INTERNAL MEDICINE

INTRODUCTION AND GENERAL DIAGNOSIS

Internal diseases have envolved as a discipline from general medicine as one of the first
specializations.

Later it was divided into a number of new specialized fields: cardiology, pulmonology,
nephrology, gastroenterology, hematology, rheumatology, endocrinology, diabetology etc.

The advantage of this should be better utilization of both technical and human recourses
(qualifications)

The disadvantages is the loss of the generalized (holistic) approach to the patient.

Traditional internal diseases are defined as a field of diagnosis and medical treatment (as
opposed to intervention/surgery).

In the last few years, this definition has been made obsolete in the face of interventions in the
diagnostic and treatment methods: cardiology, gastroenterology, nephrology, pulmonology.

Basic concepts of general diagnosis of internal diseases. The approach to the patient in internal
disease ward-stages:

1. Emergency procedures
2. Diagnostics:
a. History (general integrated curriculum examinations, special interviews
concerning health, social and professional status, style of life, etc.)
b. Physical examination (doctor and nurses)
c. Addition test: laboratory image (RTG,CT, ultrasound, MRI), invasive
(gastroscopy, bronchofiberoscopy, ERCP)
3. Treatment
a. The symptoms
b. Specific according to disease
c. Evaluation of the use of treatment used
4. Rehabilitation
a. Physical
b. Psychosocial
5. Appropriate ambulatory care
a. Basic health care
b. Specialists
c. Psychological guidance
d. Support groups

The main parts of the diagnosis

- Pathological
- Etiological
- Anatomical
- Prognostic
Medical examination

1. Patient history
2. Physical examination
3. Laboratory and instrumental examination

Patient history:

0. Introduction: date of the history, identifying data, source of referral, reliable of the
history
1. Chief complaint(s)
2. Present illness: location, quality, quantity of severity, timing (onset, during, frequency),
setting in which it developed, factors that aggravated or relieved, associated
manifestations, treatments.
3. Past history: most important diseases in chronological order (hospitalisations);
operations, injuries, accidents; allergies (drug, food, pollens etc.), transfusion(s),
screening test.
4. Current health status: social circumstances, occupation (recent and past),
environmental hazards (home, school, workplace), diet (incl. beverages), alcohol and
illicit drugs (type, amount, frequency, duration of use), tobacco (type, amount,
duration), current medication, exercise and leisure activities, sleep patterns, sexual
history.
5. Family history: parents, siblings, spouse, children, other relatives: age; age and cause
of death; health status; important diseases. Occurrence of: diabetes; hypertension,
heart diseases, stroke; infective diseases; malignant diseases; coagulation disorders;
psychiatric diseases, alcoholism, drug addition; symptoms like those the patient.
6. Review of organ systems. General: general status, usual weight, weight change,
fatigue, fever. According to organs: skin, head, eyes, ears, nose, mouth, neck, breast,
respiratory, cardiac, gastrointestinal, urinary, genital etc.

Physical examination

1. Observation
2. Palpation
3. Percussion/tapping
4. Auscultation

General appearance:

a. General features, nutritional status.

b. Temperature of the body
c. Mental state

Skin:

1. Color, dye, changes

2. Exanthema
3. Scars
4. Hair
5. Fatty padding
6. Warming, dryness, nails
Lymph nodes

1. Sensible, location
2. Mobility, painfulness

Face, head, scull, eyes

1. eye movements, stare, collapse

2. pupils
3. Conjunctiva
4. Eyelids
5. Vision

Ears

Nose

Mouth

Chest:

1. skin, nipples
2. shape
3. movement
4. type of breathing, symmetry, number of breaths
5. Pain

Respiratory system:

1. pulmonary tapping
2. physiological and ancillary airbone rhales/sounds

Circulatory system:

1. watch the heart area

2. heart rate tapping
3. listening to the murmurs, the tones
4. Heart Rate
5. Pressure
6. peripheral vessels

Abdomen:

1. shape
2. peristalsis
3. Soreness, muscle defense.
4. deep palpation - internal organs
5. tumors
6. percussion/tapping
7. hernia
8. per rectum examination
External genital

1. external genitalia
2. The pubic hair

Urinary tract:

1. kidney area - the symptom of shaking

2. palpation of the bladder area

Motion system:

1. bones and joints

2. edema
3. limitation of motility
4. spine

The nervous system:

1. basic symptoms - hypoaesthesia, hyperalgesia

2. symptoms of paralysis-paralysis
3. symptoms of neuralgia, etc.
PATHOPHYSIOLOGY AND RISK FACTORS OF CORONARY ARTERY DISEASE
Overview

- Cardiovascular disease
- Atherogenesis and response to injury (Endothelial Dysfunction)
- Manifestations and diagnosis of CAD
- Treatment of CAD
- Risk factors contributing to CAD: modifiable vs no modifiable

Cardiovascular Diseases

Arteriosclerosis: loss of elasticity of the arteries; thickening and hardening of artery walls.

Atherosclerosis: process where fatty material is deposited along walls of arteries. This material
thickens, hardens, and can eventually block the artery. Atherosclerosis is just one type of
Arteriosclerosis.

Our understanding of the development and progression if the atherosclerosis (atherogenesis)

is still incomplete.

Vascular anatomy

Endothelium; barrier between blood and arterial wall

3 layers in arterial wall:

- Tunica Intima - connective tissue; where lesions form

- Tunica Media - smooth muscle
• advanced atherosclerosis characterized by proliferation of smooth muscle cells
here
- Tunica Adventitia - connective tissue; highly vascularized to provide nutrients

Endothelial functions

- Regulates vasomotion
- Regulates thrombosis
- Regulates transport of substances to and from vascular space
- Regulates growth and apoptosis of vascular wall
- Regulates LDL oxidation

Endothelial Dysfunction

- Inadequate vasodilation
- Prothrombotic
- Altered permeability
- Increased secretion of growth factors
- Increased oxidation of LDL
Atherogenesis. Response to injury

Arterial injury

- Can result from smoke, hypertension, cholesterol, glycated substances,

vasoconstriction, homocysteine or infectious agents.
- Normal endothelial function is not repaired by inherent mechanisms.

Endothelial Dysfunction and Inflammatory Response

- Arterial homoeostasis is altered by injury, results in inflammatory response

- Increased adhesiveness endothelial cells lose selective permeability

Platelet aggregation

- Platelets adhere to damaged endothelium and form small blood clots on vessel wall
(mural thrombi)
- Release growth factors and vasoconstrictor substances
- Can cause obstruction to blood flow

LDL oxidation

- Excess oxidized LDL particles accumulate in arterial wall, attracting monocytes and
other cells into intima.
- Monocytes mature into macrophages and cause proliferation of smooth muscle cells
and promote uptake of more lipids, particularly LDL
- These cells move from the media to the intima, becoming foam cells, producing fatty
streaks or lesions
- Continued release of vasoactive substances and growth factors

Foam cells

- Release cholesterol into extracellular space

Fatty streaks

- Earliest visually detectable lesion of atherosclerosis

- As the process continues, smooth muscle cells accumulate in the intima and form a
fibrous plaque.

Fibromuscular plaque

- With continued accumulation, lesion progresses in size and appearance to

Fibromuscular plaque with an Atheroma (cholesterol core)
Remodeling

- Outward growth of artery & increased lumen size

- Lumen size increases to compensate for atherosclerotic plaque
- If plaque bulk continues to increase, lumen diameter is decreased and blood flow
obstruction occurs

Plaque rupture, thrombus formation, incorporation

- Layered appearance to lesion and increased plaque progression

- Rupture may result from local stress or chemical factors and exposes contents or
lesion to blood
- Plaques that are most vulnerable to rupture typically have a large lipid core, thinned
fibrous cap, and outward remodeling of arterial wall

Advanced atherosclerotic plaque

Progression of Atherosclerosis

Atherogenesis

- Does not occur in a predictable linear pattern.

- Some lesions develop slowly and are stable for long periods of time, others develop
quickly
- Partial regression of fatty, soft lesions is possible with aggressive risk reduction
- Endothelial dysfunction can be reversed
▪ Exercise, dietary fat intake control, decreasing stress, maintaining
optimal blood pressure and blood glucose levels
Manifestations of the atherosclerosis

- The heart: myocardial ischemia, angina, myocardial infarction

- Brain:
▪ Transient ischemic attack (TIA)
▪ Cerebrovascular accident (stroke)

Cerebrovascular accident (stroke)

- Legs:
▪ Intermittent claudication

Myocardial ischemia- ischemia cascade

- LV stiffening & decreased diastolic filling (diastolic dysfunction)

- Impaired LV systolic emptying
- ECG changes associated with altered repolarization
- Angina Pectoris – transient, referred cardiac pain resulting from ischemia

Angina – types:

- Silent ischemia: no pain

- Anginal equivalent: shortness pf breath, diaphoresis, etc.
- Typical angina: occurs with exertion, emotions & relieved with rest of NTG.
- Atypical angina: similar symptoms, but no exertion etc.
- Stable angina: reproducible, predictable.
- Unstable angina: new onset, increased freq, intensity, duration, or occurs at rest.

Diagnosis of coronary artery disease

Interventions and treatment of coronary artery disease

No cure !!!!

Risk factor modification

Treat to target

Non -modifiable and modifiable

Non modifiable risk factors

Family history

- Twice the risk of MI if one first-degree relative with MI

- Triple the risk of MI if 2+ first-degree relatives with MI
- Risk is strongest if MI occurred at age 55 or less
Advancing age:

- Risk of CAD Increases as we get older

Gender:

- Men are at risk at an earlier age than women

- Women’s risk of heart disease increases after menopause and soon equals men’s

Modifiable risk factors

Tobacco smoking

Dyslipidaemia

Hypertension

Obesity

Sedentary lifestyle

Diabetes

Emerging risk factors

Tobacco smoking

The MOST preventable risk factor

Smokers have 2 to 5 times the risk of CAD as non-smokers

Risk factor if one is currently smoking, has quit within the past 6 months, or has exposure to
environmental tobacco smoke.

Increase workload to heart

- Increased HR and BP

Endothelial dysfunction

- Increased vasoconstriction
- Decreased HDL
- Increased LDL and Triglycerides
- Increased LDL oxidation
- Increased platelet aggregation
- Decreased O2 carrying capacity of red blood cells
Dyslipidaemia

2 main types of lipids:

- Cholesterol
- Triglycerides (TGs)

Lipids are an essential component of healthy body functioning, including:

- Structural component of cell walls

- Hormones
- Energy source

Much research to support the link between abnormal serum lipid levels and CAD

 LDL =  risk of CAD

 HDL =  risk of CAD

 TGs =  risk of CAD

Abnormal lipid levels are known to be the basis of the atherosclerotic process

Endothelial Dysfunction

- Elevated cholesterol levels

• Reduce vasodilation
• Increase thrombosis
- Elevated triglyceride levels
• Mechanism is unclear

Lipid Targets for CAD

2009 Canadian Cholesterol Guidelines

Primary Targets:

- LDL-C < 2.0mmol/L (75 mg/dl) or 50% reduction

Secondary Targets: (once LDL cholesterol is at goal)

- Total Cholesterol to High-Density Lipoprotein (HDL) cholesterol ratio less than

4.0
- Non HDL cholesterol < 3.5 mmol/L
- Triglycerides < 1.7 mmol/L
- Apolipoprotein B to apolipoprotein AI ratio < 0.8
- High-sensitivity C-reactive protein (CPR) < 2 mg/L
Hypertension

- Primary risk factor for CAD

- Hypertension is associated with three to four times increased risk for CAD, MI and CVA
& PVD
- Hypertension as a precursor or consequence of endothelial dysfunction?
- Vasoconstriction (increases SBP)
- Vascular wall injury
▪ Increased platelet aggregation
- Myocardium
▪ increased wall stress
▪ increased myocardial O2 demand

Blood Pressure Targets

ACSM Guidelines

Optimal 120 / <80*

Normal 120-129 / 80-84*

High Normal 130-139 / 85-89*

Hypertension >140 / >90*

*All units in mmHg

Obesity

The risk for CVD is greater in person’s with central (android) obesity than those with peripheral
(gynoid) obesity

Obesity is often associated with …

- Diabetes
- Hypertension
- Dyslipidemia
- Inactivity

Body Mass Index (BMI)

▪ Measured in Kg/m2

ACSM BMI Targets

Underweight <18.5

Normal 18.5-24.9

Overweight 25.0-29.9

Obese >30
 - Waist Circumference
- ACSM Waist Circumference Targets

Men < 102 cm

Women < 88 cm

Sedentary lifestyle

Lower fitness level is associated with increased risk of CAD in men and women.

The relative risk of CAD associated with physical inactivity is comparable to that observed for
cigarette smoking, hypercholesterolemia and hypertension.

Persons who are physically inactive after a heart attack have significantly high mortality rates
than active individuals.

Physical activity reduces the risk of CAD through:

- Improved balance between myocardial O2 supply and demand

- Decreased platelet aggregation
- Decreased susceptibility to malignant ventricular arrhythmias
- Improved endothelial tone
- Beneficial effect on other CAD risk factors (ie. diabetes, dyslipidemia, hypertension,
obesity, stress)

Diabetes

People with diabetes have 2 to 7 times increased risk of developing CAD than people without
diabetes

Mechanism of atherosclerosis is unclear

- Endothelial damage
Increased platelet aggregation

▪ Insulin promotes synthesis of lipids and uptake of lipids by smooth

muscle

Excess sugar in vessels damages the lining making it vulnerable to plaques and clots.

Stress

Psychosocial factors associated with CAD risk:

- Type A personality
- Hostility/Anger
- Depression/Anxiety

3 to 4 times increased risk of death in first year following MI

Stress (Canadian)

Influence CAD risk via 2 main mechanisms:

Catecholamine release

- increased BP
- increased HR
- vasoconstriction
- increased O2 demand

Decreased adherence to lifestyle modification recommendations

Atherogenic diet

Diets high in fruits, vegetables, whole grains and unsaturated fatty acids have lower risk for
CAD

This influence goes beyond what is explained by other risk factors that may be related to diet.

Emerging risk factors

Nontraditional factors that are associated with increased risk of CVD, but a causal link has not
yet been proved with certainty.

- Poor oral health

- Dietary trans fat intake
- Homocysteine
- Lipoprotein A
- Infectious agents
- Adhesion molecules
- Cytokines
- Fibrogen
- High sensitive C-reactive protein
 ISCHEMIC HEART DISEASE. ANGINA PECTORIS. ACUTE CORONARY
SYNDROME
Cardiovascular disease

Cost of Coronary artery disease and cardiovascular disease

Historically:

• 17,600,000 Americans adults have a history of CAD.

• 8,500,000 American adults have a history of MI.

• 400,000 deaths annually (approx. 1 of every 6 deaths).

• 300,000 die from their initial Acute Coronary Syndrome (ACS) event.

Today…

• 785,000 will have their initial cardiac event.

• 470,000 will have a recurrent event.

• 195,000 will have a silent cardiac event.

• Estimated direct and indirect costs for Cardiovascular Disease – $503.2 billion.

• Estimated direct and indirect costs for Coronary Artery Disease – $177.1 billion.

Ischemia heart disease

Ischemia heart disease (IHD) is a condition in which there is a inadequate supply of blood and
oxygen to a portion of myocardium. It typically occurs when there is an imbalance between
myocardial oxygen supply and demand.

The most common, serious, chronic, life-threatening disease in the developed countries.

The most common cause is atherosclerotic disease of an epicardial coronary artery.

Pathophysiology of myocardial ischemia

Myocardial oxygen supply is decreased:

- Narrowed coronary arteries (sclerosis, thrombus, spasmus, coronary embolism,

vasculitis)
- Hypotension
- Severe anemia
- Methemoglobinemia, increased carboxyhemoglobin

Myocardial oxygen demand is increased:

- Left ventricle hypertrophy

- Fever
- Hyperthyroidism
- Tachycardy

Coronary atherosclerosis

High LDL-cholesterol, low HDL-cholesterol, cigarette smoking, hypertension, and diabetes

mellitus disturb the normal function of vascular endothelium of epicardial coronary arteries.

Segmental atherosclerotic narrowing of epicardial coronary arteries is caused most commonly

by formation of plaque, which is subjectc to rupture or erosion of the cap separating plaque
from the bloodstream.

When a stenosis reduces the diameter of coronary artery

- by 50%, there is a limitation on the ability to increase flow,to meet increased

myocardial demand
- by 80%, blood flow at rest may be reduced

With progressive worsening of epicardial artery stenosis, the distal resistance vessels
maximally dilate. Without reserve capacity in cases of increased oxigen demand – exercise,
stress, tachycardy – the ischemia manifest clinically by angina.

The clinical manifestations of ischemic heart disease

Ischemic heart disease without clinical symptoms. Sudden death can be the presenting
manifestation.

Cardiomegaly and heart failure that may have caused no symptoms prior the development of
heart failure – ischemic cardiomyopathy.

Angina pectoris. Stable angina pectoris.

Unstable angina/Non ST-elevation myocardial infarction (NSTEMI)/STEMI = acut coronary

syndromes
Heart attack

Angina pectoris

Angina pectoris or stenocardia means chest pain because of episodic myocardial ischemia

Angina pectoris is the most common manifestation of the ischemic heart disease.

The prevalence of angina pectoris is 16% in male and 11% in female population between 65
and 74 year of age*.

Approach to the patient with angina

History

- Context
- Location
- Radiation
- Quality
- Timing
- Factors that aggravate or relieve
- Associated symptoms

The context of the symptom development can give clues to diagnosis and management

Effort angina

- Angina, which occurs predictably at a certain level of activity – stable exertional

pectoris
- Angina only after minor exertion (a short walk or shaving) in the morning: first effort or
warm-up angina The patient by midday may capable of much greater effort without
symptoms.
- Emotional stress situation, haevy meal, exposure to cold, or smoking induced angina

Angina (1) that occurs at rest or with minimal exertion, usually lasts more than 10 min, (2) is
severe and new of onset, and/or (3) that occurs with a crescendo pattern – more severe,
prolonged, or frequent than previously -unstable angina, acute coronary syndrome.

Focal spasm of an epicardial coronary artery (usually close to a noncritical obstruction of right
coronary artery) leading to severe myocardial ischemia. It occurs at rest, and associated with
transient ST-segment elevation. Prinzmetal’s variant angina.

The typical clinical features of angina pectoris

The typical location of pain is retrosternal.

When the patient is asked to localize the sensation, he or she will typically place their hand
over the sternum, somtetimes with a clenched fist, to indicate the squezzing. The pain can not
be localized with one finger.
Usually described as heaviness, pressure, squezzing, or choking.

Usually associates with gradual intensification of symptoms over a period of minutes.

It lasts typically 2-5 min.

It can radiate to either shoulder and to both arms (especially the ulnar surfaces of the forearm
and hand.

It can also arise in or radiate to the back, interscapular region, root of neck, jaw, teeth, and
epigastrium. Rarely localized below the umbilicus or above the mandible.

Exertional angina is typically relieved by rest and nitroglycerin.

