Trends and issues in medical surgical nursing

 1. College Of Nursing Madras Medical College Chennai-03 TRENDS AND ISSUES IN MEDICAL-
SURGICAL NURSING PRESENTED BY EDWIN JOSE.L MSc(nursing) I YEAR College of nursing
Madras medical college Chennai-03 EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 2. INTRODUCTION  The entire field of health care is changing day by day.  These changes
occurs at rapid rate.  The focus of medical –surgical nursing is not limited to a disease or a
body system but focus on holistic in nature.  Medical –surgical nursing is a speciality of
nursing that requires a specific skills such as analytical, technical,administrative and
organizational skills.  According to academy of medical –surgical nurses, it is evolving as a
speciality and is the largest group of practicing professional. EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021

 3. DEFINITIONS Trend: A general direction in which a situation is changing or developing. -

Oxford Advanced Learners Dictionary Issues: An important topic that people are discussing.
A problem or worry that somebody has with some thing EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021

 4. TRENDS IN MEDICAL SURGICAL NURSING Quantification of nursing care costs Reduced

length of stay Increasing Reliance On High Technology Requirement of advanced nursing
knowledge Need for collaboration and communication Innovation in care planning
through computerization Unification of practice and education EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021

 5. TRENDS IN MEDICAL SURGICAL NURSING  Greater investment in research and

development  Role blurring and shared competencies  New areas of nursing
specialization  Nursing seen as a cost effective approach to health  Telenursing  Robotic
nursing  Aerospace nursing  Community based nursing EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021

 6. Quantification of nursing costs • Quantification of nursing contribution to patient care

can be used to determine the cost of providing care to specific patients • Quantifying
nursing time requires the identification of the level of nursing care necessary for each
patient. • The patient care plan is an integral part of the justification of nursing care costs
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 7. Reduced length of stay The provision of personalized care must be planned and
provided with continuity as the quality of care time decreases. Many patients who leave
the hospital earlier are still need of health care. Aggressive discharge planning must begin
on admission. An effective coordinated plan of care can help ensure continuity of care.
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 8. Increase reliance on high technology The evolving technological advances in nursing are
the wave of the future in healthcare. Emerging new technologies in EHRs, AI, apps and
software development are becoming increasingly popular as more hospitals and facilities
integrate them into their health system. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021

 9. Requirement of advanced nursing knowledge • The medical –surgical nurse needs greater
clinical expertise, maturity, clinical thinking ability, assertiveness and patient management
 skills to handle patients. • Certification acknowledges the nurses attaintment of
predetermined standards established by the certifying groups. EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021

 10. NEED FOR COLLABORATION AND COMMUNICATION • The health care delivery becomes
more complex and economically centered that need communication and collaboration
among health care professionals. • Only through collaboration between departments,
services, and facilities the nursing care can be delivered effectively. EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021

 11. Innovation in planning care through computerisation  Nurses believe that their better
time can be spend at the bedside giving patient care rather than filling out paperwork 
Studies shows that institutions using computers reports increases number of plan of care
being generated EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 12. Unification of practice and education The Unification Model directs nursing education,
research, and practice. Unification is not only a philosophical approach but also an
organizational structure that operationalizes the interdependence among education,
research and practice. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 13. Greater investments and developments In the recent years the budget allocation for
nursing research has been increased in the view of increasing the quality of nursing care
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 14. Role blurring and shared competencies • Nowadays the role of nurses is not clearly
defined • The work of nurses are shared with other departments EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021

 15. Nursing –cost effective approach  The nursing procedures we are doing are evidenced
based and cost effective whwn compare to medical treatment and procedures. EDWIN JOSE
L MEDICAL SURGICAL NURSING 15.02.2021

 16. telenursing Tele nursing or telehealth nursing uses technologies to provide nursing
services through computers and mobile devices It allows patients to connect with their
nurses through mobiles devices,computers,applications etc….. EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021

 17. Robotic nursing Robots are used in nursing for monitoring elderly patient via
video ,helps in positioning,feeding,shifting etc….. EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021

 18. Community based nursing The health care delivery concept is now changing from
hospital centered to community based nursing EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021

 19. Issues in medical surgical nursing  Staff shortage  Meeting patients expectations 
Long work hours  Workplace violence  Workplace hazards  Scope of practice 
Personal health EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 20. Staff shortages The world health organization estimates that there will be shortage of
1.1 million nurses throught out the world. This may cause disturbances in health care
system EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
  21. Meeting the patients expectations Due to advanced technology and awareness, the
patients expectation are not met. This causes job dissatisfaction among nurses. EDWIN
JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 22. Long work hours Shortage of nurses forces the nurses to work for long hours which
causes physical and mental disturbances EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021

 23. Workplace hazards Needle stick injuries,sharp tools, and heavy equipments may risk the
nurses health and life. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 24. Scope of practice  The scope of practice for nurses makes nurses to work in a defined
area of practice.  Till now there is no prescribed scope of practice for nurses in India.
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 25. Personal health Working in a stressfull health care system causes physical and mental
disequilibrium. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

 26. THANKYOU EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

Trends & Issue Medical Surgical Nursing,

 1. Trends & Issues in Medical Surgical Nursing Gaje Singh MSc (N) Previous Govt. College of
Nursing Jodhpur
 2. • The entire field of health care is changing Rapidly. • The focus of medical –surgical nursing
is not limited to a disease or a body system but focus on holistic in nature. • Medical –surgical
nursing is a specialty of nursing that requires a specific skills such as analytical, technical,
administrative and organizational skills. • This presentation outlines the new trends in medical
surgical nursing in practice, research, and education. Introduction
 3. • Medical Surgical Nursing : Medical-surgical nursing is a Branch of nursing specialty area
concerned with the care of adult patients in a broad range of settings ( Medical or Surgical ). •
Trend: • A general direction in which a situation is changing or developing. - Oxford Advanced
Learners Dictionary • Issue : • An important topic that people are discussing. • A problem or
worry that somebody has with some thing Definition
 4. New Trends in Medical Surgical Nursing
 5. Nano Science Robotics Clinical pathway Tele Nursing Mobile health applications Gene
therapy Advance Nursing Skill Infection Control New Trends in Practice
 6. New Courses Simulation Learning Advance Skill Training Current Nursing SIU Norms
Innovation in care Plan Therapeutic Communication Nurses Empowerment Use of Technology/
Virtual New Trends in Education
 7. Current trends in Medical Nursing research Pandemic nursing management Oncology
nursing Bariatric nursing Entrepreneurs in medical surgical nursing Genetic nursing AI in Nursing
Peri-Operative Nursing Care Forensic Nursing New Trends in Research
 8. Covid-19 Updates The COVID-19 pandemic was not in sight when the World Health
Organization (WHO) declared 2020 as the Year of the Nurse and Midwife, with a goal to raise
awareness of the need for “nine million more nurses and midwives to achieve universal health
coverage by 2030” The multiple roles and functions played by nurses are particularly important
during this COVID-19 pandemic. These important roles and functions cover five domains
 9. Nano Science
 10. What is Nanoscience? • Nanoscience: is the study of structures and materials on an ultra-
small scale, and the unique and interesting properties these materials demonstrate. •
Nanoscience is cross disciplinary, meaning scientists from a range of fields including chemistry,
physics, biology, medicine, computing, materials science and engineering are studying it and
using it to better understand our world.
 11. Nano Science in Oncology • In cancer chemotherapy, cytostatic drugs damage both
malignant and normal cells alike. Thus, a drug delivery strategy that selectively targets the
 malignant tumor is very much needed • Cancer diagnosis and therapy remains the most
significant and has led to the development of a new discipline Nano Science in Oncology
 12. Robotics
 13. Robotics “Shams” is the first robotic nurse in Egypt Ain-Shams University • Robotic
systems are used to alleviate the burden on nursing staff, adjust reduction in workforce, while
improving patient outcome and quality of life • The contributions of robots in the health field are
wide-ranging, such as in lifting and patient mobility, patient monitoring, surgery, laboratory , tele-
consultation, and rehabilitation
 14. •“A single inhaled Nanorobot reaches, deeply inspired into the lungs and attaches to the
tissue surface” www.iub.edu.pk
 15. Advantages Of Robotics in Patient Care • Rapid elimination of disease. • robots might also
produce copies of themselves to replace worn- out units, a process called self-replication • The
major advantage of robots is thought to be their durability, in theory, they can remain operational
for years, decades or centuries.
 16. Care Pathway • Clinical pathways (CPWs) are tools used to guide evidence-based
healthcare. Their aim is to translate clinical practice guideline recommendations into clinical
processes of care within the unique culture and environment of a healthcare institution. Care
Pathway
 17. Care Pathway Care Pathway
 18. Tele Health Medical Chat Bots is useful tools that patients can use to receive advice,
education, and personalized health recommendations, as well as remind them to take their pills,
it can overcome nurses shortage. Tele Health (Nursing)
 19. Electronic Health Records -Is a digital version of a patient’s paper chart. EHRs are patient-
centered records that make information available instantly and securely to authorized users. “It is
applied in the 57357 hospital.”
 20. New Technology for Patient Assessment Pain-Free Blood Testing Technology
 21. Mobile health applications
 22. Application of Artificial Intelligence in Patient Care
 23. Application of Artificial Intelligence in Patient Care
 24. • These types of vaccine technologies have been developed over more than 20 years using
translational research for use against cancer or diseases caused by genetic disorders but the
COVID-19 vaccines are the first licensed drugs to prevent infectious diseases using RNA vaccine
technology. Gene Therapy
 25. Advance Nursing Practice • Advance Nursing Practice in Medical Unit – Cardiac care •
High Quality CPR Skill , Defibrillation Skill • Palliative Nursing Care • Neurological Care • Trauma
Care Advance Nursing Practice
 26. Infection Control Practice • Its Trends to provide Care As per latest CDC Guideline • All
Invasive /Non Invasive line care • CARE BUNDLE ( CAUTI,CLABSI,VAP ,SSI) • Proper use of
PPE Infection Control Practice
 27. New Trends in education
 28. New Courses • M.Sc. in Oncology • M.Sc. in Forensic Science • Nurse Practitioner Course
Advance Skill Training ACLS, PALS,NALS , ATCN New Courses
 29. Virtual nursing education • Virtual reality simulations show nursing students what it is like to
be in a real-world clinical setting and what problems and risks
 30. •they may encounter there, and thus, helps them develop skills, build confidence, and
prepare for clinical practice. Virtual Nursing Education
 31. •Simulation is the “process of designing a model of a real system and conducting
experiments with this model for the purpose of either understanding the behavior of the system
and/or evaluating various strategies for the operation of the system Simulation in Nursing
Education
 32. Advance Skill • BLS • ACLS • ATCN • PALS • ICN • Critical Care • Diploma in Oncology
Advance Skill
 33. Current Nursing SIU Current Nursing SIU
 34. Innovative Technologies Technology
 35. Therapeutic Communication • Therapeutic communication is a type of professional
communication defined as the purposeful, interpersonal, information-transmitting process that
leads to client understanding and participation. • Allow time to communicate with the client. Use
 therapeutic communication techniques to provide client support. Encourage the client to
verbalize feelings (e.g., fear, discomfort) Evaluate the effectiveness of communications with the
client. Therapeutic Communication
 36. • Empowerment is defined as the ability to get things done and includes a capacity to
mobilize resources and to provide support, opportunity, and information. • Example : Oxygen
Therapy , CPR ,Cold Sponging Nursing Empowerment
 37. New trends in Nursing Research
 38. Current Trends in Nursing Research Across Five Locations: The United States, South
Korea, Taiwan, Japan, and Hong Kong First published: 03 2020 https://doi.org/10.11 592 Six
themes reflecting the current trends in nursing research were extracted: (a) demographic
alterations; (b) increasing diversities and globalization; (c) technology innovation; (d)
individualized or personal care and population health initiatives; (e) health policies and
regulations; (f) nursing workforce changes. New Trends in MSN Nursing Research
 39. Current trends in Medical Nursing research Pandemic nursing management Oncology
nursing Bariatric nursing Entrepreneurs in medical surgical nursing Genetic nursing AI in Nursing
Peri-Operative Nursing Care Forensic Nursing New Trends in Research
 40. Issuesinmedicalsurgicalnursing  STAFF SHORTAGE  MEETING PATIENTS
EXPECTATIONS  LONG WORK HOURS  WORKPLACE VIOLENCE  WORKPLACE
HAZARDS  SCOPE OF PRACTICE  LACK OF FUND AND APPROVAL ISSUES FOR
RESEARCH  PERSONAL HEALTH
 41. Staff shortages THE WORLD HEALTH ORGANIZATION ESTIMATES THAT THERE
WILL BE SHORTAGE OF 6 MILLION NURSES THROUGH OUT THE WORLD. THIS MAY
CAUSE DISTURBANCES IN HEALTH CARE SYSTEM IN INDIA YET 1167929 NURSES
REGISTERED ON NRTS THROUGH ALL STATE COUNCILS.  INDIA NEED AT LEAST 4.3
MILLION MORE NURSES BY 2024 TO MEET THE WHO NORMS.
 42. Meetingthe patientsexpectations DUE TO ADVANCED TECHNOLOGY AND
AWARENESS, THE PATIENTS EXPECTATION ARE NOT MET. THIS CAUSES JOB
DISSATISFACTION AMONG NURSES. Long work hours Shortage of nurses forces the nurses
to work for long hours which causes physical and mental disturbances
 43. Workplace hazards • NEEDLE STICK INJURIES, • SHARP TOOLS, AND HEAVY
EQUIPMENT'S MAY RISK THE NURSES HEALTH AND LIFE. • EXPOSURE TO RADIATION •
RISK OF INFECTION • PERSONAL TRAUMA WHILE CARE
 44. Scope of practice  THE SCOPE OF PRACTICE FOR NURSES MAKES NURSES TO
WORK IN A DEFINED AREA OF PRACTICE.  TILL NOW THERE IS NO PRESCRIBED
SCOPE / JD OF PRACTICE FOR NURSES IN INDIA.
 45. Personal health WORKING IN A STRESS FULL HEALTH CARE SYSTEM CAUSES
PHYSICAL AND MENTAL DISEQUILIBRIUM.
 46. Summery – MSN Trends & Issues Trends in Nursing Practice , Education and Research
Issues in Medical Surgical Nursing

Trends and issues in medical surgical nursing

 1. College Of Nursing Madras Medical College Chennai-03 TRENDS AND ISSUES IN
MEDICAL- SURGICAL NURSING PRESENTED BY EDWIN JOSE.L MSc(nursing) I YEAR
College of nursing Madras medical college Chennai-03 EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 2. INTRODUCTION  The entire field of health care is changing day by day.  These changes
occurs at rapid rate.  The focus of medical –surgical nursing is not limited to a disease or a
body system but focus on holistic in nature.  Medical –surgical nursing is a speciality of nursing
that requires a specific skills such as analytical, technical,administrative and organizational skills.
 According to academy of medical –surgical nurses, it is evolving as a speciality and is the
largest group of practicing professional. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 3. DEFINITIONS Trend: A general direction in which a situation is changing or developing. -
Oxford Advanced Learners Dictionary Issues: An important topic that people are discussing. A
problem or worry that somebody has with some thing EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 4. TRENDS IN MEDICAL SURGICAL NURSING Quantification of nursing care costs
Reduced length of stay Increasing Reliance On High Technology Requirement of advanced
nursing knowledge Need for collaboration and communication Innovation in care planning
through computerization Unification of practice and education EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021
 5. TRENDS IN MEDICAL SURGICAL NURSING  Greater investment in research and
development  Role blurring and shared competencies  New areas of nursing specialization 
Nursing seen as a cost effective approach to health  Telenursing  Robotic nursing 
Aerospace nursing  Community based nursing EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 6. Quantification of nursing costs • Quantification of nursing contribution to patient care can be
used to determine the cost of providing care to specific patients • Quantifying nursing time
requires the identification of the level of nursing care necessary for each patient. • The patient
care plan is an integral part of the justification of nursing care costs EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021
 7. Reduced length of stay The provision of personalized care must be planned and provided
with continuity as the quality of care time decreases. Many patients who leave the hospital
earlier are still need of health care. Aggressive discharge planning must begin on admission.
An effective coordinated plan of care can help ensure continuity of care. EDWIN JOSE L
MEDICAL SURGICAL NURSING 15.02.2021
 8. Increase reliance on high technology The evolving technological advances in nursing are the
wave of the future in healthcare. Emerging new technologies in EHRs, AI, apps and software
development are becoming increasingly popular as more hospitals and facilities integrate them
into their health system. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 9. Requirement of advanced nursing knowledge • The medical –surgical nurse needs greater
clinical expertise, maturity, clinical thinking ability, assertiveness and patient management skills
to handle patients. • Certification acknowledges the nurses attaintment of predetermined
standards established by the certifying groups. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 10. NEED FOR COLLABORATION AND COMMUNICATION • The health care delivery
becomes more complex and economically centered that need communication and collaboration
among health care professionals. • Only through collaboration between departments, services,
and facilities the nursing care can be delivered effectively. EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021
 11. Innovation in planning care through computerisation  Nurses believe that their better time
can be spend at the bedside giving patient care rather than filling out paperwork  Studies shows
that institutions using computers reports increases number of plan of care being generated
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 12. Unification of practice and education The Unification Model directs nursing education,
research, and practice. Unification is not only a philosophical approach but also an organizational
structure that operationalizes the interdependence among education, research and practice.
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 13. Greater investments and developments In the recent years the budget allocation for nursing
research has been increased in the view of increasing the quality of nursing care EDWIN JOSE L
MEDICAL SURGICAL NURSING 15.02.2021
 14. Role blurring and shared competencies • Nowadays the role of nurses is not clearly defined
• The work of nurses are shared with other departments EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 15. Nursing –cost effective approach  The nursing procedures we are doing are evidenced
based and cost effective whwn compare to medical treatment and procedures. EDWIN JOSE L
MEDICAL SURGICAL NURSING 15.02.2021
 16. telenursing Tele nursing or telehealth nursing uses technologies to provide nursing
services through computers and mobile devices It allows patients to connect with their nurses
through mobiles devices,computers,applications etc….. EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 17. Robotic nursing Robots are used in nursing for monitoring elderly patient via video ,helps
in positioning,feeding,shifting etc….. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 18. Community based nursing The health care delivery concept is now changing from hospital
centered to community based nursing EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 19. Issues in medical surgical nursing  Staff shortage  Meeting patients expectations  Long
work hours  Workplace violence  Workplace hazards  Scope of practice  Personal health
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 20. Staff shortages The world health organization estimates that there will be shortage of 1.1
million nurses throught out the world. This may cause disturbances in health care system
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 21. Meeting the patients expectations Due to advanced technology and awareness, the
patients expectation are not met. This causes job dissatisfaction among nurses. EDWIN JOSE
L MEDICAL SURGICAL NURSING 15.02.2021
 22. Long work hours Shortage of nurses forces the nurses to work for long hours which causes
physical and mental disturbances EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 23. Workplace hazards Needle stick injuries,sharp tools, and heavy equipments may risk the
nurses health and life. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 24. Scope of practice  The scope of practice for nurses makes nurses to work in a defined
area of practice.  Till now there is no prescribed scope of practice for nurses in India. EDWIN
JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 25. Personal health Working in a stressfull health care system causes physical and mental
disequilibrium. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 26. THANKYOU EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021

EVOLUTION OF AHN.pptx.evoltion of medical surgical nrsing | PPTX

EVOLUTION OF AHN.pptx.evoltion of medical surgical nrsing

 1. ADULT HEALTH NURSING EVOLUTION OF MEDICAL SURGICAL NURSING

 2. INTRODUCTION In ancient times, when medical lore was associated with good or evil
spirits, the sick were usually cared for in temples and houses of worship. These women
had no real training by today’s standards, but experience taught them valuable skills,
especially in the use of herbs and drugs, some gained fame as the physicians of their era.

 3. HISTORY In the history of Indian medicine begins from 3000 BC. In the Indus valley
civilizations we can see the drainage and we will understand that they have given
importance to health and hygiene.

 4. HISTORY  In 2000 BC the RIGVEDA ---- marks the beginning of Indian system of
medicine. The conditions like fever, cough, constipation, diarrhoea, dropsy abscesses,
seizures, skin diseases including leprosy were treated from that time. The herbs were used
for the treatment. In 272 BC king Ashoka built number of hospitals. He had given his
emphasis on the prevention of the diseases. Doctors, Nurses and the Midwifes were also
available in that time. Nalanda and Thaxaxila were the two famous medical schools.

 5. HISTORY In 100 B C, the surgical field was the well known by surgeons Sushruta and
Charaka.

 6. HISTORY Especially two types of operation at those times were outstanding, Removal of
the gall bladder stone and the plastic surgery of the nose. Nursing in India: In the beginning
 the nursing was hindered by many difficulties like the caste system and the low status of the
women. In the beginning period the nurse has a servant image so no one was ready for
nursing.

 7.  The military nursing was the earliest type of the nursing in 1664 the British east India
company helped to start a hospital for soldiers in madras (St. George HOSPITAL). The
company appointed staff was served in the hospital.  In 1854 the government sanctioned
training school for the midwives.  1864 Miss Florence Nightingale starts the efforts to
reform the hospitals. St. Stephens Hospital Delhi .

 9. HISTORY 1864 - First to train Indian girls as nurses. . In 1871 the government, general
hospital of madras took a plan to train the nurses. The nurses from the England were the in
charge of the training and the students were those who previously received there diploma in
midwifery. 1905 – T.N.A.I established.

 10. HISTORY After 1947 the many changes begin to take place. The attitude towards the
nursing begins to change and the nursing begin to see as a profession. The Indian Nursing
Council was passed by ordinance on December 31, 1947. The council was constituted in
1949. The development of Nursing in India was greatly influenced by the Christian
missionaries, World War, British rule and by the International agencies such as the World
Health Organization UNICEF, the Red Cross, etc.

 11. HISTORY 1960 – First Masters Degree program was started in R.A.K College of Nursing
Delhi. . In 1970 the WHO recognized nursing as a profession. Nursing today provides an
ever widening scope of opportunity for service. Today nurses enjoy many rights and
privileges, but the desired standards by the complete dedication for the profession.

 12. MEDICAL SURGICAL NURSING

 13. HISTORY Medical surgical nursing : a nursing speciality which is concerned with care of
adult patients in a broad range of settings. Traditionally, medical surgical nursing was an
entry level position, a stepping stone to speciality areas.

 14. HISTORY Medical surgical nursing : Advances in medicine and surgery have resulted in
medical- surgical nursing evolving into its own specialty. The ACADEMY OF MEDICAL
SURGICAL NURSES (AMSN) is a specialty nursing organization dedicated to nurturing
medical-surgical nurses as they advance their careers.

 15. HISTORY In the 17th cent., St. Vincent de Paul began to encourage women to
undertake some form of training for their work, but there was no real hospital training
school for nurses until one was established in Kaiserwerth, Germany, in 1846. There,
Florence Nightingale received the training that later enabled her to establish, at St. Thomas’s
Hospital in London, the first school designed primarily to train nurses rather than to provide
nursing service for the hospital

 16. HISTORY During the late 19th and early 20th centuries in the United States, adult
patients in many of the larger hospitals were typically assigned to separate medical, surgical,
and obstetrical wards.

 17. TRENDS OF MEDICAL SURGICAL NURSING

 18. TRENDS IN MEDICAL SURGICAL NURSING: o Quantification of nursing care costs o

Reduced length of stay oIncreasing Reliance On High Technology o Requirement of advanced
 nursing knowledge o Need for collaboration and communication  Innovation in care
planning through computerization  Unification of practice and education  Greater
investment in research and development  Role blurring and shared competencies  New
areas of nursing specialization  Nursing seen as a cost effective approach to health 
Telenursing  Robotic nursing  Aerospace nursing  Community based nursing.

 19. TRENDS IN MEDICAL SURGICAL NURSING 1.Quantification of nursing costs :

Quantification of nursing contribution to patient care can be used to determine the cost of
providing care to specific patients Quantifying nursing time requires the identification of
the level of nursing care necessary for each patient. The patient care plan is an integral
part of the justification of nursing care costs .

 20. TRENDS IN MEDICAL SURGICAL NURSING 2.Reduced length of stay Many patients who
leave the hospital earlier are still need of health care. Aggressive discharge planning must
begin on admission. An effective coordinated plan of care can help ensure continuity of
care.

 21. TRENDS IN MEDICAL SURGICAL NURSING 3.Increase reliance on high technology

Emerging new technologies in EHRs, AI, apps and software development are becoming
increasingly popular as more hospitals and facilities integrate them into their health system.

 22. TRENDS IN MEDICAL SURGICAL NURSING 4.Requirement of advanced nursing knowledge

• The medical –surgical nurse needs greater clinical expertise, maturity, clinical thinking
ability, assertiveness and patient management skills to handle patients. • Certification
acknowledges the nurses attaintment of predetermined standards established by the
certifying groups.

 23. TRENDS IN MEDICAL SURGICAL NURSING Quantification of nursing costs : Quantification

of nursing contribution to patient care can be used to determine the cost of providing care
to specific patients Quantifying nursing time requires the identification of the level of
nursing care necessary for each patient. The patient care plan is an integral part of the
justification of nursing care costs . Reduced length of stay The provision of personalized care
must be planned and provided with continuity as the quality of care time decreases. Many
patients who leave the hospital earlier are still need of health care. Aggressive discharge
planning must begin on admission. An effective coordinated plan of care can help ensure
continuity of care. Increase reliance on high technology The evolving technological advances
in nursing are the wave of the future in healthcare. Emerging new technologies in EHRs, AI,
apps and software development are becoming increasingly popular as more hospitals and
facilities integrate them into their health system. Requirement of advanced nursing
knowledge • The medical –surgical nurse needs greater clinical expertise, maturity, clinical
thinking ability, assertiveness and patient management skills to handle patients. •
Certification acknowledges the nurses attaintment of predetermined standards established
by the certifying groups.

 24. TRENDS IN MEDICAL SURGICAL NURSING Quantification of nursing costs : Quantification

of nursing contribution to patient care can be used to determine the cost of providing care
to specific patients Quantifying nursing time requires the identification of the level of
nursing care necessary for each patient. The patient care plan is an integral part of the
justification of nursing care costs . Reduced length of stay The provision of personalized care
must be planned and provided with continuity as the quality of care time decreases. Many
 patients who leave the hospital earlier are still need of health care. Aggressive discharge
planning must begin on admission. An effective coordinated plan of care can help ensure
continuity of care. Increase reliance on high technology The evolving technological advances
in nursing are the wave of the future in healthcare. Emerging new technologies in EHRs, AI,
apps and software development are becoming increasingly popular as more hospitals and
facilities integrate them into their health system. Requirement of advanced nursing
knowledge • The medical –surgical nurse needs greater clinical expertise, maturity, clinical
thinking ability, assertiveness and patient management skills to handle patients. •
Certification acknowledges the nurses attaintment of predetermined standards established
by the certifying groups.

 26. Nano Science Robotics Clinical pathway Tele Nursing Mobile health applications Gene
therapy Advance Nursing Skill Infection Control NEW TRENDS IN PRACTICE

 27. NANO SCIENCE

 28. What is Nanoscience? •Nanoscience: is the study of structures and materials on an

ultra-small scale, and the unique and interesting properties these materials demonstrate.
•Nanoscience is cross disciplinary, meaning scientists from a range of fields including
chemistry, physics, biology, medicine, computing, materials science and engineering are
studying it and using it to better understand our world.

 29. • In cancer chemotherapy, cytostatic drugs damage both malignant and normal cells
alike. Thus, a drug delivery strategy that selectively targets the malignant tumor is very much
needed • Cancer diagnosis and therapy remains the most significant and has led to the
development of a new discipline NANO SCIENCE IN ONCOLOGY

 30. ROBOTICS

 31. 2.ROBOTICS “Shams” is the first robotic nurse in Egypt Ain-Shams University Robotic
systems are used to lessen the burden on nursing staff and adjust reduction in workforce &
quality of life of patient • The contributions of robots in the health field are wide-ranging,
such as in lifting and patient mobility, patient monitoring, surgery, laboratory , tele-
consultation, and rehabilitation

 32. •“A single inhaled Nanorobot reaches, deeply inspired into the lungs and attaches to the
tissue surface” www.iub.edu.pk

 33. ADVANTAGES OF ROBOTICS IN PATIENT CARE • Rapid elimination of disease. • robots

might also produce copies of themselves to replace worn- out units, a process called self-
replication • The major advantage of robots is thought to be their durability, in theory, they
can remain operational for years, decades or centuries.

 34. Care Pathway • Clinical pathways (CPWs) are tools used to guide evidence-based
healthcare. • Their aim is to translate clinical practice guideline recommendations into
clinical processes of care within the unique culture and environment of a healthcare
institution. 3.CARE PATHWAY

 35. Care Pathway CARE PATHWAY

 36. Tele Health Medical Chat Bots is useful tools that patients can use to receive advice,
education, and personalized health recommendations, as well as remind them to take their
pills, it can overcome nurses shortage. 4.TELE HEALTH (NURSING)
  37. ELECTRONIC HEALTH RECORDS -Is a digital version of a patient’s paper chart. EHRs are
patient-centered records that make information available instantly and securely to
authorized users. “It is applied in the 57357 hospital.”

 38. NEW TECHNOLOGY FOR PATIENT ASSESSMENT Pain-Free Blood Testing Technology

 39. 5.MOBILE HEALTH APPLICATIONS

 40. APPLICATION OF ARTIFICIAL INTELLIGENCE IN PATIENT CARE

 41. APPLICATION OF ARTIFICIAL INTELLIGENCE IN PATIENT CARE

 42. • These types of vaccine technologies have been developed over more than 20 years
using translational research for use against cancer or diseases caused by genetic disorders
but the COVID-19 vaccines are the first licensed drugs to prevent infectious diseases using
RNA vaccine technology. 6.GENE THERAPY

 43. Advance Nursing Practice • Advance Nursing Practice in Medical Unit – Cardiac care •
High Quality CPR Skill , Defibrillation Skill • Palliative Nursing Care • Neurological Care •
Trauma Care 7.ADVANCE NURSING PRACTICE

 44. •Its Trends to provide Care As per latest CDC Guideline •All Invasive /Non Invasive line
care •CARE BUNDLE ( CAUTI,CLABSI,VAP ,SSI) •Proper use of PPE 8.INFECTION CONTROL
PRACTICE

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Historical developments, trends, issues, cultural and NATIONAL HEALTH POLICY ,SPECIAL LAWS
RELATED TO OLDER PEOPLE

 1. { Historical developments, Trends, Issues, Cultural or ethical issues in Medical Surgical

Nursing Submitted to: Dr. Pallavi Pathania (Assistant Professor of Medical Surgical Nursing)
Submitted by: Priyanka Thakur (MSc. Nursing 1st year) NATIONAL HEALTH POLICY ,SPECIAL
LAWS RELATED TO OLDER PEOPLE

 2.  Definition: Medical Surgical Nursing is a specialized branch of nursing that involve the
nursing care of adult patients, whose disease condition are treated medically, surgically and
pharmacologically.

 3.  In ancient times, when medical lore was associated with good or evil spirits, the sick
were usually cared for in temples and houses of worship.

 4.  These women had no real training by today’s standards, but experience taught them
valuable skills, especially in the use of herbs and drugs and some gained fame as the
physicians of their era.

 5.  In the 17th cent., St. Vincent De Paul began to encourage women to undertake some
form of training for their work, but their was no real hospital training school for nurse until
one was established in Kaiserwerth, Germany, in 1846.
 6.  There, Florence Nightingale received the training that later enabled her to establish, at
St. Thomas’s hospital in London the first school designed primarily to train nurses rather
than to provide nursing service for the hospital.

 7.  Similar schools were established in 1873 in New York City, New Haven (Conn.), and
Boston.  Nursing subsequently became one of the most important professions open to
women until the social changes brought by the revival of the feminist movement that began
in the 1960’s.

 8.  During the late 19th and early 20th centuries in the US, adult patients in many of the
larger hospitals were typically assigned to separate medical, surgical and obstetrical wards. 
Nursing education in hospital training schools reflected these divisions to prepare nurses for
work on these units.

 9.  Early National League of Nursing Education (NLNE) curriculum guides treated medical
nursing, surgical nursing and disease prevention (incorporating personal hygiene and public
sanitation) as separate topics.

 10.  By the 1930s, however , advocates recommended that medical and surgical nursing be
taught in a single, interdisciplinary course, because the division of two was considered in an
artificial distinctions. Surgical nursing came to be seen as the care of medical patients who
were being treated surgically.

 11.  The NLNE’s 1937 guide called for a “Combined Course” of medical and surgical nursing.
 Students were expected to learn not only the theory and treatment of abnormal
physiological conditions, but also to provide total care of the patient by understanding the
role of the health .

 12.  In1960’s, nursing schools emphasized the interdisciplinary study and the practice of
medical and surgical nursing.  1960s and 1970s, standards were developed for many
nursing specialties, including medical surgical nursing.

 13.  Standards, Medical- Surgical Nursing practices, written by committee of the division on
medical- surgical nursing of the American Nurses Association (ANA), was published in 1974.

 14.  It focused on the collection of data, development of nursing diagnoses and goals for
nursing, and development, implement of nursing diagnoses and goals for nursing, and
development and evaluation of plans of care.  A statement on the Scope of Medical-
Surgical Nursing Practice followed in 1980.

 15.  In 1991, the Academy of Medical Surgical Nurses (AMSN) was formed to provide an
independent specially professional organization for medical- surgical and adult health
nurses.  In 1996, the AMSN published its own Scope and Standards of Medical- Surgical
Nursing Practice.

 16.  The second edition appeared 2000. Both the ANA and AMSN documents stated that
while only clinical nurse specialists were expected to participate in research, all medical-
surgical nurses must incorporate research findings in practice.

 18.  A Trend is a change or development towards something new or different.

 19. 1. Education changes due to changes in demographics. 2. Embracing of technology. 3.
Advancements in communication and technology. 4. Working with more educated
consumers. 5. Increasing complexity of patient care.

 20. 6. Increased cost of health care. 7. Changes in federal and state regulation. 8.
Interdisciplinary skills. 9. Nurses working beyond retirement age. 10. Advances in nursing
and science research.

 21. Transitions taking place in health care: Curative Specialized care Medical diagnosis
Discipline stovepipes - Preventive approach - Primary health care - Patient emphasis -
Programme stovepipes

 22. Cont… Professional identity Trial and error practice Self-regulation Focus on quality
- Team identity - Evidence based practice - Questioning of professions - focus on costs

 23.  High tech  Competition  Need to supervise  Hierarchies

 24.  Humanistic  Cooperation  Caching, mentoring  Decentralized approach

 25. • Continued competencies • Hospital environment • Quality as excellence • Clear role •

Competencies a condition • Community environment • Quality as safe • Blurring roles

 27.  An issue is an important subject that people are arguing about or discussing.

 28. Confiden -tiality Family organisation Health beliefs Death and dying Communi- cation
cultural Diet and nutrition Ethical Patient care

 29.  Related to diet  Religion  Rituals  Refusal of medical procedures Health belief issues 
Black magic

 30.  Privacy  Personal information Family organization issues  Communication on behalf

of individual

 31.  Wrong medication  Malpractices Diet And Nutrition Issues  Poverty  Cultural myths

 32. Communication issues Cont…  Culture value modesty  Cared by female health
providers  Conflicts

 33. Standards of care Incompetence Negligence Liability: • Administrative • Civil • criminal

 34.  Unexpected death  Advance directives  Organ and tissue donation  Child
abandonment

 35.  Beauchamp and Childress(2009) developed four principles: 1) Respect for Autonomy 2)
Beneficence 3) Non-maleficence 4) Justice

 36. RESPECT FOR AUTONOMY: Autonomy can be defined as…”self-rule with no control,
undue influence or interference from other”. BENEFICENCE: This can be defined as ”the
principle of the doing well and providing care to others” Promotion of well being.

 37.  Non –maleficence: 1. “Obligation not to inflict harm on others” 2. Goes hand in hand
with beneficence. Justice: 1. Simply defined as “equal treatment of equal cases” 2. Treating
everyone the same.

 38.  Fairness  Respect for autonomy  Integrity  Seeking the most beneficial and least
harmful consequences or results  Fidelity  Veracity
 39. Nursing shortage Health care reforms Low salaries Standard care

 40. Informed consent Assault and battery Invasion of privacy Report it/Tort it

 42. compassionately listen communicate identify acknowledge recognize

 43. involve document Up to date advice Look after yourself

 46. INTRODUCTION : A health policy generally describes fundamental principles regarding

which health providers are expected to make value decisions . “ Health policy provides a
broad framework of decisions for guiding health actions that are useful to its community in
improving their health, reducing the gap between the health status of haves and have not
and ultimately contributes to the quality of life.

 47.  The National Health Policy of 1983 and the National Health Policy of 2002 have served
well in guiding the approach for the health sector in Five – Year Plans . Now 14 years after
the last health policy, a new is introduced.  The primary aim of the National Health Policy ,
2017 is to inform, clarify ,strengthen the role of the Government in shaping health systems
in all its dimensions .

 48.  Health priorities are changing , there is growing burden on account of non-
communicable diseases and some infectious diseases .  A rising economic growth enables
enhanced fiscal capacity. Therefore , a new health policy responsive to these contextual
changes is required .

 49.  The emergence of a robust health care industry estimated to be growing at double digit
.  Growing incidences of catastrophic expenditure due to health care costs, which are
presently estimated to be one of the major contributors to poverty .

 50. Improve health status concerted policy actions in all sectors and expand preventive,
promotive, curative , palliative and rehabilitative services provided through the public health
sector with focus on quality. Objectives are outlined under three broad components :-

 51.  Health status and Programme Impact  Health systems Performance  Health System
Strengthening

 52. Life expectancy and healthy life a. Increase life Expectancy at birth from 67.5 to 70 by
2025 b. Establish regular tracking of Disability Adjusted Life Years (DALY) Index as a measure
of burden od disease .

 53. Mortality by age and/ or cause a. Reduce infant mortality rate to 28 by 2019 b. Reduce
Under Five Mortality to 23 by 2025 and MMR from current levels to 100 by 2020 .

 54. Coverage of Health Services a. More than 90% of the new born are fully immunized by
one year of age by 2025 b. 80% of known hypertensive and diabetic individuals at household
level maintain ‘controlled disease status’ by 2025

 55. Health finance a. Increase State sector health spending to >8% of their budget by 2020
b. Increase health expenditure by government as a percentage of GDP from the existing
1.15% to 2.5 by 2025.

 56. Health Management Information a. Ensure district – level electronic database of

information on health system components by 2020 b. Strengthen the health surveillance
system and establish registers for diseases of public health importance by 2020
 57. Cross Sectional objectives related to Health a. National/State level tracking of selected
health behaviour . b. Access to safe water and sanitation to all by 2020( Swatch Bharat
Mission)

 58. 1. Professionalism, Integrity and Ethics The health policy commits itself to the highest
professional standards, integrity and ethics to be maintained in the entire system of health
care delivery in the country, supported by a credible, transparent and responsible regulatory
environment .

 59.  Reducing inequity would mean affirmative action to reach the protest.  It would mean
minimizing disparity on account of gender, poverty, caste , disability , other forms of social
exclusion and geographical barriers.  It would imply greater investments and financial
protection for the poor who suffer the largest burden of disease.

 60. As costs of care increases, affordability, as district from equity , requires emphasis.
Catastrophic household health care expenditures exceeding defined as health expenditure
exceeding 10% of its total monthly consumption expenditure or40% of its monthly non- food
consumption expenditure ,are unacceptable .

 61.  Prevention of exclusions on social, economic or on grounds of current health status. In

this backdrop , systems and services are envisaged to be designed to cater to the entire
population – including special groups.

 62. Financial and performance accountability , transparency in decision making , and

elimination of corruption in health care systems , both in public and private .

 63. Decentralization of decision making to a level as is consistent with practical

considerations and institutional capacity . Community participation in health planning
processes , to be promoted side by side .

 64. Constantly improving dynamic organization of health care based on new knowledge and
evidence with learning from the communities and from national and international
knowledge partners is designed .

 65.  Increase Life Expectancy from 67.5 to 70 by 2025 .  Establish regular tracking of
Disability Adjusted Life Years (DALY) Index as a measure of burden of disease by 2022 . 
Reduction of TFR to 2.1 at national and sub- national level by 2025 .  Reduction Under Five
Mortality to 23 by 2025 and MMR from current levels to 100 by 2020 .

 66.  Reduce infant mortality rate to 28 by 2019 .  Reduce neo- natal mortality to 16 and
still birth rate to ‘single digit’ by 2025.  Achieve and maintain elimination status of Leprosy
by 2018.  Kala-Azar by 2017 and lymphatic Filariasis in endemic pockets by 2017.

 67.  Achieve global target of 2020 which is also termed as target of 90:90:90, for HIV AIDS. 
To achieve and maintain a cure rate of >85% in new sputum positive patients for TB and
reduce incidence of new cases, to reach elimination status by 2025.

 68.  To reduce the prevalence of blindness to 0.251000 by 2025.  To reduce premature

mortality from cardiovascular diseases, cancer, diabetes or chronic respiratory diseases by
25% by 2025.  Increase utilization of public health facilities by 50% from current levels by
2025.
 69.  Ante-natal care coverage to be sustained above 90% and skilled attendance at birth
above 90% by 2025.  More than 90% of the newborn are fully immunized by 1 year of age
by 2025.

 70.  80% of known hypertensive and diabetic individuals at household level maintain
‘controlled disease status by 2025.  Meet need of family planning above 90% at national
and sub national level by 2025.

 71.  Relative reduction in prevalence of current tobacco use by 15% by 2020 and 30%
by2025.  40% reduction in prevalence of stunting of under-5 children by 2025.

 72.  Safe water and sanitation to all by 2020 (Swachh Bharat Mission).  Reduction of
occupational injury by half from current levels of 334 per lakh agricultural workers by 2020.

 73.  Increase health expenditure by Government from the existing 1.15% (GDP) to 2.5%
(GDP) by 2025.  Increase state sector health spending to >8% of their budget by 2020.

 74.  Decrease in proportion of household facing catastrophic health expenditure from the
current levels by 25%, by 2025.  Ensure availability of paramedics and doctors as per IPHS
norm in high priority districts by 2020.

 75.  Establish primary and secondary care facility in high priority districts by 2025.  Ensure
district-level electronic database of information on health system components by 2020.

 76.  Strengthen the health surveillance system by 2020.  Establish federated integrated
health information architecture, Health Information Exchanges and National Health
Information Network by 2025.

 77.  Establish federated integrated health information architecture, Health Information

Exchanges and National Health Information Network by 2025.

 78. 1.The Swachh Bharat Abhiyan. 2.Balanced, healthy diets and regular exercises.
3.Addressing tobacco, alcohol and substance abuse. 4.Yatri Suraksha - preventing deaths
due to rail and road traffic accidents.

 79. 5.Nirbhaya Nari action gender violence. 6.Reduced stress and improved safety in the
work place. 7.Reducing indoor and outdoor air pollution.

 80. The 7 key policy shifts in organizing health care services are: 1. In primary care from
selective care to assured comprehensive care with linkages to referral hospitals. 2. In
secondary and tertiary care from an input oriented to an output based strategic purchasing .

 81. 3. In infrastructure and human resource from normative approach to targeted approach
to reach under-serviced area. 4. In public hospitals from user fees at cost recovery to
assured free drugs , diagnostic and emergency services to all.

 82. 5. In urban health from token interventions to on-scale assured interventions, to

organize Primary Health Care delivery and referral support for urban poor. Collaboration
with other sectors to address wider determinants of urban health is advocated.

 83. 6. In national health programmes integration with health systems for programme
effectiveness and intern contributing to strengthening of health systems for efficiency . 7. In
AYUSH services from stand alone to a 3 dimensional mainstreaming.
 84. 1. RMNCH + A services 2. Child and Adolescent Health 3. Universal immunisation 4.
Communicable diseases 5. Mental health 6. Non communicable diseases 7. Population
stabilization

 85.  This policy aspires to elicit developmental action of all sectors to support Maternal
and Child survival. The policy strongly recommends strengthening of general health system
to prevent and manage maternal complications, to ensure continuity of care and emergency
services for maternal health.

 86.  The policy endorses the national consensus on accelerated achievement of neonatal
mortality targets and ‘ single digit ’ stillbirth rates through improved home based and facility
based management of sick new borns .  School health programmes as a major focus area ,
health and hygiene being a part of the school curriculam

 87.  It emphasis to the health challenges of adolescents and long term potential of investing
in their health care.

 88.  Priority would be to improve immunization coverage with quality and safety, improve
vaccine security as per National Vaccine Policy 2011 and introduction of newer vaccines
based on epidemiological considerations. The focus will be to build upon the success of
Mission Indradhanush and strengthen it .

 89.  The policy recognizes the interrelationship between communicable disease control
programmes and public health system strengthening .  It advocates the need for districts
to respond to the communicable disease priorities of their locality .

 90.  The policy acknowledges HIV and TB co infection and increased incidence of drug
resistant tuberculosis as key challenges in control of Tuberculosis .

 92.  An integrated approach for screening the most prevalent NCDs with secondary
prevention would make a significant impact on reduction of morbidity and preventable
mortality with incorporation into the comprehensive primary health care network with
linkages to specialist consultations and follow up at the primary level .

 93.  Screening for oral, breast and cervical cancer and Chronic Obstructive Pulmonary
Disease will be focused in addition to hypertension and diabetes .

 94. This policy will take action on the following fronts :  Increase creation of specialists
through public financing and develop special rules to give preference to those willing to
work in public systems .

 95.  Create network of community members to provide psycho-social support to

strengthen mental health services at primary level facilities.

 96.  Policy imperative is to move away from camp based services to a situation where
these services are available on any day of the week .  And to increase the proportion of
male sterilization from less than 5% to at least 30% and if possible much higher .

 97. While the public health initiates over the years have contributed significantly to the
improvement of the health indicators, it to be acknowledged that public health indicators /
disease burden statistics are the outcome of several complementary initiatives under the
wider umbrella of the development sector, covering rural development, agriculture, food
production , sanitation , drinking water supply, education etc.
 99.  Throughout the world , large number of older people face challenges such as
discrimination , poverty and abuse that severely restrict their human rights and their
contribution to society .  Although concerns involving the ageing population are not new,
they have traditionally been seen as problems requiring solutions that are functional and
reactive .

 100.  The rights of older people are the entitlements claimed for senior citizens . Elderly
rights are one of the fundamental rights of India .  The International Day of older persons is
celebrated annually on October 1 .  The 2001 census of India demonstrated that aged
people in India have crossed over 100 million .

 101. The NPOP in India has been formulated as a forward – looking vision of the government
for improving quality of life of older people in India through i. Increased income security, ii.
Health and Nutrition ,

 102. iii. Shelter, iv. Education, empowerment and welfare .

 103. 1. To encourage individuals to make various provisions such as health and social
insurance for their own as well as their spouse`s old age. 2. To encourage families to take
care of their older family members .

 104. 3. To enable and support voluntary and non-governmental organizations to supplement

the cate provided by the family, with greater emphasis on non institutional care . 4. To
provide care and protection to the vulnerable elder especially widows, physically,
challenged, abused and destitute elderly .

 105. 5. To provide health care facilities specially suited to elderly . 6. To promote research
and training to train geriatric care givers and organisers of services for the elderly.

 106. 7. To facilitate and strengthen inter sectoral partnerships in the field and 8. To create
awareness regarding elder persons to develop themselves into fully independent citizens .

 107. 1.Financial Security :  Pension scheme ( in public and private sector)  Lower income
tax rate and exemptions .

 108. 2. Health care and Nutrition :  Setting up Geriatric wards and training on Geriatric
Specialized care  Expanding Mental Health Services for elderly .

 109. 3. Shelter :  Government and Private Housing Schemes for elderly .  Disposal of cases
relating to property transfer, mutation of property and tax .

 110. 4. Education  Information to elderly about Concept of wellness in old age  Evolving
changes in lifestyle and living style .

 111.  Identifying extremely vulnerable elderly who are disabled, chronically sick and
destitute .  Assistance to voluntary organisations to construct and maintain old age homes,
day care centre , multi – services citizens centres, supply of disability – related aids and
appliances .

 112. 6. Research and Training :  Encourage medical colleges, training institutions for Nurses
and Para medical institutes to introduce COURSES ON GERIATRIC CARE.
  113.  Research and Documentation in elderly care  NGO supported specialized training in
Geriatric care. 7. Sensitizing the Media :  Involvement of social medias and internet to
create awareness .

 114. 1. Pradhan Mantri Suraksha Bima Yogana : 2015 All savings bank account holders 18 –
70 years old can join the scheme. It offers a coverage of rupees 200,000 for death or total
and irrevocable loss of both eyes and rupees 100,000 coverage for the loss of an eye .

 116.  The government started the Swavalamban Scheme in 2010/11 which was replaced by
the Atal Pension Yojana (APY) in June 2015 for those persons engaged in the unorganized
sector , who are not members of any statutory social security scheme .

 118.  Low premium life insurance (Pradhan Mantri Jeevan Jyoti Bima Yojana)  General
insurance (Pradhan Mantri Suraksha Bima Yojana) .  The pension plan (Atal Pension
Yojana). It is proposed to link this to the accounts .

 120.  This scheme is a part of the government`s commitment to financial inclusion and
social security during old age and to protect those aged 60 years and above against a future
fall in their interest income due to uncertain market conditions. The scheme will be
implemented through LIC .

 124. How the Money is Used

 125. A regional body South Asia Senior Citizens`s Working Group aims to work closely with
the respective governments, NGOs and civil society members of the region in order to
improve the well –being of the ageing population .

 129.  The policy should emphasise the need for expansion of social and community
services for older persons , particularly vulnerable women group to get accessible to the
user friendly client oriented services.

 130.  Special efforts will be made to implement the policy at the rural populations and
unorganised sectors where most of the older population lives .

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Critical care unit: The CCU is designed for patients experiencing severe illnesses or injuries, such as
those requiring emergency surgery, severe infections, or organ failure.

 1. SEMINAR ON CRITICAL CARE UNIT

 2. SUBMITTED TO: SUBMITTED BY: Dr. Pallavi Pathania Group A : Adisha

Amisha ,Anjali ,Bharti Associate professor Bharti Bhardwaj ,Dikshika ,Diya , Shimla nursing
college Himanshi ,Isha , Kashish Gupta B.Sc. 4th semester.

 4. INDEX  MEANING OF CCU  INTRODUCTION OF CCU  DEFINITION OF CCU  CRTICAL

CARE NURSE  CRITICAL CARE UNIT  7 C’s OF CRITICAL CARE UNIT  RESEARCH STATISTICS
 HISTORY OF CCU  LEVELS OF CCU  PURPOSE AND PRINCIPLES OF CCU  ORGANIZATION
MODLE OF CCU  ORIENTATION{LAYOUT,EQUIPMENT,BEDDING}  PATIENT AREA 
STAFFING PATTERN
 5. INDEX  PROTOCOLS AND POLICY  STANDARD PRECAUTION  LEAGAL AND ETHICAL
ASPECTS OF CCU  ADMISSION OF PATIENT IN CCU  MANAGEMENT OF CRITICALLY ILL
PATIENT  MAINTAINING RECORDS  TRANSITONAL CARE  BREAKING BAD NEWS TO
PATIENT,FAMILY  END OF LIFE CARE  SUMMARIZATION  CONCLUSION 
RECAPTUALIZATION  ASSIGNMENT

 6. MEANING The word CCU C- critical C- care U- unit In a critical care unit, the word "critical"
signifies that the patient's condition is life-threatening and requires immediate, specialized,
and intensive care. This means the patient needs constant monitoring, potentially life-
sustaining interventions, and the attention of a team of highly trained healthcare
professionals.  In a critical care unit, the term "care unit" refers to a specialized area within
a hospital that provides intensive medical care for seriously ill or injured patients

 7. INTRODUCTION  Critical care unit is one of the specialized area in the hospital where the
patient with complex and potentially life threatening illness are admitted.  In CCU, nurse
provide round the clock patient care and observation .  Usually nurse and patient ratio is
1:1.  CCU can vary in size and design and patient from different discipline are admitted . 
The NURSE who work in the CCU must be trained to work effectively.

 8. DEFINITION  A unit catering to the needs of patient who require constant individual
nursing attention throughout 24hrs and the immediate availability of medical help.
{INTENSIVE CARE SOCIETY}  The comprehensive care of a critically ill patient ,who is
deemed recoverable. {BARRIEN SHEVLIEN}  A critical care unit (CCU), also known as an
intensive care unit (ICU) or intensive therapy unit (ITU), is a specialized hospital ward that
provides intensive medical care to critically ill or injured patients.

 9. CRITICAL CARE NURSE  A critical care nurse is a licensed professional nurse who is
responsible for ensuring that acutely and critically ill patients and their family receive
optimal care.  Critical care nursing is that specialty within nursing that deals specifically
with human responses to life- threatening problems and unstable patients..  They utilize
advanced skills and knowledge to assess, monitor, and treat critically ill patients, including
those who may be on life support systems.

 10. CRITICAL CARE UNIT  Critical Care Unit is a specially design and equipped facility staffed
by skilled personnel to provide effective and safe care for patient with a life- threatening
problem that is potentially reversible.  Critical Care unit is an organized system for the
provision of care to critically ill patients that provide intensive and specialized medical and
nursing care, an enhanced capacity for monitoring and multiple modalities pf physiologic
organ support to sustain life during a period of life threatening organ system.  Eg. Multiple
organ support

 11. 7C’s OF CCU  COMPASSION  COMMUNICATION  CONSIDERATION {of

patients ,relatives and colleagues} and avoidance of conflict.  COMFORT :protection of
patient from suffering .  CAREFULNESS :avoidance of injury  CONSISTENCY: {of
observation and care}  CLOSURE: {ethics and withdrawal of treatment}

 12. CRITICAL CARE UNIT RESEARCH STATISTICS o As per the study of, Mahatma Gandhi
medical college and research institute found that critical care nurses had better knowledge
of code blue protocols compared to general ward nurse , with a mean knowledge score of
19.30 vs 15.23. o In India, a survey of critical care units (CCUs) found that - Patient-to-Nurse
 Ratio: 36.6% of CCUs had a 2:1 ratio, while 9.7% had a 1:1 ratio for complicated patients. o
{acc. To 2024 report}

 13.  Public Knowledge- There is limited data available on the general public's knowledge
about critical care units. However, it's clear that critical care nursing requires specialized
knowledge and training.  Student Nurses- While there isn't specific data on student nurses'
knowledge about critical care units, nursing education programs typically cover critical care
nursing principles, including patient assessment, vital signs, diagnostic tests, medication, and
more .

 14. HISTORY  The first modern critical care units (CCUs) emerged in the 1950s, primarily in
response to the devastating Copenhagen polio epidemic of 1952.  The concept was further
popularized by Max Harry Weil, who established a "shock ward" in the early 1960s in Los
Angeles.  In ,1965- 1st specialized CCU- the coronary care unit was formed.

 16. LEVEL III LEVEL II LEVEL I LEVELS OF CRITICAL CARE UNIT

 17. LEVEL I  CCU referred to as high dependency  Resuscitation, short term mechanical
ventilation and simple invasive cardio vascular monitoring for <24 hrs.

 18. LEVEL II  CCU located in general hospital, undertake more prolonged ventilation  CCU
provides a high standards of general intensive care , including complex multi-system life
support .

 19. LEVEL III  Tertiary referral unit for intensive care patient  It provides comprehensive
critical care including complex multi-system life support for an indefinite period. 
Demonstrated commitment to academic education and research.

 20. PURPOSE OF CRITICAL CARE UNIT  Provide close monitoring: closely monitor patients
vital sign and organ  Deliver life sustaining intervention: such as mechanical ventilation,
cardiac support and renal replacement therapy.  Support organ function : helps to prevent
further complication.

 21. Principles of critical care unit The core principle of critical care unit revolve around
providing specialised comprehensive and continuous care to critically ill patient Other
important principle encompass :  patient centred care  effective communication 
evidenced based practice  Rapid decision making  Mastery of technical skill  Stress
management

 23. ORIENTATION 

 25. EQUIPMENTS OF CCU Vital Signs Monitoring and Support:  Ventilators: Machines that
assist or control breathing, crucial for patients who cannot breathe on their own.  Patient
Monitors: Devices that continuously track vital signs like heart rate, blood pressure, oxygen
saturation, and respiratory rate.  ECG Machines: Used to monitor and diagnose heart
rhythm abnormalities.  Pulse Oximeters: Non-invasive devices that measure blood oxygen
saturation levels.  Suction Machines: Used to clear airways of secretions.  Endotracheal
Tubes: Tubes inserted into the trachea to facilitate mechanical ventilation.

 26. EQUIPMENTS

 27. MEDICATION AND FLUID ADMINISTRATION. •Infusion Pumps: Devices that deliver
medications and fluids intravenously with precise control and accuracy. •Syringe Pumps:
 Similar to infusion pumps, but used for smaller volumes of medication, often in. Feeding
Tubes: Used to deliver nutrition to patients who cannot eat or drink normally. •Urinary
Catheters: Tubes inserted into the bladder to drain urine and monitor output.

 28. GENERAL MEDICATION USED IN CRITICAL CARE UNIT

 29. HOSPITAL BEDS  12% of the total no. of beds in an acute hospital should be provided
for acute ICU.  20% of the total no. of beds in a tertiary care hospital should be provided for
ICU.  Bed space 150-200sq.ft.area per open bed with 8 ft. between beds.  225-
250sq.ft,area per bed if in a single room.  KEY FEATURE OF BEDS:-  Electric adjustability 
Trendelenburg and reverse Trendelenburg position  Cardiac chair position  Wheel and
brakes  IV pole mount  Side rails  Removable headboard

 30. PATIENT AREA  Multi channel invasive monitors ,ventilators , infusion pumps , portable
X-ray unit , fluid and bed warmers , portable light , defibrillators , anesthesia machine and
difficult air way management equipment are necessary.  A cardiac arrest/emergency alarm
button must be present at every bed side within the CCU . The alarm should be
automatically sound in the hospital telecommunications center , central nursing station, CCU
conference room , staff lounge , and any on call rooms .

 31. STAFFING PATTERN Intensivists Junior Doctor Head nurse Registered nurse Auxiliary
nurse Respiratory therapist Physiotherapist ICU technician Dietician Radiographer Data entry
operator Biomedical engineer Security guard

 32. CLASSIFICATION OF CRITICAL CARE UNIT  GENERAL  Medical intensive care unit
(MICU).  Surgical Intensive Care Unit.  Medical Surgical Intensive Care Unit (MSICU). 
SPECIALIZED  Neonatal Intensive Care Unit (NICU).  Special Care Nursery (SCN).  Pediatric
Intensive Care Unit (PICU).  Coronary care unit (CCU).  Cardiac surgery intensive care unit
(CSICU).  Neurosurgery intensive café unit(NSICU).  Burn Intensive care unit (BICU). 
Trauma Intensive Care Unit.

 33. Medical intensive care unit (MICU)  A Medical Intensive Care Unit (MICU) is a
specialized area in a hospital designed for patients with severe or life-threatening illnesses
that require intensive monitoring and treatment.  The MICU provides round-the-clock care
from a highly trained team of healthcare professionals, including doctors and nurses. 
Families play a crucial role in the care process, supporting patients while they recover.  The
MICU is equipped with specialized technology and resources to monitor and manage critical
health issues.

 34. SURGICAL INTENSIVE CARE UNIT The surgical intensive care unit is a specialized area in
the hospital where critically ill patients who have undergone some major surgeries receive
intensive care and monitoring. PURPOSE AND FUNCTION  Post surgical care :- The SICU
provides care for patients recovering from complex surgeries including general, thoracic ,
trauma , vascular , orthopaedic , obstetric surgeries.  Critical monitoring:- Patients in SICU
requires close monitoring and support due to their severity of their conditions. This includes
continuous monitoring of vital signs , advanced respiratory support and management of
complex medical assessment.

 35. MEDICAL SURGICAL INTENSIVE CARE UNIT  The medical surgical intensive care unit
(MSICU) is a specialized unit that provides post surgical care for children and young adults
following general surgery , transplantation, neurosurgery , craniofacial reconstruction ,
 orthopaedic surgery and trauma .  The unit is equipped with advanced technology such as
sophisticated bedside monitors , ventilators and defibrillators.

 36. NEONATAL INTENSIVE CARE UNIT  A neonatal intensive care unit (NICU), also known as
an intensive care nursery (ICN), is an intensive care unit (ICU) specializing in the care of ill or
premature newborn infants. The NICU is divided into several areas, including a critical care
area for babies who require close monitoring and intervention, an intermediate care area for
infants who are stable but still require specialized care, and a step down unit where babies
who are ready to leave the hospital can receive additional care before being discharged. 
Neonatal refers to the first 28 days of life. Neonatal care, as known as specialized nurseries
or intensive care, has been around since the 1960s.

 37. PEDIATRIC INTENSIVE CRITICAL CARE UNIT  The PICU, or pediatric intensive care unit, is
the unit of a hospital that provides the highest level of care to children. It is similar to the
intensive care unit (ICU), where adults receive special care, but the staff in the PICU
specialize in working with children.  The equipment available in the PICU is best suited for
children, and the environment may be more child-friendly in general. This unit provides a
level of care that is generally not available in other areas of the hospital ,although not all
hospitals have PICUs.

 38. CARDIAC CARE UNIT (CCU)  A coronary care unit (CCU) or cardiac intensive care unit
(CICU) is a hospital ward specialized in the care of patients with heart attacks, unstable
angina, cardiac dysrhythmia and (in practice) various other cardiac conditions that require
continuous monitoring and treatment.

 39. BURN INTENSIVE CARE UNIT (BISU)  A Burn Intensive Care Unit (ICU), also known as a
trauma/burn ICU, provides specialized care for patients with severe burns who require
intensive medical support. These units are equipped to manage critically ill patients, offering
advanced monitoring, medication, and therapies to stabilize their condition and facilitate
healing.

 40. TRAUMA INTENSIVE CARE UNIT  It is also known as highly dependency unit (HDU) .A
Trauma Intensive Care Unit (TICU) is a specialized hospital unit equipped to provide highly
advanced care for critically injured patients. It focuses on stabilizing, treating, and
monitoring patients with severe trauma, aiming to prevent further complications and
improve outcomes

 41. GENITO URINARY CARE UNIT  A genitourinary care unit focuses on the medical and
surgical treatment of conditions affecting the urinary tract and the male reproductive
system. It encompasses a range of specialties, including urology, nephrology, and in some
cases, reproductive endocrinology.

 42. NEUROLOGICAL CRITICAL CARE UNIT  A Neurological care unit (Neuro- ICU) is a
specialized intensive care for patient with life threatening neurological problems. These
problems can include strokes, brain tumor , brain injuries, spinal cord injuries and seizures .
Neuro-ICUs can also provide complex surgical procedures and interventional treatments for
the patients.

 43. SEPSIS CRITICAL CARE UNIT  Sepsis covers a wide range of conditions which usually do
not require admission to the intensive care unit (ICU) unless it becomes severe. When this
occurs patients will often need ICU and broadly account for about 30% of admissions
 according to the patient population Whatever the source, infection leading to sepsis remains
a major intensive care problem that has a mortality of at least 38%.1

 44. POLICIES & PROTOCOLS  Critical Care Unit have protocols and policies focused on
providing specialised care for critically ill patients.  These protocols covers areas like
Infection Control, Airway Management, Hemodynamic Monitoring , and more.  Policies
ensures standardized procedures for communication , quality improvement and resource
allocation within the unit.

 45. KEY PROTOCOLS AND POLICIES IN CCU  Infection Control  Airway Management 
Hemodynamic Management  Communication  Continuous Quality Improvement 
Equipment & Monitoring  Renal Replacement Therapy  Nutritional Support

 46. VARIOUS PROTOCOLS AND POLICIES OF CCU  CLINICAL PROTOCOL: ventilator

management , hemodynamic monitoring , pain management.  INFECTION CONTROL
PROTOCOL: hand hygiene, isolation precaution, central line care .  PATIENT SAFETY
PROTOCOL : fall prevention , medication safety, restrain use  STAFFING AND TRAINNING
PLOCIY: staffing ratio training and education assessing staff and competencies in CCU care. 
QUALITY IMPROVEMENT PLOICY: continuos quality improvement ,incident reporting.

 47. STANDARD PRECAUTION  Hand hygiene  Personal protective equipment 

Respiratory hygiene  Safe injection practice  Environmental cleaning and disinfection 
Sharp safety  Sterile instruments and devices

 48. ETHICS AND LEGAL ASPECTS IN CRITICAL CARE UNIT ETHICS IN CCU DEFINITION It
refers to the study of philosophical ideas of right and wrong behavior . Ethical principles
that nurse should must consider when providing care of patient in CCU are as follows:

 49. 1.Informed consent 2.end of life care 3.resource allocation 4.confidentiality and privacy
5.cultural sensitivity 6.decision making 7.futility of care 8.family support

 50. LEGAL ASPECTS  ‘Legal aspects’ refers to the rules regulations and laws that govern a
specific situation, action and decision. These aspects encompass all the legal considerations,
implications and issues related to a to a particular matter. Ensuring fair practices and
maintaining legal compliance. LEGAL ASPECTS IN NURSING  Legal aspects of nursing
encompass the laws and regulations that govern nursing practice, ensuring patient safety
and ethical conduct. These aspects define the scope of nursing practice, outline ethical
obligations, and detail potential legal repercussions for nurses.  Essentially, they provide
the framework for nurses to operate within the law and avoid legal liability.

 51. Admission of Patient in critical care unit A patient is admitted to critical care unit when
they are severely ill and require intensive treatment, monitoring or organ support.
ADMISSION CRITERIA  ORGAN SUPPORT :- If a patient requires life sustaining treatment like
a ventilator for breathing ,they may be admitted.  ALTERED LEVEL OF CONSCIOUSNESS :-
Significant changes in a patients alertness or ability to respond can indicate a need for
critical care.  HEMODYNAMIC INSTABILITY :-Conditions like shock or life threatening
arrhythmias require close monitoring , interventions that are best managed in a critical care
setting.  SPECIFIC MEDICAL CONDITION :- Conditions like acute coronary syndromes, life
threatening arrythmias , acute heart failure , sepsis , and respiratory failure are common
reasons for critical care admission .
 53. GOALS  Provide comfort and supportive care during process .  Improve the quality of
remaining life.  Help to ensure dignified death . PRINCIPLES  Respecting patient’s goal ,
preferences and choices .  Attention of medical , emotional , social , and spiritual needs of
the dying person .  Acknowledging and addressing care giver concerns .

 54. TYPES OF ADMISSION IN CCU PLANNED ADMISSION. • EMERGENCY ADMISSION.

 55. PLANNED ADMISSIONS o Some patients are planned for admission into CCU prior to the
commencement of the surgery or afterwards. o Underlying condition. o Related ailment.

 56. EMERGENCY ADMISSIONS  Medical personnel from the A and E or regular ward refer
patients for higher level of monitoring or specialist treatment for reversible life threatening
condition.  Patients frequently require a period of stabilization before it is save to move
them to the intensive care unit.  It may be necessary to perform emergency investigation
including radiological investigation before the patient goes to intensive care.

 57. DISCHARGE CRITERIA The status of patient admitted to an CCU should be reviewed
continuously to identify patients who may no longer need CCU care:  When a patients
physiologic status has stabilized and the need for CCU monitoring and care is no longer
necessary.  When a patients physiological status has deteriorated and become irreversible
and active intervention are no longer beneficial , withdrawal of therapy should be carried
out in the CCU. Patient should only be discharged to the ward if bed is required.

 58. MONITORING OF CRITICALLY ILL PATIENTS  Monitoring of critically ill patient is done
systematically :  CARDIOVASCULAR SYSTEM • ECG monitoring • Non invasive blood
pressure monitoring • Invasive vascular pressure monitoring • Cardiac output measurement.
 RESPIRATORY SYSTEM • Bedside spirometry • ABG analysis • Pulse oximetry

 59.  RENAL FUNCTION • Hourly urine output • Renal function tests  CNS FUNCTION •
Clinical examination • Glasgow coma scale • Intracranial pressure monitoring • Transcranial
doppler scan  GASTROINTESTINIAL MONITORING  HEMATOLOGICAL MONITORING 
METABOLISM AND NUTRITION

 61. VENTILATOR  Mechanical ventilation can be defined as the technique through which
gas is moved toward and from the lungs through an external device connected directly to
the patient. INDICATION  Upper airway obstruction  Lower airway obstruction  CNS
disease  Certain lung disease  Major post operative

 62. CARE OF PATIENT WITH VENTILATOR KEY CONSIDERATION  Ventilator setting 

Monitoring  Sedation and analgesia NURSING CARE  Airway management  Positioning 
Infection prevention  Asses breath sound and oxygen saturation  Communication  Family
support

 63. ENDOTRACHIAL SUCTIONING  An airway catheter inserted into the trachea(windpipe)

via the mouth or nose in endotracheal intubation.  IT is a process of applying a negative
pressure to the distal ETT or trachea by introducing a suction catheter to clear excess , or
abnormal secretions. INDICATIONS  Coarse breath sound by auscultation of lungs. 
Patients inability to generate an effective spontaneous cough.  Change in monitor flow and
pressure graphics.  Deterioration of anterior blood gas values.

 65. CARE OF PATIENT WITH ENDOTRACHIAL SUCTIONING 1) PRE-SUCTIONING PREPERATION

3) POST-SUCTIONING CARE Asses patient stability Reoxygenate Prepare equipment Monitor
 vitals signs Hyper oxygenate Document 2) SUCTIONING TECHNIQUES 4) COMPLICATION
PREVENTION Use sterile techniques Hypoxia Insert catheter Tracheal trauma Apply suction
Cardiac instability Limit suction time

 66. BUNDLE PROTOCOL  The Institute of Healthcare Improvement (IHI) developed the
concept of bundles a bundle is a group of evidence-based care components for a given
disease that when executed together may results in better outcomes then if implemented
individually GENERAL PRINCIPLES: 1. The implementation of care bundles can assist in
enhancing compliance to evidence-based quality process measures to improve patient care.
2. Care bundles include a set of evidence-based measures that when implemented together
have shown to produce better outcomes and have a greater impact than that of the isolated
implementation of individual measures. 3. Bundles also help to create reliable and
consistent care systems in hospital settings since they are simple, clear, and concise.

 67. TYPES OF BUNDLE PROTOCOL  1. Ventilator Associated Pneumonia (VAP)  2. Catheter

Associated Urinary Tract Infection (CAUTI)  3. Central line associated blood stream infection
(CLABSI)  4. Surgical Site Infection (SSI)  5. Needle Stick Injury (NSI)

 68. VENTILATOR ASSOCIATED PNEMONIA {VAP}  Pneumonia due to infective causes

occurring in a patient on mechanical ventilation is termed ventilator-associated pneumonia
or VAP. (INFECTION DISEASE SOCIETY) CAUSES:  Aspiration of oropharyngeal and gastric
secretion.  colonization of endotracheal tube and ventilator circuit.  infection caused by
bacteria , virus and fungi.

 69. CATHETER ASSOCIATED URINARY TRACT INFECTION {CAUTI}  Catheter-associated

urinary tract infection (CAUTI) is usually defined as, a UTI (significant bacteriuria plus
symptoms and signs attributable to the urinary tract with no other identifiable source) in a
patient with current urinary tract catheterization or who has been catheterized in the past
48 hours. CAUSE :  Primary cause is the presence of indwelling catheter.

 70. CENTRAL LINE ASSOCIATED BLOOD STREAM INFECTION {CLABSI}  A bloodstream

infection that occur in a patient who has a central line in place at the time of infection or
within 48 hrs prior to the onset of infection symptoms . CAUSES:  Improper insertion
technique  Hub contamination  Skin flora  Contaminated IV sets.

 71. SURGICAL SITE INFECTION {SSI}  SSI refers to an infection that occurs after surgery in
the part of the body where the surgery took place. SSIs can sometimes be superficial
infections involving the skin only. Other SSIs are more serious and can involve tissues under
the skin, organs, or implanted material. CAUSE:  Bacterial contamination  Inadequate
surgical techniques  Wound contamination  Poor wound care  smoking

 72. NEEDLE STICK INJURY {NSI}  A needle stick injury (NSI) is an accidental skin -
penetrating stab wound from a hollow –bore needle containing another person’s blood and
body fluid.  CAUSES:  Improper handling during disposal  Needle recapping  Suturing 
Waste disposal

 73. Prevention of bundle protocol

 75. TRACHEOSTOMY CARE  The surgical formation of an opening into the trachea through
the neck especially to allow the passage of air. A tracheostomy is an incision into trachea the
2nd , 3rd or 4th tracheal ring. INDICATION • To relieve upper airway obstruction • To
improve respiratory function • Respiratory paralysis POST-OPERATIVE CARE 1. Maintain
 patency of airway and tracheotomy tube 2. Frequent atraumatic suction 3. Humidification of
inspired air and oxygen 4. Fowlers position to aid in breathing 5. Maintain adequate fluid
intake

 76. TRACHEOSTOMY CARE  Gather the supplies  Wah your hands  Put clean pair of
gloves  Make cleaning solution. Pour hydrogen peroxide and sterile water or normal saline
into one of the clean containers.  Change inner cannula. Place two fingers of one hand on
the neck plate of the trach. With the other hand, unlock the inner cannula by turning it
clockwise.  Insert clean inner cannula. Insert clean inner cannula. To do this, place two
fingers from one hand on the neck plate while gently inserting the cannula into the trach
tube.  Clean trach area. Soak the cotton tipped applicators in the hydrogen peroxide
mixture for 10 seconds. Using the soaked cotton tipped applicators, clean around the trach
tube using a sweeping motion in one direction.

 77.  Change drain sponge. Change this daily but more often as it becomes wet. To avoid
skin problems , do not leave a wet drain sponge in place for a long period of time.  Change
trach ties.  Clean dirty inner cannula. Place used inner cannula into the ½ strength solution
of hydrogen peroxide. Store clean inner cannula.  Throw out used supplies.  Clean
containers

 78. PERFORMING & MAINTAINING CENTAL VENOUS PRESSURE (CVP)  Central Venous
Pressure (CVP) is the blood pressure in the superior vena cava, near the right atrium of the
heart. CVP reflects the amount of blood returning to the heart & ability of the heart to pump
the blood back into the arterial system. INDICATION • Major procedures involving large fluid
shifts and / or blood loss. • Intravascular volume assessment when urine output is not
reliable. • Major trauma • Surgeries with high risk air embolism • Venous access for
vasoactive / irritating drugs and for long term drug administration.

 79. NURSING RESPONSBILITY 1. Monitor for sign of complications. 2. Assess for patency of
CVP line. 3. Sterile dressing should be done to prevent infection (CVP care as per the hospital
policy). 4. The length of indwelling catheter should be recorded and regularly monitored. 5.
Replacement of CVL tubing every 72 hrs. 6. Whole procedure must be done with strict
asepsis.

 80. DEFIBRILLATION  Defibrillator is an apparatus used to control heart fibrillation by

application of an electric current to the chest wall or heart.  Defibrillation is the stopping of
the heart by administering a controlled electric shock, to allow restoration of the normal
rhythm. INDICATION  Atrial Flutter  Atrial fibrillation  Ventricular tachycardia 
Supraventricular tachycardia

 81. NURSING RESPONSBILITY  As defibrillation is an emergency procedure, the equipment

should be ready at all times.  It should be kept functioning all the time and should be
checked before each shift.  Each staff should be aware of its functioning.  The defibrillator
should be tested daily for its proper functioning .  Set the defibrillator at 300 joules. 
Depress the charge button on the defibrillator until the display number matches the joules
setting.  Leave the paddles in their resting place on the defibrillator and simultaneously
press. the discharge buttons on both paddles.  Patient should be continuously monitored
after defibrillation.

 82. MAINTAINING RECORDS Every CCU keeps some kinds of records .The clinical record is a
brief account the personal and medical history of patient ,result and diagnostic test finding
 of medical examination ,treatment and nursing care ,daily progress notes and advice on
discharge Documentation in the CCU is carried out for a number of reasons . It ensures
continuity of care and provides up-to –date patient status .It fulfills hospitals policies which
furnish the legal aspects of duty of care .

 83. TYPES OF CCU RECORDS  PATIENT RECORDS  Every CCU maintains complete patient
records .This will contain the –  Bio data of the patient ,  Diagnosis ,  Family history , 
History of the past and present illness ,  Treatments and medications ,  Progress notes and
 Summary made at the discharge of the patient.

 84. NURSE RECORD  A nurse record , also known as nursing documentation, is a systematic
collection of information about a patients health and the nursing care they receive .  It’s a
crucial part of the patients medical record and serves as a primary communication tool
between healthcare professionals , including nurses , doctors and other caregivers . KEY
ASPECTS OF A NURSE RECORD  Comprehensive documentation.  Patient centered care 
Communication and continuity  Legal and ethical requirement

 85. COMPONENTS OF MEDICAL RECORDS -Patient Identification -Medical History -Current

Health Status -Test Results -Treatment Plans

 86. TRANSITIONAL CARE  Transitional care in critical care unit refers to the process of
planning and co ordinating care as patients transition from the CCU to other care settings . 
Transitional care refers to the support provided to the patients as they move from one
phase of illness or treatment to another TYPES OF TRANSITION CARE  CCU to step down
unit : patients are transferred to a step down unit for continued monitoring and care  CCU
to general ward : patients are transferred to a general ward for continued care and recovery
 CCU to rehabilitation unit : patients are transferred to a rehabilitation unit for focused
therapy and recovery  CCU to home : patients are discharged home with ongoing care and
support

 87. ELEMENTS OF TRANSITIONAL CARE  CARE COORDINATION :Coordinate care among

health care providers ,patients and families .  COMMUNICATION :communicate effectively
with patients ,families and health care providers about patient care plans and needs 
PATIENTS EDUCATION :educate patients and families about their care plans ,medications
and follow up appointments  DISCHARGE PLANNING : planned for discharge and post
discharge care ,including arranging for follow up appointments and home care services .

 88. BENEFITS OF TRANSITIONAL CARE  IMPROVED PATIENT OUTCOMES :transitional care

can improve patient outcomes by ensuring that patient receive the right care and support at
right time .  REDUCE RE ADMISSIONS : transitional care can reduce hospital re admission by
ensuring that patient receive adequate care and support after discharge .  ENHANCED
PATIENT SATISFACTION : transitional care can enhance patient satisfaction by ensuring that
patients and families are informed and involved in care decision .

 89. BREAKING THE BAD NEWS TO THE PATEINT AND THE FAMILY.  Breaking bad news in a
medical context refers to the difficult process of conveying information to a patient and/or
their family that is likely to have a significant and negative impact on their future, such as a
serious diagnosis, poor prognosis, or unfavorable treatment outcome. It's a sensitive
communication skill requiring empathy, clear language, and awareness of the patient's and
family's emotional response.
  90. END OF LIFE CARE  End-of-life care is the support and medical care given to individuals
in the period leading up to their death, encompassing physical, emotional, social, and
spiritual needs, as well as practical support for both the person and their family. It aims to
provide comfort, dignity, and a peaceful passage for the dying individual.

 92. SUMMARIZATION  A Critical Care Unit (CCU) is a specialized hospital ward that
provides continuous monitoring and treatment for patients with different critical conditions
requiring intensive care . It focuses on providing immediate and ongoing care to stabilize
critically ill patients. A team of specially trained healthcare providers gives 24 hours of care
to every patient.

 93. CONCLUSION  Critical care unit is a specially designed and equipped facility staffed by
skilled personnel to provide effective and safe care for dependent patients with a life
threatening problem.  CCU is a vital area in the hospital and organization of a critical care
unit and it is strategically planned process.  There should be a single entry and exit .
However, it is required to have emergency exit point in case of emergency and disaster.