Associated symptoms and physical signs of angina pectoris

Associated symptoms

- Dyspnoe
- Fatique, faintness
- Nausea, vomiting
- Sweating
- Sense of impending doom (mostly in case of myocardial infarction)

Physical signs

- Third and fourth heart sounds

- Apical systolic murmur due to mitral regurgitation (impaired papillary muscle function)
- Pulmonary congestion

Summary of the characteristics of angina pectoris

Typical angina pectoris:

- Retrosternal chest pain (discomfort)

- Complaints occur after exertion or emotional stress
- The pain is relieved by rest and nitroglycerin

Atypical angina pectoris: only two from three characteristics (especially in women and
diabetics, angina may be atypical in location and not strictly related to provocing factors)

Pseudoangina: Only one or no one out of three characteristics.

Heart Attack Symptoms - MEN

Chest pain

Discomfort in other areas of the upper body

- One or both arms

- Back, neck or jaw
- Stomach
Shortness of breath

Other signs

- Cold sweat
- Nausea
- Lightheadedness
- Fatigue

Heart Attack Symptoms - WOMEN

As with men, chest pain or discomfort

More likely- other symptoms:

- Shortness of breath
- Nausea/vomiting
- Back or jaw pain
- Not feeling right
- Fatigue
- Palpitations
- Musculoskeletal complaints
- Hot flashes

Management of angina pectoris

General measures

A careful assessment of the likely extent and severity of arterial disease

The identification and control of risk factors such as smoking, hypertension and hyperlipidemia

The use of measures to control symptoms

The identification of high-risk patients for treatment to improve life expectancy

Antiplatelet therapy

Low-dose (75mg) aspirin reduces the risk of adverse events such as MI and should be
prescribed for all patients with coronary artery disease indefinitely.

Invasive treatment

1. Percutaneous coronary intervention (PCI) (angioplasty with stent)

• Is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small
structure called a stent to open up blood vessels in the heart that have been narrowed
by plaque buildup.

• A catheter is inserted into the blood vessels either in the groin or in the arm. Using a
special type of X-ray called fluoroscopy, the catheter is threaded through the blood
vessels into the heart where the coronary artery is narrowed
When the tip is in place, a balloon tip covered with a stent is inflated. The balloon tip
compresses the plaque and expands the stent. Once the plaque is compressed and the stent is
in place, the balloon is deflated and withdrawn

2. Coronary artery bypass grafting (CABG) (Revascularization)

• Coronary artery bypass grafts (CABG) deliver a new source of blood to regions of the
heart served by blocked arteries. Surgeons use segments of the patient's own veins
and arteries to go around, or bypass these blockages. If left untreated, severely
blocked arteries may lead to heart attack or death. Coronary bypass operations are
performed half a million times a year with an overall success rate of almost 98 percent.

Treatment for stable angina

Drug

- Nitrates
- Beta blockers
- Calcium Channel Blockers
- Atherosclerotic disease tx (HTN, Lipids)

Surgery

- Bypass
- PCI (PTCA, Stent)
- Experimental

Drugs

Antiplatelet

- ASA (prostaglandin)
- Clopidogrel (ADP)
- Integrilin (GP IIb/IIIa)

Anti Clotting factors

- Heparins (intrinsic)
• UF Heparin
• LMWH
- Fondaparinux (intrinsic)
- Warfarin (extrinsic)

Cardial and extracardial causes of chest discomfort

CARDIOVASCULAR DISEASES

- Ischemic heart disease

- Pericarditis
- Aortic dissection
 - Congestive heart failure
- Aortic stenosis and regurgitation
- Hypertrophic cardiomyopathy
- Pulmonary hypertension

LUNG DISEASES

- Pulmonary embolism
- Pneumothorax
- Pleuro-pneumonia
- Pleuritis

GASTROESOPHAGEAL DISEASES

- Gastroesophageal reflux
- Esophageal motility disorders
- Paptic ulcer
- Gallstones

NEUROMUSCULOSKELETAL DISEASES

- Fracture of sternum or rib

- Spondylarthrosis
- Periarthritis humeroscapularis
- Intercostal muscle cramp
- Tietze’ s syndrome

MISCELLANEOUS

- Subphrenic abscess
- Herpes zoster
- Splenic infraction
- Psychiatric disease

Differential diagnosis of chest discomfort

Acute myocardial infarction

- The duration of the pain often more than 30 min

- Often more severe than angina
- Unrielived by nitroglicerin
- May be associated with evidence of heart failure or arrhythmia

Aortic dissection

- Tearing, ripping pain with abrupt onset

- Associated with hypertension, and/or connective tissue disorder
- Depending on the location of dissection:
• Loss of peripheral pulse
• Pericardial tamponad
• Murmur of aortic insufficiency
Pericarditis

- The duration of the pain is hours to days

- Sharp, retrosternal pain that is aggravated by coughing, deep breath, or changes in
body position (relieved by sitting and leaning forward)

Pulmonary embolism

- Abrupt onset of the pain. Location is often lateral

- Associated symptoms are dyspnea, tachycardy,and occasionally hemoptysis

Pneumothorax

- Sudden onset of pleuritic chest pain. Location:lateral to side of pneumothorax

- Dyspnea, decreased breath sounds, tympanic percussion sound.

Pneumonia or pleuritis

- Localized sharp, knifelike pain

- Pain is aggravated by inspiration and coughing
- Dyspnea, fever, rales, occasionally pleural rub

Esophageal reflux

- Deep, burning discomfort that may be exacerbated by alcohol, aspirin, or some foods
- Worsened by postprandial recumbency, relieved by antacids

Ulcer disease

- Symptoms do not associated with exertion

- Prolonged burning pain
- Typically occurs 60 to 90 min after meals, when postprandial acid production is no
longer neutralized by food in the stomach

Gallbladder disease

- Prolonged colic pain

- Occurs an hour or more after meals

Neuromusculoskeletal diseases

- Cervical disk disease: compression of nerve roots –dermatomal distribution (pain in

dermatomal distribution can also be caused by intercostal muscle cramp and herpes
zoster)
- The pain is aggravated by movement
- Costochondral and chondrosternal syndromes (Tietze’s syndrome)

▪ direct pressure on the costochondral-costosternal junctions may

reproduce the pain.

Psychiatric conditions

- Th symptoms are frquently described as visceral tightness or aching that last more
than 30 min.
Pathophysiology of acute coronary syndrome

• UA/NSTEMI: Caused by a reduction in oxygen supply and/or by an increase in

myocardial oxygen demand superimposed on an atherosclerotic coronary plaque.

• STEMI: coronary blood flow decreases abruptly after a thrombotic occlusion of a

coronary artery previously affected by atherosclerosis.

Diagnostic tests in patients with chest discomfort 1.

• ECG and X-ray are essential test for adults with chest discomfort

First the physician schould be focused on life-threatening problems:

- Presence of electrocardigraphic changes consistent with ischemia or infarction:

• Serum cardiac biomarkers of myocardial injury (Troponin I or T)

• Coronarography,Primary percutaneous coronary intervention

Eval & Tx

ECG

Cardiac Enzymes X 4

- If Ruled in

• Anticoagulation, antiplatelet

• Thrombolytic Therapy

• Cath lab, Emergency bypass

- If Ruled out

• Stress test

• Angiogram

MONA: Morphine, O2, Nitrates, ASA

Coronary heart disease: clinical manifestations and pathology
MI Manifestations

• Prodromal

- Symptoms usually appear 24-72 hours before

- Malaise, Tiredness, Weakness fatigue
- Visual disturbance

• Acute Phase

- Symptoms: Chest Pain, Dyspnea, Nausea, Diaphoresis, weakness, fatigue,

anxiety
- Signs: Gray/ashen, gasping, clutching, loss of consciousness, confused, ECG
changes, tachycardia, tachypnea

ECG changes

• Conductile cells of heart are most sensitive to hypoxia

• Classic: T-wave inversion, ST-elevation, Q waves

• Non-Q wave MI: no Q waves, possibly normal ST segment

• R/O CANNOT be made with ECG alone!!!

Diagnostic evaluation

• Patient's history

• Cigarette smoking

• Hypertension

• Hyperlipidemia

• Family history of coronary artery disease

• Male gender

• Obesity

• Diabetes mellitus

• Lack of regular exercise

• Type A personality

• Diagnostic tests
• Resting ECG, is often normal, even in patients with severe coronary artery disease.
• Exercise ECG, is usually performed using a standard treadmill while monitoring the
patient's ECG, BP and general condition.
• Coronary arteriography, this provides detailed anatomical information about the
extent and nature of coronary artery disease, and is usually performed with a view to
coronary artery bypass graft (CABG) surgery or percutaneous coronary intervention(
PCI).
Time is muscle

- Reduce patient symptoms

- Decrease amount of myocardial necrosis
- Preserve heart function
- Prevent major adverse cardiac events
- Treat life threatening complications

Complications of Acute Myocardial Infarction

- Arrhythmic Complications
- Mechanical Complications
- Ischemic Complications
- Miscellaneous Complications

[DVT, PE, Pericarditits, TPA complications, Pneumonia]

Arrhythmic Complications
[Early < 24 hrs & late >24 hrs]

• Ventricular – PVC, V tach/V Fib

• Atrial – PAC, SVT, A Fib

• Bradycardia – Sinus
 • AV block – Complete Heart Block

• LAFB, LPHB, LBBB & RBBB

Mechanical Complications of Acute Myocardial Infarction

• Papillary Muscle Rupture – Acute MR

• Ventricular Septal Defect

• Right Ventricular MI

• Free Wall Rupture

• Cardiogenic shock

• Cardiac Tamponade

Sudden death

- 250,000 deaths in the US per year are caused by what is referred to as

“sudden” cardiac death
- Sudden Cardiac Death is also known as a “Massive Heart Attack” in which the
heart converts from sinus rhythm to ventricular fibrillation
- In V-Fib, the heart is unable to contract fully resulting in lack of blood being
pumped to the vital organs
- V-Fib requires shock from defibrillator “SHOCKABLE RHYTHM”

CT of patients with stroke as a complication of MI (a)

Management of Acute Myocardial Infarction

Pre discharge work up

- Secondary prevention – Diet, Exercise, Weight control, Smoking cessation

- Lipid control
- B Blockers, ACE Inhibitors, ASA, Statins
- Cardiac Rehabilitation
- Discharge planning
- Pre discharge ECHO, Stress test
 CONGESTIVE HEART FAILURE
Definition

Heart failure describes the clinical syndrome that develops when the heart cannot maintain an
adequate cardiac output. The heart pumps blood inadequately, leading to reduced blood
flows, back-up (congestion) of blood in the veins and lungs, and other changes that may
further weaken the heart.

The vicious cycle of congestive heart failure

Types of heart failure

Low-Output heart failure:

- Systolic heart failure:

✓ Decreased cardiac output
✓ Decreased left ventricular ejection fraction
- Diastolic heart failure:
✓ Elevated left and right ventricular end-diastolic pressures
✓ May have normal LVEF

High-Output heart failure:

- Seen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism,

beri-beri, carcinoid, anemia.
- Often have normal cardiac output
Right-Ventricular failure:

- Seen with pulmonary hypertension, large RV infarctions.

Causes of low-output heart failure

Systolic dysfunction

- Coronary artery disease

- Idiopathic dilated cardiomyopathy (DCM)
✓ 50% idiopathic (at least 25% familial)
✓ 9% myocarditis (viral)
✓ Prepartum, hypertension, HIV, connective tissue disease, substance
abuse, doxorubicin
- Hypertension
- Valvular heart disease

Diastolic dysfunction

- Hypertension
- Coronary artery disease
- Hypertrophic obstructive cardiomyopathy (HCM)
- Restrictive cardiomyopathy
Compensatory mechanism of heart failure

- Renin-angiotensin-aldosterone system
- Sympathetic nervous system
- Enlargement of the muscular walls of ventricles (ventricular hyper..)

Clinical presentation of heart failure

- Due to excess fluid accumulation:

▪ Dyspnea (most sensitive symptom)
▪ Edema
▪ Hepatic congestion
▪ Ascites
▪ Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
- Due to reduction in cardiac ouput:
• Fatigue (especially with exertion)
• Weakness
Physical examination in heart failure

- S3 gallop: low sensitivity, but highly specific

- Cool, pale, cyanotic extremities: have sinus tachycardia, diaphoresis and peripheral
vasoconstriction
- Crackles or decreased breath sounds at bases (effusions) on lung exam
- Elevated jugular venous pressure
- Lower extremity edema
- Ascites
- Hepatomegaly
- Splenomegaly
- Displaced PMI
• Apical impulse that is laterally displaced past the midclavicular line is usually
indicative of left ventricular enlargement.

Lab analysis in heart failure

- CBC: since anemia can exacerbate heart failure

- Serum electrolytes and creatinine: before starting high dose diuretics
- Fasting blood glucose: to evaluate for possible diabetes mellitus
- Thyroid function tests: since thyrotoxicosis can result in A. Fib, and hypothyroidism can
results in HF.
- Iron studies: To screen for hereditary hemochromatosis as cause of heart failure.
- ANA: To evaluate for possible lupus
- Viral studies: If viral mycocarditis suspected
Laboratory analysis (cont.)

BNP

- With chronic heart failure, atrial mycotes secrete increase amounts of atrial natriuretic
peptide (ANP) and brain natriuretic pepetide (BNP) in response to high atrial and
ventricular filling pressures
- Usually is > 400 pg/mL in patients with dyspnea due to heart failure.

Chest X-ray in heart failure

- Cardiomegaly
- Cephalization of the pulmonary vessels
- Kerley B-lines
- Pleural effusions
Cardiac testing in heart failure

Electrocardiogram:

- May show specific cause of heart failure:

• Ischemic heart disease
• Dilated cardiomyopathy: first degree AV block, LBBB, Left anterior fascicular
block
• Amyloidosis: pseudo-infarction pattern
• Idiopathic dilated cardiomyopathy: LVH

Echocardiogram:

- Left ventricular ejection fraction

- Structural/valvular abnormalities

Further Cardiac Testing in Heart Failure

Exercise Testing

- Should be part of initial evaluation of all patients with CHF.

Coronary arteriography

- Should be performed in patients presenting with heart failure who have angina or
significant ischemia
- Reasonable in patients who have chest pain that may or may not be cardiac in origin,
in whom cardiac anatomy is not known, and in patients with known or suspected
coronary artery disease who do not have angina.
- Measure cardiac output, degree of left ventricular dysfunction, and left ventricular
end-diastolic pressure.

Endomyocardial biopsy

- Not frequently used

- Really only useful in cases such as viral-induced cardiomyopathy
Classification of Heart Failure (cont.)

ACC/AHA Guidelines

- Stage A – High risk of HF, without structural heart disease or symptoms

- Stage B – Heart disease with asymptomatic left ventricular dysfunction
- Stage C – Prior or current symptoms of HF
- Stage D – Advanced heart disease and severely symptomatic or refractory HF

Chronic Treatment of Systolic Heart Failure

Correction of systemic factors

- Thyroid dysfunction
- Infections
- Uncontrolled diabetes
- Hypertension

Lifestyle modification

- Lower salt intake

- Alcohol cessation
- Medication compliance

Maximize medications

- Discontinue drugs that may contribute to heart failure (NSAIDS, antiarrhythmics,

calcium channel blockers)
Order of therapy

1. Loop diuretics

2. ACE inhibitor (or ARB if not tolerated)

3. Beta blockers

4. Digoxin

5. Hydralazine, Nitrate

6. Potassium sparing diuretics

Diuretics

Loop diuretics

- Furosemide, buteminide
- For Fluid control, and to help relieve symptoms

Potassium-sparing diuretics

- Spironolactone, eplerenone
- Help enhance diuresis
- Maintain potassium
- Shown to improve survival in CHF

ACE Inhibitor

Improve survival in patients with all severities of heart failure.

Begin therapy low and titrate up as possible:

- Enalapril – 2.5 mg po BID

- Captopril – 6.25 mg po TID
- Lisinopril – 5 mg po QDaily

If cannot tolerate, may try ARB

Beta Blocker therapy

Certain Beta blockers (carvedilol, metoprolol, bisoprolol) can improve overall and event free
survival in NYHA class II to III HF, probably in class IV.

Contraindicated:

- Heart rate <60 bpm

- Symptomatic bradycardia
- Signs of peripheral hypoperfusion
- COPD, asthma
- PR interval > 0.24 sec, 2nd or 3rd degree block
Hydralazine plus Nitrates

Dosing:

- Hydralazine
• Started at 25 mg po TID, titrated up to 100 mg po TID
- Isosorbide dinitrate
• Started at 40 mg po TID/QID

Decreased mortality, lower rates of hospitalization, and improvement in quality of life.

Digoxin

Given to patients with HF to control symptoms such as fatigue, dyspnea, exercise intolerance.

Shown to significantly reduce hospitalization for heart failure, but no benefit in terms of
overall mortality.

Other important medication in Heart Failure – Statins

Statin therapy is recommended in CHF for the secondary prevention of cardiovascular disease.

Some studies have shown a possible benefit specifically in HF with statin therapy

- Improved LVEF
- Reversal of ventricular remodeling
- Reduction in inflammatory markers (CRP, IL-6, TNF-alpha II)

Meds to AVOID in heart failure

NSAIDS

- Can cause worsening of preexisting HF

Thiazolidinediones

- Include rosiglitazone (Avandia), and pioglitazone (Actos)

- Cause fluid retention that can exacerbate HF

Metformin

- People with HF who take it are at increased risk of potentially lethic lactic acidosis
Implantable Cardioverter-Defibrillators for HF

Sustained ventricular tachycardia is associated with sudden cardiac death in HF.

About one-third of mortality in HF is due to sudden cardiac death.

Patients with ischemic or nonischemic cardiomyopathy, NYHA class II to III HF, and LVEF ≤ 35%
have a significant survival benefit from an implantable cardioverter-defibrillator (ICD) for the
primary prevention of SCD.
Management of Refractory Heart Failure

Inotropic drugs:

- Dobutamine, dopamine, milrinone, nitroprusside, nitroglycerin

Mechanical circulatory support:

- Intraaortic balloon pump

- Left ventricular assist device (LVAD)

Cardiac Transplantation

- A history of multiple hospitalizations for HF

- Escalation in the intensity of medical therapy
- A reproducable peak oxygen consumption with maximal exercise (VO2max) of < 14
mL/kg per min. (normal is 20 mL/kg per min. or more) is relative indication, while a
VO2max < 10 mL/kg per min is a stronger indication.
Acute Decompensated Heart Failure

- Cardiogenic pulmonary edema is a common and sometimes fatal cause of acute

respiratory distress.
- Characterized by the transudation of excess fluid into the lungs secondary to an
increase in left atrial and subsequently pulmonary venous and pulmonary capillary
pressures.
Acute Decompensated Heart Failure (cont.)

Causes:

- Acute MI
• Rupture of chordae tendinae/acute mitral valve insufficiency
- Volume Overload
• Transfusions, IV fluids
• Non-compliance with diuretics, diet (high salt intake)
- Worsening valvular defect
• Aortic stenosis

Decompensated Heart Failure

Symptoms

- Severe dyspnea
- Cough

Clinical Findings

- Tachypnea
- Tachycardia
- Hypertension/Hypotension
- Crackles on lung exam
- Increased JVD
- S3, S4 or new murmur
Labs/Studies in Acute Decompensated Heart Failure

- Chemistry, CBC
- EKG
- Chest X-ray
- May consider cardiac enzymes
- 2D-Echo
Decompensated Heart Failure

Treatment

- Strict I’s and O’s, daily weights

- Oxygen, mechanical ventilation if needed
- Loop diuretics (Lasix!)
- Morphine
- Vasodilator therapy (nitroglycerin)
- Nesiritide (BNP) – can help in acute setting, for short term therapy
 HYPERTENSION

1. Overview, definition, classification

2. Detection
3. Evaluation
4. Non-pharmacologic Intervention
5. Treatment

Problem Magnitude

Hypertension( HTN) is the most common primary diagnosis in America.

35 million office visits are as the primary diagnosis of HTN.

50 million or more Americans have high BP.

Worldwide prevalence estimates for HTN may be as much as 1 billion.

7.1 million deaths per year may be attributable to hypertension.

Definition

A systolic blood pressure ( SBP) >139 mmHg and/or

A diastolic (DBP) >89 mmHg.

Based on the average of two or more properly measured, seated BP readings.

On each of two or more office visits.

Accurate Blood Pressure Measurement

The equipment should be regularly inspected and validated.

The operator should be trained and regularly retrained.

The patient must be properly prepared and positioned and seated quietly for at least 5
minutes in a chair.

The auscultatory method should be used.

Caffeine, exercise, and smoking should be avoided for at least 30 minutes before BP
measurement.

An appropriately sized cuff should be used.

BP Measurement

At least two measurements should be made and the average recorded.

Clinicians should provide to patients their specific BP numbers and the BP goal of their
treatment.
Classification
Follow-up based on initial BP measurements for adults*

*Without acute end-organ damage

Prehypertension

SBP >120 mmHg and <139mmHg and/or

DBP >80 mmHg and <89 mmHg.

Prehypertension is not a disease category rather a designation for individuals at high risk of
developing HTN.

Pre-HTN

Individuals who are prehypertensive are not candidates for drug therapy but

Should be firmly and unambiguously advised to practice lifestyle modification

Those with pre-HTN, who also have diabetes or kidney disease, drug therapy is indicated if a
trial of lifestyle modification fails to reduce their BP to 130/80 mmHg or less.

Isolated Systolic Hypertension

Not distinguished as a separate entity as far as management is concerned.

SBP should be primarily considered during treatment and not just diastolic BP.

Systolic BP is more important cardiovascular risk factor after age 50.

Diastolic BP is more important before age 50.

Frequency Distribution of Untreated HTN by Age

Hypertensive Crises

Hypertensive Urgencies: No progressive target-organ dysfunction. (Accelerated Hypertension)

Hypertensive Emergencies: Progressive end-organ dysfunction. (Malignant Hypertension)

Hypertensive Urgencies

Severe elevated BP in the upper range of stage II hypertension.

Without progressive end-organ dysfunction.

Examples: Highly elevated BP without severe headache, shortness of breath or chest pain.

Usually due to under-controlled HTN.

Hypertensive Emergencies

Severely elevated BP (>180/120mmHg).

With progressive target organ dysfunction.

Require emergent lowering of BP.

Examples: Severely elevated BP with:

- Hypertensive encephalopathy
- Acute left ventricular failure with pulmonary edema
- Acute MI or unstable angina pectoris
- Dissecting aortic aneurysm
Types of Hypertension

Primary HTN:

also known as essential HTN.

accounts for 95% cases of HTN.

no universally established cause known.

Secondary HTN:

less common cause of HTN ( 5%).

secondary to other potentially rectifiable causes.

Causes of Secondary HTN

Common

- Intrinsic renal disease

- Renovascular disease
- Mineralocorticoid excess
- Sleep Breathing disorder

Uncommon

- Pheochromocytoma
- Glucocorticoid excess
- Coarctation of Aorta
- Hyper/hypothyroidism

Secondary HTN-Clues in Medical History

Onset: at age < 30 years ( Fibromuscular dysplasia) or > 55 (atherosclerotic renal artery
stenosis), sudden onset (thrombus or cholesterol embolism).

Severity: Grade II, unresponsive to treatment.

Episodic, headache and chest pain/palpitation (pheochromocytoma, thyroid dysfunction).

Morbid obesity with history of snoring and daytime sleepiness (sleep disorders)

Secondary HTN-clues on Exam

Pallor, edema, other signs of renal disease.

Abdominal bruit especially with a diastolic component (renovascular)

Truncal obesity, purple striae, buffalo hump (hypercortisolism)

Secondary HTN-Clues on Routine Labs

Increased creatinine, abnormal urinalysis (renovascular and renal parenchymal disease)

Unexplained hypokalemia (hyperaldosteronism)

Impaired blood glucose (hypercortisolism)

Impaired TFT (Hypo-/hyper- thyroidism)

Secondary HTN-Screening Tests

Renal Parenchymal Disease

Common cause of secondary HTN (2-5%)

HTN is both cause and consequence of renal disease

Multifactorial cause for HTN including disturbances in Na/water balance, vasodepressors/

prostaglandins imbalance

Renal disease from multiple etiologies.

Renovascular HTN

Atherosclerosis 75-90% ( more common in older patients)

Fibromuscular dysplasia 10-25% (more common in young patients, especially females)

Other

• Aortic/renal dissection

• Takayasu’s arteritis

• Thrombotic/cholesterol emboli

• CVD
 • Post transplantation stenosis

• Post radiation

Complications of Prolonged Uncontrolled HTN

Changes in the vessel wall leading to vessel trauma and arteriosclerosis throughout the
vasculature

Complications arise due to the “target organ” dysfunction and ultimately failure.

Damage to the blood vessels can be seen on fundoscopy.

Target Organs

- CVS (Heart and Blood Vessels)

- The kidneys
- Nervous system
- The Eyes

Effects On CVS

- Ventricular hypertrophy, dysfunction and failure

- Arrhythmia
- Coronary artery disease, Acute M
- Arterial aneurysm, dissection, and rupture.

Effects on The Kidneys

Glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease.

Ischemic kidney disease especially when renal artery stenosis is the cause of HTN

Nervous System

- Stroke, intracerebral and subarachnoid hemorrhage.

- Cerebral atrophy and dementia

The Eyes

Retinopathy, retinal hemorrhages and impaired vision.

Vitreous hemorrhage, retinal detachment

Neuropathy of the nerves leading to extraocular muscle paralysis and dysfunction

Retina Normal and Hypertensive Retinopathy

Stage I- Arteriolar Narrowing

Stage II- AV Nicking

AV Nicking

Stage III- Hemorrhages (H), Cotton Wool Spots and Exudates (E)

Stage IV- Stage III+Papilledema

Patient Evaluation Objectives

1. To assess lifestyle and identify other cardiovascular risk factors or concomitant disorders
that may affect prognosis and guide treatment

2. To reveal identifiable causes of high BP

3. To assess the presence or absence of target organ damage and CVD

1. Cardiovascular Risk factors

- Hypertension
- Cigarette smoking
- Obesity (body mass index ≥30 kg/m2)
- Physical inactivity
- Dyslipidemia
- Diabetes mellitus
- Microalbuminuria or estimated GFR <60 mL/min
- Age (older than 55 for men, 65 for women)
- Family history of premature cardiovascular disease (men under age 55 or
women under age 65)
 2. Identifiable Causes of HTN
- Sleep apnea
- Drug-induced or related causes
- Chronic kidney disease
- Primary aldosteronism
- Renovascular disease
- Chronic steroid therapy and Cushing’s syndrome
- Pheochromocytoma
- Coarctation of the aorta
- Thyroid or parathyroid disease

3. Target Organ Damage

Heart

Left ventricular hypertrophy

Angina or prior myocardial infarction

Prior coronary revascularization

Heart failure

Brain

Stroke or transient ischemic attack

Chronic kidney disease

Peripheral arterial disease

Retinopathy

History

Angina/MI Stroke: Complications of HTN, Angina may improve with b-blokers

Asthma, COPD: Preclude the use of b-blockers

Heart failure: ACE inhibitors indication

DM: ACE preferred

Polyuria and nocturia: Suggest renal impairment

Claudication: May be aggravated by b-blockers, atheromatous RAS may be present

Gout: May be aggravated by diuretics

Use of NSAIDs: May cause or aggravate HTN

Family history of HTN: Important risk factor

Family history of premature death: May have been due to HTN

Family history of DM : Patient may also be Diabetic

Cigarette smoker: Aggravate HTN, independently a risk factor for CAD and stroke

High alcohol: A cause of HTN

High salt intake: Advice low salt intake

Examination

Appropriate measurement of BP in both arms

Optic fundi

Calculation of BMI ( waist circumference also may be useful)

Auscultation for carotid, abdominal, and femoral bruits

Palpation of the thyroid gland.

Thorough examination of the heart and lungs

Abdomen for enlarged kidneys, masses, and abnormal aortic pulsation

Lower extremities for edema and pulses

Neurological assessment

Routine Labs

EKG.
Urinalysis.

Blood glucose and hematocrit; serum potassium, creatinine ( or estimated GFR), and calcium.

HDL cholesterol, LDL cholesterol, and triglycerides.

Optional tests

urinary albumin excretion.

albumin/creatinine ratio.

Goals of Treatment

Treating SBP and DBP to targets that are <140/90 mmHg

Patients with diabetes or renal disease, the BP goal is <130/80 mmHg

The primary focus should be on attaining the SBP goal.

To reduce cardiovascular and renal morbidity and mortality

Benefits of Treatment

Reductions in stroke incidence, averaging 35–40 percent

Reductions in MI, averaging 20–25 percent

Reductions in HF, averaging >50 percent.

Lifestyle modifications

Lifestyle Changes Beneficial in Reducing Weight

Decrease time in sedentary behaviors such as watching television, playing video games, or
spending time online.

Increase physical activity such as walking, biking, aerobic dancing, tennis, soccer, basketball,
etc.

Decrease portion sizes for meals and snacks.

Reduce portion sizes or frequency of consumption of calorie containing beverages.

DASH Diet

Dietary approaches to Stop Hypertension

As effective as one medication

JNC 7 Reference Card
Causes of Resistant Hypertension

Improper BP measurement

Excess sodium intake

Inadequate diuretic therapy

Medication

- Inadequate doses
- Drug actions and interactions (e.g., (NSAIDs), illicit drugs, sympathomimetics,
OCP)
- Over-the-counter drugs and some herbal supplements

Excess alcohol intake

Identifiable causes of HTN

CONCLUSION - TAKE HOME MESSAGE

• Hypertension is a major cause of morbidity and mortality, and needs to be treated

• It is an extremely common condition; however it is still under-diagnosed and

undertreated

• Hypertension is easy to diagnose and easy to treat

• Aim of the management is to save the target organ from the deleterious effect
• Besides pharmacology we have other choices and one has to be acquainted with that
choice

• Life style modification should always be encouraged in all Hypertensive patients

 RESPIRATORY PHYSIOLOGY
Basic concepts
Basics of the Respiratory System

- Functions & functional anatomy

Gas Laws

Ventilation

Diffusion & Solubility

Gas Exchange

- Lungs
- Tissues

Gas Transport in Blood

Regulation of Ventilation & Impacts on

- Gas levels, Ph

General Functions

Exchange of gases

• Directionality depends on gradients!

– Atmosphere to blood

– Blood to tissues

Regulation of pH

- Dependent on rate of CO2 release

Protection

Vocalization

Synthesis

Respiration

What is respiration?

- Respiration = the series of exchanges that leads to the uptake of oxygen by the cells,
and the release of carbon dioxide to the lungs

Step 1 = ventilation

- Inspiration & expiration

Step 2 = exchange between alveoli (lungs) and pulmonary capillaries (blood)

- Referred to as External Respiration

Step 3 = transport of gases in blood

Step 4 = exchange between blood and cells

- Referred to as Internal Respiration

Cellular respiration = use of oxygen in ATP synthesis

Schematic View of Respiration

Exchange II: lung to blood → External respiration

Exchange III: blood to cells → Internal respiration

Functional Anatomy

What structural aspects must be considered in the process of respiration?

- The conduction portion

- The exchange portion
- The structures involved with
ventilation

• Skeletal & musculature

• Pleural membranes

• Neural pathways

All divided into

- Upper respiratory tract

• Entrance to larynx

- Lower respiratory tract

• Larynx to alveoli (trachea

to lungs)
Bones, Muscles & Membranes

Function of these Bones, Muscles & Membranes

Create and transmit a pressure gradient

- Relying on
+ the attachments of the muscles to the ribs (and overlying tissues)

+ the attachment of the diaphragm to the base of the lungs and

associated pleural membranes

+ the cohesion of the parietal pleural membrane to the visceral pleural

membrane

+ expansion & recoil of the lung and therefore alveoli with the
movement of the overlying structures
Functional Anatomy

Pleural Membrane Detail

- Cohesion between parietal and visceral layers is due to serous fluid in the pleural
cavity

• Fluid (30 ml of fluid) creates an attraction between the two sheets of

membrane

• As the parietal membrane expands due to expansion of the thoracic

cavity it “pulls” the visceral membrane with it

– And then pulls the underlying structures which expand as well

• Disruption of the integrity of the pleural membrane will result in a rapid

equalization of pressure and loss of ventilation function = collapsed
lung or pneumothorax

The Respiratory Tree

- connecting the external environment to the exchange portion of the lungs

- similar to the vascular component
- larger airway = higher flow & velocity

• small cross-sectional area

- smaller airway = lower flow & velocity

• large cross-sectional area

- Upper respiratory tract is for all intensive purposes a single large conductive tube
- The lower respiratory tract starts after the larynx and divides again and again… and
again to eventually get to the smallest regions which form the exchange membranes.

Conductive portion:

• Trachea

• Primary bronchi

• Secondary bronchi

• Tertiary bronchi

• Bronchioles

• Terminal bronchioles

Exchange portion

• Respiratory bronchioles with start of alveoli outpouches

• Alveolar ducts with outpouchings of alveoli

Structures of the Lower Respiratory Tract

What is the function of the upper respiratory tract?

- Warm: raises incoming air to 37 celsius

- Humidify: raises incoming air to 100% humidity
- Filter: forms mucociliary escalator
- Vocalize

What is the function of the lower respiratory tract?

- Exchange of gases …. Due to

• Huge surface area = 1x105 m2 of type I alveolar cells (simple squamous

epithelium)

• Associated network of pulmonary capillaries

– 80-90% of the space between alveoli is filled with blood in

pulmonary capillary networks

• Exchange distance is approx 1 um from alveoli to blood!

- Protection

• Free alveolar macrophages (dust cells)

• Surfactant produced by type II alveolar cells (septal cells)

Characteristics of exchange membrane

- High volume of blood through huge capillary network results in

• Fast circulation through lungs

– Pulmonary circulation = 5L/min through lungs….

– Systemic circulation = 5L/min through entire body!

• Blood pressure is low…

– Means

» Filtration is not a main theme here, we do not want a

net loss of fluid into the lungs as rapidly as the
systemic tissues

» Any excess fluid is still returned via lymphatic system

Gas Laws

- Basic Atmospheric conditions

– Pressure is typically measured in mm Hg

– Atmospheric pressure is 760 mm Hg

– Atmospheric components

• Nitrogen = 78% of our atmosphere

• Oxygen = 21% of our atmosphere

• Carbon Dioxide = .033% of our atmosphere

• Water vapor, krypton, argon, …. Make up the rest

How does Boyle’s Law work in us?

- As the thoracic cavity (container) expands the volume must up and pressure goes
down

• If it goes below 760 mm Hg what happens?

- As the thoracic cavity shrinks the volume must go down and pressure goes up

• If it goes above 760 mm Hg what happens

Ventilation

Terminology

- Inspiration = the movement of air into the respiratory tracts (upper & lower)
- Expiration = movement of air out of the respiratory tracts
- Respiratory cycle is one inspiration followed by an expiration

Cause of Inspiration?

- Biological answer

• Contraction of the inspiratory muscles causes an increase in the thoracic

cavity size, thus allowing air to enter the respiratory tract

- Physics answer

• As the volume in the thoracic cavity increases (due to inspiratory muscle

action) the pressure within the respiratory tract drops below
atmospheric pressure, creating a pressure gradient which causes
molecular movement to favor moving into the respiratory tract

- Cause of Expiration?

Besides the diaphragm (only creates about 60-75% of the volume change) what are the
muscles of inspiration & expiration?
What are the different respiratory patterns?

- Quiet breathing (relaxed)

- Forced inspirations & expirations

Respiratory volumes follow these respiratory patterns…

Inspiration

- Occurs as alveolar pressure drops below atmospheric pressure

• For convenience atmospheric pressure = 0 mm Hg

– A (-) value then indicates pressure below atmospheric P

– A (+) value indicates pressure above atmospheric P

• At the start of inspiration (time = 0),

– atmospheric pressure = alveolar pressure

» No net movement of gases!

• At time 0 to 2 seconds

– Expansion of thoracic cage and corresponding pleural

membranes and lung tissue causes alveolar pressure to drop
to -1 mm Hg

– Air enters the lungs down the partial pressure gradient

Expiration

- Occurs as alveolar pressure elevates above atmospheric pressure due to a shrinking

thoracic cage

• At time 2-4 seconds

– Inspiratory muscles relax, elastic tissue of corresponding

structures initiates a recoil back to resting state
 – This decreases volume and correspondingly increases alveolar
pressure to 1 mm Hg

» This is above atmospheric pressure, causing…?

• At time 4 seconds

– Atmospheric pressure once again equals alveolar pressure and

there is no net movement

Both inspiration and expiration can be modified

- Forced or active inspiration

- Forced or active expiration
- The larger and quicker the expansion of the thoracic cavity, the larger the gradient and

• The faster air moves down its pressure gradient

Things to consider

- surfactant effect
- airway diameter
- Minute volume respiration (ventilation rate times tidal volume) & anatomical dead
space

• Leading to a more accurate idea of alveolar ventilation rates

- Changes in ventilation patterns

Surfactant is produced by the septal cells

- Disrupts the surface tension & cohesion of water molecules

- Impact?

• prevents alveoli from sticking together during expiration

Airway diameter & other factors that affect airway resistance?

Manifestations of Pulmonary Disease

Sneezing = reflex response to irritation of upper respiratory tract

Coughing = reflex response to irritation of lower respiratory tract

Sputum production

- If yellowish- green ------ infection

- If rusty ------- blood + pus = pneumococcal pneumonia
- If bloody , called “hemoptysis” ---- usually frothy --- seen in pulm. Edema

• Also seen in pulm. TB & cancer

- Large amounts & foul = bronchiectasis

- Thick & sticky = asthma, cystic fibrosis

Breathing patterns

- Eupnia, labored (dyspnea) , wheezing, stridor

Breath sounds

- Normal, rales, rhonchi, decreased breath sounds

Dyspnea --- discomfort feeling when can’t get enough air

- Orthopnea = dyspnea lying down

Cyanosis --- not a reliable early indicator of hypoxia

Respiratory System Diseases
General Outline

Infectious diseases

- Upper

• URI

• Croup

• Epiglottitis

• Flu (Influenza)

- Lower

• Bronchiolitis (RSV)

• Pneumonia

• SARS

• TB

• Fungal diseases

- Obstructive lung diseases

– Cystic fibrosis

– Cancer

– Aspiration pneumonia

– Asthma

COPD (chronic obstr. pulm. dis)

– Emphysema

– Chronic bronchitis

• Restrictive lung diseases

– Chest wall abnormalities

– Connective tissue abnormalities

• Pneumoconioses

• Vascular disorders

– Pulmonary edema

– Pulmonary embolism

• Expansion disorders
– Atelectasis

– Pleural effusion

– Pneumothorax

– Resp. distress syndrome

• Infant

• adult
 GLOBAL INITIATIVE FOR ASTHMA

Burden of asthma

Asthma is one of the most common chronic diseases worldwide with an estimated 300 million
affected individuals.