 94. RECAPTUALIZATION MULTIPLE CHOICE QUESTIONS (MCQ) 1)When was the first modern
critical care unit emerged? a. 1954 b. 1950 c. 1947 d. 1948

 95. 2) Central line associated blood stream infection is caused by : a. Smoking b. Waste
disposal c. Improper insertion technique d. None of the above 3)Choose the key features of
hospital beds : a) Electric adjustability b) Side Rails c) Wheel and Brakes d) All of the above

 96. 4) What is the purpose of a VENTILATOR A) Used for removing obstruction like mucus ,
saliva , blood , or secretion from airway B) Used to deliver a very small amount of
medications C) Used to investigate symptoms of possible heart problems D) Helps you
breath when sick injured or sedated for an operation 5) what is the purpose of a PATIENT
MONITOR ? A) Used to investigate symptoms of possible heart problems B) Sends an electric
pulse or shock to the heart to restore a normal heartbeat. C) Used to deliver a very small
amount of medications D) Show your heart rate ,blood pressure , body temperature,SpO2

 97. ASSIGNMENT  Define Critical Care Unit (CCU).  Explain about the classification of CCU.
 Briefly explain the management and care of critically ill patient.  What are the 7c’s of
Critical Care Unit ?  What is the Transitional Care Role of Nurse ?  Enlist the equipment
used in CCU.  Enlist the drugs used in CCU for emergency conditions.

Elderly Care and Management: ursing care involves creating a safe living environment, addressing
potential hazards, and implementing preventive measures. This ensures a secure space for the
elderly, minimizing the risk of accidents and injuries

 1. SEMINAR ON CARE OF THE ELDERLY

 2. SUBMITTED TO :- HOD, MSN Dr. Pallavi Pathania SUBMITTED BY:- Kashish, Kanika, Kavita,
Kirti, Komal, Leena, Manisha, Meena, Mehak, Muskan.

 3. INDEX S.NO. CONTENT 1. Meaning of elderly 2. Introduction of elderly 3. Concept of aging

4. Definition of aging 5. Aging process in elderly 6. Age related body changes in elderly 7.
Theories of aging in elderly 8. Factors contributing to long and healthy life of elderly 9. Stress
and coping strategies for elderly 10. Sexual abuse in elderly 11. Use of aids and prosthesis in
elderly 12. Legal aspects in elderly 13. National , State ,District and Community Programmes
 and Services for elderly 14. Home and Institutional care of elderly 15. Role of nurse and
conclusion

 4. RESEARCH STATISTICS • The World Health Organization analysis of the world values
survey has revealed the widespread prevalence of negative or ageist attitudes toward older
adults . • This comprehensive survey involved over 85,000 participants from 60 countries,
uncovering significant variations in the roles assigned to older adults across different nations
and cultures. • The demographic aging of the population is one of humanity’s most
significant achievements, but it also constitutes a major challenge . • It is estimated that by
2050 the population aged 60 or older is expected to increase from 962 million in 2017 to 2.1
billion in 2050.

 5. • Studies conducted in different countries showed that nurses have limited knowledge
and practice level in caring for geriatric patients like as Nigeria (40%), Saudi Arabia (14%),
Ghana (88.7%) And Zanzibar (82.6%). • In Ethiopia , it was found that most caregivers,
around 57.30% of them have little knowledge of caring for older adults. The provision of
geriatric care requires specialized skills and is a discipline that is challenging to meet its
staffing needs . • Nurses’ knowledge and practice of caring for older patients has a
significant impact on patient outcomes by reducing hospital stays, reducing readmission
rates, and increasing patient’s and families’ satisfaction.

 6. MEANING OF ELDERLY • An "elderly person" generally refers to someone who is

advanced in age, typically 65 years old or older The term can also be used more broadly to
refer to people who are quite old, perhaps even frail, and have started to show the physical
changes associated with old age.

 7. INTRODUCTION OF ELDERLY • The Elderly refers to individuals who are considered old,
typically 65 years of age or older, but can also be defined by social roles or capabilities. •
While often associated with chronological age, the experience of aging and the transition to
old age can be influenced by factors like health, social status, and cultural norms.

 8. CONCEPT OF AGING • Aging, progressive physiological changes in an organism that lead

to senescence, or a decline of biological functions and of the organism's ability to adapt to
metabolic stress. • Aging takes place in a cell, an organ, or the total organism with the
passage of time.

 9. DEFINITION OF AGING • Aging is defined as the point in a person’s life when aging
changes significantly interfere with functioning. • "A persistent decline in the age-specific
fitness components of an organism due to internal physiological degeneration". - BY
MICHAEL ROSE

 10. • Aging is the process during which structural and functional changes accumulate in an
organism as timepasses. • The changes manifest as a decline in fertility and physiological
functions from the organism’s peak until death.

 12. AGING PROCESS • The aging process in elderly individuals involves a decline in biological
functions, impacting physical, mental, and social aspects. • This process is gradual and
continuous, leading to changes in various bodily systems and increasing susceptibility to age-
related diseases.
 13. • Age groups  Infancy (birth to 1 year)  Toddlerhood (1-3 years)  Early childhood (3-5
years)  Middle childhood (6-11 years)  Adolescence (12-18 years).  Young adults(19-30
years)  Middle aged adults (31-59 years)  Old adults (60-100 years)

 14. PHYSIOLOGICAL CHANGES IN ELDERLY • Nurse must understand that each elderly
person is different. Each person’s age related changes are different in term of type and
extent. • It involve alterations across various organ systems, leading to a decline in
functional reserve and a greater susceptibility to illness. • These changes include decreased
lung elasticity, stiffening of blood vessels, reduced muscle mass and strength, and changes in
the nervous system, among others.

 15. INTEGUMENTRY SYSTEM • EPIDERMIS: The outermost layer of skin thins, becoming
more transparent and susceptible to damage. • DERMIS : Collagen and elastin production
decreases, leading to wrinkles, sagging skin, and reduced elasticity. • HYPODERMIS:
Subcutaneous fat, which provides insulation and cushioning, also thins with age, increasing
the risk of pressure ulcers and heat intolerance.

 16. • GLANDS: Sebaceous and sweat glands produce less oil and sweat, causing dry, itchy
skin and reduced ability to regulate body temperature. • BLOOD VESSELS: Blood vessels
become more fragile, increasing the risk of bruising and slowing wound healing.

 17. MUSCULOSKELETEAL SYSTEM • PAIN : Bone mass and density decrease, making bones
more brittle and prone to fractures, particularly in the spine and hips. This is often linked to
osteoporosis, especially in women after menopause. • CHANGES IN BONE STRUCTURE: The
shape and architecture of bones can change, impacting their strength and ability to
withstand stress. • DISEASE CONDITION – Osteoporosis , Osteoarthritis , Fracture , Back And
Neck Pain , Rheumatoid Arthritis .

 18. CHANGES IN MUSCLE COMPOSITION: Lipofuscin (an age-related pigment) and fat are
deposited in muscle tissue, further reducing muscle strength and function. REDUCED
REFLEXES: Nerve function and reflexes may be slower in older age, increasing the risk of falls
and injuries. INCREASED RISK OF INJURY: Changes in bone, muscle, and joint function can
increase the risk of fractures, sprains, and other injuries.

 19. RESPIRATORY SYSTEM • The qualitative deterioration in both elastic fibers and collagen
fibers, lung tissues becomes less elastic and expansile. • Even if there is no changes in the
number of alveoli, the amount of elastic fibers in the alveolar wall is decreased and the size
of alveoli is smaller with slight expansion. • The elderly are at high risk of atelectasis and
post operative pneumonia. • Weakened respiratory muscles and a stiff diaphragm are
exhibited from the age of 55.

 20. CHANGES OF RESPIRTORY SYSTEM IN ELEDERLY

 21. CARDIOVASCULAR SYSTEM • ARTERIAL STIFFNESS: Arteries become stiffer, leading to

higher systolic blood pressure and pulse pressure. This stiffness can also impair the heart's
ability to pump blood effectively. • AUTONOMIC NERVOUS SYSTEM: The heart's response to
stress, such as exercise, may be blunted due to decreased responsiveness to sympathetic
(fight-or-flight) signals. This can reduce the heart's ability to increase its rate and contractility
during exertion. • DISEASE CONDITIONS:- DVT, Hypertension, Heart Failure, Increased
Cholesterol, Atrial Fibrillation, CAD, MI.
 22. • CONDUCTION SYSTEM: The natural pacemaker system (sinoatrial or SA node) may lose
some cells, potentially causing a slightly slower heart rate and increasing the risk of
arrhythmia. • BLOOD VOLUME: Total body water decreases with age, leading to a reduction
in blood volume.

 23. CHANGES OF CARDIOVASCULAR IN ELDERLY Cardiomyopathy

 24. HEMATOPOIETIC AND LYMPHATIC SYSTEM HEMATOPOIETIC SYSTEM • REDUCED

HEMATOPOIESIS:- The bone marrow, the site of blood production, shows a decline in
cellularity and decrease in overall no. Of hematopoietic stem cell. • MYELOID SWELLING :-
The aging process leads to a shift in the hematopoietic system towards a more myeloid-
based production, meaning more myeloid cells are produced as compared to lymphoid cells.
• IMPAIRED LYMPHOPOIESIS:- The production of lymphocytes, crucial for adaptive
immunity, decreases with age, leading to a decline in the number to naive t and b cells and a
shift towards memory t cells.

 25. LYMPHATIC SYSTEM • ALTERED LYMPHATIC VESSEL FUNCTION :- The lymphatic vessels,
which transport fluid and immune cells, experience changes in their contractility and
responsiveness to inflammatory stimuli, potentially affecting their and ability to respond to
infections. • IMPAIRED IMMUNE RESPONSE :- The overall immune system in the elderly is
less efficient in responding to new or previously encountered antigens, potentially leading to
increase susceptibility to infections. • DISEASE CONDITION:- Lymphedema, Lymphatic vessel
dysfunction, Lymphoma

 26. GASTROINTESTINAL SYSTEM • DECREASED PERISTALSIS:- The rhythmic contractions that

move food through the digestive tract can slow down, leading constipation. • REDUCED
GASTRIC EMPTYING:- The stomach emptier food into the small intestine at a slower rate. •
MALABSORPTION:- The ability to absorb nutrients can decline, potentially leading to
malabsorption vitaminb12 and calcium.

 27. CHANGES IN GUT MICROBIOTA :- The composition of the gut bacteria can shift, affecting
the digestion and increases risk of infections. INCREASES RISK OF DIGESTIVE DISORDERS:-
Conditions like peptic ulcers, atrophic gastritis and small intestinal bacterial overgrowth
become more common. REDUCED LIVER BLOOD FLOW:- This can impair drug metabolism
and increases the risk of adverse drug reactions.

 29. URINARY SYSTEM • The kidney is known to be the organ with the most notable
anatomical and physiological changes caused by aging. • The size, weight and volume of the
cortex and the number of glomeruli of kidney is are reduced with increase in age.

 30. • MALE URINARY SYSTEM :-Changes include a reduction in kidney function, bladder
capacity, and urethral pressure, as well as an increase in bladder contractions. Prostate
enlargement, often benign prostatic hyperplasia (BPH), is a common issue that can obstruct
urine flow. • FEMALE URINARY SYSTEM:- Changes that can lead to decreased bladder
capacity, increased bladder contractions, and reduced urinary flow rate. These changes can
manifest as urinary incontinence, urinary tract infections, and other urinary problems.

 31. CHANGES OF REPRODUCTIVE SYSTEM IN ELDERLY (IN FEMALES)

 32. CHANGES OF REPRODUCTIVE SYSTEM (IN MALES)

 33. NERVOUS SYSTEM • BRAIN STRUCTURE AND FUNCTION :- Brain volume and weight
decreases, cerebral blood flow decline, neurotransmitters decreases, slow nerve conduction.
• SENSORY FUNCTION:- Sensory receptors in the skin, ears and eyes decline reducing
sensitivity to touch, pressure, hearing and vision, pain perception decreases, reduced
sensitivity to vibration and temperature increases the risk of injury.

 34. MOTOR FUNCTION:- Increases risk of fall due to decreased balance and proprioception.
COGNITIVE FUNCTION:- Reduced learning ability, slower recall of information potential
decline in memory (especially short term & episodic memory) and difficulty with complex
tasks.

 35. CHANGES OF NERVOUS SYSTEM IN ELEDERLY

 36. WHAT IS THEORY OF AGING? The theory of aging “Why we age?” “How do we get
older?”

 37. THEORIES OF AGING Theories Of Aging Are Mainly Divided Into Three Categories
Psychological theories of aging Sociological theories of aging Biological theories of aging

 38. PSYCHOLOGICAL THEORIES OF AGING GIVEN BY :-ERIK ERIKSON, ROBERT HAVIGHURST,

AND CARL JUNG Psychological theories Clarify maturing in terms of mental forms , feeling,
demeanors, inspiration and identity advancement that is characterized by life organize
moves. Human Needs Five essential needs spur human behavior in a deep rooted prepare
toward require fulfillment. Individualism Identity comprises a sense of self and individual
and collective obviousness that sees life from an individual or outside viewpoints. More
seasoned grownups look for life meaning and adjust to utilitarian and social misfortunes.
Stage of Personality Identity creates in 8 successive stages with comparing life advancement
errands The 8th stage astuteness versus loose hope, is characterized by assessing life
achievements, battles incorporate letting go, tolerating care separation and physical and
mental decay. Life Span Life stages are unsurprising and organized by parts, connections,
values, advancement and objectives. People adjust to changing parts and connections. Age
gather and characteristics are a vital portion of the life course. Selective Optimization
Individual cope up with aging losses through activity/role selection, optimization and
compensation and compensation. Critical life points are morbidity and quality of life
Selective optimization with compensation facilitates successful aging. THEORY DESCRIPTION

 39. SOCIOLOGICAL THEORIES OF AGING (ELAINE CUMMING, HENRY) Disengagement

Withdrawing gradually from relationships and society helps to preserve social harmony and
encourages introspection. Subculture The old people want to live apart from society in a
subculture known as “aging”, where they share a decline in status and societal
discrimination against the elderly The major factors are social status and health and
mobility. Continuity Role and life satisfaction are influenced by personality, which endures
throughout life. Finding new duties after retirement, finding a new home that
accommodates one’s restrictions and identifying with one’s group are difficult undertaking.
Age Satisfaction Age division in society serve as the foundation for obtaining resources,
roles, status, and respect from others. Person- environment fit Ego strength, mobility,
health, intellect, sensory perception and the environment all have an impact on function.
Gerotranscendence The elderly shift their outlook away from materialism and towards
oneness with the cosmos. An outward focus, embracing one’s eventual mortality,
meaningful relationships and unification with the universe are all necessary for successful
 transformation. THEORY DESCRIPTION Sociological Theories The capacity of older adults to
adapt is impacted by shifting roles , relationship status and generational cohort. Activity A
fulfilling late life requires staying active and engaged.

 40. BIOLOGICAL THEORIES OF AGING -(AUGUST WEISMANN, PETER MEDAWAR)

 41. IMPORTANCE OF APPLYING THEORIES OF AGING IN NURSING • Understanding the

individual's life experiences and preferences: Tailor care to their unique needs and goals. •
Promoting activity and social engagement: Encourage participation in meaningful activities
and social connections. • Addressing potential challenges: Recognize and address concerns
related to loneliness, isolation, cognitive decline, or physical limitations.

 42. Promoting successful aging: Focus on maintaining physical and mental health, social
well-being, and environmental security. Advocacy and social support: Nurses can use their
knowledge of aging theories to advocate for the needs of older adults, including accessing
resources, addressing social isolation, and promoting policies that support their well-being.

 43. FACTORS CONTRIBUTING TO LONG AND HEALTHY LIFE • Diet:- Reducing saturated fats
in the diet, limiting daily fat consumption to under 30% of caloric intake, avoiding weight
gain, reducing the amount of animal resourced food, substituting natural complex starches
for refined sugar and increasing the use of whole grain, vegetables and natural products all
contribute to a positive health state that can extend life span. • Exercise and meditation:-
Exercise is a critical component of good health and meditation increases strength and
endurance, improves cardiovascular capacity and has other positive effects that can aid in
the maturation process.

 44. • Playing and laughter:- Endorphins are released, the resistive framework is energized
and pressure when you laugh. Seeing comedy in everyday life and finding joy in the face of
adversity contributes to a sense of well being. • Stress management:- By adopting healthy
lifestyle choices and stress-reducing techniques, individuals can improve their physical and
mental well-being.

 46. CONCEPT OF STRESS Concept of stress STRESS: Is a condition in which the person
experience changes in normal balanced state. STRESSOR: In any event or stimulus that
caused as individual to experience stress

 47. Sources of stress Internal External Situatio -nal Develop- mental

 48. PHYSICAL SIGNS OF STRESS IN BODY BODY SYSTEM CHANGES SEEN WITH STRESS
Cardiovascular Feeling of pounding or rushing heart. Increased heart rate, elevated BP.
Hands and feet are cold and clammy. Elevated blood sugar level. Respiratory Increased
breathing depth and rate if the acid base balance is significantly disturbed, symptoms could
include seizures, fainting, dizziness and even hyperventilation with tingling in the
extremities. Musculoskeletal Increased blood glucose level to provide energy for muscles.
Increased muscle tension in the back neck and head. Complain of tension headache, teeth
grinding and backaches. Gastrointestinal Production of digestive enzymes is decreased.
Nausea, vomiting, abdominal pain, loss of appetite and heartburn may speed up the onset of
duodenal or stomach ulcers. Constipation and excessive intestinal gas are caused b
decreased peristalsis but diarrhea is also extremely prevalent. Urinary Decreased urine
production but increased urine frequency.
 49. EMOTIONAL SIGNS OF STRESS EMOTIONAL SIGNS DESCRIPTION Changes in mood
Increased irritability,, anxiety, sadness, indifference or unusual elation/overactivity.
Irritability & Anger Experiencing frequent anger, frustration, or being easily annoyed Anxiety
& Fear Feeling anxious or worried particularly about potential threats or unknown situations
Depression Persistent low mood, feeling of sadness, hopelessness or loss of interest in
activities Difficulty Concentrating Trouble focusing or staying on task Memory Problems
Difficulty with short – term memory or recalling information Social Withdrawal Isolating
from people or activities, feeling lonely or detached Change in Appetite Significant changes
in appetite, either loss or gain or eating habits Sleep Disturbance Difficulty sleeping,
insomnia or changes in sleep patterns. Helplessness/ Hopelessness Feeling overwhelmed,
unable to cope or a sense of losing control

 50. COGNITIVE SIGNS OF STRESS COGNITIVE SIGNS DESCRIPTION Memory Problems

Forgetfulness, difficulty remembering dates or names, misplacing objects Difficulty
Concentrating Trouble focusing, losing train of thoughts, easily distracted Slowed Thinking
Overall slowness in thoughts processes, brain fog Decision-Making Challenges Trouble
making decisions, feeling overwhelmed by choices Racing Thoughts Anxious or racing
thoughts, constant worrying Poor Judgement Making universe decisions, neglecting
responsibilities Negative Thinking Seeing only negative, feeling pessimistic

 51. STRESS COPING AND TECHNIQUES INTRODUCTION Stress is universal phenomenon. All
people experience it. Parents refers to the stress of raising children, working people talk of
the stress of their job, at students at all levels talk of the stress of school. Stress can result
from both positive and negative. FOR EXAMPLE:- A bride preparing for her wedding, A
graduate preparing to start a new job

 52. STRESS REDUCTION AND COPING TECHNIQUES PROBLEM FOCUSED TECHNIQUE

EMOTION BASED TECHNIQUE COGNITIVE FOCUSED TECHNIQUE COMPLEMENTARY AND
ALTERNATIVE TECHNIQUE

 53. 1.PROBLEMS FOCUSED TECHNIQUES • Problem focused coping strategies involve

directly addressing and changing the source of stress. • This approach focuses on identifying
and eliminating the stressor or at least lessening its impact. • STRATEGIES INCLUDE :-
Problem solving, time management, seeking information or support, and directly
confronting the stressor. • PROBLEM SOLVING :- Identifying the issue and brainstorming
solutions to after the circumstances that are causing stress.

 54. • TIME MANAGEMENT :- Prioritizing tasks, creating schedules and using tools like
calendar to stay organized and avoid feeling overwhelmed. • SEEKING INFORMATION:-
Gathering knowledge about the stressful situation to better understand it and develop
effective coping strategies.. • DIRECT CONFRONTATION:- Directly addressing the source of
stress, such as talking to a supervisor about a work issue or addressing a conflict with a
family member` • CHALLENGING NEGATIVE THOUGHTS:- Recognizing and changing negative
thought patterns that contribute to stress. • REDUCING EXPECTATIONS :- Lowering
expectations about what is achievable or possible, particularly when dealing with situations
that are difficult of beyond your control.

 55. 2.EMOTION BASED STRATEGIES • Emotion focused coping strategies aim to manage the
emotional response to stress by directly addressing feelings rather than the problem itself . •
STRATEGIES INCLUDE:- Journaling, Meditation, Positive thinking, Reframing and Seeking
 social support. • JOURNALING :- Writing down thoughts and feelings can help individuals
understand their emotions better and develop coping mechanism. • MEDITATION :-
Practicing meditation can help calm the mind and promote a sense of well-being, which can
be particularly helpful for managing stress and anxiety.

 56. • POSITIVE THINKING :- Focusing on the positive aspects of a situations can help shift
perspective and reduce negative emotions. • REFRAMING :- Changing how you perceive a
stressful situation can alter your emotional response. • SEEKING SOCIAL SUPPORT:- Talking
about your feelings with trusted friends, family or a therapist can provide emotional support
and help you feel less alone.

 57. 3.COMPLEMENTARY AND ALTERNATIVES TECHNIQUES It includes a range of practices

and therapies used alongside or instead of conventional medicine to address health
concerns improve well being and enhance quality of life in elderly. GERIATRIC MASSAGE-It is
a modification of standard massage designed to improve circulation , relief of pain ,increase
range of motion decrease anxiety or depression , improve sleep and enhance sense of well
being in elderly. ACUPUNCTURE-It is a traditional ,Chinese medicine practice ,can help
manage pain and other health conditions. AROMA THERAPY-Essential oils can be used to
enhance mood reduce stress and improve sleep.

 58. 4.COGNITIVE FOCUSED COPING TECHNIQUES • Involve using mental strategies to

manage stress and difficult emotions by reframing thoughts and changing perceptions of
situations . • These techniques aim to improve emotional regulation , reduce distress . KEY
FEATURES : • Distraction – shifting attention away from the stress full situation or emotion
to engage in a more pleasant . • Journaling – write down thoughts and feelings to gain
insight into emotional responses and patterns . • Self monitoring – tracking thoughts ,
feelings and behaviors related to a specific stressor to gain a better understanding of coping
patterns

 59. SEXUALABUSE IN ELDERLY • Abuse refers to “a single or repeated act or lack of

appropriate action, occurring within any relationship where there is an expectation of trust
which cause harm or distress to an older person.” • Sexual abuse against the elderly is a part
of the overall maltreatment of the elderly there are several forms of sexual abuse
perpetrated against the elderly. WHAT IS ELDER SEXUAL ABUSE? ELDER SEXUAL ABUSE
INCLUDES:- • Unwanted touching, sexual assault or rape • Forced nudity or exposure to
sexual content • Inappropriate sexual comments or advances • Sexual activity with someone
who cannot give consent due to cognitive impairment ( e.g. Dementia )

 60. WHO ARE THE VICTIM? • Most victims are elderly women, but men can also be affected.
• Victims often have physical or cognitive disabilities. • Many live in nursing homes, assisted
living facilities or depend on caregivers WHO ARE THE ABUSERS? • Caregivers( formal or
informal) • Family members • Other members in care facilities • Health professionals

 61. WARNING SIGNS OF SEXUALABUSE IN ELDERLY • Bruises around the genital area or
breasts. • Unexpected sexually transmitted infections. • Panic attacks, withdrawal or
fearfulness. • Torn or stained underwear. • Refusal to be left alone with certain people
PREVENTION AND ACTION: • Educate caregivers and staff about elder abuse. • Provide safe
and confidential ways to report abuse. • Monitor the behavior of staff and other residents in
care facilities. • Encourage regular visits and open communication with family.
 62. LEGAL PROTECTIONS USED FOR SEXUALABUSE IN ELDERLY • Most countries have elder
abuse laws, including sexual abuse as a criminal offense. • Adult protective services (aps) or
similar organizations help investigate and protect victims.

 63. USE OF AIDS AND PROSTHESIS • Hearing aid • Assistive listening and adaptive devices •
Cochlear implants • Wheelchairs • Crutches • Walkers • Artificial limbs • Orthotic
devices(braces)

 64. LEGAL ASPECTS IN ELDERLY • Gerontological nursing, a specialty focusing on the care of
older adults, involves numerous legal aspects. • These include understanding informed
consent, advance directives, and the legal implications of caregiving for individuals with
diminished capacity. • Nurses must also be aware of laws related to abuse and neglect,
mandatory reporting, and the legal consequences of negligence or malpractice. •
Circumstances that increment the gamble of risk incorporate working with deficient assets,
neglecting to follow strategy and methods, pursuing faster routes or working feeling
profoundly worried.

 65. Larceny Negligence Constitutions Battery & Fraud Assault Attorney General Opinions
Regulations Statues Court Decisions Invasion of Privacy False Imprisonment Defamation of
Character

 66. • NEGLIGENCE :- Medical attendants are supposed to offer types of assistance to

patients in a cautions, able as per a norm of care is viewed as the standard for what a
sensible person in a comparative situation would do. • CONSTITUTIONS :- State essential
privileges, award powers and put limits on government offices that guide regulations
improvement by those organizations • COURT DECISIONS :- Lay out points of reference from
cases heard in state or government courts.

 67. • STATUTES :- Regulations laid out by neighborhood, state and government regulations •
REGULATIONS :- Regulation instituted by state and government managerial organization that
explicitly characterize the techniques to accomplish objectives and goals of rules. •
ATTORNEY GENERAL OPINIONS :- Regulations got form the assessments of the main lawyer
for the state or central government • ASSAULT :- A deliberate threat or attempt to harm
someone else that the individual consents

 68. NATIONAL HEALTHCARE PROGRAMMES 1. THE AYUSHMAN BHARAT – 23 SEPTEMBER

2018 • Pradhan Mantri Jan Arogya Yojana (AB-PMJAY), which aims to provide universal
health coverage. It's a comprehensive health insurance scheme offering up to Rs 5 lakhs per
family per year for secondary and tertiary care hospitalization. 2. THE NATIONAL
PROGRAMME FOR HEALTH CARE OF THE ELDERLY (NPHCE):- 2010 • This program focuses on
providing accessible, affordable, and high-quality long-term care services for the aging
population.

 69. 3. NATIONAL VIRAL HEPATITIS CONTROL PROGRAMME (NVHCP):- 28 JULY 2018 • Aims
to eliminate hepatitis C by 2030 and reduce hepatitis B and C related morbidity. 4.NATIONAL
PROGRAMME FOR PREVENTION AND CONTROL OF CANCER, DIABETES, CARDIOVASCULAR
DISEASES & STROKE (NPCDCS):- OCTOBER 2010 • Aims to prevent and control major non-
communicable diseases through infrastructure development and resource allocation.

 70. 5. NATIONAL MENTAL HEALTH PROGRAMME (NMHP):- 1982 Focuses on providing

mental health services, including treatment, counseling, and rehabilitation. 6.NATIONAL
 PROGRAMME FOR CONTROL OF BLINDNESS & VISUAL IMPAIRMENT (NPCB&VI):Works to
prevent and control blindness and visual impairment. - 1976

 71. STATE LEVEL HEALTHCARE PROGRAMS • THE HIMACHAL PRADESH GOVERNMENT offers
several state-level healthcare programs for the elderly, including:- 1. THE OLD AGE PENSION
SCHEME:- A unfunded pension scheme financed on a pay-as-you-go (payg) basis in which
current revenues of the government funded the pension benefit for its retired employees. 2.
THE HIMCARE SCHEME (HIMACHAL PRADESH SWASTHYA BIMA YOJANA):- It is a health
insurance scheme in Himachal Pradesh, providing cashless treatment coverage up to
5,00,000 ₹ per year per family. 3. THE INTEGRATED SCHEME FOR OLDER PERSONS:- It is a
central sector scheme aimed at improving the quality of life and maintaining the dignity of
older persons. THESE PROGRAMS AIM TO PROVIDE FINANCIALASSISTANCE, HEALTH
INSURANCE, AND BASIC AMENITIES TO SENIOR CITIZENS.

 72. DISTRICT LEVEL PROGRAMMES FOR ELDERLY • INDIRA GANDHI NATIONAL OLD AGE
PENSION: For individuals aged 60 and above, with eligibility based on BPL status and other
criteria.• OLD AGE PENSION SCHEME: Provides monthly financial assistance to seniors aged
60 and above, with varying amounts based on age and income. • DISABILITY RELIEF
ALLOWANCE: For individuals with 40% or more disability. • PENSION SCHEME FOR
WIDOW/DESTITUTE/SINGLE WOMEN: For women aged 18 and above with specific income
criteria. • SENIOR CITIZEN FACILITATION CENTRE :-The himachal pradesh government has
plans to establish senior citizen facilitation centres in Shimla, Dharamshala, Mandi and
Hamirpur.

 73. COMMUNITY BASED PROGRAMMES FOR ELDERLY • THIKANA SHIMLA SENIOR

COMMUNITY:- Offers residential and day care services, medical support, activities and social
engagement for seniors. • DEV BHOOMI DARSHAN YOJANA:- Free or subsidized pilgrimage
travel for himanchal pradesh’s senior citizens. • PANCHVATI YOJANA:- Development of parks
with facilities for elderly like walking tracks and meditation areas. • SAMARTH ELDER CARE
(HOME CARE SERVICES):- Health care, safety, companionship and convenience services for
seniors at home.

 74. OLD AGE HOME IN HIMACHAL PRADESH

 75. Old Age Home ,Basantpur Distt- SHIMLA CAPACITY-50 Old Age Home Chopal ,Distt -
SHIMLA CAPACITY-25 Old Age Home Kalath Manali, Distt-KULLU CAPACITY-50 Old Age Home
Bhangrotu Distt-MANDI CAPACITY-100

 76. The Suket Citizen Home,Sundernagar Distt-MANDI CAPACITY-25 Old Age Home Dari,
(Dharamshala)Distt- KANGRA CAPACITY-50 Old Age Home Distt- BILASPUR CAPACITY-25 Old
Age Home Muthan,Distt-HAMIRPUR CAPACITY-50

 79. HOME CARE OF ELDERLY • Home care encompasses all medical and supportive services
provided in the home. • These services may include visits by physicians or nurses:
intravenous therapy, physical, speech and occupational therapy; social work and home
health aide services. FUNCTIONS OF HOME CARE FOR ELDERLY:- Complete or partial physical
care Psychological assistance/ care Emotional assistance/ care Medical assistance/ care
Entertainment and Exercise

 80. • COMPLETE CARE :- This means the elderly person is fully dependent on caregivers for
all aspects of personal care . • PARTIAL CARE :- This means the elderly person can perform
 some adls independently but needs help with others. • PSYCHOLOGICAL ASSISTANCE:-
Providing emotional, cognitive, social and spiritual support. Providing counselling, therapy,
education and empowerment & creating a supportive environment.

 81. • ENTERTAINMENT FOR ELDERLY :- To reduce loneliness, improve mood and enhance
quality of life. Common entertainment:- music therapy, games, reading, storytelling, art &
craft. • EXERCISE FOR ELDERLY:- To maintain mobility , balance, strength and independence.
Types of exercise:- physical exercise & mental exercise.

 82. • MEDICAL ASSISTANCE :- Administering prescribed medications on time, monitoring

vital signs regularly, management of chronic disease conditions, providing care to wound
and skin, providing mobility and safety support. monitoring nutrition and hydration and
preventing infection. • EMOTIONAL ASSISTANCE FOR ELDERLY :- It involves providing a
supportive and empathetic presence to address the emotional needs of seniors, fostering a
sense of well-being and security. This can include companionship, encouragement, and
active listening to help them navigate the challenges of aging and maintain their mental
health.

 83. INSTITUTIONAL CARE FOR ELDERLY • Institutional care for the elderly refers to living and
receiving care in a facility like a nursing home, assisted living center, or continuing care
retirement community. • This type of care is often chosen when individuals experience
declining health, need constant medical support or lack family support for their needs. •
Institutional settings provide a range of services, including 24-hour supervision, assistance
with daily activities, skilled nursing care, rehabilitation and social activities. TYPES IF
INSTITUTIONAL CARE 1. Independent Living 2. Nursing Homes 3. Adult Day Care 4.
Continuing Care Retirement Communities 5. Speciality Care Units

 84. 1. INDEPENDENT LIVING:- For seniors who can manage daily activities independently but
desire community living, these facilities offer apartments or homes with recreational and
social amenities. 2. NURSING HOMES:- Offer around-the-clock medical and personal care for
seniors with more significant health needs, including rehabilitation and skilled nursing. 3.
ADULT DAY CARE:- Provides daytime supervision and activities in a structured environment
for seniors who need daytime support while their caregivers are at work.

 85. 4. CONTINUING CARE RETIREMENT COMMUNITIES (CCRCS):- Combine independent

living, assisted living, and skilled nursing care on one campus, allowing residents to transition
to higher levels of care as needed. 5. SPECIALTY CARE UNITS:- These units within nursing
homes or other facilities specialize in caring for residents with specific conditions like
dementia or alzheimer's, providing specialized care and environment.

 86. ADVANCE CARE FOR ELDERLY • INDIA - Advance care for elderly in India involves
medical, emotional, and legal planning to support aging individuals, especially during serious
illness. key areas : medical services: geriatric clinics, home healthcare (like portea), palliative
care ( NGOs like pallium India ).social support: senior living communities (e.g., antara), day
care centers, elder helplines (14567).legal and financial planning: living wills (legal since
2018), senior citizen pension and insurance schemes.

 87. ADVANCE CARE FOR ELDERLY • NORWAY: known for its exceptional elder care services,
Norway's system is funded by taxes and provides financial security for older adults. the
country emphasizes independence, social engagement and re-ablement programs to help
seniors regain their abilities. • SWEDEN: Sweden's healthcare system is publicly funded and
 accessible to all residents. The country prioritizes aging in place, allowing seniors to live
independently with support from home care services

 88. • SWITZERLAND: Switzerland offers high-quality healthcare services and advanced

medical technology. The country provides personalized care plans, emphasizing research
and development in geriatric medicine. • FRANCE: France is recognized for its excellence in
geriatric medicine and patient care, providing comprehensive services for the elderly,
including geriatric units and rehabilitation services.

 89. • AUSTRALIA: Australia is known for innovative approaches to elderly care, including
research in geriatric medicine and comprehensive healthcare services. • SINGAPORE:
Singapore blends traditional practices with modern medical technology in geriatric medicine,
making it a hub for medical tourism.

 90. • GERMANY: Germany's healthcare system is robust, with specialized geriatric care
facilities and a cohabiting care model that promotes independence among seniors. •
PORTUGAL: Portugal's universal healthcare system provides low-cost medical care to
foreigners, making it an attractive option for retirees

 91. • UNITED STATES: The US offers advanced geriatric research and treatment, with
reputable assisted living programs and skilled nurses. • CANADA: Canada's publicly funded
universal healthcare system provides medical services to all residents. The country offers
financial assistance programs for elderly citizens, including old age security and guaranteed
income supplement.

 92. • KEY FEATURES OF ADVANCE CARE FOR ELDERLY • HOME CARE: Many countries
prioritize home care, allowing seniors to live independently with support from caregivers
and medical professionals. • PERSONALIZED CARE PLANS: Countries like switzerland and
norway emphasize personalized care plans, tailoring services to individual needs and goals.

 93. • RE -ABLEMENT PROGRAMS: Norway's re- ablement approach focuses on helping

seniors regain their abilities, reducing healthcare spending and improving overall well-being.
• FINANCIAL SECURITY: Countries like Norway and Sweden provide financial security for
older adults through pension plans and government-funded care systems

 94. BENEFITS FOR ELDERLY • HEALTHCARE BENEFITS: 1) AYUSHMAN BHARAT PRADHAN

MANTRI JAN AROGYA YOJANA: This scheme provides free health insurance coverage to
senior citizens aged 70 and above, regardless of their income. 2) HEALTH INSURANCE: Many
insurance companies offer health insurance specifically designed for senior citizens. 3)
MEDICAL EXPENSES DEDUCTION: Senior citizens can claim deductions under section 80D for
medical expenses, even without health insurance. 4) OLD AGE HOMES: Government and
private old age homes provide care and support for senior citizens,

 95. • TRANSPORT BENEFITS: 1) INDIAN RAILWAYS : Fare concessions 40% for men, 50% for
women on all classes of tickets 2) STATE ROAD TRANSPORT: Fare concessions free or
discounted travel, with specific details varying by state. 3) PRIORITY LANES AND LIFTS:
Facilitates easier movement through stations. 4) FREE TRAVEL: Some public transport routes
offer free travel for senior citizens aged 80 and above. 5) URBAN TRANSIT SUBSIDY: Reduced
rates for e-rickshaws and taxis in some cities.

 96. • FINANCIAL BENEFITS 1) PENSION SCHEMES: Government-backed pension schemes like

Pradhan Mantri Vaya Vandana yojana (PMVVY) and senior citizen savings scheme (SCSS)
 provide regular pension payouts. 2) NO ADVANCE TAX: Senior citizens may be exempt from
paying advance tax if their income is solely from pension and interest. 3) EXEMPTION FROM
FILING INCOME TAX RETURNS: Senior citizens aged 75 and above with income solely from
pension and interest may be exempt from filing income tax returns.

 97. DIAGNOSTIC EVALUATIONS FOR ELDERLY 1. VISION AND HEARING TESTS: Assess visual
and auditory abilities to detect age-related changes. 2. COMPLETE BLOOD COUNT (CBC):
Provides information about red and white blood cell counts, which can indicate infection,
anemia, or other blood-related issues. 3. THYROID FUNCTION TESTS: Measures thyroid
hormone levels to detect hypothyroidism or hyperthyroidism. 4. KIDNEY FUNCTION TESTS:
Evaluates kidney health and function. 5. LIVER FUNCTION TESTS: Assesses liver health and
function. 6. MENTAL STATUS EXAMINATION: Evaluates cognitive function, including
orientation, memory, and judgment. 7. IMAGING STUDIES : X Ray, CT Scan, Bone Density
Scan (DEXA)

 99. NURSING MANAGEMENT FOR ELDERLY NURSING ASSESSMENT • HISTORY

COLLECTION :- The history should include demographic data, chief complaint, history of
present illness, past medical history, family history, medication list, social history, and a
review of systems. • PHYSICAL EXAMINATION:- A physical assessment of geriatric patients
should be a comprehensive evaluation that considers the whole person, focusing on their
physical health, functional abilities, cognitive status, and social environment.

 100. METHODS OF PHYSICAL EXAMINATION • 1. Inspection -observing general appearance.

• (example , Posture, hygiene, mobility). • Look for signs of malnutrition, dehydration, skin
changes • (example ., Pressure sores, bruises). • Note facial expressions, gait, and any
assistive devices (example : Walkers). 2 Palpation: This Technique uses the sense of touch to
feel the body, assessing temperature, texture, size, shape, and tenderness of organs and
tissues. . Check skin turgor for hydration . Be cautious of fragile skin and decreased
subcutaneous fat.

 101. • 3. Percussion: This involves tapping on the body to elicit sounds that can indicate the
presence or absence of fluid, air, or solid tissue. • example , Lungs, liver. • May be less
reliable due to altered tissue density (example , Osteoporosis). • 4. Auscultation - This
method involves listening to internal body sounds, typically using a stethoscope, to assess
heart, lung, and bowel function. HEART - check for murmurs, irregular rhythms (example -
atrial fibrillation ). LUNGS – Assess breath sounds . ABDOMEN – listen for bowel sounds ,
assess for bruits

 102. NURSING DIAGNOSIS S.NO. DESCRIPTION 1. PAIN RELEATED TO JOINT STIFFNESS AND
INFLAMMATION. 2. RISK OF IMPAIRED SKIN INTEGRITY RELEATED TO IMMOBILITY AND
SENSORY LOSS. 3. IMPAIRED URINARY RETENTION RELEATED TO INABILITY TO VOID
SPONTANEOUSLY. 4. DISTURBED SENSORY PERCEPTION RELEATED TO MOTOR AND
SENSORY IMPAIRMENT. 5. INEFFECTIVE BREATHING PATTERNS RELEATED TO WEAKNESS OR
PARALYSIS OF ABDOMINAL AND INTERCOSTAL MUSCLE. 6. CONSTIPATION RELATED TO
PRESENCE OF ATONIC BOEWL. 7. INEFFECTIVE COPING RELEATED TO LACK OF FAMILY
SUPPORT, CHRONIC ILLNESS.

 103. 1. PAIN RELATED TO JOINT STIFFNESS, AND INFLAMMATION NURSING GOALS : •

Patient will report reduced pain levels within 30 minutes of intervention. • Patient will
demonstrate improved mobility. NURSING INTERVENTIONS : • Assess pain intensity using a
 pain scale. • Administer prescribed analgesics and anti-inflammatory medications. •
Encourage gentle range-of-motion exercises . apply warm or cold compresses as indicated.
NURSING EVALUATION : • Patient verbalizes decreased pain. • Patient shows improved
range of joint movements.

 104. 2. RISK OF IMPAIRED SKIN INTEGRITY RELATED TO IMMOBILITY AND SENSORY LOSS:
NURSING GOALS : • Patient’s skin will remain intact during hospital stay . • Patient and
family will verbalize understanding of skin care techniques . NURSING INTERVENTIONS : •
Inspect skin daily for signs of breakdown . • Reposition patient every 2 hours . • Keep skin
clean and dry . • Use pressure-relieving devices (e.G., Air mattresses). NURSING
EVALUATION : • No evidence of pressure ulcers . • Patient and caregiver demonstrate
proper skin care techniques.

 105. 3. IMPAIRED URINARY RETENTION RELATED TO INABILITY TO VOID SPONTANEOUSLY:

NURSING GOALS : • Patient will void spontaneously within 8 hours . • Patient will maintain
adequate urinary output . NURSING INTERVENTIONS : • Monitor bladder distention and
urinary output . • Encourage adequate fluid intake (if not contraindicated). • Assist patient
to bathroom or use bedpan regularly . • Provide privacy and comfort during toileting .
NURSING EVALUATION : • Patient voids without discomfort . • No signs of bladder distention
observed.

 106. 4. DISTURBED SENSORY PERCEPTION RELATED TO MOTOR AND SENSORY IMPAIRMENT

: NURSING GOALS : • Patient will demonstrate improved awareness of surroundings . •
Patient will remain free from injury . NURSING INTERVENTIONS : • Assess sensory deficits
(touch, pain, temperature). • Provide a safe environment to prevent injuries . • Reorient
patient frequently if necessary . • Educate patient and family about sensory changes .
NURSING EVALUATION : • Patient identifies objects by touch . • Patient remains injury-free.

 107. 5. INEFFECTIVE BREATHING PATTERNS RELATED TO WEAKNESS OR PARALYSIS OF

ABDOMINALAND INTERCOSTAL MUSCLE: NURSING GOALS : • Patient will maintain effective
respiratory patterns . • Patient’s oxygen saturation will remain within normal range .
NURSING INTERVENTIONS : • Monitor respiratory rate, depth, and effort . • Position patient
in semi-fowler’s or high fowler’s position . • Encourage deep breathing and coughing
exercises . • Administer oxygen therapy if prescribed . NURSING EVALUATION : • Patient
maintains spo above 95%. ₂ • Breath sounds are clear on auscultation.

 108. NON-PHARMACOLOGICAL MANAGEMENT • Management for elderly patients

encompasses a holistic approach to ensuring their well-being, focusing on maintaining their
independence, improving their quality of life, and addressing their unique needs. • This
involves planning and coordinating healthcare, social support, and other services to help
them live as independently • KEY ASPECTS 1. GERIATRIC CARE MANAGEMENT: This involves
working with individuals and their families to assess needs, develop care plans, and
coordinate services to meet their long-term care requirements.

 109. 2. PREVENTIVE CARE: Focusing on fall prevention, nutrition, exercise, and regular
health screenings to address safety concerns and reduce the risk of accidents and
hospitalizations. 3. COMMUNICATION: Effective communication is crucial, involving speaking
to patients as fellow adults, making them comfortable, and avoiding rushing or using jargon.
4. INDIVIDUALIZED CARE PLANS: Recognizing that older adults have diverse needs and
tailoring care plans accordingly to promote their independence and well-being.
 110. 5. ADDRESSING COGNITIVE AND PHYSICAL CHANGES: Providing interventions for
cognitive impairment, such as frequent reorientation, calm environments, and assistive
devices, while also addressing physical needs like pain management and mobility. 6.
FINANCIAL PLANNING: Navigating funding sources, pricing models, and other financial
considerations to ensure access to quality care. 7. NUTRITIONAL MANAGEMENT FOR
ELDERLY PATIENTS: Focuses on ensuring adequate intake of essential nutrients to maintain
health and prevent deficiencies. This includes a balanced diet, adequate protein, hydration
and consideration of individual needs and health conditions.

 111. • EXAMPLES OF CARE MANAGEMENT FOR ELDERLY 1. Medication management:

Ensuring that medications are taken correctly, and addressing potential drug interactions
and side effects. 2. Physical activity: Encouraging regular exercise and physical activity to
maintain mobility and overall health. 3. Nutrition: Promoting a healthy diet and addressing
any nutritional deficiencies. 4. Social engagement: Encouraging social interactions and
activities to combat isolation and promote mental well-being. 5. Mental stimulation:
Providing cognitive stimulation and activities to keep the mind active. 6. Pain management:
Addressing pain effectively through a variety of approaches, including medication, physical
therapy, and other non-pharmacological treatments. 7. Home safety: Making homes safer by
addressing potential hazards and ensuring accessibility.

 112. ROLE OF NURSE • A gerontological nurse, also known as a geriatric nurse, is a

registered nurse (RN) specializing in the care of older adults. • They work to promote
healthy aging, maximize function, and improve the quality of life for their patients. • This
specialization requires a unique set of skills and knowledge related to the specific health
needs and challenges faced by the elderly. • A gerontological nurse is a specialized
healthcare professional who is dedicated to providing comprehensive and holistic care to
older adults, promoting their well-being and independence.

 113. CONCLUSION The elderly are humans ; they undergo changes due to increasing age
that may result in reduced physical and mental capacities and in long run disabilities and
death if not taken care of. They constitute a significant proportion of the population and can
be resourceful to the society and lessen dependency burden if taken care of . hence, caring
of elderly is an investment and not an economical or health system burden. Promotion of
healthy habits, prevention of disease, early detection and management of disease,
rehabilitation and creation of age friendly environment and policies are all key in optimum
adult care.

 114. RECAPITULATION 1. Which of the following is a common age-related change in the

cardiovascular system? (A) Increased heart rate (B) Decreased blood pressure (C) Decreased
stroke volume (D) Increased elasticity of blood vessels 2. What is the primary goal of
geriatric assessment? (A) To diagnose specific diseases (B) To identify strengths and
weaknesses of the elderly person (C) To plan for a long-term care plan (D) To provide a
complete physical exam

 115. 3. What immunoglobulin is the first class of antibodies to respond to infection and
decreases in production with aging? (A) Ig A (B) Ig D (C) Ig E (D) IgM 4. Which of the following
is increased in the renal system with aging ? (A) Glomerular Filteration Rate (B) ADH and
Thirst Response (C) Ability to regulate salts and volume (D) Glucose content in urine
  116. 5. Which of the following changes seen in the elderly is an important as it increases te
risk of falling? (A) Two Point Discrimination (B) Proprioception (C) Steregnosis (D) Vibratory
Sense

 117. ASSIGNMENT LONG QUESTIONS 1. Write about the nursing intervention for age
related body changes. 2. Elaborate national programmes for elderly. SHORT QUESTIONS 3.
Discuss about the role of family, caregiver in elderly care. 4. Explain about the psychological
aspects of aging. 5. Legal and ethical issues in geriatric nursing.

OSCE Series ( Questions & Answers ) - Set 6.pdf

 1. OSCE SERIES : SET 6
 2. 1 A 45 year old patient presented to the OPD with episodes of giddiness. On examination , he
was found to have bradycardia. An ECG was taken ( shown in the next slide ) 1. Mention any 4
etiologies of sinus bradycardia. 1 2. Mention any 2 causes of pseudo bradycardia. 1 3. What is
the ECG finding ? 1 4. How to proceed in this case ? 2
 4. Answers 1. Hypothyroidism , Hypothermia , Sleep apnoea , Increased intracranial pressure
2. Ventricular bigeminy , Frequent nonconducted early atrial premature beats 3. Sinus rhythm ,
Unifocal premature ventricular complexes in a bigeminy fashion 4. ● Admit the patient ● ECHO
to rule out structural heart disease ● Measurement of Hb , TSH , serum electrolytes ● Holter
monitoring to look for significant arrhythmias ● Rule out other causes of syncope also
 6. 2 An 8 year old child was brought to the OPD by parents with complaints of decreased height
for age. Parents told that the child has history of recurrent fractures and is on vitamin D
supplements. Her CBC was normal. She had normal blood sugars , hypokalemia , a low urine pH
, glycosuria and phosphaturia. An ABG was done which showed normal anion gap metabolic
acidosis. X rays showed severe osteopenia. 1. What is the likely diagnosis ? 1 2. What are the
factors contributing to osteopenia ? 1.5 3. How does hypokalemia occur in this condition ? 1.5 4.
Mention any 4 causes of non anion gap metabolic acidosis. 1
 7. Answers 1. Renal tubular acidosis ( Proximal RTA due to Fanconi syndrome ) 2. ● Chronic
metabolic acidosis increases alkali mobilization from the bone and thus demineralisation of bone
● Chronic hypophosphatemia due to renal phosphate wasting ● Reduced level of the active form
of vitamin D because of the inability of the proximal tubule to convert 25 ( OH ) vitamin D to 1,25
(OH)2 vitamin D 3.Due to loss of NaHCO3 in the urine , there is intravascular volume depletion.
This leads to activation of renin angiotensin aldosterone system. Due to impaired proximal
reabsorption of sodium , there is increased distal delivery of sodium. Because of the associated
hyperaldosteronism and increased distal nephron Na+ reabsorption, there is increased K+
secretion. The net result is renal potassium wasting and the development of hypokalemia.
4.Diarrhoea , Renal tubular acidosis , Drug induced hyperkalemia , Mineralocorticoid resistance
 8. CAUSES OF NON ANION GAP METABOLIC ACIDOSIS
 9. 3 A 60 year old man came to the OPD complaining of inability to attain a firm erection over the
last few months. He is a smoker , and has DM and CAD. The physical examination of the
genitalia was within normal limits. 1. What is the likely cause of erectile dysfunction ( ED ) in this
patient ? 1 2. Which are the drugs associated with ED ? 1 3. Mention any 3 pharmacologic
agents approved to treat ED ? 1.5 4. What are the interventions other than pharmacologic agents
useful in ED ? 1.5
 10. Answers 1. Vasculogenic ( atherosclerosis due to DM & smoking ) 2. Antidepressants
( SSRIs , TCAs ) ; Antihypertensives ( Thiazide diuretics , Beta blockers ) 3. Sildenafil , Tadalafil ,
Vardenafil , Avanafil 4. Vacuum constriction devices , Surgery ( implantation of a semirigid or
inflatable penile prosthesis / vascular surgery ) , Sex therapy
 12. 4 A patient with DM , HTN , coronary artery disease and chronic liver disease presented to
the emergency dept with gradually progressing breathlessness. A chest X ray was taken ( shown
in the next slide ) 1. What will be the examination findings in this case ( palpation , percussion
and auscultation of the chest ) ? 3 2. How to differentiate between hepatic hydrothorax and
pleural effusion due to heart failure ? 1 3. Assuming this is hepatic hydrothorax , how will you
manage ? 1
 14. Answer 1. ● Palpation - Decreased chest expansion & Decreased vocal fremitus on right
side ● Percussion - Dull note to percussion on right side ● Auscultation - Decreased breath
sounds , Decreased vocal resonance on right side 2. ● Clinical assessment ● Serum and pleural
fluid NT proBNP 3. - Thoracentesis as the pleural effusion is symptomatic - Dietary sodium
restriction - Diuretics - Appropriate management of CLD Serum / Pleural fluid assay of NT-pro
BNP > 1500 pg/mL is suggestive of pleural effusion due to heart failure.
 15. 5 A 60 year old lady came to the OPD complaining of low back ache. The physical
examination was unremarkable. The X ray of the LS spine showed osteopenia. You decided to
do lab tests. You asked the patient to perform CBC , RBS , RFT , TSH & Vitamin D. 1. Which is
the blood test done to assess vitamin D deficiency ? o.5 2. Which are the major causes of
vitamin D deficiency ? 2 3. How to treat vitamin D deficiency ? 1.5 4. How to assess the response
to treatment ? 1
 16. Answer 1. 25 ( OH ) vitamin D 2. Impaired cutaneous production , Liver disease , Chronic
Kidney Disease 3. ● Assess the cause of vitamin D deficiency and appropriate management ●
Vitamin D & calcium supplementation ➔ If the pathway required for vitamin D activation is intact ,
severe vitamin D deficiency be treated with pharmacologic repletion initially ( 50,000 IU weekly
for 3-12 weeks ) , followed by maintenance therapy ( 800 IU /day ) ➔ Calcium supplementation
should include 1.5 - 2 g/day of elemental calcium 4. ● Measurement of serum and urinary
calcium levels. In patients who are vitamin D replete and are taking adequate calcium
supplementation , the 24 hr urinary calcium level should be in the range of 100 - 250 mg / 24
hours. ● Vitamin D levels should be rechecked 3 months after initiating supplementation
 18. 6 A 70 year old male came to the OPD with tiredness. On examination , he was pale. Upon
enquiry , he reported the passage of black tarry stools for the last 2 months. You ordered for a
CBC and a stool occult blood test. The CBC showed a Hb level of 7.6 g/dL and the stool occult
blood was positive. a. List any 4 causes of melena in an elderly individual ? 2 b. Which are the
clues to iron deficiency anemia in CBC ? 1.5 c. How to proceed in this case ? 1.5
 19. Answers 1. Peptic ulcers , Esophageal varices , Erosive disease , Neoplasms 2. Anemia ,
Decreased mean corpuscular volume , Increased red cell distribution width , Thrombocytosis 3. ●
GI endoscopy & CECT abdomen to look for the site and etiology of bleeding , and once the
etiology is identified , its appropriate management ● Correction of anemia
 20. 7 A 26 year old male presented with history of recurrent headache , vomiting and seizures.
The MRI of the patient is given below. 1. Comment about the MRI findings. 2 2. List any two
causes for this particular lesion in an immunocompromised and immunocompetent individuals. 2
3. Which are the treatment options for raised ICT ? 1
 22. Answers 1. (A) Axial contrast-enhanced T1-weighted magnetic resonance imaging
showing ring-enhancing lesions (white arrows) (B) Axial T2-weighted images showing ring-
enhancing lesions surrounding hyperintensity, consistent with vasogenic edema (white arrows).
2. ● In the immunocompetent host : tumours ( primary & metastatic ) & pyogenic abscesses ● In
the immunocompromised host , toxoplasmosis & primary CNS lymphoma 3. ● Elevate head of
the bed ; Midline head position ● Osmotic agents ( mannitol / 3 % hypertonic saline ) ●
Glucocorticoids are useful in vasogenic cerebral edema ● Sedation ; Add neuromuscular
paralytic agents if necessary ● Pressor therapy ( to maintain adequate mean arterial pressure ) ●
Decompressive craniectomy ● Extraventricular drainage of CSF
 25. 8 A 40 year old male presented to the emergency department with history of gradually
progressive exertional breathlessness and edema of lower extremities. He denied history of
substance abuse. On examination , he had no pallor , bilateral pitting pedal edema , elevated
JVP and a prominent second heart sound. A 2D ECHO was taken which showed an EF of 55% ,
severe right ventricular and atrial dilatation and elevated pulmonary artery pressure. 1. Mention
any 4 causes of exertional breathlessness. 1 2. What are the ECG changes seen in right
ventricular hypertrophy ? 1 3. How is pulmonary hypertension classified ? 2 4. Mention any two
pharmacological agents approved to treat pulmonary arterial hypertension. 1
 26. Answers 1. COPD , Left ventricular failure , Interstitial lung disease , Pulmonary
hypertension 2. ● Right axis deviation ● Dominant R wave in V1 ( R/S ratio > 1 or R wave > 7
mm ) ● Dominant S wave in V5 or V6 ( S wave > 7 mm or R/S < 1 ) ● QRS duration < 120 ms 3.
Pulmonary hypertension ( PH ) is divided into 5 categories (as per the Sixth World Symposium
on Pulmonary hypertension 2018 ) ● Pulmonary arterial hypertension ( PAH ) ● PH due to left
heart disease; ● PH due to chronic lung disease or sleep-disordered breathing; ● Chronic
 thromboembolic PH; and ● A group of miscellaneous diseases that rarely (or inconsistently)
cause PH 4. Sildenafil , Macitentan
 28. 9 A 50 year old HIV patient presented to the OPD with fever , non productive cough and
breathlessness. The patient was non compliant to ART. On examination , the patient was
tachypnoeic with an Spo2 of 90%. There were bibasal crackles on chest auscultation. The
physician suspected pneumocystis jiroveci pneumonia 1. How to confirm the diagnosis ? 1.5 2.
How to treat this patient ? 2 3. Comment about the prophylaxis to prevent pneumocystis
pneumonia. 1.5
 29. Answers 1. Histopathologic or cytopathologic demonstration of the organism in tissue ,
bronchoalveolar lavage fluid or induced sputum 2. The patient likely has mild to moderate PCP. ●
Admit the patient ● Oxygen supplementation ● TMP : SMX ( 160 mg / 800 mg ) 2 tablets orally
TDS x 21 days ● TMP SMX needs to be given IV if the patient has severe PCP. ● Steroids need
to be given if PaO2 < 70 mm of Hg or if the A-a gradient is > 35 mm of Hg. ● Ensure strict
compliance to ART ● Secondary prophylaxis after treatment completion 3. ● Primary prophylaxis
against PCP is offered if CD4 cell count is < 350 cells / mm3 or if the patient is in WHO clinical
stage 3 or 4. ● The secondary prophylaxis is offered to all patients who have successfully
completed treatment for PCP until CD4 count > 350 cells/mm3 ( at least on two occasions , done
at least 6 months apart ) ● The preferred regimen is Cotrimoxazole 1 DS tablet daily.
 30. 10 A patient presented to the emergency department with acute onset of breathlessness.
He is a known case of HTN & CAD. On examination , he was found to have low SpO2 and
bibasal crackles on chest auscultation. A bedside ultrasound was done , and an image of the
same is shown ( in the next slide ) 1. What is the image shown ? 0.5 2. What is the likely cause
of dyspnoea ? 0.5 3. What is BLUE protocol ?. 2 4. How to manage this patient ? 2
 32. Answers 1. B lines 2. Pulmonary edema 3. Bedside Lung Ultrasound in Emergency 4. The
clinical and the radiologic picture is suggestive of acute pulmonary edema ● Admit the patient ●
Non invasive ventilation ● Oxygen supplementation ● IV loop diuretics ● Cardiac evaluation
( ECG , ECHO , cardiac biomarkers )
 33. BEDSIDE LUNG ULTRASOUND IN EMERGENCY ➔ The BLUE protocol is a lung
ultrasound technique used to diagnose acute respiratory failure. ➔ It is a rapid, step-by-step
approach that uses a universal probe and standardized points of analysis to diagnose the main
causes of acute respiratory failure, including pulmonary edema, pulmonary embolism,
pneumonia, pneumothorax
 34. 11 Shown is the pedigree of two families having the same disorder. 1. Describe this
pedigree 2 2. What is the mode of inheritance ? 1 3. List any 4 disorders that are inherited in this
manner. 2
 35. Answers 1. ● In the first pedigree , when a female has a disorder , all of her offsprings have
the disorder. ● In the second pedigree , the females having the disorder does not transmit it to all
of her offsprings. 2. Mitochondrial inheritance ( the first pedigree shows that the inheritance is
maternal , the second pedigree shows the inheritance is variable ) 3. Leigh’s syndrome ,
MELAS , MERRF , Pearson’s syndrome The expression of mitochondrial conditions is variable.
Inside each cell, there are several mitochondria. The number of mitochondria that carry the
mutation can vary. A certain proportion of mutant mitochondria within a cell can be tolerated and
the disease will not be expressed in the organism. A larger proportion of mutant mitochondria
however, may cause the disease to be expressed in the organism.
 37. 12 The image shows a fingertip pulse oximeter. 1. What is the difference between SpO2
and SaO2 ? 1 2. What is “ PI “ shown in the pulse oximeter ? 1 3. Mention any two situations
where pulse oximeter is not reliable.2 4. State Beer Lambert law. 1
 38. Answers 1. SaO2 measures the oxygen saturation of arterial blood, while SpO2 measures
the oxygen saturation of peripheral blood using a pulse oximeter 2. Perfusion index (PI). PI is the
ratio of pulsatile blood flow to non-pulsatile static blood flow in a patient’s peripheral tissue.The
normal perfusion index (PI) ranges from 0.02% to 20%. 3. Presence of nail polish , Excessive
motion of the pulse oximeter placed site : Can lead to inaccurate readings 4. The Beer-Lambert
law defines that the light attenuation through a medium is proportional to the concentration of the
light absorbers present in the substance , the optical properties of the light absorber and the
optical path length traveled by the light beam.
 40. 13 A 70 year old diabetic patient presented to the OPD with complaints of burning and
tingling sensation in both his feet. On examination , there was hypoaesthesia of both the feet ,
 decreased vibratory sensation and absent ankle jerk. A diagnosis of peripheral neuropathy was
made. 1. Which are the different forms of peripheral neuropathy seen in patients with diabetes ?
1 2. Which is the most common form of diabetic neuropathy ? 1 3. Which are the treatment
options ? 2 4. What specific advice should be given to patients with peripheral neuropathy ? 1
 41. Answer 1. Distal symmetric sensory or sensorimotor polyneuropathy , Autonomic
neuropathy , Radiculopathies , Mononeuropathies 2. Distal symmetric sensory or sensorimotor
polyneuropathy 3. ● Glycemic control ● Lifestyle modifications ● Treat hypertension and
dyslipidemia ● Avoid neurotoxins like tobacco and alcohol ● Correction of vitamin deficiencies if
present - For pain relief , duloxetine , gabapentin , pregabalin , tricyclic antidepressants ,
venlafaxine , carbamazepine , tramadol or topical capsaicin products may be used. 4. Meticulous
foot care : Check feet daily ; Prevent the formation of calluses or ulcerations in the foot.
 42. 14 A 56 year old female who was recently diagnosed with hepatitis C related chronic liver
disease presented to the OPD with the following oral lesion. 1. Identify the lesion 1 2. Mention
any 2 cutaneous lesions seen in patients with chronic liver disease 2 3. Describe the treatment
for hepatitis C related chronic liver disease 2
 43. Answers 1.Oral lichen planus 2. Spider angioma , Palmar erythema 3. ● If a patient with
chronic hepatitis C related CLD has compensated cirrhosis , start the patient on sofosbuvir ( 400
mg ) and Velpatasvir ( 100 mg ) for 12 weeks ● If the patient has decompensated cirrhosis , start
the patient on sofosbuvir ( 400 mg ) , Velpatasvir ( 100 mg ) & Ribavirin ( 600 - 1200 mg ) for 12
weeks ● Test HCV RNA levels 12 weeks after completion of treatment ● If HCV RNA is not
detected , treatment is completed. However if HCV RNA is detected , refer the patient to a higher
centre for further management
 46. 15 You are planning to liberate a patient from mechanical ventilation. 1. What are the
criteria to check for prior to extubation ? 2 2. What is RSBI ? 1 3. What is spontaneous
awakening trial ( SAT ) and spontaneous breathing trial ( SBT ) ? 2
 47. Answers 1.The important criteria indicating a patient may be ready for extubation include
the following : - Underlying disease process has improved - The patient is awake and largely off
sedative medications - FiO2 ≤ 0.5 - PEEP < 8 cm of H2o - SaO2 > 88% - Stable hemodynamics -
Manageable respiratory secretions with adequate cough 2. The RSBI ( Rapid Shallow Breathing
Index ) is defined as the ratio of respiratory rate in breaths / minute to tidal volume in litres.
People on a ventilator who cannot tolerate independent breathing tend to breathe rapidly and
shallowly (low tidal volume), and will therefore have a high RSBI. It can be used in intubated
patients breathing spontaneously who meet other clinical criteria for weaning from mechanical
ventilation. The RSBI should not be the sole determinant of extubation. A normal rapid shallow
breathing index (RSBI) is less than 105 breaths per minute per liter (breaths/min/L). An RSBI of
105 or higher is associated with a higher likelihood of weaning failure.
 48. 3. SPONTANEOUS AWAKENING TRIAL
 49. 3. SPONTANEOUS BREATHING TRIAL
 50. 16 A 32 year old female was brought to the emergency department with low back ache. X
ray showed that she had a compression fracture of the lumbar spine. Upon enquiry , she
reported amenorrhoea of 3 months duration. The physician was called in for evaluation. On
examination , she had facial hair , acne , high BP recordings , proximal muscle weakness and
striae in the abdomen. 1. What is the most probable diagnosis ? 1 2. How will you screen for this
disease ? 2 3. How to confirm the diagnosis ? 2
 51. Answers 1. Cushing’s syndrome 2. ● 24 hour urinary free cortisol excretion increased
above normal ( ≥ 2 times ) ● Dexamethasone overnight test ( 1 mg of dexamethasone is given at
11 PM. Plasma cortisol is measured at 8 -9 AM the next day ; Plasma cortisol > 50 nmol/L is a
positive test ) ● Midnight salivary cortisol > 5 nmol/L 3. ● Determine if Cushing’s is ACTH
dependent or not , by assessing the ACTH levels ● If ACTH levels are high , it suggests ACTH
dependent Cushing’s syndrome. Look for the source of ACTH - MRI pituitary to look for a
pituitary lesion or if an ectopic source is suspected , CT chest / abdomen should be done. A CRH
test and/or a high dose dexamethasone test may be also be done to know if the source is
pituitary lesion. ● If ACTH levels are suppressed , image the adrenals.
 52. The most important first step in the management of patients with suspected Cushing’s
syndrome is to establish the correct diagnosis. Most mistakes in clinical management, leading to
unnecessary imaging or surgery, are made because the diagnostic protocol is not followed . This
protocol requires establishing the diagnosis of Cushing’s beyond doubt prior to employing any
 tests used for the differential diagnosis of the condition. In principle, after excluding exogenous
glucocorticoid use as the cause of clinical signs and symptoms, suspected cases should be
tested if there are multiple and progressive features of Cushing’s, particularly features with a
potentially higher discriminatory value.
 53. 17 A nurse is ordered to give an injection to a patient. The wastes generated as a part of the
procedure are Gloves , Swab , Plastic syringe , Needle , wrapper of syringe , Wrapper of needle ,
Vial of injection , Packaging of injection & instruction leaflet 1. As per the BMW rules 2016 , in
which bag / container would you dispose these items ? 2 2. Mention any 3 universal precautions.
3
 54. Answers 1. ● Gloves - Red ● Swab - Yellow ● Plastic syringe - Red ● Needle -White ●
Injection vial - Blue ● Wrapper of syringe & Wrapper of needle , packaging of injection &
instruction leaflet - General wastes - Green 2. ● Handwashing ● Personal protective equipment
( Barrier protection ) ● Proper disposal of contaminated materials
 55. 18 A patient with long standing rheumatoid arthritis (RA) presented to the OPD. An image of
his hand is shown. 1. What is the deformity ? 1 2. Mention any 2 classes of drugs used to treat
rheumatoid arthritis with examples. 2 3. Mention any four extra articular manifestations of RA. 2
 56. Answers 1. Swan neck deformity 2. ● NSAIDs - Aceclofenac , Ibuprofen ● Conventional
DMARDs - Hydroxychloroquine , Methotrexate 3. Rheumatoid nodules , Pleuritis , Pericarditis ,
Interstitial lung disease
 57. 19. Watch the attached video - 3rd nerve palsy 1. Describe the eye movements. 3 2. What is
the likely diagnosis ? 1 3. List any two etiologies. 1
 58. Answers 1. There is ptosis in the right eye ; Abduction is normal in the right eye , however
adduction , supraduction and infraduction are impaired. The movements of left eye are normal. 2.
Right 3rd nerve palsy. 3. Stroke , Diabetes , Trauma , Compression from neoplasm & aneurysm
 59. 20. Watch the attached video - Left parasternal heave 1. What does left parasternal heave
indicate ? 1 2. Mention any 2 causes of left parasternal heave. 2 3. Describe Grade 2 & Grade 3
left parasternal heave. 2
 60. Answers 1. Right ventricular hypertrophy 2. Pulmonary stenosis , Pulmonary
hypertension

Historical developments, trends, issues, cultural and NATIONAL

HEALTH POLICY ,SPECIAL LAWS RELATED TO OLDER
PEOPLE
 1. { Historical developments, Trends, Issues, Cultural or ethical issues in Medical Surgical
Nursing Submitted to: Dr. Pallavi Pathania (Assistant Professor of Medical Surgical Nursing)
Submitted by: Priyanka Thakur (MSc. Nursing 1st year) NATIONAL HEALTH POLICY ,SPECIAL
LAWS RELATED TO OLDER PEOPLE
 2.  Definition: Medical Surgical Nursing is a specialized branch of nursing that involve the
nursing care of adult patients, whose disease condition are treated medically, surgically and
pharmacologically.
 3.  In ancient times, when medical lore was associated with good or evil spirits, the sick were
usually cared for in temples and houses of worship.
 4.  These women had no real training by today’s standards, but experience taught them
valuable skills, especially in the use of herbs and drugs and some gained fame as the physicians
of their era.
 5.  In the 17th cent., St. Vincent De Paul began to encourage women to undertake some form of
training for their work, but their was no real hospital training school for nurse until one was
established in Kaiserwerth, Germany, in 1846.
 6.  There, Florence Nightingale received the training that later enabled her to establish, at St.
Thomas’s hospital in London the first school designed primarily to train nurses rather than to
provide nursing service for the hospital.
 7.  Similar schools were established in 1873 in New York City, New Haven (Conn.), and
Boston.  Nursing subsequently became one of the most important professions open to women
until the social changes brought by the revival of the feminist movement that began in the 1960’s.
 8.  During the late 19th and early 20th centuries in the US, adult patients in many of the larger
hospitals were typically assigned to separate medical, surgical and obstetrical wards.  Nursing
education in hospital training schools reflected these divisions to prepare nurses for work on
these units.
 9.  Early National League of Nursing Education (NLNE) curriculum guides treated medical
nursing, surgical nursing and disease prevention (incorporating personal hygiene and public
sanitation) as separate topics.
 10.  By the 1930s, however , advocates recommended that medical and surgical nursing be
taught in a single, interdisciplinary course, because the division of two was considered in an
artificial distinctions. Surgical nursing came to be seen as the care of medical patients who were
being treated surgically.
 11.  The NLNE’s 1937 guide called for a “Combined Course” of medical and surgical nursing. 
Students were expected to learn not only the theory and treatment of abnormal physiological
conditions, but also to provide total care of the patient by understanding the role of the health .
 12.  In1960’s, nursing schools emphasized the interdisciplinary study and the practice of
medical and surgical nursing.  1960s and 1970s, standards were developed for many nursing
specialties, including medical surgical nursing.
 13.  Standards, Medical- Surgical Nursing practices, written by committee of the division on
medical- surgical nursing of the American Nurses Association (ANA), was published in 1974.
 14.  It focused on the collection of data, development of nursing diagnoses and goals for
nursing, and development, implement of nursing diagnoses and goals for nursing, and
development and evaluation of plans of care.  A statement on the Scope of Medical- Surgical
Nursing Practice followed in 1980.
 15.  In 1991, the Academy of Medical Surgical Nurses (AMSN) was formed to provide an
independent specially professional organization for medical- surgical and adult health nurses.  In
1996, the AMSN published its own Scope and Standards of Medical- Surgical Nursing Practice.
 16.  The second edition appeared 2000. Both the ANA and AMSN documents stated that while
only clinical nurse specialists were expected to participate in research, all medical-surgical
nurses must incorporate research findings in practice.
 18.  A Trend is a change or development towards something new or different.
 19. 1. Education changes due to changes in demographics. 2. Embracing of technology. 3.
Advancements in communication and technology. 4. Working with more educated consumers. 5.
Increasing complexity of patient care.
 20. 6. Increased cost of health care. 7. Changes in federal and state regulation. 8.
Interdisciplinary skills. 9. Nurses working beyond retirement age. 10. Advances in nursing and
science research.
 21. Transitions taking place in health care: Curative Specialized care Medical diagnosis
Discipline stovepipes - Preventive approach - Primary health care - Patient emphasis -
Programme stovepipes
 22. Cont… Professional identity Trial and error practice Self-regulation Focus on quality -
Team identity - Evidence based practice - Questioning of professions - focus on costs
 23.  High tech  Competition  Need to supervise  Hierarchies
 24.  Humanistic  Cooperation  Caching, mentoring  Decentralized approach
 25. • Continued competencies • Hospital environment • Quality as excellence • Clear role •
Competencies a condition • Community environment • Quality as safe • Blurring roles
 27.  An issue is an important subject that people are arguing about or discussing.
 28. Confiden -tiality Family organisation Health beliefs Death and dying Communi- cation
cultural Diet and nutrition Ethical Patient care
 29.  Related to diet  Religion  Rituals  Refusal of medical procedures Health belief issues 
Black magic
 30.  Privacy  Personal information Family organization issues  Communication on behalf of
individual
 31.  Wrong medication  Malpractices Diet And Nutrition Issues  Poverty  Cultural myths
 32. Communication issues Cont…  Culture value modesty  Cared by female health providers
 Conflicts
 33. Standards of care Incompetence Negligence Liability: • Administrative • Civil • criminal
 34.  Unexpected death  Advance directives  Organ and tissue donation  Child abandonment
 35.  Beauchamp and Childress(2009) developed four principles: 1) Respect for Autonomy 2)
Beneficence 3) Non-maleficence 4) Justice
 36. RESPECT FOR AUTONOMY: Autonomy can be defined as…”self-rule with no control,
undue influence or interference from other”. BENEFICENCE: This can be defined as ”the
principle of the doing well and providing care to others” Promotion of well being.
 37.  Non –maleficence: 1. “Obligation not to inflict harm on others” 2. Goes hand in hand with
beneficence. Justice: 1. Simply defined as “equal treatment of equal cases” 2. Treating
everyone the same.
 38.  Fairness  Respect for autonomy  Integrity  Seeking the most beneficial and least
harmful consequences or results  Fidelity  Veracity
 39. Nursing shortage Health care reforms Low salaries Standard care
 40. Informed consent Assault and battery Invasion of privacy Report it/Tort it
 42. compassionately listen communicate identify acknowledge recognize
 43. involve document Up to date advice Look after yourself
 46. INTRODUCTION : A health policy generally describes fundamental principles regarding
which health providers are expected to make value decisions . “ Health policy provides a broad
framework of decisions for guiding health actions that are useful to its community in improving
their health, reducing the gap between the health status of haves and have not and ultimately
contributes to the quality of life.
 47.  The National Health Policy of 1983 and the National Health Policy of 2002 have served
well in guiding the approach for the health sector in Five – Year Plans . Now 14 years after the
last health policy, a new is introduced.  The primary aim of the National Health Policy , 2017 is
to inform, clarify ,strengthen the role of the Government in shaping health systems in all its
dimensions .
 48.  Health priorities are changing , there is growing burden on account of non- communicable
diseases and some infectious diseases .  A rising economic growth enables enhanced fiscal
capacity. Therefore , a new health policy responsive to these contextual changes is required .
 49.  The emergence of a robust health care industry estimated to be growing at double digit . 
Growing incidences of catastrophic expenditure due to health care costs, which are presently
estimated to be one of the major contributors to poverty .
 50. Improve health status concerted policy actions in all sectors and expand preventive,
promotive, curative , palliative and rehabilitative services provided through the public health
sector with focus on quality. Objectives are outlined under three broad components :-
 51.  Health status and Programme Impact  Health systems Performance  Health System
Strengthening
 52. Life expectancy and healthy life a. Increase life Expectancy at birth from 67.5 to 70 by 2025
b. Establish regular tracking of Disability Adjusted Life Years (DALY) Index as a measure of
burden od disease .
 53. Mortality by age and/ or cause a. Reduce infant mortality rate to 28 by 2019 b. Reduce
Under Five Mortality to 23 by 2025 and MMR from current levels to 100 by 2020 .
 54. Coverage of Health Services a. More than 90% of the new born are fully immunized by one
year of age by 2025 b. 80% of known hypertensive and diabetic individuals at household level
maintain ‘controlled disease status’ by 2025
 55. Health finance a. Increase State sector health spending to >8% of their budget by 2020 b.
Increase health expenditure by government as a percentage of GDP from the existing 1.15% to
2.5 by 2025.
 56. Health Management Information a. Ensure district – level electronic database of
information on health system components by 2020 b. Strengthen the health surveillance system
and establish registers for diseases of public health importance by 2020
 57. Cross Sectional objectives related to Health a. National/State level tracking of selected
health behaviour . b. Access to safe water and sanitation to all by 2020( Swatch Bharat Mission)
 58. 1. Professionalism, Integrity and Ethics The health policy commits itself to the highest
professional standards, integrity and ethics to be maintained in the entire system of health care
delivery in the country, supported by a credible, transparent and responsible regulatory
environment .
 59.  Reducing inequity would mean affirmative action to reach the protest.  It would mean
minimizing disparity on account of gender, poverty, caste , disability , other forms of social
 exclusion and geographical barriers.  It would imply greater investments and financial protection
for the poor who suffer the largest burden of disease.
 60. As costs of care increases, affordability, as district from equity , requires emphasis.
Catastrophic household health care expenditures exceeding defined as health expenditure
exceeding 10% of its total monthly consumption expenditure or40% of its monthly non- food
consumption expenditure ,are unacceptable .
 61.  Prevention of exclusions on social, economic or on grounds of current health status. In this
backdrop , systems and services are envisaged to be designed to cater to the entire population –
including special groups.
 62. Financial and performance accountability , transparency in decision making , and
elimination of corruption in health care systems , both in public and private .
 63. Decentralization of decision making to a level as is consistent with practical considerations
and institutional capacity . Community participation in health planning processes , to be promoted
side by side .
 64. Constantly improving dynamic organization of health care based on new knowledge and
evidence with learning from the communities and from national and international knowledge
partners is designed .
 65.  Increase Life Expectancy from 67.5 to 70 by 2025 .  Establish regular tracking of Disability
Adjusted Life Years (DALY) Index as a measure of burden of disease by 2022 .  Reduction of
TFR to 2.1 at national and sub- national level by 2025 .  Reduction Under Five Mortality to 23 by
2025 and MMR from current levels to 100 by 2020 .
 66.  Reduce infant mortality rate to 28 by 2019 .  Reduce neo- natal mortality to 16 and still
birth rate to ‘single digit’ by 2025.  Achieve and maintain elimination status of Leprosy by 2018. 
Kala-Azar by 2017 and lymphatic Filariasis in endemic pockets by 2017.
 67.  Achieve global target of 2020 which is also termed as target of 90:90:90, for HIV AIDS. 
To achieve and maintain a cure rate of >85% in new sputum positive patients for TB and reduce
incidence of new cases, to reach elimination status by 2025.
 68.  To reduce the prevalence of blindness to 0.251000 by 2025.  To reduce premature
mortality from cardiovascular diseases, cancer, diabetes or chronic respiratory diseases by 25%
by 2025.  Increase utilization of public health facilities by 50% from current levels by 2025.
 69.  Ante-natal care coverage to be sustained above 90% and skilled attendance at birth above
90% by 2025.  More than 90% of the newborn are fully immunized by 1 year of age by 2025.
 70.  80% of known hypertensive and diabetic individuals at household level maintain ‘controlled
disease status by 2025.  Meet need of family planning above 90% at national and sub national
level by 2025.
 71.  Relative reduction in prevalence of current tobacco use by 15% by 2020 and 30% by2025.
 40% reduction in prevalence of stunting of under-5 children by 2025.
 72.  Safe water and sanitation to all by 2020 (Swachh Bharat Mission).  Reduction of
occupational injury by half from current levels of 334 per lakh agricultural workers by 2020.
 73.  Increase health expenditure by Government from the existing 1.15% (GDP) to 2.5% (GDP)
by 2025.  Increase state sector health spending to >8% of their budget by 2020.
 74.  Decrease in proportion of household facing catastrophic health expenditure from the
current levels by 25%, by 2025.  Ensure availability of paramedics and doctors as per IPHS
norm in high priority districts by 2020.
 75.  Establish primary and secondary care facility in high priority districts by 2025.  Ensure
district-level electronic database of information on health system components by 2020.
 76.  Strengthen the health surveillance system by 2020.  Establish federated integrated health
information architecture, Health Information Exchanges and National Health Information Network
by 2025.
 77.  Establish federated integrated health information architecture, Health Information
Exchanges and National Health Information Network by 2025.
 78. 1.The Swachh Bharat Abhiyan. 2.Balanced, healthy diets and regular exercises.
3.Addressing tobacco, alcohol and substance abuse. 4.Yatri Suraksha - preventing deaths due to
rail and road traffic accidents.
 79. 5.Nirbhaya Nari action gender violence. 6.Reduced stress and improved safety in the work
place. 7.Reducing indoor and outdoor air pollution.
 80. The 7 key policy shifts in organizing health care services are: 1. In primary care from
selective care to assured comprehensive care with linkages to referral hospitals. 2. In secondary
and tertiary care from an input oriented to an output based strategic purchasing .
 81. 3. In infrastructure and human resource from normative approach to targeted approach to
reach under-serviced area. 4. In public hospitals from user fees at cost recovery to assured free
drugs , diagnostic and emergency services to all.
 82. 5. In urban health from token interventions to on-scale assured interventions, to organize
Primary Health Care delivery and referral support for urban poor. Collaboration with other sectors
to address wider determinants of urban health is advocated.
 83. 6. In national health programmes integration with health systems for programme
effectiveness and intern contributing to strengthening of health systems for efficiency . 7. In
AYUSH services from stand alone to a 3 dimensional mainstreaming.
 84. 1. RMNCH + A services 2. Child and Adolescent Health 3. Universal immunisation 4.
Communicable diseases 5. Mental health 6. Non communicable diseases 7. Population
stabilization
 85.  This policy aspires to elicit developmental action of all sectors to support Maternal and
Child survival. The policy strongly recommends strengthening of general health system to
prevent and manage maternal complications, to ensure continuity of care and emergency
services for maternal health.
 86.  The policy endorses the national consensus on accelerated achievement of neonatal
mortality targets and ‘ single digit ’ stillbirth rates through improved home based and facility
based management of sick new borns .  School health programmes as a major focus area ,
health and hygiene being a part of the school curriculam
 87.  It emphasis to the health challenges of adolescents and long term potential of investing in
their health care.
 88.  Priority would be to improve immunization coverage with quality and safety, improve
vaccine security as per National Vaccine Policy 2011 and introduction of newer vaccines based
on epidemiological considerations. The focus will be to build upon the success of Mission
Indradhanush and strengthen it .
 89.  The policy recognizes the interrelationship between communicable disease control
programmes and public health system strengthening .  It advocates the need for districts to
respond to the communicable disease priorities of their locality .
 90.  The policy acknowledges HIV and TB co infection and increased incidence of drug
resistant tuberculosis as key challenges in control of Tuberculosis .
 92.  An integrated approach for screening the most prevalent NCDs with secondary prevention
would make a significant impact on reduction of morbidity and preventable mortality with
incorporation into the comprehensive primary health care network with linkages to specialist
consultations and follow up at the primary level .
 93.  Screening for oral, breast and cervical cancer and Chronic Obstructive Pulmonary
Disease will be focused in addition to hypertension and diabetes .
 94. This policy will take action on the following fronts :  Increase creation of specialists
through public financing and develop special rules to give preference to those willing to work in
public systems .
 95.  Create network of community members to provide psycho-social support to strengthen
mental health services at primary level facilities.
 96.  Policy imperative is to move away from camp based services to a situation where these
services are available on any day of the week .  And to increase the proportion of male
sterilization from less than 5% to at least 30% and if possible much higher .
 97. While the public health initiates over the years have contributed significantly to the
improvement of the health indicators, it to be acknowledged that public health indicators /
disease burden statistics are the outcome of several complementary initiatives under the wider
umbrella of the development sector, covering rural development, agriculture, food production ,
sanitation , drinking water supply, education etc.
 99.  Throughout the world , large number of older people face challenges such as
discrimination , poverty and abuse that severely restrict their human rights and their contribution
to society .  Although concerns involving the ageing population are not new, they have
traditionally been seen as problems requiring solutions that are functional and reactive .
 100.  The rights of older people are the entitlements claimed for senior citizens . Elderly rights
are one of the fundamental rights of India .  The International Day of older persons is celebrated
annually on October 1 .  The 2001 census of India demonstrated that aged people in India have
crossed over 100 million .
 101. The NPOP in India has been formulated as a forward – looking vision of the government for
improving quality of life of older people in India through i. Increased income security, ii. Health
and Nutrition ,
 102. iii. Shelter, iv. Education, empowerment and welfare .
 103. 1. To encourage individuals to make various provisions such as health and social
insurance for their own as well as their spouse`s old age. 2. To encourage families to take care
of their older family members .
 104. 3. To enable and support voluntary and non-governmental organizations to supplement the
cate provided by the family, with greater emphasis on non institutional care . 4. To provide care
and protection to the vulnerable elder especially widows, physically, challenged, abused and
destitute elderly .
 105. 5. To provide health care facilities specially suited to elderly . 6. To promote research and
training to train geriatric care givers and organisers of services for the elderly.
 106. 7. To facilitate and strengthen inter sectoral partnerships in the field and 8. To create
awareness regarding elder persons to develop themselves into fully independent citizens .
 107. 1.Financial Security :  Pension scheme ( in public and private sector)  Lower income
tax rate and exemptions .
 108. 2. Health care and Nutrition :  Setting up Geriatric wards and training on Geriatric
Specialized care  Expanding Mental Health Services for elderly .
 109. 3. Shelter :  Government and Private Housing Schemes for elderly .  Disposal of cases
relating to property transfer, mutation of property and tax .
 110. 4. Education  Information to elderly about Concept of wellness in old age  Evolving
changes in lifestyle and living style .
 111.  Identifying extremely vulnerable elderly who are disabled, chronically sick and destitute .
 Assistance to voluntary organisations to construct and maintain old age homes, day care
centre , multi – services citizens centres, supply of disability – related aids and appliances .
 112. 6. Research and Training :  Encourage medical colleges, training institutions for Nurses
and Para medical institutes to introduce COURSES ON GERIATRIC CARE.
 113.  Research and Documentation in elderly care  NGO supported specialized training in
Geriatric care. 7. Sensitizing the Media :  Involvement of social medias and internet to create
awareness .
 114. 1. Pradhan Mantri Suraksha Bima Yogana : 2015 All savings bank account holders 18 – 70
years old can join the scheme. It offers a coverage of rupees 200,000 for death or total and
irrevocable loss of both eyes and rupees 100,000 coverage for the loss of an eye .
 116.  The government started the Swavalamban Scheme in 2010/11 which was replaced by
the Atal Pension Yojana (APY) in June 2015 for those persons engaged in the unorganized
sector , who are not members of any statutory social security scheme .
 118.  Low premium life insurance (Pradhan Mantri Jeevan Jyoti Bima Yojana)  General
insurance (Pradhan Mantri Suraksha Bima Yojana) .  The pension plan (Atal Pension Yojana).
It is proposed to link this to the accounts .
 120.  This scheme is a part of the government`s commitment to financial inclusion and social
security during old age and to protect those aged 60 years and above against a future fall in their
interest income due to uncertain market conditions. The scheme will be implemented through LIC
.
 124. How the Money is Used
 125. A regional body South Asia Senior Citizens`s Working Group aims to work closely with the
respective governments, NGOs and civil society members of the region in order to improve the
well –being of the ageing population .
 129.  The policy should emphasise the need for expansion of social and community services
for older persons , particularly vulnerable women group to get accessible to the user friendly
client oriented services.
 130.  Special efforts will be made to implement the policy at the rural populations and
unorganised sectors where most of the older population lives .

2. TRENDS AND ISSUES IN MEDICAL-SURGICAL NURSING 2
 3. WHAT DO YOU MEAN BY ISSUES? 3
 4. WHAT DO YOU MEAN BY TRENDS? 4
 5. INTRODUCTION Nursing has been called the oldest of the art, and the youngest of the
profession. As such, it has gone through many stages and has been an integral part of social
movements. Nursing has been involved in in the existing culture, shaped by it and yet beeping to
develop it. The trend analysis and future scenarios provide a basis for sound decision making
through mapping of possible futures and aiming to create preferred futures. 5
 6. The world health organization (who) has been considering the future and predicts that by
2000 the world experiences:  Major growth in the elderly population  Decline in birth rate,
especially in western counteries  Increase in chronic illness  Continuing social unrest  AIDS a
major problem  Many infectious diseases under control  Mental health a key issue  Poverty
continuing to plague mach of the world 6
 7. TRENDS IN NURSING: 1. Education changes due to changes in demographics 2. Embracing
of technology 3. Advancements in communication and technology 4. Working with more
educated consumers 5. Increasing complexity of patient care 7
 8. TRENDS IN NURSING(continue): 6. Increased cost of health care 7. Changes in federal and
state regulation 8. Interdisciplinary skills 9. Nurses working beyond retirement age 10. Advances
in nursing and science research. 8
 9. TRANSITIONS TAKING PLACE IN HEALTH CARE:  Curative - Preventive approach 
Specialized care - Primary health care  Medical diagnosis - Patient emphasis  Discipline
stovepipes - Programme stovepipes  Professional identity - Team identity  Trial and error -
Evidence based practice  Self – regulation - Questioning of professions  Focus on quality -
Focus on costs 9
 10. IN THE WORKPLACE:  High tech - Humanistic  Competition - Cooperation  Need to
supervise - Caching, mentoring  Hierarchies - Decentralized approach 10
 11. IN NURSING  Continued competencies - Competencies a condition  Hospital environment
- Community environment  Quality as excellence - Quality as safe  Clear role - Blurring roles 11

4. ETHICAL PRINCIPLES IN NURSING CARE • Religious Issues • Communication Issues •
Family Organization Issues • Ethical Issues
 5. MAJOR TRENDS IN MEDICAL SURGICAL NURSING • Quantification of nursing care costs •
Reduced length of stay • Increasing reliance on high technology • Requirement for advanced
nursing knowledge. • Innovations in care planning through computerization.
 6. SIGNIFICANCE OF CULTURE IN NURSING • DEFINITION OF CULTURE: • Culture
represents a unique way of perceiving, behaving and evaluating the external environment and
such provides a blue print for determining values beliefs and practices (Boyle, 2003)
 7. CULTURAL VALUES Cultural values are unique expressions of a particular culture that have
been accepted as appropriate over time. They guide actions and decisions making that facilitate
self worth and self esteem (LEININGER, 1985)
 9. INDIAN CULTURE • Religion • Language • Family Structure • Health Beliefs • Death And
Dying • Cultural Beliefs
 11. ETHICAL ISSUES IN NURSING PRACTICE • Clinical • Professional • Philosophical •
Organisational and societal
 13. CONCLUSION • Rapid changes in the health care environment, with continuous
technological advancements, increasing severity of illness, budget constraints, and expanding
nursing knowledge, have greatly increased the responsibilities, facing today’s nurses. To fulfil
these responsibilities, planning and documentation of care are essential to satisfy patient needs
and meet legal obligations. Documentation of the impact of nursing on patient care also provides
information for continuing care needs, legal concerns, and payments.
 14. BIBLIOGRAPHY • NANCY.M.HOLLOWAY “MEDICAL SURGICAL CARE PLANNING” 4TH
EDITION, LIPPINCOTT PUBLICATIONS PAGE NO: 2-5. • USHA RAVINDRAN “TEXT BOOK
OF MEDICAL SURGICAL” JAYPEE PUBLICATIONS PAGE NO: 14-15. • PRISCILLA LEMONE,
KAREN BRUKE “MEDICAL SURGICAL NURSING CRITICAL THINKING IN CLIENT CARE”
PAGE NO:8 • LYNDA JUALL CARPENITO {2004} “NURSING CARE PLANS AND
DOCUMENTATION” 4TH EDITION PUBLISHED BY LIPPINCOTT WILLIAMS AND WILKINS.
 15. CONT... • GAYLE ROUX, ET.AL “ISSUES AND TRENDS IN NURSING: ESSENTIAL
KNOWLEDGE FOR TODAY AND TOMMOROW” JONES AND BARTLETT PUBLISHERS PAGE
NO:14-16 • BARBARA CHERRY, SUSAN R JACOB “CONTEMPORARY NURSING, ISSUES,
TRENDS AND MANAGEMENT” 6TH EDITION ELSEVIER PUBLICATIONS PAGE NO:5-8 •
PERLE SALVIK COWEN SUE MOORHEAD “CURRENT ISSUES IN NURSING” 8TH EDITION
MOSBY ELSEVIER PUBLICATIONS PSGE NO:23-25 • BRUNNER AND SUDDARTH “TEXT
BOOK OF MEDICAL SURGICAL NURSING” VOLUME 1 12TH EDITION, LIPPINCOTT
WILLIAMS AND WILKINS PUBLICATIONS, PAGE NO: 25-26

Trends and issues in medical surgical nursing

 1. College Of Nursing Madras Medical College Chennai-03 TRENDS AND ISSUES IN
MEDICAL- SURGICAL NURSING PRESENTED BY EDWIN JOSE.L MSc(nursing) I YEAR
College of nursing Madras medical college Chennai-03 EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 2. INTRODUCTION  The entire field of health care is changing day by day.  These changes
occurs at rapid rate.  The focus of medical –surgical nursing is not limited to a disease or a
body system but focus on holistic in nature.  Medical –surgical nursing is a speciality of nursing
that requires a specific skills such as analytical, technical,administrative and organizational skills.
 According to academy of medical –surgical nurses, it is evolving as a speciality and is the
largest group of practicing professional. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 3. DEFINITIONS Trend: A general direction in which a situation is changing or developing. -
Oxford Advanced Learners Dictionary Issues: An important topic that people are discussing. A
problem or worry that somebody has with some thing EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 4. TRENDS IN MEDICAL SURGICAL NURSING Quantification of nursing care costs
Reduced length of stay Increasing Reliance On High Technology Requirement of advanced
nursing knowledge Need for collaboration and communication Innovation in care planning
through computerization Unification of practice and education EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021
 5. TRENDS IN MEDICAL SURGICAL NURSING  Greater investment in research and
development  Role blurring and shared competencies  New areas of nursing specialization 
Nursing seen as a cost effective approach to health  Telenursing  Robotic nursing 
Aerospace nursing  Community based nursing EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 6. Quantification of nursing costs • Quantification of nursing contribution to patient care can be
used to determine the cost of providing care to specific patients • Quantifying nursing time
requires the identification of the level of nursing care necessary for each patient. • The patient
care plan is an integral part of the justification of nursing care costs EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021
 7. Reduced length of stay The provision of personalized care must be planned and provided
with continuity as the quality of care time decreases. Many patients who leave the hospital
earlier are still need of health care. Aggressive discharge planning must begin on admission.
An effective coordinated plan of care can help ensure continuity of care. EDWIN JOSE L
MEDICAL SURGICAL NURSING 15.02.2021
 8. Increase reliance on high technology The evolving technological advances in nursing are the
wave of the future in healthcare. Emerging new technologies in EHRs, AI, apps and software
development are becoming increasingly popular as more hospitals and facilities integrate them
into their health system. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 9. Requirement of advanced nursing knowledge • The medical –surgical nurse needs greater
clinical expertise, maturity, clinical thinking ability, assertiveness and patient management skills
to handle patients. • Certification acknowledges the nurses attaintment of predetermined
standards established by the certifying groups. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 10. NEED FOR COLLABORATION AND COMMUNICATION • The health care delivery
becomes more complex and economically centered that need communication and collaboration
 among health care professionals. • Only through collaboration between departments, services,
and facilities the nursing care can be delivered effectively. EDWIN JOSE L MEDICAL
SURGICAL NURSING 15.02.2021
 11. Innovation in planning care through computerisation  Nurses believe that their better time
can be spend at the bedside giving patient care rather than filling out paperwork  Studies shows
that institutions using computers reports increases number of plan of care being generated
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 12. Unification of practice and education The Unification Model directs nursing education,
research, and practice. Unification is not only a philosophical approach but also an organizational
structure that operationalizes the interdependence among education, research and practice.
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 13. Greater investments and developments In the recent years the budget allocation for nursing
research has been increased in the view of increasing the quality of nursing care EDWIN JOSE L
MEDICAL SURGICAL NURSING 15.02.2021
 14. Role blurring and shared competencies • Nowadays the role of nurses is not clearly defined
• The work of nurses are shared with other departments EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 15. Nursing –cost effective approach  The nursing procedures we are doing are evidenced
based and cost effective whwn compare to medical treatment and procedures. EDWIN JOSE L
MEDICAL SURGICAL NURSING 15.02.2021
 16. telenursing Tele nursing or telehealth nursing uses technologies to provide nursing
services through computers and mobile devices It allows patients to connect with their nurses
through mobiles devices,computers,applications etc….. EDWIN JOSE L MEDICAL SURGICAL
NURSING 15.02.2021
 17. Robotic nursing Robots are used in nursing for monitoring elderly patient via video ,helps
in positioning,feeding,shifting etc….. EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 18. Community based nursing The health care delivery concept is now changing from hospital
centered to community based nursing EDWIN JOSE L MEDICAL SURGICAL NURSING
15.02.2021
 19. Issues in medical surgical nursing  Staff shortage  Meeting patients expectations  Long
work hours  Workplace violence  Workplace hazards  Scope of practice  Personal health
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 20. Staff shortages The world health organization estimates that there will be shortage of 1.1
million nurses throught out the world. This may cause disturbances in health care system
EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 21. Meeting the patients expectations Due to advanced technology and awareness, the
patients expectation are not met. This causes job dissatisfaction among nurses. EDWIN JOSE
L MEDICAL SURGICAL NURSING 15.02.2021
 22. Long work hours Shortage of nurses forces the nurses to work for long hours which causes
physical and mental disturbances EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 23. Workplace hazards Needle stick injuries,sharp tools, and heavy equipments may risk the
nurses health and life. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 24. Scope of practice  The scope of practice for nurses makes nurses to work in a defined
area of practice.  Till now there is no prescribed scope of practice for nurses in India. EDWIN
JOSE L MEDICAL SURGICAL NURSING 15.02.2021
 25. Personal health Working in a stressfull health care system causes physical and mental
disequilibrium. EDWIN JOSE L MEDICAL SURGICAL NURSING 15.02.2021


3. UNIT OUTLINE Review of Anatomy and Physiology of Endocrine System Nursing
Assessment—History and Physical Assessment ™ Diabetes Mellitus ™ Disorders of Thyroid
and Parathyroid, Adrenal and Pituitary ™ (Hyper, Hypo, Tumors)

 4. • The endocrine system is consisting of glands, its manifest and release hormones,
chemical substances in the human body. It controls the function of human cells or organs. •
 The pituitary, thyroid, parathyroid, adrenal, pineal and thymus glands, the pancreas, and the
gonads are major endocrine organs in the human body

 5. Function of Endocrine System • It is controls water balance through regulating the solute
absorption of the blood. • It regulates the growth of bone and muscle tissues. • It regulates
bone and muscles metabolism of tissues • It helps to maintain the normal body temperature
and normal mental functions. • Its aids to maturation of tissues, it seems in the growth of
adult features and adult behavior. • Its supports to managing the heart rate and blood
pressure.

 6. CONTI…. • It aids in formulating the body for physical gesture. • Its helps control the
immune cell’s function and production. • It normalizes the males and females’ reproductive
systems development and the functions. • Its maintain the contractions of uterus during the
delivery of the newborn and during lactation period stimulates milk release from the
breasts. • It stabilizes Na+, K+, and Ca2+ absorptions in the blood.

 7. Endocrine glands.

 8. DIABETES MELLITUS (DM) • Diabetes mellitus is a chronic multi-system involved disease.

‘Siphon’ is a Greek word. • It means that made lot is urine, ‘Diabetes’ comes from the Greek
word. ‘Mellitus’ is derived from the Latin word. ‘Mel’ implies that ‘honey’ indicates that
urine is sweet. • Worldwide, diabetes is one of the significant health issues. Its prevalence
keeps on increasing rapidly in the world.

 9. Classification of DM Type 1 diabetes: It occurs due to the destruction of Β-cell. Insulin

production is deficient, and it leads to absolute insulin deficiency. Type 2 diabetes occurs
due to insulin resistance with relative insulin deficiency, and mainly an insulin secretory
defect with insulin resistance. Gestational diabetes mellitus (GDM): Gestational diabetes
mellitus occurs when pregnant women start glucose intolerance diagnosed as diabetes
during pregnancy. It is caused by insulin receptor dysfunction during pregnancy due to the
human placental lactogeninhibition of vulnerable insulin receptors, preventing insulin
uptakes.

 10. Mechanism of insulin and glucose.

 11. • Type 1 and type 2 diabetes common clinical feature is inadequacies of insulin. Absolute
insulin deficiency causes Type 1 diabetes. It occurs due to the entire destruction of the beta-
cell. Insulin resistance and beta-cell dysfunction cause Type 2 diabetes. • Generally, the
pancreas secretes 40–50 units of insulin per day or 0.6 units per kilogram of body weight in
two steps: (i) Basal insulin secretion—secreted at low levels during fasting, a (ii) Prandial—
increased levels after eating. A primary flow of insulin occurs within 10 minutes of eating.

 12. Pathophysiology of type 2 diabetes mellitus.

 13. Etiology and Risk Factors of DM • Inactivity • Race • Hypertension • Stress • Age •
Pregnancy • High cholesterol • Obesity • History of CVD • Familial history—first-degree
relative history —10 times high-risk • Polycystic ovary syndrome • Gestational diabetes

 14. Clinical Manifestations

 15. Differences between type 1 and type 2 DM.

 16. CONTI…
 18. CONTI….

 19. Pathophysiology of diabetic heart failure.

 20. Management of DM

 21. Step-wise management of type 2 diabetes.

 22. Classes of oral hypoglycemic agents: • Sulfonylureas (glipalamide) increase insulin

secretion by beta- cells. • Meglitinides (repaglinide) increase insulin secretion by pancreatic
beta-cells—to target insulin secretion. • Biguanides (metformin) inhibit glucose production
by the liver. • Thiazolidinediones (rosiglitazone) increase glucose uptakes by skeletal muscle
—to target insulin resistance. • Alpha-glucosidase inhibitors (acarbose) target glucose
absorption from the intestine.

 23. Complication s of Diabetes Mellitus.

 24. CONTI….

 25. Hypoglycemia • Hypoglycemia is extreme low glucose in the blood. It is highly

associated with the diabetes treatment. Causes of Hypoglycemia • People with diabetes may
not make enough insulin or may be less responsive to it • Taking someone else’s oral
diabetes medication accidentally • Insulin overproduction due to tumor of the pancreas •
Quinine—malaria drug, heavy doses of salicylates, propranolol are triggering hypoglycemia

 26. CONTI…. • High intake of alcohol can cause the liver to stop discharging stored glucose
into the bloodstream • Drug-induced hepatitis can cause hypoglycaemia • Kidney disorders
because of problems to eliminate waste medications, follow-on in hypoglycaemia • Eating
disorders, like anorexia nervosa cause hypoglycaemia • Pancreatic tumor, trigger pancreas
to produce excess insulin • Vigorous physical activity can lead hypoglycaemia

 27. Signs and symptoms of hypoglycem ia.

 28. Management of Hypoglycaemia • Treat the hypoglycemia with “15–15 Rule”—it means
15 g of carbohydrate to raise blood glucose and check blood glucose level after 15 minutes.
• It the blood glucose level is still below 70 mg/dL give another serving.

 29. GOITER • Goiter is the enlargement of the thyroid gland. Iodine deficiency causes goiter,
which has three types: simple, toxic, and exophthalmic. The normal thyroid gland is not
palpable. • It visibly appears quite prominent in goiter.

 30. Causes • Iodine deficiency • Dyshormonogenesis • Goitrogens Clinical Manifestations of

Goiter • Airway obstruction • Compression of laryngeal nerve • Obstruction of esophageal •
Obstruction in the neck veins • Superior vena cava syndrome

 31. There are three types of simple goiter: 1. Colloid goiter—this type is prominent in areas
where the drinking water is deficient in iodine. • In order to produce normal levels of the
hormone, the gland becomes hypertrophied. • The follicles in the body are filled with
colloids. Consuming iodinated salt can help prevent this condition.

 32. CONTI…. 2. Diffuse parenchymatous goiter—the follicular epithelial cells show

hypertrophy and multiply in number due to which the lumen of the follicle becomes
obliterated. 3. Nodular goiter—nodules in the thyroid gland are the hallmark of this
particular thyroid disorder. A distinct elevation of T3 with less elevation of T4 level causes it.
  33. Management of Goitre • Supply iodine supplements in iodine-deficient areas; food
iodine fortification is one of the best prevention measures for goiters. • Thyroxin
supplementation: In patients with diffuse hyperplastic goiter for several months (0.1 to 0.2
mg daily).

 34. PITUITARY TUMOR • The pituitary gland is oval in shape, measuring 8 mm Antero
posteriorly and 12 mm transversely. • Its weight is around 600 mg, and it is situated in Sella
turcica ventral to diaphragm Sella. • It comprises anatomically and functionally distinct
anterior and posterior lobes.

 35. CONTI…. • The anterior pituitary gland produces seven major hormones: (i) Prolactin
(PRH) (ii) growth hormone (GH), (iii) adrenocorticotropin hormone (ACTH), (iv) luteinizing
hormone (LH), (v) follicle-stimulating hormone (FSH), (vi) thyroid stimulating hormone (TSH),
(vii) antidiuretic hormones (ADH).

 36. Mechanism of pituitary incidentaloma.

 37. Diagnostic Evaluations • Visual field test to study the visual changes • MRI—shows
better visualization of soft tissues and vascular structures than CT • CT scan—shows better
visualization of bony structures and calcifications within soft tissues. It is useful when MRI is
contraindicated, like when the patients have pacemakers or metallic implants. • Hormonal
evaluation: All pituitary tumours screened based on basal hormone levels like prolactin, TSH,
FT4, ACTH, AM cortisol, midnight salivary cortisol, LH, FSH, oestradiol or testosterone,
insulin-like growth factors-1

 38. Medical management: An oral dopamine agonist can prescribed for patients with micro
or macro prolactinomas. 1 Dopamine agonists suppress PRL secretion and synthesis and
lactotroph cell proliferation. 2 Drugs cabergoline-0.5 to 1 mg twice weekly, bromocriptine-
2.5 mg thrice daily, pergolide mesylate, and Lisuride are available. 3

 39. Home Care Guidelines • Instruct the patient not to stop corticosteroids abruptly and
without medical supervision because the syndrome reappears again due to lack of
corticosteroid medication • Ensure adequate calcium intake without raising the risk of
hypertension, hyperglycemia, and weight gain • Monitor blood pressure, blood glucose
levels, and weight

 40. Case Scenario • A 45-year-old female was admitted to the emergency room complaining
of thirst, excessive urination, more than 4kg weight loss in seven weeks, and no other
relevant history. • Her cousin has diabetes and is on insulin, on no regular medications, and
is a thin woman. Her blood sugar level is 240 mg. What is her diagnosis?

 41. Diabetes • A 40-year-old woman is concerned she may have diabetes. She had diabetes
during her last pregnancy, which was managed with diet. • Lately, she has been feeling tired
but otherwise has no complaints. Her mother had diabetes; she has been overweight since
her last pregnancy and has taken a tablet for blood pressure for the last 2 years. • She is
obese, and her blood pressure is 140/90 mm Hg; otherwise, her examination is regular. She
undergoes testing, and her fasting glucose is 180 mg/dL. What is her diagnosis? Ans:
 :- STUDENTS SHOULD KNOW ABOUT THE ANTICANCER DRUGES
 3. SPECIFIC OBJECTIVES • EXPLAIN ABOUT ANTICANCER DRUGS • DESCRIBE THE
DEVELOPMENT OF CANCER • EXPLAIN ABOUT MACHNISM OF CANCER • ENLIST THE
INDICATION AND CONTRAINDICATION
 4. ANTICANCER DRUGES •CANCER IS ONE OF THE LEADING CAUSES OF THE DEATH IN
THE WORLD IN INDIAALSO •CANCER ARISE FROM A SINGLE ABNORMAL CELL THAT
MULTIPLIES AND GROWS PROGRESSIVELY ABNORMAL •IT ALSO DAMAGING
SURROUNDING HEALTHY TISSUE. •THIS CANCER CELLS INTRUDE THE NORMAL CELLS
LEADING TO LOSS OF NORMAL CELLULAR FUNCTION.
 5. •AIM AND MODALITIES OF TREATMENT OF CANCER DEPENDS ON THE STAGE AT
WHICH THE DISEASE HAS BEEN DIAGNOSED . •ANTICANCER DRUGS IN COMBINATION
WITH SURGERY RADIOTHERAPY OR IMMUNOTHERAPY
 6. DEVELOPMENT OF CANCER •PRIMARY TUMOR •GROWS AND INVADES
SURROUNDING TISSUE •MOVES INTO BASEMENT MEMBRANE OF CAPILLARIES
SURROUNDING THE TUMOR •ENTERS THE BLOOD STREAM AND LYMPHATIC'S •LEAVES
THE BLOOD LYMPHATIC VESSELS THROUGH CAPILLARY WALLS •PROLIFERATES AT
THIS NEW SITE GROWS AND INVADES SURROUNDING TISSUE
 7. MECHANISM OF THE ACTION OF ANTICANCER DRUGS • ANTICANCER DRUGS ARE
TRADITIONALLY CLASSIFIED EITHER BY THEIR MECHANISM OF ACTION OR BY THEIR
ORIGINS. • ALKYLATING AGENTS ARE REACTIVE TO DNA AND CELLULAR PROTEINS
AND INHIBITING REPLICATION OF DNAAND TRANSCRIPTION OF RNA. • CHEMOTHERAPY
DAMAGES THE GENES INSIDE THE NUCLEUS OF CELLS • SOME DRUGS DAMAGE THE
CELLS AT THE POINT OF SPLITTING
 8. INDICATION • CHEMOTHERAPY IS AN AGGRESSIVE FORM OF CHEMICAL DRUGS
THERAPY MEANS TO DESTROY RAPIDLY GROWING CELLS IN THE BODY • ITS USED TO
TREAT CANCER AS CANCER CELLS GROW AND DIVIDE FASTER THAN OTHER CELLS •
KILL THE HIDDEN CANCER CELLS .
 9. CONTRAINDICATION • A CONTRAINDICATION IS A SPECIFIC SITUATION IN WHICH A
DRUG, PROCEDURE, OR SURGERY SHOULD NOT BE USED BECAUSE IT MAY BE
HARMFUL TO THE PERSON • A HIGH FEVER • BLEEDING • BRUISING • RASH • ALLERGIC
REACTION EX. SWELLING OF MOUTH OR THROAT • SEVER ITCHING • TROUBLE
SWALLOWING
 10. COMMON SIDE EFFECTS OF CHEMO • FATIGUE • HAIR LOSS • EASY BRUISING AND
BLEEDING • INFECTION • ANEMIA (LOW RED BLOOD CELL COUNTS) • NAUSEAAND
VOMITING • APPETITE CHANGES • CONSTIPATION • DIARRHEA
 11. • MOUTH, TONGUE, AND THROAT PROBLEMS SUCH AS SORES AND PAIN WITH
SWALLOWING • PERIPHERAL NEUROPATHY OR OTHER NERVE PROBLEMS, SUCH AS
NUMBNESS, TINGLING, AND PAIN • SKIN AND NAIL CHANGES SUCH AS DRY SKIN AND
COLOR CHANGE • URINE AND BLADDER CHANGES AND KIDNEY • WEIGHT LOSS •
MOOD CHANGES • CHANGES IN LIBIDO AND SEXUAL FUNCTION • FERTILITY PROBLEMS
 12. ROLE OF NURSE • THE NURSE IS RESPONSIBLE FOR THE SAFE. • APPROPRIATE
ADMINISTRATION OF CANCER THERAPY • MEDICATIONS (CHEMOTHERAPY,
BIOLOGICAL THERAPY, TARGETED THERAPY • ASSOCIATED SUPPORTIVE
MEDICATIONS) IN ACCORDANCE WITH REQUIREMENTS, NATIONAL STANDARDS AND
LOCAL
 13. • ONCOLOGY NURSES ARE HEALTHCARE PROFESSIONALS WHO ARE SPECIALLY
TRAINED TO ADMINISTER CHEMOTHERAPY AND RADIATION TREATMENTS. • THEY ARE
ALSO RESPONSIBLE FOR MONITORING CANCER PATIENTS' VITAL SIGNS • OVERALL
WELL-BEING, HELPING THEM MANAGE PAIN . • LESSEN SIDE EFFECTS AS THEY
UNDERGO TREATMENT.
 14. • The oncology nurse will monitor patients' lab results and make sure about the treatment . •
The oncology nurse's role in cancer treatment is to advocate for the patient • Their families and
to treat the whole person, not just the cancer.
 15. THE CHEMOTHERAPY NURSE HAS FOUR KEY ROLES: • EDUCATING PATIENTS, •
ADMINISTERING CHEMOTHERAPY DRUGS, • MANAGING SIDE EFFECTS • SUPPORTING
PATIENTS EMOTIONALLY. • NURSES WORK IN A MULTI-DISCIPLINARY TEAM. • IN BOTH
IN-PATIENT AND OUTPATIENT SETTINGS • ALSO INCLUDING HOSPITAL WARDS AND
COMMUNITY HEALTHCARE CENTERS.
 16. •NURSE PROVIDE PHYSICAL CARE SUCH AS DRESSING CHANGES, MEDICATION
AND CHEMOTHERAPY. • ADMINISTRATION MONITORING OF BLOOD AND VITAL SIGNS, •
 ALSO EDUCATE, SUPPORT AND CARE FOR PATIENTS AND THEIR FAMILIES ON AN
EMOTIONAL LEVEL. •.
 17. USING THE NURSING PROCESS, NURSES CAN PLAY A KEY ROLE IN: 1) IDENTIFYING
INDIVIDUALS WHO HAVE THIS ABNORMAL MOLE PATTERN 2) EDUCATING PATIENTS
ABOUT MELANOMA RISK- REDUCTION METHODS 3) COORDINATING PIGMENTED
LESION SURVEILLANCE PROGRAMS AIMED AT BOTH PRIMARY PREVENTION AND
EARLIER DETECTION AND TREATMENT
 18. PRIOR TO ADMINISTRATION TAKE MEASURES TO PREVENT MEDICATION ERRORS:
• PERFORM INDEPENDENT DOUBLE-CHECK OF ORIGINAL ORDERS WITH A SECOND
CHEMOTHERAPY-CERTIFIED NURSE •DOUBLE CHECK FOR ACCURACY OF TREATMENT
REGIMEN, CHEMOTHERAPY AGENT, DOSE, CALCULATIONS OF BODY SURFACE AREA,
SCHEDULE, • ROUTE OF ADMINISTRATION.
 19. NURSING INTERVENTIONS • MONITOR AND ASSESS THE PATIENT'S PAIN LEVEL
USING A STANDARD 0-TO-10 PAIN SCALE. ... • IF APPROPRIATE, REFER PATIENTS WITH
FATIGUE FOR PHYSICAL THERAPY, WHICH CAN IMPROVE STAMINA. • OBTAIN A
COMPLETE LIST OF THE PATIENT'S MEDICATIONS AND MONITOR FOR DRUG
INTERACTIONS. • EVERY DAY THAT NURSE WORK WITH A CANCER PATIENT IS
 20. NURSING IMPLICATIONS • ARRANGE FOR BLOOD TEST PERIODICALLY BEFORE
DURING AND FOR AT LEAST 3 WEEKS AFTER THERAPY TO MONITOR BONE MARROW
FUNCTION • ADMINISTER MEDICATION ACCORDING TO SCHEDULED PROTOCOL AND
COMBINATION WITH THE DRUGS AS INDICATED TO IMPROVE EFFECTIVENESS •
ENSURE THAT THE PATIENT IS WELL HYDRATED TO DECREASE RISK OF RENAL
TOXICITY • PROTECT THE PATIENT FROM EXPOSURE TO INFECTION LIMIT INVASIVE
PROCEDURES WHEN BONE MARROW SUPPRESSION LIMITS THE PATIENTS IMMUNE
/INFLAMMATORY RESPONSES .
 21. • PROVIDE SMALL FREQUENT MEALS • FREQUENT MOUTH CARE • DIETARY
CONSULTATION TO MAINTAIN NUTRITION WHEN GI EFFECTS ARE SEVER • PROVIDE
ANTIEMETIC DRUGS • ARRANGE FOR PROPER HEAD COVERING AT EXTREMES OF
TEMPERATURE IF ALOPECIA • USE WIG , SCARF , CAP TO MAINTAIN BODY
TEMPERATURE • COVER HEAD WITH WIG OR SCARF OR CAP TO MAINTAIN SELF
ESTEEM AND POSITIVE BODY IMAGE • MONITOR THE RESPONSE TO THE DRUG
 22. •MONITOR THE ADVERSE EFFECTS EX. GI TOXICITY , NEUROTOXICITY ALOPECIA
RENAL OR HEPATIC DYSFUNCTION •HEALTH EDUCATION ABOUT DRUG DOSE
ADVERSE EFFECT TO WATCH AND SPECIFIC MEASURES TO HELP AVOID ADVERSE
EFFECT
 23. SUMMERY :- • TODAY WE HAVE DISCUSS ABOUT ANTICANCER DRUGS
 24. CONCLUSION : • STUDENTS KNOW ABOUT ANTICANCER DRUGS .EFFECT
SIDEFFECT DRUGS INTERATION NURSESROLE
 25. • REFERENCES • KESHAB R P . HANDBOOK OF PHARMACOLOGYFOR NURSING
SECOND EDITION, JAYPEE BROTHERS MEDICAL PUBLISHRS • PADMAJA
U ,PHARAMOCOLOGY FOR NURSES 4TH EDETION THE HEALTH SCIENCES PUBLISHER
NEW DELHI • JOGINDER S P RUPENDRA K B , PHARAMOCOLGY FOR BSC NURSING 1
EDITION CBC PUBLISHERS
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 Introduction to chemotherapy | PPT

 CHEMOTHERAPY MODE OF ACTION CLASSIFICATION SIDE EFFECTS HEALTH
EDUCATION PROTOCOLS Introduction to cancer chemotherapy http://surgicaltechie.com
 3. Cancer cell characterised by •Uncontrolled proliferetion •Dedifferentiation(anaplsia)
•Invasiveness •metastasis
 6. Chemotherapy may be used conventionally to: •Cure patients-Wilm’s tumor, ALL, Testicular
cancer, Burkitt’s lymphoma, NHL Prolong survival-Prolong remission Decreases rate of relapse
•Palliative care symptom control-Relive symptoms and improved quality of life
 7. 1. Primary Chemotherapy 2. Adjuvant Chemotherapy 3. Neoadjuvant chemotherapy 4.
Concurrent chemotherapy •Chemotherapy is main modality of treatment •Can be single drug or
combination chemotherapy •e.g. Hematological malignancy- •ABVD regimen for hodgkins
lymphoma. •Combined with radiation or surgery. •For advanced cancer •e.g. Ca breast after
surgery to remove microscopic focci. •Chemotherapy is given before surgery. •Shrink a large
cancerous tumour to make surgery easy. •e.g. Laryngeal carcinoma before surgery.
•Simultaneously with radiation. •Mainly act as radiation sensitizer, encourages the cancer cells to
take radiotherapy. •e.g. Head and neck ca, Rectal ca, Lung ca.
 8. Anti neoplastic drugs
 9. •Oral •Intravenous •Intramuscular •Intrathecal •Subcutaneous •Intraperitoneal •Central
venous catheter •Inplantable access
 10. •A cycle- one dose followed by several days or weeks usually 21 to 28 days but may vary
according to protocols . •Number of cycles-based on the type and stages of cancer and side
effect as well •Dose calculationDosage of chemotherapy are difficult: If the dose is too low, it will
be ineffective , whereas excessive causes toxicity . In most cases, the dose is adjusted for the
patient's body surface area (BSA), a measure that correlates with blood volume. • W is weight in
kg, and H is height in cm.
 11. Platelet - 1,00,000 cumm , Red Blood Cell (Hb)- 8 gms% • Total Leucocyte Count-2,000
cumm, Absolute Neutrophil Count- 1,000 cumm, Liver function test , Renal function test
 14. 1.Cytotoxic agents 2.Targeted therapies
 15. CLASS DRUGS Nitrogen Mustards Cyclophosphamide Ifosfamide
Etylenimine ThioTEPA- ca breast Alkyl sulfonte Busulfan Nitrosoureas Carmustine Lomustine-
CNS tumors Triazine Dacarbazine
 16. CLASS DRUGS Folic acid analogue Methotrexate – choriocarcinoma,ca breast,ALL
Pemetrexed Pyrimidine analogue 5 Fluorouracil Cytarabine Gemcitabine Purine analogue and
related inhibitors Mercaptopurine Fludarabine
 17. Obtained from microorganisms yet intercalated between specific base pair as
adenine,guanine,cytosine thiamine CLASS DRUGS Antibiotics Dactinomycin (actinomycin D)
Daunorubicin Doxorubicin Mitoxantrone Bleomycin Mitomycin Enzymes L-Asparaginase
 18. CLASS DRUGS Vinca alkaloids –obtained from vinca rosea plants Vinblastine Vinorelbine
Vincristine Taxanes Paclitaxel, Docetaxel Epipodo- phyllotoxins Etoposide Camptothecins
Topotecan, Irinotecan
 19. Act on specific receptors on tumour cell and not inhibit normal cells rituximab CLL cetximab
CA colon trastuzumab CA breast
 20. CLASS DRUGS Glucocorticoides Prednisone Estrogens Diethylstilbestrol, Ethinyl
estradiol Substituted urea Hydroxyurea Differentiating agents Arsenic trioxide cisplatin Acts
analgouly to alkylating agents
 22. Febrile neutropenia-Temperature greater than or equal to 38.3 deg c Absolute Neutrophil
count (ANC) less than 1.0 One of the few Oncologic EMERGENCIES Wash your hands Note
signs of infections: sore throat,chills,productive cough and burning urination. Meet your doctor as
early as possible
 23. Bleeding-if the platelet count are low notice •Bruises or small purple spots on body •Nose
bleed •Bleeding gums •Bloody stool or urine •MUCOSITIS-Presents with mouth sores,
inflammation, sometimes sloughing of mucosa •MAGIC MOUTHWASH •SALT WATER
GARGLES •TOPICAL ANALGESIA ie Xylocainviscous, tantum
 24. Nausea- Types of Nausea Anticipatory—conditioned reflex to sight and smell of
chemotherapy area Acute—within 24hrs and related to chemotherapeutic agents Delayed—more
than 24 hrs. post chemotherapy--specific agents—cisplatin, cyclophosphamide, adriamycin
•Take antiemetics as and when prescribed eg ondensetron •Take small but frequent meal and
water. Loss of appetite (anorexia)-try to avoid spicy and smelly food. Eat high caloric and
proteineous food.avoid fluid with food.
 25. Diarrhea-GI tract consist of rapidly growing cells thats why diarrhea occurs •Take lots of
fluid and blend diet and small but frequent meal. Take prescribed medicines and go to
emergency if more than 24 hours Constipation-increas fluid ,fiber,cooked fruits and cooked
vegetables •Speak to your doctor and take medicine at bed time
 26. Hair loss -may have total hair loss,thinning or no loss at all. •Wear caps and wigs •Take care
of scalp •Skin changes -may develop skin sensitivity •Use sunscreams •Wear hat and keep
 covered when outdoor •Fatigue and anemia •Plan activities and rest time.never overburden •Do
regular exercise •Inform to doctor if unmanageable and blood tranfusion may be needed.
 27. DISEASE PROTOCOLS CANCER BREAST FEC / Docetaxel Gastro – esophageal
carcinoma PF Carcinoma of gall bladder Gem+Cis(Gemcitabine +CDDP) Neuro endocrine
tumour EP (Etoposide+Platinum) Ovarian cancer TP Cervix cancer CDDP Hodgkin lymphoma
ABVD Non hodgkin lymphoma Rituximab,CHOP CARCINOMA OF HEAD AND NECK PF
CARCINOMA OF LUNG TP
 28. STS IA PNET VAC IE GCT BEP TIP Bone metastases(Ca.breast,MM) Zoledronic acid
Cancer prostate Docetaxel Urinary bladder carcinoma GEM+CDDP GEM+CARBO GTN EMA –
CO http://surgicaltechie.com
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 is one of the most common diseases in the developed world: • 1 in 4 deaths are due to
cancer • 1 in 17 deaths are due to lung cancer • Lung cancer is the most common cancer in
men • Breast cancer is the most common cancer in women • There are over 100 different
forms of cancer

 3. • Cancer is a group of diseases characterized by uncontrolled growth and spread of

abnormal cells. • Cancer is caused by external factors and internal factors which may act
together to initiate or promote carcinogenesis. – External Factors – chemicals, radiation,
viruses, and lifestyle – internal Factors – hormones, immune condition, and inherited
mutations

 4. Factors Believed to Contribute to Global Causes of Cancer

 6. Cancer prevention? • Cancer prevention is defined as active measures to decrease the

risk of cancer. • Cancer is considered as the largely preventable disease. • Prevention offers
the most cost-effective long-term strategy for the control of cancer as 30- 40% of cancers
can be prevented, and one-third of cancers can be cured through early diagnosis and
treatment.

 7. Preventable risk factors • Tobacco • Obesity • Physical inactivity • Alcohol • Sun exposure
• Infections • Pollution

 8. STRATEGIES FOR CANCER PREVENTION AND MANAGEMENT

 9. What Is Chemoprevention? • The science of trying to apply natural and synthetic

compounds to interfere with the earliest stages of carcinogenesis, before invasive cancer
appears

 10. The Ideal Chemo preventive Agent • Is effective • Easily administered • Preferably
once/twice day • Little or ideally no toxicity • Affordable

 11. Mechanisms of Chemoprevention • Antioxidants: defense against radicals • Anti-

proliferative agents • Anti-hormonal compounds • Disruption of mutational gain or loss of
function

 12. Strategy#1-dietary strategy for cancer prevention • 30% to 40% of all cancers may be
prevented by changes in diet and physical activity. • Increase antioxidants by eating a variety
of anti-oxidant rich fruits and vegetables including nuts, seeds , herbs and spices. •
Antioxidants supplements mainly contain:- 1.Vitamin a,c,e,d and k 2.alpha-lipoic acid 3.co-
 enzyme q10 4. Falvanoids from plants including lycopene, resveratrol and quercetin. 5.
Carotenoids 6.selenium

 13. Foods that contain antioxidants: • VITAMIN A- CARROTS, SWEET POTATOES, MEAT •
VITAMINC- CHERRIES, PEPPERS, BERRIES, CABBAGE, BROCOLI, CITRUS • VITAMIN E-
WALNUTS, SESAME SEEDS • VITAMIN D- COD LIVER OIL, SALMON, EGGS, FORTIFIED FOODS
• VITAMIN K-CAULIFLOWER, SPROUTS, BEANS • SELENIUM-INCLUDES SEAFOODS • ALPHA
LIPOIC ACID-SPINACH, BROCOLI • CO-ENXYME Q10-MEAT, SEAFOOD

 14. FLAVONOIDS • CLASS OF PLANT SECONDARY METABOLOITIES • HAVE ANTIOXIDANTL

ACTIVITY • Knowns as vitamin p • Found in fruits and vegetables

 15. classification • Flavonols- compounds:- quercetin , kaempferol (e.g- cherry tomato,

apple, blueberry) • Flavones-compounds:- apegenin, tricetin, heptamethoxyflavone (e.g-
parsley, celery) • Flavanones-compounds:-dihydroquercetin, hesperetin (e.g-orange juice) •
Flavanols-compounds-taxifolin (e.g-cocoa, chocolates) • Catechins-compounds-
egcg(epigallocatechin gallate) (e.g-tea, apricot) • Isoflavones-compounds:- genistein (e.g-
soy, cheese) • Anthocyanins-componds-cyaniding (e.g-grapes, strawberry)

 17. Strategy#2 lifestyle strategy for cancer prevention • Maintain a healthy body weight. •
Be active, whether you walk with friends or sign up for yoga class, set a fitness goal. • Don’t
miss regular check –ups with doctor • Reduce your sodium intake. • Switch to whole grains.
Instead of white rice go for brown rice. • Choose water when you are thirsty. Reduce intake
of sweet drinks such as iced tea • Avoid smoked or grilled food

 18. • Quit smoking • Protect your skin • Limit red meat and animal fat • Know your personal
and family medical history • Get screened for cancer regularly • Increase your physical
activity

 19. Modalities of treatment: • 1-local therapy: – -surgery. – -radiation therapy. • 2-systemic

treatment: – chemotherapy. – Monoclonal antibodies. – Radioactive material. • 3-supportive
care. • 4-non-conventional therapy.

 20. Surgery: • Surgery was the first modality used successfully in the treatment of cancer. •
It is the only curative therapy for many common solid tumors. • The most important
determinant of a successful surgical therapy are the absence of distant metastases and no
local infiltration.

 21. Cont: • Microscopic invasion of surrounding normal tissue will necessitate multiple
frozen section. • Resection or sampling of regional lymph node is usually indicated. • Surgery
may be used for palliation in patients for whom cure is not possible. • Has significant role in
cancer prevention.

 22. Surgery for prevention: • Patients with conditions that predispose them to certain
cancers or with genetic traits Associated with cancer can have normal life span with
prophylactic surgery. -colectomy . -oophorectomy. -thyroidectomy. -removal of
premalignant skin lesion .

 23. Radiation therapy:

 24. Radiation therapy: • Radiation therapy: is a local modality used in the treatment of
cancer . • Success depend in the difference in the radio sensitivity between the tumor and
normal tissue. • It involves the administration of ionizing radiation in the form of x-ray or
 gamma rays to the tumor site. • Method of delivery: External beam(teletherapy). Internal
beam therapy(Brachytherapy).

 25. BRACHYTHERAPY • Internal radiation treatment achieved by implanting radioactive

material directly into the tumor or very close to it. • Sometimes called internal radiation
therapy. • Prefix “brachy” – from Greek for “short range”

 26. WHY BRACHYTHERAPY • Delivering the high dose of radiation to the tumor • Sparing of
the surrounding normal tissues • Delivered in a short period of time – Tumor repopulation •
Limited to localized tumors

 27. TELETHERAPY • Teletherapy or External Beam Radiation Therapy" involves delivery of

therapeutic radiation from a source • that is placed away • from the body.

 28. Cont: • Radiation therapy is planned and performed by a team of nurses,

dosimetrists,physician and radiation oncologist. • A course of radiation therapy is preceded
by a simulation session in which low-energy beam are used to produce radiograghic images
that indicate the exact beam location.

 29. Cont: • Radiation therapy is usually delivered in fractionated doses such as 180 to 300
cGy per day,five times a week for a total course of 5-8 weeks. • Radiation therapy with
curative intent is the main treatment in limited stage Hodgkin’s disease,some NHL,limited
stage of prostate,gynecologic tumors&CNS tumor . • Also can use in palliative &emergency
setting.

 30. DOSE • The amount of radiation used in photon radiation therapy is measured in gray
(Gy), • A unit of absorbed radiation equal to the dose of one joule of energy absorbed per
kilogram of matter, or 100 rads. • For curative cases, the typical dose for a solid epithelial
tumor ranges from 60 to 80 Gy, while lymphomas are treated with 20 to 40 Gy. • Preventive
(adjuvant) doses are typically around 45–60 Gy in 1.8–2 Gy fractions (for breast, head, and
neck cancers.)

 31. Complication of radiation: • There is two types of toxicity ,acute and long term toxicity.
• Systemic symptoms such as Fatigue,local skin reaction,GI toxicity,oropharyngeal
mucositis&xerostomia.myelosuppression. • Long-term sequelae:may occur many months or
years after radiation therapy. • Radiation therapy is known to be
mutagenic,carcinogenic,and teratogen,and having increased risk of developing both
secondary leukemia and solid tumor.

 32. Chemotherapy:

 33. Chemotherapy: • Systemic chemotherapy is the main treatment available for

disseminated malignant diseases. • Progress in chemotherapy resulted in cure for several
tumors. • Chemotherapy usually require multiple cycles.

 34. Classification of cytotoxic drug: • Cytotoxic agent can be roughly categorized based on
their activity in relation to the cell cycle. cytotoxic drug phase nonspecific. phase specific

 35. Cont : • What is the difference between phase specific & phase non specific?….. • Phase
non-specific: – The drugs generally have a linear dose-response curve( the drug
administration ,the  the fraction of cell killed). • Phase specific: – Above a certain dosage
level,further increase in drug doesn’t result in more cell killing.but you can play with
duration of infusion.
 36. What are the chemotherapeutic agent?…..

 37. Chemotherapeutic agents: • Alkylating agents: Cyclophosphamide • Antitumor antibiotic

• Antimetabolites

 38. Antitumor Antibiotics Cell cycle non-specific agents Variety of mechanisms: prevents
DNA replication, RNA production, or both Anthracyclines Anthracenediones Actinomycin
D (dactinomycin) – DNA intercalator, inhibits topoisomerase II also Bleomycin – inhibits
DNA synthesis, G2-phase specific Mitomycin C – functions as alkylator

 39. Antimetabolites They interfere with DNA and RNA growth by substituting for the normal
building blocks of RNA and DNA. These agents damage cells during the S phase Commonly
used to treat...... •leukemias, •cancers of the breast •ovary, •intestinal tract, as well as
other types of cancer.

 40. Cell-cycle Directed Anti-neoplastic Drugs Cell Cycle Phase Drug Target Go – G1 Taxol
Microtubules (stabilize) S-Phase Ara-C (Cytosine arabinoside) DNA synthesis S- G2 VP-16
(Etoposide) Topoisomerase II M Vinca-alkaloids Taxol Microtubule disrupters Microtubule
stabilizer Non-cell-cycle specific Alkylating agents: Cis-platinum Cyclophosphamide
Nucleophiles (e.g. DNA)

 41. Complication of Chemotherapy: • Every chemotherapeutic will have some deleterious

side effect on normal tissue . • E.G; Myelosuppression,nausea&vomiting, Stomatitis,and
alopecia are the most frequently observed side effects.

 42. • Chemotherapy targets cells which are dividing rapidly. • Chemotherapy cannot
distinguish between normal cells and cancer cells • Healthy Cells which have a high rate of
growth and multiplication include cells of the bone marrow, hair, GI mucosa and skin.

 43. Combined Modality Therapies for Cancer Surgery and Radiation Adjuvant
Chemotherapy: Surgery and Chemotherapy Radio-sensitizers: Chemotherapy and Radiation
Chemotherapy and Host-Response Modification • Induction of Differentiation by
Chemotherapeutic Agents • Induction of Apoptosis by Chemotherapeutic Agents
Immunotherapy and Gene Therapy Genetically Engineered T-Cells Chemotherapy with Ultra-
sonic Disruption? Combined

 44. Immunotherapy of Cancer • Potentially Highly Tumor-Specific • Can be Effective Against

Disseminated Disease Including Unrecognized Micro-metastases • Probably of Limited Value
Against Extensive Advanced Disease • Can Involve Severe, Sudden Onset Life-threatening
Treatment-limiting Side-Reactions • Limited by Tumor Heterogeneity, Selection for
Unresponsive Variants, and Emergence of Immune-Escape

 45. Host-Response Modification in Cancer Management Potentially Less Intrusive than

Other More-Aggressive Modalities Treating Host Supporting Cells to Reduce their ability to
promote tumor growth (e.g. anti-angiogenesis) Host stromal cell interactions supporting
tumor growth:

 46. Gene Therapy for Cancer • Potentially Highly Tumor-Specific • Accessibility of Cell
Targets Is a Major Obstacle for General Application • May Have Great Value in Combined
Modality Approaches • Potentially Dangerous Side-Reactions from Viral Vector Delivery
Agents
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
the growth of abnormal cells in the body. The symptoms are dependent upon the type of
cancer. Some cancers show no symptoms at all and there are many cancers of which the
cause remains unknown. There are a range of tests used to diagnose cancer. Most cancers
are diagnosed through biopsies. Treatment depends upon the type of cancer and the stage
the cancer is in. The stage of any cancer is determined by how much the tumor has grown
and whether it has spread. A diagnosis of cancer causes much anxiety for both the patient
and loved ones. There are support groups across the country to help cope with this terrible
disease. A patient’s prognosis depends on the type of cancer. Even with the same type of
cancer, the outcomes vary depending on the stage of the tumor and how early the diagnosis
was made. Works Cited Grady, D. (2008, August 2). Cancer patients, lost in a maze of uneven
care. New York Times ,
http://health.nytimes.com/health/guides/disease/cancer/overview.html.

 3. # 1 What is Cancer? The human body is made up of many living cells. Normal cells grow,
divide, and die. Cancer is a disease of the cells; it often begins when abnormal cells divide
without control. They then can invade tissues and even spread to other parts of the body
through the blood and lymph systems called metastasis.

 4. # 1 What is Cancer? (continued) Cells can become cancerous because of damage to the
cell’s DNA (DNA directs all of the cells’ actions). In cancer cells damaged DNA is not repaired,
and the cell will go on making new cells with the damaged DNA. These mutations in the DNA
may promote cell growth, interfere with growth restraint, or prevent cell death. Cancer can
often arise slowly developing over several decades. The abnormal mass of cells is called a
tumor. Cancer is not just one disease but many diseases. There are more than 100 different
types of cancer; they have different characteristics, occur in different locations of the body,
take different courses, and require different treatments. Works Cited -What is Cancer?
National Cancer Institute. http://www.cancer.gov/cancertopics/what-is-cancer. Updated
5/11/09 -Whiney, E. a. (2008). Understanding Nutrition. Belmont: Thomson Wadsworth. -
What is Cancer? American Cancer Society.
http://www.cancer.org/docroot/CRI/content/CRI_2_4_1x_What_Is_Cancer.asp . Updated
2010

 5. # 2 Cancer Prevention There are many things that affect your risk of getting cancer. Some
of those things are within your power to control such as what you consume, your activity
level and other life style behaviors. Let’s look at seven simple things to do to prevent
increasing your risk of cancer. 1. Don’t smoke. Smoking is one of the most preventable
causes of death in our nation. 2. Keep a healthy weight. Obesity has been determined to be
a risk factor in contracting colon, breast, endometrial, kidney and esophageal cancers.
(Whitney, 2008) 3. Exercise for 45 minutes a day. People with a vigorous lifestyle have been
shown to have a reduced risk of colon cancer (Whitney, 2008) 4. Eat less red meat and more
vegetables, fruits and whole grains. Saturated and trans-fat have been connected to a higher
risk of cancer while fruits, vegetables and whole grains have a protective effect.
 6. # 2 Cancer Prevention (continued) 5. Limit alcohol consumption to no more than one
drink per day for women, or two for men. Alcohol use has been linked to increased risk
mouth, throat, voice box, esophagus, liver, breast, colon and rectum and the risk increases
with the amount of alcohol consumed. 6. Practice safe sex. Both HPV, the most common
STD, and Hepatitis B can cause cancer. 7. Protect your skin from sun exposure . The sun's UV
rays cause the vast majority of skin cancers includi.ng melanoma, which can be life-
threatening. Sun screen alone is not a good enough preventative measure. One needs to
wear protective clothing or seek shade as well. Works Cited Greviskes, A. (April 15, 2010).
The cancer blog: Develop a cancer prevention program, http://www.thecancerblog.com/ .
Whiney, E. a. (2008). Understanding Nutrition. Belmont: Thomson Wadsworth.

 7. # 3 Treatments There are several types of treatments that can help to reduce and
eliminate cancer cells: chemo therapy, radiation therapy, biologic therapy, surgery and bone
marrow transplant. There are also some natural types of treatments such as herbs and
vitamins to help boost the immune system. There are many factors that go into deciding
which treatment is the best option. Factors include the type of cancer, location, whether or
not the cancer has spread and the patient’s general health as well as other things. (Denton,
2010) Chemotherapy The use of chemical agents to stop cancer cells from growing.
(Abramson Cancer Center at the University of Pennsylvania, 2010) Radiation Radiation
damages the DNA of cells with high energy x-ray which kills them or at least slows their
reproduction. Radiation also damages regular cells but because they grow more slowly than
the cancer cells, they can more easily repair themselves. (Abramson Cancer Center at the
University of Pennsylvania, 2010) Biologic Therapy This therapy may encourage your body to
produce more of its natural defenses, or the therapy may be a man-made version of a
naturally occurring substance itself. There are also therapies that use cells which have been
removed from the patient's body and altered in a laboratory and then returned back into the
patient’s body. (Abramson Cancer Center at the University of Pennsylvania, 2010)

 8. # 3 Treatments (continued) Surgery This is the oldest form of cancer treatment. It usually
involves the removal of cancerous tumors. It could be to remove the cancer all together, to
allow easier access to other tumors or as pain management if the tumor is pressing on a
nerve or bone. (Mayo Staff, 2009) Bone Marrow Transplant Usually a patient first receives
radiation or chemotherapy to destroy the cancer cells within the bone. The marrow is
harvested either from the patient themselves or a donor and then transplanted with the
hopes that the new young cells will go into the now open spaces and regenerate healthy
cells. (Abramson Cancer Center at the University of Pennsylvania, 2010) Natural Alternatives
Vitamin E is recommended for prostate cancer. Acupuncture can help alleviate vomiting and
nausea. Massage is recommended to also alleviate nausea as well as stress and lymph
drainage for lymphoma. (Whitney, 2008) Works Cited Abramson Cancer Center at the
University of Pennsylvania. (2010). Cancer treatment information . Retrieved April 27, 2010,
from Oncolink: http://www.oncolink.org/treatment/ Denton, L. (2010, April 27). Blog Be a
cancer survivor– Advice about successful treatment met. Retrieved April 27, 2010, from
Cancer Help Center: http://www.cancer-helpcenter.com/be-a-cancer-survivor-advice-about-
successful-treatment-met/ Mayo Staff (2009, August 22). Cancer surgery: Physically
removing cancer. Retrieved April 27, 2010, from Cancer:
http://www.mayoclinic.com/health/cancer-surgery/CA00033 Whiney, E. a. (2008).
Understanding Nutrition. Belmont: Thomson Wadsworth.
 9. # 4 Side Effects and Symptoms ANEMIA -can be caused by radiation or chemotherapy,
making red blood cell count drop. -get plenty of rest and conserve energy -do daily exercise
such as walking -be sure to eat -sit and stand slowly -follow your doctors advice and keep
them up informed of your symptoms FATIGUE -can be cause by cancer type and treatment,
and is usually worse just after treatment -can be caused by anemia, malnutrition due to
suppressed appetite, or depression -remember to eat healthy foods -keep your doctor
informed -engage in moderate exercise -plan a rest regimen with 15-20 minute naps
throughout the day -massage, acupuncture, and relaxation therapies may be helpful HAIR
LOSS -caused when chemotherapy and radiation kill fast growing cells -not all treatments
cause hair loss -use baby shampoo, or other protein based shampoos and conditioners -use
satin or silk pillow cases -avoid daily washing, braids, driers, straighteners, other processing,
or dyes. -in cases of hair loss, remember to use sunblock -insurance may cover the cost of a
wig

 10. # 4 Side Effects and Symptoms (continued ) CONSTIPATION -can be caused by a decrease
in activity and fluids, and an increase in medication -drink 8-10 glasses of decaffeinated
beverages daily -eat foods containing fiber -use laxatives and stool softeners with the advice
of your doctor LYMPHEDEMA -accumulation of lymphatic fluids that can cause abnormal
body swelling -can occur after cancer treatment -can induce bacterial infections -take
caution with personal hygiene and follow doctors orders -lymphedema can occur up to 15
years after surgery CHEMOTHERAPY INDUCED DIARRHEA -you may use immodium, stopping
only once all signs of diarrhea are gone for 12 hours -stay hydrated with at least 6-8 glasses
of non-caffeinated fluid per day -drink a little at a time as often as you can using water, clear
soups, or gatorade -do not drink milk, coffee, alcohol, very hot or very cold beverages. -do
not eat fatty, spicy or high fiber foods, raw fruits or vegetables, beans, popcorn, nuts, or
chocolate Dana-Farber Cancer Institute. Symptom Management. http://www.dana-
farber.org/can/symptom-management/ Visited 4/26/10. CLICK HERE FOR A YOUTUBE VIDEO
ON SYMPTON MANAGEMENT Cancer patients should eat small meals frequently and rotate
between drinking and eating. Patients should also avoid lying down after meals. Vitamins
and minerals may help manage symptoms and enhance treatment, but should only be taken
under the advice of a doctor. Cathcart, David. Chemotherapy Cancer Treatments and Side
Effects: Nutrition for Chemotherapy Side Effects. http://www.youtube.com/watch?
v=MEqhDOOCKKU. Visited 4/26/10

 11. # 5 Screening and Testing Cancer screening refers to processes by which cancer can be
detected before symptoms occur. This often increases chances for recovery. TYPES OF TESTS
for SCREENING There are over 200 different types of cancer, and many different methods of
testing. The following are basic categories of screening for cancer. 1.) Physical Examination
and History: -A doctor examines the body for lumps, changes, and any other abnormalities.
The doctor also considers age and personal history. This is the primary and least invasive of
all screening methods. 2.) Laboratory Tests: -Samples of blood, urine, tissue biopsies, or
other bodily substances are used to detect cancer. 3.) Imaging Procedures: - Images of the
internal body systems can be obtained and analyzed through X-ray, MRI, CT Scans,
Colonoscopy, Endoscopy, Mammography etc. 4.) Genetic Tests: -Tests that screen for
mutations in DNA which can cause cancer.

 12. # 5 Screening and Testing (continued) FACTS ABOUT SCREENING AND TESTING -
Screening tests have risks which should be discussed with your doctor -Screening tests,
particularly exploratory procedures, can cause trauma to internal organs -False positive and
 false negative results are possible. -Follow ups are important. -Detecting certain cancers may
not improve health. Some cancers do not cause symptoms and are not life threatening, but
if detected, treatment may cause harmful side-effects. National Cancer Institute. Cancer
Screening Overview. http://www.cancer.gov/cancertopics/pdq/screening/overview/patient.
Visited 4/28/10.

 13. # 5 Screening and Testing (continued) Bone marrow biopsy Bone marrow or stem cell
transplant Fiberoptic colonoscopy Exfoliative cytology Laparoscopy Mammography Needle
biopsy Radionuclide scans Stool DNA Tests http://www.youtube.com/watch?v=7u08itoH_sk
Tests to detect Cancer

 14. # 6 Foods That Fight Unfortunately there is no single food that can prevent and protect
you from cancer. There is evidence that minerals, vitamins, and phytochemicals in plant
based foods may interact in ways that can boost anti cancer effects. What is most important
before you have cancer and while you have cancer is essentially the same- taking in
nutrients with a whole foods diet and trying to avoid excess chemicals. Some established
dietary guidelines are to eat a healthy, balanced diet that is low in fat and rich in high-fiber
grains, fruits, and vegetables. Eating a predominantly plant based diet can not only prevent
weight gain but can protect against those cancers whose risk is increased by body fat.
Legumes - Contain saponins, protease inhibitors and phytic acid. These phytochemicals
appear to protect our cells from damage that can eventually lead to cancer. Beans are rich in
fiber and has been proven to decrease the risk of colon cancer . Berries - are among the
most powerful anti-cancer food, they are rich in ellagic acid. This phytochemical acts as an
antioxidant and helps the body to destroy specific carcinogens. Cruciferous and Dark Green
Vegetables - are high in both B-complex and D vitamins. Examples of cruciferous vegetables
include cauliflower, broccoli, brussel sprouts, and cabbage. In laboratory studies, these
vegetables have been shown to shrink prostrate and colon cancer tumors. Eating them is
believed to reduce the development of colon polyps (a precursor to colon cancer), even in
those people who are genetically predisposed to them. Dark Green veggies contain
carotenoid. Researchers believe that carotenoids prevent cancer by acting as antioxidants
(removing free radicals from the body before they can do any harm).

 15. # 6 Foods That Fight (continued) Garlic- Can boost your immune system and breakdown
cancer causing substances. Garlic contains allium compounds these are known to block
carcinogens from entering your cells and later developing into cancer. In animal studies,
Allium vegetables have slowed the development of cancer in stomach, breast, esophagus,
colon and lung cancers. Flaxseed- is full of antioxidants and high in omega-3 fatty acids. It
has shown to protect against breast and colon cancer. Grapes and Grape Juice- Grapes are
rich in resveratrol, a natural phytochemical. Studies suggest that resveratrol possess potent
antioxidant and anti-inflammatory properties. In lab studies resveratrol demonstrated the
ability to slow the growth of cancer cells and inhibit the formation of tumors in lymph, liver,
stomach and breast cells. Green Tea- Black and green teas contains polyphenols and
flavonoids which have antioxidant properties. Polyphenols shut down and prevent tumors
from growing by cutting off the blood supply. green tea has been shown to slow or
completely prevent cancer in colon, liver, breast and prostate cells. Whole Grain- means that
all three parts of the grain kernel (germ, bran and endosperm) are included. Whole grains
are rich in fiber, vitamins, minerals and hundreds of natural plant compounds. In addition
research points to specific substances in whole grains that have been linked to lower cancer
risk including antioxidants, phenols, lignans, and saponins. Works Cited Coomer, Cynara Dr .,
 10 Cancer-Fighting Foods . Fox News.Com Health Blog. Feb 8, 2010.
http://health.blogs.foxnews.com/2010/02/08/10-cancer-fighting-foods/ American Institute
for Cancer Research. Foods That Fight Cancer? http://www.aicr.org/site/PageServer?
pagename=foodsthatfightcancer_home http://www.youtube.com/watch?v=Fab-0KyoJNU

 16. # 6 Foods that Fight (continued)

 17. # 7 Causes of Cancer Environmental Factors –Exposure to sun, water, air pollution,
smoking are all known to cause cancer. Dietary Factors- certain foods can be carcinogenic,
especially those that contain additives or pesticides Genetics- Cancer can sometimes be
more predominant in families for examples Breast cancer is common in families with BRCA1
and BRCA2 genes. Hereditary cancers occur when a person is born with a change or
mutation in a single copy of a protective gene pair. Because people with an inherited
mutation have only one working copy of a protective gene, damage to that remaining gene
may occur in fewer steps and over a shorter period of time. This change can increase the risk
for certain cancers in different parts of the body Infectious Agents- can increase a persons
risk for cancer such as H.pylori and Human Papillomavirus Radiation - radiation exposure has
been known to cause cancer for example cellular phone use Weight and Physical Activity-
lack of physical activity and weight play a role in the development of cancer Works Cited
http://www.cancer.gov/cancertopics/prevention-genetics-causes/causes -Whiney, E. a.
(2008). Understanding Nutrition. Belmont: Thomson Wadsworth. Nelson, N. (2004) The
majority of cancer are linked to the environment.
http://www.cancer.gov/newscenter/benchmarks-vol4-issue3/page , Retrieved April 2009.
http://www.facingourrisk.org/hereditary_cancer/hereditary_cancer_and_genetics.html#wh
atis

 18. # 8 Cancer Support Groups There are several support groups that can be a valuable
resource for cancer patients and their families. Community cancer support groups are the
one of the best ways to actively get support and become more active in your cancer
community. These types of support groups can be held in hospitals, churches, and
community centers. There are also support groups on line .If you are experiencing side
effects from therapy and have difficulty leaving your home, an online community can be the
simplest, most effective way to get the support you need during treatment. America Cancer
Society, Make A wish foundation, American Lung Associations and several others.

 19. # 9 Mental Health Cancer patients experience significant physical and psychological
stress. Many suffer from depression and anxiety disorders. Cancer treatment programs
include a holistic approach to treating cancer which includes treating the body and mind.
Among them are Pet therapy, healing hands, art, and music therapy Studies have shown that
cancer patients undergoing chemotherapy can benefit from stress management training that
helps them cope with pain, fatigue, anxiety and depression. Pet Therapy is the use of
certified dogs to visit and comfort cancer patients while hospitalized. Cancer patients have
also reported benefits from Healing hands a type of energetic and spiritual massage therapy.
Hill, P. (2006). Therapy dogs comfort kids in stressful places. Albany Times Union.

 20. # 10 New Developments CANCER SCREENING IN THE NEWS Cancer screening tests,
procedures, and standards of care are constantly being changed and updated. Be sure to
keep up with the news and talk to your doctor.
http://www.reuters.com/article/idUSLDE63Q1QS20100427 This article is from Reuters, April
27th 2010. It explains that HPV tests are proving more effective for cervical cancer screening
 than the traditional pap smear for women aged 30 and over. This could mean less frequent
testing (every 5 years) because cervical cancer is a slow growing cancer. A new five-minute
test, conducted at age 55, could save 3,000 lives a year, the researchers said. The test
involves examining the lower bowels with a scope and removing any polyps which could
eventually become cancerous. (2010, Smith) The U.S. Food and Drug Administration just
approved Dendreon's Provenge® (sipuleucel-T) to treat certain men with advanced prostate
cancer . This heralds an advance in the development of biological therapy for cancer
treatment. Provenge is the first product approved in a new therapeutic class known as active
cellular immunotherapies. (Kilbert,, 2010) For more on Cancer Research check out
http://cancerres.aacrjournals.org/ Kellen, Kate. HPV tests better for cervical screening -
experts. Reuters. April 27, 2010. http://www.reuters.com/article/idUSLDE63Q1QS20100427
Kilbert, A. FDA Approval of new Prostate Treatment Shows Promise of Cancer
Immunotherapy. PRWeb. April 29, 2010. http://
www.prweb.com/releases/2010/04/prweb3944074.htm Smith, R. New cancer test cuts
deaths by 40 per cent. Telegraph. April 28, 2010.
http://www.telegraph.co.uk/health/healthnews/7638601/New-cancer-test-cuts-deaths-by-
40-per-cent.html
 prof of Medical -Surgical Nursing Faculty of Nursing Benha University
 3. OBJECTIVES OBJECTIVES Identify the meaning of cancer  List types of cancer. 
Enumerate risk factors of cancer.  List common clinical manifestation of cancer  Identify
diagnostic tests  Classify treatment modalities  Apply nursing process for patient with cancer
 4. Definition of cancer Definition of cancer Cancer is a collective term describing a large group
of diseases characterized by uncontrolled growth and spread of abnormal cells.
 5. Types of tumor  Tumor can be classified as : 1- Benign tumor is a simple new growth is
similar in substance to the tissue in which it arises and is named accordingly. 2- Malignant tumor
is growth and spread of the abnormal cells which continue to reproduce until they form a mass of
tissue known as cancer.
 6. the difference between benign and malignant tumor. According Characteristic of benign and
malignant tumor. 1- Cell Characteristics 2- Mode of growth 3- Rate of growth 4- Metastasis 5-
General effects 6- Tissue destruction 7- Ability to cause death
 7. Types of cancer  Carcinoma: Malignant cells of epithelial tissue and skin.  Sarcomas:
Malignant cells of connective tissue, muscle and bone.  Leukemia: Malignant cells of blood or
blood forming organs.  Lymphomas: Malignant cells of lymph nodes. There are different types of
cancer, including: - - Breast cancer - skin cancer - lung cancer - colon cancer - prostate cancer -
lymphoma
 8. Etiology& risk factors for cancer A) Controllable risk factors for cancer 1-Tobacco use 2-
Obesity, diet and exercise 3-Alcohol and drugs abuse 4-Ultraviolet (UV) radiation 5-Occupational
exposure 6-Psychosocial factors 7-Reproductive and hormonal factors.
 9. etiology& risk factors for cancer B -Uncontrollable risk factors for cancer: 1- Age. 2-Family
history of cancer.. 3-Genetic conditions; 4-Previous history of cancer; 5-Radiation therapy or
chemotherapy; 6-Virus exposure
 10. Clinical manifestation of cancer  The clinical manifestations of cancer are numerous. 
Each variant of the disease has its unique manifestations that may be  -vague complaints of
unexplained fatigue  -weight loss - fever - pain - life threatening medical emergencies
 11. The following sings may be associated with cancer and it called warning signs 1) Changes
in bowel or bladder habits, 2) A sore that does not heal, 3) Unusual bleeding or discharge, 4)
Thickening or lump in breast or any other part of the body 5) Indigestion or difficulty swallowing
6) Cough or hoarseness
 12. Detection and prevention of cancer  It includes primary and secondary prevention. A)
Primary Prevention : concerned with reducing the risks of cancer in healthy people through
community education about cancer risk, assisting patients to avoid known carcinogens, and
adopting dietary and varies lifestyle changes that epidemiologic and laboratory studies show
influence the risk of cancer.
 13. Ten steps to reduce the risk of cancer 1. Increase consumption of fresh fruits and
vegetables especially those of cabbage family. 2. Increase intake of vitamin A, C which act as
protective against many cancers. 3.Increase fiber intake and choose whole grains instead of
refined (processed) grains and sugars. 4. Maintain ideal body weight. 5. Limit consumption of red
meat, especially processed meats.
 14. steps to reduce the risk of cancer 6. Reduce intake of dietary fat especially taken from
animal source. 7. Limit salt intake, salt-cured food, and smoked foods. 8. Stop smoking. 9.
Reduce alcohol intake. 10. Avoid exposure to direct sun light especially at the duration from
10am to 3pm.
 15. American cancer society (ACS) recommendations for cancer checkup breast - Routine
monthly breast self-examination starting at age 20 Clinical breast examination every 3 years
from age 20-40 and yearly thereafter. Screening mammography every 2 years from age 40 to
50 and yearly thereafter
 16. B) Secondary Prevention  It involves screening and early detection for cancer to achieve
early diagnosis and prompt intervention to stop the cancer process.  Directed towards nursing
and medical management of cancer as disease effect and side effect of therapy management 
palliative care of advanced cancer signs and symptoms.
 17. Diagnoses of cancer  Medical diagnosis require obtaining a complete patient history and
physical examination in addition to Radiological studies; X-rays, a CT scan, and MRI 
Endoscopy; for example, colonoscopy to look inside the colon).  Laboratory tests; such as blood
and urine tests Biopsy; a biopsy is the only sure way to know whether the problem is cancer.
 18. Treatment modalities and nursing care of clients with cancer  Goals of treatment:  1-
Complete eradication of malignant disease (cure).  2-Prolonged survival and containment of
cancer cell growth (control).  3-Relief of symptoms associated with the disease (palliation).
 19. Considerations in choosing therapy Disease and results obtained from each type of
therapy. Patient’s general conditions and co- existing disease.
 20. Multiple modalities are commonly used in cancer treatment including: 1) Surgery 2)
Radiation therapy 3) Chemotherapy 4) Hyperthermia 5) Acupuncture 6) Hormone therapy 7)
Gene therapy 8) Bone marrow transplantation and steam cell
 21. 1-surgery Types of surgical application: a ) Diagnostic surgery ,a variety of methods are
used such as. Incisional biopsy: removal of a small portion of tumor for examination by
endoscopic examinations. - Excisional biopsy: removal of entire tumor. d) Needle biopsy:
aspiration of core tissue samples through a needle. - Endoscopy: removal of small portions of
tumor with forceps following visual examination.
 22. b) Treatment of disease by surgery: It involve the following: (1)Local excision: is the simple
excision of a tumor and a small margin of normal tissue. Most commonly used to treat skin
cancer. (2) Wide excision: is the removal of the primary tumor, regional lymph nodes, lymphatic
channels, and neighboring structures (e.g.) radical mastectomy
 23. 2- Radiation Therapy Definition: Irradiation means application or exposure of body tissues
to radiation energy which may occur either accidentally or for therapeutic purposes. Uses of
Radiation therapy  to cure the cancer, When a tumor cannot be removed surgically or when
local nodal metastasis is present.  It can be used prophylactically  Palliative radiation therapy
 24. Effect of radiation  A- Systemic effect Radiation causing nausea, vomiting, and depression
poor appetite, weight loss, and anemia  B- Local effect Skin: Erythema – Edema-Chronic -Loss
of hair Bone and cartilage: Bone necrosis and pathological fracture GIT: Ulceration and
hemorrhage-Atrophy of lymphoid tissue-Necrosis and perforation Kidney: Radiation nephritis-
Chronic renal failure-  Testes and ovaries: Atrophy of germ cells leading to sterility Bone marrow
and blood: Anemia-Leucopenia- Thrombocytopenia-Leukemia.
 25. . . Nursing care related to side effects that results from radiation therapy: 1- Impaired skin
integrity related to radiation therapy. Nursing interventions: Assess skin integrity. Instruct patient
to minimize trauma Clean skin with lukewarm water. Avoid use of soap, powders Avoid
shaving and protect skin from cold, heat, sun.- Avoid adhesive tape on irradiated skin
 26. 2-Fatigue or activity intolerance related to radiation therapy.  Assess fatigue.  Monitor
blood counts for anemia.  Help the pt to plan for assistance with transportation, preparation of
food.  Help pt to taking a nap immediately after returning home to have energy for the rest of
the day.  Help the pt to maintain an adequate nutritional intake
 27. 3-Altered nutrition less than body requirements related to anorexia.  Nursing
interventions:- • Assess loss of appetite in pt. receiving radiation therapy. • Instruct the patient
that small meals allow more food to be consumed throughout the day. • Instruct the patient to
have high-calorie, high- protein foods at all times
 28. Altered oral mucous membrane related to stomatitis secondary to radiation therapy of head
and neck. • Mouth care. -Tooth brushing and if painful, warm saline rinses and gentle swabbing
with moist gauze. -Inspecting oral cavity each day. -- Instruct the patient to use soft diet to make
chewing and swallowing easier. - control minor areas of bleeding in the mouth or systemic
antibiotics to control oral infections
 29. Ineffective individual coping related to alopecia.  Instruct the patient to use a scarf or
turban to protect scalp from the wind, cold, and sun. A mild shampoo may be used, but avoid
excessive shampoo. • Help the patient to cope with alopecia or allowing verbalization of fears,
grief, and anger.
 30. 6-Altered nutrition, less than body requirements related to nausea and vomiting • Assess
for occurrence and pattern of nausea and vomiting. • Prophylactic use of antiemetic before
treatment each day . • Relaxation techniques and distraction such as listening to soothing music
and engaging in enjoyable activity. • Provide diet that is low in fat, low in sugar. and easily
digested. • Soups, broths and other fluids should be consumed to maintain fluid intake and
prevent dehydration
 31. 3- Chemotherapy  Chemotherapeutic is an agent are effective in destroying or preventing
the multiplication of cancer cell, normal tissue is also affected.  a cytotoxic drugs in the
treatment of cancer, chemotherapy is a systemic as opposed to localized therapy such as
surgery and radiation therapy.
 32. The goals of chemotherapy  To reduce tumor size preoperatively.  To destroy any
remaining tumor cells postoperatively.  To treat some forms of leukemia.  Cure, control,
palliation (20% to 99%, depending on dosage) of tumor cells is destroyed.
 33. Side effects of chemotherapy  Bone marrow suppression: - ↓Red blood cells carry oxygen,
Risk for anemia- - ↓white blood cells that fight infection, Risk for fatigue, and infection --
↓platelets that help the blood to clot, Risk for bleeding  mouth sores, nausea, vomiting, and
diarrhea  Hair loss, also called "alopecia": Chemotherapy affects the cells of the hair and nails
 34. Nursing care related to side effects that results From chemotherapy:  1- Disturbance in
self-concept related to alopecia.  Nursing Intervention Inform patient that hair loss is temporary
and hair will regrow when the treatment is stopped (it usually returns 2-6months). - Provide
resources for purchase/loan of wigs, scarves, and caps).  Inform patient about health care
measures for scalp protection: use of gentle shampoos, and wear protective covering when out
doors.
 35. Altered nutrition less than body requirements related to anorexia.  -Nursing Intervention -
Assess loss of appetite in pt receiving chemo therapy. - Instruct the patient that small meals
allow more food to be consumed throughout the day. - Instruct the patient to have high-calorie,
high-protein foods at all times  - Promote relaxed, quite, environment during mealtime with
increased social interaction as desired

 1. An overview of Cancer

 3.  9.6 million people die from cancer every year.  At least one third of common cancers
are preventable.  Cancer is the second-leading cause of death worldwide.  70% of cancer
deaths occur in low-to- middle income countries.  Up to 3.7 million lives could be saved
each year by implementing resource appropriate strategies for prevention, early detection
and treatment.