Prevalence is increasing in many countries, especially in children.

Asthma is a major cause of school and work absence.

Health care expenditure on asthma is very high:

▪ Developed economies might expect to spend 1-2 percent of total health care
expenditures on asthma.

▪ Developing economies likely to face increased demand due to increasing

prevalence of asthma.

▪ Poorly controlled asthma is expensive.

▪ However, investment in prevention medication is likely to yield cost savings in

emergency care.

Prevalence of asthma in children aged 13-14 years

Stepwise approach to control asthma symptoms and reduce risk

Definition and diagnosis of asthma

What is known about asthma?

Asthma is a common and potentially serious chronic disease that can be controlled but not
cured

Asthma causes symptoms such as wheezing, shortness of breath, chest tightness and cough
that vary over time in their occurrence, frequency and intensity

Symptoms are associated with variable expiratory airflow,

i.e. difficulty breathing air out of the lungs due to

▪ Bronchoconstriction (airway narrowing)

▪ Airway wall thickening

▪ Increased mucus

Symptoms may be triggered or worsened by factors such as viral infections, allergens, tobacco
smoke, exercise and stress.

Asthma can be effectively treated

When asthma is well-controlled, patients can

✓ Avoid troublesome symptoms during the day and night

✓ Need little or no reliever medication

✓ Have productive, physically active lives

✓ Have normal or near-normal lung function

✓ Avoid serious asthma flare-ups (also called exacerbations, or severe attacks)

Definition of asthma

Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation.

It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest
tightness and cough that vary over time and in intensity, together with variable expiratory
airflow limitation.

Diagnosis of asthma

The diagnosis of asthma should be based on:

- A history of characteristic symptom patterns

- Evidence of variable airflow limitation, from bronchodilator reversibility testing or
other tests

Document evidence for the diagnosis in the patient’s notes, preferably before starting
controller treatment

- It is often more difficult to confirm the diagnosis after treatment has been started

Asthma is usually characterized by airway inflammation and airway hyperresponsiveness, but

these are not necessary or sufficient to make the diagnosis of asthma.
Diagnosis of asthma – symptoms

Increased probability that symptoms are due to asthma if:

- More than one type of symptom (wheeze, shortness of breath, cough, chest tightness)
- Symptoms often worse at night or in the early morning
- Symptoms vary over time and in intensity
- Symptoms are triggered by viral infections, exercise, allergen exposure, changes in
weather, laughter, irritants such as car exhaust fumes, smoke, or strong smells

Decreased probability that symptoms are due to asthma if:

- Isolated cough with no other respiratory symptoms

- Chronic production of sputum
- Shortness of breath associated with dizziness, light-headedness or peripheral tingling
- Chest pain
- Exercise-induced dyspnea with noisy inspiration (stridor)
Diagnosis of asthma – variable airflow limitation

Confirm presence of airflow limitation

- Document that FEV1/FVC is reduced (at least once, when FEV1 is low)
- FEV1/ FVC ratio is normally >0.75 – 0.80 in healthy adults, and
>0.90 in children

Confirm variation in lung function is greater than in healthy individuals

- The greater the variation, or the more times variation is seen, the greater probability
that the diagnosis is asthma
- Excessive bronchodilator reversibility (adults: increase in FEV1 >12% and >200mL;
children: increase >12% predicted)
- Excessive diurnal variability from 1-2 weeks’ twice-daily PEF monitoring (daily
amplitude x 100/daily mean, averaged)
- Significant increase in FEV1 or PEF after 4 weeks of controller treatment
- If initial testing is negative:

• Repeat when patient is symptomatic, or after withholding

bronchodilators

• Refer for additional tests (especially children ≤5 years, or the elderly)

Typical spirometric tracings

Diagnosis of asthma – physical examination

Physical examination in people with asthma

- Often normal
- The most frequent finding is wheezing on auscultation, especially on forced expiration
Wheezing is also found in other conditions, for example:

- Respiratory infections
- COPD
- Upper airway dysfunction
- Endobronchial obstruction
- Inhaled foreign body

Wheezing may be absent during severe asthma exacerbations (‘silent chest’)

Assessment of asthma

1. Asthma control - two domains

▪ Assess symptom control over the last 4 weeks

▪ Assess risk factors for poor outcomes, including low lung function

2. Treatment issues

▪ Check inhaler technique and adherence

▪ Ask about side-effects

▪ Does the patient have a written asthma action plan?

▪ What are the patient’s attitudes and goals for their asthma?

3. Comorbidities

▪ Think of rhinosinusitis, GERD, obesity, obstructive sleep apnea, depression,

anxiety

▪ These may contribute to symptoms and poor quality of life

GINA assessment of symptom control

Assessment of risk factors for poor asthma outcomes
The role of lung function in asthma

Diagnosis

- Demonstrate variable expiratory airflow limitation

- Reconsider diagnosis if symptoms and lung function are discordant

• Frequent symptoms but normal FEV1: cardiac disease; lack of fitness?

• Few symptoms but low FEV1: poor perception; restriction of lifestyle?

Risk assessment

- Low FEV1 is an independent predictor of exacerbation risk

Measure lung function to monitor progress

- At diagnosis and 3-6 months after starting treatment (to identify personal best)
- Periodically thereafter, at least every 1-2 years for most adults;
more often for high risk patients and for children, depending on age and asthma
severity
- Consider long-term PEF monitoring for patients with severe asthma or impaired
perception of airflow limitation

Adjusting treatment?

- Utility of lung function for adjusting treatment is limited by between-visit variability of

FEV1 (15% year-to-year)

Assessing asthma severity

How?

- Asthma severity is assessed retrospectively from the level of treatment required to

control symptoms and exacerbations

When?

- Assess asthma severity after patient has been on controller treatment for several
months
- Severity is not static – it may change over months or years, or as different treatments
become available

Categories of asthma severity

- Mild asthma: well-controlled with Steps 1 or 2 (as-needed SABA or low dose ICS)
- Moderate asthma: well-controlled with Step 3 (low-dose ICS/LABA)
- Severe asthma: requires Step 4/5 (moderate or high dose ICS/LABA ± add-on), or
remains uncontrolled despite this treatment
Goals of asthma management

The long-term goals of asthma management are

1. Symptom control: to achieve good control of symptoms and maintain normal

activity levels

2. Risk reduction: to minimize future risk of exacerbations, fixed airflow

limitation and medication side-effects

Achieving these goals requires a partnership between patient and their health care providers

3. Ask the patient about their own goals regarding their asthma

4. Good communication strategies are essential

5. Consider the health care system, medication availability, cultural and personal
preferences and health literacy

Key strategies to facilitate good communication

Improve communication skills

- Friendly manner
- Allow the patient to express their goals, beliefs and concerns
- Empathy and reassurance
- Encouragement and praise
- Provide appropriate (personalized) information
- Feedback and review

Benefits include:

- Increased patient satisfaction

- Better health outcomes
- Reduced use of health care resources

Initial controller treatment for adults, adolescents and children 6–11 years

Start controller treatment early

- For best outcomes, initiate controller treatment as early as possible after making the
diagnosis of asthma

Indications for regular low-dose ICS - any of:

- Asthma symptoms more than twice a month

- Waking due to asthma more than once a month
- Any asthma symptoms plus any risk factors for exacerbations

Consider starting at a higher step if:

- Troublesome asthma symptoms on most days

 - Waking from asthma once or more a week, especially if any risk factors for
exacerbations

If initial asthma presentation is with an exacerbation:

- Give a short course of oral steroids and start regular controller treatment (e.g. high
dose ICS or medium dose ICS/LABA, then step down)

Before starting initial controller treatment

- Record evidence for diagnosis of asthma, if possible

- Record symptom control and risk factors, including lung function
- Consider factors affecting choice of treatment for this patient
- Ensure that the patient can use the inhaler correctly
- Schedule an appointment for a follow-up visit

After starting initial controller treatment

- Review response after 2-3 months, or according to clinical urgency

- Adjust treatment (including non-pharmacological treatments)
- Consider stepping down when asthma has been well-controlled for 3 months
-

Stepwise management - pharmacotherapy

Stepwise management – additional components

Step 4 – two or more controllers + as-needed inhaled reliever

Before considering step-up

- Check inhaler technique and adherence

Adults or adolescents: preferred option is combination low dose ICS/formoterol as

maintenance and reliever regimen*, OR
combination medium dose ICS/LABA with as-needed SABA

Children 6–11 years: preferred option is to refer for expert advice

Other options (adults or adolescents)

- Tiotropium by mist inhaler may be used as add-on therapy for patients aged ≥12 years
with a history of exacerbations
- Adults: consider adding SLIT (see Non-pharmacological therapy)
 - Trial of high dose combination ICS/LABA, but little extra benefit and increased risk of
side-effects
- Increase dosing frequency (for budesonide-containing inhalers)
- Add-on LTRA or low dose theophylline

Step 5 – higher level care and/or add-on treatment

Preferred option is referral for specialist investigation and consideration of add-on treatment

- If symptoms uncontrolled or exacerbations persist despite Step 4 treatment, check

inhaler technique and adherence before referring
- Add-on tiotropium for patients ≥12 years with history of exacerbations
- Add-on anti-IgE (omalizumab) for patients with severe allergic asthma
- Add-on anti-IL5 (mepolizumab (SC) or reslizumab (IV)) for severe eosinophilic asthma
(≥12 yrs)

Other add-on treatment options at Step 5 include:

- Sputum-guided treatment: this is available in specialized centres; reduces

exacerbations and/or corticosteroid dose
- Add-on low dose oral corticosteroids (≤7.5mg/day prednisone equivalent): this may
benefit some patients, but has significant systemic side-effects. Assess and monitor for
osteoporosis
- See ERS/ATS Severe Asthma Guidelines (Chung et al, ERJ 2014) for more detail
Low, medium and high dose inhaled corticosteroids
Adults and adolescents (≥12 years)

Reviewing response and adjusting treatment

How often should asthma be reviewed?

- 1-3 months after treatment started, then every 3-12 months

- During pregnancy, every 4-6 weeks
- After an exacerbation, within 1 week

Stepping up asthma treatment

- Sustained step-up, for at least 2-3 months if asthma poorly controlled

• Important: first check for common causes (symptoms not due to asthma,
incorrect inhaler technique, poor adherence)

- Short-term step-up, for 1-2 weeks, e.g. with viral infection or allergen

• May be initiated by patient with written asthma action plan

- Day-to-day adjustment

• For patients prescribed low-dose ICS/formoterol maintenance and

reliever regimen*

Stepping down asthma treatment

- Consider step-down after good control maintained for 3 months

- Find each patient’s minimum effective dose, that controls both symptoms and
exacerbations
General principles for stepping down controller treatment

Aim

- To find the lowest dose that controls symptoms and exacerbations, and minimizes the
risk of side-effects

When to consider stepping down

- When symptoms have been well controlled and lung function stable for
≥3 months
- No respiratory infection, patient not travelling, not pregnant

Prepare for step-down

- Record the level of symptom control and consider risk factors

- Make sure the patient has a written asthma action plan
- Book a follow-up visit in 1-3 months

Step down through available formulations

- Stepping down ICS doses by 25–50% at 3 month intervals is feasible and safe for most
patients (Hagan et al, Allergy 2014)
- See GINA 2017 report Box 3-7 for specific step-down options

Stopping ICS is not recommended in adults with asthma because of risk of exacerbations (Rank
et al, JACI 2013)

Treating modifiable risk factors

Provide skills and support for guided asthma self-management

- This comprises self-monitoring of symptoms and/or PEF, a written asthma action plan
and regular medical review

Prescribe medications or regimen that minimize exacerbations

- ICS-containing controller medications reduce risk of exacerbations

- For patients with ≥1 exacerbations in previous year, consider low-dose ICS/formoterol
maintenance and reliever regimen*

Encourage avoidance of tobacco smoke (active or ETS)

- Provide smoking cessation advice and resources at every visit

For patients with severe asthma

- Refer to a specialist centre, if available, for consideration of add-on medications

and/or sputum-guided treatment

For patients with confirmed food allergy:

- Appropriate food avoidance

- Ensure availability of injectable epinephrine for anaphylaxis
Non-pharmacological interventions

Avoidance of tobacco smoke exposure

- Provide advice and resources at every visit; advise against exposure of children to
environmental tobacco smoke (house, car)

Physical activity

- Encouraged because of its general health benefits. Provide advice about exercise-
induced bronchoconstriction

Occupational asthma

- Ask patients with adult-onset asthma about work history. Remove sensitizers as soon
as possible. Refer for expert advice, if available

Avoid medications that may worsen asthma

- Always ask about asthma before prescribing NSAIDs or beta-blockers

Remediation of dampness or mold in homes

- Reduces asthma symptoms and medication use in adults

Sublingual immunotherapy (SLIT)

- Consider as add-on therapy in adult HDM-sensitive patients with allergic rhinitis who
have exacerbations despite ICS treatment, provided FEV1 is 70% predicted

See GINA Box 3-9 and online Appendix for details

Guided asthma self-management and skills training

Essential components are:

- Skills training to use inhaler devices correctly

- Encouraging adherence with medications, appointments
- Asthma information
- Guided self-management support

▪ Self-monitoring of symptoms and/or PEF

▪ Written asthma action plan

▪ Regular review by a health care provider

Check adherence with asthma medications

Poor adherence:

- Is very common: it is estimated that 50% of adults and children do not take controller
medications as prescribed
- Contributes to uncontrolled asthma symptoms and risk of exacerbations and asthma-
related death

Contributory factors

- Unintentional (e.g. forgetfulness, cost, confusion) and/or

- Intentional (e.g. no perceived need, fear of side-effects, cultural issues, cost)

How to identify patients with low adherence:

- Ask an empathic question, e.g. “Do you find it easier to remember your medication in
the morning or the evening?”, or
“Would you say you are taking it 3 days a week, or less, or more?”
- Check prescription date, label date and dose counter
- Ask patient about their beliefs and concerns about the medication

Investigations in patients with severe asthma

Confirm the diagnosis of asthma

- Consider alternative diagnoses or contributors to symptoms, e.g. upper airway

dysfunction, COPD, recurrent respiratory infections

Investigate for comorbidities

- Chronic sinusitis, obesity, GERD, obstructive sleep apnea, psychological or psychiatric

disorders

Check inhaler technique and medication adherence

Investigate for persistent environmental exposure

- Allergens or toxic substances (domestic or occupational)

Management of severe asthma

Optimize dose of ICS/LABA

- Complete resistance to ICS is rare

- Consider therapeutic trial of higher dose

Consider low dose maintenance oral corticosteroids

- Monitor for and manage side-effects, including osteoporosis

Add-on treatments without phenotyping

- Tiotropium - reduces exacerbations (history of exacerbations, age ≥12 years)

 - Theophylline, LTRA – limited benefit

Phenotype-guided treatment

- Severe allergic asthma: add-on omalizumab (anti-IgE)

- Severe eosinophilic asthma: add-on mepolizumab or reslizumab (anti-IL5)
- Sputum-guided treatment to reduce exacerbations and/or steroid dose
- Aspirin-exacerbated respiratory disease: consider add-on LTRA

Non-pharmacological interventions

- Consider bronchial thermoplasty for selected patients

- Comprehensive adherence-promoting program

Asthma flare-ups (exacerbations)

Definition and terminology

A flare-up or exacerbation is an acute or sub-acute worsening

of symptoms and lung function compared with the patient’s usual status

Terminology

- ‘Flare-up’ is the preferred term for discussion with patients

- ‘Exacerbation’ is a difficult term for patients
- ‘Attack’ has highly variable meanings for patients and clinicians
- ‘Episode’ does not convey clinical urgency

Consider management of worsening asthma as a continuum

- Self-management with a written asthma action plan

- Management in primary care
- Management in the emergency department and hospital
- Follow-up after any exacerbation

Identify patients at risk of asthma-related death

Patients at increased risk of asthma-related death should be identified

- Any history of near-fatal asthma requiring intubation and ventilation

- Hospitalization or emergency care for asthma in last 12 months
- Not currently using ICS, or poor adherence with ICS
- Currently using or recently stopped using OCS

• (indicating the severity of recent events)

- Over-use of SABAs, especially if more than 1 canister/month

- Lack of a written asthma action plan
- History of psychiatric disease or psychosocial problems
- Confirmed food allergy in a patient with asthma

Flag these patients for more frequent review

Written asthma action plans

All patients should have a written asthma action plan

- The aim is to show the patient how to recognize and respond to worsening asthma
- It should be individualized for the patient’s medications, level of asthma control and
health literacy
- Based on symptoms and/or PEF (children: only symptoms)

The action plan should include:

- The patient’s usual asthma medications

- When/how to increase reliever and controller or start OCS
- How to access medical care if symptoms fail to respond

Why?

- When combined with self-monitoring and regular medical review, action plans are
highly effective in reducing asthma mortality and morbidity
Managing exacerbations in primary care
Follow-up after an exacerbation

Follow up all patients regularly after an exacerbation, until symptoms and lung function return
to normal

- Patients are at increased risk during recovery from an exacerbation

The opportunity

- Exacerbations often represent failures in chronic asthma care,

and they provide opportunities to review the patient’s asthma management

At follow-up visit(s), check:

- The patient’s understanding of the cause of the flare-up

- Modifiable risk factors, e.g. smoking
- Adherence with medications, and understanding of their purpose
- Inhaler technique skills
- Written asthma action plan
Diagnosis and initial treatment of asthma, COPD and asthma-COPD overlap (ACO)

Background

For patients with respiratory symptoms, infectious diseases and non-pulmonary conditions
need to be distinguished from chronic airways disease

In patients with chronic airways disease, the differential diagnosis differs by age

- Children and young adults: most likely to be asthma

- Adults >40 years: COPD becomes more common, and distinguishing asthma from
COPD becomes more difficult

Many patients with symptoms of chronic airways disease have features of both asthma and
COPD

- This has been called asthma-COPD overlap (ACO)

ACO is not a single disease

- It is likely that a range of different underlying mechanisms and origins will be identified

Patients with features of both asthma and COPD have worse outcomes than those with
asthma or COPD alone

- Frequent exacerbations
- Poor quality of life
- More rapid decline in lung function
- Higher mortality
- Greater health care utilization

Reported prevalence of overlap varies by definitions used

- Concurrent doctor-diagnosed asthma and COPD are found in

15–20% of patients with chronic airways disease
- Reported rates of overlap are between15–55% of patients with chronic airways
disease, depending on the definitions used for ‘asthma’ and ‘COPD’, and the
population studied
- Prevalence varies by age and gender
Definitions
Stepwise approach to diagnosis and initial treatment

For an adult who presents with respiratory symptoms:

1. Does the patient have chronic airways disease?

2. Syndromic diagnosis of asthma, COPD and overlap

3. Spirometry

4. Commence initial therapy

5. Referral for specialized investigations (if necessary)

Step 1 – Does the patient have chronic airways disease?