 4.  A disease which occurs when changes in a group of normal cells within the body lead to
uncontrolled, abnormal growth forming a lump called a tumour – true of all cancers except
 leukaemia (cancer of the blood).  If left untreated, tumours can grow and spread into the
 surrounding normal tissue, or to other parts of the body  the bloodstream and lymphatic
systems, and can affect the digestive, nervous and circulatory systems or release hormones
that may affect body function.

 5. Division of Tumours Benign Malignant Precancerous

 6. Benign • grows quite slowly, • do not spread to other parts of the body • usually made up
of cells quite similar to normal or healthy cells. • cause a problem if they grow very large,
becoming uncomfortable or press on other organs - for example a brain tumour inside the
skull. • are not cancerous Malignant •Grows faster than benign tumours • ability to spread
and destroy neighbouring tissue. •Cells of malignant tumours can break off from the main
(primary) tumour and spread to other parts of the body through a process known as
metastasis. • invades healthy tissue at the new site they continue to divide and grow.
•These secondary sites are known as metastases and the condition is referred to as
metastatic cancer. Precancerous •describes the condition involving abnormal cells which
may (or is likely to) develop into cancer.

 7. • Arises from the epithelial cells • Invade surrounding tissues, organs, metastasis to the
Lymph nodes and other area of the body • Common forms of cancer are breast , prostrate,
lung and colon Carcinoma • malignant tumour of the bone or soft tissue (fat, muscle, blood
vessels, nerves and other connective tissues that support and surround organs). • common
forms of sarcoma are leiomyosarcoma, liposarcoma and osteosarcoma Sarcoma • Arise in
the cells of the immune system • Lymphoma is a cancer of the lymphatic system • Myeloma
(or multiple myeloma) starts in the plasma cells, a type of white blood cell that produces
antibodies to help fight infection. Lymphoma & Myeloma

 8. • Occurs in the white blood cells and bone marrow, the tissue that forms blood cells. •
There are several subtypes; common are lymphocytic leukaemia and chronic lymphocytic
leukaemia Leukemia • central nervous system cancers. • Some are benign while others can
grow and spread. Brain and Spinal Cord

9. ⦿ Modifiable risk factors Alcohol Being overweight or obese Diet and nutrition
Physical activity Tobacco Ionizing radiation Work place hazards Infection ⦿ Non-


modifiable risk factors  Age  Cancer-causing substances (carcinogens)  Genetics  The

immune system

 10. Unusual lumps or swelling – cancerous lumps are often painless and may increase in size
as the cancer progresses

 11. Coughing, breathlessness or difficulty swallowing – be aware of persistent coughing

episodes, breathlessness or difficulty swallowing

 12. Changes in bowel habit – such as constipation and diarrhoea and/or blood found in the
stools Unexpected bleeding – includes bleeding from the vagina, anal passage, or blood
found in stools, in urine or when coughing

 13. Unexplained weight loss – a large amount of unexplained and unintentional weight loss
over a short period of time (a couple of months) Fatigue – which shows itself as extreme
tiredness and a severe lack of energy. If fatigue is due to cancer, sufferers normally also have
other symptoms
 14. Pain or ache – includes unexplained or ongoing pain, or pain that comes and goes New
mole or changes to a mole – look for changes in size, shape, or colour and if it becomes
crusty or bleeds or oozes

 15. Complications with urinating – includes needing to urinate urgently, more frequently, or
being unable to go when you need to or experiencing pain while urinating Unusual breast
changes – look for changes in size, shape or feel, skin changes and pain

 16. A sore or ulcer that won’t heal – including a spot, sore wound or mouth ulcer Appetite
loss – feeling less hungry than usual for a prolonged period of time

 17. Heartburn or indigestion – persistent or painful heartburn or indigestion Heavy night

sweats – be aware of very heavy, drenching night sweats

 18. Over a third of all cancers can be prevented by reducing your exposure to risk factors
such as tobacco, obesity, physical inactivity, infections, alcohol, environmental pollution,
occupational carcinogens and radiation. Prevention of certain cancers may also be
effective through vaccination against the Hepatitis B Virus (HBV) and the Human Papilloma
Virus (HPV), helping to protect against liver cancer and cervical cancer respectively.
Reducing exposures to other carcinogens such as environmental pollution, occupational
carcinogens and radiation could help prevent further cancers.

 19.  There are a number of cancers which can be identified early which helps to improve
the chances of successful treatment outcomes, often at lower costs and with fewer (or less
significant) side effects for patients.  There are cost-effective tests that help detect
colorectal, breast, cervical and oral cancers early and further tests are being developed for
other cancers.

 21. Treatment depends on the type of cancer where cancer is, how big it is, whether it has
spread General health.

 22. Types of Treatment Surgery Chemo therapy Radio therapy Hormone therapy Immunot
herapy Gene therapy

 23. Surgery ⦿ If a cancer has not metastasized (spread), surgery can remove the entire

prostate or a breast or testicle. Radiotherapy ⦿ Radiation treatment or radiotherapy uses

cancer which may completely cure the disease. Often, this is effective in removing the

high-energy rays to reduce a tumour or destroy cancer cells as a stand-alone treatment and
in some cases in combination with other cancer treatments.

 24. Chemotherapy Chemotherapy uses chemicals to interfere with the way cells divide -
damaging of DNA - so that cancer cells will destroy themselves. These treatments target
any rapidly dividing cells (not necessarily just cancer cells), but normal cells usually can
recover from any chemical- induced damage while cancer cells cannot. Chemotherapy is
generally used to treat cancer that has spread or metastasized because the medicines travel
throughout the entire body. It is a necessary treatment for some forms of leukaemia and
lymphoma.

 25. Immunotherapy Immunotherapy uses the body's own immune system to fight the
cancer tumour. Immunotherapy may treat the whole body by giving an agent that can
shrink tumours. Hormone therapy Several cancershave been linked to some types of
 hormones, including breast and prostate cancer.  Hormone therapy works to change
hormone production in the body so that cancer cells stop growing or are killed completely.

 26. Gene therapy The goal of gene therapy is to replace damaged genes with ones that
work to address a root cause of cancer: damage to DNA.  Other gene-based therapies
focus on further damaging cancer cell DNA to the point where the cell destroys themselves.
However, gene therapy is new and has not yet resulted in any successful treatments.

 27. Survivorship Survivorship focuses on health and the physical,psychological, social

and economic issues affecting people after the end of the primary treatment for cancer,
including people who have no disease after finishing treatment, people who continue to
receive treatment to reduce the risk of the cancer coming back and people with well
controlled disease and few symptoms, who receive treatment to manage cancer as a chronic
disease.

 28.  Survivorship care includes issues related to  follow-up care,  the management of
late side-effects of treatment,  the improvement of quality of life and psychological and
emotional health.  Survivorship care includes also future anticancer treatment where
applicable.  Family members, friends and caregivers should also be considered as part of
the survivorship experience.

 29. Palliative care  Palliative care runs throughout a patient’s journey from diagnosis to
cure or end of life, and is designed to relieve symptoms and improve a cancer patient’s
quality of life.  It can be used to respond to troubling symptoms such as pain or sickness,
and also to reduce or control the side effects of cancer treatments.  In advanced cancer,
palliative treatment might help someone to live longer and to live comfortably, even if they
cannot be cured.

 30. Awareness, understanding, myths and misinformation Access to information and

knowledge about cancer can empower us all.

 31. Prevention and risk reduction Over one third of cancers are preventable, which means
we all can reduce our cancer risk.

 32. Equity in access to cancer services Life-saving cancer diagnosis, treatment and care
should be equal for all – no matter where you live, what your income, your ethnicity or
gender.

 33. Government action and accountability Governments can influence many of the levers
to reduce and prevent cancer.

 34. Beyond physical: mental and emotional Impact The impact of cancer goes far beyond
physical health, impacting the mental and emotional wellbeing of patients and their
caregivers.

 35. Saving lives saves money The financial impact on nations, individuals and families have a
huge impact on sustainable economic and human development. By focusing on saving lives,
we can also save money

 36. Reducing the skills gap A shortage of skilled healthcare workers is one of the greatest
barriers in delivering quality cancer care. Working together as one By joining forces, we help
to strengthen efforts that stimulate powerful advocacy, action and accountability at every
level.
 37. The Cancer Atlas: History of Cancer ⦿ Explore a timeline of the history of cancer from BCE
to 2011 ⦿ National Cancer Institute: Dictionary of Cancer Terms ⦿ Cancer terms explained


International Agency for Research on Cancer: Global Cancer Observatory ⦿ An interactive

web-based platform presenting global and national cancer statistics to inform cancer control
and research

 38. World Health Organization: Cancer Country Profiles Synthesized national cancer data by

⦿ Understanding risk factors and causes of cancer

country, including data on mortality, incidence and risk factors The Cancer Atlas: Risk Factors

39. The Cancer Atlas: How to take action ⦿ Discover the opportunities for controlling cancer
World Cancer Research Fund: Facts and Figures on specific cancers ⦿ World Cancer Research


Fund International is the world’s leading authority on cancer prevention research related to
diet, weight and physical activity

 40. World Cancer Research Fund International: Cancer prevention recommendations ⦿

each type of cancer ⦿ Access over 120 individualized and oncologist- approved guides
Explore the recommendations on helping to prevent cancer Cancer.Net: Individual guides on

Cancer.Net: Questions to ask your doctor ⦿ Find guidance on what to ask your health team,
as approved by the American Society of Clinical Oncology

41. ⦿ National Comprehensive Cancer Network: Cancer Staging ⦿ Understand what cancer
stages mean ⦿ National Cancer Institute: Types of treatment ⦿ Understand the treatment


options for cancer

 42. National Comprehensive Cancer Network: Patient and Caregiver Resources ⦿ These

caregivers Rethink Breast Cancer: Care guidelines ⦿ This guide is aimed at young women with
guidelines and video resources are aimed specifically at individuals with cancer and their

breast cancer to help them navigate their treatment

43. UICC and Bupa: Working with cancer ⦿ A resource for both employers and employees
International Psycho Oncology Society: Survivorship ⦿ Download a practical guide for


patients and caregivers

44. Medical News Today: Most recent research breakthroughs ⦿ Read about how close we
are to finding more effective treatments Union for International Cancer Control: Members ⦿


Find a national cancer organization near you

 1. Carrington College Summer 2012 N254
 2. Terminology to know  All key terms on page 260  Overall Survival (OS) in Lewis et al 
Quality of Life (QOL)  Prevalence  Benign  Incidence  Malignant  Mortality  Node  Morbidity
 Biopsy  Survival  Cachexia  Progression Free Survival  Cure (PFS)  Control  Disease Free
Survival (DFS)  Palliation  Adjuvant  Hospice
 3. Who gets cancer?  Men – Prostate, Lung, Colon/rectum, Bladder, NHL, melanoma, Head
and neck  Women – Breast, Lung, Colon/rectum, Uterus, NHL, Thyroid, Melanoma, Ovary 
Adult age variables – the older the person, the higher the risk of cancer  Children – very specific
childhood cancers, significant genetic components  Ethnicity variables – page 261  US and rest
of the world  Developing nations – very different issues
 4. How do people get cancer? Risk factors  Age, Gender  Environmental influences –
carcinogens  Chemical/Radiation/Smoke/Smog/ Water Quality/ Infections/Food Processing 
Genetics – 10-15% have genetic link  New research increasing our ability to detect links 
Behaviors  Smoking  Dietary  Exercise  ETOH
 5. Statistics
 7. Classification  Anatomic site  Histology  Solid/Blood  Origin  Can have breast cancer in
the brain, for example
 8. Staging  T – Primary Tumor  is: in situ, x: can’t be found, 0: no evidence of primary tumor 
1 – 4: Ascending size  N – Node  0: no evidence of disease, x: unable to assess  1 – 4:
Ascending degrees of nodal involvement  M – distant metastases  0: no evidence of distant
mets, x: cannot be determined  1 – 4: Ascending degrees of metastatic involvement  Staging
related to the formula for the TNM  Stage 0 – 4: the higher the number, the more serious the
disease  Guides decision making about treatment, advises about prognosis
 9. Grading  Grade 1  Differ slightly from normal cells – low grade  Grade 2  Moderate
differentiation – intermediate grade  Grade 3  Severe differentiation – high grade  Grade 4 
Immature and primitive  The cells of Grade 1 tumors resemble normal cells, and tend to grow
and multiply slowly.  Conversely, the cells of Grade 3 or Grade 4 tumors do not look like normal
cells of the same type. Grade 3 and 4 tumors tend to grow rapidly and spread faster than tumors
with a lower grade.
 10. Diagnostic tests to ID cancer  Routine screening  Mammogram  Colonoscopy  PAP
Smear  Others not as established – Lung CT, Specific blood tests  Issues are often r/t cost,
insurance coverage, controversy  See ACS website for complete list of screening guidelines
 11. Example of screening guidelines
 12. Diagnostic tests to ID cancer  Labs  CBC, Chem Panel, Liver studies  Some cancer
specific tests, called tumor markers (PSA, CA 125, CEA, etc)  Genetic markers – (BRCA, etc) 
Diagnostic tests  Imaging – Ultrasound, CT, MRI, PET CT, Endoscopy, Radio- isotope scans 
Often biopsy done with Imaging guidance  Often require a series of tests, and the entire time,
the patient is anxiously waiting!
 15. Biopsy  Definitive identification of histological type of cancer  Determines type of
treatment necessary  Role of Tumor Board  Role of Clinical Trials
 16. Tumor Board  Group meets, usually weekly  MDs - Radiologist, Pathologists, Medical
Oncologists, Surgeons, Radiation Oncologists, Geneticists, Psychiatrists, Palliative Care,
Hospice, Primary Care  Psychologists, Social workers, Nurse Navigators, Infusion Room
nurses, Radiation Therapy staff and nurses, Nutrition, Physical and Occupational Therapy,
Surgical and Oncology nurses, Research nurses, Cancer Registry staff  Others: Medical and
Nursing Students – have to sign confidentiality agreement  If you get a chance to go, do it!
Fascinating stuff!
 17. Tumor Board  Present all Imaging results  Present all lab results, including biopsy 
Present patient’s H & P  Compare to National standards and guidelines  Discuss cancer and
best therapy for that patient  Recommend treatment options, including clinical trials and referrals
to other facilities (UCSF, Stanford)  ALL participants discuss, all cite evidence and research 
Often lively discussion and debate about recommendations
 18. Clinical Trials  Variety of trials available – prevention, screening, diagnostic, treatment,
QOL, genetics  Patient may leave clinical trial at any time  Some trials have been stopped
abruptly  Significant negative outcomes  Significant positive outcomes  Nurse has huge role in
Clinical Trials  Assisting people in finding appropriate trial  Data collection and monitoring 
Clinical follow-up  Examples of CT/research in Reno
 20. Surgery  Goal – removal of as much of tumor as possible  Other goals:  Placement of
treatment devices  Cure  Control  Support/Palliative  Rehab
 22. Surgery side effects  Loss of function/motion  Altered body image  Altered sexuality 
Social isolation  Infection
 23. Chemotherapy  Huge number of chemicals that we can give to people – more being
developed all the time.  Cure  Control  Support/palliative
 24. Types of chemo administration  Oral  IV – most common today  Usually given in cycles,
sometimes RTC  Peripheral  Central  Intracavity or into organ  Intrathecal or into ventricles
 25. Issues r/t chemo  Toxicity  Patient  Nurse safety  Side effects  Long therapies  Cycles
 Continuous infusions  More and more chemo given in outpatient setting  Chemo in all patient
waste for 2-3 days or longer
 26. Biologic and Targeted Therapy  Alter or modify the relationship between the host and
tumor  Classic example – hormone therapy for prostate, breast cancers  Many of the newer
targeted therapies are specific for one type of cancer, or have only been tested with one type of
cancer  Many are still under patent, and quite expensive  Examples:  Gleevec for CML: $6-
 7K/month for rest of life  Herceptin for breast cancer: $54K/year x 1 year  Patient assistance
programs  Patients may reach lifetime maximum of insurance quickly
 28. Side effects of chemo  Immediate  Skin and nail changes  N&V  N & V – up to 2 weeks 
Stomatitis, mucousitis after chemo  Fluid shifts  Bowel changes  Falls  Peripheral neuropathy
 Delayed  Cognitive changes  Bone marrow  Cachexia suppression  FATIGUE  Alopecia –
about 2 weeks after chemo
 29. Side effects of chemo  Long term  People who had chemo  Infertility as children now are
 Cardiac dealing with a variety of  Secondary cancers issues – need to continue to see MD for
follow-up  Permanent skin and hair changes  Emerging area of study  Some chemos cause
chronic cardiac and/or pulmonary changes
 30. Mitigating side effects  N&V  RBCs  WBCs  Mouth care  Fatigue  Cachexia  Physical
changes
 31. Nausea and vomiting  Much research on this with medications and complementary
therapies  Multiple reasons that people are nauseated/vomit  Anticipatory – “Elevator vomiting”
 Immediate  Delayed  Long term  Currently, meds include:  High doses of steroids  Anti-
emetics – many specific to cancer therapy
 32. Nausea and vomiting  Complementary therapies that have been shown to be effective: 
Acupressure  Acupuncture  Guided imagery  Music therapy  Muscle relaxation 
Psychoeducational support and information  Many more are being researched and may show
effectiveness
 33. RBCs and WBCs and platelets  RBCs  Transfusions  Erythropoietin  Oxygen  WBCs 
GCSF – Granulocyte Colony Stimulating Factor  Often given right after chemo, so that patient
never has nadir  Platelets  Transfusion uncommon  Often simply put on bleeding precautions
until platelets rise  Meds in the works, so far have not been effective
 34. Mouth care  Prevention of mouth sores is crucial for many reasons:  Impaired comfort,
Impaired nutrition, Impaired body image, Impaired communication, Risk for infection and
bleeding to name a few!  Frequent mouth care crucial, but a challenge  Soft toothbrush, no
alcohol mouthwash, careful attention to dentist visits, flossing, avoiding irritating foods
 35. Radiation Therapy  Local  Internal  Brachytherapy  External  Systemic very rarely used
 Cure  Control  Support/Palliation  Rehab
 38. Side effects of radiation  Immediate  Rare  With head and neck – Skin issues, N&V,
mouth sores  Delayed  Usually begin to manifest during treatment to end of treatment and
several weeks beyond  Skin burns, fatigue  GI issues if getting radiation to belly
 39. Side effects of radiation  Long term  Chronic fibrous changes in lungs, heart  Prostate –
incontinence, impotence  Scar tissue
 40. Mitigating side effects  Skin – creams and lotions  Mouth – special rinses and meticulous
care  N&V – anti emetics  Fatigue – exercise during and after radiation!  Prostate – Urinary
exercises, Kegels, Viagra
 41. Combination therapies  Surgery, chemo and radiation may all be used, sometimes at the
same time  These patients are very ill, often with a compounded bunch of side effects  Biggest
risks/concerns:  Infection leading to sepsis  N&V leading to severe dehydration  Anorexia
leading to severe malnutrition  Pain from cancer itself, as well as side effects of treatment
 42. Stem cell transplantation/ Bone marrow transplantation  Used to treat variety of cancers
often blood tumors  Patient receives “induction” chemo to eliminate cancer cells  Cells
harvested from patient or donor  If patient cells, they are treated to remove any remaining
cancer cells  Patient usually gets more chemotherapy/ sometimes radiation  Receives stem
cells which proliferate and form new cells that are cancer free  Very intensive process with many
risks  Significant long term issues
 44. Complementary Therapies  Used with western medicine – best treatments are evidence
based, have had clinical trials  Effective for cancer treatments:  Pet therapy  Healing touch 
Music therapy  Support groups  Exercise  Imagery  Ongoing study  Nutrition  Herbal
supplements
 46. Alternative Therapies  Used instead of western medicine  Hallmarks:  Cash payments 
No clinical trials  Often ingredients not revealed  Anecdotal or celebrity evidence  Many of the
practitioners do not have hospital privileges or board certifications, may not be physicians 
Doesn’t mean they don’t work, but no data collected on them – can’t tell if they work or not
 47. Advanced Cancers  Diagnosed late – Stage 3 or 4  Usually already have metastasis from
primary cancer  Often treatable, can often give significant DFS or PFS  Lance Armstrong –
example  Recurrence – originally, was the end  Now, often treatable and can give significant
PFS  Some patients on their 3rd or 4th recurrence, related to aggressive and newer chemos 
Secondary cancer  Problem is often that the patient can’t have as much chemo or radiation –
has reached lifetime limit of one or the other or both, so surgery may be only option available
 50. Common cancers and the treatments commonly used  Lung (p. 560-564)  Breast (p.
1311-1326) Lotsa pages!  Leading cause of cancer deaths in  Most frequently occurring cancer
in US at present, expected to continue women to rise for women  Screening – mammogram,
breast  New screening may diagnosis at exam earlier stage – improve survival  Hallmarks: 
Hallmarks:  Usually found in screening  Worsening cough with sputum, mammograms, or small
lump weight loss, fatigue, chest pain palpated – usually no symptoms  Treatments include
surgery, chemo,  Highly treatable, very often curable sometimes radiation  Treatments include
surgery, chemo,  Issues include shortness of breath, radiation and hormone therapy fear and
anxiety  Issues include fatigue and body  In 2011, @226,000 diagnosed and image @160,000
died with lung cancer  In 2011, @ 288,480 diagnosed, @40,000 died with breast cancer
 51. Common cancers and the treatments commonly used  Prostate (p. 1386-1391) 5 pages 
Colon/rectum (p. 1035 - 1038)  Most frequently occurring cancer in  Screening test:
Colonoscopy, FOBT men  Hallmark:  Screening test Exam, PSA  Abdominal pain, change in
bowel  Hallmark: Similar to BPH – pattern, blood in stool, anemia problems urinating or change
in  Treatment includes surgery, urination patterns chemotherapy, radiation  Treatment – varies
according to  Issues include body image, change stage – sometimes watch and wait in bowel
habits, pain  Other treatments include surgery,  In 2011, @ 143,000 diagnosed and radiation,
hormonal therapy @51,000 died with colon/rectal  Issues include impotence cancer
incontinence  In 2011, @ 241,000 diagnosed with and @ 28,000 died with prostate cancer
 52. Common cancers and the treatments commonly used  Leukemias (p. 694-697) 
Lymphomas (p. 699-703)  Screening – not done.  Screening - not done  Hallmark: fatigue,
patient presents  Hallmark: Often few symptoms with infection, has very abnormal until
substantial lymph node labs, esp. WBC involvement. Sometimes patient  Treatments include
chemo, rarely presents with infection or chest radiation, and transplant. pain, and abnormal labs
are found.  Some of the new treatments are oral Fever, night sweats and weight loss – and
VERY effective – hold out a lot indicate poorer prognosis. of promise. Incredibly expensive as 
Treatments are chemo, radiation well. and for some, bone marrow or stem  Issues include
infections, fear, cell transplants anxiety and post transplant  Issues include fear, anxiety and
post problems transplant problems  In 2011, @ 47,000 diagnosed and  In 2011, @79,ooo
diagnosed and 23,000 died of leukemias @20,000 died with lymphomas
 54. Common cancers and the treatments commonly used  Multiple Myeloma (p. 703-704) 
Skin cancers – specifically  Screening – not done Malignant Melanoma (p. 451 – 453) 
Hallmark: bone destruction,  Screening – annual skin inspection skeletal pain  Other than MM –
surgical removal,  One “new” drug is thalidomide – usually not a problem significant patient
education  MM – Hallmark – VERY rapid necessary growth and metastasis  Problems with
calcium and uric acid  Requires wide excision, lymph node – may lead to renal failure excision
and aggressive  Emphasis on preventing chemotherapy complications from bone damage 
Issues with body image, VERY  Issues with pain, fractures difficult treatment (some new  In
2011, @ 21,000 diagnosed, meds on the way, but cost is @10,ooo died of multiple myeloma
concern)  In 2011, @ 76,000 diagnosed, @9000 died of malignant melanoma
 55. Common cancers and the treatments commonly used  Liver cancer (p. 1086-1087) 
Pancreatic cancer (p. 1094-1095)  In the US, rarely a primary site for cancer,  Screening not
done in other nations, a common primary site  Hallmarks are abdominal pain and  Screening –
not done unexplained weight loss, sometimes jaundice if bile duct blocked  Hallmarks: History of
cirrhosis, Hep B  Surgery done sometimes, usually or Hep C, jaundice, anorexia, nausea,
chemo, sometimes radiation for vomiting palliation  Treatment is directed toward primary 
Issues include pain, fear site  In 2011, @ 43,000 diagnosed, @ 37,000 died with pancreatic
cancer –  If liver is primary, surgery, chemo just have not made a lot of headway transplantation
sometimes an option on this cancer yet, because the  New technique of radiofrequency and/
cancer has often metastasized by the time of diagnosis or chemoablation may be more effective
  Issues include pain, fear  In 2011, @ 28,000 were diagnosed and @20,000 died with Liver
cancer
 56. Complications of cancer  Nutritional issues  Infections  Cancer emergencies  Pain 
Skin Integrity  Financial
 57. Nutritional issues  Some cancers and some  Some cancers are treated treatments are
hard on the with high doses of steroids GI system that make a person  People often need more
REALLY hungry, and they nutrition during and after gain water and food weight treatment, but
they are not during treatment. They hungry, don’t want to cook get bloated, striae, and feel or
eat. lousy.  Nutritional supplements  They need to eat healthy necessary, sometimes G
frequent small meals, with tubes even. an emphasis on high nutrition and low salt. Right.
 58. Infections  We create new openings:  Surgical sites  IV sites  We give meds/treatments
that decrease the immune response  We give meds/treatments that may mask symptoms of
infection  These are people who have a fever of 100.5, feel lousy and turn out to be septic. 
End up in hospital on IV broad spectrum antibiotics.
 59. Cancer Emergencies  There are many of these – I do a whole 2 hour lecture on them, if
you would like to see it.  Suffice to say, most need to be addressed immediately, and vary with
the type of cancer and the type of treatment.  Oncology nurses and doctors will give patients
information about the ones for which they are at highest risk. Patients need to CALL if they have
these symptoms.
 60. Cancer Emergencies – a few  Malignant pleural effusion  Cardiac tamponade  Superior
vena cava syndrome  Bone metastases and fractures Spinal cord compression  Increased
intracranial pressure  DVTs
 61. Pain  Cancer pain is no different than other pain IMHO – it is just more persistent and
feared  Related to either cancer itself occupying space, or rubbing against something, or
treatment side effects  Very treatable with appropriate methods  ATC meds are the best for
some pain BUT!  Examples:  Surgery, chemo and radiation all can be used to reduce pain 
Pains specialists can be called in to do nerve blocks, ablations to reduce pain
 62. Skin integrity  Serious concern, as any open lesions predispose for infection  Many
treatments dry skin out (some chemos), damage hair and nails (chemo) and may cause nerve
damage, decreasing the ability to feel  Radiation may cause skin damage, and although it is
temporary, it can be very problematic  Skin folds, pannus, neck, mouth, face, perineum –
breakdown is a serious problem  May need wound consult
 63. Financial  People without insurance  Limited options for treatment  Depend on charity 
Meds may be donated by drug companies  Patient may choose not to have treatment at all 
People with insurance  May need to continue working to keep insurance  Co pays and
deductibles may be very high  Billing very confusing at best!  Insurance may refuse some
treatments, need to appeal  Insurance may have cap on treatment costs  Other costs – non-
reimbursable  Time off work  Travel  Meals out  What else?  Many people, even with
insurance, end up declaring medical bankruptcy  Try getting individual policy type life insurance
after having had cancer – not happening
 64. Psychosocial impact of cancer  Fear  Pain  Death  Long treatment regimen  Unknown
 Coping mechanisms  Support groups  Navigators  Cancer Survival Toolbox/Stress
thermometer  Entire family needs assistance, not just patient
 65. Fear  Diagnosis of cancer very stressful for patient and family  Often comes at the end of
several stressful weeks of diagnostic tests  Unfamiliar doctors, unfamiliar terms, scary
treatments  Radiation  Chemotherapy  Cutting  Cannot promise that treatment will work! 
Significant time between beginning and end of treatment, so chronic stressor
 66. Fear of pain  Common concern  Media and others have told of severe, unrelievalbel
cancer pain  Need to address this head on and right away  Need to assess beliefs about pain 
Not inevitable  Treatable  Will not make patient an addict  What else?
 67. Fear of death  People do die of cancer, no doubt about it  Some cancers are very deadly –
which ones did you identify in this talk?  Need to address this head on as well  Ask questions 
Help with advanced directives  Talk about options if needed (Hospice, refusal of treatment, etc.)
 68. Fear of long treatment regimen  Compare with heart attack  Chest pain – go to ER – go to
cath lab – go to OR – recovery and cardiac rehab. First line can all happen within one day. 
Breast cancer – get a routine mammo – get called to come back for more mammos – get called
to come back for a biopsy – go to MD for diagnosis – presented to Tumor Board – have a
 lumpectomy – wait for results – go to oncologist – discuss treatment options – start treatment.
Treatment may take up to 4 months for chemo, then 2 months for radiation, with a month off in
between. So all of the above can take over a year! At which point the oncologist says “Well it’s all
gone, so we are good for now. Come back and see me in 3 months.”
 69. Fear of unknown  How many words have I used so far today that were new to you?  You
don’t have cancer!  Think how hard it would be to hear these words if you were also dealing with
a new diagnosis!  No wonder that people say “The doctor didn’t tell me anything.” What they
meant was “I didn’t hear anything.”
 70. Coping – Support Groups  Research and surveys have indicated that this is VERY helpful
for some people  Some people find on-line groups better than face-to- face, or that may be only
choice for some  Caregiver support groups are very beneficial as well, to help family and loved
ones cope with the changes that cancer, its treatment and its ramifications bring  Usually led by
a nurse or social worker, to guide group and make sure information is accurate
 71. Coping - Navigators  Research and surveys indicate that patients with navigation are seen
faster, more likely to complete treatment and more satisfied with their experience than others. 
Issues:  Navigators do not generate revenue for hospitals, and may in fact cost money  Hard to
quantify the work  Probably will be required in the future to get accreditation by American
College of Surgeons and other groups
 72. Coping – Cancer Survival Toolbox  Series of CDs or downloadable talks that address the
common issues that cancer patients and their families experience  Developed by Oncology
Nurses and Oncology Social Workers  Highly regarded by professional groups as helpful and
accurate  Currently developing more on specific cancers  Go to web site!
 73. Coping – Stress Thermometer  See handouts  Great tool to quickly ID issues and or
problems that you can address each visit  Monitor whether things are getting better or worse 
Clearly indicates (if you use and follow through!) that you know how stressful the cancer
treatment is  Provides you with suggestions for referrals  Fact G sheet – similar tool, but takes
longer
 74. Fact-G Use and Referral Guidelines for Nurse Navigators All Cancer Center patients have
FACT-G completed w/in 2 mos of initial contact w Nurse Navigator Physical Social/Family
Emotional Functional T Score >50 T Score >50 T Score >50 T Score >50 No referral required No
referral required No referral required No referral required T Score <50 T Score <50 T Score <50
T Score <50 Nurse Navigator assesses specific issues contributing to low score Intensify Nurse
Intensify Nurse Navigator contact Navigator contact Referral if appropriate to: Referral if
appropriate to: Referral if appropriate to: Referral if appropriate to: • Med Onc / Rad Onc for •
Med Onc / Rad Onc for • Support Groups • Support Groups symptom mgmt symptom mgmt •
Individual Counseling • Individual Counseling • PT / Cancer Rehab for • PT / Cancer Rehab for •
Spiritual Care • Spiritual Care functional issues fatigue •Physician if medication • Financial
Counseling • Nutrition if related to issues • Nutrition if related to issues possibly needed • Support
groups Repeat FACT-G w/in 1 month end of tx and at 6 mos post-tx if contact continues Draft
8/9/11 Powerpoint Presentations – Flowchart Fact-G Use
 75. Psychosocial impact of cancer  Family issues  Patient advocacy  Lifestyle changes 
Valley of the Shadow of Death
 76. Family issues  Guilt, blame, shame  Body image changes affect the whole family  Role
changes within the family may be significant  Not unusual to have a family member not able to
deal with diagnosis  Can bring some family conflicts to the forefront, especially related to end of
life issues
 77. Patient advocacy  Nurses need to advocate for patients:  Physicians  Pharmacy 
Insurance  Sometimes family!  Sometimes employers  Tale of two breast cancer patients 
“What can we do for Kelly.”  “Take all the time you want – you’re fired.”
 78. Lifestyle changes  Examples:  Patient who scuba dives + new colostomy  Patient with
breast cancer + clothes don’t fit  Patient with pancreatic cancer + well meaning friends who
suggest alternative therapy  Patient who is newly married + prostate cancer and possible
impotence  Patient with stem cell transplant who needs to live in a very clean environment + has
chickens he loves (Has to get rid of them)
 79. Valley of the Shadow of Death  We take people, some of whom have few or no symptoms,
and put them through a terrible ordeal. It is truly amazing that they usually trust us!  You have
seen, or will see, people in the hospital with terrible complications from the treatments: 
 Neutropenia with fever  Awful mouth sores that bleed constantly  Dehydration from ongoing
nausea and vomiting or uncontrollable diarrhea  Malnutrition from anorexia and fatigue
 80. Survivorship  Begins the day person is diagnosed  Whole family/group is survivor 
http://www.cancer.org/Cancer/News/ExpertVoices/po st/2012/06/14/ACS-releases-new-data-on-
survivorship.aspx
 81. Death and Cancer  Still kills a lot of folks.  However:  Cancer gives you time  Usually we
can give you wide awake, alert pain-free quality time  Opportunity for spiritual growth
 82. So why be a cancer nurse?  Always changing, new info  Improvements every day in care 
Research opportunities  Autonomy of practice  People teach you how to live/how to die –
personal growth  Advanced degrees, certifications
 84. Emerging issues  Genetic testing  Survivorship – beyond 5 years  Mitigation of risk
factors – ex. Gardisil  Increasing use of aggressive regimens, especially on elders  When to
stop – 1st recurrence? 2nd recurrence? 3rd recurrence?  Some cancer becoming chronic
illnesses  Incredible cost of care, especially new drugs
 86. Sources of reliable information  American Cancer Society http://www.cancer.org/ 
American Society of Clinical Oncology http://www.asco.org/  Oncology Nursing Society -
research and evidence based guidelines for nursing care http://www.ons.org/  National Cancer
Institute http://www.cancer.gov/  National Coalition of Cancer Survivorship
http://www.canceradvocacy.org/  National Comprehensive Cancer Network – guidelines for all
types of cancer – updated at least yearly http://www.nccn.com/
 1. Care of client with cancers Presenter Dr. F. A. Affey (PhD, MscN, ) LECTURER UMMA
UNIVERSITY
 2. PATHOPHYSIOLOGY OF CANCER Cancer is characterized by abnormal, unrestricted cell
growth beyond their usual boundaries that can then invade adjoining parts of the body and/or
spread to other organs  NEOPLASMS/TUMORS-new growth of abnormal tissue CLASSIFIED
BY: Origin  Manner of growth benign – not invasive or spreading malignant – invasive &
capable of spreading – Metastatic
 3. Classification of tumors cells CARCINOMAS – originate from epithelial Cells
LYMPHOMAS – originate from organs that fight infection LEUKEMIAS – originate from organs
that form blood SARCOMAS – originate from connective , tissue, like bone or muscle
 4. CT Classification of tumors cells METASTASIS or spreading Primary site – areas where
the tumor first forms Secondary site – areas where the cancerous cells move or metastasis 
BENIGN TUMORS – do not move, may just slowly grow larger
 5. ETIOLOGY Cancer is the second leading cause of death globally, and was responsible for
8.8 million deaths in 2015. 1 in 6 every death is caused by cancer Globally, Lung (1.69 million
deaths), Liver (788 000 deaths), Colorectal (774 000 deaths), Stomach (754,000 deaths)& Breast
(571 000 deaths). 70% of cancer deaths occurs in developing countries Cancer is the third
leading cause of death after infectious and cardiovascular diseases in Kenya & among NCD
Second leading cause of death after cardiovascular diseases  annually there are 37, 000 new
cases & over28,000 mortality An average of about 10 new cases per month at GCRH
 6. ETIOLOGY Cancers in women: cervix uteri (40.1/100,000),breast (38.3/100,000) &
oesophagus (15.1/100,000) Cancers in men, prostate (31.6/100,000), Kaposi sarcoma
(16/100,000) and oesophagus (20.5/100,000) (Ferlay et,al 2013). Behavioral risk factors
( tobacco use, harmful use of alcohol, unhealthy diet and physical inactivity) (90-95%) Biological
risk factors (overweight, obesity, age, sex of the individual (30–35%) ? Environmental risk
factors (exposure to environmental carcinogens such as chemicals, Asbestos , aflatoxin,
ultraviolent & ionizing radiation, infectious agents e.g virus, bacteria &parasites ( 15- 20%
infections ) Genetic factors(5-10%) ?
 7. DIAGNOSTIC TESTS Labs & Tumor markers Radiological & Imaging Tests  Xrays  CT
Nuclear medicine scans using radioisotopes  MRI PET(positron emission tomography) scans
Radioimmunoconjugates Ultrasound Fluoroscopy
 8. SIGNS & SYMPTOM OF CANCERS Change in bowel/bladder function Sores that do not
heal Unusual bleeding or discharge Thickening or lump in breast or other body parts
Indigestion or difficulty in swallowing Recent change in a wart or mole Nagging cough or
hoarseness
 9. DIAGNOSTIC TESTS Labs & Tumor markers Radiological & Imaging Tests - Xrays ,CT,
Ultrasound ,MRI Nuclear medicine scans using radioisotopes PET(positron emission
tomography) scans Radioimmunoconjugates Fluoroscopy
 10. OTHER DIAGNOSTIC STUDIES BIOPSY – tissue examined under microscope FROZEN
SECTION – sample frozen and then thinly sliced to see under microscope – for quicker decision
maker ENDOSCOPY – done with scope to upper or lower GI system CYTOLOGY – cells
examined under microscope
 11. STAGING OF TUMOURS Stage I – Malignant cells are confined to the tissue of origin, no
signs of metastasis Stage II – Spread of cancer is limited to the local area, usually to area
lymph nodes Stage III – Tumor is larger, probably has invaded surrounding tissue or both
Stage IV – Cancer has invaded or metastasized to other parts of the body
 12. SURGERY RANGE OF SURGICAL INTERVENTION  Extent of the disease Actual
pathology Age and physical condition of patient anticipated results
 13. TYPES SURGERY Primary treatment used when tumors are confined &have not invaded
vital organs; considered curative Salvage surgery is when there has been a local recurrence of
cancer Prophylactic surgery is when the client is at considerable risk for cancer Palliative
surgery is used to relieve uncomfortable symptoms or prolong life Reconstructive or plastic
surgery done after extensive surgery or to correct defects caused by the original surgery
 14. RADIATION THERAPY Uses high-energy ionizing radiation to destroy cancer cells
External radiation therapy – aimed at specific body location; usually done daily for a specified
number of times; outpatient Internal radiation therapy – sealed brachytherapy done as inpatient
-radioactive source implanted directly into the tumor Possible side effects: alopecia, n/v/d
cystitis, pneumontitis, fatigue, stomatitis, leukopenia, thrombocytopenia, fibrosis Nursing
interventions of client & family teaching
 15. NURSING CARE OF PT. RECEIVING RADIATION Provide information on procedure
&possible side effects Protect skin  Maintain intact oral mucous membrane Provide emotional
support Monitor for s/s of bone marrow suppression Monitor for s/s of bleeding due to low
platelet count
 16. CHEMOTHERAPY Drug Therapy  Antineoplastic drugs are used to destroy Tumor
cells by interfering with cellular function and reproduction Cell Cycle-Specific Drugs – work
when the cell is in a specific stage of reproduction –used for rapidly growing tumors Cell Cycle-
Nonspecific drugs – effective during any phase of the cell cycle or even when not reproducing
 17. ROUTES & DEVICE Oral & IV are the most common routes IV – must monitor for s/s of
extravasation at site or leakage of the drug into the surrounding tissue – Common Vascular
Devices: PICC lines, Hickman or Broviac Catheters, implanated ports – Advantages  long
term use  less venipunctures  less problems when a client has poor veins, drug can go
directly into the heart & central circulation
 18. ADVERSE EFFECTS& NURSING CARE Adverse effects are : n/v most common within
first 24 hrs Stomatitis Alopecia bone marrow Depression fatigue Nursing care-Guidelines
on Safety measures for nurses when administering chemotherapy monitor for s/s of
anaphylactic reactions increase fluid intake administer antiemetic Drugs dietary
 19. BONE MARROW TRANSPLANTATION  Autologous – client receives own bone marrow
that was harvested Allogeneic – receives bone marrow from a histocompatible, but unrelated
donor Syngeneic – client receives bone marrow from an identical twin Stem cell – receive their
own stem cells that have been grown due to infusion of hematopoietic growth factors
 20. OTHER CANCER TREATMENT Immunotherapy uses biologic response modifiers (BRM)
to stimulate the body’s natural immune system to restrict & destroy the cancer cells
Hyperthermia uses temperatures > 106.4F to destroy tumor cells Gene therapy replaces
altered genes with correct genes Clinical trials – testing new treatments for specific cancers
 1. An overview of Cancer
 3.  9.6 million people die from cancer every year.  At least one third of common cancers are
preventable.  Cancer is the second-leading cause of death worldwide.  70% of cancer deaths
occur in low-to- middle income countries.  Up to 3.7 million lives could be saved each year by
implementing resource appropriate strategies for prevention, early detection and treatment.
 4.  A disease which occurs when changes in a group of normal cells within the body lead to
uncontrolled, abnormal growth forming a lump called a tumour – true of all cancers except 
leukaemia (cancer of the blood).  If left untreated, tumours can grow and spread into the
 surrounding normal tissue, or to other parts of the body  the bloodstream and lymphatic
systems, and can affect the digestive, nervous and circulatory systems or release hormones that
may affect body function.
 5. Division of Tumours Benign Malignant Precancerous
 6. Benign • grows quite slowly, • do not spread to other parts of the body • usually made up of
cells quite similar to normal or healthy cells. • cause a problem if they grow very large, becoming
uncomfortable or press on other organs - for example a brain tumour inside the skull. • are not
cancerous Malignant •Grows faster than benign tumours • ability to spread and destroy
neighbouring tissue. •Cells of malignant tumours can break off from the main (primary) tumour
and spread to other parts of the body through a process known as metastasis. • invades healthy
tissue at the new site they continue to divide and grow. •These secondary sites are known as
metastases and the condition is referred to as metastatic cancer. Precancerous •describes the
condition involving abnormal cells which may (or is likely to) develop into cancer.
 7. • Arises from the epithelial cells • Invade surrounding tissues, organs, metastasis to the
Lymph nodes and other area of the body • Common forms of cancer are breast , prostrate, lung
and colon Carcinoma • malignant tumour of the bone or soft tissue (fat, muscle, blood vessels,
nerves and other connective tissues that support and surround organs). • common forms of
sarcoma are leiomyosarcoma, liposarcoma and osteosarcoma Sarcoma • Arise in the cells of the
immune system • Lymphoma is a cancer of the lymphatic system • Myeloma (or multiple
myeloma) starts in the plasma cells, a type of white blood cell that produces antibodies to help
fight infection. Lymphoma & Myeloma
 8. • Occurs in the white blood cells and bone marrow, the tissue that forms blood cells. • There
are several subtypes; common are lymphocytic leukaemia and chronic lymphocytic leukaemia
Leukemia • central nervous system cancers. • Some are benign while others can grow and

9. ⦿ Modifiable risk factors Alcohol Being overweight or obese Diet and nutrition Physical
spread. Brain and Spinal Cord

activity Tobacco Ionizing radiation Work place hazards Infection ⦿ Non-modifiable risk


factors  Age  Cancer-causing substances (carcinogens)  Genetics  The immune system

 10. Unusual lumps or swelling – cancerous lumps are often painless and may increase in size
as the cancer progresses
 11. Coughing, breathlessness or difficulty swallowing – be aware of persistent coughing
episodes, breathlessness or difficulty swallowing
 12. Changes in bowel habit – such as constipation and diarrhoea and/or blood found in the
stools Unexpected bleeding – includes bleeding from the vagina, anal passage, or blood found in
stools, in urine or when coughing
 13. Unexplained weight loss – a large amount of unexplained and unintentional weight loss
over a short period of time (a couple of months) Fatigue – which shows itself as extreme
tiredness and a severe lack of energy. If fatigue is due to cancer, sufferers normally also have
other symptoms
 14. Pain or ache – includes unexplained or ongoing pain, or pain that comes and goes New
mole or changes to a mole – look for changes in size, shape, or colour and if it becomes crusty
or bleeds or oozes
 15. Complications with urinating – includes needing to urinate urgently, more frequently, or
being unable to go when you need to or experiencing pain while urinating Unusual breast
changes – look for changes in size, shape or feel, skin changes and pain
 16. A sore or ulcer that won’t heal – including a spot, sore wound or mouth ulcer Appetite loss –
feeling less hungry than usual for a prolonged period of time
 17. Heartburn or indigestion – persistent or painful heartburn or indigestion Heavy night sweats
– be aware of very heavy, drenching night sweats
 18. Over a third of all cancers can be prevented by reducing your exposure to risk factors such
as tobacco, obesity, physical inactivity, infections, alcohol, environmental pollution,
occupational carcinogens and radiation. Prevention of certain cancers may also be effective
through vaccination against the Hepatitis B Virus (HBV) and the Human Papilloma Virus (HPV),
helping to protect against liver cancer and cervical cancer respectively. Reducing exposures to
other carcinogens such as environmental pollution, occupational carcinogens and radiation could
help prevent further cancers.
 19.  There are a number of cancers which can be identified early which helps to improve the
chances of successful treatment outcomes, often at lower costs and with fewer (or less
significant) side effects for patients.  There are cost-effective tests that help detect colorectal,
breast, cervical and oral cancers early and further tests are being developed for other cancers.
 21. Treatment depends on the type of cancer where cancer is, how big it is, whether it has
spread General health.
 22. Types of Treatment Surgery Chemo therapy Radio therapy Hormone therapy Immunot

23. Surgery ⦿ If a cancer has not metastasized (spread), surgery can remove the entire cancer
herapy Gene therapy


breast or testicle. Radiotherapy ⦿ Radiation treatment or radiotherapy uses high-energy rays to

which may completely cure the disease. Often, this is effective in removing the prostate or a

reduce a tumour or destroy cancer cells as a stand-alone treatment and in some cases in
combination with other cancer treatments.
 24. Chemotherapy Chemotherapy uses chemicals to interfere with the way cells divide -
damaging of DNA - so that cancer cells will destroy themselves. These treatments target any
rapidly dividing cells (not necessarily just cancer cells), but normal cells usually can recover from
any chemical- induced damage while cancer cells cannot. Chemotherapy is generally used to
treat cancer that has spread or metastasized because the medicines travel throughout the entire
body. It is a necessary treatment for some forms of leukaemia and lymphoma.
 25. Immunotherapy Immunotherapy uses the body's own immune system to fight the cancer
tumour. Immunotherapy may treat the whole body by giving an agent that can shrink tumours.
Hormone therapy Several cancershave been linked to some types of hormones, including
breast and prostate cancer.  Hormone therapy works to change hormone production in the
body so that cancer cells stop growing or are killed completely.
 26. Gene therapy The goal of gene therapy is to replace damaged genes with ones that work
to address a root cause of cancer: damage to DNA.  Other gene-based therapies focus on
further damaging cancer cell DNA to the point where the cell destroys themselves. However,
gene therapy is new and has not yet resulted in any successful treatments.
 27. Survivorship Survivorship focuses on health and the physical,psychological, social
and economic issues affecting people after the end of the primary treatment for cancer,
including people who have no disease after finishing treatment, people who continue to
receive treatment to reduce the risk of the cancer coming back and people with well controlled
disease and few symptoms, who receive treatment to manage cancer as a chronic disease.
 28.  Survivorship care includes issues related to  follow-up care,  the management of late
side-effects of treatment,  the improvement of quality of life and psychological and emotional
health.  Survivorship care includes also future anticancer treatment where applicable.  Family
members, friends and caregivers should also be considered as part of the survivorship
experience.
 29. Palliative care  Palliative care runs throughout a patient’s journey from diagnosis to cure
or end of life, and is designed to relieve symptoms and improve a cancer patient’s quality of life.
 It can be used to respond to troubling symptoms such as pain or sickness, and also to reduce
or control the side effects of cancer treatments.  In advanced cancer, palliative treatment might
help someone to live longer and to live comfortably, even if they cannot be cured.
 30. Awareness, understanding, myths and misinformation Access to information and
knowledge about cancer can empower us all.
 31. Prevention and risk reduction Over one third of cancers are preventable, which means we
all can reduce our cancer risk.
 32. Equity in access to cancer services Life-saving cancer diagnosis, treatment and care should
be equal for all – no matter where you live, what your income, your ethnicity or gender.
 33. Government action and accountability Governments can influence many of the levers to
reduce and prevent cancer.
 34. Beyond physical: mental and emotional Impact The impact of cancer goes far beyond
physical health, impacting the mental and emotional wellbeing of patients and their caregivers.
 35. Saving lives saves money The financial impact on nations, individuals and families have a
huge impact on sustainable economic and human development. By focusing on saving lives, we
can also save money
 36. Reducing the skills gap A shortage of skilled healthcare workers is one of the greatest
barriers in delivering quality cancer care. Working together as one By joining forces, we help to

37. The Cancer Atlas: History of Cancer ⦿ Explore a timeline of the history of cancer from BCE
strengthen efforts that stimulate powerful advocacy, action and accountability at every level.

to 2011 ⦿ National Cancer Institute: Dictionary of Cancer Terms ⦿ Cancer terms explained


International Agency for Research on Cancer: Global Cancer Observatory ⦿ An interactive web-
based platform presenting global and national cancer statistics to inform cancer control and
research

country, including data on mortality, incidence and risk factors The Cancer Atlas: Risk Factors ⦿
 38. World Health Organization: Cancer Country Profiles Synthesized national cancer data by

39. The Cancer Atlas: How to take action ⦿ Discover the opportunities for controlling cancer
Understanding risk factors and causes of cancer

World Cancer Research Fund: Facts and Figures on specific cancers ⦿ World Cancer Research


Fund International is the world’s leading authority on cancer prevention research related to diet,

40. World Cancer Research Fund International: Cancer prevention recommendations ⦿ Explore
weight and physical activity


cancer ⦿ Access over 120 individualized and oncologist- approved guides Cancer.Net: Questions
the recommendations on helping to prevent cancer Cancer.Net: Individual guides on each type of

to ask your doctor ⦿ Find guidance on what to ask your health team, as approved by the

41. ⦿ National Comprehensive Cancer Network: Cancer Staging ⦿ Understand what cancer
American Society of Clinical Oncology

stages mean ⦿ National Cancer Institute: Types of treatment ⦿ Understand the treatment options


42. National Comprehensive Cancer Network: Patient and Caregiver Resources ⦿ These
for cancer


caregivers Rethink Breast Cancer: Care guidelines ⦿ This guide is aimed at young women with
guidelines and video resources are aimed specifically at individuals with cancer and their

43. UICC and Bupa: Working with cancer ⦿ A resource for both employers and employees
breast cancer to help them navigate their treatment

International Psycho Oncology Society: Survivorship ⦿ Download a practical guide for patients


44. Medical News Today: Most recent research breakthroughs ⦿ Read about how close we are
and caregivers

to finding more effective treatments Union for International Cancer Control: Members ⦿ Find a


national cancer organization near you

 1. SHOCK DR MEMBA NYANDIGISI MODERATOR DR.GATHIRI
 2. OBJECTIVES • DEFINITION OF SHOCK • CLASSIFICATION OF SHOCK • ETIOLOGY OF
SHOCK • PATHOPHYSIOLOGY OF THE DIFFERENT TYPES OF SHOCK • CLINICAL
MANIFESTATIONS • DIAGNOSIS • COMPLICATIONS OF SHOCK • MANAGEMENT
 3. SHOCK • DEFINITION • Shock is a global state of tissue hypoperfusion,in short it is a state in
which blood supply is insufficient to provide enough oxygen to tissues to support normal cellular
functions or metabolism,leading organ failure through tissue hypoxia and death.
 4. Definition of Terms • Cardiac Output-the amount of blood pumped by the heart • Mean
Arterial Pressure-average arterial pressure through one cardiac cycle.[usually 60-65]. • Systemic
Vascular Resistance-resistance in the circulatory system used to create blood pressure • Central
Venous Pressure-is the BP in the vena cava near the right atrium. • Pulmonary Wedge Pressure-
pressure in the left atrium of the heart.
 5. Definition Of Terms… -Afterload-the amount of pressure that the heart needs to exert to
eject blood during ventricular contraction • Preload-stretch of the myocardium or end diastolic
volume of the ventricles. • Stroke Volume-the volume of blood pumped out of the hearts left
ventricle during each systolic cardiac contraction.
 6. Cardiac Physiology • How Blood Circulates Occurs in 2 phases i.e -]Pulmonary circulation-
from heart to lungs to heart. -]Systemic Circulation-from heart to rest of the body to heart.
 7. diagram
 10. PHYSIOLOGY OF SHOCK • The circulatory system is a circuit in which blood continually
circulates through a series of vessels and generates blood pressure. • MAP is the driving force
that pushes blood into the tissues. • This is summerised by the equation
MAP=HR*SV*SVR+CVP,whereby MAP is the pressure on the arterial side, CVP is the pressure
 on the venous side,Flow is cardiac output [CO],and SVR is the resistance within the blood
vessels,That must be overcome for blood to flow to tissues.
 11. Frank sterling curve
 12. This curve describes the relationship between the volume of the blood filling the heart and
volume it ejects,directly proportional. • Stroke volume is dependant on • -Preload-which is the
filling pressure or volume of the heart,the amount of blood in the ventricles • -contractility-which is
the hearts ability to squeeze. • Stroke volume increases as end diastolic volume rises within
physiologic limits.
 13. Compensatory Mechanisms of Shock. • A decrease in MAP will cause • -Decreased
baroreceptor stimulation from stretch of large arteries • -Decreased stimulation of atrial stretch
receptors • -Decreased chemoreceptor stimulation of vasomotor centres which are sensitive in • -
oxygen tension,which decreases in shock, • C02 content,which increases in shock, • Hydrogen
ion concentration which increases in shock
 14. • Aftermath of this will be decreased parasympathetic nervous system activity and increased
sympathetic activity,,and also an increase in neurohormonal responses, • These responses are
aimed at increasing SVR,CO,and CVP.
 15. Compensatory mechanisms in: • Cardiovascular-increased SNS,activity leads to
stimulation of alpha -1 adrenergic receptors resulting in • -increased vasoconstriction leading to
increase which helps increase in SVR • -Redistribution via shunting of blood from
intestine,kidney • -overall effects lead to increased SVR • -increased inotropy
 16. • Hormonal • -there is a role of hormones such catecholamines and pro-inflammatory
cytokines which stimulate the release of corticotropin releasing hormone from hypothalamus
resulting in the release of ACTH from pituitary ,causing • -release of cortisol-by retention of
sodium. • -release of aldosterone leads to retention of sodium ions effect
 17. Pathophysiology Of Shock.and IRREVERSIBLE SHOCK • Shock occurs when the bodys
compensatory mechanisms are inadequate to counteract the reason for hypoperfusion • Shock
when prolonged occurs in 3 phases which represents progressive failure of bodys compensatory
mechanisms to offset the primary cause • If shock progresses,the eventual result is cellular and
mitochondrial damage.
 18. The 3 phases • Compensated-this is where the bodys neurohormonal responses counteract
the initial loss of blood pressure,hemodynaics are maintained and MAP is normalized. •
Decompensated –if the primary cause of the hypoperfusion is not corrected,the bodys
compensatory mechanisms are overwhelmed,ongoing hypoperfusion and cellular death lead to
micro-circulatory dysfunction • Irreversible phase-this is the phase whereby there is extensive
tissue damage,mitochondrial dysfunction,prolonged and any intervention to reverse this phase is
difficult ,however how much you try to intervene.
 19. Vicious cycle of shock.
 20. Understanding types of shock • Shock that occurs when the pump is affected- something
here prevents the heart from moving blood forward[e.g in cardiogenic,bradycardic,obstructive
shocks] • Shock that occurs when the tank is affected-here there is no enough blood volume to
fill the circuit[e.g hypovolemic/hemorrhagic] • Shock that occurs when the pipes are affected-here
the blood vessels don’t have adequate tone,which impaires the distribution of blood to tissues[e.g
in septic shock]
 21. image
 22. Types of Shock. • Hypovolemic shock[hemorrhagic shock] • Cardiogenic shock • Obstructive
shock • Bradycardic shock • Vasodilatory/Distributive shock[septic,neurogenic, shocks].
 23. receptors
 24. Drug vs receptors
 25. Image
 26. HYPOVOLEMIC SHOCK • Hypovolemic shock occurs due to loss of circulating
volume,while this is commonly due to blood loss,that is termed as hemorrhagic shock,other
examples include,fluid losses example in severe vomiting,diarrhea,surgical fluid losses,NGT
losses. • Hemmorhagic shock is the most common type of shock in trauma patients.
 27. Hemorrhagic shock • Occurs when there is massive blood loss,usually in trauma ,patient
and it is classified in classes. • Typically, this is shock that occurs when the tank is affected.
 28. Classes of Hemorrhagic Shock.
 29. Causes of hemorrhagic shock • Penetrating abdominal trauma • Blunt abdominal trauma
e.g at the level of the chest ,abdomen and retroperitoneum,pelvis,major long bones and their
surrounding soft tissues.
 30. Common bleeding cavities.
 31. Diagnosing Hemorrhagic shock. • There are 4 parameters used in the diagnosis of
hemorrhagic shock.i.e • -systolic blood pressures • -base deficit • -serum lactate • -hemoglobin
and hematocrit
 32. • SBP • -of less than 90mmHg is defines hypotension and hypoperfusion • Serum lactate-
usually elevated during shock,indicating inadequate tissue perfusion after switching to anaerobic
metabolism • Base deficit-usually elevated in connection to anaerobic metabolism and metabolic
acidosis,during shock. • Hemoglobin/hematocrit-there is an automatic decrease during
hemorrhagic shock
 33. Clinical signs • Tachycardia • Hypotension • Cold,clammy skin • Delayed capillary refill •
Low urine output • Mental status changes
 34. Imaging • Chest x ray • Pelvic radiograph • FAST • Efast-also assess hemopneithothoraces,
• DPL • CT scans.
 35. Complications of hemorrhagic shock • Multi Organ Failure • AKI • DIC • Death
 36. Traumatic shock • This results from soft tissue injuries,long bone fractures and the
associated blood loss. • Traumatic shock causes a more extreme physiologic insult than simple
hemorrhagic shock ,e.g ,Multi organ failure,including ARDS,develops relatively ,often in the blunt
trauma patient but but rarely after pure hemorrhagic shock • Can also occur as a combination of
hypovolemic,neurogenic or obstructive shock..
 37. • Traumatic Shock • It is vital to correct the things that worsen the inflammatory cascade
and activate pro-inflammatory cytokines. These include: prompt control of hemorrhage,
adequate volume resuscitation to correct O2 deficit, debridement of nonviable tissue,
stabilization of bony injuries, and appropriate treatment of soft tissue injuries.
 38. Treatment • Stop the bleeding • Secure airway • Restore circulation –initially crytsalloids,but
limited,definitive is early blood transfusion,via the MTP in a ratio of 1:1:1 of
PRBCs:FFP:Platelets, • Role of tranexamic acid-within 3 hrs in trauma • Role of vasopressors •
Permissive hypotension? • Close monitoring of vital signs • NB-early recognition and intervention
is KEY.
 39. Stop the bleeding • If external bleeding is visible from injury to a major vessel,apply direct
pressure • If unstable patients with possible intrathoracic bleeding,empiric chest tube
thoracostomy is indicated • If pelvic bleeding is suspected as the source,a pelvic binder is placed
• In a patient with GI bleeds,NGT decompression and lavage will be critical to diagnosis and
management. • In a patient with post –operative bleeding,complications management,typically
requires returning to the OR.,to identify and control bleeding
 40. Restore the circulating volume. • Obtain a vascular access promptly-can range from a
normal gauge 18 cannulae,to I.O,CVC, • Restore circulating volumes-guidelines have shifted
from giving crystalloids,to giving blood in the setting of active bleeding.if you don’t have blood
you can bolus with 1-2 L if ringers. • For patients with ongoing active bleeding,give red blood
cells ,FFP,Platelets in a ration of 1:1:1 • If cross –matched blood is unavailable,give type O-ve
uncrossed blood
 41. • For females of child bearing age ,Rh-ve is preferred to prevent sensitization,but only if
Rh+ve is available,the patient needs to be treated with rhogam./anti-D. • Continuous infusion of
large volumes of fluid and blood is not a substitute for definitive control of bleeding. • Definitive
management of bleeding is achieved in the operating room.
 43. MASSIVE TRANSFUSION PROTOCOL • This the administration of 10 or more units of
PRBCs within 24 hrs ,or more than 4 PRBCs within 1 hour. • The primary objective of a massive
transfusion is to prevent fatal outcomes resulting from shock,while striving to attain hemostasis •
Patients across medical specialties may require massive transfusion,although cardiac and
vascular surgeries are the most common scenarios,that necessitate massive transfusion.
 44. • The primary goal of massive transfusion is to sustain cardiac output and optimize on
oxygen carrying capacity. • MTPS should prioritize the delivery of of PRBCs,along with platelets
and FFPs. • It is give in the ratio of 1:1:1[plasma,platelets and RBCs]
 45. Assessment of Blood Consumption. • Th assessment of need for MTP is based on the ABC
score ,which has 4 parameters which are • -peneratrating mechanism-1 point • -SBP less than
90-1 point • -heart rate more than 120-1 point • -FAST[positive]-1 point.
 46. Interpretation ABC [assessment of blood consumption score] of 2 or more is used a
threshold to activate a massive transfusion.
 47. Setting up MTP • Effective communication with blood banks • Sufficient number of personnel
• A blood warmer • A blood refrigerator with blood inside[8 units of o negative,PRBCs ,8 units,of
thawed group AB or low titer anti-B group A plasma.] • Inclusion of in line fluid warmers and
surface warmers • Continuous core temperature monitors • An invasive arterial blood pressure
monitor • Iv calcium preperations • Point of care testing for various bodily functions,including
ABGs,hb,electrolytes,lactate and thromboelastography, • Rapid infusion pumps
 48. • Continuous monitoring through out the resuscitation should include steps for assessing
coagulopathy and treatment of acid base disorders,hypothermia and electrolyte abnormalities. •
Ideal monitoring involves measuring pH,blood gases,electrolytes and metabolites such as
glucose every 20 to 30 minutes.
 49. Goals For MTP. • MAP of 60 to 65 • Hb btn 7-9 g/dl • INR below 1.5 • Fibrinogen levels
within 1.5 to 2g/l • Platelet count above 50000 micromole/L • PH btn 7.35 to 7.45 • Core temp of
above 35 degrees celcius.
 50. Complications of MTP • hypothermia • dilutional coagulopathy •
hypocalcemia,hypomagnesemia,citrate toxity, • metabolic acidosis • hypokalemia/hyperkalemia •
air embolism • TRALI[transfusion related acute lung injury] • TACO[transfusion related circulatory
overload] • infection,sepsis. • hemolytic transfusion reaction. • GVHD
 51. Role of vasopressors in hemorrhagic shock • During hemorrhagic shock,blood loss causes
a fall in decrease cardiac output and consequently oxygen transport, • The current
guidelines ,recommend the administration of vasopressor together with fluids in order to maintain
arterial pressure when life threatening hypotension occurs. • Nor-epinephrine has shown to
increase the MAP via,a-1 and b-1by increased SVR and C.O respectively.
 52. • Limitations with vasopressors can lead to worsening ischemia secondary to prolonged
vasoconstriction . • NOR-EPINEPHRINE • -potent a1 and weak b1 agonist,causes
vasocontriction,and increases vascular tone. -is the vasopressor of choice in septic shock -dose
is 2-30 micrograms /min
 53. Epinephrine • Potent a1,2 and b1,2 ,agonist • Causes vasoconstriction through
a1,chronotropy through b1,and inotropy through b1 • Dose 1-20ug • Used as a vasopressor for
inotropic support,though has risk of tachyarrythmias • Used in cardiogenic shock,late
septic,pediatric,anaphylactic shock
 54. vasopressin • Works via the vasopressin receptor[v1] • Usual dose is 0.03 to 0.04 units/min
• Used in septic shock,as an adjunct to catecholamines • Works by constricting blood vessels
hence increase in blood pressure.
 55. ephedrine • A sympathomimetic working as a direct and indirect alpha and beta receptor
agonist • Causes an indirect release of nor-epinephrine,inhibits nor epinephrine re-uptake plus
replace norepinephrine from storage vesicles. • Raises blood pressure by causing an increase in
myocardial contractility,and heart rate,hence increase in cardiac output. • Also causes peripheral
vasoconstriction
 56. dopamine • Works via Dopamine receptor agonist,b1agonist,a1 agonist at higher doses. •
Given in 1-20ug/kg/min • Used in septic shock if nor-epinephrine is unavailable,also carries a
higher risk of tachyarrythmias. • No clear data on renovascular dilation .
 57. phenylephrine • Pure a1 agonist, • A weak vasoconstrictor • Dose is 25 to 300ug/min • Used
in neurogenic shock by improving vascular tone.
 58. dobutamine • Primarily b1 agonist with weak b2 agonist, • Causes inotropy and some
vasodilation • Dose is 2-10ug/min • Used in cardiogenic shock to improve cardiac function and
reduce afterload.
 59. Milrinone • A PDE inhibitor increasing cAMP and augmenting LV relaxation,causes inotropy
and vasodilation. • Dose is 0.5mcg/kg/min • Used in cardiogenic shock to improve cardiac
function and reduce afterload.
 60. Permissive hypotension. • Is a strategy used in trauma care where a lower than normal
blood pressure is deliberately maintained in patients with active bleeding, • The goal of this is to
maintain adequate organ perfusion without causing further bleeding. • By avoiding aggressive
 fluid resuscitation[which increases blood pressures],permissive hypotension helps to prevent
dislodging clots that may have formed at the site of injury and reduce risk of further bleeding.
 61. • This strategy is employed in trauma patients with active hemorrhage ,particularly those
with penetrating injuries or internal bleeding , • Permissive hypotension is a balancing act ,it
involves careful monitoring of the patients vital signs and adjusting the level of hypotension •
Limitations of permissive hypotension,are organ dysfunction or brain injury if there is prolonged
hypotension. • Exclusions of permissive hypotension are those with spinal cord injuries and
TBI,and very elderly patients.
 62. Excessive crystalloid resuscitation can cause.. • A rise in cardiac output,hence increasing
MAP-more bleeding • Dilution coagulopathy • Popping the clot/clot dislodgement • Hypothermia •
Edema causing abdominal compartment syndrome • Organ failure
 63. Choice of fluids during in hypovolemic shock. • In hypovolemic shock fluid resuscitation
aims to quickly restore adequate blood volume and perfusion to vital organs. • Initial treatment
involves rapid administration of isotonic crystalloid solutions like Ringers/Normal saline in
boluses of 1 -2 L, • Close monitoring of vital signs is key. • In hemorrhagic shock ,the fluid of
choice is blood products,
 64. BRADYCARDIC SHOCK This is where severely low heart rate causes/leads to inadequate
cardiac output ,hence a state of hypoperfusion of vital organs. Bradycardia is when the heart rate
is less than 60b/min • Many patients will tolerate lower heart rate without impaired tissue
perfusion. • Assessing perfusion in response to bradycardia will determine need for intervention.
 65. Determinants of MAP in relation to Bradycardic shock
 66. Causes • Sick sinus syndrome • A-V BLOCKS [Complete heart blocks]. • MI[esp.inferior wall
MI.] • Medications[beta blockers,ccb,digoxin’] • Electrolyte imbalance. • Hypothyroidism •
Hypothermia • Increased vagal tone [during intubation/suctioning]. • Spinal cord injuries
 68. A word about sick sinus syndrome • A group of abnormal heart rythms caused by
malfunction of the SA node,the hearts primary pacemaker. • It is caused by intrinsic and extrinsic
factors that affect the functioning of the SA node. • Intrinsic causes tend to be responsible for
permanent SA node dysfunction,while extrinsic causes are more commonly temporary. •
Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which t he arrythmia
alternates between fast and slow heart rates.
 69. Intrinsic causes • Age related degenerative changes of SA node.[most common] • Heart
failure • Atrial fibrillation • Sarcoidosis • Amyloidosis • Hemochromatosis • Rheumatic fever •
Chagas • Lyme disease • Atheroslerotic and ischemic changes to SA node artery.
 70. Extrinsic Causes • Beta –blockers • CCBs • Digoxin • Hyperkalemia • Hypokalemia •
Hypocalcemia • Hypothyroidism • hypoxia • hypothermia
 71. Signs and symptoms • HR less than 50 • Hypotension sbp less 90/MAP less than 65 •
Altered mental status • Cold,clammy skin, • Syncope/pre-syncope • Dizziness • Shortness of
breath • Chest pain or discomfort.
 72. Treatment. • Atropine 1 mg every 3-5 mins[max 3 mg] • Transcutaneous pacing • Iv
dopamine [2-10mcg/kg/min] • Iv epinephrine 2-10 mcg/min] • Manage the underlying cause.-stop
AV nodal blockers via beta blockers,correct hyperkalemia,hypothyroidism • Role of calcium
gluconate • Glucagon • Insulin+glucose in CCB /beta blocker overdose
 73. CARDIOGENIC SHOCK • Cardiogenic shock is similar to bradycardic shock in that cardiac
output is impaired. • However, rather than a low heart rate, the issue is decreased heart muscle
contractility, which leads to decreased stroke volume.
 75. Causes The most common cause of cardiogenic shock is myocardial ischemia due to
myocardial infarction. The degree of ischemia determines the degree of tissue injury and whether
enough heart muscle is involved to impair contractility. Other causes include blunt cardiac injury
or penetrating injury from trauma; arrhythmias; cardiomyopathies; myocardial depression from
systemic illnesses, such as sepsis; papillary muscle rupture; valvular disorders, for instance, as
can be seen with severe mitral regurgitation; and congestive heart failure.
 76. Diagnosis Signs and Symptoms of Hypoperfusion + Hypotension that persists for > 30
minutes Reduced cardiac index < 2.2 L/min/m2. The cardiac index (CI) is simply total cardiac
output based on the patient's size as body surface area. For instance, if a patient's cardiac output
is 4.5 liters/minute, and his body surface area is 1.25 m2, his CI would be: CO/BSA = 4.5/1.25 =
3.6 L/min/m2. Increased pulmonary capillary wedge pressure (PCWP) > 15 mmHg Additional
investigations ECG ECHO Chest Xray
 77. treatment  Identify the cause and reverse those things that are reversible. For instance, if
myocardial ischemia is the cause, revascularization  Fluid administration or diuresis may be
helpful depending on fluid status.  Inotropic agents may be helpful as supportive agents to
improve cardiac contractility. These include milrinone and dobutamine, though both may cause
vasodilation, worsening hypotension. In this situation, dopamine, epinephrine, or norepinephrine
can be added as they also have some inotropic effects but can counteract vasodilation.
 78. • Though relatively uncommon, blunt cardiac injury is a cause of cardiogenic shock • Blunt
cardiac injury (BCI) is the injury sustained to the heart in blunt trauma. • The most common type
of BCI is a myocardial contusion with the right side more commonly affected than the left
 80. OBSTRUCTIVE SHOCK. • This is the type of shock caused by physical obstruction to blood
flow,either into or out of the heart or great vessels., • This obstruction prevents adequate blood
flow to the body leading to tissue hypoxia • In obstructive shock there is: • - reduced cardiac
output, • -impaired blood flow,
 81. OBSTRUCTIVE SHOCK.
 82. • Obstructive shock should be suspected in patients with evidence of tissue hypoperfusion
and a history of trauma (tension pneumothorax and pericardial tamponade must be ruled out in
this situation), central line placement (tension pneumothorax), mechanical ventilation, or risk
factors for pulmonary embolism. • Treatment is relieving the obstruction through tube
thoracostomy, pericardial drainage, Thrombolytics etc
 83. Causes • Pulmonary embolism • Cardiac tamponade • Tension pneumothorax • Restrictive
cardiomyopathy • Constrictive pericarditis • Tumors compressing the heart or great vessels,
 84. Symptoms/signs • Hypotension • Tachycardia • Tachypnea • Cool,clammy skin • Altered
mental status • Decreased urine output • Raised JVP,
 85. treatment • Addressing the underlying cause • -cardiac tamponade-periacardiocentesis • -
tension pneumothorax-needle decompression • -pulmonary embolism-thrombolysis/embolectomy
• -aortic stenosis-valve replacement • -aortic dissection-surgical repair • -tumor or mass -resect
 86. Supportive management • Fluid resuscitation • Vasopressors • Oxygen therapy •
Monitoring
 87. DISTRIBUTIVE SHOCK • In distributive shock, also known as vasodilatory shock, the
underlying cause is profound vasodilation of the vascular beds or a decrease in systemic
vasculature resistance (SVR). • This either occurs because there is an impairment in control of
vasomotor tone, as happens with neurogenic shock, or because of the release of inflammatory
mediators that cause vasodilation, as with septic shock. • Thus, in distributive shock, hypotension
results from failure of the vascular smooth muscle to constrict appropriately • Also referred to as
the Final Common pathway for all progressive shock
 89. Types of Distributive shock. • Septic • Neurogenic • Anaphylactic
 90. Anaphylactic shock • Is a severe life threatening allergic reaction after exposure to some
allergen, • Occurs after the immune system produces antibodies which fights the antigen from
the allergen and elicits an antibody -antigen reaction. • Pathophysiology is widespread systemic
vasodilation and increased vascular permeability
 91. Signs and symptoms • Flushing • Hives • Rapid ,irregular pulse • Swelling of the throat and
tongue,with breathing difficulty. • Rhinitis/asthma • Vomiting,diarhoea,stomach cramps •
Hypotension,light headedness.
 92. causes • Insect bites • Stings • Food allergies • medications
 93. treatment • Involves supportive care • -oxygen • -epinephrine • -antihistamines • -
 94. SEPTIC SHOCK • Sepsis is a life-threatening organ dysfunction caused by a dysregulated
host response to infection. • Septic shock is when sepsis is complicated by organ dysfunction
and systemic hypotension refractory to an adequate fluid challenge. • Pathophysiology • When
cells are damaged, they release specific molecules or triggers that initiate the inflammatory
process, thus alerting the immune system to the presence of damage to initiate the inflammatory
response. These include damage-associated molecular patterns (DAMPs) and pathogen-
associated molecular patterns (PAMPs) eg endotoxin LPS found in cell wall of Gram Negative
bacteria
 95. • The gram-negative, gram-positive, or fungal PAMPs trigger an inflammatory response,
which can be appropriate and beneficial or dysregulated and harmful. • The dysregulated or
uncontrolled host immune response to these PAMPs causes the lethal consequences of sepsis •
Signs and Symptoms • Tachycardia (increased SV and CO) • Altered mental status • Tachypnea
 96. • Patients may also have signs and symptoms related to infection: • Fever, chills, rigors •
Leukocytosis • Hyperglycemia • SOFA • The sequential organ failure assessment (SOFA) is
useful in identifying organ dysfunction in patients suspected to have sepsis. This score assesses
six systems - respiratory, neurologic, cardiovascular, renal, hepatic, and hematologic - to
determine organ dysfunction. Each system receives a score of 0-4. A change in SOFA ≥2 above
baseline indicates organ dysfunction.
 98. • SOFA score correlates with mortality. A score of < 9 carries a mortality of < 33%. For a
score of 9-11, mortality is 40-50%. A SOFA score > 11 points is associated with a mortality of >
95% • Due to the complex nature of the SOFA score a modified qSOFA score has been adopted
which has a similar predictive value outside the ICU setting • qSOFA is a bedside screening test
that is rapid and repeatable. It uses only three criteria, all of them based on observation or vital
signs, and the patient is assigned 1 point for each abnormality: • RR ≥ 22 • ANY alteration in
mental status (GCS < 15) • SBP ≤ 100
 99. • Once the qSOFA score has been determined, apply the following rules: • 0-1 The patient is
not at a high risk and management should continue as appropriate • Any concern should prompt
a search for an infectious source. • qSOFA ≥ 2 should prompt assessment of organ dysfunction
(such as through the use of the full SOFA score).
 100. Treatment • As per The Surviving Sepsis Guidelines • Managing infection: • HOUR-1
BUNDLE-emphasizes on • -obtaining blood cultures before antibiotics • -administration of broad
spectrum antibiotics • -starting of fluid resuscitation with crystalloids • -measuring lactate levels • -
beginning vasopressors • • Antibiotics: Administer broad-spectrum intravenous • antimicrobials
for all likely pathogens within 1 hour after • sepsis recognition
 101. • • Source control: Obtain anatomic source control as rapidly • as is practical • • Antibiotic
stewardship: Assess patients daily for de- escalation • of antimicrobials; narrow therapy based on
cultures and/or • clinical improvement
 102. • Managing resuscitation: • • Fluids: For patients with sepsis-induced hypoperfusion,
provide • 30mL/kg of IV crystalloid within 3hours with additional fluid based on frequent •
reassessment (BPS), preferentially using dynamic variables to • assess fluid responsiveness. • •
Resuscitation targets: For patients with septic shock requiring • vasopressors, target a mean
arterial pressure (MAP) of 65 mmhg -Use Norepinephrine as the first line vasopressor of choice
 103. • Early Vs late Septic Shock • The initial phase of septic shock is also known as Warm
shock because Peripheral vasodilation maintains the warm peripheries. • This phase is
associated with more stroke volume and cardiac output • If shock persists, SIRS progresses
leading to myocardial damage which results in poorer conductivity and Cardiac Output
 104. Neurogenic shock • Neurogenic shock is a form of distributive shock due to loss of
vasomotor tone resulting from disruption of the autonomic pathways in the spinal cord. • Loss of
vasoconstrictor impulses results in increased vascular capacity and decreased venous return •
However, there is bradycardia in neurogenic shock due to autonomic disruption, as contrasted to
the tachycardia in other forms of distributive shock. This causes a decreased cardiac output
rather than increased cardiac output typically associated with other forms of distributive shock
 105. • Neurons controlling the cardiac and vascular systems are found between T1 and T4.
Pathology at or above this level will interfere with autonomic sympathetic pathways and, as a
result, the sympathetic tone of the heart and vascular system. Such pathologies may include:
Spinal cord Trauma Spinal cord Neoplasms -spinal or epidural anesthesia
 106. spinal shock vs neurogenic shock • spinal shock refers to flaccidity and loss of reflexes
after spinal cord injury below the level of the injury and is typically reversible. • it refers to cord
injury and has nothing to do with blood pressure or tissue perfusion.
 107. • Pathophysiology • Sympathetic input is disrupted: To peripheral vasculature. To the
heart, which usually increases heart rate and contractility. To the adrenal medulla, which
normally releases catecholamines. • Disruption of sympathetic stimulation leads to:
Hypotension and bradycardia. Loss of regular reflex tachycardia. This results in low cardiac
output.
 108. Diagnosis When making a diagnosis of neurogenic shock, it is important to note that the
severity of the spinal cord injury correlates to the severity of the shock. Further, complete motor
injury is more likely to have neurogenic shock than partial cord injury. Physical examination may
show:  Hypotension  Bradycardia  Warm extremities  Motor and sensory deficits  Altered
thermoregulation[poikilothermia]
 109. Treatment • The goals of treatment in neurogenic shock are to: • Restore tissue perfusion,
which should occur before operative intervention to stabilize vertebral fractures. • Prevent
secondary tissue injury. Recall that hypotension, if ongoing, will continue to cause hypoperfusion,
which will worsen damage to the brain, spinal cord, and other tissues. • Maintaining spinal
stabilization. A cervical collar should be kept on the patient for cervical spinal cord injuries. Spinal
motion should be restricted, including throughout any procedures and intubation.
 110. • Treatment • Fluid resuscitation. This is an essential part of care for patients with
neurogenic shock and is sufficient for the treatment of hypotension in most.isotonic crystalloids
commonly normal saline is used. • Vasopressor administration. Hypovolemia must be excluded
as a cause and treated. If patients remain hypotensive, vasopressors are the next-line treatment
and improve peripheral vascular tone. Dopamine or phenylephrine (pure -agonist) are the
vasopressors of choice. ɑ • A brief duration of vasopressors is sufficient (24-48 hrs). However,
hypotension or dysrhythmias may occur up to 14 days after injury. • There is no evidence of
benefit from steroids, which are not routinely recommended,but methylprednisolone has been
shown to have positive effects during early stages of spinal cord injury.[within 8 hours of injury]
 111. Undiffrentiated shock • In this Scenario the patient meets the criteria for diagnosis of
shock but the cause is uncertain • A 70 year old patient with a history of longstanding Diabetes
and Hypertension undergoes a Right Hemicolectomy, 3 hours post op you are called to review
him. On Examination, the patient's heart rate is 124 bpm and his blood pressure is
86/61mmHg.He is oliguric and confused. • 1.Does he meet the criteria for a diagnosis of shock? •
2.How would you approach this patient?
 113. Approach to a patient with shock. • When shock is suspected, the priority, as with all
critically ill patients, is the ABCs. • This involves ensuring a secure airway and adequate
breathing and establishing intravenous access. • A fluid bolus should be initiated as most causes
of shock will respond to IV fluids, which should improve blood pressure and perfusion even as
you look for the reason for the shock. • The cause of the shock may become apparent based on
the initial assessment of ABCs, eg in the case of a tension pneumothorax in a trauma patient
with absent breath sounds and tracheal deviation
 114. • 2.Brief and Focused history and examination. Has the patient been involved in a trauma?
Does the patient complain of chest pain or shortness of breath? Are they vomiting blood? Is there
a known exposure to an allergen? In addition to helping you determine the cause of the shock,
this brief assessment may allow you to immediately identify life-threatening issues that require
emergent intervention, such as needle decompression of a tension pneumothorax or emergent
administration of epinephrine in anaphylaxis. • If the cause is not identifiable, the focused history
and exam will guide on interventions • Point of care ultrasound has emerged as a valuable tool in
the initial assessment of shock
 115. ultrasound in shock • there are many approaches and algorithms,that use ultrasound to
reacha diagnostic conclusion,e.g • -RACE[rapid assessment by cardiac echo] • -FOCUS[focused
cardiac ultrasound] • -ACES[abdominal and cardiac evaluation with sonography for shock] •
RUSH[rapid ultrasound for shock and hypotension] • This methods normaly examine the
heart,and other organs,to obtain further information about potential cause of shock
 116. point of care ultrasound in shock. • is a valuable tool for diagnosingand mnaging patients in
shockby providing rapid,bedside assessment of multiple organ sysytems. • it aids in
differentiating between various shock etiologies,guiding treatment and monitoring response to
interventions.
 117. POCUS • For evaluation of the heart; • Pericardium. A finding of a pericardial effusion,
especially with impaired cardiac function or a compressed right ventricle, supports tamponade as
the cause of shock. • Left ventricle. A finding of reduced function may indicate pump failure
(cardiogenic shock), whereas small, underfilled chambers that are rapidly contracting may
indicate hypovolemia or sepsis. • Right ventricle. A finding of reduced function may indicate
pump failure. In contrast, an enlarged or dilated right ventricle, especially with the septum bulging
toward the left
 118. • The IVC is assessed 2 cm distal to where the hepatic vein or veins enter it. The goal is to
determine the change in IVC diameter with respiration. This varies depending on whether the
patient is mechanically ventilated or breathing spontaneously. • The maximum IVC diameter is
seen at the end of expiration for patients who are breathing spontaneously because that is when
intrathoracic pressure is the greatest. Recall that normal inspiration occurs due to negative
 intrathoracic pressure. • For mechanically ventilated patients, the maximum IVC diameter is seen
at the end of inspiration because that is when intrathoracic pressure is the greatest. Recall that
inspiration during mechanical ventilation occurs due to positive pressure.
 119. • In a patient in shock, a finding of IVC collapse > 50% of the IVC diameter with respiration
or IVC diameter < 1.5 cm at maximum diameter may indicate volume depletion. This may
indicate hypovolemia, hemorrhage, or even sepsis • A larger (>2.5cm) and noncompressible IVC
or one with minimal change with respiration shows volume overload. This is seen in shock states
with poor cardiac output, like cardiogenic or obstructive shock • Peritoneal Cavity • A finding of
free fluid in any of the dependent areas of the abdomen (RUQ, LUQ, pelvis) can indicate
hemoperitoneum, as with trauma or a ruptured abdominal aortic aneurysm.
 120. Pulmonary Artery Catheters • These catheters are placed much like a central venous line
and are floated by a balloon with blood flow into the pulmonary circulation. • They can measure
or calculate several hemodynamic parameters, including cardiac output (and cardiac index),
central venous pressure, pulmonary capillary wedge pressure, systemic and pulmonary vascular
resistance, core body temperature, and mixed venous oxygen saturation. • Their use has
significantly decreased over the years due to newer and less invasive methods of hemodynamic
assessment of patients, such as ultrasound and echocardiography.
 121. Pulmonary Artery Catheters
 122. Resuscitation. • Hypovolemic Shock • The most commonly encountered Hypovolemic
Shock subtype in Trauma is Hemorrhagic Shock • The primary treatment of hemorrhagic shock
is to control the source of bleeding as soon as possible and to replace fluid.
 123. • the normal range may mask bleeding. The fourth edition of the guideline on management
of major bleeding and coagulopathy following trauma, by the pan-European Multidisciplinary
Task Force for Advanced Bleeding Care in Trauma, includes the following  Early imaging
(ultrasonography or contrast-enhanced CT) should be used for detection of free fluid in patients
with suspected torso trauma.  CT assessment should be provided for hemodynamically stable
patients.  Low initial Hb should be considered an indicator for severe bleeding associated with
coagulopathy.  Repeated Hb measurements should be used as a laboratory marker for
bleeding, as an initial Hb value in
 124. Serum lactate and/or base deficit measurements are sensitive tests to estimate and
monitor the extent of bleeding and shock. Repeated monitoring of coagulation, using a
traditional laboratory determination (prothrombin time [PT], activated partial thromboplastin time
[APTT], platelet counts, and fibrinogen) and/or a viscoelastic method, should be provided.
Target systolic blood pressure is 80-90 mm Hg until major bleeding has been stopped in the
initial phase following trauma without brain injury. In patients with severe traumatic brain injury
(TBI) (GCS ≤8), mean arterial pressure ≥80 mm Hg should be maintained.
 125.  Fluid therapy using isotonic crystalloid solutions should be initiated in the hypotensive
patient with bleeding trauma.  Excessive use of 0.9 % NaCl solution should be avoided. 
Hypotonic solutions such as lactated Ringer’s solution should be avoided in patients with severe
head trauma.  Use of colloids should be restricted due to adverse effects on hemostasis. 
Target Hb is 7-9 g/dL.  In initial management of patients with expected massive hemorrhage,
one of the following strategies should be used: Plasma (FFP or pathogen- inactivated plasma)
should be provided at a plasma-to-RBC ratio of at least 1:2 as needed, with fibrinogen
concentrate and RBC according to Hb level
 126.  Tranexamic acid should be administered as early as possible to the trauma patient who
is bleeding or is at risk of significant hemorrhage, at a loading dose of 1 g infused over 10
minutes, followed by an IV infusion of 1 g over 8 hours.  Tranexamic acid should be
administered to the bleeding patient with trauma within 3 hours after injury.  Protocols for
treatment of bleeding patients should consider administration of the first dose of tranexamic acid
en route to the hospital.  If a plasma-based coagulation resuscitation strategy is used, plasma
(FFP or pathogen-inactivated plasma) should be administered to maintain PT and APTT < 1.5
times normal control values.  Plasma transfusion should be avoided in patients without
substantial bleeding.
 127.  If a concentrate-based strategy is used, treatment with fibrinogen concentrate or
cryoprecipitate should be provided if significant bleeding is accompanied by viscoelastic signs of
a functional fibrinogen deficit or a plasma fibrinogen level less than 1.5-2.0 g/L.  Initial
fibrinogen supplementation of 3-4 g is used, which is equivalent to 15-20 single donor units of
 cryoprecipitate or 3-4 g of fibrinogen concentrate. Repeat doses must be guided by viscoelastic
monitoring and laboratory assessment of fibrinogen levels.  Platelets should be administered to
maintain a platelet count above 50 × 109/L.  Platelet count above 100 × 109/L should be
maintained in patients with ongoing bleeding and/or TBI.  Initial dose is 4-8 single platelet units
or 1 apheresis pack.
 128. Septic shock resuscitation • As per The Surviving Sepsis Guidelines • Managing infection:
• • Antibiotics: Administer broad-spectrum intravenous • antimicrobials for all likely pathogens
within 1 hour after • sepsis recognition
 129. • • Source control: Obtain anatomic source control as rapidlyAs per The Surviving Sepsis
Guidelines • Managing infection: • • Antibiotics: Administer broad-spectrum intravenous •
antimicrobials for all likely pathogens within 1 hour after • sepsis recognition • as is practical • •
Antibiotic stewardship: Assess patients daily for de-escalation
 130. • Managing resuscitation: • • Fluids: For patients with sepsis-induced hypoperfusion,
provide • 30mL/kg of IV crystalloid within 3hours with additional fluid based on frequent •
reassessment (BPS), preferentially using dynamic variables to • assess fluid responsiveness. • •
Resuscitation targets: For patients with septic shock requiring • vasopressors, target a mean
arterial pressure (MAP) of 65 mm • Hg. Use Norepinephrine as the first line vasopressor of
choice
 131. Pediatric Shock. • Pathophysiology Is similar to adults • All infants younger than 3
months who present in shock should be considered to have a serious bacterial infection until
proven otherwise • General, nonspecific symptoms may manifest in the child with shock.
Lethargy, weakness, a sense of malaise, decreased urine output, fussiness, and poor feeding
are all nonspecific symptoms that may accompany shock.
 132. Pediatric shock • Infants and children have a remarkable ability to preserve their central
blood pressure in an attempt to protect their heart and brain in many forms of shock while
critically reducing perfusion to the extremities, gastrointestinal tract, kidneys, and other end
organs. As a result, shock is characterized in these patients by the following: • Tachycardia (may
be absent in the hypothermic patient) • Signs of impaired organ perfusion (eg, decreased urine
output, altered mental status) or delayed peripheral perfusion (eg, weak peripheral pulses,
delayed capillary refill >2 sec, cool extremities) • Temperature instability (hyperthermia,
hypothermia) • Tachypnea
 133. • To differentiate between compensated and decompensated shock, the patient’s blood
pressure is compared to the American Heart Association (AHA)'s fifth- percentile systolic blood
pressures for age, which are as follows [13] : • Newborn: 60 mmHg • Infant (1 mo to 1 y): 70
mmHg • Child (1 to 10 y): 70 + (2 × age [in years]) mmHg • Child older than 10 years: 90 mmHg •
Children with a systolic blood pressure above the normal
 134. • Hypotension in the pediatric shock patient is a late and ominous clinical finding. Such
children, if not quickly and aggressively resuscitated, experience additional organ damage, and
their condition may progress to irreversible shock, cardiovascular collapse, and cardiac arrest. •
Regardless of the cause of shock, the ABCs (airway, breathing, circulation) must be immediately
evaluated and stabilized without delay for further diagnostic workup or imaging studies. Place the
patient on appropriate noninvasive monitors, such as a pulse oximeter and cardiorespiratory
monitor. • Glucose and Calcium Stabilization • Children in shock, particularly when due to sepsis,
are at risk for both hypoglycemia and hypocalcemia. These conditions should be rapidly
identified and corrected.
 135. • Hypoglycemia is common as a result of inadequate glycogen stores, increased glucose
consumption, and metabolic failure. Neonates and infants have limited glycogen stores, which
may become rapidly depleted during shock and lead to hypoglycemia • Alternatively, high levels
of endogenous and exogenous catecholamines may cause a relative insulin-resistant state that
can result in serum hyperglycemia. • Shock may also cause alterations in available levels of
serum ionized calcium, despite normal total serum calcium levels. Hypocalcemia in the shock
state is due to impaired parathyroid hormone function, decreased hepatorenal vitamin D
hydroxylation, and end-organ resistance. Furthermore, administered blood products (which
contain citrate) may bind free available calcium, thereby additionally decreasing the available
ionized calcium levels.
 136. • Calcium mediates excitation-contraction coupling in muscle cells, including cardiac
muscle; low levels of ionized calcium have been shown to be associated with cardiac dysfunction
 and more severe organ dysfunction. • Can be corrected by either calcium gluconate or calcium
chloride. However, calcium chloride has been shown to produce higher and more consistent
levels of available calcium and, therefore, is recommended in the acute resuscitation of a child in
shock. • dosage is usually 0.3mls/kg/dose of a 10% solution,iv
 137. • Fluid management • Administer 20 mL/kg of an isotonic crystalloid infusion, such as 0.9%
isotonic sodium chloride or lactated Ringer solution, over 5 minutes or less. This may be most
rapidly achieved by a disconnect-reconnect technique using large volume syringes. In this
technique, one provider prepares syringes of normal saline or lactated Ringer solution while the
other pushes the fluid filled syringe into an IV or IO line • As soon as the initial bolus of fluid (20
mL/kg) has been infused, reevaluate the patient. If the patient retains the clinical appearance of
shock, immediately infuse another 20 mL/kg of fluid and repeat the cycle. Additional boluses are
titrated to clinical improvement with improved mental status, hemodynamics, perfusion, and
urinary output. Ultimately, a child with severe hypovolemia or sepsis should receive 60 mL/kg of
volume in the first 15 minutes of early goal-directed therapy (EGDT).
 138. • If more than 2-3 volumes of crystalloid have been infused into a patient at risk for
hemorrhage (eg, from trauma), administer blood or packed red blood cells (PRBCs). If rales or
hepatomegaly develop at any point during the volume resuscitation, the resuscitation should
transition from volume administration to inotropic therapy initiation • Antibiotics • If septic shock is
a concern, initial coverage with empiric antibiotics is essential to eliminating the precipitating
cause of shock. The current standard of care is to initiate empiric antibiotics within the first hour
of the diagnosis of severe sepsis. Delayed antimicrobial therapy, specifically greater than 3 hours
after recognition of sepsis, has been associated with increased mortality and prolonged organ
dysfunction
 139. • Blood • In a hemodynamically unstable child with reduced oxygen saturation target Hb
should be 10g/dl • If Hemodynamically stable with resolving shock a lower threshold of 7g/dl may
suffice • Vasopressors • Following the initial fluid resuscitation, if shock persists, then it is
described as fluid-refractory shock. In this situation, the early initiation of inotropic catecholamine
infusions is recommended to potentially help restore sufficient total arterial flow of oxygen (DO2)
through improved perfusion and cardiac
 140. • For the patient with persistent, catecholamine resistant shock despite appropriate volume
and blood and electrolyte repletion, conduct additional evaluation to rule out alternate causes.
Pericardial effusion, pneumothorax, and pulmonary embolism all should be ruled out. • Any
malignant arrhythmias should be converted to normal sinus rhythm as soon as possible. •
Consideration of a potential endocrine emergency, such as relative/absolute adrenal insufficiency
or hypothyroidism is also necessary.
 141. • Adrenocortical failure or infarction, known as Waterhouse-Friderichsen syndrome, may
result in cardiovascular failure and hyporesponsiveness to catecholamines. In affected patients,
initiation of stress- dose hydrocortisone, in the range of 50-100 mg/m2/day IV, may be beneficial
and lifesaving. A serum cortisol level may be drawn prior to initiating the first dose of
corticosteroids, and if this random serum cortisol level is low, then replacement doses may be
beneficial • Sodium Bicarbonate, To give or not and discuss why?

 2. DR. LEONARDO BALLESTAS MALDONADO VASCULAR SURGERY RESIDENT UNIVERSIDAD

DE ANTIOQUIA DR. IVAN ARISMENDI VASCULAR SURGERY TEACHER IPS UNIVERSITARIA
UNIVERSIDAD DE ANTIOQUIA

 3. INTRODUCTION • The term ischemic stroke is used to describe a variety of condictions in

which blood flow to part or all of the brain is reduced, resulting in tissue damage • Although
in some cases this may be a chronic condition, most strokes occurs acutely • The stroke is
currently the second leading cause of death in western world Scott Kinlay .Changes in Stroke
Epidemiology, Prevention, and Treatment. Circulation. 2011;124:e494-e496

 4. OBJETIVE The goal of this review is to provide an overview of the underlying factors, such
as hemodinamic changes and mollecular and celular pathways, wich are involved in stroke-
realted brain injury AND correlate these events with reperfusion syndrome and its treatment
 5. EVIDENCE • A SEARCH OF EVIDENCE IN THE DATABASE: MEDLINE, EMBASE, COHCRANE,
TRIPDATABASE, SCIELO • KEY WORDS: ISCHEMIC STROKE, BRAIN DAMAGE,
PATHOPHYSIOLOGY, CEREBRAL ARTERY OCLUSSION, MECHANISMS, REPERFUSION
SYNDROME, HIPERPERFUSION

 6. STROKE SUBTYPES • Acute ischemic stroke subtypes are often classified in clinical studies
using a system developed by investigators of the TOAST trial, based upon the underlying
cause • Strokes are classified into the following categories: Large artery atherosclerosis
Cardioembolism Small vessel oclussion Stroke of other, unusual, determined etiology
Stroke of undetermined etiology Adams HP Jr., Bendixen BH, et al. Classification of suptype
of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org
10172 in acute Stroke treatment. Stroke 1993; 24:35

 7. • Ischemic strokes are due to a reduction or complete blockage of blood flow • This
reduction can be due to decreased systemic perfusion, severe stenosis or occlusion of a
blood vessel • Ischemic strokes represent about 80 percent of all strokes Caplan LR. Basic
pathology, anatomy, and pathophysiology of stroke. In: Caplan's Stroke: A Clinical Approach,
4th ed, Saunders Elsevier, Philadelphia 2009. p.22

 8. CEREBRAL ARTERY OCCLUSION • Thrombosis refers to obstruction of a blood vessel due

to a localized occlusive process within a blood vessel • The obstruction may occur acutely or
gradually • Atherosclerosis may cause narrowing of the diseased vessel

 9. CEREBRAL ARTERY OCCLUSION • This may lead to restriction of blood flow gradually •
Platelets may adhere to the atherosclerotic plaque forming a clot leading to acute occlusion
of the vessel • Atherosclerosis usually affects larger extracranial and intracranial vessels

 11. CEREBRAL AUTOREGULATION • Under normal conditions, the rate of cerebral blood
flow is primarily determined by the amount of resistance within cerebral blood vessels,
which is directly related to their diameter • Cerebral blood flow is also determined by
variation in the cerebral perfusion pressure Markus HS. Cerebral perfusión and stroke. J
Neurol Neurosurg Psychiatry 2004; 75:353

 12. CEREBRAL AUTOREGULATION • Is the phenomenon by which cerebral blood flow is

maintained at a relatively constant level despite moderate variations in perfusion pressure •
The mechanism by which autoregulation occurs is not well understood, and may involve
multiple pathways R Aaslid, K F Lindegaard, W Sorteberg and H Nornes. Cerebral
autoregulation dynamics in humans. Stroke. 1989;20:45-52

 13. CEREBRAL AUTOREGULATION SMOOTH MUSCLE IN CEREBRAL VESSELS

 14. CEREBRAL AUTOREGULATION Maintenance of cerebral blood flow by autoregulation

typically occurs within a mean arterial pressure range of 60 to 150 mmHg

 15. CEREBRAL AUTOREGULATION DURING STROKE CEREBRAL PERFUSION PRESSURE FALLS

CEREBRAL BLOOD VESSELS DILATE INCREASE CEREBRAL BLOOD FLOW OXYGEN EXTRACTION
FRACTION IS INCREASED AUTOREGULATION IMPAIRED LOW LEVELS OF OXYGEN DELIVERY
TO THE BRAIN

 16. CEREBRAL AUTOREGULATION DURING STROKE Aries MJ, Elting JM, et al. Cerebral
autoregulation in stroke: a review of transcranial Doppler studies. Stroke 2010; 41:2697
 17. CONSEQUENCES OF REDUCTION IN BLOOD FLOW DURING STROKE • The human brain is
exquisitely sensitive and susceptible to even short durations of ischemia • The brain is
responsible for a large part of the body's metabolism and receives about 20 percent of the
cardiac output although it is only 2 percent of total body weight • The brain contains little or
no energy stores of its own, and therefore relies on the blood for their delivery Markus HS.
Cerebral perfusión and stroke. J Neurol Neurosurg Psychiatry 2004; 75:353

 18. CONSEQUENCES OF REDUCTION IN BLOOD FLOW DURING STROKE FOCAL ISCHEMIA

CENTRAL CORE PENUMBRA

 19. MECHANISM OF ISCHEMIC CELL INJURY AND DEATH • DEPLETION ATP • CHANGES IN
IONIC CONCENTRATIONS OF NA, K AND CA • INCREASED LACTATE ACIDOSIS •
ACCUMULATION OF OXYGEN FREE RADICALS • INTRACELLULAR ACCUMULATION OF WATER
• ACTIVATION OF PROTEOLYTIC PROCESSES

 20. MECHANISM OF ISCHEMIC CELL INJURY AND DEATH ISCHEMIA ELECTRICAL FAILURE

 21. MECHANISM OF ISCHEMIC CELL INJURY AND DEATH MULTIPLE PATHWAYS

 22. EXITOTOXICITY SODIUM – INFLUX OF WATER Sodium causes reversal of the normal
process of glutamate uptake by astrocyte glutamate transporters NA NITRIC OXIDE FREE
RADICALS DNA DAMAGE MITOCHONDRIAL FAILURE APOPTOSIS

 23. INFLAMATORY RESPONSE

 24. Cell death following cerebral ischemia or stroke can occur by either necrosis or by
apoptosis:

 25. APOPTOSIS

 27. LOSS OF BRAIN STRUCTURAL INTEGRITY • Cerebral edema complicating stroke can cause
secondary damage by several mechanisms, including : INTRACRANEAL PRESSURE DECREASE
CEREBRAL BLOOD FLOW MASS EFFECT

 28. • Cytotoxic edema is caused by the failure of ATP-dependent transport of sodium and
calcium ions across the cell membrane • The result is accumulation of water and swelling of
the cellular elements of the brain, including neurons, glia, and endothelial cells

 29. • Vasogenic edema is caused by increased permeability or breakdown of the brain

vascular endothelial cells that constitute the BBB • This allows proteins and other
macromolecules to enter the extracellular space, resulting in increased extracellular fluid
volume

 30. REPERFUSION SYNDROME

 31. INTRODUCTION • Cerebral hyperperfusion, or reperfusion syndrome, is a rare, but

serious, complication following revascularization • Restoration of blood flow following
ischemic stroke can be achieved by means of thrombolysis or mechanical recanalization
(endarterectomy) • In the treatment of acute stroke, restoration of the blood supply can
reduce more extensive brain tissue injured by salvaging a reversibly damage penumbra of
tissue Schaller B, Graf R (2004) Cerebral ischemia and reperfusion: the pathophysiologic
concept as a basis for clinical therapy. J Cereb Blood FlowMetab 24:351–371
 32. INTRODUCTION • Hyperperfusion is defined as a major increase in ipsilateral cerebral
blood flow (CBF) that is well above the metabolic demands of the brain tissue • The terms
hyperperfusion and reperfusion are often used interchangeably • When patients are
identified and treated early, the prognosis is better and the incidence of intracraneal
hemorrage is decreased Karapanayiotides T, Meuli R, Devuyst G, Piechowski-Jozwiak B,
Dewarrat A, Ruchat P, et al. Postcarotid endarterectomy hyperperfusion or reperfusion
syndrome. Stroke. Jan 2005;36(1):21-6.

 33. INTRODUCTION • Outcomes are dependent on timely recognition and prevention of

precipitating factors • Most important is the treatment of hypertension before it can inflict
damage in the form of edema or hemorrahge • The prognosis following hemorrhagic
transformation is poor Yoshimoto T, Shirasaka T, Yoshizumi T, Fujimoto S, Kaneko S,
Kashiwaba T. Evaluation of carotid distal pressure for prevention of hyperperfusion after
carotid endarterectomy. Surg Neurol. Jun 2005;63(6):554-7; discussion 557-8.

 34. INTRODUCTION • Mortality in such cases is 36-63%, and 80% of survivors have
significant morbidity • Damage to the blood-brain barrier (BBB), an important factor in
reperfusion injury Wagner WH, Cossman DV, Farber A, Levin PM, Cohen JL. Hyperperfusion
syndrome after carotid endarterectomy. Ann Vasc Surg. Jul 2005;19(4):479-86

 35. SYMPTOMS OF CEREBRAL REPERFUSION SYNDROME HEADACHE HYPERTENSION seizure

contralateral neurological deficits • The time frame in which symptoms arise can be from
immediately after restoration of blood flow to up to 1 month after restoration • Patients are
usually symptomatic within the first week Coutts SB, Hill MD, Hu WY. Hyperperfusion
syndrome: toward a stricter definition. Neurosurgery. Nov 2003;53(5):1053-58; discussion
1058-60.

 36. CAUSES OF CEREBRAL REPERFUSION INJURY • Postoperative hypertension • High-grade

stenosis with poor collateral flow • Decreased cerebral vasoreactivity • Increased peak
pressure, such as in contralateral carotid occlusion • Recent contralateral CEA (< 3 months) •
Intraoperative distal carotid pressure of less than 40 mm Hg • Intraoperative ischemia peak
flow velocity Adhiyaman V, Alexander S. Cerebral hyperperfusion syndrome following
carotid endarterectomy. QJM. Apr 2007;100(4):239-44

 37. HYPERTENSION • Elevated blood pressure is the most common factor found in
syntomatic patients • During acute ischemic stroke, systemic blood pressure often rises as a
physiologic compensation of cerebral ischemia • The key to reperfusion injury in this
scenario is ischemic disruption of the blood-brain barrier (BBB) McCabe DJ, Brown MM,
Clifton A. Fatal cerebral reperfusion hemorrhage after carotid stenting. Stroke. Nov
1999;30(11):2483-6.

 38. DYSAUTOREGULATION • Cerebral autoregulation protects the brain against changes in

systemic blood pressure • In patients with high-grade stenosis, CBF is maintained at the
expense of maximal arteriolar vasodilatation • Chronic cerebral hypoperfusion (eg, critical
stenosis) leads to the production of carbon dioxide and nitric oxide • Correction of a critical
stenosis causes rapid and large changes in the CBF, which can lead to edema or hemorrhage
Hosoda K, Kawaguchi T, Shibata Y, Kamei M, Kidoguchi K, Koyama J, et al. Cerebral
vasoreactivity and internal carotid artery flow help to identify patients at risk for
hyperperfusion after carotid endarterectomy. Stroke. Jul 2001;32(7):1567-73.
 39. ISCHEMIA - REPERFUSION • Is characterized by oxidant production, complement
activation, and increased microvascular permeability • At the site of ischemia itself,
activated leukocytes release free radicals and toxins, causing further destruction • The
combination results in an impaired BBB, which can lead to cerebral edema and/or
hemorrhage

 40. REPERFUSION INJURY AFTER REVASCULARIZATION • Symptomatic hemorrhagic

transformation rates within 24- 36 hours of stroke are increased in the setting of
revascularization therapy, regardless of modality • In the absence of revascularization
therapy, hemorrhagic transformation is a common and natural consequence of infarction •
Hemorrhagic transformation is now known to be a multifactorial process • Patient selection
based on physiologic parameters is likely important to reduce late hemorrhage attributable
to revascularization Khatri P, Wechsler LR, Broderick JP. Intracranial hemorrhage associated
with revascularization therapies. Stroke. Feb 2007;38(2):431-40.

 41. ASSESMENT OF RISK FOR REPERFUSION INJURY Preoperative transcranial Doppler

ultrasonography • Low preoperative distal carotid artery pressure (< 40 mm Hg) and an
increased peak blood flow velocity have been found to be predictive of postoperative
hyperperfusion • TCD can be used to select patients for aggressive postprocedure
observation and management Ogasawara K, Inoue T, Kobayashi M, Endo H, Fukuda T, Ogawa
A. Pretreatment with the free radical scavenger edaravone prevents cerebral hyperperfusion
after carotid endarterectomy. Neurosurgery. Nov 2004;55(5):1060-7.

 42. ASSESMENT OF RISK FOR REPERFUSION INJURY Preoperative acetazolamide SPECT

scanning • Cerebrovascular reactivity (CVR) to carbon dioxide can be used to test cerebral
hemodynamic reserve • Normally, administration of acetazolamide (a carbonic anhydrase
inhibitor that causes a local increase in carbon dioxide) induces a rapid increase in CBF • This
iatrogenic CBF surge is measured using single-photon emission computed tomography
(SPECT) scanning Cikrit DF, Burt RW, Dalsing MC, Lalka SG, Sawchuk AP, Waymire B, et al.
Acetazolamide enhanced single photon emission computed tomography (SPECT) evaluation
of cerebral perfusion before and after carotid endarterectomy. J Vasc Surg. May
1992;15(5):747-53; discussion 753-4.

 43. PREVENTION OF REPERFUSION INJURY • The most important factor in preventing

reperfusion syndrome is early identification and control of hypertension • The use of TCD
ultrasonography preoperatively and postoperatively can aid in identifying patients with
increased CBF and, consequently, increased risk of hyperperfusion • Blood pressure should
then be controlled aggressively if CBF elevates Naylor AR, Evans J, Thompson MM, London
NJ, Abbott RJ, Cherryman G, et al. Seizures after carotid endarterectomy: hyperperfusion,
dysautoregulation or hypertensive encephalopathy?. Eur J Vasc Endovasc Surg. Jul
2003;26(1):39-44.

 44. PREVENTION OF REPERFUSION INJURY • Pressures can be reduced gently with

antihypertensives that do not increase CBF or cause excessive vasodilatation • According to
the American Stroke Association stroke and intracerebral hemorrhage guidelines, the blood
pressure goal for an acute intracerebral hemorrhage is a mean arterial pressure (MAP) of
less than 110 mm Hg

 45. PREVENTION OF REPERFUSION INJURY Free-radical scavengers and antiadhesion

therapy • Free radicals produced during ischemia are a purported culprit in reperfusion
 injury • Free-radical scavengers and antiadhesion therapy have shown promise in decreasing
the incidence of endothelial injury • Animal studies using various methods of modulating the
cytokine response have shown beneficial effects from modulation of IL-1 and TNF

 46. PREVENTION OF REPERFUSION INJURY Free-radical scavengers and antiadhesion

therapy


2. CEREBRAL ISCHEMIA • It is potentially reversible altered state of brain physiology and
biochemistry that occurs when substrate delivery is cut off or substantially reduced by
vascular stenosis or occlusion. • Stroke is defined as an acute neurologic dysfunction of
vascular origin with sudden (within sec) or atleast rapid occurrence of symptoms and signs
corresponding to involvement of focal areas in the brain.

 3. Pathological alterations in cerebral vessel function 1. Platelets and PMN release

vasoactive amines include ADP,TXA2 and serotonin reduce or inhibit NO Vasoconstriction. 2.
Atherosclerosis excess production of ROS decrease NO bioavailabilty impaired endothelial
dep relaxation. 3. Statins are pleotropic improve vascular function by increase in NOS and
reduced NADPH oxidase and Rho kinase. 4. Chronic hypertension oxidative stress and
elevated ROS inactivation of NO and endothelial dysfunction

 5. 6.Impaired function of many K+ channels leads in cerebral artery dysfunction and

vasoconstriction

 6. 6.SAH leads to cerebrovascular depolarisation and results in vasospasm due to impaired

endothelial dep relaxation,reduced guanyl cyclase, bilirubin oxidation products and reduced
K+ channel function

 7. 7)Diabetes – hyperglycemia leads to impaired endothelial vascular dilatation due to

activation of EDCF protein C kinase. 8. Hyperhomocystenemia leads to endothelial
dysfunction due to increased levels of S adenosine methionine levels.

 8. Cerebral stroke subtypes ischemic thrombotic embolic hemorrhagic intracerebral

subarachnoid

 9. Risk factors

 10. Thrombosis • Refers to an obstruction of blood flow due to a localised occlusive process
within one or more blood vessels. • The lumen of the vessel is narrowed or occluded by an
alteration in the vessel wall or by superimposed clot formation. • The most common type of
vascular pathology is atherosclerosis.

 12. Atherosclerosis • Fibrous and muscular tissues overgrow in the sub intima. • Fatty
materials form plaques that can encroach on the lumen. • Platelets adhere to plaque and
form clumps that serve as nidus for the deposition of fibrin, thrombin, and clot. • Affects
chiefly the larger extracranial and intracranial arteries. • The smaller, penetrating arteries
are more often damaged by hypertension than by atherosclerotic processes.

 14. • Less common vascular pathologies leading to obstruction include Fibromuscular

dysplasia Arteritis Dissection of the vessel wall Hemorrhage into plaque • At times, the
 focal vascular abnormality is a functional change in the contractility of blood vessel • Intense
focal vasoconstriction can lead to decreased blood flow and thrombosis.

 15. Embolism • Material formed else where within the vascular system lodges in an artery
and blocks blood flow. • Blockage can be transient or may persist for hours or days. • Most
commonly :heart • Other sources: 1)major arteries such as aorta, carotid and vertebral
arteries. 2)systemic veins.

 16. Decreased systemic perfusion • Diminished flow to brain tissue is caused by low
systemic perfusion pressure. • Most common causes are: 1)Cardiac pump failure: due to
Myocardial infarction. 2)Systemic hypotension: due to blood loss or hypovolemia. • Lack of
perfusion is more generalised than in localised. • Poor perfusion is most critical in border
zone or called as watershed regions.

 17. Damage caused by ischemia • All 3 mechanisms lead to temporary or permanent tissue
injury. • Permanent injury is termed as infarction. • Capillaries or other vessels within the
ischemic tissue may also be injured. • Reperfusion can lead to leakage of blood into the
ischemic tissue resulting in hemorrhagic infarction. • Extent of brain damage depends on 1)
Location and duration of the poor perfusion. 2) Ability of collateral vessels to reperfuse the
tissues at risk.

 18. • The systemic blood pressure, blood volume, and blood viscosity also affect blood flow
to the ischemic areas. • In acute phase: Brain and vascular injuries may lead to brain edema
during the hours and days after stroke. • In chronic phase: Macrophages gradually ingest the
necrotic tissue debris within the infarct leading to shrinkage of infarct and forms gliotic scars.

 19. Cerebral microvessel response to focal ischemia 1. Loss of barrier leading to endothelial
cell permeability with subsequent edema 2. Loss of basal lamina and extracellular matrix
with haemorrhagic transformation 3. Alteration in cell matrix adhesion 4. Loss of microvessel
patency 5. Generation endothelial and leucocyte adhesion molecules

 20. • Capilllary permeabilty barrier function is lost in 30 min after ischemia swelling of
endothelial and astrocytes with cytoplasm reorganization Capillary expands and rupture
Accumulation of fluid in extravascular space Swelling leads to focal no flow phenomena •
Bradykinin,vegf,MMP,thrombin and protease leads to loss of BBBand microvas ECM •
Decrease in laminin and fibronectin leads to leakage of blood • Beta integrin, p selectin and
E selectin are involved in ECM disturbed due to cytokines by glial cells

 21. • Proteolysis of microvascular matrix Loss of basal lamina Increase in pro MMP 2,
urokinase and plasminogen activator inhibitor Leads to matix and parenchymal degeneration
• Microvessel cell adhesion- after injury beta integrins and dystroglycan on endothelial cell
reduces the adhesion. • Focal no flow phenomenon and secondary injury-transient occlusion
of brain supplying artery significantly reduces patency of distal microvascular bed . • Could
be external or internal compression

 22. • Initiation of cellular inflammation Ischemia secondary injury to vessels inflammation

obstruction by WBC and platelet adhesion • Leucocyte diapedesis. Leucocytes interact with
endothelial cells expressing P selectins through P-selectin glycoprotein 1 (PSGL-1), leading to
their“rolling” on the endothelial surface. Interaction of leucocyte integrins CD11a/CD18 and
CD11b/CD18 with intercellular adhesion molecule 1 (ICAM-1) leads to firm adherence and
 aggregation of leucocytes. Diapedesis of leucocytes is facilitated by platelet-endothelial cell
adhesion molecule 1 (PECAM-1).

 23. • Fibrin formation and deposition Fibrinogen exposed to tissue factor leads to formation
of fibrin Activated platelets +fibrin Vascular obstruction in capillaries and venules •
Hemostasis Occurs by expression of activators and inhibitors of thrombosis in vessel walls or
by cross talk between vascular cell components TF is the activator of coagulation and breach
in endothelium leads to contact of TF and coagulation.

 25. Physiology and pathophysiology of brain ischemia Normal Metabolism and Blood Flow:
• Brain uses glucose as its sole substrate for energy metabolism. • Glucose metabolism leads
to conversion of ADP to ATP. • A constant supply of ATP is needed to maintain neuronal
integrity and to keep the major extracellular Ca++ and Na+ outside the cells and the
intracellular K+ within the cells. • Production of ATP is much more efficient in the presence
of oxygen.

 26. • In absence of oxygen anaerobic glycolysis leads to formation of ATP and lactate, the
energy yield is relatively small, and lactic acid accumulates within and outside the cells. •
Brain requires 75 to 100 mg of glucose each minute. • Normal CBF =50-55ml/100g/minute. •
Cerebral oxygen consumption, is normally 3.5ml/100g/minute. • By increasing oxygen
extraction from the blood stream, compensation can be made to maintain until CBF is
reduced to a level of 20 to 25ml/100g/minute.

 27. • Brain energy use and blood flow depend on the degree of neuronal activity. • In
response to ischemia , the cerebral autoregulatory mechanisms compensate for a reduction
in CBF.

 28. Autoregulation • The capacity of the cerebral circulation to maintain relatively constant
levels of CBF despite changing blood pressure.(80-150mmHg) • The range of autoregulation
is shifted to the right, i.e. to higher values, in patients with hypertension and to left during
hypercarbia.

 29. Maintenance of cerebral blood flow by autoregulation typically occurs within a mean
arterial pressure range of 60-150mmHg

 30. Autoregulatory mechanisms • The myogenic theory of autoregulation: changes in vessel

diameter caused by the direct effect of blood pressure variations on the myogenic tone of
the vessel walls. 1) By local vasodilatation 2) Opening the collaterals. 3) Increasing the
extraction of oxygen and glucose from the blood.

 31. Cerebral autoregulation during stroke

 32. Between CBF Values of 22ml/100mg/min to 8mL/100mg/min,brain tissue maintains its

structural integrity and can be salvaged with reperfusion.

 33. • Development of permanent neurologic sequelae is a time dependent process; for any
given blood flow level, low CBF values are tolerated only for short period

 35. • Core of the infarct: • Center of the zone where the blood flow is lowest • Neurons
undergoes necrosis. • CBF ranges from 0 to 10ml/100g/min. • Ischemic penumbra: • Zone of
reduced perfusion in the periphery. • CBF ranges from 10 to 20ml/100g/min. • Electrical
failure but not permanent damage. • Restoration of blood results in survival. • If blood flow
is not restored cells undergo death by apoptosis.
 36. • Area of oligemia- represents mildly hypoperfused tissue from the normal range down
to around 22ml/100mg/min. • Usually not at risk of infarction. • In hypotension, fever, or
acidosis, oligemic tissue can be incorporated into penumbra and subsequently undergo
infarction.

 37. impaired perfusion >3min decrease in ATP ↓ mitochondria –loss of incoming oxygen ↓
anaerobic glycolysis release of free radicals accumulation of lactic acid inflammation Damage
Edema to BBB

 38. Local Brain Effects of Ischemia • Survival of the at-risk tissue depends on 1. Intensity and
duration of the ischemia. 2. The availability of collateral blood flow. CBF:
-approx.=20ml/100g/min-EEG activity is affected. -<20ml/100g/min-cerebral O2
consumption falls. -<10ml/100g/min-membranes and functions are affected
-<5ml/100g/min-neurons cannot survive for long. • When neurons become ischemic, a
number of biochemical changes potentiate and enhance cell death.

 40. These biochemical effects are: • K+ moves out the cell and Ca2+ moves into the cell
leads to failure of membrane function and mitochondrial failure. • Decreased oxygen
availability leads to formation of oxygen free radicals. • These free radicals cause
peroxidation of fatty acids in cell organelles and plasma membranes, causing severe cell
dysfunction. • Anerobic glycolysis leads to an accumulation of lactic acid and decrease in pH.
• The resulting acidosis also greatly impairs cell metabolic functions.

 41. • Excitatory neurotransmitters(glutamate, aspartate ) is significantly increased in

regions of brain ischemia. • Hypoxia , hypoglycemia and ischemia all contribute to cause
energy depletion and an increase in glutamate release but a decrease in glutamate uptake. •
Glutamate entry opens membranes and increases Na+ and Ca2+ influx into cells. • Large
influxes of Na are followed by entry of chloride ions and water, causing cell swelling and
oedema. • Glutamate is an agonist at both NMDA and non NMDA receptors types, but only
NMDA receptors are linked to membrane channel with high calcium permeability.

 42. • All these metabolic changes cause a self perpetuating cycle leading to more local
biochemical changes, which in turn cause more neuronal damage. • At some point, the
process of ischemia becomes irreversible, despite of reperfusion. • At times, although the
severity of ischemia is insufficient to cause neuronal necrosis, ischemia may cause
programmed cell death referred to as apoptosis.

 43. Effects at cellular level

 44. Excitotoxicity • Pathological process by which neurons are damaged by the

overstimulation of receptors by the excitatory neurotransmitter glutamate, such as the
NMDA receptor and AMPA receptor.

 45. Fig. 1. The dual role of NMDA receptors in determining the fate of neurons: binding of
glutamate to extrasynaptic NMDARs dephosphorylates cAMPresponsive element-binding
protein (CREB), inactivates the extracellular signal-regulated kinase (ERK) pathway and
promotes cell death, while binding of glutamate to synaptic NMDARs promotes cell survival
through activation of the phosphoinositide-3-kinase (PI3K)/Akt pathway, which inactivates
glycogen synthase kinase 3β (GSK3β), the pro-apoptotic Bcl-2 associated death promotor
(BAD), pro-apoptotic p53, and c-Jun N-terminal kinase (JNK)/p38 activator apoptosis signal-
regulating kinase 1 (ASK1)
 46. • In the ischemic zone, the glutamate binds to postsynaptic receptors which triggers
increased calcium influx through glutamate receptor-coupled ion channels. • Glutamate
overstimulates NMDA, AMPA, Kainite type glutamate receptors. • Results in sodium influx
and potassium efflux through the glutamate receptor activated membrane channels. •
NMDA channels are highly permeable to calcium and contribute to influx of calcium from
extracellular space and results in cell death after ischemic stroke.

 47. increased calcium levels in cytosol ↓ Increased activation of calcium dependent

synthases and proteases ↓ Degradation of cytoskeletal and enzymatic proteins Increased
levels of NO and peroxynitrite within the cell through activation of degrading enzymes such
as phospholipase, proteases and endonucleases.

 48. • Potassium efflux through NMDA channels can increase caspase activity, triggering
apoptosis. • Primary caspases responsible for apoptosis due to ischemic stroke are caspases
9 and 3. • Caspase 9 activates caspase 3. • Caspase 3 degrade substrate proteins within the
cell and produce internucleosomal endonuclease activity and DNA fragmentation.

 50. Oxidative stress • A potential pathway for cellular damage in ischemic stroke may be the
occurrence of oxidative stress, which is the increased occurrence of ROS above physiological
levels. • Free radicals can cause membrane damage through peroxidation of unsaturated
fattyacids in the phospholipids making up the cell membrane.

 54. Apoptosis • Programmed cell death. Which involves: Shrinkage of the cell cytoplasm
Cleavage of DNA within the nucleus Condensation of chromatin in the nucleus
Formation of apoptotic bodies Cell death

 56. Mitochondria mediated • Translocation of pro-apoptotic Bcl-2 members like Bax into
the mitochondria, a cascade of events are triggered. • This leads to mitochondria releasing
substances such as cytochrome c ,procaspase 9 from its intermembrane space.

 57. Main pathways are leading to apoptosis. Opening of the mitochondrial permeability
transition pore (MPTP) leads to the release of cytochrome C (cyt C), which together with the
cytosolic apoptotic-protease-activating factor-1 (Apaf-1) activates procaspase-9. Active
caspase-9 further activates caspases-3 and 7, leading to the execution phase of caspase-
dependent apoptosis. The mitochondria also release apoptosis-inducing factor (AIF), high-
temperaturerequirement protein A (HtrA2/OMI), as well as a second mitochondrion-derived
activator of caspase/direct inhibitor of apoptosis-binding protein with low pI
(SMAC/DIABLO), which inhibits the antiapoptotic X chromosome-linked inhibitor-of-
apoptosis protein (XIAP), thereby leading to apoptosis The binding of Fas ligands (FasL) to
Fas receptors recruits the cytoplasmic Fas-associated death domain (FADD) and pro-caspase-
8, forming together the death-inducing signaling complex (DISC), which leads to activation of
pro-caspase-8 and triggering of the extrinsic pathway of apoptosis.

 58. Endoplasmic reticulum • ER initiates unfolded protein response(UPR). • Three ER

transmembrane effector proteins are activated(PERK,IRE1,and ATF-6). • IRE1 has been
shown to be involved in the activation of caspase-12.

 59. Cerebral edema and increased intracranial pressure • There are 2 types of cerebral
edema: 1)Cytotoxic edema 2)Vasogenic edema leads to shifts in position of brain tissue and
herniation of brain contents from one compartment to another.
  60. Cytotoxic edema: • Water accumulation inside cells. • Caused by energy failure, with
movement of ions and water across the cell membranes into cells. • Brain swelling caused
by cytotoxic edema means a large volume of dead or dying brain cells, which implies bad
outcome. • Usually seen after arterial occlusion due to energy failure.

 61. Vasogenic edema • Fluid within the extracellular space. • Influenced by hydrostatic
pressure factors and by osmotic factors. • Breakdown of BBB→proteins and other
macromolecules enter the Extracellular space→exert osmotic gradient→pulling water into
the extracellular space. • Preferentially involves cerebral white matter.

 63. Ischemic cascade Lack of oxygen supply to ischemic neurones ATP depletion Membrane
ions system stops functioning Depolarisation of neuron Influx of calcium Release of
neurotransmitters, including glutamate, activation of N-metyl -D- aspartate and other
excitatory receptors at the membrane of neurones Further depolarisation of cells Further
calcium influx

 67. Thank you

 68. References • J P Mohr Stroke patho physiology, diagnosis and management 5th edition.
• Jurcau A, Ardelean IA. Molecular pathophysiological mechanisms of ischemia/reperfusion
injuries after recanalization therapy for acute ischemic stroke. J Integr Neurosci. 2021 Sep
30;20(3):727- 744. doi: 10.31083/j.jin2003078. PMID: 34645107. • Kuriakose D, Xiao Z.
Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. Int J Mol
Sci. 2020 Oct 15;21(20):7609. doi: 10.3390/ijms21207609. PMID: 33076218; PMCID:
PMC7589849. • Qin, C., Yang, S., Chu, YH. et al. Signaling pathways involved in ischemic
stroke: molecular mechanisms and therapeutic interventions. Sig Transduct Target Ther 7,
215 (2022). • Lo EH, Dalkara T, Moskowitz MA. Mechanisms, challenges and opportunities in
stroke. Nat Rev Neurosci. 2003 May;4(5):399-415. doi: 10.1038/nrn1106. PMID: 12728267.

CANCER SeminarCancer Overview Type of Cancer.pptx

 1. PREVENTIVE MEDICINE Dr. Babasaheb Ambedkar Technological University
 2. Social & Preventive Pharmacy STAGED BY MR. Stavan U. Kadam Final Year
B.PHARMACY Dr. Babasaheb Ambedkar Technological University • CANCER
 3. KEYNOTE • Introduction • Cancer Overview • Variety Of Cancer • Etiology & Risk FactorsOf
Cancer • Symptoms & sign Of Cancer • Diagnosis Of Cancer • Treatment Of Cancer • Cancer
Myth & Misconception • Government Policy and Program on Cancer • Role of Pharmacist •
Leading Cancer Research Institute in India
 4. INTRODUCTION  Cancer is an abnormal growth of functioning cell not in the control of body
hormonal system and hampering functioning of other body system  Cancer is the general name
for a group of more than 100 diseases. All cancers start because abnormal cells grow out of
control.  When cells continue multiplying when the body doesn't need them. The result is a
mass or growth, also called a TUMOR.
 5. Cancer Overview These growths are considered either BENIGN or MALIGNANT 
NEOPLASM - abnormal growth of cells  BENIGN -neoplasms are not cancerous 
MALIGNANT - neoplasms are cancerous
 6. CHARACTERISTICS OF CANCER CELLS Lack differentiation Have abnormal nuclei
Form tumors Mitosis controlled by contact with neighboring cells Cancer cells have lost
contact inhibitor
 7. STAGES OF CANCER • Stage 0. This stage describes cancer in situ. In situ means "in place."
Stage 0 cancers are still located in the place they started. They have not spread to nearby
tissues. This stage of cancer is often curable. Surgery can usually remove the entire tumor. •
Stage I. This stage is usually a cancer that has not grown deeply into nearby tissues. It also has
 not spread to the lymph nodes or other parts of the body. It is often called early-stage cancer. •
Stage II and Stage III. In general, these 2 stages are cancers that have grown more deeply into
nearby tissue. They may have also spread to lymph nodes but not to other parts of the body. •
Stage IV. This stage means that the cancer has spread to other organs or parts of the body. It
may be also called advanced or metastatic cancer.
 8. Cancer Patient Reported Worldwide 2019-23 15500000 16000000 16500000 17000000
17500000 18000000 18500000 19000000 19500000 20000000 20500000 2019 2020 2021 2022
2023 Series 1
 9. Cancer Death Reported 2019-23 594000 596000 598000 600000 602000 604000 606000
608000 610000 612000 2019 2020 2021 2022 2023 Series 1 Series 1
 10. Name of Cancer • Name of Cancer is given according to cell of origin , site of origin , stage
of disease • About 200 cancer are estimated • Broadly Classified as Blood related Cancer
( leukemia, Myeloma, lymphoma) And then other Big Category is solid tumors and this are fether
branded as squamous cell carcinomas , adenocarcinomas , sarcomas
 11. Continue • In male Lung , larynx, tongue , Prostrate cancer is common • In female breast,
Cervical , Gall Bladder , Endometrial cancer is common
 12. Healing Hands, Healing Hearts
 13. TYPES OF CANCER The following five broad categories indicate the tissue and blood
classifications of cancer
 14. Carcinoma A carcinoma is a cancer found in body tissue known as epithelial tissue that
covers or lines surfaces of organs, glands, or body structures. For example, a cancer of the lining
of the stomach is called a carcinoma. Many carcinomas affect organs or glands that are involved
with secretion, such as breasts that produce milk. Carcinomas account for 80-90% of all cancer
cases.
 15. Continue Types of carcinoma include: • Melanoma • Basal cell carcinoma • Squamous cell
• skin cancer • Merkel cell carcinoma
 16. Sarcoma A sarcoma is a malignant tumor growing from connective tissues, such as
cartilage, fat, muscle, tendons, and bones. The most common sarcoma, a tumor on the bone,
usually occurs in young adults. Examples of sarcoma include osteosarcoma (bone) and
chondrosarcoma (cartilage).
 17. Continue • Types of sarcoma include: • Soft tissue sarcoma • Osteosarcoma • Ewing's
sarcoma • Chrondrosarcoma
 18. Lymphoma Lymphoma refers to a cancer that originates in the nodes or glands of the
lymphatic system, whose job it is to produce white blood cells and clean body fluids, or in organs
such as the brain and breast. Lymphomas are classified into two categories: Hodgkin's
lymphoma and non Hodgkin's lymphoma.
 19. Continue Types of lymphoma include: • Hodgkin's lymphoma • Non-Hodgkin's lymphoma •
Cutaneous lymphoma
 20. Leukemia Leukemia, also known as blood cancer, is a cancer of the bone marrow that
keeps the marrow from producing normal red and white blood cells and platelets. White blood
cells are needed to resist infection. Red blood cells are needed to prevent anemia. Platelets keep
the body from easily bruising and bleeding.
 21. Continue Types of leukemia include: • Acute lymphocytic leukemia • Acute myeloid
leukemia • Agnogenic myeloid leukemia • Chronic lymphocytic leukemia • Chronic myeloid
leukemia • Essential thrombocythemia (ET) • Hairy cell leukemi
 22. Myeloma Myeloma grows in the plasma cells of bone marrow. In some cases, the myeloma
cells collect in one bone and form a single tumor, called a plasmacytoma. However, in other
cases, the myeloma cells collect in many bones, forming many bone tumors. This is called
multiple myeloma.
 23. Radiating Strength, Illuminating Lives
 24. Etiology & Risk Fact Of Cancer
 25. • The main cause of cancer is mutations, or changes to the DNA in your cells. Genetic
mutations can be inherited. They can also occur after birth as a result of environmental forces. •
These external causes, called carcinogens, can include: • physical carcinogens like radiation and
ultraviolet (UV) light • chemical carcinogens like cigarette smoke, asbestos, alcohol, air pollution,
and contaminated food and drinking water • biological carcinogens like viruses, bacteria, and
parasites • According to the WHOTrusted Source, about 33 percent of cancer deaths may be
 caused by tobacco, alcohol, high body mass index (BMI), low fruit and vegetable consumption,
and not getting enough physical activity.
 26. Risk factors • tobacco use • high alcohol consumption • an unhealthy diet, characterized by
red and processed meat, sugary drinks and salty snacks, starchy foods, and refined
carbohydrates including sugars and processed grains, according to a 2017 review • a lack of
physical activity • exposure to air pollution • exposure to radiation • unprotected exposure to UV
light, such as sunlight • infection by certain viruses including H. pylori, human papillomavirus
(HPV), hepatitis B, hepatitis C, HIV, and the Epstein-Barr virus, which causes infectious
mononucleosis • The risk of developing cancer also increases with age. In general, the risk of
developing cancer appears to increase until the age of 70 to 80Trusted Source and then
diminish, according to the National Cancer Institute (NCI).
 27. SIGN & SYMTOMS
 28. Its to simple to remember sign and symptoms By word : Caution • Change in bowel or
bladder habits C • A sore that does not heal A • Unusual bleeding or discharge, unexplained
weight loss U • Thickening or lump in a breast or elsewhere T • Indigestion or difficulty
swallowing I • Obvious change in a wart or mole o • Nagging cough or hoarseness N
 29. C:-Change in bowel or bladder habit
 30. A:-A sore that does not heal
 31. U:-Unusual bleeding or discharge, unexplained weight loss
 32. T:- Thickening or lump in a breast or elsewhere
 33. I:-Indigestion or difficulty swallowing
 34. O:-Obvious change in a wart or mole
 35. N:-Nagging cough or hoarseness
 37. Diagnosis Of Cancer
 38. Main methods of cancerdiagnosis • Radiological diagnosis • Cytological diagnosis •
Histological diagnosis • Frozen section • Tumour markers
 39. RADIOLOGICAL DIAGNOSIS It include, • X-ray • Ultrasound • CT scan • MRI These are
one of the best early, non-invasive methods of cancer diagnosis.
 40. CYTOLOGICAL DIAGNOSIS 1. Fine needle aspiration cytology (FNAC)• Fine needle
aspiration cytology is a popular method of tumor diagnosis particularly for palpable tumors •
Lymph nodal tumors • Breast tumors • Salivary gland tumors • •Thyroid tumors
 41. HISTOLOGICAL DIAGNOSIS : For histological diagnosis the following methods of
sampling is done: Biopsy- biopsy is a surgical removal of small piece of tissue For microscopic
examination for the presence of cancer cell. There are three ways tissues can be removed for•
Biopsy:-• • Endoscopy • Needle biopsy • Surgical biopsy
 42. FROZEN SECTION • Frozen section is quick diagnosis method. • The tissue is quickly
frozen at around -20' c in frozen section • cryostant which makes the tissue hard. • tissue is
immediately sectioned & stained • the whole process from receiving, staining to diagnosis can be
completed within 10 to 15 days.
 43. TUMOR MARKER Some tumors release substance is called tumor markers Blood test can
be performed to detect the blood Cells as well as for specific tumor markers Tumor marker is
biochemical indicators of Tumors these may be: • Antigens • Cytoplasmic proteins • Enzymes •
Hormones • Use in support diagnosis
 44. A Joke about Cancer Awareness A • A cancer patient was sitting in the infusion center
receiving their 14th infusion. Their hair was totally gone, their toenails missing and they had lost
one half their body weight. • A young, handsome and clearly very healthy man approached the
patient and with a beaming smile offered a cancer awareness ribbon. • “What are you kidding
me, I am pretty aware, thank you very much!”
 45. Treatment of Cancer
 46. Treatment of cancer Cancer can be treated by:- • Surgery • Chemotherapy • Radiation
therapy • Hormonal therapy • Synthetic lethality The choice of therapy depends upon the location
and grade of the tumor and the stage of the disease, as well as the general state of the patient
(performance status).
 47. Surgery:- In theory, non-hematological cancers can be cured if entirely removed by
surgery, but this is not always possible. When the cancer has metastasized to other sites in the
body prior to surgery, complete surgical excision is usually impossible. In the Halstedian model of
cancerprogression, tumors grow locally, then spread to the lymph nodes, then to the rest of the
 body. This has given rise to the popularity of local-only treatments such as surgery for small
cancers.
 48. Continue Even small localized tumors are increasingly recognized as possessing
metastatis potential.Examples:- Examples of surgical procedures for cancer include for non-small
cell lung cancer:- Such as- mastectomy for breast cancer, prostatectomy for prostate cancer,
lung cancer surgery. The goal of the surgery can be either the removal of only the tumor, or the
entire organ.A single cancer cell is invisible to the naked eye but can regrow into a new tumor, a
process called recurrence.
 49. Chemotherapy It is one of the most common treatments for cancer.It uses certain drugs to
kill cancer cells or to stop them from growing and spreading to other parts of your body. Your
doctor might prescribe chemo by itself or with surgery or radiation therapy. Why You Need
Chemotherapy? Even after surgery to remove a tumor, your body might still have cancer cells.
These cells can grow new tumors or spread the cancer to other parts of your body
Chemotherapy drugs help destroy, shrink, ar control those cells. It might also treat symptoms the
cancer causes, like pain. You might also get chemo to shrink a tumor before your doctor
removes it in surgery.
 50. Continue • Common Chemotherapy Drugs • chemo drug interferes with the normal
metabolism of cells, which makes them stop growing. • These drugs are called antimetabolites.
Doctors often use them to treat leukemia and cancer in the breasts, ovaries, and intestines.
Drugs in this group include 5-fluorouracil,6- mercaptopurine, cytarabine, gemcitabine, and
methotrexate • Anthracycline chemotherapy attacks the enzymes inside cancer cells' DNA that
help them divide and grow. They work for many types of cancer. Some of these drugs are
actinomycin-D, bleomycin, daunorubicin, and doxorubicin.
 51. Radiation therapy Radiation therapy (also called radiotherapy, X-ray therapy, or
irradiation) is the use of ionizing radiation to kill cancer cells and shrink tumors.Radiation therapy
can be administered externally via external beam radiotherapy (EBRT) or internally via
brachytherapy. How Does It Work? Cells in your body are always dividing and making new
copies. When you have cancer, though, some cells start to divide way too fast.That's where
radiation therapy can help. It uses high-energy particles to make tiny breaks in the DNA of
cancer cells to destroy or damage them, so they can no longer make new copies. The aim is to
treat your cancer by slowing or stopping tumor growth.Your doctor may sometimes suggest you
get radiation therapy to shrink a tumor before you get surgery. Or he may recommend it
 52. Continue If cancer cells have spread to other parts of your body, radiation therapy can kill
them before they grow into new tumors.If you have a cancer that can't be cured, your doctor may
still suggest you use "palliative" radiation therapy. The goal is to shrink tumors and ease
symptoms of your disease. Types of Radiation Therapy: • The kind of radiation therapy you get
depends on things like. • Type of cancer you have. • How big your tumors are. • Where your
tumors are. • How close your tumors are to other tissues. • Your general health • Other
treatments you're getting
 53. Continue • Radiation Therapy side effects:- may include fatigue, temporary hair loss,
sexual and fertilityproblems, blurry vision, and skin changes.
 55. Cancer Myth & Misconception
 56. • There is Nothing I can do to prevent Cancer • Most Cancer are hereditary • Its too late too
stop Smoking • What to eat What not to eat • Drinking Alcohol decreases Risk of cancer • Only
people with risk of cancer need to get cancer Screening • There is Cure for Cancer but drug
companies wont let it come • Cancer is contagious
 57. Government Policy and Program on Cancer
 58. Rastriya Arogya Nidhi - Health Minister’s Cancer Patient Fund • The “Health Minister’s
Cancer Patient Fund (HMCPF) within the Rashtriya Arogya Nidhi (RAN)” was set up in 2009. • It
is a scheme to provide financial assistance to poor patients living below poverty line and
suffering from cancer, for their treatment at 27 Regional cancer centers (RCCs). Revolving
Funds have been created in all the 27 Regional Cancer Centres (RCCs) and funds up to Rs. 50
lakhs will be placed at their disposal. • The financial assistance to a Cancer Patient up to Rs.
2,00,000/- (Rs. Two lakh only) is processed by the Institute/Hospitals concerned through the
revolving fund placed at their disposal. • Individual cases, which require assistance of more than
Rs. 2.00 lakh is to be sent to the Ministry for processing
 59. List of the treatments under this scheme • Radiation treatment of all kinds including Radio
Therapy and Gama Knife Surgery/GRT/MRT/Brachytherapy. • Anti-Cancer Chemotherapy with
supportive medication including hormonal therapy. • Bone Marrow Transplantation- Allogenic&
Autologous • Diagnostic Procedures- including PET scan. • Surgery for operable malignant
tumours.
 60. NATIONAL PROGRAMME FOR PREVENTION & CONTROL OF CANCER, DIABETES,
CARDIOVASCULAR DISEASES & STROKE (NPCDCS) • India is facing a health transition with
a growing burden of Non-Communicable Diseases (NCDs), accounting for around 60% of all
deaths. The National Programme for Prevention and Control of Cancer, Diabetes,
Cardiovascular Diseases and Stroke (NPCDCS) was launched in 2010 to prevent and control
major NCDs. The program focuses on infrastructure, human resource development, health
promotion, early diagnosis, management, and referral. NCD cells are established at national,
state, and district levels, and clinics are set up at district and CHC levels. The program aims to
cover the entire country by March 2017.
 61. Continue The National Cancer Control Programme (NCD) is implemented in all 36
states/UTs, with 298 District NCD Cells and 293 Clinics established. Over 1.29 crore persons
were screened in clinics between 2015-2016, with 8% diagnosed as diabetics and 12% as
hypertensives. Around 90,000 were diagnosed with cardiovascular diseases and over 13,000
had common cancers.
 62. Role of Pharmacist
 63. Oncology pharmacists play various roles, including inpatient, ambulatory, infusion center,
specialty, practice manager, and investigational drug pharmacist. They manage chemotherapy
administration, medication therapy, and patient education. They work closely with nursing staff to
coordinate chemotherapy administration and provide patient education. Infusion center
pharmacists compound anticancer treatments and support direct patient care functions. Specialty
pharmacists distribute and dispense oral anticancer treatments, providing patient education and
adherence monitoring. Oncology practice managers oversee pharmacists, manage resources,
and develop policies and procedures. Investigational drug pharmacists coordinate oncology
investigational drug studies, ensuring patient access and serving as medication experts. Other
roles include academia, medical communications, population health management, informatics,
and regulatory agencies. Oncology pharmacists have demonstrated value in patient care,
supportive care management, laboratory monitoring, and increased documentation in electronic
medical records. They have become important members of informatics teams, leading to
increased medication error identification and cost-savings. They can also decrease physician
and advanced practice provider (APP) time by developing independent practice models. The
global shortage of oncology physicians is expected to continue, but oncology pharmacists can
help prevent a reduction in cancer patient visits and prevent burnout.
 64. Leading Cancer Research Institute in India
 65. Tata Memorial Hospital, Parel, Mumbai Tata Memorial Hospital in Mumbai, established in
the year 1952, is one of the best Advanced Cancer Research Centre for Treatment, Research,
and Education in Cancer. This hospital provides free treatment to almost 70% of its cancer
patients.
 66. Regional Cancer Centre (RCC), Thiruvananthapuram RCC is a state-owned cancer
research institute sponsored by the Government of Kerala and the Government of India. It also
gets some financial aid from the Indian Cancer Society.
 67. Adyar Cancer Hospital, Chennai Adyar Cancer Hospital is one of the most famous cancer
research centers in India and it is a public charitable voluntary institute for cancer care since the
last 60 years. It is also known as the cancer institute (WIA). This cancer hospital is equipped with
the latest technologies and has both research and preventive facilities for cancer patients. This
hospital successfully performs numerous cancer surgeries every year.
 68. Other  Kidwai Institute of Oncology (KMIO), Bangalore  Apollo Hospitals  Jawaharlal
Nehru Institute of Post Graduate Medical Education And Research  Max Institute of Cancer
Care  Postgraduate Institute of Medical Education and Research Institute, Chandigarh 
Institute of Cytology and Preventive Oncology  Central Drug Research Institute, Lucknow, Uttar
Pradesh
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COMMUNICABLE DISEASE - Part 1......................................... | PPTX


2. INDEX S.NO. CONTENT 1. 2. Communicable disease Types of communicable disease 
Tuberculosis  Acute diarrheal disease  Hepatitis  Herpes simplex  Chicken Pox  Small
pox  Typhoid fever  Meningitis  Gas gangrene  Leprosy  Dengue  COVID-19 
Plague  Malaria  Poliomyelitis  Diphtheria  Pertusis

 3. Cont… S.NO. CONTENT Measles Mumps Influenza Tetauns Yellow fever Filarsis Hiv/AIDS
Rubella Cholera Rabies Ebola Zika virus disease Chikungunya Swine flu

 4. Communicable disease  An infectious disease that is contagious and that can be

transmitted either directly or indirectly from one source to another by an infectious agent or
its toxins.

 5. OR  An illness due to a specific infectious agent or its toxic products capable of being
directly or indirectly transmitted from man to man, animal to animal, or from the
environment (through air, dust, soil, food etc.) to man or animal.

 6. Cont…  Communicable period: A time period require for transmission of infectious agent
from reservoir to a susceptible host.

 7. Mode of transmission of communicable disease Direct Indirect Droplet spread Direct

Contact Airborne Vehicle borne Vector borne Biological Mechanical

 8. Mode of transmission of communicable disease Cont…  Airborne transmission 

Contaminated water, soil

 9. CONTD….  Contact and faeces  Pathogens in blood- stream and tissues

 10. Types of communicable disease Depending upon source:  Respiratory infections: e.g:
tuberculosis etc.  Intestinal infections: e.g: hepatitis etc.

 11. Cont…  Arthropod borne infection: e.g: plague etc.  Surface infections: e.g: leprosy 
Sexually transmitted disease: e.g: AIDS etc.

 12. Causes of transmission Viruses: The smallest and simplest disease- organism Bacteria:
Tiny one- celled organisms that live nearly everywhere Fungi: Primitive life- forms, such as
molds or yeast, that can’t make their own food Protozoa: One – celled organisms that have a
more complex structure than bacteria

 13. Controlled By:  Improvement of personal hygiene  Improvement of social hygiene 

Awareness about health  Awareness about disease  Immunization  Medication

 14.  According to recent information, the most prevalent communicable diseases in India
include tuberculosis (TB), malaria, HIV/AIDS, typhoid, influenza, hepatitis, measles, and
COVID-19, with a significant burden of these diseases concentrated in specific regions and
high-risk populations; while the government is actively working to manage these issues
through vaccination campaigns and disease surveillance programs.
 15.  Prevalence: While the burden of non-communicable diseases has increased,
communicable diseases still represent a substantial part of the disease burden in India. 
Leading communicable diseases: Respiratory infections (like pneumonia), acute diarrheal
diseases, and viral hepatitis are considered the top communicable diseases causing deaths in
India.  Underreporting: A significant number of communicable disease cases likely go
unreported, impacting the accuracy of reported statistics.  Impact on health system:The
continued presence of communicable diseases places a significant strain on India's
healthcare system.

 16. RESPIRATORY SYSTEM

 17.  Respiratory infections includes:  Through respiration: Tuberculosis Chicken pox,

Small Pox Measles, Mumps, Influenza Diphtheria Whooping cough SARS

 19. • Tuberculosis Phthisis, Phthisis pulmonalis , Consumption White plague  TB is a

potentially fatal contagious disease that can affect almost any part of the body but is mainly
an infection of the lungs.  It also affect all other vital organs like intestine, brain, bones,
joints, lymph glands, skin etc.

 20.  Incubation period : -from weeks, months to years depending upon dose of infection
and immunity of patient.

 21. Causative organism  Mycobacterium tuberculosis Human  Mycobacterium Bovis

Animal

 23. Predisposing Factors 1. Over crowded population 2. Malnutrition 3. Poverty 4.

Alcoholism 5. Drug addiction 6. HIV infection 7. Immuno compromised status 8. Close
Contact

 24. Classification Pulmonary TB -Primary TB -Secondary TB Extra pulmonary TB -Lymph

node TB -Pleural TB -TB of upper Airways -Genitourinary TB -Skeletal TB -Miliary TB -
Pericardial TB -Gastrointestinal TB

 25. Mode of transmission Tuberculosis is mainly spread by:  Droplet infection (produced by
sputum of positive patient i.e. 0.5-5 μm)  Coughing

 27. Sign and symptoms  Tiredness  Loss of appetite  Loss of weight  Anemia  Evening
rise in temperature  Cough for long time etc.

 30. Cont…  Sputum examination and culture  Biopsy of affected tissue  Chest CT 
Tuberculin Skin Test (PPD)

 31. Contd… -Interferon gamma release blood test such as the QFT- Gold test for TB infection
-Thoracentesis

 33. Treatment  Antitubercular drugs: First line:  Isoniazid- 5mg/Kg  Rifampin- 10mg/Kg 
Pyrazinamide-15-25mg/Kg  Ethambutol- 15-25 mg/Kg  Streptomycin- 15mg/Kg

 34. Cont…  2nd Line Drugs: Cycloserine-15mg/kg Capreomycin-12-15mg/kg

Paraaminosalicyilate sodium -200-300mg/kg Ethionamide-15mg/kg Vitamin b
(Pyridoxine)

 35. Cont….  3rd Line drugs:  Linezolid  Thioacetazone  Arginine  Rifabutin 

Clarithromycin
 38. Cont…  DOTS therapy  Multidrug therapy

 39. Prevention and control Preventive measures: 1. Mask 2. BCG Vaccine 3. Regular Medical
Follow Up 4. Isolation of patient 5. Ventilation 6. Natural sunlight 7. UV Germicidal
Irradiation

 40. Cont… Control programmes: 24th march celebrated as TB day The National
Tuberculosis Programme (NTP) The district Tuberculosis programme (DPT) (RNTCP) 
National Tuberculosis Elimination Program (NTEP)

 43.  The Glory of Life ( film) The Glory of Life is a 2023 German drama film about Franz
Kafka and his final romance with Dora Diamant, which takes place while he is suffering from
tuberculosis The film is based on the best-selling novel by Michael Kumpfmüller. It tells the
story of Kafka's last year, when he met Dora in 1923 while convalescing from tuberculosis on
the Baltic Sea coast. The two moved in together in Berlin and then to a sanatorium in
Austria, where Dora joined him

 44. Acute diarrheal disease  Acute diarrheal disease is a sudden onset of diarrhea that lasts
less than 14 days. It's characterized by frequent loose, watery stools.

 45. Causes Infectious agents: These include bacteria, viruses, and parasites. For example,
cholera, rotavirus, and adenoviruses can cause acute diarrhea. Toxins: These can be
produced by bacteria or other infectious agents. Abnormalities in the gut lining: These can
cause the gut to secrete too much fluid. Travel: Common pathogens affect different regions
of the world. Animal exposure: Some animals, like cats and dogs, can carry pathogens that
cause diarrhea. Poor hygiene: Poor personal hygiene, unsafe water storage, and unhygienic
food preparation can all contribute to diarrhea.

 46. Pathophysiology  Bacteria attach to the wall of the small bowel  enterotoxins are
released,  drawing fluid electrolytes from the mucosa into the lumen,  causing profuse
watery diarrhea.

 48. Types Watery diarrhea  Acute watery diarrhea: Lasts a few hours to a few days, and can
be caused by cholera, rotavirus, or entero virus  Secretory diarrhea: Large volumes of
watery diarrhea, often more than a liter per day  Osmotic diarrhea: Caused by excess sugar
or small molecule intake, or poor absorption, such as with lactose intolerance Bloody
diarrhea: Acute bloody diarrhea  Also known as dysentery, and can be caused by bacteria
like Shigella, Campylobacter, or Salmonella, or parasites like intestinal amoebiasis Bloody
diarrhea: A subtype of diarrhea where all or most stools have visible blood, which indicates
inflammation in the bowel wall

 49. The incubation period for acute diarrheal disease can vary from a few hours to 10 days,
depending on the cause.  Bacterial diarrhea: The incubation period is usually a few hours to
5 days after exposure.  Viral diarrhea: The incubation period is usually 1 to 3 days after
exposure.  Enteric adenovirus infection: The incubation period is usually 8 to 10 days after
exposure.