Clinical history: consider chronic airways disease if

- Chronic or recurrent cough, sputum, dyspnea or wheezing, or repeated acute lower

respiratory tract infections
- Previous doctor diagnosis of asthma and/or COPD
- Previous treatment with inhaled medications
- History of smoking tobacco and/or other substances
- Exposure to environmental hazards, e.g. airborne pollutants

Physical examination

- May be normal
- Evidence of hyperinflation or respiratory insufficiency
- Wheeze and/or crackles

Radiology (CXR or CT scan performed for other reasons)

- May be normal, especially in early stages

- Hyperinflation, airway wall thickening, hyperlucency, bullae
- May identify or suggest an alternative or additional diagnosis, e.g. bronchiectasis,
tuberculosis, interstitial lung disease, cardiac failure

Screening questionnaires

- Designed to assist in identification of patients at risk of chronic airways disease

- May not be generalizable to all countries, practice settings or patients
- See GINA and GOLD reports for examples

Step 2 – Syndromic diagnosis of asthma, COPD and asthma-COPD overlap

Assemble the features that, when present, most favor a diagnosis of typical asthma or typical
COPD

Compare the number of features on each side

- If the patient has ≥3 features of either asthma or COPD, there is a strong likelihood
that this is the correct diagnosis

Consider the level of certainty around the diagnosis

- Diagnoses are made on the weight of evidence

- The absence of any of these features does not rule out either diagnosis, e.g. absence
of atopy does not rule out asthma
- When a patient has a similar number of features of both asthma and COPD, consider
the diagnosis of asthma-COPD overlap
Step 3 – Spirometry

Essential if chronic airways disease is suspected

- Confirms chronic airflow limitation

- More limited value in distinguishing between asthma with fixed airflow limitation,
COPD and asthma-COPD overlap

Measure at the initial visit or subsequent visit

- If possible measure before and after a trial of treatment

- Medications taken before testing may influence results

Peak expiratory flow (PEF)

- Not a substitute for spirometry

- Normal PEF does not rule out asthma or COPD
- Repeated measurement may confirm excessive variability, found in asthma or in some
patients with asthma-COPD overlap
Step 4 – Commence initial therapy

Initial pharmacotherapy choices are based on both efficacy and safety

If syndromic assessment suggests asthma as single diagnosis

- Start with low-dose ICS

- Add LABA and/or LAMA if needed for poor control despite good adherence and correct
technique
- Do not give LABA alone without ICS

If syndromic assessment suggests COPD as single diagnosis

- Start with bronchodilators or combination therapy

- Do not give ICS alone without LABA and/or LAMA

If differential diagnosis is equally balanced between asthma and COPD, i.e. asthma-COPD
overlap

- Start treatment as for asthma, pending further investigations

- Start with ICS at low or moderate dose
- Usually also add LABA and/or LAMA, or continue if already prescribed
For all patients with chronic airflow limitation:

- Treat modifiable risk factors including advice about smoking cessation

- Treat comorbidities
- Advise about non-pharmacological strategies including physical activity, and, for COPD
or asthma-COPD overlap, pulmonary rehabilitation and vaccinations
- Provide appropriate self-management strategies
- Arrange regular follow-up

See GINA and GOLD reports for details

 GLOBAL INICIATIVE FOR CHRONIC OBSTRUCTIVE LUNG DISEASE

Chronic Obstructive Pulmonary Disease (COPD)

COPD is currently the fourth leading cause of death in the world.

COPD is projected to be the 3rd leading cause of death by 2020.

More than 3 million people died of COPD in 2012 accounting for 6% of all deaths globally.

Globally, the COPD burden is projected to increase in coming decades because of continued
exposure to COPD risk factors and aging of the population.

COPD Etiology, Pathobiology & Pathology

 1. Definition and Overview

OVERALL KEY POINTS (1 of 2):

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable

disease that is characterized by persistent respiratory symptoms and airflow limitation that is
due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious
particles or gases.

The most common respiratory symptoms include dyspnea, cough and/or sputum production.
These symptoms may be under-reported by patients.

The main risk factor for COPD is tobacco smoking but other environmental exposures such as
biomass fuel exposure and air pollution may contribute.

OVERALL KEY POINTS (2 of 2):

Besides exposures, host factors predispose individuals to develop COPD. These include genetic
abnormalities, abnormal lung development and accelerated aging.

COPD may be punctuated by periods of acute worsening of respiratory symptoms, called

exacerbations.

In most patients, COPD is associated with significant concomitant chronic diseases, which
increase its morbidity and mortality.
Prevalence of COPD

Estimated 384 million COPD cases in 2010.

Estimated global prevalence of 11.7% (95% CI 8.4%–15.0%).

Three million deaths annually.

With increasing prevalence of smoking in developing countries, and aging populations in high-
income countries, the prevalence of COPD is expected to rise over the next 30 years.

By 2030 predicted 4.5 million COPD related deaths annually.

Economic and Social Burden

Economic burden of COPD

COPD is associated with significant economic burden.

COPD exacerbations account for the greatest proportion of the total COPD burden.

European Union:

- Direct costs of respiratory disease ~6% of the total healthcare budget

- COPD accounting for 56% (38.6 billion Euros) of the cost of respiratory disease.

USA:

- Direct costs of COPD are $32 billion

- Indirect costs $20.4 billion.

Global Burden of Disease (GBD) study

Disability-Adjusted Life Year (DALY) = sum of years lost because of premature mortality and
years of life lived with disability, adjusted for the severity of disability.

COPD is an increasing contributor to disability and mortality around the world.

In 2013 COPD was 5th leading cause of DALYs lost.

In the United States, COPD is the second leading cause of reduced DALYs, trailing only ischemic
heart disease

Factors that influence disease progression

- Genetic factors
- Age and gender
- Lung growth and development
- Exposure to particles
- Socioeconomic status
- Asthma & airway hyper-reactivity
- Chronic bronchitis
- Infections
Pathology, pathogenesis & pathophysiology

Pathology

- Chronic inflammation
- Structural changes

Pathogenesis

- Oxidative stress
- Protease-antiprotease imbalance
- Inflammatory cells
- Inflammatory mediators
- Peribronchiolar and interstitial fibrosis

Pathophysiology

- Airflow limitation and gas trapping

- Gas exchange abnormalities
- Mucus hypersecretion
- Pulmonary hypertension

2. Diagnosis and Initial Assessment

OVERALL KEY POINTS (1 of 2):

COPD should be considered in any patient who has dyspnea, chronic cough or sputum
production, and/or a history of exposure to risk factors for the disease.

Spirometry is required to make the diagnosis; the presence of a post-bronchodilator FEV1/FVC

< 0.70 confirms the presence of persistent airflow limitation.

The goals of COPD assessment are to determine the level of airflow limitation, the impact of
disease on the patient’s health status, and the risk of future events (such as exacerbations,
hospital admissions, or death), in order to guide therapy.

OVERALL KEY POINTS (2 of 2):

Concomitant chronic diseases occur frequently in COPD patients, including cardiovascular

disease, skeletal muscle dysfunction, metabolic syndrome, osteoporosis, depression, anxiety,
and lung cancer. These comorbidities should be actively sought and treated appropriately
when present as they can influence mortality and hospitalizations independently.

Symptoms of COPD

- Chronic and progressive dyspnea

- Cough
- Sputum production
- Wheezing and chest tightness
- Others – including fatigue, weight loss, anorexia, syncope, rib fractures, ankle swelling,
depression, anxiety.
Medical History

Patient’s exposure to risk factors

Past medical history

Family history of COPD or other chronic respiratory disease.

Pattern of symptom development

History of exacerbations or previous hospitalizations for respiratory disorder

Presence of comorbidities

Impact of disease on patient’s life

Social and family support available to the patient.

Possibilities for reducing risk factors, especially smoking cessation.

Spirometry
Classification of severity of airflow limitation

Choice of thresholds

COPD Assessment Test (CAT TM )

Chronic Respiratory Questionnaire (CCQ® )

St George’s Respiratory Questionnaire (SGRQ)

Chronic Respiratory Questionnaire (CRQ)

Modified Medical Research Council (mMRC) questionnaire

Assessment of Exacerbation Risk

COPD exacerbations are defined as an acute worsening of respiratory symptoms that result in
additional therapy.

Classified as:

- Mild (treated with SABDs only)

- Moderate (treated with SABDs plus antibiotics and/or oral corticosteroids) or
- Severe (patient requires hospitalization or visits the emergency room). Severe
exacerbations may also be associated with acute respiratory failure.

Blood eosinophil count may also predict exacerbation rates (in patients treated with LABA
without ICS).
ABCD Assessment Tool

Alpha-1 antitrypsin deficiency (AATD)

AATD screening

The World Health Organization recommends that all patients with a diagnosis of COPD should
be screened once especially in areas with high AATD prevalence.

AATD patients are typically < 45 years with panlobular basal emphysema

Delay in diagnosis in older AATD patients presents as more typical distribution of emphysema
(centrilobular apical).

A low concentration (< 20% normal) is highly suggestive of homozygous deficiency.

Differential Diagnosis

3. Evidence Supporting Prevention & Maintenance Therapy

OVERALL KEY POINTS (1 of 3):

Smoking cessation is key. Pharmacotherapy and nicotine replacement reliably increase long-
term smoking abstinence rates.

The effectiveness and safety of e-cigarettes as a smoking cessation aid is uncertain at present.

Pharmacologic therapy can reduce COPD symptoms, reduce the frequency and severity of
exacerbations, and improve health status and exercise tolerance.

Each pharmacologic treatment regimen should be individualized and guided by the severity of
symptoms, risk of exacerbations, side-effects, comorbidities, drug availability and cost, and the
patient’s response, preference and ability to use various drug delivery devices.

Inhaler technique needs to be assessed regularly.

OVERALL KEY POINTS (2 of 3):

Influenza vaccination decreases the incidence of lower respiratory tract infections.

Pneumococcal vaccination decreases lower respiratory tract infections.

Pulmonary rehabilitation improves symptoms, quality of life, and physical and emotional
participation in everyday activities.
In patients with severe resting chronic hypoxemia, long-term oxygen therapy improves
survival.

In patients with stable COPD and resting or exercise-induced moderate desaturation, long-
term oxygen treatment should not be prescribed routinely. However, individual patient factors
must be considered when evaluating the patient’s need for supplemental oxygen.

OVERALL KEY POINTS (3 of 3):

In patients with severe chronic hypercapnia and a history of hospitalization for acute
respiratory failure, long-term non-invasive ventilation may decrease mortality and prevent re-
hospitalization.

In select patients with advanced emphysema refractory to optimized medical care, surgical or
bronchoscopic interventional treatments may be beneficial.

Palliative approaches are effective in controlling symptoms in advanced COPD.

Smoking Cessation

Smoking cessation has the greatest capacity to influence the natural history of COPD.

If effective resources and time are dedicated to smoking cessation, long-term quit success
rates of up to 25% can be achieved.
Pharmacologic Therapy
Bronchodilators in Stable COPD

Anti-inflammatory Therapy in Stable COPD

Rehabilitation, Education & Self-Management

Palliative, End of Life & Hospice Care

In many patients, the disease trajectory in COPD is marked by a gradual decline in health status
and increasing symptoms, punctuated by acute exacerbations that are associated with an
increased risk of dying.

Although mortality rates following hospitalization for an acute exacerbation of COPD are
declining, reported rates still vary from 23% to 80%.

Oxygen Therapy & Ventilatory Support in Stable COPD

During exacerbations of COPD. Noninvasive ventilation (NIV) in the form of noninvasive

positive pressure ventilation (NPPV) is the standard of care for decreasing morbidity and
mortality in patients hospitalized with an exacerbation of COPD and acute respiratory failure
Interventional Therapy in Stable COPD

Lung volume reduction surgery (LVRS). LVRS is a surgical procedure in which parts of the lungs
are resected to reduce hyperinflation, making respiratory muscles more effective pressure
generators by improving their mechanical efficiency.

4. Management of Stable COPD

OVERALL KEY POINTS:

The management strategy for stable COPD should be predominantly based on the
individualized assessment of symptoms and future risk of exacerbations.

All individuals who smoke should be strongly encouraged and supported to quit.

The main treatment goals are reduction of symptoms and future risk of exacerbations.

Management strategies are not limited to pharmacologic treatments, and should be

complemented by appropriate non-pharmacologic interventions.

Once COPD has been diagnosed, effective management should be based on an individualized
assessment to reduce both current symptoms and future risks of exacerbations.
Identify and reduce exposure to known risk factors

Identification and reduction of exposure to risk factors is important in the treatment and
prevention of COPD.

Cigarette smoking is the most commonly encountered and easily identifiable risk factor for
COPD, and smoking cessation should be continually encouraged for all individuals who smoke.

Reduction of total personal exposure to occupational dusts, fumes, and gases, and to indoor
and outdoor air pollutants, should also be addressed.

Treatment of Stable COPD

Pharmacologic treatment

Pharmacologic therapies can reduce symptoms, and the risk and severity of exacerbations, as
well as improve health status and exercise tolerance.

Most of the drugs are inhaled so proper inhaler technique is of high relevance.

Pharmacologic treatment algorithms

A proposed model for the initiation, and then subsequent escalation and/or de-escalation of
pharmacologic management of COPD according to the individualized assessment of symptoms
and exacerbation risk is shown.

We suggest escalation (and de-escalation) strategies.

The recommendations made are based on available efficacy as well as safety data.

It should be noted that there is a lack of direct evidence supporting the therapeutic
recommendations for patients in groups C and D. These recommendations will be re-evaluated
as additional data become available.
Non-Pharmacologic Treatment

Education and self-management

Physical activity

Pulmonary rehabilitation programs

Exercise training

Self-management education

End of life and palliative care

Nutritional support

Vaccination

Oxygen therapy

Oxygen therapy

Long-term oxygen therapy is indicated for stable patients who have:

- PaO2 at or below 7.3 kPa (55 mmHg) or SaO2 at or below 88%, with or without
hypercapnia confirmed twice over a three week period; or
- PaO2 between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg), or SaO2 of 88%, if there is
evidence of pulmonary hypertension, peripheral edema suggesting congestive cardiac
failure, or polycythemia (hematocrit > 55%).
Interventional bronchoscopy and surgery

In selected patients with heterogeneous or homogenous emphysema and significant

hyperinflation refractory to optimized medical care, surgical or bronchoscopic modes of lung
volume reduction (e.g., endobronchial one-way valves or lung coils) may be considered.

In selected patients with a large bulla, surgical bullectomy may be considered.

In selected patients with very severe COPD and without relevant contraindications, lung
transplantation may be considered.

Monitoring and Follow-up

Monitoring disease progression and development of complications and/or comorbidities

Measurements. Decline in FEV1 can be tracked by spirometry performed at least once a year.

Symptoms. At each visit, information on symptoms since the last visit should be collected,
including cough and sputum, breathlessness, fatigue, activity limitation, and sleep
disturbances.

Exacerbations. The frequency, severity, type and likely causes of all exacerbations should be
monitored.

Imaging. If there is a clear worsening of symptoms, imaging may be indicated.

Smoking status. At each visit, the current smoking status and smoke exposure should be
determined followed by appropriate action.

5. Management of Exacerbations

OVERALL KEY POINTS (1 of 3):

An exacerbation of COPD is defined as an acute worsening of respiratory symptoms that

results in additional therapy.

Exacerbations of COPD can be precipitated by several factors. The most common causes are
respiratory tract infections.

The goal for treatment of COPD exacerbations is to minimize the negative impact of the
current exacerbation and to prevent subsequent events.

Short-acting inhaled beta2-agonists, with or without short-acting anticholinergics, are

recommended as the initial bronchodilators to treat an acute exacerbation.

OVERALL KEY POINTS (2 of 3):

Maintenance therapy with long-acting bronchodilators should be initiated as soon as possible

before hospital discharge.

Systemic corticosteroids can improve lung function (FEV1), oxygenation and shorten recovery
time and hospitalization duration. Duration of therapy should not be more than 5-7 days.
Antibiotics, when indicated, can shorten recovery time, reduce the risk of early relapse,
treatment failure, and hospitalization duration. Duration of therapy should be 5-7 days.

Methylxanthines are not recommended due to increased side effect profiles.

OVERALL KEY POINTS (3 of 3):

Non-invasive mechanical ventilation should be the first mode of ventilation used in COPD
patients with acute respiratory failure who have no absolute contraindication because it
improves gas exchange, reduces work of breathing and the need for intubation, decreases
hospitalization duration and improves survival.

Following an exacerbation, appropriate measures for exacerbation prevention should be

initiated (see GOLD 2017 Chapter 3 and Chapter 4).

COPD exacerbations are defined as an acute worsening of respiratory symptoms that result in
additional therapy.

They are classified as:

- Mild (treated with short acting bronchodilators only, SABDs)

- Moderate (treated with SABDs plus antibiotics and/or oral corticosteroids) or
- Severe (patient requires hospitalization or visits the emergency room). Severe
exacerbations may also be associated with acute respiratory failure.

Classification of hospitalized patients

No respiratory failure:

Respiratory rate: 20-30 breaths per minute; no use of accessory respiratory muscles; no
changes in mental status; hypoxemia improved with supplemental oxygen given via Venturi
mask 28-35% inspired oxygen (FiO2); no increase in PaCO2.

Acute respiratory failure — non-life-threatening: Respiratory rate: > 30 breaths per minute;
using accessory respiratory muscles; no change in mental status; hypoxemia improved with
supplemental oxygen via Venturi mask 25-30% FiO2; hypercarbia i.e., PaCO2 increased
compared with baseline or elevated 50-60 mmHg.

Acute respiratory failure — life-threatening:

Respiratory rate: > 30 breaths per minute; using accessory respiratory muscles; acute changes
in mental status; hypoxemia not improved with supplemental oxygen via Venturi mask or
requiring FiO2 > 40%; hypercarbia i.e., PaCO2 increased compared with baseline or elevated >
60 mmHg or the presence of acidosis (pH < 7.25).
Pharmacologic treatment

The three classes of medications most commonly used for COPD exacerbations are:

Bronchodilators

- Although there is no high-quality evidence from RCTs, it is recommended that short-

acting inhaled beta2-agonists, with or without short-acting anticholinergics, are the
initial bronchodilators for acute treatment of a COPD exacerbation.

Corticosteroids

- Data from studies indicate that systemic glucocorticoids in COPD exacerbations

shorten recovery time and improve lung function (FEV1). They also improve
oxygenation, the risk of early relapse, treatment failure, and the length of
hospitalization.

Antibiotics

Respiratory support

6. COPD and Comorbidities

OVERALL KEY POINTS (1 of 2):

COPD often coexists with other diseases (comorbidities) that may have a significant impact on
disease course.

In general, the presence of comorbidities should not alter COPD treatment and comorbidities
should be treated per usual standards regardless of the presence of COPD.

Lung cancer is frequently seen in patients with COPD and is a main cause of death.

Cardiovascular diseases are common and important comorbidities in COPD.

OVERALL KEY POINTS (2 of 2):

Osteoporosis and depression/anxiety are frequent, important comorbidities in COPD, are often
under-diagnosed, and are associated with poor health status and prognosis.

Gastroesophageal reflux (GERD) is associated with an increased risk of exacerbations and

poorer health status.

When COPD is part of a multimorbidity care plan, attention should be directed to ensure
simplicity of treatment and to minimize polypharmacy.