 50. Acute diarrheal disease is a short-term illness that causes frequent loose or watery
stools. Other symptoms include:  Abdominal pain or cramps  Bloating  Fever  Nausea and
vomiting  Urgent need to use the bathroom  Loss of control of bowel movements  Fatigue
 Soreness, itching, or burning in the anus  Acute diarrheal disease is usually mild and goes
away on its own. However, severe cases can lead to dehydration and shock
 51. Diagnostic investigation Acute diarrheal disease is diagnosed through a physical exam,
medical history, and a variety of tests.  Physical exam  Blood pressure and pulse: Check for
signs of dehydration or fever  Abdominal exam: Listen for sounds and check for tenderness
or pain  Digital rectal exam: Check for signs of diarrhea Medical history  Ask about travel
history, family medical history, and sick contacts  Ask about gastroenterologic disease,
endocrine disease, and factors that increase the risk of immunosuppression Tests  Stool
test: Check for blood, parasites, and bacterial infections  Blood tests: Check for electrolyte
levels, kidney function, and other conditions  Hydrogen breath test: Check for lactose
intolerance or bacterial overgrowth  Endoscopy: Check the stomach, upper small intestine,
or colon for growths or other structural issues  Flexible sigmoidoscopy or colonoscopy:
Check the lower or entire colon for growths or other structural issues  Upper endoscopy:
Check the stomach and upper small intestine for growths or other structural issues

 52. Treatment Acute diarrheal disease is treated by rehydrating the body with fluids and
electrolytes, and taking medications to help ease symptoms.  Rehydration  Drink water,
broths, sports drinks, or oral rehydration solutions (ORS)  If you have diarrhea, you may lose
your appetite, but you can eat your normal diet when it returns For children, ask a doctor
about using an oral rehydration solution like Pedialyte If you have severe dehydration or
shock, you may need intravenous fluids  Medications  Loperamide (Imodium) and
simethicone can help with watery diarrhea and abdominal discomfort  Antibiotics can treat
some types of diarrhea,  Zinc supplements can reduce the duration of diarrhea Other
treatments  Probiotics may shorten the duration of diarrhea  Nutrient-rich foods can help
break the cycle of malnutrition and diarrhea

 54. Vaccine There are licensed vaccines for cholera, rotavirus, and typhoid fever, but no
combination vaccine for diarrheal diseases. However, vaccines are one of the most effective
ways to protect children from diarrheal diseases. Rotavirus vaccines  Rotarix and RotaTeq:
These vaccines are safe and effective at preventing rotavirus illness.  ROTAVAC and
ROTASIIL: These vaccines were developed in India and approved by the WHO for safety and
efficacy.  Benefits: Rotavirus vaccines reduce hospitalizations and deaths, and help stop the
spread of rotavirus in the community. Cholera vaccines  Dukoral: A monovalent vaccine
based on formalin and heat-killed whole-cells of V. cholerae O1  Shanchol and mORCVAX:
Bivalent vaccines based on serogroups O1 and O139  Benefits: These vaccines have been
effective in controlling epidemic diseases

 55. Prevention Acute diarrheal disease can be prevented by practicing good hygiene,
sanitation, and food safety. Hygiene  Wash hands with soap and water, especially after
using the bathroom, before eating, and after changing diapers  Avoid sharing towels,
utensils, and handkerchiefs with someone who has diarrhea  Stay home from work or
school until symptoms resolve  Sanitation Ensure access to clean drinking water, Treat
wastewater and sewage properly, Dispose of human waste properly, Clean and disinfect
frequently touched surfaces, and Maintain proper drainage systems. Food safety  Buy fresh
food from reliable sources  Cook food thoroughly, especially seafood and shellfish  Wash
and peel fruits yourself  Avoid raw vegetables  Avoid drinks with ice of unknown origin
Other measures  Get the rotavirus vaccine for infants  Educate yourself about how
infections spread  Breastfeed exclusively for the first six months of a baby's life

 57. Hepatitis  Hepatitis refers to an inflammatory condition of the liver. It is commonly the
result of a viral infection, but there are other possible causes of hepatitis. These include
 autoimmune hepatitis and hepatitis that occurs as a secondary result of medications, drugs,
toxins, and alcohol.  Autoimmune hepatitis is a disease that occurs when body makes
antibodies against liver tissue.  The five main viral classifications of hepatitis are hepatitis A,
B, C, D, and E. A different virus is responsible for each type of viral hepatitis.  Hepatitis is an
inflammation of the liver and caused by viral infection, alcohol consumption, several health
conditions, or even some medications. Treatment varies based on the type and underlying
cause.

 59. Types  Hepatitis A: This form of hepatitis does not lead to a chronic infection and
usually has no complications. The liver usually heals from hepatitis A within several months.
However, occasional deaths from hepatitis A have occurred due to liver failure, and some
people have required a liver transplant for acute hepatitis A infection. Hepatitis A can be
prevented by vaccination.  Hepatitis B: Around 22,000 new cases of hepatitis B occurred in
2017, and around 900,000 people are living with the disease in the US. Approximately 95%
of adults recover from hepatitis B and do not become chronically infected. However, a few
cases cause a life-long, chronic infection. The earlier in life hepatitis B is contracted, the
more likely it is to become chronic. People can carry the virus without feeling sick but can
still spread the virus. Hepatitis B can be prevented by getting a vaccine.

 60. Types  Hepatitis C: Hepatitis C is one of the most common causes of liver disease in the
U.S., and used to be the number one reason for liver transplant. About 75% to 85% of
patients with hepatitis C develop a chronic liver infection. Roughly 2.4 million people in the
U.S. are estimated to have chronic hepatitis C infection. It often does not show any
symptoms. No vaccine is yet available to prevent hepatitis C.  Hepatitis D: Hepatitis D only
happens to people who are infected by the hepatitis B virus. If you are vaccinated against
hepatitis B, you will be protected against hepatitis D virus.  Hepatitis E: This type of hepatitis
is spread by ingesting contaminated food or water. Hepatitis E is common throughout the
world. Even though vaccines exist, they are not available everywhere.

 61.  Hepatitis A: A food-borne illness that's usually mild and self- limiting. It's the easiest
type of hepatitis to transmit, especially in children.  Hepatitis B: A chronic infection that can
lead to liver damage, liver cancer, and cirrhosis. It can be transmitted through contaminated
blood, needles, syringes, or bodily fluids.  Hepatitis C: A chronic infection that can lead to
liver damage, liver cancer, and cirrhosis. It's only transmitted through infected blood or from
mother to newborn during childbirth.  Hepatitis D: A chronic infection that only occurs in
people who are also infected with hepatitis B.  Hepatitis E: An acute infection that's most
prevalent in Africa, Asia, and South America.  Autoimmune hepatitis: A non-viral cause of
hepatitis caused by autoimmune disorders.  Alcoholic hepatitis: A non-viral cause of
hepatitis caused by excessive alcohol consumption.  Drug-induced hepatitis: A non-viral
cause of hepatitis caused by certain medications or toxins.

 62. Type of hepatitis Common route of transmission Hepatitis A exposure to HAV in food or
water Hepatitis B contact with HBV in body fluids, such as blood, vaginal secretions, or
semen Hepatitis C contact with HCV in body fluids, such as blood, vaginal secretions, or
semen Hepatitis D contact with blood containing HDV Hepatitis E exposure to HEV in food or
water Causes of hepatitis

 63. Causes of non-infectious hepatitis  Although hepatitis is most commonly the result of
an infection, other factors can cause the condition. Alcohol and other toxins  Excess alcohol
consumption can cause liver damage and inflammation. This may also be referred to as
 alcoholic hepatitis.  The alcohol directly injures the cells of your liver. Over time, it can
cause permanent damage and lead to thickening or scarring of liver tissue (cirrhosis) and
liver failure. Other toxic causes of hepatitis include misuse of medications and exposure to
toxins. Autoimmune system response  In some cases, the immune system mistakes the liver
as harmful and attacks it. This causes ongoing inflammation that can range from mild to
severe, often hindering liver function. It’s three times more common in women than in men.

 64. Risk factors  Hepatitis A: Poor sanitation, lack of safe water, living with an infected
person, and traveling to areas with high rates of hepatitis A  Hepatitis B: Contact with
blood, semen, or other bodily fluids from an infected person, sharing needles, and traveling
to areas with high rates of hepatitis B  Hepatitis C: Sharing needles, birth from a mother
who is infected with hepatitis C, and receiving a blood transfusion  Hepatitis D: Being
infected while pregnant, carrying the hepatitis B virus, and receiving many blood
transfusions  Hepatitis from tattoos and piercings: Getting a tattoo or piercing in an
unregulated setting  Hepatitis from grooming items: Sharing personal care items that may
have come into contact with infected blood, such as razors, nail clippers, or toothbrushes 
Hepatitis from medications: Taking medicine that can weaken the immune system, such as
chemotherapy  Hepatitis from sexual contact: Having sex without a condom with multiple
sex partners or with someone who's infected  Hepatitis from HIV: Being HIV positive 
Hepatitis from homelessness: Being homeless  Hepatitis from recreational drugs: Using any
type of recreational drugs

 65. Pathophysiology  Viral hepatitis: Viruses enter the bloodstream, infect liver cells, and
cause the body's immune system to attack the infected cells. This attack damages the liver
and can lead to liver fibrosis and cirrhosis.

 67. Transmission

 68. Sign and symptoms

 69.  Hepatitis may start and get better quickly. It may also become a long-term condition. In
some cases, hepatitis may lead to liver damage, liver failure, cirrhosis, liver cancer or even
death.  There are several factors that can affect how severe the condition is. These may
include the cause of the liver damage and any illnesses you have. Hepatitis A, for example, is
most often short-term and does not lead to chronic liver problems.  The symptoms of
hepatitis include:  Pain or bloating in the belly area  Dark urine and pale or clay-colored
stools  Fatigue  Low grade fever  Itching  Jaundice (yellowing of the skin or eyes)  Loss of
appetite  Nausea and vomiting  Weight loss

 70. Diagnostic investigation

 71.  Hepatitis is diagnosed using a combination of blood tests, imaging tests, and
sometimes a liver biopsy. The type of test used depends on the type of hepatitis being
investigated. Blood tests  Hepatitis B: Blood tests can detect the hepatitis B virus,
determine if the infection is acute or chronic, and if you are immune.  Hepatitis C: Blood
tests can detect the hepatitis C virus, and determine if the infection is acute or chronic. 
Hepatitis A: Blood tests can confirm a suspected case of hepatitis A.  Autoimmune hepatitis:
Blood tests can help diagnose autoimmune hepatitis. Imaging tests  Liver ultrasound: A
special ultrasound called transient elastography can show the amount of liver damage. 
Abdominal ultrasonography: Can help exclude other conditions that resemble acute
hepatitis.  Computed tomography (CT): Can help exclude other conditions that resemble
 acute hepatitis. Liver biopsy  A small sample of liver tissue is removed for testing to check
for liver damage. Other tests  Elastography  Uses sound waves to measure the stiffness of
the liver and check for fibrosis. Paracentesis  Fluid from the patient's abdomen is tested to
help differentiate among many potential causes of liver disease.

 72. Hepatitis treatment depends on the type of hepatitis and the severity of liver damage.
Treatments include:  Antiviral medications: These can prevent the virus from replicating,
reverse liver damage, and eliminate the virus from the bloodstream.  Interferon shots:
These can help your immune system fight the virus.  Liver transplant: This is an option if
your liver has been badly damaged.  Rest and hydration: These can help you feel better and
prevent dehydration.  Nutritious diet: This can help you get enough calories and prevent
malnutrition.  Abstaining from alcohol: Alcohol can damage your liver.  Hepatitis A: Rest,
hydration, and a healthy diet: These can help you feel better and prevent dehydration. 
Vaccination: This can prevent you from getting hepatitis A.  Hepatitis B : Antiviral
medications: These can help fight the virus and slow its ability to damage your liver. 
Interferon shots: These can help your immune system fight the virus.  Liver transplant: This
is an option if your liver has been badly damaged.  Hepatitis C : Direct-acting antiviral (DAA)
tablets: These are the safest and most effective medicines for treating hepatitis C.

 73.  Hepatitis prevention involves practicing good hygiene, avoiding contact with
contaminated objects, and getting vaccinated. Hepatitis A  Get the hepatitis A vaccine,
which is safe and effective  Practice good hand hygiene  Avoid contact with contaminated
water and food  Avoid tap water, fresh fruit, and vegetables unless you can peel them 
Wash your hands frequently Hepatitis B  Get the hepatitis B vaccine  Avoid sharing
needles, syringes, or other drug equipment  Practice safe sex  Avoid sharing toothbrushes,
razors, or needles  Wash your hands thoroughly with soap and water after coming into
contact with blood, body fluids, or contaminated surfaces Hepatitis C  Avoid behaviors that
can spread the disease  Avoid sharing needles, syringes, or other drug equipment  Practice
safe sex  Avoid contact with anything that has contaminated blood on it Hepatitis D 
Hepatitis D only infects people with hepatitis B Hepatitis E  Ensure high levels of sanitation
and access to safe food and water

 74. Vaccination  Hepatitis vaccinations are safe and effective ways to prevent hepatitis A
and B. The CDC recommends that children get the hepatitis A vaccine between 12 and 23
months of age. The hepatitis B vaccine is recommended for all newborns and children, and
for adults at risk. Hepatitis A vaccine  There are single-antigen and combination vaccines. 
The combination vaccine protects against both hepatitis A and B, but can only be given to
people 18 years or older.  The CDC recommends that children get the hepatitis A vaccine
between 12 and 23 months of age. Hepatitis B vaccine  The first dose is recommended for
newborns within 24 hours of birth.  The vaccine is given in 2 or 3 doses.  The second dose
is given 1 month after the first, and the third dose is given 6 months after the second.

 76. As of current information, there is no officially designated "Herpes Simplex Day" in India,
and there is no widely recognized national awareness day for herpes in the country;
however, if you're looking for a global reference point, "Herpes Awareness Day" is often
observed on October 13th.

 77. Herpes simplex  Herpes simplex virus (HSV) can infect many different parts of body,
most commonly mouth area (oral herpes) and genitals ( genital herpes). HSV causes fluid-
filled blisters that break open and crust over wherever the infection is. This is known as a
 herpes outbreak.  HSV is highly contagious. It spreads from person to person through skin-
to-skin contact. A herpes simplex infection occurs when the virus enters body through skin
and mucous membranes (mucosa). The virus uses cells to make copies of itself (replication).
 Once infected, the virus stays in body for life. It’s usually asleep (dormant) but may “wake
up” (reactivate) and cause outbreaks. How HSV affects depends on many factors, including
the specific virus type and overall health.

 78. Types There are two types of herpes simplex virus:  Herpes simplex virus type 1 (HSV-
1).  Herpes simplex virus type 2 (HSV-2).  Both HSV-1 and HSV-2 can cause oral herpes or
genital herpes. They also cause infections in other areas of your body.

 79. Herpes simplex incubation period  The incubation period for herpes simplex infections
ranges from one to 26 days but is typically six to eight days. This is how long it takes for you
to develop symptoms after first getting infected with HSV.  Some people get infected but
don’t develop symptoms right away. Instead, symptoms may not appear for months or even
years until the virus reactivates. Herpes simplex virus (HSV) type 1 (HSV-1) and type 2 (HSV-
2) are both contagious viral infections that cause painful blisters or ulcers. HSV-1 usually
causes cold sores around the mouth, while HSV-2 usually causes genital herpes.

 80. Type of contact How HSV spreads Genital-to-genital contact HSV spreads from one
person’s genital area to another person’s genital area (giving them genital herpes). Oral-to-
oral contact HSV spreads from one person’s mouth to another person’s mouth (giving them
oral herpes). Oral-to-genital contact HSV spreads from one person’s mouth to another
person’s genitals (giving them genital herpes). Genital-to-oral contact HSV spreads from one
person’s genitals to another person’s mouth (giving them oral herpes). Skin-to-sore contact
It’s less common but possible to spread HSV by touching an oral or genital sore or other
infected areas. Transmission/ HSV usually spreads in the following ways:

 82. Stages

 84. Sign and symptoms

 86. Treatment Prescription antiviral medications are the main treatment for HSV infections.
These come in different forms, including:  Pills you swallow.  Cream or ointment you apply
to your skin.  Medication your provider gives you intravenously (through an IV).  Drops you
put into your eyes (for ocular herpes). Your provider will tell you which type(s) of medication
are best for you based on:  The type of infection you have.  Its severity.  How well your
immune system is working.  They’ll also tell you the proper dose and how long you’ll need
the medication. Treatment for oral and genital herpes falls into two categories: episodic
therapy and chronic suppressive therapy.

 89. Prevention  To prevent herpes simplex virus (HSV), you can avoid risky behaviors and
maintain a healthy immune system.  Avoid risky behaviors  Avoid oral contact: Don't share
objects that have touched saliva,.  Avoid sexual activity:  Wash hands: Wash your hands
with soap and water after touching sores or the area around them.  Wash objects: Wash
objects that may have touched sores, like eating utensils, drinking glasses, washcloths, and
towels.  Maintain a healthy immune system Eat nutritious food, Exercise regularly, Get
enough rest, and Reduce stress.

 90. • Chicken pox  Chicken pox is a viral infection in which a person develops extremely
itchy blisters all over the body.  It is used to be one of the classic childhood disease.
 91. Incubation period:  About 14 - 16 days Causative Organism Human (alpha) herpes virus
(Varicella- Zoster virus :VZV)  Occur mainly in children under 10 years of age.  Uncommon
in adults.

 92. Mode of transmission Chicken pox is mainly spread by, 1) Droplet infection
2)Contaminated clothing and direct contact with open blisters. 3) Virus can cross placental
barrier and may affect fetus.

 94. Sign and Symptoms  Fever  Loss of appetite  Cold  Abdominal pain  Headache 
Fatigue  Sore throat  Rash

 95. Cont…  The rash starts on the chest and back, and spread to the face, scalp, arms and
legs.  The rash can develop all over the body, inside the ears, on the eyelids, inside the nose
and within the vagina, everywhere.

 96. Stages of Chicken Pox

 97. Diagnosis  History collection  Physical examination  Blood Sample  Blood Cultures 
Stained smears from vesicular scrapings  Serology test for Varicella IgM  ELISA test is also
useful

 98. Treatment  Drugs:  Antiviral – Acyclovir  Antipyretics- Paracetamol  Antihistamine-

Fexofenadine (allegra)  Antibiotic- Amoxicillin

 99. Vaccination  The chickenpox vaccine, also known as the varicella vaccine, protects
against chickenpox. The CDC recommends that children, adolescents, and adults get two
doses of the vaccine.  Who should get the vaccine?  Children under 13 should get two
doses of the vaccine  People 13 and older who have never had chickenpox or the vaccine
should get two doses  People who have only had one dose of the vaccine should get a
second dose  People at higher risk of getting chickenpox, like healthcare workers, should
get the vaccine

 100. Prevention and control  By administering specific V. Zoster immunoglobulin.  Use of

local antiseptics like chlorhexidine.  Transmission prevented by isolation of patient for 5-7
days.  Sterilization of all articles used by patient after cure.

 101. Complications  Pneumonia  CNS involvement : Encephalitis, Transverse myelitis,

Reye’s Syndrome  Myocarditis, Nephritis, Arthritis

 102. Movies Chicken Pox (2008)  A movie that some say is a piece of art that expresses
emotions in a way that words cannot. Varicella (2015)  An Italian short film also known as
Chickenpox that was selected for the 2015 The One with the Chicken Pox  A 1996 episode
of Friends where Ryan develops chickenpox after staying with Phoebe who was sick when he
arrived.

 103. Small pox  Smallpox was a serious illness that killed hundreds of millions before its
eradication. It caused a hard, blistering rash that often led to disfiguring scars.  Beginning in
the 1960s, the World Health Organization (WHO) led efforts to stop the spread of smallpox
worldwide. By vaccinating and controlling outbreaks, they rid the world of smallpox. It was
eradicated in 1980. The last naturally occurring case was in 1977.

 104.  Smallpox vaccines are not routinely given in India because smallpox has been
eradicated. However, health officials would use the vaccine to control any future outbreaks.
  Explanation: The first smallpox vaccine lymph arrived in India in 1802.  In 1962, India
launched the National Smallpox Eradication Program (NSEP).  The program focused on mass
vaccination and involved hiring healthcare workers and investing in vaccine manufacturing. 
The World Health Organization (WHO) also played a critical role in the eradication of
smallpox.

 105. Causes  The variola virus causes smallpox. There are two variants of variola: variola
major and variola minor (or variola alastrim). Variola major caused most cases of smallpox
and the most deaths. Variola minor caused similar, but less severe, symptoms. It was only
fatal in 1% of cases, compared to over 30% of cases of variola major.

 106. Transmission  Smallpox spread through close, face-to-face contact. For instance,
someone with smallpox could transmit it by coughing or talking to someone nearby. It was
also possible to spread it through contact with infected items (like bedsheets or clothing).

 107. Pathophysiology  Initial infection: The virus enters the respiratory tract through
droplets from an infected person's cough, sneeze, or talk.  Replication: The virus multiplies
in the respiratory tract and lymph nodes.  Viremia: The virus spreads throughout the body,
causing a massive asymptomatic viremia.  Skin infection: The virus localizes in the skin,
causing a rash that progresses through stages.  Cell-mediated immune response: The body's
immune response causes the rash to develop into pustules.  Scarring: The pustules can
cause deep scarring, especially in the most lethal cases.

 108. Types  There are a few types of smallpox that cause slightly different symptoms: 
Ordinary smallpox. Ordinary smallpox was the most common type of smallpox and caused
the symptoms described above. It caused about 85% of cases. About 1 in 3 people with
ordinary smallpox died.  Modified-type smallpox. People who had been vaccinated
sometimes got modified-type smallpox. This was similar to ordinary smallpox, but the rash
was less severe and didn’t last as long. Most people survived modified-type smallpox.  Flat-
type (malignant) smallpox. Flat-type smallpox caused more severe initial symptoms than
ordinary smallpox. The bumps from the rash merged together and never got hard or fluid-
filled. This made a flat, soft rash that didn’t form scabs. Flat-type smallpox happened more
often in children. It was almost always fatal.  Hemorrhagic smallpox. Hemorrhagic smallpox
was more common in pregnant people. It caused severe initial symptoms. The rash usually
didn’t get hard and fluid-filled. Instead, the skin underneath it bled, causing it to look black
or burnt. It also caused internal bleeding and organ failure. Hemorrhagic smallpox was
almost always fatal.

 109. Sign and symptoms Early symptoms  High fever, often between 101° and 104°
Fahrenheit  Feeling generally unwell (malaise)  Severe headache and backache 
Abdominal pain and vomiting  Mouth sores  Rash  A rash of flat spots that turn into raised
bumps, then fluid-filled blisters, and finally scabs  The rash starts on the face and hands,
then spreads to the rest of the body  The rash appears 2–3 days after the initial symptoms 
Other symptoms  Diarrhea  Lesions in the mucous membranes of the nose and mouth 
Ulceration of the lesions in the mouth and throat Infectious period  A person with smallpox
is infectious from the time they develop a fever until the last scabs fall off  Smallpox is a
highly contagious disease that can cause blindness, encephalitis, and other serious
complications.
 110. Diagnostic assessment Laboratory testing  Real-time polymerase chain reaction (PCR):
The preferred method for detecting the variola virus  Culture of fluid or scab: From blisters,
pustules, or scabs  Blood test: During the fever stage to identify antibodies made in
response to the virus  Electron microscopy: Of fluid or scab  Smallpox is diagnosed in
specialized laboratories that have the proper testing techniques and safety measures.

 111. Treatment  Smallpox treatment is generally supportive care in a hospital setting.

There is no specific treatment that has been proven effective in people who are sick with
smallpox.  Supportive care : Patients are treated in a hospital setting with strict isolation
and infection controls.  Vaccination: Vaccination with replication-competent smallpox
vaccines, can prevent or lessen the severity of the disease if given within 2 to 3 days of
exposure.  Antiviral drugs: Some antiviral drugs, like brincidofovir (TEMBEXA) and
tecovirimat (Tpoxx), have been tested in animals and in labs. However, they have not been
tested in people who are sick with smallpox.  Isolation : Patients should be kept in a room
with negative air pressure.  The room should have a private shower and bathroom. 
Unvaccinated personnel should wear protective clothing, including gowns, masks, gloves,
and eye protection.  Smallpox has been eradicated worldwide due to vaccination efforts.
There are currently no cases circulating.

 112. Prevention  Smallpox is prevented by vaccination. The smallpox vaccine is made from
a virus called vaccinia, which is similar to smallpox but less harmful. How to prevent
smallpox  Get vaccinated  The smallpox vaccine can protect you from getting sick or make
the disease less severe if you get it before or within a week of exposure.  Vaccinate people
at risk  If there is a potential exposure, vaccinate all people who are susceptible.  Dispose
of contaminated materials properly  Incinerate disposable materials and sterilize reusable
equipment or clothing.

 113. • Typhoid Fever • Acute infectious illness • Affect GIT. • Enteric fever – Typhoid &
Paratyphoid fever.  Typhoid fever is characterized by a fever that is usually lowest in the
morning and highest in the afternoon or evening.  Incubation Period : About 6–30 days.

 114. Typhoid fever  Typhoid fever is an illness caused by the bacterium Salmonella Typhi (S.
Typhi). It infects small intestines (gut) and causes high fever, stomach pain and other
symptoms. Typhoid fever is also called enteric fever.  Paratyphoid fever is similar to typhoid
with more mild symptoms. It’s caused by Salmonella Paratyphi (S. Paratyphi).  S. Typhi and
S. Paratyphi are different than the Salmonella bacteria that cause salmonellosis, a common
type of food poisoning.

 115. Causative Organism Salmonella typhi, Salmonella parathyphi A, Salmonella parathyphi

B, Mode of Transmission  Mainly transmit by, 1. Through fecal – oral route. 2.
Contaminated drinking water by sewage. 3. Contaminated of food from flies

 116. Stages  Stage 1. You can start getting typhoid symptoms anywhere from five to 14
days after coming in contact with S. Typhi. The first symptom is a fever that gets higher over
a few days — called “stepwise” since it goes up in steps. The bacteria is moving into your
blood in this stage.  Stage 2. Around the second week of fever, the bacteria is multiplying in
your Peyer’s patches (part of your immune system that identifies harmful invaders). You’ll
start experiencing abdominal pain and other stomach symptoms, like diarrhea or
constipation. You might get “rose spots,” small pink dots on your skin that look like a rash. 
Stage 3. If not treated with antibiotics, the bacteria can cause severe damage, usually
 around the third week after your symptoms start. Some people get serious complications,
like internal bleeding and encephalitis (inflammation in your brain).  Stage 4. Stage four is
when most people begin to recover. Your high fever begins to come down. S. Typhi can live
in your gallbladder without causing symptoms, which means you may still be contagious
even after you feel better.

 117. Pathophysiology  Ingestion: The bacteria enter the body through contaminated food
or drink.  Survival: The bacteria survive stomach acid and pass into the small intestine. 
Invasion: The bacteria invade the intestinal epithelium, triggering an inflammatory response.
 Dissemination: The bacteria spread to the lymph nodes, gallbladder, liver, spleen, and
other parts of the body.  Systemic disease: The bacteria can spread to the liver, spleen, and
bone marrow, causing systemic disease.

 118. Sign and symptom cont…

 120. Diagnostic investigation  Blood. Your provider will use a needle to take a small tube of
blood from your arm.  (stool). Your healthcare provider will give you a sterile container and
instructions on how to collect a sample.  Pee (urine). You may be asked to pee into a cup
given to you by your healthcare provider.  Your provider might numb your skin and take a
sample with a small razor or scalpel.  Bone marrow. Your provider will numb your skin and
use a special needle to get a sample of the inside of your bones. It’s rare that you’d ever
need this test for diagnosis.  You provider may also take X-rays (pictures of the inside of
your body) to look for changes in your lungs.

 121. Prevention & Control cont… 1. Strict personal hygiene. 2. Using boiling drinking water.
3. Early detection of cases. 4. Proper and immediate treatment. 5. Disinfection of infective
discharges & clothing. 6. Sanitation should be maintained. 7. For prevention use vaccine. i.
Monovalent anti typhoid vaccine ii. Bivalent vaccine iii. TAB 8. Treatment is done by, a. By
antibiotics

 122. Management  Typhoid is treated with antibiotics. Some newer types of the bacteria
are able to survive antibiotic treatments, so you’ll be treated with different antibiotics
depending on what type of typhoid you have and where you got sick. Paratyphoid fever is
also treated with antibiotics. treat typhoid fever with antibiotics, which may include: 
Ciprofloxacin, levoflaxin or ofloxacin.  Ceftriaxone, cefotaxime or cefixime.  Azithromycin. 
Carbapenems.  Conservative management .

 123.  The typhoid vaccine for adults is available in injectable and oral forms. The World
Health Organization (WHO) recommends the typhoid conjugate vaccine (TCV) for routine
use. Injectable vaccines  Vi polysaccharide vaccine (Vi-PS): A single injection given to people
aged two and older.  Typhoid conjugate vaccine (TCV): An injectable vaccine that can be
given to children and adults. Oral vaccines  Ty21a vaccine: A live-attenuated vaccine given
in four capsules taken on alternate days. It's approved for adults and children aged six and
older.

 124. Name Typhoid conjugate vaccines (TCV) Ty21a Vi capsular polysaccharide vaccines
(ViCPS) Tradename(s) (Manufacturer) Typbar TCV® (Bharat Biotech) TYPHIBEV® (Biological E)
SKYTyphoid™ (SK bioscience) ZyVac® TCV (Zydus Lifesciences Limited) Vivotif® (PaxVax)
Typhim Vi® (Sanofi Pasteur) Typherix® (GlaxoSmithKline) Administration Intramuscular
injection Oral capsules Intramuscular injection Age >6 months of age >6 years of age >2
years of age Number of doses 1 dose 3 to 4 doses 1 dose with boosters every 2 to 3 years
 Duration of protection > 4 years 7 years 2 years Effectiveness 79% to 85% 50% to 80% 50%
to 80%

 125. Gas gangrene  Gas gangrene, also called clostridial myo-necrosis, is a bacterial
infection that destroys tissues. It’s usually caused by Clostridium bacteria (most commonly,
C. perfringens).  Clostridium bacteria release toxins that destroy blood cells, blood vessels
and muscle tissue. This causes severe blisters, swelling and skin discoloration. The bacteria
create gas that makes wounds smell bad when they open. The toxins also cause widespread
inflammation.  Gas gangrene can be life-threatening within hours of symptoms starting.

 126. Causes  The bacterium Clostridium perfringens causes most cases of gas gangrene.
Other species (types) of Clostridium and group A Streptococcus bacteria can also cause it. 
These bacteria live in dirt and in the intestines (GI tract) of people and animals. They release
toxins that destroy your cells, including your blood cells, blood vessels and muscle tissue. 
They reproduce best in areas with little oxygen. Destroying your blood cells means that less
oxygen gets to your tissues. That makes it easier for them to keep reproducing and creating
toxins, spreading the damage very quickly. Breaking down nutrients without oxygen
(fermentation) is also what causes the pockets of gas.

 127. Risk factor  Severe injuries and abdominal surgeries put you at higher risk for
traumatic gas gangrene. You’re at higher risk for spontaneous gas gangrene — not caused by
an injury — if you have certain underlying conditions, including:  Colon cancer. 
Diverticulitis, which can damage your colon.  Diabetes.  Blood vessel disease, such as
atherosclerosis.  Keep in mind that, even if you have one of these risk factors, it’s still
extremely unlikely that you’ll ever be affected by gas gangrene.

 128. Pathophysiology

 129. Sign and symptoms  Gas gangrene causes discoloration, large blisters and swelling on
your skin where you have a wound. It can also cause other symptoms, including:  Pain near
your injury. This might be severe, even if your wound doesn’t look serious.  Fever.  Fast
heart rate (tachycardia).  Sweating.  Anxiety.  Yellow skin (jaundice).  Light-headedness. 
Low blood pressure (hypotension).

 130. Diagnostic investigation  A diagnosis by looking at tissue or fluids from your wounds
under a microscope. They might order imaging tests, such as X-rays, CT scans or MRIs to
check for tissue damage.  Imaging. X-rays, CT scans or MRIs can show gas bubbles or
changes in your muscle tissue.  Bacterial staining or culture. A provider takes fluid from
your wound and looks at it under a microscope for the types of bacteria that cause gas
gangrene. They may also try to grow (culture) the bacteria.  Biopsy. A provider takes a
sample of the tissue from your wound to look for damage or changes.

 131. Treatment  Gas gangrene must be treated immediately. Health provider will give you
high doses of antibiotics and surgically remove as much of the infected tissue as possible.
You may need other treatments depending on the severity of your infection. You’ll need to
stay in the hospital to be monitored throughout your treatment. Medications and
procedures used to treat gas gangrene:  Debridement. A provider will surgically remove
dead and damaged tissue or debris from your wound.  Antibiotics. Providers often use a
combination of penicillin and clindamycin to kill the bacteria causing the gas gangrene. 
Amputation. In some cases, the best way to prevent further damage and life- threatening
illness is to remove the infected limb. About 1 in 5 people with gas gangrene need an
 amputation.  Hyperbaric oxygen therapy. Hyperbaric oxygen therapy can help gas gangrene
heal. A provider puts you in a special chamber that delivers 100% oxygen (about five times
more than room air). This increases the amount of oxygen getting to your tissues, helping
them to heal. It can also slow down the infection, since oxygen kills Clostridium bacteria.

 132. Prevention  Healthcare providers take precautions to prevent any infections during
surgery and other procedures. This includes the bacterial infections that cause gas gangrene.
Ways for you to reduce your risk of gas gangrene and other bacterial infections include: 
Clean out wounds with soap and water.  Get medical attention immediately for any deep
wounds. This includes wounds you’re unable to clean completely by washing with soap and
water.  Keep an eye on injuries. Let a provider know if you see changes in your skin or
experience severe pain.  Wear protective gear that covers your arms and legs when riding a
motorcycle or bicycle.  Work with a provider to treat underlying conditions that affect your
blood vessels or circulation, or that weaken your immune system.

 134. Meningitis  Meningitis is an inflammation of the area surrounding brain and spinal
cord (meninges). It’s sometimes called spinal meningitis.  Meninges protect brain and spinal
cord from injury and provide support and structure. They contain nerves, blood vessels and
protective fluid (cerebrospinal fluid).  Infectious diseases, like viruses and bacteria, and non-
infectious conditions, like cancer or head injuries, can cause meningitis.  The incubation
period for meningitis is usually 4 days, but can range from 2 to 10 days. Symptoms typically
appear 3 to 7 days after exposure.

 135. Causes of bacterial meningitis  Streptococcus pneumonia.  Group B Streptococcus. 

Neisseria meningitides.  Haemophilus influenza.  Listeria monocytogenes.  E. coli. 
Mycobacterium tuberculosis. Causes of viral meningitis  Non-polio enteroviruses.  Mumps.
 Herpesviruses (including those that cause mononucleosis, chickenpox and shingles). 
Measles.  Influenza.  Arboviruses, such as West Nile virus.  Lymphocytic choriomeningitis
virus. Causes of fungal meningitis  Coccidioides. Causes of parasitic meningitis (eosinophilic
meningitis)  Angiostrongylus cantonensis.  Baylisascaris procyonis.  Gnathostoma
spinigerum. Causes of amebic meningitis (PAM)  Naegleria fowleri causes amebic
meningitis. Causes of non-infectious meningitis  Systemic lupus erythematosus (lupus). 
Certain medications, like NSAIDs and antibiotics.  Head injuries.  Brain surgery.

 136. Transmission Most bacterial and viral causes of meningitis can be spread from person
to person. There are many ways can get meningitis, depending on whether the cause is
infectious or not:  From a contagious illness passed person-to-person, like a virus or
bacteria.  From food contaminated with something infectious.  From swimming in or
drinking water contaminated with something infectious.  From fungi in the environment
that you breathe in.  As a complication of non-infectious illnesses, like cancer or lupus.  As
the result of a head injury or brain surgery.  As a side effect of a medication.

 137. Types of meningitis are typically named for the cause or for how long you’ve had
symptoms. They include:  Bacterial meningitis.  Viral meningitis.  Fungal meningitis. 
Parasitic meningitis. Meningitis caused by certain parasites is called eosinophilic meningitis
or eosinophilic meningoencephalitis (EM).  Primary Amebic Meningitis (PAM). Meningitis
can be caused by the ameba Naegleria fowleri.  Drug-induced aseptic meningitis (DIAM).
Rarely, certain medications cause drug-induced aseptic meningitis (DIAM). Non-steroidal
anti-inflammatory drugs (NSAIDS) and antibiotics are the most common causes of DIAM. 
Chronic meningitis. When meningitis has lasted a month or more, it’s called chronic
 meningitis.  Acute meningitis. Bacterial meningitis is often acute, meaning that symptoms
are severe and come on suddenly.

 138. Risk factors  Are under 5 years old. About 70% of all bacterial meningitis cases affect
children under age 5.  Have a weakened immune system. medications that suppress your
immune system.  Have a CSF leak.  Don’t have a spleen or have a damaged spleen.  Live in
or travel to places where infectious diseases that cause meningitis are common.  Have
chronic nose and ear infections, pneumococcal pneumonia or a widespread blood infection.
 Have a head injury, traumatic brain injury (TBI) or spinal cord injury.  Are living with sickle
cell disease.  Are living with alcohol use disorder.

 139. Pathophysiology

 141. Symptoms of meningitis in children and adults  Neck stiffness.  Nausea or vomiting. 
Sensitivity to light (photophobia).  Confusion or altered mental state.  Lack of energy
(lethargy), extreme sleepiness or trouble waking up.  Lack of appetite.  Small round spots
that look like a rash (petechiae). Additional symptoms of amebic meningitis  You might
experience additional symptoms of amebic meningitis a few days after your initial
symptoms:  Hallucinations.  Loss of balance.  Lack of attention or focus. Meningitis signs
and symptoms in babies  Your baby might not experience the same meningitis symptoms as
adults (like headache, neck stiffness and nausea) and it can be hard to tell even if they are.
Some signs of meningitis you can look for in babies include:  Bulging “soft spot” (fontanelle)
on baby’s head.  Poor eating.  Sleepiness or trouble waking up from sleep.  Low energy or
slower responses (lethargy).

 143. Diagnostic Investigation  Some tests your healthcare provider may use to diagnose
meningitis include:  Nasal or throat swab. Your provider uses a soft-tipped stick (swab) to
take a sample from your nose or throat. A lab will test your sample for signs of infection. 
Lumbar puncture/spinal tap. Your healthcare provider inserts a needle into your lower back
to collect a sample of your cerebrospinal fluid (CSF). A lab tests your CSF sample for signs of
infection.  Blood tests. Your provider takes a sample of blood from your arm with a needle.
A lab tests your blood for signs of infection.  Your healthcare provider can use a CT scan or
MRI to take pictures of your brain and look for inflammation. This is sometimes called a
brain scan.  Stool sample. You give a sample of your poop (stool) to your provider. A lab will
test your stool sample for signs of infection.

 144. Treatment  Meningitis treatment depends on the cause. Antibiotics are used to treat
bacterial meningitis and antifungals are used to treat fungal meningitis. Antivirals can be
used to treat some viral causes of meningitis. Non-infectious causes of meningitis are
treated by addressing the underlying illness or injury.  There are no specific treatments for
other infectious causes of meningitis. Medications might be used to reduce inflammation or
relieve your symptoms. Medications and other therapies that might be used to treat
meningitis include:  Antibiotics for bacterial meningitis.  Antifungals for fungal meningitis. 
Antivirals for certain cases of viral meningitis, like herpesvirus and influenza. 
Corticosteroids, like dexamethasone or prednisone, to reduce inflammation.  Pain relievers.
 IV fluids to keep you hydrated.

 145. Prevention  The best way to reduce your risk of meningitis is to take simple
precautions to protect yourself from the infectious diseases that most often cause it.  Get
vaccinated against the bacterial and viral infections that can cause meningitis. Ask your
 providers which ones might be recommended for you or your child. Take care to avoid
fungal infections.  Wash your hands frequently with soap and water.  Avoid contact with
others when sick with a contagious illness. Cover your mouth and nose when you cough or
sneeze, and disinfect frequently touched surfaces.  Don’t swim in or drink water that could
be contaminated. Use distilled or treated water for nasal irrigation.  Practice safe food prep.
Don’t drink unpasteurized milk or eat food made from unpasteurized milk.  Take
precautions to avoid mosquito and tick bites.

 146.  There are 3 types of meningococcal vaccines used  1. Meningococcal conjugate or

MenACWY vaccines  2. Serogroup B meningococcal or MenB vaccines  3. Pentavalent or
Men ABCWY vaccine

 147.  World Leprosy Day is observed every year on the last Sunday of January. In India, it is
observed on 30 January every year, coinciding with the death anniversary of Mahatma
Gandhi.  The aim of observing the World Leprosy Day is to create awareness against the
stigma attached to the disease, by making the general community aware that it is a disease
spread by a type of bacteria and it can be easily cured.

 148. • Leprosy  Leprosy (also called Hansen’s disease) is an infectious disease caused by the
bacteria Mycobacterium leprae. It can affect eyes, skin, mucous membranes and nerves,
causing disfiguring sores and nerve damage. Leprosy has been around since ancient times. •
Chronic infections of human. • Affect & damage superficial tissue especially skin and
peripheral nerves. • Incubation Period : About 3–5 years

 149. Causative Organism Mycobacterium leprae Mode of Transmission  Mainly spread by,
1. Direct transmission: Prolonged close contact with an infected person. 2. Through air borne
droplets

 150. The incubation period for leprosy, also known as Hansen's disease, can range from 9
months to 20 years, with an average of around 5 years. The incubation period is difficult to
determine because the leprosy bacillus multiplies very slowly. 1. Initially nerve damage
causes numbness of skin on face, hands & feet. 2. Affected skin may become thickened &
discolored. 3. Loss of sensation 4. Lack of sensation leads to injury or even loss of fingers or
toes.

 151. Types There are three main types of leprosy, including:  Tuberculoid leprosy. Someone
with this type of leprosy usually has mild symptoms, developing only a few sores. This is
because of a good immune response. Tuberculoid leprosy is also called paucibacillary
leprosy.  Lepromatous leprosy. People with this type of leprosy have widespread sores and
lesions affecting nerves, skin and organs. With lepromatous leprosy, the immune response is
poor and the disease is more contagious. Lepromatous leprosy is also called multibacillary
leprosy.  Borderline leprosy. This type of leprosy involves symptoms of both tuberculoid
and lepromatous leprosy. Borderline leprosy is also called dimorphus leprosy.

 153. Symptoms The three main symptoms of leprosy (Hansen's disease) include:  Skin
patches that may be red or have a loss of pigmentation.  Skin patches with diminished or
absent sensations.  Numbness or tingling in your hands, feet, arms and legs.  Painless
wounds or burns on the hands and feet.  Muscle weakness. Additionally, people with
leprosy (Hansen's disease) may develop:  Thick or stiff skin.  Enlarged peripheral nerves. 
Loss of eyelashes or eyebrows.  Nasal congestion.  Nosebleeds. When the disease is in the
advanced stages, it can cause:  Paralysis.  Vision loss.  Disfigurement of the nose. 
 Permanent damage to the hands and feet.  Shortening of the fingers and toes.  Chronic
ulcers on the bottom of the feet that don’t heal.

 154. Diagnostic investigation  Perform a skin biopsy. During this procedure, they’ll take a
small sample of tissue and send it to a lab for analysis.

 155. Treatment  Leprosy (Hansen's disease) is treated with multidrug therapy (MDT), an
approach that combines different types of antibiotics. In most cases, your healthcare
provider will prescribe two to three different kinds of antibiotics at the same time. This helps
prevent antibiotic resistance, which occurs when bacteria mutate (change) and fight off the
antibiotic drugs that usually kill them. Common antibiotics used in the treatment of Hansen's
disease include dapsone , rifampin and clofazimine.  Antibiotics can’t treat the nerve
damage that may occur as a result of Hansen's disease. Your healthcare provider may also
prescribe anti- inflammatory drugs, such as steroids, to manage any nerve pain.  On
average, leprosy (Hansen's disease) treatment takes one to two years to complete. During
this time, your healthcare provider will monitor your progress.

 156. Prevention & Control cont… 1. Isolation of patient 2. Early diagnosis & chemotherapy 3.
Treated with some specific drugs such as dapsone etc. 4. Create awareness about leprosy 
Avoid over crowding  Bad personal hygiene  Avoid of sharing of cloths etc 4. For
prophylactic purposes use BCG vaccine

 157.  National Dengue Day in India is celebrated on May 16th every year. It is a day to raise
awareness about dengue, a viral infection spread by mosquitoes.

 158. Dengue  Dengue fever is an illness can get from the bite of a mosquito carrying one of
four types of dengue virus (DENV). The virus is most commonly found in tropical and
subtropical regions, including Central and South America, Africa, parts of Asia and the Pacific
Islands.  Dengue isn’t contagious from person to person except when passed from a
pregnant person to their child. Symptoms are usually mild with your first infection, but if you
get another infection with a different version of DENV, your risk of severe complications
goes up.

 159.  Dengue fever is caused by one of four dengue viruses. When a mosquito infected with
the dengue virus bites you, the virus can enter your blood and make copies of itself. The
virus itself and your immune system’s response can make you feel sick.  The virus can
destroy parts of your blood that form clots and give structure to your blood vessels. This,
along with certain chemicals that your immune system creates, can make your blood leak
out of your vessels and cause internal bleeding. This leads to the life-threatening symptoms
of severe dengue.

 160. Risk factors  Living in tropical areas: Dengue fever is caused by a virus that's more
prevalent in tropical and subtropical areas.  Travel to tropical areas: Travelers who spend a
lot of time in areas with dengue are at higher risk.  Previous dengue infection: Having
dengue fever before increases the risk of developing severe dengue if you get it again. 
Urbanization: Unplanned urbanization can increase the risk of dengue transmission.  Age:
Extreme age can be a risk factor for severe dengue.  Mosquito feeding activity: Dengue is
more likely to spread during periods when mosquitoes are feeding the most, which is usually
in the early evening and two to three hours after dawn.  Community practices: How a
community stores water, keeps plants, and protects itself from mosquito bites can affect the
risk of dengue.
 161. Transmission  Dengue is spread by Aedes mosquitos, which also carry viruses like Zika
and chikungunya. The mosquitos bites someone with dengue fever and then bites someone
else, causing them to become infected.  Dengue fever isn’t contagious directly from one
person to another like the flu. The only way to get dengue from another person is if a
pregnant person becomes infected. If you’re pregnant and get dengue, you can pass it to
your baby during pregnancy or childbirth.

 162. Pathophysiology

 163. Sign and symptoms Dengue fever is a flu-like illness caused by an infected mosquito
bite. Symptoms include: Fever: A sudden high fever of 104°F (40°C) Headache: A severe
headache, especially in the front of the head Pain: Pain behind the eyes that worsens when
moving the eyes, as well as muscle and joint pain Nausea and vomiting: Frequent vomiting
that can lead to dehydration Rash: A rash that looks like measles, appearing on the chest and
upper limbs Swollen glands: Swollen lymph nodes in the neck, armpits, and groin Other
symptoms: Loss of appetite, sore throat, red eyes, facial flushing, and easy bruising Dengue
fever usually begins 4–10 days after being bitten by an infected mosquito and lasts for 2–7
days. However, many people don't experience any symptoms. Warning signs of severe
dengue Severe abdominal pain Persistent vomiting Bleeding from the nose, gums, or under
the skin Rapid breathing Lethargy or change in alertness Giddiness when standing or sitting
up Decreased urine output Severe dengue can lead to dengue shock syndrome (DSS), which
can be life-threatening. Seek immediate medical attention if you experience these
symptoms. .

 164. Diagnostic investigation  Dengue fever is diagnosed using a blood test that checks for
the presence of the dengue virus. The test may involve a nucleic acid amplification test
(NAAT), an NS1 antigen test, or an IgM antibody test.  Tests  Nucleic acid amplification test
(NAAT)  A test that can detect dengue virus RNA in blood, serum, or plasma. A positive
NAAT result usually means you currently have dengue.  NS1 antigen test  A test that looks
for the presence of the dengue virus non-structural protein 1 (NS1) in your blood. A positive
NS1 test result usually means you currently have dengue.  IgM antibody test  A test that
looks for the presence of IgM antibodies against the dengue virus. IgM levels are usually
positive 4–5 days after symptoms appear and can be detected for about 12 weeks.  Other
tests  Complete blood count (CBC): A test that looks for low platelet count, anemia, and
other blood changes.  Viral isolation in cell culture: A test that involves growing the virus in
a lab to identify it. This test is considered the gold standard for dengue detection.  When to
get tested  You should get tested for dengue if you have symptoms like fever, headache,
muscle aches, joint pain, or rash. You should also get tested if you've recently traveled to an
area where dengue is prevalent.

 165.  Dengue fever is treated with supportive care, such as rest, fluids, and pain relievers.
There is no specific cure for dengue.  Supportive care  Acetaminophen: Can help with fever
and muscle pain. Acetaminophen is available over-the-counter under brand names like
Tylenol.  Hydration: Drink plenty of fluids to stay hydrated.  Bed rest: Get enough rest to
help your body fight the virus.  Tepid sponge baths: Can help manage fever.  Home
remedies: Turmeric may help reduce the severity of symptoms. Warm milk can provide
comfort and hydration.  Avoid certain medications : Aspirin, Ibuprofen (Advil, Motrin IB),
Naproxen sodium (Aleve)  Non-steroidal anti-inflammatory drugs (NSAIDs)  Severe cases 
May require hospitalization  May require intravenous (IV) fluids and electrolyte
 replacement  May require blood pressure monitoring  May require blood transfusion 
May require careful fluid management  May require prompt treatment of hemorrhagic
complications  Prevention  Use mosquito repellents  Wear clothes that cover as much of
your body as possible  Use mosquito nets  Remove standing water  Repair holes in
screens  Keep windows and doors closed

 166.  There are a number of medicines and natural remedies that can help increase platelet
count in dengue patients, including: Papaya leaf extract  A natural remedy that can be
taken as a juice or supplement. It's made from fresh papaya leaves that are washed, cut,
blended, and strained. PLT-NORM  A natural herbal medicine that contains a blend of herbs
that can help increase platelet count. Nplate (romiplostim)  A once-weekly platelet booster
that works by increasing the activity of cells that produce platelets. Giloy (Tinospora
Cordifolia)  An Ayurvedic herb that can help improve platelet count by boosting the
immune system. Pomegranate  A fruit that's rich in iron, which can help maintain a healthy
platelet count. Pumpkin  A vegetable that contains vitamin A and antioxidants, which can
help increase platelet count. Spinach  A leafy green vegetable that's rich in vitamin K, which
is important for blood clotting and platelet production.

 167. Vaccination  The dengue vaccine, Dengvaxia, is a safe and effective vaccine that helps
protect against dengue fever. It's recommended for people who have had a previous dengue
infection and live in an area where dengue is common. How it works  Dengvaxia is a live-
attenuated vaccine that protects against all four dengue virus serotypes.  It's made by
Sanofi Pasteur and approved by the U.S. Food and Drug Administration.  The vaccine is
given subcutaneously in three doses, with each dose administered six months apart. Who
can get the vaccine?  People aged 6 to 45 who have had a previous dengue infection 
Children and adolescents aged 9–16 who have had a previous dengue infection and live in an
area where dengue is common

 168. Prevention  To reduce your risk of dengue, you can:  Wear long-sleeved shirts, long
pants, socks, and closed-toe shoes.  Use mosquito repellent.  Empty standing water from
around your home.  Spray clothing with insecticide.  Use vector control methods like
insecticide sprays and thermal fogging.

 169. • SARS (Severe Acute respiratory syndrome)  It is a contagious and sometimes fatal
respiratory illnesss.  SARS appears first in China 2002 and then spread in world wide by
travelers.

 170. Incubation Period:  2 to 7 days  1 to 14 days  Mode of transmission: -Direct or

Indirect method

 171. Causative agent  Corona Virus: Family is coronaviridae Risk Factors:  Recent travel 
Close Contact

 173. Types of SARS  Respiratory: common cold, pneumonia  Gastrointestinal : generalized

mild disease

 174. Severe type of causes of SARS  SARS: CoV -2003 in China  MERS- Cov – 2012 in Saudi
Arab  19- SARS – 2019 in China as COVID-19 (2019 Novel Corona Virus)

 175. Sign and Symptoms:

 176. Diagnosis  PCR (Polymerase Chain Reaction)  Serologic Testing  Viral Culture  Chest
X-Ray  Throat Swab

 177. Treatment  No uniform treatment for SARS- CoV  Broad –spectrum antibiotics 
Antiviral agents  Immunomodulatory therapy  Supportive Care  Require Mechanical
Ventilation in severe

 178. Prevention  Wash hands  Use PPE  Pay attention to what surfaces you touch surface
 Isolation  Intake of Warm Water

 179.  SARS Wars (Thai: ขุนกระบี่ผีระบาด or Khun krabi phirabat, also subtitled
Bangkok Zombie Crisis) is a 2004 Thai action fantasy comedy horror film directed and co-
written by Taweewat Wantha.  The story involves people who are infected with a fictional
Type 4 strain of the SARS virus and turned into zombies. The outbreak is contained to one
apartment building in Bangkok, and the Health Ministry is determined to keep it contained
at all costs. But the building also happens to be the hideout for a gang that has kidnapped a
teenage schoolgirl. She is to be rescued by a sword-wielding superhero crime fighter, who
must not only contend with the criminals, but also the zombies in a race against the
government's plan to blow the building up.

 180. COIVID -19  COVID-19, also called coronavirus disease 2019, is an illness caused by a
virus. The virus is called severe acute respiratory syndrome coronavirus 2, or more
commonly, SARS-CoV-2. It started spreading at the end of 2019 and became a pandemic
disease in 2020.

 181.  COVID-19 is caused by infection with the severe acute respiratory syndrome
coronavirus 2, also called SARS-CoV-2.  The coronavirus spreads mainly from person to
person, even from someone who is infected but has no symptoms. When people with
COVID-19 cough, sneeze, breathe, sing or talk, their breath may be infected with the COVID-
19 virus.  The coronavirus carried by a person's breath can land directly on the face of a
nearby person, after a sneeze or cough, for example. The droplets or particles the infected
person breathes out could possibly be breathed in by other people if they are close together
or in areas with low air flow. And a person may touch a surface that has respiratory droplets
and then touch their face with hands that have the coronavirus on them.  It's possible to
get COVID-19 more than once.  Over time, the body's defense against the COVID-19 virus
can fade.  A person may be exposed to so much of the virus that it breaks through their
immune defense.  As a virus infects a group of people, the virus copies itself. During this
process, the genetic code can randomly change in each copy. The changes are called
mutations. If the coronavirus that causes COVID-19 changes in ways that make previous
infections or vaccination less effective at preventing infection, people can get sick again. 
The virus that causes COVID-19 can infect some pets. Cats, dogs, hamsters and ferrets have
caught this coronavirus and had symptoms. It's rare for a person to get COVID-19 from a pet.

 182.  The main risk factors for COVID-19 are:  If someone you live with has COVID-19.  If
you spend time in places with poor air flow and a higher number of people when the virus is
spreading.  If you spend more than 30 minutes in close contact with someone who has
COVID-19.  Many factors affect your risk of catching the virus that causes COVID-19. How
long you are in contact, if the space has good air flow and your activities all affect the risk.
Also, if you or others wear masks, if someone has COVID-19 symptoms and how close you
are affects your risk. Close contact includes sitting and talking next to one another, for
 example, or sharing a car or bedroom.  It seems to be rare for people to catch the virus that
causes COVID- 19 from an infected surface. While the virus is shed in waste, called stool,
COVID-19 infection from places such as a public bathroom is not common.

 183. Pathophysiology

 184.  Typical COVID-19 symptoms often show up 2 to 14 days after contact with the virus. 
Symptoms can include:  Dry cough.  Shortness of breath.  Loss of taste or smell.  Extreme
tiredness, called fatigue.  Digestive symptoms such as upset stomach, vomiting or loose
stools, called diarrhea.  Pain, such as headaches and body or muscle aches.  Fever or chills.
 Cold-like symptoms such as congestion, runny nose or sore throat.  People may only have
a few symptoms or none. People who have no symptoms but test positive for COVID-19 are
called asymptomatic. For example, many children who test positive don't have symptoms of
COVID-19 illness. People who go on to have symptoms are considered presymptomatic. Both
groups can still spread COVID-19 to others.  Some people may have symptoms that get
worse about 7 to 14 days after symptoms start.

 186.  Most people with COVID-19 have mild to moderate symptoms. But COVID-19 can
cause serious medical complications and lead to death. Older adults or people who already
have medical conditions are at greater risk of serious illness.  COVID-19 may be a mild,
moderate, severe or critical illness.  In broad terms, mild COVID-19 doesn't affect the ability
of the lungs to get oxygen to the body.  In moderate COVID-19 illness, the lungs also work
properly but there are signs that the infection is deep in the lungs.  Severe COVID-19 means
that the lungs don't work correctly, and the person needs oxygen and other medical help in
the hospital.  Critical COVID-19 illness means the lung and breathing system, called the
respiratory system, has failed and there is damage throughout the body.  Rarely, people
who catch the coronavirus can develop a group of symptoms linked to inflamed organs or
tissues. The illness is called multisystem inflammatory syndrome. When children have this
illness, it is called multisystem inflammatory syndrome in children, shortened to MIS-C. In
adults, the name is MIS-A.

 187. Diagnostic investigation Molecular tests. These tests look for genetic material from the
COVID-19 virus.  Polymerase chain reaction tests, shortened to PCR tests, are molecular
tests. You may also see this type of test called an NAAT test, short for nucleic acid
amplification test.  PCR tests are more accurate than the other type of COVID-19 test, called
an antigen test. PCR tests may be done at home. But they are much more likely to be done
by a healthcare professional and processed in a lab. Antigen tests. These tests look for viral
proteins called antigens.  Antigen tests also may be called rapid COVID-19 tests or at-home
COVID-19 tests. These tests are useful if you need a quick result.  Antigen tests are reliable
and accurate, but they are less accurate than PCR tests. This is especially true if you don't
have symptoms. If you take an antigen test and are negative for COVID-19, take another
antigen test after 48 hours to get the most accurate result.  computed tomography (CT)
based medical imaging technologies are being used for diagnosing the COVID-19 infection
and pathological status, respectively, in clinical settings [

 188. Treatment Therapeutic Type of treatment Start time after symptoms first appear
Paxlovid Oral antiviral (pills) As soon as possible and up to 5 days Lagevrio (molnupiravir)
Oral antiviral (pills) As soon as possible and up to 5 days Veklury® (remdesivir) IV infusion
antiviral As soon as possible and up to 7 days Symptomatic treatment : antibiotic therapy,
antipyretics, respiratory therapies, yoga, meditation, nutritional therapy, supportive therapy.
 Use cough medications containing guaifenesin, such as Robitussin, Mucinex, and Vicks.
keeping you from getting rest. Coughing is useful because it brings up mucus from the lungs
and helps prevent bacterial infections.

 189.  For people who are in the hospital for COVID-19 care, care is given based on a
person's immune system response and the need for oxygen support.  Added oxygen may be
given through a tube in the nose. Some people may need to have a tube placed in their
airway to push air into the lungs. That's called mechanical ventilation. In very severe
situations, a machine called extracorporeal membrane oxygenation, also known as ECMO,
can be used to mimic the function of the heart and lungs.  Medicines for severe COVID-19
may be remdesivir, baricitinib (Olumiant) and tocilizumab (Actemra), or a corticosteroid such
as dexamethasone.  Baricitinib is a pill. Tocilizumab is an injection. Dexamethasone may be
either a pill or given through a needle in a vein.  Another option may come from blood
donated by people who have recovered from COVID-19, called convalescent plasma. The
blood is processed to remove blood cells, leaving behind a liquid called plasma that has
immune system proteins called antibodies. Convalescent plasma with high antibody levels
may be used to help people with a weakened immune system recover from COVID-19. 
Mechanical ventilator support  Palliative care

 191. Part -2 Topics in Next Slide  Plague  Malaria  Poliomyelitis  Diphtheria  Pertusis
 Measles  Mumps  Influenza  Tetauns  Yellow fever  Filarsis  Hiv/AIDS  Rubella
 Cholera  Rabies  Ebola  Zika virus disease  Chikungunya  Swine flu

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
2. Anti cancer or neoplastic drugs Instructor: Dr. Homan “Mohib" Pharmacology
presentation Prepared By: Nasir Ahmad Danish

 3. ANTI NEOPLASTIC DRUGS Subtitle

 4. Discussable topics

 5. NUM CONTENT SLIDE 1 INTRODUCTION/DIFINTION 2 EPIDEMIOLOGY OF CANCER 3 RISK

FACTORS 4 CHARACTERISTIC OF CANCER 5 THE SEVEN WARNING SIGNS OF CANCER 6
CANCER TYPES 7 CELL CYCLE 8 CARCINOGENESIS FORMATION OF MALIGNAT CELL BY
MUTATION 10 TREATMENT OPTIONS OF CANCER 11 DIAGNOSIS OF CANCER 12 CELL CYCLE
SPECIFIC /NON- SPECIFIC DUGS 13 ANTI CANCER DRUG CLASSIFICATION 14
CHEMOTHERAPEUTIC DRUGS AFFECTING RNA /DNA PRECURSORS 15 COMPARISON OF
MYELOSUPPRESSIVE POTENTIAL OF CHEMOTHERAPEUTIC DRUGS 16 MECHANISAM OF
ANTICANCER DRUGS 17 TOXIC EFFECTS OF ANTI CANCER DRUGS 18 CONCLUSION.

 6. INTRODUCTION/DIFINTION • Cancer is the rapid creation of abnormal cells that grow

beyond their usual boundaries, and which can then invade adjoining parts of the body and
spread to other organs. This process is referred to as metastasis. Metastases are the major
cause of death from cancer. (WHO) • Cancer known medically as a malignant neoplasm, is a
broad group of diseases involving unregulated cell growth. In cancer, cellsdivide and grow
 uncontrollably, forming malignant tumors, and invading nearby parts of the body. The
cancer may also spread to more distant parts of the body through the lymphatic system or
blood stream. • Not all tumors are cancerous; benign tumours do not invade neighbouring
tissues and do not spread throughout the body. There are over 200 different known cancers
that affect humans.

 7. Creeping =crab

 8. Anti neoplastic A=Anticancer drugs cause N=Nausea and vomiting T=Treatment regimen
must be followed I=Individualized dosage N=New drugs appear on the market E=Exposure
time kept to a minimum O=Only a physician can administer P=Protect yourself L=Look, listen,
and learn A=Assessment of laboratory tests S=Safe dosage based on weight T=Toxicities
I=Inform patients C=Classification of agents

 9. 9 EPIDEMIOLOGY OF CANCER

 11. 11 RISK FACTORS 1. Tobacco 2. Age 3. Sunlight 4. Ionizing radiation 5. Certain chemicals
and other substances 6. Some viruses and bacteria 7. Certain hormones 8. Family history of
cancer 9. Alcohol 10. Poor diet, lack of physical activity, or being overweight

 17. 17 Cancer arises as a result of a series of genetic and epigenetic changes, the main
genetic lesions being: 1. inactivation of tumour suppressor genes 2. the activation of
oncogenes (mutation of the normal genes controlling cell division and other processes).
Cancer cells have four characteristics that distinguish them from normal cells: 1.
uncontrolled proliferation 2. loss of function because of lack of capacity to differentiate 3.
invasiveness 4. the ability to metastasise. Cancer cells have uncontrolled proliferation
because of changes in: 1. growth factors and/or their receptors 2. intracellular signalling
pathways, particularly those controlling the cell cycle and apoptosis 3. telomerase
expression 4. tumour-related angiogenesis CHARACTERISTIC OF CANCER

 19. THE SEVEN WARNING SIGNS OF CANCER The American Cancer Society uses the word C-
A-U-T-I-O-N to help recognize the seven early signs of cancer: 1. Change in bowel or bladder
habits 2. A sore that does not heal 3. Unusual bleeding or discharge 4. Thickening of breast
tissue or a lump in, testicles, or elsewhere. 5. Indigestion or difficulty swallowing 6. Obvious
change in the size, color, shape, or thickness of a wart, mole, or mouth sore 7. Nagging
cough or hoarseness 19

 22. 22 categorized based on the functions/locations of the cells from which they originate: 
Carcinoma: a tumor derived from epithelial cells, those cells that line the surface of our skin
and organs (80-90% of all cancer cases reported)  Sarcoma: a tumor derived from muscle,
bone, cartilage, fat or connective tissues.  Leukemia: a cancer derived from white blood
cells or their precursors.  Lymphoma: a cancer of bone marrow derived cells that affects
the lymphatic system.  Myelomas: a cancer involving the white blood cells responsible for
the production of antibodies (B lymphocytes) CANCER TYPES

 23. Methods of treatment 1. Local treatment(1/3) 1. Surgery 2. radiotherapy 2. General

treatment 1. chemotherapy 3. Sever local treatment 1. Chemotherapy + radiotherapy
Chemotherapy – Primary inductive therapy(SDM-NOT OTHER THERAPY) – Primary new
helper therapy(local cancer and surgical /radiotherapy are not benefit.chemotherapy+
radiotherapy – Maybe done at the same time or sepratly

 24. CANCER CELL CYCLE KINETICS A. Cell Cycle Kinetics B. The Log-Kill Hypothesis
 25. Cell Cycle Kinetics A. Cell Cycle Kinetics Cancer cell population kinetics and the cancer
cell cycle are important determinants of the actions and clinical uses of anticancer drugs. 1.
cell cycle-specific [CCS] drugs) 2. cell cycle-nonspecific [CCNS] drugs CCS drugs are usually
most effective when cells are in a specific phase of the cell cycle . Both types of drugs are
most effective when a large proportion of the tumor cells are proliferating (ie, when the
growth fraction is high).

 26. B. The Log-Kill Hypothesis 1. Cytotoxic effect of anticancer drug follows killing of
logarithmic cell…. 2. Drug when meet a constant or specific amount of cells-so will destroy a
specific amount of cell 3. For exa:if a drug 3 log of carcinogen cell 4. So burden of tumor will
decrease from 1010 to 107----105 to 102---- 5. Rule is due to a relation 6. So this is the rule
of chemotherapy

 27. The Log-Kill Hypothesis 1. DARK BLUE LINE: Infrequent scheduling of treatment courses
with low (1 log kill) dosing and a late start prolongs survival but does not cure the patient
(i.e., kill rate < growth rate) 1. LIGHT BLUE LINE: More intensive and frequent treatment,
with adequate (2 log kill) dosing and an earlier start is successful (i.e. kill rate>growth rate) 2.
GREEN LINE: Early surgical removal of the primary tumour decreases the tumour burden.
Chemotherapy will remove persistant secondary tumours, and the total duration of therapy
does not have to be as long as when chemotherapy alone is used.

 28. Combination rule of drugs A. Uses of drugs only(choriocarcinoma and burkitt lymphoma)
B. In other case combination regime.. A. High killing of CC B. Increase an broad interaction
between drugs and tumor cell with a differ genitical in a differ population turmeric cells. C.
Prevention from future drug resistant . • Rule in selection of drugs combination: 1. tumor
sensitive 2. Toxicity 3. Timing and dosage 4. Mechanism of interaction(for high effect) 5.
Prevent from optional changing (without Dr consult)

 29. Pharmacokinetic of Anticancer Agents

 30. Resistance Intrinsic and Acquired A. Intrinsic: Some tumor types, e.g. malignant
melanoma, renal cell cancer, and brain cancer, exhibit primary resistance, i.e. absence of
response on the first exposure, to currently available standard agents(p53 mutation-
uncomplete reparing) B. Acquired: – Single drug: change in the genetic apparatus of a given
tumor cell with amplification or increased expression of one or more specific genes –
Multidrug resistance: • Resistance to a variety of drugs following exposure to a single variety
of drug • increased expression of a normal gene (the MDR1 gene) for a cell surface
glycoprotein (P-glycoprotein) involved in drug efflux

 31. Normal Cell DNA Damage Mutations in the genome of somatic cells Alteration of genes
that regulates apoptosis Expression of altered gene products Loss of regulatory gene
product MALIGNANT NEOPLASM Activation of growth promoting oncogene Inactivation of
cancer suppressor genes Acquired (environmental DNA damaging agents) Chemicals
Radiation viruses Successful DNA repair Failure of DNA repair CARCINOGENESIS •Clonal
expansion •Additional mutations •Heterogeneity

 32. Go – Resting phase Restriction checkpoint 8hrs or more 6-8 hrs 2-5 hrs

 33. ANTI CANCER DRUGS

 34. CELL CYCLE SPECIFIC /NON- SPECIFIC DUGS CON… 34

 36. 36 MECHANISAM OF ANTICANCER DRUGS 1. Alkylating agents and related compounds,
which act by forming covalent bonds with DNA and thus impeding replication . 2.
Antimetabolites, which block or subvert one or more of the metabolic pathways involved in
DNA synthesis 3. Cytotoxic antibiotics, i.E. Substances of microbial origin that prevent
mammalian cell division 4. Plant derivatives (vinca alkaloids, taxanes, campothecins) - most
of these specifically affect microtubule function and hence the formation of the mitotic
spindle. 5. Hormones, of which the most important are steroids, namely glucocorticoids,
oestrogens and androgens, as well as drugs that suppress hormone secretion or antagonise
hormone action.

 37. CHEMOTHERAPEUTIC DRUGS AFFECTING RNA /DNA PRECURSORS. 37

 38. Anti metambolit -Pyrimidine antagonists Fluorouracil （5-Fu） Mechanism: convert to 5F-
dUMP and inhibit thynidylate synthase,block the synthesis of dTMP Clinical uses: good effect
on cancer of digestive tract, breast cancer Toxicity : myelosuppression and mucositis Dose: 1
gm orally on alternative days. Branded Name: Fluracil, five fluro250 mg cap, 5 ml for i.v. inj.
Cytarabine （Ara-C ） Ara-C →Ara-CMP →→Ara-CTP, competitively inhibit DNA polymerase.
The triphosphate of Cytarabine is an inhibitor of DNA polymerase. Clinical uses: acute
granulocytic leukemia, mononuclearcyte leukemia Toxicity: severe myelosuppression ,
nausea etc Dose: 1.5-3 mg/kg i.v. BD for 5-10 days Branded Name: Cytarabine, cytosar &
cytabin 100, 500, 1000 mg inj.

 40. Antimetabolites  Mercaptopurine & thioguanine: Converted into monoribonucleotides

which inhibit the conversion of IMP to adenine & guanine nucleotide. Uses: acute leukemia
& solid tumors Dose: 6- Mercaptopurine – 2.5 mg/kg/day 6 Thioguanine: 100-200 mg/ day
Toxicity : myelosuppression and gastrointestinal symptoms Generic: Purinethol, Empurine –
50 mg Tab

 42. Alkylating agents HN N N N R O H2N Guanine in DNA R-X HN N N N R O H2N R HN N N N

R O H2N R HN N N N R O H2N R Produce Highly reactive carbonium Ion which transfer alkyl
group to position 7 of guanine by the covalent bond.

 43. Cyclophosphamide: • Supress DNA by its methabolite. • Usage: CLL-SOLID TUMOR AND
LYPHOMA • SIDE EFFECT: Hemorrhagic inflammation in bladder Intereuption-fluid therapy in
24-48 will prevent of this effect Contra indication: pregenency and lactation Caution :renal
and liver problem • Dose: Oral - 2-3 mg/kg/day, i.v. – every 10-15 mg/kg, i.m. – 7-10
mg/kg/day • Branded Name: Endoxan, Cycloxan 50 mg tab, 200, 500, 1000 mg inj.

 44. Cytotoxic drugs Doxorubicin & Daunorubicin 1. Mechanism : Bind with high affinity to
DNA through intercalation and then block the synthesis of DNA and RNA 2. Clinical uses 1.
One of the most important anticancer drugs , treatment of carcinoma of the breast,
endometrium, ovary, testicle, thyroid, lung and many sarcoma, acute leukemia, Hodgkin’s
disease 2. Daunorubicin: acute leukemia 3. Dose: Doxorubicin 60-75 mg slow i.v. inj. every 3
weeks. 4. Daunorubicin: 30-60 mg daily for 3 days repeat weekly. 5. Branded Name:
Daunocin 20 mg/vial inj

 46. Vinka Alkaloids Mechanism of action Bind specifically to the micro tubular protein
tubulin in dimeric form, terminate assembly of microtubules and result in mitotic arrest at
metaphase, cause dissolution of the mitotic spindle and finally interfere with chromosome
segregation.
  47. Vincristine: • Use: in childhood acute leukemia, Hodgkin's disease, wilm’s
tumor(nephroblastoma), ewing’s sarcoma & carcinoma lung. • Dose: 1.5-2 mg/m2 BSA i.v.
weekly • Generic: Oncovin & cytocristin 1 mg/ vial inj • Side effect: constipitation,abdomen
swallow,loss deep tendon reflex • Contra indication:pregenancy and lactation

 48. 48 Tamoxifen binds to the estrogen receptor and the complex fails to induce estrogen-
responsive genes, and RNA synthesis does not ensue.  The result is depletion (down-
regulation) of estrogen receptors, and the growth-promoting effects of the natural hormone
and other growth factors are suppressed. The action of tamoxifen is not related to any
specific phase of the cell cycle. Usage :breast cancer Contra indication:pregenancy Side
effect:bright or hotness,hypercalcemis,ovary cyst,emboli with cytotoxic drugs MECHANISM
OF ACTION OF TAMOXIFEN

 49. 49 1. Bone marrow toxicity (myelosuppression) with decreased leucocyte production

and thus decreased resistance to infection 2. Impaired wound healing 3. Loss of hair
(alopecia) 4. Damage to gastrointestinal epithelium 5. Depression of growth in children 6.
Sterility 7. Teratogenicity TOXIC EFFECTS OF ANTI CANCER DRUGS

 50.  Acute toxicity  Vomiting  Allergic reactions  Arrhythmias  Delayed effects 

Mucositis  Alopecia  Bone marrow suppression  Chronic toxicities  Heart  Kidney 
Liver  Lungs 50

 51. Causes of weight loss Weight loss often begins with appetite loss. This may result from
the following side effects of cancer or treatment: 1. Changes to the immune system or
metabolism. Metabolism is the body’s process of breaking down food and turning it into
energy. 1. Nausea and vomiting 2. Constipation 3. Mouth sores 4. Difficulty chewing 5.
Difficulty swallowing 6. Loss of taste 7. Depression 8. Pain

 52. 52 CONCLUSION 1. Every year, more than 1 million Americans and more than 10 million
people worldwide are expected to be diagnosed with cancer, a disease commonly believed
to be preventable. 2. Only 5–10% of all cancer cases can be attributed to genetic defects,
whereas the remaining 90–95% have their roots in the environment and lifestyle. 3. The
evidence indicates that of all cancer-related deaths, almost 25–30% are due to tobacco, as
many as 30–35% are linked to diet, about 15–20% are due to infections, and the remaining
percentage are due to other factors like radiation, stress, physical activity, environmental
pollutants etc. 4. Therefore, cancer prevention requires smoking cessation, increased
ingestion of fruits and vegetables, moderate use of alcohol, caloric restriction, exercise,
avoidance of direct exposure to sunlight, minimal meat consumption, use of whole grains,
use of vaccinations, and regular check-ups.