Some common comorbidities occurring in patients with COPD with stable disease include:

- Cardiovascular disease (CVD)

- Heart failure
- Ischaemic heart disease (IHD)
- Arrhythmias
- Peripheral vascular disease
- Hypertension
- Osteoporosis
- Anxiety and depression
- COPD and lung cancer
- Metabolic syndrome and diabetes
- Gastroesophageal reflux (GERD)
- Bronchiectasis
- Obstructive sleep apnea

COPD as part of multimorbidity

An increasing number of people in any aging population will suffer from multi-morbidity,
defined as the presence of two or more chronic conditions, and COPD is present in the
majority of multi-morbid patients.

Multi-morbid patients have symptoms from multiple diseases and thus symptoms and signs
are complex and most often attributable to several causes in the chronic state as well as during
acute events.

There is no evidence that COPD should be treated differently when part of multi-morbidity;
however, it should be kept in mind that most evidence comes from trials in patients with COPD
as the only significant disease.

Treatments should be kept simple in the light of the unbearable polypharmacy that these
patients are often exposed to.
 PNEUMONIA

Normal Chest X-Ray

What is pneumonia?

• Infection of the lung parenchyma

• Causative agents include bacteria, viruses, fungi

Is often misdiagnosed, mistreated, and underestimated

Was typically classified as :

1. Community-Acquired Pneumonia (CAP)

2. Health Care–Associated Pneumonia (HCAP)

- subcategories of HCAP including

▪ Hospital-acquired pneumonia (HAP)
▪ Ventilator-associated pneumonia (VAP)
- Factors responsible for infection with multidrug-resistant (MDR) pathogens include :
▪ development and widespread use of potent oral antibiotics
▪ earlier transfer of patients out of acute-care hospitals to their homes or
various lower-acuity facilities
▪ increased use of outpatient IV antibiotic therapy
▪ general aging of the population
▪ more extensive immunomodulatory therapies
Pathophysiology

Pneumonia results from the proliferation of microbial pathogens at the alveolar level and the
host's response to those pathogens

Microorganisms gain access to the lower respiratory tract in several ways:

- The most common is by aspiration from the oropharynx

- Many pathogens are inhaled as contaminated droplets
- pneumonia occurs via hematogenous spread
- contiguous extension from an infected pleural or mediastinal space

Mechanical factors are critically important in host defense: »»»»»»»»»»»»

- hairs and turbinates of the nares catch larger inhaled particles

- branching architecture of the tracheobronchial tree traps particles on the airway lining
- mucociliary clearance and local antibacterial factors either clear or kill the potential
pathogen
- gag reflex and the cough mechanism
- normal flora adhering to mucosal cells of the oropharynx
- resident alveolar macrophages

Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is
exceeded does clinical pneumonia become manifest »»»»»»»»»»»» the alveolar
macrophages initiate the inflammatory response to bolster lower respiratory tract defenses

The host inflammatory response, rather than the proliferation of microorganisms, triggers the
clinical syndrome of pneumonia

- The release of inflammatory mediators, such as IL-1 and TNF »»»»»»»»»»»» fever
- Chemokines, such as IL-8 and GCSF, stimulate the release of neutrophils and their
attraction to the lung »»»»»»»»»»» peripheral leukocytosis and increased purulent
secretions
- Even erythrocytes can cross the alveolar-capillary membrane, with consequent
hemoptysis
- The capillary leak results in a radiographic infiltrate and rales detectable on
auscultation
- hypoxemia results from alveolar filling
- some bacterial pathogens appear to interfere with the hypoxic vasoconstriction that
would normally occur with fluid-filled alveoli, and this interference can result in severe
hypoxemia

Dyspnea due to :

- Decreased compliance due to capillary leak hypoxemia

- increased respiratory drive increased secretions
- infection-related bronchospasm
 1. The initial phase »»»»»»»» edema

presence of a proteinaceous exudate—and often of bacteria—in the alveoli

This phase is rarely evident in clinical or autopsy specimens because it is so rapidly followed by
a red hepatization

2. The second stage »»»»»»»»» red hepatization

presence of erythrocytes in the cellular intraalveolar exudate

neutrophils are also present and are important from the standpoint of host defense

Bacteria are occasionally seen in cultures of alveolar specimens

3. The third phase »»»»»»»» gray hepatization

no new erythrocytes are extravasating, and those already present have been lysed and
degraded

The neutrophil is the predominant cell

fibrin deposition is abundant

bacteria have disappeared

This phase corresponds with successful containment of the infection and improvement in gas
exchange

4. The final phase »»»»»»»»» resolution

the macrophage is the dominant cell type in the alveolar space

the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory
response

CAP

CAP = pneumonia in person not hospitalized or residing in a long-term care facility for  14
days

CAP - Why do we care about it?

5.6 million cases annually

1.1 million require hospitalization

Mortality rate =12% in-hospital; near 40% in ICU patients

CAP – Patient Stratification

CAP – Testing

• CXR

• Sputum Gram Stain and culture

• Pulse oximetry

• Routine lab testing – CBC, BMP, LFTs

• ABG

• Thoracentesis if pleural effusion present

CAP – Modifying Factors

MODIFYING FACTORS THAT INCREASE THE RISK OF INFECTION WITH SPECIFIC PATHOGENS

Penicillin-resistant and drug-resistant pneumococci

Age > 65 yr

B-Lactam therapy within the past 3 mo

Alcoholism

Immune-suppressive illness (including therapy w/ corticosteroids)

Multiple medical comorbidities

Exposure to a child in a day care center

Enteric gram-negatives

Residence in a nursing home

Underlying cardiopulmonary disease

Multiple medical comorbidities

Recent antibiotic therapy

Pseudomonas aeruginosa

Structural lung disease (bronchiectasis)

 Corticosteroid therapy (10 mg of prednisone per day)

Broad-spectrum antibiotic therapy for > 7 d in the past month

Malnutrition

CAP – Algorithms
Duration of Therapy

- ? ? ? ? ? ?
- 5 -7 days – outpatients
- 7-10 days – inpatients, S. pneumoniae
- 10-14 days – Mycoplasma, Chlamydia, Legionella
- 14+ days - chronic steroid users

CAP -The Switch to Oral Antibiotics

Switch if patient meets the following:

- Improved cough and dyspnea

- Afebrile on 2 occasions 8 hours apart

• If otherwise improving way waive this criteria

- Decreasing WBC count

- Functional GI tract with adequate PO intake

CAP – Prevention

- Influenza Vaccine
- Pneumococcal Vaccine

Remember

Influenza Vaccine

Pneumococcal Vaccine

• BEFORE DISCHARGE!!!!

After discharge – Follow up CXR to exclude cancer

HAP

Pneumonia occurring ≥48 h post admission

Excludes infection incubating at time of admission

HAP – Epidemiology

5 to 10 cases per 1,000 hospital admissions

Incidence MUCH higher with mechanical ventilation (6-20 fold higher)

Second most common nosocomial infection but number one for M & M

Mortality near 70% in patients with HAP

Increased length of stay by 7-9 days

HAP – Stratification
HAP – Failure of Therapy

Incorrect diagnosis – it is not pneumonia

- Atelectasis, CHF, PE with infarction, lung contusion, chemical pneumonitis, ARDS,

pulmonary hemorrhage

Pathogen resistance

Host factors that increase mortality

- Age > 60, prior pneumonia, chronic lung disease

- immunosuppression

Antibiotic resistance
HAP – Prevention

Hand washing

Vaccination

- Influenza
- Pneumococcus

Isolation of patients with resistant respiratory tract infections

Enteral nutrition

Choice of GI prophylaxis

Subglottic secretion removal?

Pneumocystis Carinii /Pneumocystis jiroveci Pneumonia (PCP)

Uncommon until 1980’s with emergence of HIV disease

Caused by organism most closely related to fungi

Mode of transmission unclear, but felt to represent reactivation of latent infection

PCP Pneumonia

Gradual onset of symptoms

Common symptoms include fever, cough, progressive dyspnea

Many patients asymptomatic

May present as a spontaneous pneumothorax

PCP – Lab Work

CD4 <200

LDH

- Elevated in HIV+ persons w/ PCP

- Very high values and increasing levels in face of therapy correlate w/ poorer prognosis

ABG

- PaO2 <70 indication for steroids

Lung sampling

- Definitive diagnosis dependent on isolation of Pneumocystis

PCP – Treatment

TMP/SMX (trimethoprim/sulfamethoxazole)

- Drug of choice
- High incidence of side effects in HIV+ pts

Dapsone + TMP

Clindamycin + primaquine

Atovaquone

Pentamadine IV

PCP – Prophylaxis

TMP/SMX* –

Dapsone +/- pyrimethamine*

Aerosolozed pentamadine

Atovaquone

*= also prophylaxis for Toxoplama

 LUNG CANCER

Bronchial carcinoma

Most common fatal lung malignancy account for 95% of lung cancer

Leading cause of cancer death.

Peak incidence occur between ages 55-65 years .

There is a 3:1 male : female ratio.

Aetiology :

- smoking is the most common aetiological factor.

-others: passive smokers , exposure to asbestos, chromium , iron oxide and products of cool
combustion
Types:

There are 4 major types

1. epidermoid [squamous] -35%

2. adeno carcinoma -30%
3. large cell carcinoma -15%
4. small cell lung cancer -20%

Epidermoid carcinoma -35% :

Occurs most frequently in men and old people

Usually starts on one breathing tubes.

Tend to be localized in the chest longer than other types of lung cancer.

Does not tend to metastasize early.

It is strongly associated with smoking

Adenocarcinnoma-30%:

Most common cancer among women.

Usually started near the outer edges of the lung.

Invasion of pleura and mediastinal lymph node is common.

May spread to other parts of the body.

Can be seen in non smoker.

Large cell carcinoma – 15% :

Less well – differentiated.

May occur at any part of the lung.

Tumors are large by the time they are diagnosed.

Has greater possibility of spreading to brain and mediastinum.

Small cell lung cancer:

Small cell lung cancer also called oatcell because SCLC cells have oat grain appearance.

It arises from endocrine cells [kulchitisky cells] where many hormones are secreted

Spread to lymph nodes and other organs more quickly than NSCLC .

Usually started in one larger breathing tube.

Tend to grow rapidly .

Commonly has spread by the time and is considered a systemic disease.

It is the only one of the bronchial carcinomas that respond to chemotherapy

Presentations:

Lung cancer may present in number of different ways :

Most commonly symptoms reflect local involvement of the bronchus.

May also arise from spread to the chest wall or mediastinum or from distant blood-borne
spread.

Local effects of tumor within the bronchus:

1. Cough ( in 80% of cases ) :

- It is the most common early symptoms.
- Sputum is purulent if there is sec. infection.
- A change in the character of the (regular cough) associated with other new
respiratory symptoms increase the possibility of B.C.
2. Hemoptysis ( in 70% of cases) :
- Repeated episodes of scanty cough hemoptysis or blood –streaking of sputum
in smokers are highly suggestive of B.C and should be always investigated.
3. Dyspnea ( 60% of cases ):
- reflect occlusion of a large bronchus resulting in collapse of a lobe of the
lung or development of pleural effusion.
4. Pleural pain :
- reflect malignant invasion of the pleura or reflect infection distal to a
tumor (which is recurrent and fail to resolve).
Direct spread:

Involvement of pleura and ribs .

Pancoast’s tumor:

- involvement of lower part of the brachial plexus ( C8 , T1,T2) causing severe

pain of the shoulder and down inner surface of the arm.
- Horner syndrome: due to involvement of the sympathetic ganglion.
- recurrent laryngeal nerve palsy : causing unilateral vocal cord paresis with
hoarseness of voice and a bovine cough.

Invasion of phrenic nerve , causing paralysis of the diaphragm.

Involvement of esophagus , causing dysphagia.

Cardiovascular: atrial fibrillation, tamponade ,pericarditis, pericardial effusion.

Superior vena cava obstruction causing early morning headache, facial congestion and edema
involving the upper limb, distention of jugular vein and veins of the chest

Nonmetastatic extra pulmonary manifestations:

1. Endocrine manifestation:

12% of tumors, in particular small cell tumors present with SIADH, ACTH secretion (SCLC),
hypercalcemia (sq.cell carcinoma), bone metastasis gynecomastia(LCLC).

2. Neurological manifestation:

e.g: sensory polyneuropathy ,myelopathy, cerebellar degeneration.

3. Others:

Digital clubbing , hypertrophic pulmonary osteo-arthropathy (sq.cell cancer) , nephrotic

syndrome, DIC, hyper coagulopathy (adenocarcinoma), ,thrombophlebitis migricans.

Blood borne metastasis:

Bony metastasis giving severe bony pain and pathalogical fractures.

Liver metastasis (Jundice)

Brain metastasis (change in personality, epilpsy,focal neurological symptoms).

Physical signs:

Examination is usually normal unless there is significant bronchial obstruction or tumor has
spread to pleura or mediastinum.

1. physical signs of collapse (in large obstructing tumor) which may rise to
pneumonia.
2. monophonic or unilateral wheeze (fixed bronchial obstruction).
3. stridor (obstruction at or above the lever of main carina.
4. hoarsness of voice associated with bovine cough (recurrent laryngeal nerve
palsy).
5. dullness percussion and absent breath sounds at the lung base (unilateral
diaphragmatic palsy due to involvement of phrenic nerve)
6. physical signs of pleursy or pleural effusion (involvement of pleura).
7. bilateral engorgement of the jangular vein and later edema affecting face, neck, arms.
8. tenderness and pain of long bone and joints (HPOA).

Management

Investigation:

Sputum cytology: high yield for endobronchial tumors such as squamous cell and small cell
carcinoma.

Chest x-ray:

common radiological presentation of bronchial carcinoma.

1. unilateral hilar-enlagement.
2. peripheral pulmonary opacity.
3. lung, lobe or segmental collapse.
4. pleural effusion .
5. broadening of the mediastinum, enlarged cardiac shadow, elevation of
hemidiaphram.
6. rib distruction.
Pleural fluid cytology in pleural effusion.

Bronchoscopy: gives high yield in excess of 90% (allows biopsy and bronchial brush samples)
if fail precautious fine needle aspiration under CT.

CT thorax and upper abdomen.

Head CT scan.

Radio nuclide bone scanning.

Liver US.

Bone marrow biopsy

Treatment:

1. surgery : in patient with localized disease and non-small cell cancer.

2. solitary pulmonary nodule, resection if : age ≥ 35, cigarette smoking, large (>2 cm)
lesion, lack of calcification, chest symptoms, growth of lesion compared old CXR
 3. for unresectable non-small cell cancer, metastatic disease, or refusal of surgery:

radio therapy +chemo therapy

may reduce death risk by 13% at 2 years.

4. small cell lung cancer : combination

chemotherapy is standard mode of

therapy with long-term survival.

5. laser obliteration of tumor though

bronchoscopy in presence of

bronchial obstruction

6. Radio therapy for brain metastasis,

spinal cord comprission, symptomatic

mass, bone lesion.

7. Encourage cessation of smoking.

 STANDARS OF MEDICAL CARE IN DIABETES

1. Promoting Health and Reducing Disparities in Populations

Key Recommendations

Treatment decisions should be timely and based on evidence-based guidelines that are
tailored to patient preferences, prognoses, and comorbidities. B

Providers should consider the burden of treatment and self-efficacy of patients when
recommending treatments. E

Treatment plans should align with Chronic Care Model, emphasizing productive interactions
between a prepared proactive practice team and an informed activated patient. A

When feasible, care systems should support team-based care, community involvement,
patient registries, and decision support tools to meet patient needs. B

Care Delivery Systems

33-49% of patients still do not meet targets for A1C, blood pressure, or lipids.

14% meet targets for all A1C, BP, lipids, and nonsmoking status.

Progress in CVD risk factor control is slowing.

Substantial system-level improvements are needed.

Delivery system is fragmented, lacks clinical information capabilities, duplicates services & is
poorly designed.

Chronic Care Model

Six Core Elements:

1. Delivery system design

2. Self-management support
3. Decision support
4. Clinical information systems
5. Community resources & policies
6. Health systems
Objective 2: Support Patient Self-management

Implement a systematic approach to support patient behavior change efforts, including:

- Healthy lifestyle
- Disease self-management
- Prevention of diabetes complications
- Identification of self-management problems and development of strategies to
solve those problems

Objective 3: Change the Care System (2)

Successful practices prioritize providing a high quality of care. Changes that have been shown
to increase quality of care include:

- Removing financial barriers and reducing patient out-of-pocket costs

- Identifying community resources and public policy that supports healthy
lifestyles
- Coordinated primary care, e.g., through Patient-Centered Medical Home
- Changes to reimbursement structure

System-Level Interventions

Key Recommendations

Patients should be referred to local community resources when available. B

Patients should be provided with self-management support from lay health coaches,
navigators, or community health workers when available. A

1. Classification and Diagnosis of Diabetes

Classification & Diagnosis
- Classification
- Diagnostic Tests for Diabetes
- Prediabetes
- Type 1 Diabetes
- Type 2 Diabetes
- Gestational Diabetes
- Monogenic Diabetes Syndromes
- Cystic Fibrosis-Related Diabetes
Classification of Diabetes

1. Type 1 diabetes

– β-cell destruction

2. Type 2 diabetes

– Progressive insulin secretory defect

3. Gestational Diabetes Mellitus (GDM)

4. Other specific types of diabetes

– Monogenic diabetes syndromes

– Diseases of the exocrine pancreas, e.g., cystic fibrosis

– Drug- or chemical-induced diabetes

Staging of Type 1 Diabetes

Criteria for the Diagnosis of Diabetes

Recommendations: Type 1 Diabetes

Blood glucose rather than A1C should be used to diagnose type 1 diabetes in symptomatic

individuals. E

Screening for type 1 diabetes with an antibody panel is recommended only in the setting of

a clinical

research study or in a first-degree family members of a proband with type 1 diabetes. B

Recommendations: Prediabetes

Screening for prediabetes with an informal assessment of risk factors or validated tools should

be considered in asymptomatic adults. B

Testing should begin at age 45 for all people. B

Consider testing for prediabetes in asymptomatic adults of any age w/ BMI ≥25 kg/m2 or ≥23

kg/m2 (in Asian Americans) who have 1 or more add’l risk factors for diabetes. B

If tests are normal, repeat at a minimum of 3-year intervals. C

Recommendations: Prediabetes (2)

FPG, 2-h PG after 75-g OGTT, and A1C, are equally appropriate for prediabetes testing. B

In patients with prediabetes, identify and, if appropriate, treat other CVD risk factors. B

Consider prediabetes testing in overweight/obese children and adolescents with 2 or more add’l

diabetes risk factors. E

Prediabetes
Recommendations: Testing for Type 2 Diabetes

Screening for type 2 diabetes with an informal assessment of risk factors or validated tools

should be considered in asymptomatic adults. B

Consider testing in asymptomatic adults of any age with BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian

Americans who have 1 or more add’l dm risk factors. B

For all patients, testing should begin at age 45 years. B

If tests are normal, repeat testing carried out at a minimum of 3-year intervals is reasonable. C

Risk factors for Prediabetes and T2D

Criteria for Testing for T2DM in Children & Adolescents

Overweight plus any 2 :

• Family history of type 2 diabetes in 1st or 2nd degree relative

• Race/ethnicity
• Signs of insulin resistance or conditions
associated with insulin resistance
• Maternal history of diabetes or GDM

Age of initiation 10 years or at onset of puberty

Frequency: every 3 years

Test with FPG, OGTT, or A1C

Recommendations: Detection and Diagnosis of GDM

Test for undiagnosed T2DM at the 1st prenatal visit in those with risk factors. B

Test for GDM at 24–28 weeks of gestation in women not previously known to have diabetes. A
Screen women with GDM for persistent diabetes at 4–12 weeks postpartum, using the OGTT. E

Recommendations: Detection and Diagnosis of GDM (2)

Women with GDM history should have lifelong screening for development of diabetes or

prediabetes at least every 3 years. B

Women with GDM history found to have prediabetes should receive lifestyle interventions or

Metformin to prevent diabetes. A

Screening for & Diagnosis of GDM

One-Step Strategy

At 24-28 weeks gestation in women not previously dx’d with overt diabetes

75-g OGTT; Measure plasma glucose at fasting and at 1 and 2 hours.

GDM dx’d when plasma glucose exceeds:

• Fasting: 92 mg/dL (5.1 mmol/L)

• 1 h: 180 mg/dL (10.0 mmol/L)

• 2 h: 153 mg/dL (8.5 mmol/L)

• Comprehensive Medical Evaluation and Assessment of Comorbidities

Patient-Centered Collaborative Care

A patient-centered communication style that uses active listening, elicits patient preferences, and

assesses literacy, numeracy, and potential barriers to care should be used to optimize patient

health outcomes and health-related quality of life. B

Comprehensive Medical Evaluation

A complete medical evaluation should be performed at the initial visit to:

• Confirm & classify diagnosis B

• Detect complications & potential comorbid conditions E

• Review prior treatment & risk factor control E

• Begin formulation of care management plan B

• Develop a continuing care plan B

Components of the Comprehensive Diabetes Evaluation

Medical history:

• Age and characteristics of onset of diabetes

• Eating patterns, nutritional status, weight history, sleep behaviors, physical activity habits,

nutrition education

• Presence of common comorbidities and dental disease

• Screen for psychosocial problems and other barriers to self-management

• History of tobacco use, alcohol consumption, and substance use

Components of the Comprehensive Diabetes Evaluation (2)

Medical History (2):

• Diabetes education, self-management, and support history & needs

• Previous treatment regimens and response to therapy (A1C records)

• Results of glucose monitoring and patient’s use of data

• DKA frequency, severity, and cause

• Hypoglycemia episodes, awareness, frequency & causes

• Assess medication-taking behaviors/barriers to adherence

Components of the Comprehensive Diabetes Evaluation (3)

Medical History (3):

• History of increased blood pressure, abnormal lipids

• Microvascular: retinopathy, nephropathy, and neuropathy (sensory, including history of

foot lesions; autonomic, including sexual dysfunction and gastroparesis)

• Macrovascular: coronary heart disease, cerebrovascular disease, and peripheral arterial

disease

• For women with childbearing capacity, review contraception and preconception planning

Components of the Comprehensive Diabetes Evaluation (4)

Physical Examination:

• Height, weight, and BMI; growth and pubertal development in children and adolescents
 • Blood pressure determination, including orthostatic measurements when indicated

• Fundoscopic examination

• Thyroid palpation

• Skin examination

• Comprehensive foot examination

Components of the Comprehensive Diabetes Evaluation (5)

Laboratory Evaluation

• A1C, if results not available within past 3 months

• If not performed/available within past year:

• Fasting lipid profile

• Liver function tests

• Spot urinary albumin-to-creatinine ratio

• Serum creatinine and eGFR

• Thyroid-stimulating hormone in patients with type 1 diabetes

Recommendation: Autoimmune Disease

Consider screening patients with type 1 diabetes for autoimmune thyroid disease and celiac

disease soon after diagnosis. E

Recommendation: Cognitive Dysfunction

In people with cognitive impairment/dementia, intensive glucose control cannot be expected to

remediate deficits. Treatment should be tailored to avoid significant hypoglycemia. B

• Lifestyle Management

Recommendations: Diabetes Self-Management Education & Support

• All people with diabetes should participate in DSME and DSMS both at diagnosis and as needed

thereafter. B

• Effective self-management, improved clinical outcomes, health status, and quality-of-life are key

outcomes of DSME and DSMS and should be measured and monitored as part of care. C
• DSME/S should be patient-centered, respectful, and responsive to individual patient preferences,

needs, and values that should guide clinical decisions. A

DSME / DSMS Delivery

Four critical time points for DSME/S delivery:

• At diagnosis

• Annually for assessment of education, nutrition, and emotional needs

• When new complicating factors arise that influence self-management; and

• When transitions in care occur

Goals of Nutrition Therapy

• Promote & support healthful eating patterns, emphasizing a variety of nutrient-dense foods in

appropriate portion sizes, to improve health and to:

• Achieve and maintain body weight goals

• Attain individualized glycemic, blood pressure, and lipid goals

• Delay or prevent complications of diabetes

• Address nutrition needs based on personal & cultural preferences, health literacy & numeracy,

access to healthful foods, willingness and ability to make behavioral changes & barriers to change.

Goals of Nutrition Therapy (2)

• To maintain the pleasure of eating by providing non-judgmental messages about food

choices.

• Provide practical tools for developing healthful eating patterns rather than focusing on

individual macronutrients, micro-nutrients, or single foods.

Recommendations: Nutrition

Effectiveness of Nutrition Therapy:

• An individualized MNT program is recommended for all people with type 1 and type 2
diabetes. A
 • For people with T1D or T2D on a flexible insulin program, education on carb counting and,
in some cases, fat and protein gram estimation can improve glycemic control. A
• For people whose daily insulin dosing is fixed, a
consistent pattern of carb intake can result in improved glycemic control and a reduced
risk of hypoglycemia. B

Recommendations: Nutrition (2)

Effectiveness of Nutrition Therapy (2):

• Emphasizing healthy food choices and portion control may be more helpful for those with
type 2 diabetes who are not taking insulin, who have limited health literacy or
numeracy, and who are elderly and prone to hypoglycemia. B
• Because diabetes nutrition therapy can result in cost savings B and improved outcomes
(e.g., A1C reduction) A, MNT should be adequately reimbursed by insurance and
other payers. E

Recommendations: Nutrition (3)

Energy Balance:

• Modest weight loss achievable by the combination of lifestyle modification and the

reduction of calorie intake benefits overweight or obese adults with type 2 diabetes and also those

with prediabetes. Intervention programs to facilitate this process are recommended. A

Recommendations: Nutrition (4)

Eating patterns & macronutrient distribution:

• Macronutrient distribution should be individualized while keeping total calorie and

metabolic goals in mind. E
• Carbohydrate intake from whole grains, vegetables, fruits, legumes, and dairy products, with
An emphasis on foods higher in fiber and lower in glycemic load, should be advised
over other sources, especially those containing sugars. B
Recommendations: Nutrition (5)

Eating patterns & macronutrient distribution (2):

• People with diabetes and those at risk should avoid sugar-sweetened beverages to control
weight and reduce their risk for CVD and fatty liver B and should minimize the
consumption of foods with added sugar that have the capacity to displace healthier,
more nutrient-dense food choices. A
• A variety of eating patterns are acceptable for the management of type 2 diabetes and
prediabetes including Mediterranean, DASH, and plant-based diets. B

Recommendations: Nutrition (7)

Dietary Fat:

• An eating plan emphasizing elements of a Mediterranean-style diet rich in monounsaturated

fats may improve glucose metabolism and lower CVD risk and can be an effective
alternative to a low-fat, high-carb diet. B
• Eating foods containing long-chain ω-3 fatty acids, such as fatty fish, nuts, and seeds, is
recommended to prevent or treat CVD B; however, evidence does not support a
beneficial role for ω-3 dietary supplements. A

Recommendations: Nutrition (9)

Alcohol:

• Adults with diabetes should drink alcohol only in moderation (no more than one drink

per day for adult women and no more than two drinks per day for adult men). C

• Alcohol consumption may place people with diabetes at an increased risk for hypoglycemia,

especially if taking insulin or insulin secretagogues. Education and awareness regarding the

recognition and management of delayed hypoglycemia are warranted. B

Recommendations: Nutrition (10)

Sodium:

• As for the general population, people with diabetes should limit sodium consumption
to less than 2,300 mg/day, although further restriction may be indicated for those with both
diabetes and hypertension. B

Recommendations: Nutrition (11)

Nonnutritive sweeteners:

• - The use of nonnutritive sweeteners has the potential to reduce overall calorie and
Carbohydrate intake if substituted for caloric sweeteners and without compensation by
intake of additional calories from other food sources. Nonnutritive sweeteners are
generally safe to use within the defined acceptable daily intake levels. B

Recommendations: Physical Activity (1)

• Children with diabetes/prediabetes: at least 60 min/day physical activity B

• Most adults with type 1 C and type 2 B diabetes: 150+ min/wk of moderate-to-vigorous

activity over at least 3 days/week with no more than 2 consecutive days without exercise.

Shorter durations (minimum 75 min/week) of vigorous-intensity or interval training may be

sufficient for younger and more physically fit individuals.

• Adults with type 1 C and type 2 B diabetes should perform resistance training in 2-3

sessions/week on nonconsecutive days

Recommendations: Smoking Cessation

• Advise all patients not to use cigarettes, other tobacco products A or e-cigarettes E.

• Include smoking cessation counseling and other forms of treatment as a routine component

of diabetes care. B

Recommendations: Psychosocial Care

Psychosocial care should be provided to all people with diabetes, with the goals of optimizing health

outcomes and QOL . A

Psychosocial screening and follow-up include:

• Attitudes

• Expectations for medical mgmt. & outcomes

• Affect/mood

• Quality-of-life (QOL)

• Resources- financial, social & emotional

• Psychiatric history E

Diabetes Distress

• Diabetes distress

– Very common and distinct from other psychological disorders

– Negative psychological reactions related to emotional burdens of managing a

demanding chronic disease

• Recommendation: Routinely monitor people with diabetes for diabetes distress, particularly

when treatment targets are not met and/or at the onset of diabetes complications. B

5. Prevention or Delay of Type 2 Diabetes

Recommendations: Prevention or Delay of T2DM

Patients with prediabetes should be referred to an intensive diet and physical activity behavioral

counseling program adhering to the tenets of the DPP targeting a loss of 7% of body weight, and

should increase their moderate physical activity to at least 150 min/week. A

Recommendations: Prevention or Delay of T2DM (4)

Monitor at least annually for the development of diabetes in those with prediabetes. E

Screening for and treatment of modifiable risk factors for CVD is suggested. B

Recommendations: Prevention or Delay of T2DM (5)

DSME and DSMS programs are appropriate for people with prediabetes to receive education and

support to develop and maintain behaviors that can prevent or delay the onset of diabetes. B
Technology assisted tools can be useful elements of effective lifestyle modification to prevent

diabetes. B

6. Glycemic Targets

Assessment of Glycemic Control

Two primary techniques available for health providers and patients to assess effectiveness of

management plan on glycemic control

1. Patient self-monitoring of blood glucose (SMBG)

2. A1C

CGM or interstitial glucose may have an important role assessing the effectiveness and safety of

treatment In selected patients.

Recommendations: Glucose Monitoring (2)

Most patients on multiple-dose insulin (MDI) or insulin pump therapy should do SMBG B

– Prior to meals and snacks

– At bedtime

– Prior to exercise

– When they suspect low blood glucose

– After treating low blood glucose until they are normoglycemic

– Prior to critical tasks such as driving

– Occasionally postprandially

Recommendations: A1C Testing

• Perform the A1C test at least 2x annually in patients that meet treatment goals (and have

stable glycemic control). E

• Perform the A1C test quarterly in patients whose therapy has changed or who are not

meeting glycemic goals. E

• Use of point-of-care (POC) testing for A1C provides the opportunity for more timely

treatment changes. E
Mean Glucose Levels for Specified A1C Levels

Recommendations: Glycemic Goals in Adults

• A reasonable A1C goal for many nonpregnant adults is <7% (53 mmol/mol). A

• Consider more stringent goals (e.g. <6.5%) for select patients if achievable without

significant hypos or other adverse effects. C

• Consider less stringent goals (e.g. <8%) for patients with a history of severe hypoglycemia,

limited life expectancy, or other conditions that make <7% difficult to attain. B

A1C and CVD Outcomes

• DCCT: Trend toward lower risk of CVD events with intensive control (T1D)

• EDIC: 57% reduction in risk of nonfatal MI, stroke, or CVD death (T1D)

• UKPDS: nonsignificant reduction in CVD events (T2D).

• ACCORD, ADVANCE, VADT suggested no significant reduction in CVD outcomes with

intensive glycemic control. (T2D)

Approach to the Management of Hyperglycemia

Glycemic Recommendations for Nonpregnant Adults with Diabetes

Classification of Hypoglycemia
Recommendations: Hypoglycemia

• Individuals at risk for hypoglycemia should be asked about symptomatic and asymptomatic

hypoglycemia at each encounter. C

• Glucose (15–20 g) preferred treatment for conscious individual with blood glucose < 70

mg/dL. E

• Glucagon should be prescribed for those at increased risk of clinically significant

hypoglycemia, defined as blood glucose < 54 mg/dL, so it is available if needed. E

• Hypoglycemia unawareness or episodes of severe hypoglycemia should trigger treatment

re-evaluation. E

7. Obesity Management for the Treatment of Type 2 Diabetes

Benefits of Weight Loss

• Delay progression from prediabetes to type 2 diabetes

• Positive impact on treatment of type 2 diabetes

– Most likely to occur early in disease development

• Improves mobility, physical and sexual functioning & health-related quality of life

Recommendations: Assessment

At each patient encounter, BMI should be calculated and documented in the medical record. B

– Discuss with the patient

– Asian American cutpoints:

Overweight/Obesity Treatment

* Asian-American individuals

┼ Treatment may be indicated for selected, motivated patients

Recommendations: Diet, physical activity & behavioral therapy

• Diet, physical activity & behavioral therapy designed to achieve >5% weight loss should be

prescribed for overweight & obese patients with T2DM ready to achieve weight loss. A

• Interventions should be high-intensity (≥16 sessions in 6 months) and focus on diet, physical

activity & behavioral strategies to achieve a 500 - 750 kcal/day energy deficit. A

• Diets should be individualized, as those that provide the same caloric restriction but differ

in protein, carbohydrate, and fat content are equally effective in achieving weight loss. A

• Patients who achieve short-term weight loss goals should be prescribed long-term

maintenance programs. A

Recommendations: Pharmacotherapy

Consider impact on weight when choosing glucose-lowering meds for overweight or obese

patients. E

Minimize the medications for comorbid conditions that are associated with weight gain. E

Weight loss meds may be effective adjuncts to diet, physical activity & behavioral counseling for

select patients. A

Metabolic Surgery

Evidence supports gastrointestinal operations as effective treatments for overweight T2DM

patients.
Randomized controlled trials with postoperative follow-up ranging from 1 to 5 years have

documented sustained diabetes remission in 30–63% of patients, though erosion of remission

occurs in 35-50% or more.

With or without diabetes relapse, the majority of patients who undergo surgery maintain

substantial improvement of glycemic control for at least 5 to 15 years

Adverse Effects

Costly

Some associated risks

Outcomes vary

Patients undergoing metabolic surgery may be at higher risk for depression, substance abuse,

and

other psychosocial issues

8. Pharmacologic Approaches to Glycemic Treatment

Recommendations: Pharmacologic Therapy For Type 1 Diabetes

• Most people with T1DM should be treated with multiple daily injections of prandial insulin

and basal insulin or continuous subcutaneous insulin infusion (CSII). A

• Individuals who have been successfully using CSII should have continued access after they

turn 65 years old. E

Recommendations: Pharmacological Therapy For Type 1 Diabetes (2)

• Consider educating individuals with T1DM on matching prandial insulin dose to

carbohydrate intake, premeal blood glucose, and anticipated activity. E

• Most individuals with T1DM should use insulin analogs to reduce hypoglycemia risk. A

Recommendations: Pharmacologic Therapy For T2DM

• Metformin, if not contraindicated and if tolerated, is the preferred initial pharmacologic

agent for T2DM. A

 • Consider insulin therapy (with or without additional agents) in patients with newly dx’d

T2DM who are markedly symptomatic and/or have elevated blood glucose levels (>300 mg/dL)

Or A1C (>10%). E

New Recommendation: Pharmacologic Therapy For T2DM

• Long-term use of metformin may be associated with biochemical vitamin B12 deficiency,

and periodic measurement of vitamin B12 levels should be considered in metformin-treated

patients, especially in those with anemia or peripheral neuropathy. B

• If noninsulin monotherapy at maximal tolerated dose does not achieve or maintain the A1C

target over 3 months, add a second oral agent, a GLP-1 receptor agonist, or basal insulin. A

• Use a patient-centered approach to guide choice of pharmacologic agents. E

• Don’t delay insulin initiation in patients not achieving glycemic goals. B

Insulin Therapy in T2DM

• The progressive nature of T2DM should be regularly & objectively explained to

T2DM patients.

• Avoid using insulin as a threat, describing it as a failure or punishment.

 • Give patients a self-titration algorithm.

New Recommendation: Pharmacologic Therapy For T2DM

In patients with long-standing suboptimally controlled type 2 diabetes and established atherosclerotic

cardiovascular disease, empagliflozin or liraglutide should be considered as they have been shown to

reduce cardiovascular and all-cause mortality when added to standard care. Ongoing studies are

investigating the cardiovascular benefits of other agents in these drug classes. B

9. Cardiovascular Disease and Risk Management

Cardiovascular Disease

• CVD is the leading cause of morbidity & mortality for those with diabetes.

• Largest contributor to direct/indirect costs

• Common conditions coexisting with type 2 diabetes (e.g., hypertension, dyslipidemia) are

clear risk factors for ASCVD.

• Diabetes itself confers independent risk

• Control individual cardiovascular risk factors to prevent/slow CVD in people with diabetes.

• Systematically assess all patients with diabetes for cardiovascular risk factors.
Hypertension

• Common DM comorbidity

• Prevalence depends on diabetes type, age, BMI, ethnicity

• Major risk factor for ASCVD & microvascular complications

• In T1DM, HTN often results from underlying kidney disease.

• In T2DM, HTN coexists with other cardiometabolic risk factors.

Blood Pressure Control & T2DM

Action to Control Cardiovascular Risk in Diabetes (ACCORD):

• Does SBP <120 provide better cardiovascular

protection than SBP 130-140? No.

ADVANCE-BP:

• Significant risk reduction

Recommendations: Hypertension/ Blood Pressure Control (2)

Systolic Targets:

• People with diabetes and hypertension should be treated to a systolic blood pressure goal

of <140 mmHg. A

• Lower systolic targets, such as <130 mmHg, may be appropriate for certain individuals at

high risk of CVD, if they can be achieved without undue treatment burden. C

Recommendations: Hypertension/ Blood Pressure Control (3)

Diastolic Targets:

• Patients with diabetes should be treated to a diastolic blood pressure <90 mmHg. A

• Lower diastolic targets, such as <80 mmHg, may be appropriate for certain individuals at

high risk for CVD if they can be achieved without undue treatment burden. C

Recommendations: Hypertension/ Blood Pressure Treatment (2)

Patients with confirmed office-based blood pressure >160/100mmHg should, in addition to

lifestyle therapy, have prompt initiation and timely titration of two drugs or a single pill combination

of drugs demonstrated to reduce cardiovascular events in patients with diabetes. A

Lifestyle intervention including:

– Weight loss if overweight

– DASH-style diet

– Moderation of alcohol intake

– Increased physical activity

Recommendations: Hypertension/ Blood Pressure Treatment (3)

• Treatment for hypertension should include A

– ACE inhibitor

– Angiotensin II receptor blocker (ARB)

– Thiazide-like diuretic

– Dihydropyridine calcium channel blockers

• Multiple drug therapy (two or more agents at maximal doses) generally required to

achieve BP targets.