 53. References 1. www.journals.elsevier.com/cancer-epidemiology 2. robboins Basic

pathology-9th edition 3. www.medicinenet.com/cancer_causes/page6.htm 4.
www.retireeasy.com/health/7-warning-signs-of-cancer 5. Clinical pharmacology and drug
treatment 6. Basic and clinical pharmacology {Bertram G.Katzung}-2015- 13th edition 7.
Medscape.com 8. Wekipedia.com

Cancer chemotherapy
 1. Cancer Chemotherapy •Dr. P. Suganya •Assistant Professor •Sri Kaliswari College
(Autonomous) •Sivakasi
 2.  Introduction : • Also known as Neoplasm / Tumor. • Define : The term cancer refers to a
disease of cells that show uncontrolled proliferation, dedifferentiation, invasiveness and the
 ability to metastasise. • When such cells proliferate excessively, they form local tumors. • The
extent of metastasis and deterioration in metabolic processes resulting from cancer leads to
eventual death of the patient.
 4. The origin of cancer chemotherapy..... • WW (I) exposure to mustard gas led to the
observation that alkylating agents caused BMD and lymphoid hypoplasia which was further
studied during WW(II). • This observation led to the direct application of such agents to patients
with Hodgkin’s disease and lymphocytic lymphomas at Yale Cancer Centre in 1943, Luis
Goodman and Alfred Gillman demonstrated it for the first time.
 5. • 1948, Sydney Farber successfully used Antifolates to induce remission in children with all. •
1955, National chemotherapy program begins at National cancer institute, a systematic
programme for drug screening. • 1958, Roy Hertz and Min Chiu Li demonstrated Methotrexate as
a single best agent for choriocarcinoma, the first solid tumour that can be cured by
chemotherapy. • 1959, FDA approved the alkylating agent, Cyclophosphamide • 1965, The era of
combination chemotherapy begins.
 6. Introduction • The use of chemicals to treat cancer began in the early 1940’s • The era of
modern chemotherapy begun in 1948 with the introduction of nitrogen mustard • It is only in the
last 10 to 15 yrs, however , that chemotherapy has become a major treatment modality.
 7. Objectives of chemotherapy….. To maximize the death of malignant tumor cells To cure
the client with cancer Control the tumor growth when cure is not possible To extend the life
span and improve the quality of life of client with cancer
 8. Cell cycle
 9. Chemotherapeutic drugs act through variety of mechanism….. Limiting DNA synthesis and
expression Cross linking polymer DNA DNA double stand breaks Preventing formation of mitotic
apparatus
 10. Classification of chemotherapeutic drugs ….. According to activity on cell • Cell cycle
phase specific •G1 phase :Bleomycin, Corticosteroids, Hormones •G2 phase: Bleomycin,
Etoposide, Topotecan, Taxol etc. •S phase: Cytarabin, 5-fluorocil, Methotrexate •M phase :
Vinblastin, Vincristine, Paclitaxel • Cell cycle phase non-specific • Busulfan • Cisplatin •
Cyclophosphamide
 11. Classification…………… According to chemical groups Alkylating agents
Antimetabolites Anti tumor antibiotics Nitrosureas Plant alkaloids Hormonal agents
Miscellaneous agents
 12. Alkylating agents • Eg : Buzalfan ,Cyclophosphamide, Carboplatin Antimetabolites • Eg:
Cladribine , Methotrexate Sodium, 5- flurouracil Antitumor antibiotics • Eg: Bleomycin Sulfate,
Dactinomycin , Epirubicin
 13. Nitrosureas • Eg: Carmustine, Lomustine, Semustine Pant alkaloids /natural products • Eg :
Docetaxel, Etoposide, Pacltitaxel Miscellaneous agents • Eg: Altetramine, Amsrcrine,
Asparaginase
 14. Concepts in chemotherap y Combination chemotherapy (use of cytotoxic drugs in
combination Neoadjuvant chemotherapy ( initial use of chemotherapy to reduce the bulk and
lower the stage of tumor , making it amenable to cure with subsequent local therapy ) Adjuvant
chemotherapy (along with surgery and radiation)
 15.  Treatment of Cancer : 1. Chemotherapy 2. Surgical resection 3. Radiotherapy 4.
Immunotherapy • Chemotherapy :- - Cancer cells are more sensitive to antineoplastic drugs
when the cells are in the process of growing and dividing. - Chemotherapeutic drug having many
side effect …. - BMD - Loss of hair - Nausea & vomiting - Increase susceptibility to infection -
Teratogenicity in pregnant women
 16. Classification of the anticancer agents: • Cell cycle specific agents Go phase – Alkylating
agent G1 phase – Asparaginase & steroids S phase –antimetabolite,camptothecin,
cisplatin,doxorubicin,hydroxyurea G2 phase- Bleomycin,epipodophylotoxin M phase – taxans
&Vinca alkaloids
 17. Alkylating agents : A) Nitrogen mustards :
chlorambucil,cyclophosphamide,mechlorethamine HCl, uracil mustard, Ifosfamide B)
Ethylenimines: thiotepa, hexamethylmelamine,triethylenemelamine C) Nitrosoureas : carmustine,
lomustine, semustine, streptozotocin D) Alkylsulfonates : busulphan E) Thiazenes : decarbazine
F)Platinium based alkylating agent : cisplatine, carboplatin, oxaliplatin G) Methylhydrazines :
Procarbazine
 18. Antimetabolites : - Folic acid antagonist : methotrexate (Mtx) - Pyrimidin analogues : 5-
FU, cytarabine, azarabine, floxuridine - Purine analogues : 6-MP, 6- TG, azathioprine,
fludarabine Natural products : - Vinca alkaloids : - Epipodophylotoxin : - Taxane deri. : -
Campothesins deri.: vincristine, vinblastine etoposide, teniposide paclitaxel, docelatel irinotecan,
topotecan  Antibiotics :  Enzymes : actinomycin- D, daunorubicin,doxorubicicn, mitomycin,
bleomycin L- Asparaginase Monoclonal antibody : Rituximab, Trastuzumab
 19. Hormonal drugs : • Glucocorticoids – Prednisolone and others • Estrogen – Fosfestrol,
Ethinylestradiol • Selective estrogen receptor modulators - Tamoxifen ,Toremifene • Selective
estrogen receptor down regulators – Fulvestrant • Aromatase Inhibitors – Letrozole,
Anastrozole , Exemestane • Anti androgens – Flutamide,Bicalutamide • 5-α reductase Inhibitors
– Finasteride, Dutasteride • GnRH analogues – Nafarelin,Leuprorelin,triptorelin • GnRH
antagonists – Cetorelix, Ganirelix, Abarelix • Progestins – Hydroxyprogesterone acetate, etc.
 20. Alkylating agents • MOA : -this are compound that are capable to introduce alkyl group into
N site Of DNA , RNA or any enzyme through covalent bond or may cause…. a) Miscoding b)
Destuction of guanine c) Distruption of nucleic acid function -act on 7 position of G-base in each
double stranded DNA to give 7- alkyl guanine & causing cross linking that interfere with
seperation of strand & prevent mitosis. - the effect of base alkylation include misreading of DNA
codon & single strand breakage of DNA chain. Long time effect may cause mutation & cell death.
-Most favoured site on DNA is N-7 POSITION OF A,G,C & even sugar phosphate group. •
Nitrogen mustards & ethyleneimines act by above mech. • Busulfan act by ‘sulfur stripping’. •
Nitrosoureas act through liberation of alkylation moiety. (stz produce S.E. on pancreas.)
 21. A) Nitrogen mustards: cyclophosphamide, chlorambucil, mechlorethamine HCl, uracil
mustard, Ifosfamide • This are cytotoxic chemotherapeutic agent similar to mustard gas. a)
Cyclophosphamide : - Inactive invitro but when it administered ,it is metabolized by liver into
phosphoramide & acrolein. ( active comp.) - Phosphoramide : cytotoxic to cancer cell - Acrolein :
toxic to bladder - Not propely absorb by oral route so better to be given by I.V. - USED :in treat to
lymphosarcoma,breast,ovarian,lung cancer - A.E. : N/V/D, BMD, darkening of skin/nails ,
pulmonary fibrosis, UTI - Dose – 2-3 mg/kg/day oral , 10-15 mg/kg i.v every 7- 10 days
 22. b) mechlorethamine HCl : - Taken by I.V. infusion - Used to treat prostate cancer - A.E. :
allergic reaction, thrombophlebitis, herpes zooster infection,mutagenic & carcinogenic effect on
bone marrow stem cell. - Dose- 0.1 mg/kg iv daily x 4 days ; courses may be repeated at suitable
intervals c) Chlorambucil : – Slow acting alkylating agent, esp. active against lymphoid tissues,
myeloid tissues – largely spared (Ch. Lymphatic leukaemia and non- Hodgkin's lymphoma) -
Dose – orally 0.1-0.2 mg/kg daily for 3-6 weeks, then 2 mg daily for maintenance - A.E. : muscle
problem, numbness of hands/feet, hepatotoxicity
 23. B) Nitrosoureas :carmustine, lomustine, semustine, streptozotocin - 2 functional group :
Nitroso + Urea - highly lipid soluble, & having ability to cross BBB ( So used in brain tumor,
meningeal leukaemia ) (i.v.) - A.E. : pulmonary toxicity, nephrotoxicity, N,V - common , CNS
effects BMD –delayed -6 weeks , Visceral fibrosis and Renal damage C) Alkylsulfonates :
busulphan(i.v.) - alkyl sulfonate , - highly selective for myeloid elements; Granulocyte
precursors(most sensitve) > Platelets and RBC - USED : to treat chronic myelogenous
leukaemia (CML) in bone marrow transplantation patients. - A.E. :N/V/D, Constipation, Seizure,
little effect on lymphoid tissue and GIT Hyperuricemia(common); Pulmonary fibrosis and skin
pigmentation – specific adverse effect
 24. D) Ethylenimines: Thio-TEPA (i.v) - High Toxicity - USED – Ovarian and Bladder Cancer
E) Thiazenes : decarbazine (i.v.) - after activation in liver – methylating DNA , - most imp.
Indication – malignant melanoma, also – Hodgkin's lymphoma F) Methylhydrazines :
Procarbazine(i.v./orally(gel capsule)) - In vivo they convert into azo der. Or active against tumor
cells. - Used : in Hodgkin's disease with combination of MVPP. M – mechlorethamine V -
vincristine P - Procarbazine P - prednisone
 25. G) Platinium based alkylating agent : cisplatine, carboplatin, oxaliplatin- They having no
alkyl group , but also damage DNA, & trigger apoptosis. - platin is only heavy metal comp. used
in cancer. a) Cisplatine : - Act against cells which in S- phase, M-phase, - Effects resemble –
alkylating agent and radiation - Plasma protein bound, penetrates tissues ,Slowly excreted in
urine, - T1/2 – 72 hrs - Used : ovarian, testicular, endometrial , bladder ,Lung and Oesphageal
Cancer - A.E. : N,V,(ondensetron) Aloplacia,maylosuppression,nephrotoxicity , Ototoxicity,
Electrolyte disturbances : Hypokalemia, Hypocalcemia and Hypomagnesemia ,Rarely
 Anaphylactic shock , Mutagenic , Teratogenic and Carcinogenic properties, - Dose – Cisplatin
adm. Slow i.v infusion 50-100 mg/m2 BSA every 3-4 weeks
 26. Antimetabolites : • They are structurally related to normal compounds that present with in
cell. • They generally interfere with… a) availability of purine or pyrimidine nucleotide precursors.
b) Either by inhibiting their synthesis c) or by competing with them in DNA or RNA synthesis. •
Their max. cytotoxic effect are in S –phase ( there for, cell cycle specific )
 27. A) Folic acid antagonist : methotrexate (Mtx)  MOA : • Folic acid is an essential dietary
factor. • It is converted by enzymatic reduction to a series of tetrahydrofolate cofactors that
provide carbon groups for synthesis of precursors of DNA & RNA. • Mtx inhibits the enzyme
DHFR. Which leads to depletion of tetrahydrofolate cofactor used for DNA & RNA synthesis. •
Also used to inhibite thymidylate synthase (TS)
 28. • In inhibition of DHFR can only be reversed by a thousand fold excess of the natural
sub. ,DHF , by adm. Of leucovorin. • Folinic acid, thymidine also counteracts Mtx toxicity. • Dose
– choriocarcinoma; 15-30 mg/day for 5 days orally or 20-40 mg/m2 BSA i.m. or i.v. twice weekly,
• Low dose Mtx ( 7.5-30 mg once weekly) – Rheumatoid Arthritis, psoriasis,  RESISTANCE : -
Reduction of affinity of DHFR to MTX - Diminished entry of MTX into cancer cells - Over
production of DHFR enzyme  USES : • combine with other drug in.. - Lymphocytic leukaemia,
breast cancer, head & neck carcinoma • In low dose effective against some inflammatory
disease, like…. - severe psoriasis , rheumatoid arthritis, crohn disease , etc.. - Other Uses –
Psoriasis, IBD and in Organ transplantation
 29. • PK : - Routes of Adm. : oral, I.M., I.V., I.T. - 50% bound to plasma proteins, Poorly crosses
BBB - Metabolism : Mtx to polyglutamate deri., or at high dose undergo hydroxylation at 7
position & form 7- OHMtx. - Less water soluble, so produce crystalluria. - Excreted by urine. •
A.E. : - stomatitis, rash, urticaria, alopecia, myelosuppression, - Most frequent toxicities : n/v/d -
Hepatic function : long term use of Mtx may lead to cirrhosis - Renal function : variable -
Neurological toxicities : meningeal irritation, stiff neck, fever, headache, rarely seizures • C.I. : -
because Mtx is teratogenic in exp. Animals & is an abortifacient, it should be avoided in
pregnancy
 30. B) Purine analogues :6-MP, 6- TG, azathioprine, fludarabine • Highly effective agent •
Purine antagonist used for treatment of malignant tumer (6-MP, 6-TG)but also prove beneficial
for treating neoplastic disease ( immunosuppresion (azathioprine) and in antiviral chemotherapy
(acyclovir, ganciclovir, vidarabine, zidovudine))  6-MP : • MOA : • 6-MP inhibit the conversion of
inosine monophosphate to adenine & guanine nucleotide formation, which are responsible for
RNA & DNA formation. - Nucleotide formation : 6-MP converted to the nucleotide analog,6-MP-
ribose phosphate (6- thioinosinic acid, or TIMP) - Inhibition of purine synthesis :TIMP can inhibite
the first step of De novo purine ring biosynthesis. - Incorporation into nucleic acids :TIMP
converted to thioguanine monophosphate (TGMP)which after phosphorylation to di.&
triphosphates can be incorporated into RNA. The deoxy-ribonucleotide analogs are also formed
are incorporated into DNA. This results in nonfunctional RNA & DNA.
 31. • PK : - Oral administration,well distributed except for the CSF. - Metabolized in the liver, 6-
MP is converted into 6- ethylMP deri. Or to thiouric acid. - The parent drug & its metabolites are
excreted by kideny. • AE : -BMD (major),anorexia, n/v/d -hepatotoxicity in the form of jaundice
has been reported in about one third of adult patients. - Dose : 2.5 mg/kg/day, half dose for
maintenance
 32. 6-TG • 6-TG is also purine analog,is primarily used in treatment of acute nonlymphocytic
leukemia in combination with Daunorubicin & cytarabine.  MOA : • Converted 6-TG/6-MP to
TGMP by enzyme hypoxanthineguanine phosphoribosyltransferase (HGPRT) • TGMP further
converted into di. & tri. phosphate • Which inhibite biosynthesis of GMP to guanosine
diphosphate  PK :similar to 6- MP  AE : - BMD -TG is not recommended for maintenance
therapy or continuous long term treatment due to the risk of liver toxicity. - Dose : 100-200
mg/m2 /day for 5-20 days
 33. C) Pyrimidine analogues : 5- FU, cytarabine, azarabine, floxuridine  MOA : • 5-FU
converted into 5-fluro-2-deoxyuredinemonophosphate (5-FduMP) which inhibite thymidylate
synthase and blocks the conversion of deoxyuridilic acid to deoxythymidylic acid. • 5-FU
incorporated into RNA, interferes with RNA synthesis and causing cytotoxic effect. • this drug
produce anticancer effect in the S – phase of the cell cycle  PK : • Oral absorption of 5-FU is
unreliable & Because of its severe toxicity to the GI tract, primarily used by i.v. infusion or, in the
 case of skin cancer , given topically. • 5-FU rapidly metabolized by dihydropyrimidine
dehydrogenase (DPD) resulting in a plasma T1/2 15- 20 mins after i.v. infusion • Genetic
deficiency of DPD – severe 5-FU toxicity
 34.  AE : • N/v/d, alopecia, severe ulceration in the oral & GI mucosa, myelosuppression ,
mucositis, peripheral neuropathy, BMD (with bolus injection), & anorexia are frequently
encountered. • 5-FU also cause “ HAND- FOOT SYNDROME “is seen after extended infusions.
 USED : • primarily in the treatment of slow growing solid tumors (colorectal, breast, ovarian,
pancreatic, & gastric carcinoma) • Dose – 25 mg/m2 BSA daily for 5 days every 28 days by
i.v.infusion
 35. Natural products :
 36. A)VincaAlkaloids :Vincristine & vinblastine • MOA : (mitotic spindle inhibitor) -these agent
bine specifically to protein tubulin & inhibit polymerization of microtubules. -This prevent
formation of spindles & blockade of mitotic division at metaphase. -they act primarily on the M
phase of cancer cell cycle. • PK- given parenterally, penetrate most tissues except CSF cleared
mainly via biliary secretions • AE : - leukopenia, mental depression, loss of sleep, headache, n/v,
anorexia, constipation, alopecia, peripheral neuritis
 37. • Uses : - Lymphosarcoma , Hodgkin's disease , lymphatic leukaemia , cancer of breast,
testes, kidney B) Epipodophylotoxin : etoposide,teniposide • MOA : - They act by inhibition of
mitochondrial function & nucleotide transport. - They also bind to topoisomerase ‖ & DNA,
causing breaking of DNA. - This drug are most active in late s-phase & early G2- phase.
 38. • PK : orally well absorbed and distributes to most body tissues , Elimination is mainly via
kidneys • AE : n/v , myelosuppression, alopecia • USES : testicular tumor, lung carcinoma along
with cisplatin, non- Hodgkin's lymphoma & lymphoblastic leukaemia in children C) TAXANES :
paclitaxel, docetaxel • MOA : - same as Vinca alkaloid taxans are act on microtubules & stabilize
them
 39. • AE : - bone marrow depression, alopecia, muscle pain, neurotoxicity - allergy to paclitaxel is
also common and many a time corticosteroids & antihistamines are to be used to control allergy.
• USES : - ovarian & breast cancer D) CAMPOTHECINS : Irinotecan , topotecan • MOA : - they
block Topoisomerase-І, which occure in high levels throughout the cell cycle.
 40. • AE : - by campothesin, mild & reversibile AE i.e. Myelosuppressionand Diarrhoea • PK : -
Irinotecan – prodrug – converted to active metabolite in liver , -Topotecan is eliminated renally,
whereas Irinotecan and its metabolite eliminated in bile and faeces • USES : -Topotecan - 2nd
line agent – Advanced Ovarian Cancer and for small cell lung Cancer. - Irinotecan – Metastatic
Colorectal Cancer
 41. Antibiotics : Actinomycin- D, Daunorubicin, Doxorubicin, Mitomycin, Bleomycin 1)
Actinomycin- D or Dactinomycin : • MOA :It is an anticancer antibiotic which bind with DNA &
form complex with it. Also inhibits topoisomerase ‖ & produce cytotoxicity. Also interrupts
function of DNA. • A.E. : (Dactinomycin) anorexia, n/v , BMD • USES : in lymphoma, Hodgkin's
disease
 42. 2) Daunorubicin or Doxorubicin : • MOA : - it is bind with DNA & intercalate with adjacent
pairs & disrrupts DNA activity , also inhibite DNA gyrase & produce cytotoxicity. • PK: - Doxo and
Daunorubicin must be given IV. - Metabolized in liver , excreted in bile and urine • A.E. : - This
agents are highly toxic to myocardium & produce arrhythmia, also produce BMD , HT, • Uses : -
Doxorubicin – Hodgkin's and non-Hodgkin’s lymphoma, myelomas, sarcomas, breast, lung,
ovarian and thyroid ca. - Daunorubicin – acute leukemias
 43. 3) Bleomycin : • MOA : acts in the G2 phase- generates free radicals – bind to DNA – DNA
strand breaks – inhibit DNA synthesis • PK : Given parenterally, inactivated by tissue amino
peptidases mainly • A.E. : that cause minimal BMD but produce serious effect i.e. pulmonary
fibrosis. rarely produce nausea, vomiting, headache, hypotension • cutaneous toxicity
(hyperpigmentation ,hyperkeratosis, erythema and ulcers) • bleomycin should be given prior to
radiation therapy because it’s most sensitive to radiation . • USES : used in carcinoma of skin,
upper respiratory passages, oral cavity, urinogenital tract.
 44. Enzym e 1) L-Asparaginase : • Enzyme used for treatment of leukaemia's and lymphomas •
These tumors require exogenous asparagine for growth, L- Asparaginase acts by depleting this
amino acid in serum. • Adm. by IV route • AE : hypersensitivity reactions, acute pancreatitis and
cortical vein thrombosis
 45. Monoclonal antibodies -
 46. Surgical Resection • Surgery is the oldest method of treating cancers, with the view to
complete removal of the cancer (organ) from the body. • Surgery in certain cancers is the most
important aspect of the care, and cure may not be possible without it. • This is true in patients
with breast cancer, colon cancer, stomach cancer, non-small cell lung cancer, and many other
cancers.
 47. Radiotherap y • Radiotherapy is treatment with high energy x-rays that target the area of
the cancer. • Cancer cells are more sensitive than normal cells and the x-rays damage their
genetic code. This damage means that they are unable to grow. • Treatment is designed
specifically for each individual. Why radiotherapy is given? • After surgery for cancer, there is
always a small risk of a few cells remaining in the body. Radiotherapy is given to reduce the
chance of local recurrence, i.e. cancer returning in the particular tissue. • Sometimes
radiotherapy is given to treat cancer, when surgery is not an option. • Ex. : I131 , P32, U198
 48. Planning CT scan • Before the treatment can start patient will have to come for a planning
CT scan. This scan is specifically for designing radiotherapy. • The scan can take about 30
minutes, in which time you need to lie quite still, but you can breath normally. • At the end of the
planning scan the radiographers will, give you some permanent marks,.
 49. treatmen t • The treatment will usually start a few weeks after having planning CT scan.
During these weeks consultant and the rest of the planning team will have designed a
radiotherapy plan specifically for patient. • On the day that treatment starts, one of the treatment
radiographers will first discuss the treatment with patient. • Patient will be taken into the
treatment room and placed in exactly the same position that for the planning scan. The
radiographers will set up for the first treatment and then they will leave the room. The
radiographers will be watching patient all the time from outside the room on CCTV. After that part
of the treatment has been given, the radiographers will return into the room and set up the
machine for the next. This process will continue until you have had all the required treatment in
each session.
 50. Assembly for Radiotherapye radiotherapy
 51. Immunotherap y • At the present time the treatment of cancers relies on chemotherapy and
radiation both of which have devastating effects on normal non- tumor tissues. • Because the
immune response is highly specific it was long been hoped that tumor specific immunity may be
used to selectively eradicate tumors without injuring the patient. • When cells become cancerous
they produce new, unfamiliar antigens. The immune system may recognize these antigens as
foreign, and contain or even destroy the cancer cells. • The main antitumor effectors (antibodies
and T cells) to patient strategies for cancer immunotherapy aim to provide actively immunize
patient against their tumors and stimulate the patients’ own antitumor immune responses
 52. Novel drugs for Cancer
 55. References : • WHO Global Health Observatory. Available at:
http://www.who.int/gho/map_gallery/en/ • City Mayors. Available at:
http://www.citymayors.com/statistics/largest- cities-population- 125.html • Tripathi KD, Anticancer
drugs , Chemotherapy of neoplastic diseases; 7th ed ; 857-877 • Katzung’s and Trevor’s,
Pharmacology: Examination and board review, Cancer chemotherapy, 10th ed. 465-475 •
Goodman and Gillman’s 12th ed. Images • www.google.com , images
 56. • Goodman LS, Win Trobe MM, Dameshek W,Goodman MJ, Gilman AZ, McLennan MT
(1946). "Nitrogen mustard therapy". JAMA. 132 (3): 126– 132.
doi:10.1001/jama.1946.02870380008004. • “Alkylating Agents” US National Library of Medicine.
Retrieved 2 August 2014. • McDonald AC, Vasey PA, Walling J, Lindb MJ. Bailey NP,Siddiquib
C, Twelves J, Cassidy J and Kaye SB (1996) Clinical phase I study of LY2315 14, a
multitargeted anti-folate, administered by daily x 5 q 21 schedule. AnnII Onicol 7 (suppl. 1): 85 •
Bailly, C. (2009) Ready for a comeback of natural products in oncology. Biochem Pharmacol 77:
1447– 1457.CrossRef | PubMed | CAS | Web of Science® Times Cited: 25
Pathophysiology Chemotherapy of Cancer

 1. Presented by Shaheen Begum M.Pharm, I Year I Sem Pharmacology, UCPSc, Kakatiya

University. 1
 2. • Cancer – Uncontrolled multiplication and spread within the body of abnormal forms of
body's own cells • Neoplasm – A mass of tissue formed as a result of • Abnormal • Excessive
• Uncoordinated • Autonomous and • purposeless Proliferation of cells 2 1

 3. 3

 4. Cancer cells differ from normal cells by • Uncontrolled proliferation • De-differentiation &
loss of function • Invasiveness • Metastasis 4 2,3,4

 5. Guiding principles in cancer chemotherapy • To achieve cure a TOTAL CELL KILL must be
tried • Early diagnosis and early initiation of treatment • Combination chemotherapy •
Intermittent regimens • Adjuvant and neoadjuvant chemotherapy occasionally 5 5,6,7

 6. Total cell kill • Aimed at destroying all the malignant cells, leaving none • This approach
ensures – Early recovery – Prevents relapse – Prolongs survival 6

 7. Early diagnosis and early T/t why? • Survival time inversely related to initial number of
cells • Aging cancer cells are less susceptible to chemotherapy, because there is – ↑ cell
cycle (division) time – ↓No of actively dividing cells with more resting cells – ↑ cell death
within tumor – Overcrowding of cells 7

 8. CLASSIFICATION - I: CELL CYCLE NON SPECIFIC : Kills resting cells & dividing cells •
Cyclophosphamide • Chlorambucil • Cisplatin • Actinomycin-D • L-asparaginase CELL CYCLE
SPECIFIC Kills actively dividing cells • G1 – Vinblastine • S – Methotrexate 6-Mercaptopurine
5-Fluorouracil • G2 –Bleomycin Etoposide, Topotecan Daunorubicin • M – Vincristine
Vinblastine Paclitaxel,Docetaxel 8 5

 9. • Nitrogen Mustards – Meclorethamine, Melphalan, Chlorambucil, cyclophosphamide,

ifosfamide • Ethyleneimine : Thiotepa • Alkyl Sulfonate: Busulfan • Nitrosureas –
Carmustine,lomustine, streptozocin • Triazines – Dacarbazine, temozolamide Alkylating
agents 9 5

 10. • Folate Antagonists – Methotrexate • Purine Antagonists – 6 Mercaptopurine, 6

Thioguanine, Azathioprine • Pyrimidine antagonists – 5 Fluorouracil, cytarabine, gemcitabine
Antimetabolites 10 5

 11. • Antibiotics – Actinomycin D, Doxorubicin, Daunorubicin, Bleomycin, Mitomycin C •

Vinca alkaloids – Vincristine, Vinblastine, Vinorelbine • Taxanes – Paclitaxel, docetaxel •
Enzymes – L-Asparginase Natural Products • Epipodophyllotoxins – etoposide, tenoposide •
Camptothecin analogs – Topotecan, irinotecan • Biological response modifiers – Interferons,
– Interleukins 11 5

 12. • Cisplatin • Carboplatin • Hydroxurea • Procarbazine • Mitotane • Imatinib

Miscellaneous Agents 12 5

 13. CLASSIFICATION - II: Depending on mechanism at cell level • Directly acting cytotoxic
drugs: – Alkylating agents – Antimetabolites – Natural products • Antibiotics • Vinca
alkaloids • Taxanes • Epipodophyllotoxins • Camptothecin analogs • Enzymes • Biological
response modifiers – Miscellaneous: Cisplatin, carboplatin • Indirectly acting- by altering the
hormonal mileau : – Corticosteroids – Estrogens & ERMs – 5 alpha reductase inhibitors –
Gnrh agonists – Progestins 13 5
 14. Hormones & antagonists • Corticosteroids – Prednisolone • Estrogens – Ethinyl Estradiol
• SERM – Tamoxifene, Toremifene • SERD – Fulvestrant • Aromatase Inhibitors – Letrozole,
Anastrazole, Exemestane • Progestins – Hydroxyprogesterone • Anti-androgens – Flutamide,
Bicalutamide • 5- reductase Inhibitors – finasteride, dutasteride • GnRH analogs –
Naferelin, goserelin, leuoprolide 14 5

 15. 15

 16. 16

 17. Mechanism of action Alkylating Agents Form highly reactive carbonium ion Transfer
alkyl groups to nucleophilic sites on DNA bases Results in Cross linkage Abnormal base
pairing DNA strand breakage ↓ cell proliferation Alkylation also damages RNA and proteins
17

 18. • Nausea & Vomiting • Bone marrow depression • Alopecia • Gonads: Oligospermia,
impotence, ↓ ovulation • Foetus: Abortion, foetal death, teratogenicity • Carcinogenicity •
Hyperuricaemia • Immunosupression: Fludarabine • Hazardous to staff General toxicity of
cytotoxic drugs 18

 19. • Cytotoxic action – Hemopoetic system highly susceptible • Chlorambucil – more

against lymphoid series • Busulfan – more against myeloid series – Epithelial tissues, hair
follicles – Spermatogenesis , fetopathic effect • Immunosupressant action • Miscellaneous –
Severe nausea & vomiting • Known as radiomimetic drugs Pharmacological actions 19

 20. • Very irritant drug • Dose = 0.4 mg/kg single or divided • Uses – Hematological cancers ,
lymphomas , solid tumors – Hodgkins • Adverse effects – Anorexia, nausea, vomiting – Bone
marrow depression, aplasia – Menstrual irregularities Mechlorethamine (Mustine) 20

 21. 21

 22. Uses of cyclophosphamide • Neoplastic conditions – Hodgkins and non hodgkins

lymphoma – Neuroblastoma , retinoblastoma – breast , adenocarcinoma of ovaries • Non
neoplastic conditions – Rheumatoid arthritis • Adverse effects: – Hemorrhagic cystitis, –
alopecia, – nausea & vomiting, hepatic damage 22

 23. Nitrosureas • Highly lipid soluble, Cross BBB • Uses: – Meningeal / Brain tumours • Dose
:150-200 mg/m2 BSA every 6 wks (Carmustine) • Adverse Effects: – Delayed bone marrow
suppression – Visceral fibrosis, renal damage 23

 24. Triazenes • Dacarbazine – Primary inhibitory action on RNA & protein synthesis – Used
in malignant melanoma • Temozolamide – New alkylating agent – Approved for malignant
glioma – Rapidly absorbed after oral absorption & crosses BBB 24

 25. Cisplatin • Non cell cycle specific killing • Administered IV • Highly bound to plasma
proteins • Gets conc in kidney, intestine, testes • Poorly penetrates BBB • Slowly excreted in
urine Pt NH3Cl Cl NH3 Dose: 20 mg for 5 days a week 75 – 100 mg once in 4 weeks to treat
ovarian cancer 25

 26. Mechanism of action of cisplatin Cisplatin enters cells Forms highly reactive platinum
complexes DNA damage Intra strand & interstrand cross links Inhibits cell proliferation Cl- 26
 27. Cisplatin uses and adverse effects • Uses – Testicular cancer (85% - 95 % curative ) –
Ovarian cancer – Other solid tumors: lung, esophagus, gastric • Adverse effects – Emesis –
Nephrotoxicity – Peripheral neuropathy – Ototoxicity 27

 28. Methotrexate Adenine, guanine, thymidine , methionine, serine Folic acid not useful in
toxicity Folinic acid N5 formyl FH4 should be given which is converted to N5,N10- Methylene
–FH4 and bypasses the inhibited reductase 28

 29. Pharmacological actions • Cytotoxic actions – Predominant on bone marrow – foetal

malformations and death • Immunosupressive action • Anti-Inflammatory action 29

 30. Uses of methotrexate • Antineoplastic – Choriocarcinoma and tropoblast tumor

Immuno-supressive agent • Rheumatoid arthritis, resistant asthma,Psoriasis. • Medical
termination of pregnancy • Adverse effects • Megaloblastic
anemiaThrombocytopenia,leukopenia, aplasia , Oral, intestinal ulcer , diarrhoea Alopecia ,
liver damage. 30

 31. 6 Mercaptopurine 6 MP 6 Thiouric acid Xanthine oxidase Allopurinol TPMT Inactive

metabolite 31

 32. • Use: – Acute leukemia (ALL) – Choriocarcinoma • Adverse Effects: – Bone marrow &
GIT mainly – Hepatic necrosis rarely – Hyperuricaemia 6 Mercaptopurine 32

 33. 5 fluorouracil 5 FU FdUMP dUMP Thymidine Monophosphate Thymidilate synthetase

DNA Synthesis (Selective failure) Uses : stomach , colon, breast ovaries , liver, skin cancers
FdUMP = fluorodeoxyuridine monophosphate 33

 34. • Obtained from periwinkle plant ( Vinca Rosea) • Vincristine, vinblastine, vindesine,
vinorelbine • These are microtubule damaging agents Vinca alkaloids 34

 35. Mechanism of action 35

 36. Taxanes • Paclitaxel & docetaxel • Plant product obtained from bark of Pacific Yew
( Taxus Brevifolia) & European Yew (Taxus Buccata) 36

 37. Mechanism of action Cell cycle arrested in G2 and M phase 37

 38. • Paclitaxel – Administered IV – Use: advanced breast & ovarian cancer also lungs,
esophagus, prostrate cancer – Adverse effects: • Anaphylactoid reaction because of solvent
cremaphor • Myalgia, myelosupression, peripheral neuropathy • Docetaxel – Oral – Used in
refractory breast & ovarian cancer – Major toxicity neutropenia may cause arrhythmias
hypotension 38

 39. Epipodophyllotoxins • Etoposide & tenoposide • Semisynthetic derivatives of

podophyllotoxins podophyllum peltatum (plant glycoside) • Act in S & G2 phase • Inhibit
topoisomerase II which results in breakage of DNA strands & cell death • Uses: – Testicular
tumors – cancer of lungs 39

 40. • Derived from camptotheca accuminata • Inhibit Topoisomerase I: No resealing of DNA

after strand has untwisted • Topotecan: – Used in metastatic ovarian cancer – Major toxicity
is bone marrow depression • Irinotecan – Used in metastatic cancer of colon/rectum –
Toxicity: diarrhoea, neutropenia, thrombocytopenia, cholinergic side effects Camptothecin
analogs 40
 41. • Cell cycle non specific drugs • Derived from streptomyces species • MOA: –
Intercalation in the DNA between adjoining nucleotide pairs – blocks DNA & RNA synthesis –
Generation of oxygen radicals which mediate single strand scission of DNA – Action on
Topoisomerase II Anticancer antibiotics 41

 42. • Uses: – Wilm’s tumor, – gestational chorio carcinoma • Adverse effects – bone marrow
supression – Irritant like meclorethamine – sensitizes to radiation, and inflammation at sites
of prior radiation therapy may occur – Gastrointestinal adverse effects Dactinomycin 42

 43. L-asparaginase 43

 44. L-asparaginase • Isolated from E.coli • Use: Acute Lymphocytic Leukemia (ALL) • Dose :
• 6000 to 10000U/kg IV daily for 3-4 weeks • A/E: • Hepatic damage • Hypersensitivity ,
hemorrhage • Hyperglycemia, headache, hallucinations , confusion, coma 44

 45. Hormones & antagonists • Corticosteroids – Prednisolone • Estrogens – Ethinyl Estradiol

• SERM – Tamoxifene, Toremifene • SERD – Fulvestrant • Aromatase Inhibitors – Letrozole,
Anastrazole, Exemestane • Progestins – Hydroxyprogesterone • Anti-androgens – Flutamide,
Bicalutamide • 5- reductase Inhibitors – finasteride, dutasteride • GnRH analogs –
Naferelin, goserelin, leuoprolide 45

 46. Glucocorticoids • Marked lympholytic effect so used in acute leukaemias & lymphomas,
• They also – Have Anti-inflammatory effect – Increase appetite, prevent anemia – Produce
sense of well being – Increase body weight – Supress hypersensitivity reaction – Control
hypercalcemia & bleeding – Non specific antipyretic effect – Increase antiemetic effect of
ondansetron 46

 47. Estrogens • Physiological antagonists of androgens • Thus used to antagonize the

effects of androgens in androgen dependent prostatic cancer • Fofesterol – Prodrug ,
phosphate derivative of stilbesterol – 600-1200mg IV initially later 120-240 mg orally 47

 48. • Tamoxifen : Non steroidal antiestrogen Selective Estrogen Receptor Modulators

(SERMs) Agonistic: Uterus, bone, liver, pitutary Antagonistic: Breast and blood vessels 48

 49. Tamoxifen • DOSE:10-20mg bd • Standard hormonal treatment in breast cancer •

Adverse effects: – Hot flushes , vomiting, vaginal bleeding, menstrual irregularities, venous
thromboembolism, dermatitis, rarely endometrial cancer 49

 50. • Pure estrogen antagonist • USES: Metastatic ER+ Breast Ca in postmenopausal women
• MOA: • Inhibits ER dimerization & prevents interaction of ER with DNA • ER is down
regulated resulting in more complete supression of ER responsive gene function Selective
Estrogen Receptor Down regulator (fulvestrant) 50

 51. • Letrozole • Orally active non steroidal compound • MOA : Inhibits aromatisation of
testosterone & androstenedione to form estrogen. • Uses : Breast Ca- & adj. to mastectomy
• Dose :2.5mg bd orally • Anastrozole : more potent • 1mg OD in ER+ Breast Ca • A/E : hot
flushes Aromatase Inhibitors 51

 52. • FLUTAMIDE & BICALUTAMIDE : • Androgen Receptor antagonists • Dose : 250 mg tds,
50mg od resp. • Palliative effect in metastatic Prostatic Ca after orchidectomy Anti
androgens 52
  53. 5- reductase inhibitors Finasteride • Orally active • DHT levels ↓ • Benign prostatic
hyperplasia Dose: 5mg/day Prostate volume Symptom score Peak urine flow rate DHT level
in prostate Side effects: Loss of libido & impotence in 5 % pts. Also used for prevention of
hair loss 53

 54. • NAFERELIN : nasal spray / SC inj • ↓FSH & LH release from pituitary- ↓ the release of
estrogen & testosterone • USE : Breast Cancer, Prostatic Cancer • PROGESTINS: •
Hydroxyprogesterone – used in metastatic endometrial Cancer. • A/E: bleeding GnRH
agonists 54

 55. 55

 56. Newer anticancer drugs • Inhibitors of growth factors receptors – Imatinib: CML (BCR-
ABL gene) – Gefitinib: Non small cell cancer of lungs (EGFR) – Nilotinib : CML (Tyrosine kinase
inhibitor) – Dasatinib : CML (Tyrosine kinase inhibitor) – Lapatinib : metastatic breast cancer
(HER2/neu) – Sunitinib : renal cell carcinoma (VEGF) – Sorafinib : renal cell carcinoma (VEGF)
56 9

 57. • Monoclonal antibodies – Trastuzumab : breast cancer (HER2/neu) – Bevacizumab:

metastatic colon cancer (VEGF) – Rituximab : non hodgkins lymphoma (CD-20) –
Panitumumab : metastatic colon cancer (EGFR) – Alemtuzumab : CLL (CD 52 antigen) –
Iodine tositumonab : Non hodgkins (CD-20) Newer anticancer drugs7 57

 58. References 1. Rang and Dale 5th edition ppt:693 Elsevier Publication. 2. Favoni RE 2000 -
The Role of Polypeptide growth factors in human carcinomas, Pharmacol Rev 52: 179-206. 3.
Workman P, Kaye 2002- New Potential Approaches to the development of anticancer drugs,
Mol Med Suppl8: 1-73. 4. Weinberg R A 1996, Senderowicz A M 2000- how cancer arises,
Cell Cycle Control J Natl Cancer Inst 92: 376-387 5. Essentials of Medical Phrmacology 7th
Edition- ppt:858 Jaypee Brothers Medical Publishers (P) LTD. New Delhi. 6. Talapatra S,
Thompson C B -2001 Growth factor signaling in cell survival. J Pharmacol Exp Ther 298: 873-
878 7. Sikic B I 1999- New Approaches in Cancer Treatment. Ann Oncol 10 : S149-S153
(Coverage of Monoclonal Antibodies) 58

 59. 8. Batchelor TA, Sorensen AG, di Tomaso E, et al. AZD2171, a pan-VEGF receptor tyrosine
kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma
patients. Cancer Cell, 2007, 11:83–95. 9. Sequist LV, Lynch TJ. EGFR tyrosine kinase inhibitors
in lung cancer: An evolving story. Annu Rev Med, 2008, 59:429–442. 10. Slamon DJ, Leyland-
Jones B, Shak S, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for
metastatic breast cancer that overexpresses HER2. N Engl J Med, 2001, 344:783–792. 11.
Weinstein IB, Joe AK. Mechanisms of disease: Oncogene addiction—a rationale for
molecular targeting in cancer therapy. Nat Clin Pract Oncol, 2006, 8:448–457 12. Pullarkat
ST, Stoehlmacher J, Ghaderi V, et al. Thymidylate synthase gene polymorphism determines
response and toxicity of 5-FU chemotherapy. Pharmacogenomics J, 2001, 1:65–70. 59

Chemotherapy of cancer
 1. CHEMOTHERAPY OF CANCER -BY KAVYA VAJRESH MPHARMACY (Pharmacology)
 2.  Introduction  Properties Of Cancer  Cancer Cell Transformation  Biochemical Pathway
 Types  Drugs Acting Directly On Cells  General Toxicity Of Cytotoxic Drugs  Hormones 
Radiation Therapy  Future Strategies
 3. CANCER Group of diseases involving abnormal cell growth with the potential to invade or
spread to other parts of the body. Growth regulators Killing pathways • Mutations
(physical/chemical carcinogens) • Eating habits • Virus • Inheritance
 4. Hallmarks of cancer: Immortality Rapid growth and division (Faulty check points; Lots of
growth receptors) No contact inhibition Proliferation(metastases) Low nutrient and oxygen
requirement( promoting angiogenesis)
 5. Cancer cells can go against the immune system • Natural killer cells • Cytokines Cancer cells
hide its antigenic sites ,therefore NK cells are not able to recognize
 6. CANCER CELL TRANSFORMATION • Irradiation • Virus • Lifestyle Avian Leukosis Virus
insertion leads to production of MYC without regulatory site UV Irradiation: Causes dimerization
of pyrimidine's leading to faulty DNA
 7. Oncogene : Gain of function Tumor suppressor gene : Loss of function CANCER Changes in
gene, due to mutations It can be: Point mutations: Ex: Rendering P53 inactive ;hyper activation
of Ras Chromosomal mutations: • Deletion • Translocation • Insertion
 8. BIOCHEMICAL PATHWAY NORMAL CELL CANCER CELL
 9. Cancers are classified according to the • kind of fluid or tissue from which they originate, or •
according to the location in the body where they first developed  Carcinoma : (>80%) Found in
epithelial tissue, which covers surfaces of organs, glands, or body structures. EX: cancer of the
lining of the stomach ;Many carcinomas affect organs involved with secretion, such as breasts
that produce milk.  Sarcoma : (<2%) A sarcoma is a malignant tumor growing from connective
tissues, such as cartilage(chondrosarcoma), fat, muscle, tendons, and bones osteosarcoma
TYPES
 10.  Lymphoma : Lymphoma refers to a cancer that originates in the nodes or glands of the
lymphatic system(WBC) Lymphomas are classified into two categories: • Hodgkin
lymphoma( presence of Reed-Sternberg cell, which is abnormal lymphocytes that may contain
more than one nucleus) and • Non-Hodgkin lymphoma.  Leukemia: also known as blood cancer,
is a cancer of the bone marrow
 11. DRUGS ACTING DIRECTLY ON CELLS  Alkylating Agents • Nitrogen Mustards •
Ethylenimine • Nitrosoureas  Anti metabolites • Folate antagonist • Purine antagonist •
Pyrimidine antagonist  Vinca alkaloids  Taxanes  Epipodohyllotoxin  Camptothecin
analogues  Antibiotics
 12. ALKYLATING AGENTS • Produce highly reactive carbonium ion intermediates, which
transfer alkyl groups by forming covalent bonds • Position 7 of guanine residue is susceptible •
Thus, cross linking or abnormal base pairing or scission of DNA strand occurs • cell cycle non-
specific
 13. NITROGEN MUSTARDS DRUG ROUTE A.E OTHERS Mechlorethamine Only I.V Nausea,
vomiting, sloughing(collapse due to extravasation) Cyclophosphamide (prodrug) Oral, I.V, I.M
Alopecia; cystitis *Active metabolites(Aldophosphamide; Phoshoramide)-occurs in liver
*Immunosuppressant *Chloramphenicol-Retards metabolism Ifofosfamide Hemorrhagic cystitis
(Due to acrolein-corrosive liver metabolite) (- by mesna) Use-carcinoma, sarcoma, lymphoma
Chlorambucil oral Slow acting; active on lymphoid tissue Long term maintenance therapy
Melphalan Oral, inj Bone marrow depression; Diarrhea; Use-Multiple myeloma, ovarian cancer
 14. DRUG ROUTE A.E OTHERS Thio- TEPA(Ethylenimine) inj Highly toxic(Not used) Busulfan
(Alkyl sulfonate) oral Hyperuricaemia; Pulmonary fibrosis; infertility Specific for myeloid elements
(granulocytes, RBC precursors) Nitrosoureas(Alkyl sulfonate) oral Visceral fibrosis; renal damage
Cross BBB-used in Brain tumors Dacarbazine (Triazine) inj Has inhibitory action on RNA,
Proteins; Use-Hodgkin's; Activated-liver
 15. ANTI METABOLITES Folate antagonist: (Methotrexate) • Inhibition(Primarily DNA) is
irreversible (50,000times high affinity) • Cell cycle specific(S-phase) Route: Oral(50%bound);
I.M;I.V • Salicylates, sulfonamides displace from binding sites and Inc. toxicity by decreasing
renal secretion Use: Choriocarcinoma; Leukemia; Arthritis; Psoriasis; Immunosuppressant A.E:
Low dose-megaloblastic anemia High dose-Pancytopenia Desquamation(Shedding of skin);
bleeding MOA: Competitively inhibit use of normal substrate or get incorporated forming
dysfunctional macromolecules.
 16. Purine Antagonist: DRUG USE A.E OTHERS 6- Mercaptopur ine; Thioguanine Leukemia;
Choriocarcin oma Metabolized by: Xanthine oxidase (6- MP) S- methylation (TG) Azathioprine
Immunosupp ressant (Suppress cell mediated immunity) ;Arthritis Reversible jaundice’
 Hypeuricemi a(-By Allopurinol) Route-oral Metabolized by: Xanthine oxidase or methylation
Fludarabine Lymphatic leukemia; Non- Hodgkin's lymphoma Chills; Fever; Myelosuppre ssion
Active- triphosphate form ; It also inhibits DNA polymerase
 17. Pyrimidine Antagonist: 5-fluoro2-deoxy- uridine monophosphateDeoxy uridilic
acid Deoxy thymidilic acid 5-Fluorouracil: Itself gets incorporated into nucleic acids , leading to
toxicity) Route: Oral;I.V.;Topical Use: Cutaneous carcinoma; Breast;Colon;Urinary bladder
Cytarabine: Phosphorylated(Triphosphate) Inhibits DNA-polymerase ; Blocks generation of
cytidilic acid Cell cycle specific(S phase) Route: Inj Use: Leukemia; Lymphoma
 18. VINCA ALKALOIDS  Vincristine(Oncovin): Rapidly acting Use: leukemia; sarcoma;
carcinoma; Hodgkin's A.E: Neuropathy; Alopecia  Vinblastine: Use: Hodgkin's; Testicular
carcinoma A.E: Bone marrow depression
 19. TAXANES  Paclitaxel: Obtained from bark of western yew tree Increase polymerization of
tubulin, inhibits reorganization of microtubules Use: Metastatic ovarian and breast carcinoma;
head and neck cancer; prostate cancer A.E: Myelosuppression; stocking and glove neuropathy;
arthralgia; myalgia; edema  Docetaxel: More potent Use: ovarian and breast cancer;
Pancreatic; Gastric A.E: Neutropenia; Arrhythmia; Fall in BP
 20. EPIPODOHYLLOTOXIN Etoposide:  Semisynthetic derivative of
podophyllotoxin(glycoside)  Arrests cells in G2 phase  Resealing of strand is prevented. Use:
Testicular tumor; lung cancer; Lymphoma; Bladder carcinoma A.E: Alopecia; leucopenia Route:
inj
 21. CAMPTOTHECIN ANALOGUES • Obtained rom Chinese tree • Allows single strand breaks
but not resealing after untwisting. • Act in S phase, arrests at G2 phase(Damage during
replication) Topotecan: Use: Metastatic ovary carcinoma; Lung cancer A.E: Neutropenia;
anorexia; Diarrhea Route: inj Irinotecan: • Prodrug; Decarboxylated I liver to active metabolite •
Inhibits AchE (Cholinergic effects are seen) , Can be suppressed by prior atropinization Use:
Metastatic colorectal carcinoma; Lung cancer A.E: Neutropenia; Thrombocytopenia; Diarrhea;
Hemorrhage. Route: inj
 22. ANTIBIOTICS Practically all of them intercalate between DNA strands and interfere with
template function. DRUG USE AE MOA OTHERS Actinomycin D Wilm’s tumor;
Rhabdomyosarcoma (In striated muscle); Choriocarcinoma Stomatitis(Sores in mouth); Diarrhea;
Erythema; Desquamation of skin; Alopecia; Bone marrow depression binds DNA at the
transcription initiation complex and prevents elongation of RNA chain Route: Inj Daunorubicin;
Doxorubicin Leukaemia Cardio toxicity; Arrhythmia; Hypotension; CHF; Alopecia; Stomatitis
Breaks DNA by Inhibiting TopoisomeraseII Generates quinone type free radicals Route: Inj
Mitoxantrone Lymphoma; leukemia; Breast carcinoma Marrow depression; mucosal inflammation
Route: Inj Bleomycin Testicular tumor;Squamous cell carinoma; Hodgkin’s lymphoma
Myelosuppression Chelates Cu/Fe &produce superoxide ions &intercalate causing chain
scission, Inhibits repair Route: Inj Mitomycin C Cancers of stomach, cervix, colon ,bladder
Marrow depression; Kills cells at G1-M phase Higly toxic; Inj
 23. MISCILLANEOUS 1.Hydroxyurea: MOA: Ribonucleotides Deoxy ribonucleotides
Ribonucleoside diphosphate reductase S-phase specific Use: Leukemia; Psoriasis; Polycythemia
(Inc Hb A.E: Myelosupression Route: Oral 2. Procarbazine: MOA: Depolymerizes DNA and
cause chromosomal damage; Inhibits nucleic acid synthesis • It is a weak MAO inhibitor • Alcohol
causes disulfiram like effects Use: Hodgkin’s; Non-Hodgkin lymphoma; Oat cell carcinoma of
lung A.E: Leucopenia; Thrombocytopenia; Dermatitis
 24. 3. Cisplatin: • Bound to plasma proteins, slowly excreted • Can also react with –SH groups •
Has radiomimetic poperty Use: Metastatic testicular and ovarian carcinoma Route: Inj A.E:
Emetic; Renal impairment; Tinnitus; Deafness;Hyperuricemia 4. L-Asparaginase: A.E: Liver
damage; Pancreatitis; allergy Route: Inj
 25. 5.Carboplatin: Less reactive Dose limiting toxicity-Thrombocytopenia Less protein bound
Use: Ovarian , squamous, Lung carcinoma 6. Imatinib: Inhibits tyrosine protein kinase; Ones that
are activated by platelet derived growth factor A.E: Edema; Myalgia; Liver damage
 26. GENERAL TOXICITY OF CYTOTOXIC DRUGS Majority have effect on rapidly multiplying
cells , affecting nucleic acid synthesis Bone marrow: Depression leads to granulocytopenia;
thrombocytopenia; aplastic anemia Infections and bleeding are usual complications
Lymhoreticular tissue: Lymphocytopenia results in suppression of cell mediated immunity,
damage to epithelial tissue; so susceptibility to infections is increased. Oral cavity: Oral mucosa
 has high epithelial cell turnover, many drugs produce stomatitis Also subjected to breaches,
trauma; Thrombocytopenia may cause bleeding gums
 27. GIT: Diarrhea,shedding of mucosa, heamorrhages occur due to decrease in rate of
renewal of ucosal lining; Mucositis is common Nausea,vomiting are common due to direct
stimultion of CTZ Skin: Alopecia(due to damage to cells in hair follicles) Dermatitis Gonads:
Oligozoospermia and impotence in males Inhibition of ovulation and amenorrhea in females
Foetus: Abortion, foetal deth, teratogenesis
 28. Carcinogenicity: Secondary cancers , leukemia, lymphoma tumors appear with great
frequency after many years (Might be due to cell mediatd &humoral blockage) Hyper uricaemia:
Massive desturction (Uric acid is byproduct of purine metabolism) Inhibited by allopurinol
 29. HORMONES • Modify the growth of hormone-dependent tumors. • All hormones are
palliative 1. Glucocorticoids: Mechanism: apoptosis is achieved via activation of death-inducing
genes or inhibiting the transcription of growth/survival genes. Includes: Prednisolone;
Dexamethasone Marked lympholytic action Use: Acute childhood leukemia; lymphoma; Breast
cancer Also used for controlling complications like hypercalcemia, hemolysis, bleeding,
Increased intracranial tension, edema A.E: Hypercorticism(As doses given are v.high)
 30. 2. Estrogen: Physiological antagonists of androgens Produce relief in prostate cancer,
which is anrogen depndent tumor Includes • Fosfestrol: Prodrug (Phosphatee derivative of
stillbestrol) Route: Oral,inj • Selective estrogen receptor modulator(Tamoxifen): • Aromatase
Inhibitors: Aromatase, turns the hormone androgen into estrogen in the body. This means that
less estrogen is available to stimulate the growth of hormone-receptor-positive breast cancer
cells Includes letrazole
 31. • Selective estrogen receptor down regulator (fulvestrant ): Binds to estrogen receptor
monomers, inhibits receptor dimerization, translocation of receptor to the nucleus is reduced
degradation of the estrogen receptor is accelerated. 3. Anti-Androgen: Includes flutamide,
bicalutamide Used in combination with orchiectomy(one or both testicles are removed) MOA: •
Blocks the action of both endogenous and exogenous testosterone by binding to the androgen
receptor. • Inhibitor of testosterone-stimulated prostatic DNA synthesis.
 32. 4. 5-alpha reucatse inhibitor: • Includes finasteride and dutasteide • Occasionally used •
Reduce size of prostate gland 5. GnRH agonists: Indirectly inhibit estrogen/androgen secretion
by suppressing FSH,LH release Used in combination 6.Progestins: inhibition of estradiol binding
to its specific receptors, inhibiting the formation of the estrogen-receptor system , the cause of
cell growth Use: Metastatic endometrial carcinoma, breast cancer
 33. RESISTANCE TO ANTI CANCER DRUGS It is primary(Present when drug is first given)
Acquired(developed during treatment with drug) Various mechanisms: • Drug Inactivation: Many
anticancer drugs must undergo metabolic activation in order to acquire clinical efficacy EX:
cytarabine (AraC), activated after multiple phosphorylation events. Down-regulation or mutation
in this pathway can produce a decrease in the activation and lead to drug resistance • Alteration
of Drug Targets: EX: certain anticancer drugs target topoisomerase II, mutations in this gene can
confer resistance • Decreased requirement of substrate • Drug efflux • Rapid repair of drug
induced lesions Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190567/
 34. RADIATION THERAPY High energy rays are aimed at tumor cell, which damages DNA and
destroys ability to reproduce and finally eliminates Used in 2ways- • Radical: To cure cancer
(Destroy tumors that haven't spread) • Palliative: To reduce symptoms( shrink tumors, affecting
quality of life ) Delivered 2 types: External beam radiation (Ex: Proton, neutron beam therapy)
Internal radiation: (Brachytherapy) Involves placing radioactive sources(Thin wires, capsules)
inside patient. Allows minimal radiation exposure to normal tissue.
 35. FUTURE STRATEGIES  Angiogenesis and metalloproteinase inhibitors  Cyclo-
oxygenase inhibitors  p53 as anticancer target  Antisense oligonucleotide  Gene therapy 
Reversal of multi drug resistance
 36. • RANG AND DALE’S Pharmacology page no.-718-733 • Essentials of medical
pharmacology –by KD TRIPATHI page no.-819-834

medicinal chemistry of Anticancer agents

 1. CHEMOTHERAPY OF ANTICANCER AGENTS BY GANESH D.MOTE AGCOP,SATARA 1
 2. WHAT IS CELL CYCLE??? 2
 3. 3
 4. WHAT IS CANCER??? • Cancer is a term used for diseases in which abnormal cells divide
without control and are able to invade other tissues. Cancer cells can spread to other parts of the
body through the blood and lymph systems 4
 5. 5
 6. TYPES OF CANCER • Carcinoma - cancer that begins in the skin or in tissues that line or
cover internal organs. There are a number of subtypes of carcinoma, including adenocarcinoma
basal cell carcinoma, squamous cell carcinoma and transitional cell carcinoma. • Sarcoma -
cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or
supportive tissue. • Leukemia - cancer that starts in blood-forming tissue such as the bone
marrow and causes large numbers of abnormal blood cells to be produced and enter the blood. •
Lymphoma and myeloma - cancers that begin in the cells of the immune system • Central
nervous system cancers - cancers that begin in the tissues of the brain and spinal cord. 6
 7. 7
 8. 8
 9. TYPES OF TUMORS • Not all tumors are cancerous; tumors can be benign or malignant. •
Benign tumors aren't cancerous. They can often be removed, and, in most cases, they do not
come back. Cells in benign tumors do not spread to other parts of the body. • Malignant tumors
are cancerous. Cells in these tumors can invade nearby tissues and spread to other parts of the
body. The spread of cancer from one part of the body to another is called metastasis. 9
 10. 10 Cancer Therapeutic Modalities (classical) 1. Surgery 2. Radiation 3. Chemotherapy 1/3
of patients without metastasis Respond to surgery and radiation. If diagnosed at early stage,
close to 50% cancer could be cured. 50% patients will undergo chemotherapy, to remove
micrometastasis. However, chemotherapy is able to cure only about 10-15% of all cancer
patients.
 11. GENERAL PRINCIPLES OF CHEMOTHERAPY OF CANCER 1. ANALOGOUS WITH
BACTERIAL CHEMOTHERAPY – DIFFERENCES ARE • SELECTIVITY OF DRUGS IS
LIMITED – BECAUSE “I MAY HARM YOU” • NO OR LESS DEFENCE MECHANISM –
CYTOKINES ADJUVANT NOW 2. ALL MALIGNANT CELLS MUST BE KILLED TO STOP
PROGEMY – SURIVAL TIME IS RELATED TO NO. OF CELLS THAT ESCAPE CHEMO
ATTACK 3. SUBPOPULATION CELLS DIFFER IN RATE OF PROLIFERATION AND
SUSCEPTIBILITY TO CHEMOTHERAPY 4. DRUG REGIMENS OR COMBINED CYCLE
THERAPY AFTER RADIATION OR SURGERY (BASIS OF TREATMENT NOW IN LARGE
TUMOUR BURDENS) 5. COMPLETE REMISSION SHOULD BE THE GOAL – BUT ALREADY
USED IN MAXIMUM TOLERATED DOSE – SO EARLY TREATMENT WITH INTENSIVE
REGIMENS 6. FORMERLY SINGLE DRUG – NOW 2-5 DRUGS IN INTERMITTENT PULSES –
TOTAL TUMOUR CELL KILL – COMBINATION CHEMOTHERAPY 11
 12. COMBINATION CHEMOTHERAPY - SYNERGISTIC • DRUGS WHICH ARE EFFECTIVE
WHEN USED ALONE • DRUGS WITH DIFFERENT MECHANISM OF ACTION • DRUGS WITH
DIFFERING TOXICITIES • DRUGS WITH DIFFERENT MECHANISM OF TOXICITIES • DRUGS
WITH SYNERGISTIC BIOCHEMICAL INTERACTIONS • OPTIMAL SCHEDULE BY TRIAL AND
ERROR METHOD • MORE IMPORTANTLY ON CELL CYCLE SPECIFICITY 12
 13. Antineoplastic Agent a. Cell Cycle Specific (CCS) agents b. Cell Cycle Non-Specific
(CCNS) agents c. Miscellaneous (e.g., antibodies) agents 13
 14. 14 G0 = resting phase G1 = pre-replicative phase G2 = post-replicative phase S = DNA
synthesis M = mitosis or cell division M S G G2 1 Hydrocortisone Vincristine,Vinblastine G0
Cyclophosphamide Bleomycin Actinomycin D Actinomycin D 5-Fluorouracil Cytosine arabinoside
Methotrexate 6-Mercaptopurine 6-Thioguanine Purine antagonists Methotrexate
Cyclophosphamide 5-Fluorouracil Cytosine arabinoside Daunomycin Paclitaxel, Docetaxel
resting Cell cycle specificity of Anti-Neoplastic Agents
 15. CLASSIFICATION 1. ALKYLATING AGENTS • A. Nitrogen Mustards: Cyclophosphamide,.
Chlorambucil, Melphalan, • B. Alkyl Sulfonate: Busulfan • C. Nitrosoureas : Carmustine,
Lomustine,semustine • D. Ethylenimines: Thiotepa • E. Triazenes : Dacarbazine 15
 16. 2. Antimetabolites •A. Folate antagonist: methotrexate and gemcitabine •B. Purine
analogues: thioguanine, mercaptopurine, pentostatin •C. Pyrimidine analogues: fluorouracil,
cytarabine 16
 17. • 3. Plant-derived products : vinca alkaloids( vincristine, vinblastine) epipodophyllotoxins
( etoposide) taxanes: (paclitaxel) • 4. Antibiotics : doxorubicin , daunorubicin , bleomycin,
mitomycin, dactinomycin • 5. Hormones and related drugs : tamoxifen estramustine, flutamide ,
progestins • 6. Miscellaneous agent : hydroxyurea, cisplatin , mitoxantrone, levamisole, interferon
alfa and aldesleukin. 17
 18. •7. Drugs that alters hormonal milieu 1. Glucocorticoids: Prednisolon, Prednisone 2.
Estrogen: Diethylstilbestreol 3. Anti-estrogen: Tamoxifen 4. Androgen: Testosteron 5. Progestin:
Medroxy Progesteron Acetate 18
 19. 8. Monoclonal Antibodies 1. Trantuzumab 2. Rituximab 3. Imatinib 19
 20. MECHANISM OF ACTION: ALKYLATING AGENT • Alkylating agents exert their cytotoxic
effects via transfer of their alkyl groups to various cellular constituents. • Alkylations of DNA
within the nucleus probably represent the major interactions that lead to cell death. • The major
site of alkylation within DNA is the n7 position of guanine; however, other bases are also
alkylated to lesser degrees, including n1 and n3 of adenine, n3 of cytosine, and o6 of guanine 20
 21. MOA: ANTI METABOLITES • Antimetabolites are drugs that are structurally related to
naturally occurring compounds, such as vitamins, amino acids, and nucleotides. These drugs
can compete for binding sites on enzymes or can themselves become incorporated into DNA or
RNA and thus interfere with cell growth and proliferation. 21
 22. ALKYLATING AGENTS 22
 23. • ALKYLATING AGENTS ARE COMPOUNDS THAT ARE CAPABLE OF INTRODUCING
AN ALKYL GROUP INTO NUCLEOPHILIC SITES ON DNA , RNA OR ANY ENZYME
THROUGH COVALENT BOND . • THESE AGENTS ARE THOUGHT TO REACT WITH THE 7
POSITION OF GUANINE ( OR ANY OTHER NITROGEN BASE) IN EACH OF THE DOUBLE
STRANDS OF DNA, CAUSING CROSS-LINKING THAT INTERFERES WITH SEPARATION OF
THE STRANDS AND PREVENTS MITOSIS. 23
 24. • THE EFFECTS OF BASE ALKYLATION INCLUDE MISREADING OF THE DNA CODON
AND SINGLE STRAND BREAKAGE OF THE DNA CHAIN. HOWEVER, THE LONGTIME
EFFECTS ARE MUTATION AND CELL DEATH. • THE FAVORED SITE ON DNA IS AT THE N7
POSITION OF GUANINE, ADENINE, CYTOSINE, AND EVEN THE SUGAR PHOSPHATE
GROUPS . 24
 25. NITROGEN MUSTARDS • METHCLORETHAMINE • CYCLOPHOSPHAMIDE •
MELPHALAN • CHLORAMBUCIL • IFOSFAMIDE • THE NITROGEN MUSTARDS ARE
CYTOTOXIC CHEMOTHERAPEUTIC AGENTS SIMILAR TO MUSTARD GAS WHICH WAS
USED IN WWI AND WWII 25
 26. • NITROGEN MUSTARDS CONTAIN BIS(2-CHLOROETHYL) GROUP • MODIFICATION
OF THIS GROUP CHANGE STABILITY , REACTIVITY AND LIPOPHILICITY 26
 27. MECHANISM OF ALKYLATION BY NITROGEN MUSTARDS 27
 28. • METHCLORETHAMINE (2-CHLORO-N-(2-CHLOROETHYL)-N-METHYL- ETHANAMINE)
• A STRONG VESICANT AND IS TAKEN BY IV INFUSION AND IT USED TO TREAT
PROSTATE CANCER . • A MAJOR DISADVANTAGE OF MECHLORETHAMINE IS THAT IT
HAS MUTAGENIC AND CARCINOGENIC EFFECT ON BONE MARROW STEM CELLS. 28
 29. • CYCLOPHPSPHAMIDE (CYTOXAN®) 29
 30. • CYCLOPHOSPHAMIDE (N,N-BIS(2-CHLOROETHYL)-1,3,2- OXAZAPHOSPHINAN-2-
AMINE 2-OXIDE) • THIS MOST WIDELY USED ALKYLATING AGENT • IT IS INACTIVE IN
VITRO BUT WHEN IT ADMINISTERED IT IS METABOLIZED BY LIVER INTO
PHOSPHORAMIDE MUSTARD (ACTIVE COMPOUND) 30
 31. CYCLOPHOSPHAMIDE CLINICAL APPLICATIONS: 1. BREAST CANCER 2. OVARIAN
CANCER 3. NON-HODGKIN’S LYMPHOMA 4. CHRONIC LYMPHOCYTIC LEUKEMIA (CLL) 5.
SOFT TISSUE SARCOMA 6. NEUROBLASTOMA 7. WILMS’ TUMOR 8.
RHABDOMYOSARCOMA 31
 32. CYCLOPHOSPHAMIDE MAJOR SIDE EFFECTS 1. NAUSEA AND VOMITING 2.
DECREASE IN PBL COUNT 3. DEPRESSION OF BLOOD CELL COUNTS 4. BLEEDING 5.
ALOPECIA (HAIR LOSS) 6. SKIN PIGMENTATION 7. PULMONARY FIBROSIS 32
 33. SAR OF CYCLOPHOSPHAMIDE • BIS-2-CHLOROETHYLAMINO GROUP IS ESSENTIAL •
CHLORO ATOM PROVIDES MAXIMUM ACTIVITY • LEVO-ISOMER IS INACTIVE •
TRIETHYLENE DERIVATIVE IS INACTIVE 33
 34. CYCLOPHOSPHAMIDE ACTIVATION/METABOLISM 34
 35. • PHOSPHORAMIDE MUSTARD IS CYTOTOXIC TO CANCER CELLS WHILE ACROLEIN
IS TOXIC TO THE BLADDER • CYCLOPHOSPHAMIDE MAY GIVEN ORALLY BUT ITS
ABSORPTION INCOMPLETE SO IT IS BETTER TO BE GIVEN I.V • IT USED TO TREAT
MANY TYPES OF CANCER SUCH AS LYMPHOSARCOMAS , BREAST, OVARIAN, AND
LUNG CANCER. 35
 36. NITROUREAS • CARMUSTINE (GLIADEL®) •

Chemotherapeutic agents
 1. CHEMOTHERAPEUTIC AGENTS FROM PERSPECTIVE OF RADIATION ONCOLOGIST Dr
Prachi Upadhyay Moderator- Dr. Pavan Kumar / Dr. Ayush Garg
 2. CONTENTS • History • Classification of anticancer drug • Mechanism of action •
Chemotherapy
 3. HISTORY • Chemotherapy began during the world war II after the observation of autopsy of
soldiers who died due to the use of nitrogen mustard • Aplasia of bone marrow • Dissolution of
lymphoid tissue • Ulceration of the GIT • Led to the use of these agents to treat Hodgkins and
non-Hodgkins lymphomas at Yale in 1943 • Luis Goodman and Alfred Gillmen demonstrated it
for the first time.
 4. PAUL EHRLICH 1854 - 1915 • Father of Chemotherapy • Salvarsan for Treatment of Syphilis
• Nobel Prize 1908 • “Magic Bullet Concept
 5. MODES OF CHEMOTHERAPY • PRIMARY CHEMOTHERAPY - chemotherapy is used as
the sole anti-cancer treatment in a highly sensitive tumor types Example – CHOP for Non-
Hodgkins lymphoma • ADJUVANT CHEMOTHERAPY – treatment is given after surgery to “mop
up” microscopic residual disease Example – Adriamycin, cyclophosphamide for breast cancer •
NEOADJUVANT CHEMOTHERAPY – treatment is given before surgery to shrink tumor and
increase chance of successful resection Example – Adriamycin, ifosfamide for osteosarcoma •
CONCURRENT CHEMOTHERAPY – treatment is given simultaneous to radiation to increase
sensitivity of cancer cells to radiation Example – Cisplatin, 5-fluourouracil, mitomycin C
 6. CLASSIFICATION According to chemical structure and sources of drugs: • Alkylating
Agents, Antimetabolite, Antibiotics, Plant Extracts, Hormones and Others According to
biochemistry mechanisms of anticancer action: • Block nucleic acid biosynthesis • Direct
influence the structure and function of DNA • Interfere transcription and block RNA synthesis •
Interfere protein synthesis and function • Influence hormone homeostasis According to the cycle
or phase specificity of the drug: • Cell cycle nonspecific agents (CCNSA) & Cell cycle specific
agents (CCSA)
 7. CELL CYCLE AND CLINICAL IMPORTANCE • All cells—normal or neoplastic— must
traverse before and during cell division • Malignant cells spend time in each phase - longest time
at G1, but may vary • Many of the effective anticancer drugs exert their action on cells traversing
the cell cycle - cell cycle-specific (CCS) drugs • Cell cycle-nonspecific (CCNS) drugs - sterilize
tumor cells whether they are cycling or resting in the G0 compartment • CCNS drugs can kill both
G0 and cycling cells - CCS are more effective on cycling cells
 8. • Information on cell and population kinetics of cancer cells explains, in part, the limited
effectiveness of most available anticancer drugs • Information is valuable in knowing - mode of
action, indications, and scheduling of cell cycle-specific (CCS) and cell cycle-nonspecific (CCNS)
drugs • CCS – effective against hematologic malignancies and in solid tumors with large growth
fraction • CCNS drugs – solid tumors with low growth fraction solid tumors • CCS drugs are given
after a course of CCNS
 9. DRUGS BASED ON CELL CYCLE • Nitrogen Mustards • Cyclphosphamide • chlorambucil •
carmustine dacarbazine • busulfan • L-asparginase, cisplatin, procarbazine and actinomycin D
etc. CCNS • G1 – vinblastine • S – Mtx, cytarabine, 6-thioguanine, 6- MP, 5-FU, daunorubicin,
doxorubicin • G2 – Daunorubicin, bleomycin • M – Vincristine, vinblastine, paclitaxel etc. CCS
 12. CLASSIFICATION 1. ALKYLATING AGENTS 2. ANTIMETABOLITES 3. ANTITUMOR
ANTIBODIES 4. MITOTIC SPINDLE AGENTS 5. TOPOISOMERASE INHIBITORS 6.
TYROSINE KINASE INHIBITORS 7. MONOCLONAL ANTIBODIES 8. MISCELLANEOUS
AGENTS 9. HORMONAL AGENTS 10. CYTOPROTECTIVE AGENTS
 13. ALKYLATING AGENTS • Are cell cycle non specific, i.e act on dividing as well as resting
cells. • Alkylate nucleophilic groups on DNA bases • Position 7 of guanine residues in DNA/RNA
 is specially susceptible, but other molecular sites are also involved. • Leads to cross linking of
bases, abnormal base pairing and DNA strand breakage
 14. CLASSIFIED 1. Nitrogen mustards- Cyclophosphamide, Chlorambucil, Ifosfamide 2. Alkyl
Sulfonate- Busulfan 3. Nitrosoureas- Carmustine, Lomustine 4. Triazine- Dacarbazine,
Temozolomide 5. Ethylenime- Thio- TEPA
 15. MECHANISM OF ACTION Alkylating Agents Form highly reactive carbonium ion Transfer
alkyl groups to nucleophilic sites on DNA bases Results in Cross linkage Abnormal base pairing
DNA strand breakage ↓ cell proliferation Alkylation also damages RNA and proteins
 16. CYCLOPHOSPHAMIDE • Most commonly used alkylating agent a prodrug
Cyclophosphamide Aldophosphamide Phosphoramide mustard Acrolein Cytotoxic effect
Hemorrhagic cystitis Mesna
 17. USES OF CYCLOPHOSPHAMIDE • Neoplastic conditions – Hodgkins and non hodgkins
lymphoma – ALL, CLL, Multiple myeloma – Burkits lymphoma – Neuroblastoma , retinoblastoma
– Ca breast , adenocarcinoma of ovaries • Non neoplastic conditions – Control of graft versus
host reaction – Rheumatoid arthritis – Nephrotic syndrome
 18. COMMON TOXICITIES • Hematopoietic toxicity • Gastrointestinal toxicity • Gonadal toxicity
• Pulmonary toxicity • Alopecia • Teratogenicity • Carcinogenesis • Myleosuppression
 19. ATYPICAL ALKYLATING ( PLATINUM COMPOUNDS ) • Cell cycle non specific. • Platinum
compounds act by covalently binding to DNA with preferentially binding to N7 position in guanine
and adenine . • Form strong covalent bonds – DNA cross linking
 20. COMMONLY USED PLATINUM COMPOUNDS • CISPLATIN • CARBOPLATIN •
OXALIPLATIN
 21. CISPLATIN • CDDP – Cis Di amine Dichloro platinum • Alkylating agent • Used in – in
concurrent settings and ca bladder, ca ovary ,ca oesophagus, ca testis , head and neck, ca lung ,
ca gall bladder ,ca cervix, sarcomas , melanoma , mesothelioma  Administration – iv infusion,
substituted with 2.5 lits of iv fluids , inj mannitol , inj mgso4 , inj kcl  Highly emetogenic – should
be given good anti emetic cover
 22.  Mechanism of action – it damages DNA , RNA and inhibits cell division • Side effects –
nausea / vomiting , low blood counts , renal toxicity , ototoxicity , low ca, Mg, k , peripheral
neuropathy, loss of appetite , metallic taste sensation, hair loss, diarrhoea, fatigue, oral
ulcers ,malena , anaphylactic reactions
 23. ANTIMETABOLITES • These drugs act in the S phase of cell cycle • Thus only dividing cells
are responsive • Folate antagonists - Methotrexate • Purine antagonists - 6-Mercaptopurine - 6-
Azathioprine - 6-Thioguanine • Pyrimidine antagonists - 5-Flurouracil - Cytarabine
 24. METHOTREXATE Folic acid Tetra hydro folic acid Purine synthesis - DRUG CLASS:
Antemetabolite Folate antagonist Dihydro folic acid Dihydro folate reductase DNA synthesis Cell
cycle specific: S phase AICAR TS
 25. • INTERMITTENT IV ADMINISTRATION • IT CAN ALSO BE GIVEN :  IM  ORALLY 
REGIONAL INTRA-ARTERIAL INFUSION (INTO THE SUPERFICIAL TEMPORAL OR
SUPERIOR THYROID ARTERY)
 26. Adverse effects • Megaloblastic anemia • Thrombocytopenia, leukopenia, aplasia • Oral,
intestinal ulcer , diarrhoea •Alopecia , liver damage, nephrpathy  Folinic acid (citrovorum factor,
N5 Formyl THF)  IM/IV 8 to 24 hrs after initiation of methotrexate  120 mg in divided doses in
first 24 hrs, then 25 mg oral/IM 6 hrly for next 48 hrs Treatment of methotrexate toxicity
 27. USES OF METHOTREXATE • Antineoplastic • Choriocarcinoma and tropoblast tumor15 -30
mg/day orally for 5 days • Remission of ALL in children 2.5 to 15 mg/day • Ca breast, head &
neck, bladder, ovarian cancer • Immuno-supressive agent • Rheumatoid arthritis, resistant
asthma • Crohns disease, wegeners granulomatosis • Prevention of graft versus host reaction •
Psoriasis • Medical termination of pregnancy
 28. MERCAPTOPURINE: PURINE ANTAGONIST Mechanism of action: Inhibits the formation
of nucleotides from adenine & guanine ( purine) Highly effective antineoplastic drugs. Common
side effects:  Bone marrow depression  Nausea and vomiting  Hyperurecemia DOSE Active
Phase: 2.5 mg/Kg/day I.V. Maintenance Phase: ½ Dose
 29. 5-FLUOROURACIL : PYRIMIDINE ANTAGONIST • Mechanism of action: Disrupts
pyrimidine synthesis Capecitabine is an oral pro-drug • Route of administration:  Intravenously
 Orally  continuous iv infusion
 30. • Even resting cells are affected (though rapidly multiplying cells are more susceptible) –
particularly useful for many solid tumors. • Side-effects:  Myelosuppression Hand and foot
syndrome  Mucosal ulceration/mucositis  Nausea and vomiting  Alopecia.
 31. MITOTIC SPINDLE AGENTS • M phase of cell cycle • Bind to micro tubular proteins – inhibit
micro tubular assembly --- dissolution mitotic spindle structures . • Vinka alkaloids. • Taxanes
 32. VINCA ALKALOIDS (VINCRISTINE, VINEBLASTINE) • Inhibits microtubule formation
(mitotic inhibitor) • Inhibits RNA synthesis by affecting DNA dependent RNA polymerases. • Cell
cycle specific (M phase)
 33. COMPARISON BETWEEN Vincristine • Marrow sparing effect • Alopecia more common •
Peripheral & autonomic neuropathy & muscle weakness (CNS) • Constipation • Uses: (Childhood
cancers) • ALL , Hodgkins, lymphosarcoma, Wilms tumor, Ewings sarcoma Vinblastine • Bone
marrow supression • Less common • Less common, temp. mental depresssion • Nausea,
vomiting, diarrhoea • uses • Hodgkins disease & other lymphomas , breast cancer, testicular
cancer
 34. TAXANES ( PACLITAXEL,DOCETXEL ) • Isolated from bark of yew tree ( taxus brevifolia ) •
Microtubule-stabilizing agent • Blocking of cell cycle at the G2 or M phase by promoting
microtubule polymerization.- Non functional microtubules • Commonly used agents –
paclitaxel ,docetaxel
 35. MECHANISM OF ACTION Cell cycle arrested in G2 and M phase
 36. TAXANES USED • PACLITAXEL •
 COLLEGE OF NURSING, UNIVERSITY OF BAGHDAD
 3. A condition in which part of an organ is displaced and protrudes through the wall of the cavity
containing it (often involving the intestine at a weak point in the abdominal wall) Hernia The most
important elements in the development of a hernia are: • Congenital • Muscle weakness •
Increased of the intra-abdominal pressure
 4. Classification
 6. Types of Hernia 1.) Inguinal hernia i.) Indirect inguinal hernia ii.) Direct inguinal hernia (in
contrast) 2.) Hiatal Hernia 3.) Femoral hernias (protrude through the femoral ring) 4.) Umbilical
hernia (congenital/acquire) 5.) Incisional/ventral hernias (occur at he site of previous surgical
incision)
 8. Inquinal Hernia
 9. Hiatal Hernia
 10. Femoral Hernia
 11. Umbilical Hernia
 12. Incisional Hernia
 13. Risk Factors
 14. Risk Factors
 15. • Small to moderate size hernia don’t usually causes any symptoms. • Large hernia may be
noticeable and cause same - discomfort. - Pain when lifting heavy object - Tenderness - Bulging
• Severe symptoms - Severe and sudden pain - Constipation - Nausea - Vomiting Sign and
symptoms
 16. History 1. Age of patient. (65 and above more risk) 2. Duration of hernia.(1st saw) 3. Height
and weight. (obesity more risk) 4. Pain at the hernia place. (score/ type/ duration/ specific ) 5.
Ask about the previous history of surgical .Post- operative complications (wound infection and/or
dehiscence) 6. Smoking 7. Bowel movement (constipation ) 8. Chronic cough 9. Family history of
hernia Assessment
 17. Physical examination • health care provider may ask the patient to stand and cough or
strain so the health care provider can feel for a bulge caused by the hernia as it moves into the
groin or scrotum. • The health care provider may gently try to massage the hernia back into its
proper position in the abdomen Investigation
 18. Physical examination 1. Palpate the bulge area ( standing and lying ) 2. Check for the skin
fragile 3. Type of hernia Investigation Ultrasound scan X-ray abdomen Barium swallow MRI
Blood test Assessment
 19. 1. Ultrasound may be ordered to diagnose a hernia or to characterize the contents of a
hernia and determine its reducibility Investigation
 20. 2. Barium swallow • Barium is a non-toxic chemical, that shows up clearly on x-ray. You will
be fast for 6 hours 3. MRI • MRI has more contrast resolution, which means can see the anatomy
of the groin in high details and also very sensitive for small areas of inflammations Investigation
 21. 4. X-ray abdomen • abdominal X-rays may be ordered to determine if a bowel obstruction is
present 5. Blood test • CBC - for anemia due to blood loss • WBC - detect inflammation, infection
and presence of tissue necrosis Investigation
 22. 1.) Antibiotic: cefoxitin - Ampicilin 2.) H2 receptor blocker: famotidine – ranitidine 3.) PPI:
lansoprazole - osomeprazole 4.) Antianxiety Agents: Dormicum 5.) Nonsteroidal Anti-
Inflammatory Drugs (NSAIDs): Ibuprofen Medical Pharmacology treatment
 23. 1.) Avoid food that cause acid reflux or heartburn such as spicy food 2.) Don’t lie down or
bend over after a meal 3.) Exercise 4.) stop smoking 5.) Avoid gassy drinks 6.) Avoid lift heavy
object Non-pharmacological management
 24. • Truss (Inguinal hernia) - a pad made with firm material that will held in place over the
hernia with belt to help keep the abdominal contents from protruding into the hernia sac Non-
Surgical Management Surgical Management Nissen fundoplication Laparoscopic (LEP)
Herniorrhaphy (hernia repairs)
 25. 1. Post herniarrhaphy pain syndrome/ inguinodynia 2. Hernia recurrence 3. Wound Infection
4. Ischemia 5. Necrosis COMPLICATIONS
 26. 1. PRE-OPERATIVE FOR HERNIA REPAIR Fear and anxiety related to undergoing surgery
2. POST-OPERATIVE FOR HERNIA REPAIR Acute pain related to surgical intervention Risk of
infection related to surgical site 3. HIATAL HERNIA Risk for aspiration related to reflux of gastric
content NURSING DIAGNOSES
 27. Health Education 1.) Educate patient to assess for any signs and symptoms of infection
such as redness, severe itchyness and condition at the surgical site 2.) Advise patient come for
follow-up to monitor patient progress 3.) Educate patient to avoid wearing tight clothing to
minimize abdominal pressure 4.) Encourage patient avoid lifting heavy object or doing heavy
exercise at least 6 weeks 5.) Use proper lifting technique
 28. Health Education 6.) Lose weight 7.) Exercise regularly 8.) Advice patient to eat a vitamin-
rich diet such as vitamin C and protein to promote wound healing 9.) Encourage patient to take
high fiber food to prevent constipation
 29. Keep Calm and Watch for
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 COLLEGE OF NURSING, UNIVERSITY OF BAGHDAD

 3. A condition in which part of an organ is displaced and protrudes through the wall of the
cavity containing it (often involving the intestine at a weak point in the abdominal wall)
Hernia The most important elements in the development of a hernia are: • Congenital •
Muscle weakness • Increased of the intra-abdominal pressure

 4. Classification

 6. Types of Hernia 1.) Inguinal hernia i.) Indirect inguinal hernia ii.) Direct inguinal hernia (in
contrast) 2.) Hiatal Hernia 3.) Femoral hernias (protrude through the femoral ring) 4.)
Umbilical hernia (congenital/acquire) 5.) Incisional/ventral hernias (occur at he site of
previous surgical incision)

 8. Inquinal Hernia

 9. Hiatal Hernia

 10. Femoral Hernia

 11. Umbilical Hernia

 12. Incisional Hernia

 13. Risk Factors

 14. Risk Factors

 15. • Small to moderate size hernia don’t usually causes any symptoms. • Large hernia may
be noticeable and cause same - discomfort. - Pain when lifting heavy object - Tenderness -
Bulging • Severe symptoms - Severe and sudden pain - Constipation - Nausea - Vomiting Sign
and symptoms

 16. History 1. Age of patient. (65 and above more risk) 2. Duration of hernia.(1st saw) 3.
Height and weight. (obesity more risk) 4. Pain at the hernia place. (score/ type/ duration/
specific ) 5. Ask about the previous history of surgical .Post- operative complications (wound
infection and/or dehiscence) 6. Smoking 7. Bowel movement (constipation ) 8. Chronic
cough 9. Family history of hernia Assessment

 17. Physical examination • health care provider may ask the patient to stand and cough or
strain so the health care provider can feel for a bulge caused by the hernia as it moves into
the groin or scrotum. • The health care provider may gently try to massage the hernia back
into its proper position in the abdomen Investigation

 18. Physical examination 1. Palpate the bulge area ( standing and lying ) 2. Check for the
skin fragile 3. Type of hernia Investigation Ultrasound scan X-ray abdomen Barium swallow
MRI Blood test Assessment

 19. 1. Ultrasound may be ordered to diagnose a hernia or to characterize the contents of a

hernia and determine its reducibility Investigation

 20. 2. Barium swallow • Barium is a non-toxic chemical, that shows up clearly on x-ray. You
will be fast for 6 hours 3. MRI • MRI has more contrast resolution, which means can see the
anatomy of the groin in high details and also very sensitive for small areas of inflammations
Investigation

 21. 4. X-ray abdomen • abdominal X-rays may be ordered to determine if a bowel

obstruction is present 5. Blood test • CBC - for anemia due to blood loss • WBC - detect
inflammation, infection and presence of tissue necrosis Investigation

 22. 1.) Antibiotic: cefoxitin - Ampicilin 2.) H2 receptor blocker: famotidine – ranitidine 3.)
PPI: lansoprazole - osomeprazole 4.) Antianxiety Agents: Dormicum 5.) Nonsteroidal Anti-
Inflammatory Drugs (NSAIDs): Ibuprofen Medical Pharmacology treatment

 23. 1.) Avoid food that cause acid reflux or heartburn such as spicy food 2.) Don’t lie down
or bend over after a meal 3.) Exercise 4.) stop smoking 5.) Avoid gassy drinks 6.) Avoid lift
heavy object Non-pharmacological management

 24. • Truss (Inguinal hernia) - a pad made with firm material that will held in place over the
hernia with belt to help keep the abdominal contents from protruding into the hernia sac
Non-Surgical Management Surgical Management Nissen fundoplication Laparoscopic (LEP)
Herniorrhaphy (hernia repairs)
  25. 1. Post herniarrhaphy pain syndrome/ inguinodynia 2. Hernia recurrence 3. Wound
Infection 4. Ischemia 5. Necrosis COMPLICATIONS

 26. 1. PRE-OPERATIVE FOR HERNIA REPAIR Fear and anxiety related to undergoing surgery
2. POST-OPERATIVE FOR HERNIA REPAIR Acute pain related to surgical intervention Risk of
infection related to surgical site 3. HIATAL HERNIA Risk for aspiration related to reflux of
gastric content NURSING DIAGNOSES

 27. Health Education 1.) Educate patient to assess for any signs and symptoms of infection
such as redness, severe itchyness and condition at the surgical site 2.) Advise patient come
for follow-up to monitor patient progress 3.) Educate patient to avoid wearing tight clothing
to minimize abdominal pressure 4.) Encourage patient avoid lifting heavy object or doing
heavy exercise at least 6 weeks 5.) Use proper lifting technique

 28. Health Education 6.) Lose weight 7.) Exercise regularly 8.) Advice patient to eat a
vitamin-rich diet such as vitamin C and protein to promote wound healing 9.) Encourage
patient to take high fiber food to prevent constipation

 29. Keep Calm and Watch for

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Management of anticancer toxicities

 1. TOXICITY OF ANTI CANCER DRUGS AND ITS AMELIORATION Dr. Jaya Dadhich Resident,
Department of Pharmacology SMS medical college, Jaipur

 2. Overview • Anticancer drug target • Toxicities caused by anticancer drugs • Management

of individual toxicity • Generalised approach • pharmacological intervention • Summary

 5. Toxicity of anticancer drugs Acute or in short term 1. Nausea and vomiting= CTZ or from
upper GIT impulses By cisplatin, decarbazine, lomustine, actinomycin D, all the alkylating
agents 2.Local toxicity

 6. 3. Toxicity due to effect on normal rapidly multiplying cells  Bone marrow depression 
Lymphoreticular tissue-immunosuppression  Platelets- thrombocytopenia  GIT-diarrhoea
and ulcers  Skin and hair follicles- alopecia  Wound healing-delayed  Gonads-
oligozoospermia

 7. DELAYED OR LONG TERM TOXICITY Carcinogenecity and mutagenecity Secondary

hyperuricemia Effect on foetus Effect on children

 8. Other toxicities 1.Peripheral neuropathy-vincristine, oxaliplatin 2.Cardiomyopathy-

doxorubicin,daunorubicin 3.Pnemonitis and pulmonary fibrosis-bleomycin, methotrexate
4.Dermatitis- procarbazine 5.CNS depression- mitotane 6.Renal damage-cisplatin,
streptozocin 7.Hemorrhagic cystitis- cyclophosphamide , ifosfamide 8.Stomatitis –
dactinomycin, 5-FU, Mtx
 10. Measures to reduce the toxicity 1. Pulse therapy Interval of some time eg 2 week 2.
Selective drug administration 3.Bone marrow transplantation 4. Supportive measures

 11. Agents 1. Folinic acid/leukovorin/citrovorum factor 2. Colony stimulating factor

neutopenia, sepsis, infection 3. Thiophosphate cytoprotectants Amifostine 4. Acrolein
conjugator Mesna and acetyl cystein 5. Iron chelator Dexrazoxane 6. Thrombopoietic factor
Oprelvekin, thrombopoietin

 12. Bone marrow suppression • Peripheral cytopenia from bone marrow suppression is a
frequent dose limiting side effect of chemotherapy and can manifest as acute and chronic
marrow damage. • Destruction of activity of proliferating haematopoietic precursor cells •
Deprivation of formed elements, and incidence of life threatening haemorrhage and
infection.