Recommendations: Hypertension/ Blood Pressure Treatment (4)

An ACE inhibitor or angiotensin receptor blocker, at the maximum tolerated dose indicated for

blood pressure treatment, is the recommended first-line treatment for hypertension in patients with

diabetes and urinary albumin–to– creatinine ratio >300 mg/g creatinine (A) or 30–299 mg/g

creatinine (B). If one class is not tolerated, the other should be substituted. B

Recommendations: Lipid Management

In adults not taking statins, a screening lipid profile is reasonable (E):

– At diabetes diagnosis

– At the initial medical evaluation

– And every 5 years, or more frequently if indicated

Obtain a lipid profile at initiation of statin therapy, and periodically thereafter. E

Recommendations: Lipid Management (2)

To improve lipid profile in patients with diabetes, recommend lifestyle modification A, focusing on:

– Weight loss (if indicated)

– Reduction of saturated fat, trans fat, cholesterol intake

– Increase of ω-3 fatty acids, viscous fiber,

plant stanols/sterols

– Increased physical activity

Recommendations for Statin Treatment in People with Diabetes

Recommendations: Lipid Management (5)

• Combination therapy (statin/fibrate) doesn’t improve ASCVD outcomes and is generally not

recommended A. Consider therapy with statin and fenofibrate for men with both trigs

≥204 mg/dL (2.3 mmol/L) and HDL ≤34 mg/dL (0.9 mmol/L). B

• Combination therapy (statin/niacin) hasn’t demonstrated additional CV benefit over statins

alone, may raise risk of stroke & is not generally recommended. A

• Statin therapy is contraindicated in pregnancy. B

Recommendations: Antiplatelet Agents

Consider aspirin therapy (75–162 mg/day) C

• As a primary prevention strategy in those with type 1 or type 2 diabetes at increased

cardiovascular risk.
 • Includes most men or women with diabetes age ≥50 years who have at least one

additional major risk factor, including:

– Family history of premature ASCVD

– Hypertension

– Smoking

– Dyslipidemia

– Albuminuria

Recommendations: Antiplatelet Agents (2)

• Aspirin is not recommended for ASCVD prevention for adults with DM at low ASCVD risk,

Since potential adverse effects from bleeding likely offset potential benefits. C

– Low risk: such as in men or women with diabetes aged <50 years with no major

additional ASCVD risk factors)

• In patients with diabetes <50 years of age with multiple other risk factors (e.g., 10-year risk

5–10%), clinical judgment is required. E

Recommendations: Antiplatelet Agents (3)

• Use aspirin therapy (75–162 mg/day) as secondary prevention in those with diabetes and

history of ASCVD. A

• For patients w/ ASCVD & aspirin allergy, clopidogrel (75 mg/day) should be used. B

• Dual antiplatelet therapy is reasonable for up to a year after an acute coronary syndrome. B

Recommendations: Coronary Heart Disease

Screening

• In asymptomatic patients, routine screening for CAD isn’t recommended & doesn’t improve

outcomes provided ASCVD risk factors are treated. A

• Consider investigations for CAD with:

– Atypical cardiac symptoms (e.g. unexplained dyspnea, chest discomfort)

– Signs or symptoms of associated vascular disease incl. carotid bruits, transient

ischemic attack, stroke, claudication or PAD

 – EKG abnormalities (e.g. Q waves) E

10. Microvascular Complications and Foot Care

Recommendations: Diabetic Kidney Disease

Screening

• At least once a year, assess urinary albumin and estimated glomerular filtration rate (eGFR):

– In patients with type 1 diabetes duration of ≥5 years B

– In all patients with type 2 diabetes B

– In all patients with comorbid hypertension B

Treatment

• Optimize glucose control to reduce risk or slow progression of diabetic kidney disease. A

• Optimize blood pressure control to reduce risk or slow progression of diabetic kidney

disease. A

Treatment (3)

• In nonpregnant patients with diabetes and hypertension, either an ACE inhibitor or ARB is

recommended for those with modestly elevated urinary albumin excretion (30–299 mg/g

creatinine).

B and is strongly recommended for patients w/ urinary albumin excretion ≥300 mg/g

creatinine and/or eGFR <60. A

Treatment (6)

• If patients have eGFR <30, refer for evaluation for renal replacement treatment. A

• Promptly refer to a physician experienced in the care of DKD for: B

– Uncertainty about the etiology of disease

– Difficult management issues

– Rapidly progressing kidney disease

Recommendations: Diabetic Retinopathy

• To reduce the risk or slow the progression of retinopathy

 – Optimize glycemic control A

– Optimize blood pressure control A

Screening:

• Initial dilated and comprehensive eye examination by an ophthalmologist or optometrist:

– Adults with type 1 diabetes, within 5 years of diabetes onset. B

– Patients with type 2 diabetes at the time of diabetes diagnosis. B

Screening (2):

• If no evidence of retinopathy for one or more eye exam, exams every 2 years may be

considered. B

• If diabetic retinopathy is present, subsequent examinations should be repeated at least

annually by an ophthalmologist or optometrist. B

• If retinopathy is progressing or sight-threatening, more frequent exams required. B

Treatment:

• Promptly refer patients with macular edema, severe NPDR, or any PDR to an ophthalmologist
knowledgeable & experienced in management, treatment of diabetic retinopathy. A

• Laser photocoagulation therapy is indicated to reduce the risk of vision loss in patients with
high-risk PDR and, in some cases, severe NPDR. A

Neuropathy

Early recognition & management is important because:

1. DN is a diagnosis of exclusion.

2. Numerous treatment options exist.

3. Up to 50% of DPN may be asymptomatic.

4. Recognition & treatment may improve symptoms,

reduce sequelae, and improve quality-of-life.
Recommendations: Neuropathy (1)

Screening:

• Assess all patients for DPN at dx for T2DM, 5 years after dx for T1DM, and at least

annually thereafter. B

• Assessment should include history & 10g monofilament

testing, vibration sensation (large-fiber function), and temperature or pinprick (small-fiber

function) B

• Symptoms of autonomic neuropathy should be assessed in patients with microvascular &

neuropathic complications. E

Treatment:

• Optimize glucose control to prevent or delay the development of neuropathy in patients

with T1DM A & to slow progression in patients with T2DM. B

• Assess & treat patients to reduce pain related to DPN B and symptoms of autonomic

Neuropathy and to improve quality of life. E

Recommendations: Foot Care

• Perform a comprehensive foot evaluation annually to identify risk factors for ulcers &

amputations. B

• All patients with diabetes should have their feet inspected at every visit. C

• History should contain prior hx of ulceration, amputation, Charcot foot, angioplasty or

vascular surgery, cigarette smoking, retinopathy & renal disease; and should assess current

symptoms of neuropathy and vascular disease. B

Recommendations: Foot Care (2)

• Exam should include inspection of the skin, assessment of foot deformities, neurologic

assessment & vascular assessment including pulses in the legs and feet. B

Recommendations: Foot Care (3)

• Patients with symptoms of claudication, decreased, or absent pedal pulses should be

referred for ABI & further vascular assessment. C

 • A multidisciplinary approach is recommended for individuals with foot ulcers and high-risk

feet. B

• The use of specialized therapeutic footwear is recommended for patients with high-risk

feet. B

Recommendations: Foot Care (5)

• To perform the 10-g monofilament test, place the device perpendicular to the skin; Apply

pressure until monofilament buckles.

• Hold in place for 1 second & release.

• The monofilament test should be performed at the highlighted sites while the patient’s

eyes are closed.

11. Older Adults

26% of patients aged >65 have diabetes.

Older adults have higher rates of premature death, functional disability & coexisting illnesses.

At greater risk for polypharmacy, cognitive impairment, urinary incontinence, injurious falls &

persistent pain.

Screening for complications should be individualized and periodically revisited.

At higher risk for depression

Recommendations: Older Adults

Functional, cognitively intact older adults (≥65 years of age) with significant life expectancy should

receive diabetes care using goals developed for younger adults. C

Determine targets & therapeutic approaches by assessment of medical, functional, mental, and

social geriatric domains for diabetes management. C

Recommendations: Older Adults (2)

• Glycemic goals for some older adults might be relaxed but hyperglycemia leading to

symptoms or risk of acute hyperglycemic complications should be avoided in all patients. C

• Hypoglycemia should be avoided in older adults with diabetes. It should be screened for

and managed by adjusting glycemic targets and pharmacologic interventions. B

Recommendations: Older Adults (4)

• When palliative care is needed, strict BP control may not be necessary and withdrawal of

therapy may be appropriate. Intensity of lipid management can be relaxed and withdrawal

of lipid-lowering therapy may be appropriate. E

• Screening for complications should be individualized, but attention should be paid to

complications that would lead to functional impairment. C

12. Children & Adolescents

Type 2 Diabetes

Distinguishing between type 1 and type 2 can be challenging.

Diabetes-associated autoantibodies and ketosis may be present in patients with features of type 2

such as obesity and acanthosis nigricans.

Accurate diagnosis is critical.

Recommendations: Transition from Pediatric to Adult Care

• Health care providers and families should begin to prepare youth in early to

mid-adolescence and, at the latest, at least 1 year before the transition to adult health

care. E

• Both pediatricians and adult health care providers should assist in providing support and

links to resources for the teen and emerging adult. B

Recommendations: Transition from Pediatric to Adult Care (2)

• Early & ongoing attention should be given to comprehensive coordinated planning for

seamless transition of all youth to adult health care.

• Association position statement, “Diabetes Care for Emerging Adults”

 13. Management of Diabetes in Pregnancy

Preexisting Diabetes

• Starting at puberty, preconception counseling should be incorporated into routine

diabetes care for all girls of childbearing potential. A

• Family planning should be discussed and effective contraception should be prescribed

and used until a woman is prepared and ready to become pregnant. A

Preexisting Diabetes (2)

• Provide preconception counseling that addresses the importance of glycemic control as

close to normal as safely possible, ideally <6.5%, to reduce the risk of congenital anomalies. B

Preexisting Diabetes (3)

• Women w/ preexisting type 1 or type 2 diabetes who are pregnant or planning to become

pregnant should be counseled on the risk of development and/or progression of diabetic

retinopathy. Eye exams

should occur before pregnancy or in the first trimester & then be monitored every trimester

and for 1 year postpartum as indicated by degree of retinopathy. B

Gestational Diabetes Mellitus (GDM)

• Lifestyle change is an essential part GDM mgmt. and may suffice for many women. Add

medications if needed to achieve glycemic targets. A

• Insulin is the preferred medication for treating hyperglycemia in GDM, as it does not cross

the placenta. Metformin and glyburide may be used but both, particularly metformin, cross

the placenta. All oral agents lack long-term safety data. A

Gestational Diabetes Mellitus (GDM)

• Metformin, when used to treat polycystic ovary syndrome and induce ovulation, need

not be continued once pregnancy has been confirmed. A

General Principles for Management of Diabetes in Pregnancy

• Potentially teratogenic medications (ACE inhibitors, statins, etc.) should be avoided in

sexually active women of childbearing age who are not using reliable contraception. B

• Fasting and postprandial SMBG are recommended in both GDM and preexisting diabetes

in pregnancy to achieve glycemic control. Some women with preexisting diabetes should

also test blood glucose preprandially. B

Glycemic Targets in Pregnancy

For women with gestational diabetes or preexisting type 1 or type 2 diabetes in pregnancy, the

following targets are recommended:

– Fasting ≤95 mg/dL (5.3 mmol/L)

and either

– One-hour postprandial ≤140 mg/dL (7.8 mmol/L) or

– Two-hour postprandial ≤120 mg/dL (6.7 mmol/L)

14. Diabetes Care in the Hospital

Recommendations: Diabetes Care in the Hospital

• Perform an A1C for all patients with diabetes or hyperglycemia admitted to the hospital if

not performed in the prior 3 months. B

• Insulin therapy should be initiated for treatment of persistent hyperglycemia starting at a

threshold ≥180 mg/dL. Then a target glucose of 140–180 mg/dL is recommended for the

majority of critically ill A and noncritically ill patients. C

Recommendations: Diabetes Care in the Hospital (2)

• More stringent goals, such as <140 mg/dL mmol/L) may be appropriate for selected critically

ill patients, if achievable without significant hypoglycemia. C

• Intravenous insulin infusions should be administered using validated written or

computerized protocols that allow for predefined adjustments in the infusion rate based

on glycemic fluctuations and insulin dose. E

Recommendations: Diabetes Care in the Hospital (4)

• A hypoglycemia management protocol should be adopted and implemented by each hospital

or hospital system. E

• A plan for preventing and treating hypoglycemia should be established for each patient. E

• Episodes of hypoglycemia in the hospital should be documented in the medical record and

tracked. E

Recommendations: Diabetes Care in the Hospital (5)

• A hypoglycemia management protocol should be adopted and implemented by each hospital

or hospital system. A plan for preventing and treating hypoglycemia should be established for

each patient. Episodes of hypoglycemia in the hospital should be documented in the medical

record and tracked. E

Recommendations: Diabetes Care in the Hospital (6)

• The treatment regimen should be reviewed and changed if necessary to prevent further

hypoglycemia when a blood glucose value is <70 mg/dL (3.9 mmol/L). C

• There should be a structured discharge plan tailored to the individual patient

 EPIDEMIOLOGY OF DIABETES IN US AND WORLDWIDE

Epidemiology of Diabetes

Diabetes affects 25.8 million people of all ages

8.3% of the U.S. population

- Diagnosed: 18.8 million

- Undiagnosed: 7.0 million

Leading cause of kidney failure, nontraumatic lower-limb amputation, new cases of blindness

among adults.

Major cause of heart disease and stroke.

Seventh leading cause of death.

Diagnosed and Undiagnosed Diabetes in 2010

~1.9 million people ≥20 years of age newly diagnosed; 215,000 were <20 years

Of the 25.6 million (11.3%) ≥20 years:

- Men: 13.0 million (11.8%)

- Women: 12.6 million (10.8%)
- Non-Hispanic whites: 15.7 million (10.2%)
- Non-Hispanic blacks: 4.9 million (18.7%)

>65 years, 10.9 million (26.9%)

Racial/Ethnic Differences in Diagnosed Diabetes

2007–2009 national survey data for people ages 20 years or older

Diagnosed and Undiagnosed Diabetes

County-Level Estimates of Diagnosed Diabetes (%), Adults ≥20 years, 2008

Number of Americans with Diagnosed Diabetes, 1980-2009
Number and Percentage of U.S. Population with Diagnosed Diabetes, 1958-2015

Prevalence of Overweight and Obesity Among Adults with Diabetes

CDC analysis of prevalence of overweight and obesity among U.S. adults ≥20 years with

previously diagnosed diabetes

– Overweight or obesity: 85.2%

– Obesity: 54.8%

Women aged 20-64 years had a significantly higher prevalence of obesity than women ≥65

Years of age (64.7% vs 47.4%; P<0.05) during 1999-2002.

Among men, prevalence of overweight or obesity was 86.3% and obesity, 53.0%.

SEARCH for Diabetes in Youth Results

6379 youth with diabetes in a population of ~3.5 million

- Average age at diagnosis: 8.4 years

- Average duration of diabetes 56 months (range, 38-60 months)

Estimated prevalence of U.S. youth aged 0-19 years with diabetes in 2001

- 1.82 cases per 1000 youth(95% CI: 1.78-1.87 per 1000 youth)
- Cancer: 1.24 per 1000
- Asthma: 120 per 1000
SEARCH for Diabetes in Youth 0-9 Years by Race/Ethnicity

SEARCH for Diabetes in Youth 10-19 Years by Race/Ethnicity

Prediabetes

In 2005-2008, based on fasting glucose or hemoglobin A1C levels, prediabetes was detected in

– 35% of adults ages 20 years and older

– 50% of adults ages 65 years and older

– An estimated 79 million adults ages

30 years and older
People with prediabetes have an increased risk of developing type 2 diabetes, heart disease,

and stroke.

Gestational Diabetes

Range from 2%–10% of pregnancies.

Postpartum, 5%–10% of women with gestational diabetes are found to have diabetes, usually

type 2.

Women who have had gestational diabetes have a 35%–60% chance of developing diabetes

within 10–20 years.

Using new diagnostic criteria, international multicenter study of gestational diabetes found 18%

of pregnancies were affected.

Complications of Diabetes Blindness, Eye Problems

Diabetes is leading cause of new cases of blindness among adults ages 20–74 years

Of people with diabetes aged ≥40 years, 4.2 million (28.5%) had diabetic retinopathy in 2005-2008.

655,000 (4.4% of those with diabetes) had advanced diabetic retinopathy that could lead to severe

vision loss.

Complications of Diabetes Renal Disease

In 2008, diabetes was leading cause of kidney failure, accounting for 44% of all new cases of renal

failure.

48,374 people with diabetes began treatment for end-stage renal disease (ESRD)

202,290 people with ESRD due to diabetes were living on chronic dialysis or with a kidney

transplant.

Complications of Diabetes Nervous System Disease

~60%–70% of people have mild to severe forms of nervous system damage

- Impaired sensation or pain in feet or hands

- Slowed digestion of food in the stomach
- Carpal tunnel syndrome
- Erectile dysfunction
Severe forms are a major contributing cause of lower-extremity amputations: >60% occur in

people with diabetes.

Treatment of Diabetes

Age Distribution of Deaths Associated with Diabetes

All-cause mortality rate among people with and without diabetes

CVD mortality rate among people with and without diabetes

CVD mortality rate among women with and without diabetes

All-cause mortality rate among women with and without diabetes

CVD mortality rate among men with and without diabetes

Economic Costs of Diabetes, 2007

Cost of Diabetes Model

Total cost of diabetes: $174 billion

- $116 billion: excess medical expenditures

• $27 billion to treat diabetes directly

• $58 billion to treat diabetes-related chronic complications attributed to

diabetes

• $31 billion excess medical costs

- $58 billion: reduced national productivity

Medical Expenditures Attributed to Diabetes, 2007

Hospital inpatient care (50%)

Diabetes medication and supplies (12%)

Retail prescriptions to treat complications of diabetes (11%)

Physician office visits (11%)

Costs Incurred by People with a Diagnosis of Diabetes in 2007

Average annual expenditures: $11,744

- $6,649 attributed to diabetes

On average, people with diagnosed diabetes have medical expenditures ~2.3 times higher

than those without diabetes

- ~$1 in $5 health care dollars is spent caring for someone with diagnosed diabetes
- ~$1 in $10 health care dollars is attributed to diabetes

Health Resource Use Attributed to Diabetes, 2007

Indirect Costs Attributed to Diabetes, 2007

Section 3

Future projections

IDF Global Projections for Number of People with Diabetes, 2010-2030

Total U.S. Adult Population Diabetes Prevalence Projections