 14. Approach • Management varies from dose reduction to treatment for

neutropenic,sepsis. • Patient who develop grade 4 toxicity require hospitalisation, treatment
of infection or bleeding • Colony stimulating factors like erythropoietin, Darbopoietin alpha,
G-CSF, GM-CSF, various cytokines, platelet transfusion is given • Bone marrow
transplantation

 15. Anemia The symptoms associated with mild to moderate anaemia can negatively affect
the person’s normal functional ability and quality of life. A thorough laboratory investigation
is necessary to assess the cause of anaemia. The decision for transfusion should be based on
the patient’s symptom in concert with laboratory data.

 16. Anemia causing drugs • Cisplatine • Docetaxel • Altretamine • Cytarabine • Topotecan •

Paclitaxel

 17. Management • Management 1. Packed red cell transfusion 2. Erythropoietin, Epoetin

alpha 3. Darbopoietin.

 20. Neutropenia • Definition: Absolute neutrophil count < 500cell/mm3 and count
<1000cell/mm3 with a predicted decrease to 500cell/mm Four general principles to
minimise the risk of infection in patients with cancer. a) Augment the host defence
mechanism b) Preserving the natural barrier of defence c) Reducing the environmental
organisms d) Minimising endogenous micro flora.

 21. Infections and neutropenia • Prompt intervention of empirical chemotherapy is

essential in the management of neutropenia. • The choice of antibiotics is influenced by the
ever-changing environment, individual susceptibility, pattern and emergence of resistant
strains.

 22. Interventions to promote mechanical barrier integrity include 1. Avoidance of injections

whenever possible 2. Strategies to prevent skin breakdown 3. Avoidance of bladder
catheterisation 4. Daily baths , Perineal and rectal hygiene 5. Oral care after meals

 33. Thrombocytopenia • A moderate risk of bleeding exists when the platelet count falls to
less than 50,000cells/mm3 and major risk is associated with the platelet count falls to less
than 10,000cells/mm3. • Clinical manifestations include increased bruising, purpura,
petechiae, oozing from mucosal surface.
 37. Gastrointestinal toxicity • Anorexia, nausea and vomiting are frequently observed after
chemotherapy. • It is not a pathological process but rather a physiological process in which
the body attempts to rid itself of toxic substances

 38. Emetic potential Level 1 Frequency of emesis <10% Level 2 Frequency of emesis 10-30%
Level 3 Frequency of emesis 30- 60% Level 4 Frequency of emesis 60- 90% Carboplatin
Carmustine <250mg/m2 Level 5 Frequency of emesis >90% Carmustine>250mg/m2
Cisplatine>59mg/m2 Bleomycin Docetaxel Cyclophosphamide <750mg/m2 Busulfan
Etoposide Doxorubicin 20-60mg/m2 Hydroxyurea Gemcitabine Epirubicin Cisplatine
Cyclophosphamide <90mg/m2 <50mg/m2 >1500mg/m2 Vinblastine Vincristine
Methotrexate >50mg/m2 <250mg/m2 Idarubicin Cyclophosphamide >750mg/m2 <
1500mg/m2 Dacarbazine

 39. Class of antiemetics Drug Antihistamines Cinnarizine Benzodiazepines Lorazepeam

Anticholinergic drugs Hyoscine Dopamine inhibitors Phenothiazines Corticosteroids
Dexamethasone 5-HT3antagonists Ondansetron Prokinetic drugs Metoclopramide NK1
receptor antagonists Substance P antagonists

 40. Agents causing stomatitis Antimetabolites Methotrexate, 5-Flurouracil, Cytarabine,

Irinotecan Antitumor Doxorubicin, Dactinomycin, Mitomycin, Plant alkaloids Vincristine,
Vinblastine, Etoposide Others Alkylating agents in high doses Biologic agents Interleukins

 41. Agents for oral care • Cleansing agents Normal saline, hydrogen peroxide, sodium
bicarbonate, Chlorhexidin • Lubricating agents Saliva substitutes, water or oil base lubricants
• Analgesic agents • Healing & coating agents Sucralfate, Vitamine E, Antacids, Allopurinol •
Topical anaesthetics Lidocaine, Benzocaine, Diclomine hydrochloride • Systemic analgesics
NSAID, Narcotic analgesics

 42. Agents causing diarrhoea • Methotrexate • Paclitaxel • Cytarabine • Nitrosourea •

Irinotecan • Floxuridine

 43. Management • Management of treatment related diarrhoea is symptomatic and

requires little or no alteration in cancer therapy. • Pharmacological management is given 12
to 24 hours later if inadequate response or immediately if grade 3 or 4 diarrhoea begin. • It
includes agents like kaolin, pectin, loperamide, diphenoxylate hydrochloride, Octreotide

 44. Hair follicle toxicity by • Doxorubicine • Daunorubicine • Cyclophophamaide •

Vincristine • Paclitaxel • Etoposide • Methotrexate

 45. Management • Interventions start with informing and preparing the patient for the
possibility of alopecia. • Because of the concern for scalp metastasis and sanctuary sites,
scalp hypothermia is no longer recommended. • Studies have shown that the use of Imuvert
– a membrane vesicle ribosome preparation from a bacterium either partially or completely
reverse the alopecia caused by the chemotherapeutic agents

 46. Neurotoxicity 1. Acute myelopathy Intrathecal cytarabine Intrathecal methotrexate

Intrathecal thiotepa 2. Cerebellar syndrome Cytarabine Procarbazine 5-Flurouracil 3.
Autonomic neuropathy Cisplatin Vindesine Paclitaxel Vinblastine Procarbazine Vincristine 4.
Cranial nerve toxicity Vindesine Carmustine Vinblastine Cisplatin Vincristine Ifosamide 5.
Encephalopathy Carmustine Cytarabine Procarbazine 5-Flurouracil Cisplatin Ifosamide 6.
Peripheral Neuropathy Vincristine Carboplatin Vinblastine Procarbazine Vindesin Paclitaxel
  47. • Early detection and treatment of neurotoxicity by reduction of drug dose or
discontinuation prevents permanent neurological damage • Assessment of symptoms of
neurotoxicity should be documented on a routine basis. • Tricyclic antidepressant,
anticonvulsant, high dose vitamins are used in drug therapy. • Management by a
cytoprotectant like Amifostine is promising

 48. Hepatotoxicty • Cyclophosphamide • Streptozocin • 5-Flurouracil • Methotrexate • 6-

Mercaptopurine • Doxorubicin

 49. • Depending on the condition of patient discontinuation of drugs, • reduction in dose or

• intermittent therapy is done other than supportive management. • Defibrotide can reverse
the venoocclusive disease of liver caused by all drugs at high doses except cisplatin.

 50. Renal toxicity by • Cisplatin • Ifosamide • Mitomycin • Plicamycin

 51. Renal toxicity • Assess the renal function and evaluate the risk factors before initiating
therapy. Plasma concentration of blood urea nitrogen and creatinine are common
assessment parameters. 24 hour collection of urine for creatinine clearance is recommended
to monitor patients and alter drug doses to prevent or minimize renal toxicity.34
Thiophosphate Cytoprotectants like Amifostine can counteract cisplatin induced
nephrotoxicit

 52. Pulmonary toxicity • Acute pneumonitis Bleomycin Vinca alkaloids Methotrexate

Procarbazine Carmustine Mitomycin • Pulmonary fibrosis Bleomycin • Hypersensitivity
pneumonitis Procarbazine Azathioprine Bleomycin Methotrexate • Non cardiogenic
pulmonary edema Cyclophosphamide Methotrexate Cytarabin Mitomycin

 53. Management • It includes discontinuation of the drug and administration of

corticosteroids and supportive care.

 54. Cardiac toxicity • Cardiomyopathy is the most common chemotherapy associated

cardiac toxicity and is thought to be due to free radical mediated injury • The anthracyclines
have the highest risk for cardiomyopathy which is cumulative dose response related. • The
primary management strategy of Anthracycline cardiac toxicity is prevention and early
detection. Use of cardioprotectant iron chelator, Dexrazoxane represents the primary
prevention approach

 55. conclusion

 58. Treatment option MOA Toxicity by Dose Leucovorin Mtx Allopurinol XaOi Filgrastim
Sargramostine CSF -neutrophils Neutropenia Darbopoetin Erythropoetin CSF- RBC Anemia
Amifostin Thiophos cytoprotctor Cisplatin induced nephrotoxicity Acetyl cysteine Mesna
Acrolein conjugator (trap) Cyclophosphamide Dexrazoxane Iron chelator(free radical injury
minimised) Cisplatin Oprelvekin Thrombopoietin thrompoietic factor Thrombocytopenia

Editor's Notes

 #5: 4

Unit No 4- Chemotherapy of Malignancy.pptx

 1. TOPIC WISE PRESENTATION Pharmacology-III (SEM VI) Prepared by Ashish N. Umale M.
PHARM IN PHARMACOLOGY ASSISTANT PROFESSOR SHRADDHA INSTITUTE OF
PHARMACY, WASHIM-444505
 2. • Cancer is a disease of cells characterized by Progressive, Persistent, Perverted (abnormal),
Purposeless and uncontrolled Proliferation of tissues. • Lungs cancer, prostate cancer, stomach
& colon is the most common cancer in men. • Breast cancer, Ovary cancer is most common
cancer in women. • Types of cancer 1. Carcinomas:- A carcinoma begins in the skin or the tissue
that covers the surface of internal organs and glands. 2. Sarcomas:- A sarcoma begins in the
tissues that support and connect the body. 3. Leukemia's:- Leukemia is a cancer of the blood. 4.
Lymphomas:- Lymphoma is a cancer that begins in the lymphatic system. 5. Multiple myeloma:-
It is a cancer that forms in a type of WBCcalled a plasma cell. 6. Melanoma :- It is a form of skin
cancer that begins in the cells (melanocytes) that control the pigment in your skin.
 3. CELL CYCLE OF ANTINEOPLASTIC AGENTS (1) G phase (Pre-synthetic phase) - ₁ During
which the cell determines its readiness to commit to DNA synthesis. (2) S phase (Synthesis
phase) - Involving DNA synthesis takes place. (3) G2 Phase (Post-synthetic) phase - during
which the accuracy of DNA replication is determined, and errors are corrected; (4) M Phase
(Mitotic Phase) - Mitotic cell division take place. during which the replicated chromosomes are
separated into two nuclei for the two daughter G, cells. These cell s may re-enter the cycle or
pass into the resting phase. (5 ) Go Phase (Resting Phase) - Cell stop dividing temporarily or
permanently., non proliferative
 4. In the cancer cell, the cell cycle control is disrupted by: 1. Abnormal growth factor function.
2. Abnormal DNA synthesis 2. 3 . Abnormal CDK function (Cyclin-dependent kinases) 4.
Abnormal decreases in negative regulatory forces due to mutation in the tumours suppressor
gene.  General toxicity of cytotoxic drugs  i. Bone marrow suppression ii. Loss of hair iii.
Damage to GI mucosa and ulceration  iv. Impaired wound healing v. Damage to gonads vi.
Growth inhibition in children
 7. Alkylating agents • These compounds produce highly reactive carbonium ion intermediates
which transfer alkyl groups to cellular macromolecules by forming covalent bonds. • The position
7 of guanine residues in DNA is especially susceptible. • Alkylating agents may react with
carboxyl, hydroxyl, amino, sulfhydryl and phosphate groups of bio macromolecules. • Alkylating
agents can also bind to proteins and damage them. • Mechanism of action Alkylating agents
(except platinum containing compounds) Form highly reactive carbonium ion Transfer of 'alkyl'
group(s) to various sites on DNA Results in • Cross-linkage (inhibits DNA replication). • Abnormal
base pairing (alkylated guanine base pairs with thymine rather than cytosine and results in
production of defective protein).
 8. Cyclophosphamide • Cyclophosphamide is a prodrug converted to the active metabolite
aldophosphamide in the liver • Mechanism of action • Aldophosphamide is in turn converted to
phosphoramide mustard and acrolein. • Phosphoramide is thought to be responsible for cytotoxic
activity while acrolein causes adverse effects. • Pharmacokinetics • Cyclophosphamide is well
absorbed on oral administration with high bioavailability. • It can be given orally or IV.
 9. • Adverse effect • Cyclophosphamide causes cystitis due to a metabolite acrolein. •
cyclophosphamide is severe hemorrhagic cystitis. • It is associated with dysuria and haematuria
due to irritation of bladder mucosa by acrolein. • It is dose-limiting toxicity and can be reduced by
adequate hydration and co-administration of I.V. mesna (2-mercapto-ethane-sulphonate). •
Mesna is also excreted in urine where it binds and inactivates acrolein, thus preventing
hemorrhagic cystitis. • Uses • Cyclophosphamide is a commonly used alkylating agent. • It also
has immunosuppressant properties. • It is useful in the treatment of testicular cancer and
sarcomas.
 10. Procarbazine (Methyl hydrazine) • It is not a classical alkylating agent, but has similar
properties. • After metabolic activation (it is inactive as such), Procarbazine methylates and
depolymerizes DNA causing chromosomal damage. • Inhibition of nucleic acid synthesis also
occurs. • Because of damage to DNA, mutagenic and carcinogenic potential has been detected.
• It is a component of combination regimens for Hodgkin's and lymphomas, and is an alternative
drug for brain tumours. • Procarbazine is a weak MAO inhibitor; produces sedation and other
CNS effects, and can interact with foods and drugs. • Alcohol causes hot flushing and a
disulfiram-like reaction in patients taking Procarbazine. • Males may suffer sterility. • Vomiting,
leucopenia, thrombocytopenia are the prominent toxicities
 11. Cisplatin • Mechanism of action Cisplatin Forms highly reactive platinum complexes.
Reacts with DNA(Forms both intrastrand and interstrand cross-links) DNA damage. •
Pharmacokinetics • Cisplatin is administered intravenously. • It is highly bound to plasma proteins
and gets concentrated in kidney, liver, intestines and testes. • It poorly penetrates BBB and is
slowly excreted in urine. • Adverse effects • Nephrotoxicity, Ototoxicity, Neuropathy, Anaphylactic
shock, mutagenic, teratogenic and carcinogenic • Uses • i. Cisplatin is highly effective in the
treatment of testicular, ovarian, endometrial and bladder cancer. • ii. It is also used in lung and
oesophageal cancer. • iii. Cisplatin is the most emetogenic anticancer drug.
 12. Methotrexate (MTX) • Methotrexate is one of the most commonly used anticancer drugs. •
It is a cell cycle specific (CCS) drug and acts during S phase of the cell cycle. • It has
antineoplastic, immunosuppressant and anti inflammatory effects • Methotrexate (MTX) is a folic
acid antagonist. • Mechanism of action • Methotrexate structurally resembles folic acid. • It
competitively inhibits dihydrofolate reductase enzyme and prevents the conversion of DHFA to
THFA, thus depleting the intracellular THFA. • Tetrahydrofolic acid is necessary for the synthesis
of purines and thymidylate, which, in turn, are necessary for DNA and RNA synthesis •
Pharmacokinetics • Methotrexate is well absorbed after oral administration and can also be given
I.M., I.V. • Bound to plasma proteins, poorly crosses the BBB, and the drug is excreted
unchanged in urine • Side effects:- Mucositis, Bleeding, Alopecia, Impaired wound healing etc.
 13. Purine Antagonist • Mechanism of action of purines • Purine analogs enter the cells and
get converted to active metabolites (triphosphates in most compounds) which are incorporated
into DNA in place of regular purines. • They cause breakages in DNA strands and inhibit protein
synthesis.  6-Mercaptopurine (6-MP) & 6-Thioguanine (6-TG) • Mechanism of action • 6-MP and
6-TG are activated to their ribonucleotides, which inhibit purine ring biosynthesis and nucleotide
inter conversion. • They are CCS drugs that act in S phase of cell cycle. • 6-MP also has
immunosuppressant action. • Allopurinol interferes with the metabolism of 6-MP by inhibiting the
enzyme xanthine oxidase and increases the antineoplastic effect of 6-MP.
 14. • Adverse effect • Bone marrow depression • Mucositis • Gut damage • Nausea • Vomiting •
Uses • Allopurinol is frequently used in cancer patients receiving chemotherapy to prevent
hyperuricaemia and to reduce the dose of 6-MP, thus reducing its toxicity. • 6-mp is used mainly
in acute lymphocytic leukaemia.ii. Azathioprine
 15. 5-Fluorouracil • Pyrimidine analogue sused in antineoplastic, antifungal and anti psoriatic
agents. • Mechanism of action • 5-Fluorouracil (5-FU) is a pyrimidine analog. • It is activated to a
nucleotide metabolite which inhibits the enzyme thymidylate synthetase. • Due to this, it inhibits
the synthesis of thymine and thereby inhibits DNA synthesis • The active metabolites of 5-FU are
also incorporated into DNA and RNA leading to inhibition of DNA and RNA synthesis •
Pharmacokinetics • 5-FU is given intravenously and has a short t½ of 10-20 min. • Metabolised
by an enzyme called dihydropyrimidine dehydrogenase (DPD). • Adverse effect:- Bone marrow
suppression, Mucositis, diarrhoea, nausea, vomiting. • Uses:- As anticancer drug especially of
colon, rectum, pancreas, liver, urinary bladder.
 16. Paclitaxel • It is a complex diterpin taxane obtained from bark of the Western yew tree •
Mechanism of action • Paclitaxel Binds to -tubulin ẞ Stabilizes microtubules Formation of
abnormal microtubules Inhibits mitosis • Pharmacokinetics:- Paclitaxel is administered by I.V.
infusion. • Adverse effect:- Bone marrow suppression, Peripheral neuropathy, hypersensitivity
reactions etc. • Uses:- It is useful in advanced breast, ovarian, lung, oesophageal and bladder
cancer.
 17. Actinomycin D • Actinomycin D is obtained from the fungus of Streptomyces species. • It
binds to DNA and forms a complex. • It inhibits DNA-dependent RNA synthesis and also causes
breaks in the DNA. • It is one of the most potent anticancer drugs. • Pharmacokinetics • It is given
by intravenous injection. • Uses • It is used in Wilms' tumour, and some soft tissue sarcomas. • It
is also used in Kaposi's sarcoma and Ewing's tumour. • Dactinomycin is also an
immunosuppressant and is used in renal transplants. • Adverse effect:- Erythema, Nausea,
Vomiting, Alopecia
 18. • These drugs are primarily of two types: • Specific monoclonal antibodies that need to be
given parenterally and attack cell surface targets or tumour antigens. • Synthetic small molecular
compounds, given orally, which penetrate cells and affect cancer specific enzymes or pathways
Imatinib • Mechanism of action • Imatinib inhibits a specific tyrosine protein kinase labelled
'BCR-ABL' tyrosine kinase expressed by chronic myeloid leukaemia (CML) cells and related
 receptor tyrosine kinases. • Platelet derived growth factor (PDGF) receptor that is constitutively
active in derma to fibrosarcoma protuberans, stem cell receptor and c-kit receptor active in
gastrointestinal stromal a rare tumour. • BCR-ABL tyrosine kinase is responsible for uncontrolled
cell division in tumours. Targeted Drugs
 19. • Pharmacokinetics • Imatinib is well absorbed orally, Metabolized in liver & excreted in
faeces through bile • The major degrading enzyme is CYP3A4, and potential interactions can
occur with inducers and inhibitors of this isoenzyme. • Adverse effects:- Abdominal
pain,Vomiting, fluid retention, myalgia, liver damage and CHF. Gefitinib • Mechanism of action •
Gefitinib is a synthetic compound that penetrates cells, binds to the tyrosine kinase domain of the
EGF receptor and prevents phosphorylation of regulatory proteins. • Gefitinib and Erlotinib inhibit
epidermal growth factor receptor (EGFR) tyrosine kinase • Pharmacokinetics • Oral bioavailability
of gefitinib is 60%. • It is primarily metabolized by CYP3A4 with t½ of ~ 40 hours
 20. Sunitinib & Sorafenib • Mechanism of action • Small molecular synthetic VEGF receptor-2
inhibitor, which enters cells and competitively blocks ATP binding to the tyrosine kinase domain,
thereby Preventing phosphorylation of angiogenic regulatory proteins. • Sunitinib inhibits multiple
receptor tyrosine kinases like platelet derived growth factor (PDGF) receptor a and , c-kit, ret,
etcSunitinib and sorafinib are tyrosine ẞ kinase inhibitors. • Pharmacokinetics • Sunitinib is
administered orally. • It is metabolized by CYP3A4 and t½ is ~100 hours. • Uses:- It is used in
metastatic renal cell carcinoma and imatinib resistant G.I. stromal tumour • Adverse effects :-
Hypertension, rashes, diarrhoea, fatigue, weakness, bleeding.
 21. Bortezomib • Bortezomib binds with high affinity to 26S proteosome and inhibits it,
promotes programmed cell death in neoplastic cells. • Adverse effect:-Peripheral neuropathy,
Thrombocytopenia, Bone marrow suppression • Uses:- Bortezomib is used in refractory multiple
myeloma. Rituximabi • Rituximab target antigen on the B cells causing lysis of these cells. • It
targets the CD20 antigen on B cell and is found to be effective in cell ẞ lymphomas. • Adverse
effects:- Chills, Fever, Pruritus, Dyspnoea and hypotension • Uses:- i. Rituximab is also being
used in some autoimmune diseases ii. It is indicated in -cell lymphoma, non-Hodgkin lymphoma
and chronic ẞ lymphocytic leukaemia,
 22. Prednisolone • It is 4 times more potent than hydrocortisone, also more selective
glucocorticoid, but fluid retention does occur with high doses. • It has intermediate duration of
action: causes less pituitary-adrenal suppression • Uses:- Used for allergic, inflammatory,
autoimmune diseases and in malignancies lymphocytic action and are primarily used in acute
childhood leukaemia and lymphomas. • Adverse effect:- Hypercalcaemia, Bleeding due to
thrombocytopenia, etc 2. Estrogens • They produce symptomatic relief in carcinoma prostate •
Estrogens have been superseded in carcinoma prostate by GnRH agonists used with an anti
androgen. • Physiological antagonists of androgens • It is used to antagonize the effects of
androgens in androgen dependent prostatic cancer Hormonal drugs
 23. Ethnyl estradiol • Estradiol is a major regulator of growth for the subset of breast cancers
that express the estrogen receptor (ER, ESR1). • Strategies to block ER action, via reduction of
estradiol or direct inhibition of ER, have shown major success in the prevention and treatment of
breast cancer. Tamoxifen • Non steroidal anti estrogen • Antagonistic: Breast and blood vessels
• Agonistic: Uterus, bone, liver, pitutary • Standard hormonal treatment in breast cancer •
Adverse effects:- vomiting, vaginal bleeding, menstrual irregularities, dermatitis etc. • DOSE: 10-
20mg BD
 24. Flutamide and Bicalutamide • Both drugs antagonise androgen action on prostate
carcinoma cells and have palliative effect in advanced cases. • Because they increase androgen
secretion by antagonizing androgenic action in pituitary, combination with GnRH analogues is
required to produce full therapeutic effect • Mechanism of action • Non-steroidal anti-androgen
inhibits cellular uptake of androgen steroids and inhibits nuclear binding of androgens to their
receptors - adrenal. • Used with (GnRH) agonists, photosensitivity, inform patients of urine color
changes. • Pharmacokinetics • Hepatic metabolism with renal excretion & 96% protein bound. •
Uses :- It is use in combo treatment with surgical castration for metastatic carcinoma of the
prostate.
 25.  Finasteride, Dutasteride • Finasteride and dutasteride inhibit conversion of testosterone to
dihydrotestosterone in prostate (and other tissues), have palliative effect in advanced carcinoma
prostate; occasionally used. • It is orally act & Decrease Symptom score • Dose: 5mg/day •
Uses:- Also used for prevention of hair loss GnRH analogues • They indirectly inhibit
 estrogen/androgen secretion by suppressing FSH and LH release from pituitary and have
palliative effect in advanced estrogen/androgen dependent carcinoma of breast and prostate. •
They are generally used in combination with antiandrogens or SERMS. • Naferelin • Present in
Nasal spray / SC inj also decrease FSH & LH release from pituitary and suppress the release of
estrogen & testosterone • Uses:- Breast Cancer & Prostatic Cancer
 26. Hydroxyprogesterone acetate • They bring about temporary remission in advanced or
recurrent in surgery/radiotherapy and endometrial carcinoma. • High doses are needed. • Uses:-
used in palliatibe treatment of metastatic carcinoma breast. • Adverse effect:- Bleeding
Sulvestrant • Mechanism of action • Inhibits ER dimerization & prevents interaction of ER with
DNA • ER is down regulated resulting in more complete supression of ER responsive gene
function • Pure estrogen antagonist • Uses:- Metastatic ER+ Breast Cancer in postmenopausal
women
 27.  TREATMENT OF CANCERS • Chemotherapy in most cancers (except curable cancers) is
generally palliative and suppressive. • Because of the ability of cancers for recurrence, i.e. even
if a few cells are spared during treatment, these cells can multiply and result in recurrence and
regrowth of a tumour of earlier dimensions. • To avoid this, it is essential to kill all the cancer cells
during treatment-to achieve what is known as 'total cell kill'. • Chemotherapy is just one of the
modes in the treatment of cancer. • Other modes like radiotherapy and surgery are also
employed to ensure 'total cell kill'.  Combination of drugs is preferred for: i. Synergistic effect ii.
Reduced adverse effects iii. To prevent rapid development of resistance

Chemotherapy and rdiotherapy by heena mehta

 1. MEDICAL SURGICAL NURING PRESENTED BY MRS HEENA MEHTA S.Y.M.SC NURSING
IVALUATION BY MR.P.YONATANSIR ASSOCIATE PROFESSER J G NURSING COLLEGE
 4. • INTRODUCTION OF CHEMOTHERAPY • The use of chemicals to treat cancer first began in
the early 1940.The modern chemotherapy begun in 1948 with introduction of nitrogen mustard.
Since that time Scientiests continued to search for medication to treat neoplasm. • , such as a
virus or other microorganism.
 5. • DEFINITION OF CHEMOTHERAPY • The treatment of cancer using specific chemical
agents ordrugs that are selectively destructive to malignant cells andtissues. • The treatment of
disease using chemical agents or drugsthat are selectively toxic to the causative agent of
thedisease, s uch as a virus or other microorganism.
 6. OBLECTIVES OF THECHEMOTHERAPY • *The main objective in treating patients with
chemotherapy is • to maximize the death of malignant tumor cells. • * To cure the client with
cancer. • * To control the tumor growth when cure is not possible. • *To extend the lifespan and
improve the quality of life of client with cancer.
 7. HOW CHEMOTHERAPY WORKS • it is helpful to understand the normal life cycle of a cell, or
the cell cycle. • All living tissue is made up of cells. Cells grow and reproduce to replace cells lost
through injury or normal “wear and tear.”
 8. • The cell cycle is a series of steps that both normal cells and cancer cells go through in order
to form new cells. • This discussion is somewhat technical, but it can help you understand how
doctors predict which drugs are likely to work well together and how doctors decide how often
doses of each drug should be given
 9. • The cell cycle has 5 phases which are labeled below using letters and numbers. Since cell
reproduction happens over and over, the cell cycle is shown as a circle. All the steps lead back to
the resting phase (G0), which is the starting point. • After a cell reproduces, the 2 new cells are
identical. Each of the 2 cells made from the first cell can go through this cell cycle again when
new cells are needed.
 11. • The Cell Cycle • G0 phase (resting stage): The cell has not yet started to divide. Cells
spend much of their lives in this phase. Depending on the type of cell, G0 can last from a few
hours to a few years. When the cell gets a signal to reproduce, it moves into the G1 phase. • G1
phase: During this phase, the cell starts making more proteins and growing larger, so the new
cells will be of normal size. This phase lasts about 18 to 30
 12. • S phase: In the S phase, the chromosomes containing the genetic code (DNA) are copied
so that both of the new cells formed will have matching strands of DNA. The S phase lasts about
 18 to 20 hours. • G2 phase: In the G2 phase, the cell checks the DNA and gets ready to start
splitting into 2 cells. This phase lasts from 2 to 10 hours
 13. • M phase (mitosis): In this phase, which lasts only 30 to 60 minutes, the cell actually splits
into 2 new cells. • This cell cycle is important because many chemotherapy drugs work only on
cells that are actively reproducing (not cells that are in the resting phase, G0). Some drugs
specifically attack cells in a particular phase of the cell cycle (the M or S phases, for example.
 14. CHEMOTHERAPY DRUGS
 15. • Chemotherapy drugs act through a variety of mechanism but, essentially, kill cells by: •
Limiting DNA synthesis and expression- By interfering with synthesis of buiding blocks for nucleic
acid.
 16. • Cross- linking polymer DNA-Damaging the DNA template and cross-link the twostands of
the double helix , preventing replication.
 17. • DNA double stand breaks- Bind selectively with DNA, producing complexes that block DNA
replication andformation of DNA dependent RNA. • Preventing formation of mitotic apparatus-
Prevent chromosome segregation at mitosisby producing metaphase arrest.
 18. CLASSIFICATION OF CHEMOTHERAAPY • Chemotherapeutics agents are broadly
classified as: • Cell cycle-specific Drugs: Those chemotherapeutic agents that destroy cells in
specific phases of the cell cycle . Most affect cells in the S-phase by interfering with DNA and
RNA synthesis.
 19. • Cell cyle non specific Drugs: • Those chemotherapeutic agents that act independently of
the cell cycle phase are termed cell cycle non- specific drugs. These drugs usually have a
prolonged effect on cell , leading to cellular damage or death.
 20. • Chemotherapeutic agents also classifiedaccording tovarious chemical groups eachwith a
different mechanism of action. These include
 21. 1-Alkylating agents- • Alkylating agents are so named because of their ability to alkylate
many nucleophilic functional groups under conditions present in cells. They impair cell function
by forming covalent bonds with the amino, carboxyl, sulfhydryl, and phosphate groups in
biologically important molecules. • Cisplatin and carboplatin, as well as oxaliplatin, is alkylating
agents.
 22. Polyfunctional Alkylating Drugs: Mechanism of Action • Alkyl group transfer –Major
interaction: Alkylation of DNA • Primary DNA alkylation site: N7 position of guanine • interaction
may involve single strands or both strands .
 23. –Other interactions: these drugs react with carboxyl, sulfhydryl, amino, hydroxyl, and
phosphate groups of other cellular constituents –These drugs usually form a reactive
intermediate – ethylene ammonium ion.
 24. • Polyfunctional Alkylating Drug Resistance -Increased ability to repair DNA defects -
Decreased cellular permeability to the drug -Increased glutathione synthesis
 25. • Injection site damage (vesicant effects) and systemic toxicity. • Toxicity: – dose related –
primarily affecting rapidly dividing cells • bone marrow • GI tract –nausea and vomiting within less
than an hour-- with mechlorethamine, carmustine (BCNU) or cyclophosphamide
 26. –Emetic effects: CNS »reduced by pre- treatment with phenothiazines or cannabinoids.
•gonads
 27. – Major Toxicity: bone marrow suppression • dose-related suppression of myelopoiesis:
primary effects on –megakaryocytes –platelets –granulocytes • Bone marrow suppression is
worse when alkylating agents are combined with other myelosuppressive drugs and/or radiation
(dose reduction required)
 28. • Oral Route of Administration:cycloph osphamide (Cytoxan), melphalan (Alkeran),
chlorambucil (Leukeran), busulfan (Myleran), lomustine (CCNU,CeeNU)
 29. • Nitrosoureas: – not cross reactive ( with respect to tumor resistance) with other alkylating
drugs. –Nonenzymatic by transformation required to activate compounds. –Highly lipid- soluble--
crosses the blood-brain barrier (BBB)
 30. • useful in treating brain tumors –Act by cross-linking: DNA alkylation –More effective
against cells in plateau phase than cells in exponential growth phase –Major route of
elimination:urinary excretion –Steptozocin: • sugar-containing nitrosourea
 31. Other Alkylating Drugs • Procarbazine (Matulane) – Methylhydrazine derivative – Active in
Hodgkin's disease (combination therapy) – Teratogenic, mutagenic, leukemogenic. – Side
effects: • nausea, vomiting, myelosuppression • hemolytic anemia • pulmonary effects
 32. • Dacarbazine (DTIC) –Clinical use: • Melanoma • Hodgkin's disease • soft tissue sarcoma –
Synthetic drug; requires activation by liver microsomal system. • Parenteral administration
 33. – Side effects: • nausea, vomiting, myelosuppression • Altretamine (Hexalen) – Clinical use:
• alkylating agent-resistant: ovarian carcinoma – Activated by biotransformation (demethylation)
– Side effects: • nausea, vomiting, central and peripheral nervous system neuropathies. •
relatively mild myelosuppressive effects.
 34. • Cisplatin (Platinol) – Clinical use: • Genitourinary cancers –testicular –ovarian –bladder •
In combination with bleomycin and vinblastine: curative treatment for nonseminomatous
testicular cancer
 35. Alkylating Agent Toxicity: Summary • IV mechlorethamine, cyclophosphamide, carmustine:
Nausea and Vomiting (common) • Oral cyclophosphamide: Nausea and Vomiting (less
frequently) • Most Important Toxic Effect:Bone marrow suppression, leukopenia,
thrombocytopenia
 36. –secondary to myelosuppression -- • severe infection • septicemia –hemorrhage •
Cyclophosphamide (Cytoxan):alopecia, hemorrhagic cystitis (may be avoided by adequate
hydration)
 37. 2- Anti-metabolites – • Anti-metabolites masquerade as purines ((azathioprine,
mercaptopurine)) or pyrimidines—which become the building blocks of DNA. They prevent these
substances from becoming incorporated in to DNA during the "S" phase (of the cell cycle),
stopping normal development and division. They also affect RNA synthesis. Due to their
efficiency, these drugs are the most widely used cytostatics
 38. -Tumor resistance to methotrexate: • decreased drug transport into the cell • altered
dihydrofolate reductase enzyme -- lower affinity for methotrexate • decreased polyglutamate
formation • quantitative increase in dihydrofolate reductase enzyme concentration in the cell
(gene amplification, increased message)
 39. – Adverse effects: • Bone marrow suppression • Dermatologic • GI mucosa • Adverse
effects reversed by leucovorin (citrovorum factor) –Leucovorin "rescue" may be used in cases of
over dosage or in high- dose methotrexate protocols – Other uses: • Treatment of rheumatoid
arthritis • In combination with a prostaglandin: induces abortion
 40. • Purine Antagonists – 6-Thiopurines (Mercaptopurine [6-MP]; Thioguanine [6-TG]) –
Mercaptopurine (Purinethol) • Mechanism of Action:Activation by hypoxanthine-guanine
phosphoribosyl transferase (HGPRT) to form 6-thioinosinic acid which inhibits enzymes involved
in purine metabolism. (thioguanylic acid and 6- methylmercaptopurine ribotide (MMPR) also
active) • Clinical Use: – childhood acute leukemia – the analog, azathioprine (Imuran)--
immunosuppressive agent.
 41. – Thioguanine • purine nucleotide pathway enzyme-inhibitor – decreased intracellular
concentration of guanine nucleotides – inhibition of glycoprotein synthesis – Mechanism of
Action: inhibits DNA/RNA synthesis • Clinical Use: – Synergistic with cytarabine in treating adult
acute leukemia. – Drug resistance • Decreased HGPRT activity • In acute leukemia -- increased
alkaline phosphatase, which dephosphorylates thiopurines nucleotides
 42. – Adverse Effects: • Both mercaptopurine and thioguanine, given orally, are excreted in the
urine. – 6-MP is converted to an inactive metabolite, 6-thioruric acid, by xanthine oxidase .6-TG:
requires deamination before metabolism by xanthine oxidase. – In cancer (hematologic)
chemotherapy, allopurinol is used to inhibit xanthine oxidase, to prevent hyperuricemia
associated with tumor cell lysis {xanthine oxidase inhibition blocks purine degradation -- purines
(more soluble) are excreted instead of uric acid (less soluble)}
 43. use of allopurinol thus blocks acute gout and nephrotoxicity. However, the combination of
allopurinol and 6- mercaptopurine, because of xanthine oxidase inhibition, can lead to
mercaptopurine toxicity; This interaction does not occur with 6-TG.
 44. -Fludarabine phosphate • parenteral administration; renal excretion • dephosphorylated to
active form: • Mechanism of Action:DNA synthesis inhibition • Clinical Use: –lymphoproliferative
disease • Adverse Effect:dose-limiting -- myelosuppression.
 45. – Cladribine: (Leustatin) • phosphorylated by deoxycytidine kinase –incorporated into DNA
–Mechanism of Action: increased strand breaks (inhibition of repair mechanisms) • Clinical Use:
–Hairy cell leukemia • Adverse Effects: –Transient severe myelosuppression; possibly
associated with infection.
 46. – Pentostatin: • irreversible inhibitor adenosine deaminase – results in toxic accumulation of
deoxyadenosine nucleotides (especially in lymphocytes) • Adverse Effects: –
immunosuppression (T cell mediated immunity) – myelosuppression – kidney function
impairment – CNS toxicity – liver toxicity • Pyrimidine Antagonists: – Flurouracil (5-FU), normally
given by IV administration (oral absorption erratic)
 47. • Biotransformed to ribosyl- and deoxyribosyl- derivatives. – Mechanism of Action: » One
derivative, 5-fluoro-2'-deoxyuridine 5'- phosphate (FdUMP), inhibits thymidylate synthase and its
cofactor,a tetrahydrofolate derivative, resulting in inhibition of thymidine nucleotide synthesis. »
Another derivative, 5-fluorouridine triphosphate is incorporated into RNA, interfering with RNA
function. » Cytotoxicity:effects on both RNA and DNA • Clinical Use: Systemically --
adenocarcinomas; Topically: skin cancer • Floxuridine (FUDR): similar to 5-FU, used for hepatic
artery infusion. •
 48. • Major Toxicity: myelosuppression, mucositis – Cytarabine (ara-C) IV administration •
Mechanism of Action:S phase-specific antimetabolite – Biotransformed to active forms: ara-CTP,
competitive inhibitor of DNA polymerase. » Blocks DNA synthesis; no effect on RNA or protein
synthesis – cytarabine incorporated into RNA and DNA -- interfering with chain elongation
 49. • Clearance: deamination (inactive form) • S phase specificity: highly schedule-dependent •
Clinical Use: almost exclusively for acute myelogenous leukemia • Adverse Effects: –nausea –
alopecia –stomatitis – severe myelosuppression
 50. – Azacitidine (IV administration): • Mechanism of Action: active derivatives inhibit orotidylate
decarboxylase -- reducing pyrimidine nucleotide synthesis; azacitidine -- incorporated into DNA
and RNA; inhibits DNA, RNA, and protein synthesis. • Investigational drug -- second-line agent in
treatment of acute leukemia • Adverse Effect: myelosuppression.
 51. 3- Plant alkaloids and terpenoids . • hese alkaloids are derived from plants and block cell
division by preventing microtubule function. Microtubules are vital for cell division, and, without
them, cell division cannot occur. The main examples are vinca alkaloids and taxanes.
 52. • Vinblastine -- (Velban) – Mechanism of action: microtubule depolymerization • Mitotic
arrest at metaphase; interferes with chromosome segregation – Clinical Use:: • Systemic
treatment of Hodgkin's disease • Lymphomas – Adverse Effects: • nausea • vomiting • alopecia •
bone marrow suppression
 53. • Vincristine -- (Oncovin) – Mechanism of action: microtubule depolymerization • Mitotic
arrest at metaphase; interferes with chromosome segregation – Clinical Use:: • In combination
with prednisone: induction of remission in children with acute leukemia • useful in treating some
other rapidly proliferating neoplasms – Adverse Effects: • significant frequency of neurotoxic
reactions • occasional: bone marrow depression
 54. • Podophyllotoxins (etoposide {VP- 16}and teniposide {VM-26}) – Etoposide and
teniposide: structurally similar –Mechanism of action: Block cell cycle: in late S-G2 phase •
inhibition of topoisomerase II -- DNA damage –IV administration –Urinary excretion; some in bile
 55. – Clinical Use: • Etoposide (VP-16,VePe-sid): –monocytic leukemia –testicular cancer –oat
cell lung carcinoma • Teniposide (Vumon): lymphomas – Adverse Effects: • nausea • vomiting •
alopecia • significant hematopoietic toxicity and lymphoid toxicity
 56. • Camptothecins (topotecan and irinotecan ) – Mechanism of action: interfere with activity
of topoisomerase I (cuts and religates single stranded DNA. DNA is damaged – Clinical Uses: •
Topotecan: metastatic ovarian cancer -- including cisplatin-resistant forms (as effective as
paclitaxel) • Adverse Effects: Topotecan -- –Primary »neutropenia »thrombocytopenia »anemia
 57. –Other »nausea »nominee »alopecia • Irinotecan:prodrug-metabolized active topoisomerase
I inhibitor –Used in management of colon and rectal cancer, including tumors not responding to
5-FU –Adverse Effects: Irinotecan -- »Most common: diarrhea »also common: nausea, vomiting •
Dose limiting adverse effect: myelosuppression
 58. • Taxanes (Paclitaxel (Taxol) and Docetaxel (Taxotere)) –Paclitaxel (Taxol): derivative of the
Western Yew –Mitotic spindle inhibitor: enhances tubulin polymerization –Clinical Uses: •
Ovarian • Advanced breast cancer
 59. –Dose-limiting Adverse Effects: •neutropenia •thrombocytopenia •peripheral neuropathy –
Docetaxel (Taxotere):Used in advanced breast cancer •Adverse Effects:bone marrow
suppression
 60. 4- Topoisomerase inhibitors- • Topoisomerases are enzymes our cells use to break the
DNA bonds before copying and repair of breaks after copying. Topoisomerase inhibitors interfere
 with DNA repair causing the cancer cell to die because damaged DNA cannot be translated into
proteins, such as transport and digestive proteins
 61. • Topoisomerase inhibitors are cell cycle specific, that is, they only kill cells that are in a
particular phase of cell division and generally do not have any effect on other cells. Examples of
Topoisomerase inhibitors are Etoposide and Topotecan.
 62. • Topoisomerase inhibitors are agents designed to interfere with the action of
topoisomerase enzymes (topoisomeras e I and II), which are enzymes that control the changes
in DNA structureby catalyzing the breaking and rejoining of the phosphodiester backbone of DNA
strands during the normal cell cycle.
 63. • In recent years, topoisomerases have become popular targets for cancer chemotherapy
treatments. It is thought that topoisomerase inhibitors block the ligation step of the cell cycle,
generating single and double stranded breaks that harm the integrity of the genome. Introduction
of these breaks subsequently lead to apoptosis and cell death.
 64. • Classification • Topoisomerase inhibitors are often divided according to which type of
enzyme it inhibits. • Topoisomerase I inhibitors: irinotecan, topotecan, camptothecin and
lamellarin D all target type IB topoisomerases,
 65. • Topoisomerase II inhibitors: etoposide (VP- 16), teniposide, doxorubicin, d aunorubicin,
mitoxantrone, am sacrine, ellipticines, aurintricar boxylic acid, and HU-331, a quinolone
synthesized from cannabidiol.
 66. • Numerous plant derived natural phenols (ex. EGCG, genistein, querc etin, resveratrol)
possess strong topoisomerase inhibitory properties affecting both types of enzymes. They may
express function of phytoalexins - compounds produced by plants to combat vermin and pests.
 67. • Use of topoisomerase inhibitors for antineoplastic treatments may lead to secondary
neoplasms because of DNA damaging properties of the compounds. Also plant derived
polyphenols shows signs of carcinogenity, especially in feuses and neonates who do not detoxify
the compounds sufficiently.An association between high intake of tea (containing polyphenols)
during pregnancy and elevated risk of childhood malignant central nervous system (CNS)
tumours has been found.
 68. 5- Cytotoxic antibiotics- • It is bind directly toDNA , thusinhibite the synthesis of DNA and
interfering with transcpition of RNA. • actinomycin ,anthracyclines,doxorubi cin •
Daunorubicin,valrubicin ,epirubicin are example of antibiotics.
 69. Anticancer Drugs: Antibiotics • Clinically useful anticancer antibiotics: derived from
Streptomyces • These antibiotics act by: – DNA intercalation, blocking synthesis of DNA and
RNA • Anthracyclines: Doxorubicin (Adriamycin, Rubex, Doxil) and Daunorubicin (DaunoXome) –
IV administration; hepatic metabolism; biliary excretion; some urinary excretion; enterohepatic
recirculation.
 70. • Among the most useful anticancer antibiotics – Mechanism of action: • DNA intercalation --
blocking synthesis of DNA and RNA; DNA strands scission - - by affecting topoisomerase II •
Altering membrane fluidity and ion transport • Semiquinone free radical an oxygen radical
generation (may be responsible for myocardial damage)
 71. – Doxorubicin (Adriamycin, Rubex, Doxil)-- very important anticancer agent -- •
Carcinomas-Doxorubicin • breast carcinoma • ovarian carcinoma • thyroid carcinoma •
endometrial carcinoma • testicular carcinoma • lung carcinoma • Sarcomas-Doxorubicin • Ewing's
sarcoma • osteosarcoma • rhabdomyosarcomas •
 72. • Hematologic Cancers-Doxorubicin • acute leukemia • multiple myeloma • Hodgkin's
disease • non-Hodgkin's lymphoma • Adjuvant therapy in: osteogenic sarcoma and breast cancer
• Generally used in combination protocols with: – cyclophosphamide (Cytoxan) – cisplatin
(Platinol) – nitrosoureas
 73. • Major Use: Acute Leukemia • Daunorubicin: limited utility-- limited efficacy in treating solid
tumors. • Idarubicin: approved for acute myeloid leukemia – Idarubicin in combination with
cytarabine: more active than daunorubicin in inducing complete remission in acute myelogenous
leukemia. • Adverse Effects: – Bone marrow depression (short duration) – Cumulative, dose-
related, possibly irreversible cardiotoxicity. – Total, severe alopecia
 74. • Dactinomycin (Cosmegen) – IV administration; 50 percent remains unmetabolized. –
Mechanism of action: intercalation between guanine-cytosine base pairs • inhibits DNA-
dependent RNA synthesis • blocks protein synthesis – Clinical Uses: • dactinomycin in
combination with vincristine (Oncovin)and surgery (may include radiotherapy) in treatment of
 Wilms' tumor • dactinomycin with methotrexate: maybe curative for localized or disseminated
gestational choriocarcinoma.
 75. Adverse Effects: Major dose limiting toxicity: bone marrow suppression (all blood elements
affected -- particularly platelets and leukocytes) occasional severe thrombocytopenia nausea
vomiting diarrhea oral ulcers Dactinomycin: immunosuppressive (patient should not receive live
virus vaccines) alopecia/skin abnormalities interaction with radiation ("radiation recall")
 76. • Plicamycin (Mithramycin) • Mechanism of action:binds to DNA -- interrupts DNA-directed
RNA synthesis –Also decreases plasma calcium (independent tumor cell action;acts on
osteoclasts) • Clinical Uses: –some efficacy in testicular cancer that is unresponsive to standard
treatment: –especially useful in managing severe hypercalcemia associated with cancer
 77. • Adverse Effects: –nausea –vomiting –thrombocytopenia –leukopenia –hypocalcemia –liver
toxicity –bleeding disorders
 78. • Mitomycin: (Mutamycin) – Mechanism of action: • metabolic activation to produce a DNA
alkylating agent. • Solid tumor hypoxic stem cells may be more sensitive to the action of
mitomycin. • Best available drug, in combination with x-rays, to kill hypoxic tumor cells. – Clinical
Use: • in combination chemotherapy {with vincristine and bleomycin}: squamous sell carcinoma
of the cervix
 79. • adenocarcinoma of the stomach, pancreas, and lung {along with flurouracil and
doxorubicin} • second-line drug: metastatic colon cancer • topical intravesical treatment of small
bladder papillomas. – Adverse Effects: • severe myelosuppression, especially after repeated
doses, suggest action on hematopoietic stem cells. • Vomiting • anorexia • occasional
nephrotoxicity • occasional interstitial pneumonitis
 80. • Bleomycin (Blenoxane) • Mechanism of Action:binds to DNA -- produces single- and
double-strand breaks (free radical formation) – Cell cycle specific: arrests division in G2 –
Synergistic effects with vinblastine and cisplatin (curative protocol for testicular cancer) • Clinical
Uses: – Testicular cancer – Squamous cell carcinoma: head, neck, cervix, skin, penis, and
rectum
 81. –combination treatment: lymphoma –intracavity treatment: malignant effusions in ovarian
breast cancer • Adverse Effects: –Anaphylactoid reaction (potentially fatal) –Fever –anorexia,
blistering, hyperkeratosis (palms) –pulmonary fibrosis (uncommon) • No significant
myelosuppression
 82. 6-Nitrosourceas- •It is like alkylating agents,break DNA helix.
 83. • Structural Features • Nitrosourea • Mechanism of Action • Hydrolysis of Nitrosourea group
produces two active species • Alkylating Agents with Nitro group provides crosslinking in DNA for
Chemotherapy • Carbamoylating agent O=C=N-R causing toxic effects of blocking DNA
Polymerase and DNA Repair enzymes by binding to nucleophilic sites on proteins
 84. • Toxicity • Carbamoylating agent • Carcinogenic • Mutanogenic • Infertility • Bone marrow
depression
 85. Agent Structure Details Indications Brain Tumor Hodgkins Lymphoma Side Effects
Lomustine Delayed Myelosuppressi on Pulmonary Toxicity
 86. Indications Pancreatic Cancer (Beta Cells) Side Effects GLUT-2 Transporter Substrate,
leading to Streptozocin lower levels of Insulin and a form of Type II Diabetes Renal Toxicity Drug
interactions Doxorubicin Not a GLUT-2 Ethylchloride Transporter Substrate Chlorozotocin
instead of methyl on Otherwise Per nitrosourea Streptozocin
 87. 7-Mitotic inhibitors- • Anti microtubule agent that interefere with mitosis act during the late
G2 phse and mitosis to stabilize microtubules, thus inhibiting cell division
 88. Use of mitotic inhibitors in cytogenetics • Cytogenetics, the study of chromosomal material
by analysis of G-Banded chromosomes, uses mitotic inhibitors extensively. In order to prepare a
slide for cytogenetic study, a mitotic inhibitor is added to the cells being studied.
 89. • Specific agents • Taxanes • Taxanes are complex terpenes produced by the plants of the
genus Taxus (yews). Originally derived from the Pacific yew tree, they are now synthesized
artificially. Their principal mechanism is the disruption of the cell's microtubule function by
stabilizing microtubule formation. Microtubules are essential to mitotic reproduction, so through
the inactivation of the microtubule function of a cell, taxanes inhibit the cell's division.
 90. • Paclitaxel—used to treat lung cancer, ovarian cancer, breast cancer, and advanced forms
of Kaposi's sarcoma. [5] • Docetaxel—used to treat breast, ovarian, and non- small cell lung
cancer
 91. • Vinca alkaloids • Vinca alkaloids are amines produced by the hallucinogenic plant
Catharanthus roseus (Madagascar Periwinkle). Vinca alkaloids inhibit microtubulepolymerizat
ion, thereby inhibiting mitosis.
 92. • Vinblastine—used to treat leukaemia, Hodgkin's lymphoma, non-small cell lung cancer,
breast cancer and testicular cancer. It is also a component in a large number of chemotherapy
regimens.[8] • Vincristine—used to treat lymphoma, breast cancer, lung cancer, and acute
lymphoblastic leukemia.[8] • Vindesine—used to treat leukaemia, lymphoma, melanoma, breast
cancer, and lung cancer.[8] • Vinorelbine—used to treat breast cancer and non- small-cell lung
cancer
 93. • Colchicine • Colchicine is an alkaloid derived from the autumn crocus (Colchicum
autumnale). It inhibits mitosis by inhibiting microtubule polymerization. While colchicine is not
used to treat cancer in humans, it is commonly used to treat acute attacks of gout
 94. • Podophyllotoxin • Podophyllotoxin and Podophyllin, derived from the may apple plant,
are used to treat viral skin infections. • Griseofulvin • Griseofulvin, derived from a Penicillium
mold, is an antifungal drug.
 95. • A mitotic inhibitor is a drug that inhibits mitosis, or cell division. These drugs disrupt
microtubules, which are structures that pull the cell apart when it divides. Mitotic inhibitors are
used in cancer treatment, because cancer cells are able to grow and eventually spread through
the body (metastasize) through continuous mitotic division and so are more sensitive to inhibition
of mitosis than normal cells
 96. 8-Corticosteroids- • Discrupt the cell membrain and inhibit synthesis of protein,decrease
circulting lymphocytes, inhibit mitosis.
 97. • Discrupt the cell membrain and inhibit synthesis of protein,decrease circulting
lymphocytes, inhibit mitosis. • Pharmacologic doses of steroid inhibited growth of various tumor
systems. Tissue culture studies confirmed that lymphoid cells were the most sensitive to
glucocorticoids, and responded to treatment with
 98. • ribonucleic acid (RNA), and protein synthesis. Studies of proliferating human leukemic
lymphoblasts supported the hypothesis that glucocorticoids have preferential lymphocytolytic
effects. The mechanism of action was initially thought to be caused by impaired energy use via
decreased glucose transport and/or phosphorylation; it was later discovered that glucocorticoids
induce apoptosis, or programmed cell death, in certain
 99. • Corticosteroids can be used to kill lymphoma, leukemia and multiple myeloma cells and
may also be used to ease the side effects of other chemotherapy drugs. In addition to their
chemotherapy action, corticosteroids also help reduce nausea, vomiting and allergic reactions
caused by cancer treatment
 100. 9-Hormone therapy- •Selectively attach to estrogen receptors, cuasing downregulation of
them and inhibiting tumor growth
 101. Anticancer Agents: Hormones • Introduction • Breast and prostatic cancer: palliation with
sex hormone therapy • Adrenal corticosteroid treatment-- useful in: – acute leukemia – myeloma
– lymphomas – other hematologic cancers
 102. • Pharmacological effects: –Steroid hormones bind to steroid receptors: –Efficacy of
steroid treatment depends on specific receptor presence on malignant cell surface. • Clinical
Use:Treatment of: –female and male breast cancer –prostatic cancer –endometrial cancer of
uterus
 103. • Adverse Effects: –Fluid retention (secondary to Na-retaining properties) –Androgens-
masculinization (long-term use) –Estrogens-feminization (long-term use) –Adrenocortical
steroids: • hypertension • diabetes • enhanced susceptibility to infection • cushingoid appearance
 104. • Estrogen and Androgen Inhibitors: (Tamoxifen and Flutamide) • Tamoxifen: Breast
cancer treatment –Oral administration. –Activity against progesterone- resistant endometrial
neoplasm –Chemopreventive:women -- high- risk for breast cancer
 105. – Mechanism of Action: • Competitive partial agonist-inhibitor of estrogen • Binds to
estrogen-sensitive tissues (receptors present) • Best antiestrogen effect requires minimal
endogenous estrogen presence {estradiol has a much higher affinity for the estrogen receptor
than tamoxifen's affinity for the estrogen receptor} • Suppresses serum levels of insulin-like
growth factor-1; and up-regulates local TGF-beta production. These properties may explain
 106. – Adverse Effects: • Generally mild • Most frequent: hot flashes • Occasionally: fluid
retention, nausea – Clinical Use: • Advanced breast cancer – Most likely to be effective if: » lack
 endogenous estrogens {oophorectomy; postmenopausal} » Presence of cytoplasmic estrogen
receptor;presence of cytoplasmic progesterone receptorColeman • Prolongs survival {surgical
adjuvant therapy} in postmenopausal women with estrogen receptor-positive breast cancer.
 107. • Flutamide (Eulexin): prostatic cancer –Antagonizes remaining androgenic effects after
orchiectomy or leuprolide treatment • Gonadotropin-Releasing Hormone Agonists (Leuprolide
and Goserelin (Zoladex)) • Leuprolide and goserelin: synthetic peptide analogues of
gonadotropin- releasing hormone (GnRH, LHRH)
 108. – Mechanism of Action: Analogues more potent -- behave as GnRH agonists. • pituitary
effects: when given continuously -- initial stimulation then inhibition of follicle-stimulating hormone
and leutinizing hormone. • Clinical Use: treating metastatic prostate carcinoma • Comparing
leuprolide with diethylstilbestrol (DES): – Similar suppression of androgens synthesis and serum
prostatic acid phosphatase .
 109. – Adverse Effects: Leuprolide less frequently causes: • nausea • vomiting • edema •
thromboembolism • painful gynecomastia –Leuprolide and goserelin: medication more costly, the
more cost-effective given reduced frequency of complications.
 110. • Aromatase Inhibitors (Aminoglutethimide and Anastrozole (Arimidex)) •
Aminoglutethimide: –Mechanisms of action: Reduction in estrogen concentration •
Aminoglutethimide: inhibitor of adrenal steroid synthesis ( blocks conversion of cholesterol to
pregnenolone {first-step})
 111. • Aminoglutethimide inhibits extra-adrenal estradiol and estrone synthesis. •
Aminoglutethimide inhibits an aromatase enzyme {catalyzes conversion of androstenedione to
estrone} –This conversion may occur in fat. – Clinical Use: • Metastatic breast cancer (tumors
contain estrogen or progesterone receptors) –Aminoglutethimide is administered with
adrenalreplacement doses of hydrocortisone to ensure avoidance of adrenal insufficiency.
 112. » Hydrocortisone is used in preference to dexamethasone, because dexamethasone
increases the degradation of aminoglutethimide. • Aminoglutethimide in combination with
hydrocortisone: Second-Line Therapy for women treated with tamoxifen (aminoglutethimide
causes more adverse side effects than tamoxifen) • Anastrozole (Arimidex): new, selective,
nonsteroidal aromatase inhibitor. – appears to have no effect on glucocorticoid or
mineralocorticoid synthesis – Clinical Use: • Treatment of advanced estrogen-or progesterone-
receptor positive non-- tamoxifen responsive breast cancer
 113. 10-Miscellneous- • Inhibite the protein synthesis, enzymes derived from the yeast Enwinia
used to deplete the supply of asparagines for leukemic cells that are dependent on exogenous
source of this amino acid
 114. Miscellaneous Anticancer Drugs • Amsacrine: – Hepatic metabolism – Mechanism of
Action: • DNA intercalation: produces single-and double-strand breaks • interaction with
topoisomerase II-DNA complexes – Clinical Uses: • Anthracyclines- and cytarabine-resistant
acute myelogenous leukemia • Advanced ovarian cancer • Lymphomas
 115. – Adverse Effects: • Does-limiting hepatic toxicity • Cardiac arrest has been noted with
amsacrine infusion • Asparaginase (El-spar): – Mechanism of action: depletion of serum
asparagine {forming aspartic acid and ammonia} • Decreased blood levels of asparagine and
glutamine inhibit protein synthesis in those neoplastic cells that express decreased levels of
asparagine synthase. • Most normal cells express sufficient levels of asparagine synthase to
avoid toxicity.
 116. • Hydroxyurea: – Mechanism of action: • Inhibits ribonucleotide reductase; depletes
deoxyribonucleoside triphosphate pools • Acts at S phase. – Clinical Uses: • Melanoma
[secondary role] • Chronic myelogenous leukemia [secondary role] – Adverse Effects: • Bone
marrow suppression • nausea • vomiting • diarrhea
 117. • Mitoxantrone (Novantrone): – Mechanism of action: • Induces DNA strand breaks •
Inhibits RNA and DNA synthesis – Clinical Uses: • Refractory acute leukemia • Pediatric and
adult acute myelogenous leukemia • non-Hodgkin's lymphoma's • breast cancer – Adverse
Effects: • Dose-limiting: leukopenia • mild nausea • vomiting • stomatitis • alopecia • some
cardiotoxicity {arrhythmias}
 118. • Mitotane (Lysodren): – Clinical Use:Single indication-- adrenal carcinoma • Reduces
excessive steroid secretion – Adverse Effects: • diarrhea • mental depression • skin eruption •
anorexia • nausea • somnolence • dermatitis
 119. • Retinoic acid Derivatives: – Clinical Uses: • Remissions -- acute promyelocytic leukemia •
13-cis-Retinoic acid: chemopreventive -- second primary tumors in patients with hand and neck
squamous cell carcinoma. – Adverse Effects: • skeletal effects • hepatic effects • teratogenic
effects • mucocutaneous effects
 120. • Bone Marrow Growth Factors (sargramostim and filgrastim): –Reduces neutropenic
sepsis and other complications of chemotherapy –Filgrastim shortens neutropenic state following
induction chemotherapy for acute nonlymphocytic leukemia. • Amifostine • Cytoprotective from
effects of chemotherapy
 121. CONCEPT IN CHEMOTHERAPY • ADJUVANT CHEMOTHERAPY- • Adjuvant
chemotherapy is the utilization of antineoplastics agents in additionto surgery orradiotherapy.
The rationale is to destroy cancer cells left behind in the operative field or disseminated through
the blood stream to metastaticlocation.
 122. • NEOADJUVANT CHEMOTHERAPY • It refers to the initial use of chemotherapy to reduce
the bulk and lower the stage of atumor, making it amenable to cure with subsequent
localtherapy. • COMBINATION CHEMOTHERAPY • It refers to the use of cytotoxic drugs in
combination. It isconsistently superior to single agent therapy.
 123. ADMINISTRATION OF CHEMOTHERAPY • Depending on clinical setting , chemotherapy
may be administered by the physician,staffnurse or specialized team ember,such as the
oncology clinical nurse specialist or intravenous therapist.
 124. ROUTE OF ADMINISTRATION • 1-Oral • This rout is normally used for cyclophosphamide,
capecitabine drugs. • 2-Intramuscular • This rout is normally used for Bleomycin drug. • 3-
Intravenous- • This rout is normally used for Daxarubicine, vincristine,cisplatin, 5-fu drugs.
 125. • 4- Intracavitary(pleural,peritoneal) – • This rout is normally used for radioisotopes ,
alklying agents, methotrexate. • 5-Intrathecal • For mithotraxate and cytarabine. • 6-Intraartical- •
For DTIC,5-fu, Methotraxate. • 7-Perfusion • For alkylating agents
 126. • 8-Continuous infusion- • For 5-fu,methotraxate and cytarabine. • 9-Subcutaneous- • For
cytarabine • 10-Topical • For 5-fu crem.
 127. TOXIC EFFCT OF CHEMOTHERAPY • Toxicity associated with chemotherapy can be acue
or chronic. Cell with rapid growth rates(e.g epithelium, bone marrow, hair follicles,and sperm) are
very susceptible to damage from these agents. Varius body system may also be affected by
these drugs
 128. GASTROINTESTINAL SYSTEM • Nausea and voming • Anorexia • Taste alteration •
Weight loss • Oral mucositis • Diarrhea • Constipation
 129. HEMATOPIETIC SYSTEM • Leukopenia • Anemia • Thrombocytopeniautropenia •
Neutopenia • Increase risk of infection and bleeding
 130. INTEGUMETARY SYSTEM • Alopesia • Skinreaction such as Red
patches(erythema),urticaria, • hyper pigmentation in the nailbeds, • mouth or gums or
teeth,Photosensitivity
 131. REPRODUCTIVE SYSTEM • Testicular and ovarian function impairedso result
Azoospermia,oligospermia and sterility in male and • Amenorrhea,menopausal manifestations
and • sterility in female with increase risk of abortion and fetal malformation. • In second and third
trimester result low
 132. IMMUNE SYSTEM •Risk for fatal infection •Stomatitis,enteritis,gingi vitis and more infection
•Fatique •Hair loss
 133. Damage to specific organs may occur, with resultant symptoms: • Cardiotoxicity (heart
damage) • Hepatotoxicity (liver damage) • Nephrotoxicity (kidney damage) • Ototoxicity (damage
to the inner ear), producing vertigo • Encephalopathy (brain dysfunction)
 134. Chemotherapy regimens Example of uses, and other Name Components notes
Adriamycin ABVD (doxorubicin), bleomycin, vin Hodgkin's lymphoma blastine, dacarbazine
Adriamycin AC (doxorubicin), cyclophospha Breast cancer mide Bleomycin, etoposide,
Adriamycin (doxorubicin), cyclophospha BEACOPP Hodgkin's lymphoma mide, Oncovin
(vincristine), procarbazine,pre dnisone Bleomycin, etoposide, Testicular cancer, germ cell BEP
platinum agent (cisplatin) tumors Cyclophosphamide, CA Adriamycin (doxorubicin) Breast cancer
(same as AC)
 135. Cyclophosphamide, Adriamycin CAF Breast cancer (doxorubicin), fluorouracil (5-FU)
Cyclophosphamide, CAV Adriamycin Lung cancer (doxorubicin), vincristine Cyclophosphamide,
BCNU CBV (carmustine), VP-16 Lymphoma (etoposide) Chlorambucil, vincristine (Oncovin),
 procarbazine, pre ChlVPP/EVA dnisone, etoposide, vinblasti Hodgkin's lymphoma ne,
Adriamycin (doxorubicin) Cyclophosphamide, hydroxydoxorubicin CHOP Non-Hodgkin
lymphoma (doxorubicin), vincristine (Oncovin), prednisone
 136. Non-Hodgkin Cyclophosphamide, lymphoma in patients Oncovin COP or CVP with history
(vincristine), predniso ofcardiovascular ne disease Cyclophosphamide, met CMF hotrexate,
fluorouracil ( Breast cancer 5-FU) Cyclophosphamide, Oncovin Non-Hodgkin COPP (vincristine),
procarbazi lymphoma ne, prednisone Epirubicin, cyclophosph EC Breast cancer amide Gastric
Epirubicin, cisplatin, flu
 137. Etoposide, prednisone, Oncovin, cyclophosph EPOCH amide, Lymphomas and
hydroxydaunorub icin Fluorouracil (5- FEC FU), epirubicin, cyclop Breast cancer hosphamide
Fluorouracil (5-FU), FL (Also known as leucovorin (folinic Colorectal cancer Mayo) acid)
Fluorouracil (5-FU), FOLFOX leucovorin (folinic Colorectal cancer acid), oxaliplatin Fluorouracil
(5-FU),
 138. High-risk progressive or ICE-R ICE + rituximab recurrent lymphomas Methotrexate,
bleomycin, Adriamycin m-BACOD (doxorubicin), cyclophospham Non-Hodgkin lymphoma ide,
Oncovin (vincristine), dexamethasone Methotrexate, leucovorin (folinic acid), Adriamycin
(doxorubicin), cyclophosphamid MACOP-B Non-Hodgkin lymphoma e, Oncovin
(vincristine),prednisone, bleomy cin Mechlorethamine, Oncovin MOPP (vincristine),
procarbazine, pred Hodgkin's lymphoma nisone methotrexate, vinblastine, adria MVAC
Advanced bladder cancer[2] mycin, cisplatin Procarbazine, CCNU PCV Brain tumors
 139. Prednisone, doxorubicin (a driamycin), cyclophospha mide, etoposide, cytarabine
ProMACE-CytaBOM Non-Hodgkin lymphoma , bleomycin, Oncovin (vincristine),methotrexate,
leucovorin Rituximab, fludarabine, cycl B cell non-Hodgkin R-FCM ophosphamide, mitoxantrone
lymphoma Doxorubicin, mechlorethami ne, bleomycin, vinblastine, v Stanford V Hodgkin's
lymphoma incristine, etoposide, prednis one Thal/Dex Thalidomide, dexamethasone Multiple
myeloma Paclitaxel, ifosfamide, Testicular cancer, germ cell TIP platinum agent cisplatin tumors
in salvage therapy Vincristine, Actinomycin, Cy VAC Rhabdomyosarcoma clophosphamide
 140. Vincristine, Adriamycin VAD Multiple myeloma (doxorubicin), dexa methasone Hodgkin's
Vincristine and VAMP lymphoma, leukemi others a, multiple myeloma Vincristine, Adriamycin
(doxorubicin), predn Hodgkin's VAPEC-B isone, etoposide, cyc lymphoma lophosphamide, bleo
mycin
 141. Care of the patient with chemotherapy • Before care • During care • After care
 142. RADIOTHERAPY • introduction • More than 60% of all clients with cancer receive
radiation therapy at some point during the course of their disease Radiation therapy may be used
as a primary,adjuvant or palliative treatment modality.
 143. • RT is the only treatment used and aims to achieve local cure of the cancer. • e.g. early
stage Hodkin’s disease, skincancer and carcinoma of cervix.
 144. HISTORICAL BACKGROUND • X-rays were discovered in 1885 by the German
physicist,Wilhelm Conrad Roentgen, alsocalled the father of diagnostic radiology. • Parallel to the
discovery of X-rays, Becquerel discovered radioactivity in 1898. • During the early
1900s,radiobiological experiments were conducted.
 145. TYPES OF RADIATION • ionizing radiation • non-ionizing radiation • Photons (x-rays and
gamma rays), • Particle radiation
 146. METHOD OF RADIATION • EXTERNAL RADIATION THERAPY • INTERNAL RADIATION
THERAPY • A-SEALED SOURCE RADIOTHERAPY • B-UNSEALED SOURCE RADIATION
THERAPY • MULTI-FIELD THERAPT • CONFORMAL RADIATION
 147. EXTERNAL RADIATIN THERAPY-
 148. A-Conformal radiotherapy
 149. • Conformal radiotherapy is a common type of external beam radiotherapy. It is also
called 3D conformal radiotherapy (3D CRT). Conformal radiotherapy uses the same types of
radiotherapy machine as standard beam external radiotherapy. But the radiotherapists put metal
blocks in the path of the radiation beam. The blocks change the shape of the beam so that it
‘conforms’ more closely to the shape of the tumour.
 150. B-Intensity modulated radiotherapy
 151. • Intensity modulated radiation therapy (IMRT) uses hundreds of tiny devices called
collimators to shape the radiotherapy area. The collimators also vary the intensity of the beams
during each dose of treatment. The radiotherapy beams are aimed at the tumour from different
 directions. The collimators can move during treatment so that the machine gives very precise
doses to a cancer or to specific areas within the
 152. C-Image guided radiotherapy
 153. • In image guided radiotherapy (IGRT) CT, MRI, or PET scans are taken regularly during
the treatment. The scans are processed by computers to show changes in the size and position
of the tumour.
 154. D-Tomotherapy
 155. • Part of the tomotherapy machine can rotate completely around the patient to take CT
scans and give radiotherapy to a very localised area.
 156. E-Stereotactic radiotherapy and radiosurgery
 158. • Stereotactic radiotherapy gives radiotherapy in fewer sessions, using smaller radiation
fields and higher doses than 3D conformal radiotherapy. A single treatment of this type is
sometimes called radiosurgery, Gamma Knife or Cyberknife
 159. F- Proton therapy
 160. • One of the newer ways of giving radiotherapy uses a different type of radiation beam
called a proton beam. Protons collect energy as they slow down and travel through the body.
They then release this energy at their target point – the tumour.
 161. G-Electron beam radiotherapy
 162. • Electron beams cannot travel very far through body tissue. This type of radiotherapy is
used to treatskin cancers or tumours very close to the surface of the body.
 163. • External radiation therapy may help relieve the problems caused by the tumors.
Treatment may be done to the following body areas:
 164. • Head and neck • Chest: • Arms and legs: • Bones • Abdomen: • Pelvic area
 165. 2-INTERNAL RADIATION THERAPY
 166. • Internal radiotherapy is used mainly to treat cancers in the head and neck area, the
cervix, womb, prostate or the skin. • Treatment is given in one of two ways: • Brachytherapy -
putting solid radioactive material (the source) close to or inside the tumour for a limited period of
time. • Radioisotope treatment - by using a radioactive liquid, which is given either as a drink or
as an injection into a vein
 167. Brachytherapy
 168. Radioisotope therapy
 169. A-SEALED SOURCE RADIOTHERAPY
 170. • brachytherapy /brachy·ther·a· py/ (-ther´ah-pe) treatment with ionizing radiation whose
source is applied to the surface of the body or within the body a short distance from the area
being treated
 171. • Surface Applicator or "Mould" brachytherapy. • Interstitial brachytherapy. • Intracavitary
brachytherapy places the sources inside a pre-existing body cavity.
 172. .B-UNSEALED SOURCE RADIATION THERAPY
 173. •Unsealed source radiotherapy relates to the use of soluble forms of
radioactivesubstances which are administered to the body by injection or ingestion.
 174. • 1 Iodine • 2 Other unsealed sources • 3 Experimental antibody based methods - alpha
emitters
 175. Iodine
 176. • • For example, iodine is an element selectively taken up by the thyroid gland in healthy
people. Thyroid disease (both benign conditions like thyrotoxicosis and malignant conditions like
papillarythyroid cancer) can be treated with radioactive iodine (iodine-131) which is then
concentrated into the thyroid. Iodine-131 produces beta and gamma radiation.
 177. Other unsealed sources Isotope Use Description 131I-MIBG for the treatment of
phaeochromocytoma andn (metaiodobenzylguanidine) euroblastoma the main place of use of
phosphorus is the bone 32P for overactive bone marrow marrow 89Sr 153Sm for secondary
cancer in the strontium and samarium beh & bones ave just like calcium
 178. strontium and for secondary samarium beh 89Sr cancer in the ave just like & 153Sm
bones calcium radiosynovecto my in 90Y the knee joint
 179. Experimental antibody based methods - alpha emitters • ITU work is being done on
Alpha-Immunotherapy, this is an experimental method
 180. MULTI-FIELD THERAPY • In the planning of X-ray therapy the aim is to deliver a lethal
dose to the lesion without doing significant harm to healthy tissue
 181. CONFORMAL RADIATION T • Three-Dimensional Conformal Radiation Therapy (3D-CRT)
• Tumors are not regular; they come in different shapes and sizes. Three-dimensional conformal
radiation therapy, or 3D-CRT,
 182. Common side effects of radiation therapy • skin problems • fatigue from lack of sleep; •
Diarrhea • Nausea and vomiting • Dry mouth • Trouble swallowing • Swelling • Hair loss • Sexual
problems • Urinary and bladder changes
 183. Site-specific side effects • Head and neck • Chest. • Stomach and abdomen • Pelvis.
 184. Nursing care of the patient • Before care • During care • After care
t the same time, it is crucial to minimize exposure to the surrounding healthy tissues
and critical organs to prevent significant side effects or damage. This balance is
achieved through advanced treatment planning techniques that consider the shape,
size, and location of the lesion.
• Multi-field therapy involves using several radiation beams from different angles,
which converge on the lesion. This approach allows for a higher cumulative dose to
the tumor while spreading out the radiation dose to healthy tissues, reducing the risk
of complications.
• The success of this therapy depends on precise imaging, accurate patient
positioning, and sophisticated computer algorithms that optimize the dose
distribution for effective and safe treatment.
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