PART 1- INTRODUCTION TO NURSING SELECTIVE TOXICITY- drug’s ability to attack only those found

in foreign cells w/o damaging normal human cell

PHARMACOLOGY CRITICAL CONCENTRATION- amount of drug that is needed
CHAPTER 1- Introduction to Drugs to cause a therapeutic effect
ABSORPTION- what happens to the drug when it enters &
PHARMACOLOGY- study of the biological effects of chemicals reaches the circulation
PHARMACOTHERAPEUTICS- uses drugs to treat, prevent, & SITES OF ABSORPTION:
diagnose disease  Oral, rectal
DRUGS- chemicals that cause changes  Mucous membrane
 THERAPEUTIC CLASS- pwd sa uban sakit  Skin
 PHARMACOLOGIC CLASS- pero antidiuretic jud sya  Lungs
SOURCES OF DRUGS:  Muscles
 PLANTS
 ANIMAL PRODUCTS 1. PASSIVE DIFFUSION- greater to lower concentration
o GENETIC ENGINEERING- process of altering w/ no energy required; small molecule
DNA 2. ACTIVE TRANSPORT- uses energy; larger molecule
 INORGANIC COMPOUNDS 3. FILTRATION- used in drug excretion
DRUG EVALUATION: ADMINISTRATION
1. PRECLINICAL TRIALS  ORAL ROUTE- most commonly used; not invasive;
2. PHASE I STUDIES less expensive
3. PHASE II STUDIES  IV- fastest route
4. PHASE III STUDIES  IM- least
5. CONTINUAL EVALUATION  SUB-Q- least
a. BRAND NAME- trade name DISTRIBUTION- movement of drug to the body
b. GENERIC NAME-abbreviation of chemical Factors:
name  LIPID SOLUBILITY
c. CHEMICAL NAME- chemical structure of a  IONIZATION
drug  PERFUSION OF THE REACTIVE TISSUE
d. ORPHAN DRUGS- drugs that have been  BLOOD-BRAIN BARRIER
discovered but are not financially viable BIOTRANSFORMATION (METABOLISM)
e. OVER-THE-COUNTER DRUGS- products that LIVER ENZYME SYSTEMS- liver is the most important site
are available w/o prescription of drug metabolism
HEPATIC MICROSOMAL SYSTEM- structure of hepatic
CHAPTER 2- Drugs and the Body cells’ intracellular lined up w/ enzymes
EXCRETION- removal of drug from body; skin, saliva, lungs,
bile & feces.
PHARMACODYNAMICS- how the drug affects the body
KIDNEY- plays the most important role in drug excretion
PHARMACOKINETICS- how the body reacts on the drug
HALF-LIFE- time it takes for the amount of drug to decrease
DRUG ACTIONS:
 To replace substitutes for missing chemicals
 To increase/ decrease certain cellular activities CHAPTER 3- Toxic Effects of Drugs
 To interfere w/ the functioning of foreign cells, like
invading neoplasms (CHEMOTHERAPEUTIC AGENTS) ADVERSE EFFECTS- undesired effects
RECEPTORS SITE- specific areas on cell membranes; react w/ Reasons of occurrence:
certain chemicals to cause an effect  Pt is sensitive to the drug
 SPECIFIC CHEMICAL- the key  Pt taking too much/ little of the drug
 PERFECT FIT- the lock ADVERSE DRUG REACTION- unintended & undesired reaction
AGONIST- create response to the drug
ANTAGONIST- doesn’t create response SIDE EFFECT- result of drug in addition of the desired
 COMPETITIVE ANTAGONIST- some drugs react w/ therapeutic effect
receptor sites to block normal stimulation, producing TYPES OF ADVERSE REACTIONS:
no effect 1. PRIMARY
 NONCOMPETITIVE ANTAGONIST-react w/ receptor 2. SECONDARY
sites & prevent the reaction of another chemical w/ 3. HYPERSENSITIVITY
a different receptor sire ALLERGY:
1. ANAPHYLACTIC REACTION (TYPE 1)
 “Immediate Hypersensitivity Reaction”  RECEPTOR SITES
 Sudden, widespread, potentially sever & life-  IDENTIFYING MARKERS- histocompatibility
threatening antigens/ Human Leukocyte Antigens
 Appears w/in 10 min (HLAs)- identify a cell as self-cell
S/S  CHANNELS
 Hives, rash, difficulty breathing, increased 3. CYTOPLASM
BP, dilated pupils, diaphoresis, increased  MITOCHONDRIA
heart rate, respiratory arrest  ENDOPLASMIC RETICULUM
2. CYTOTOXIC REACTION  FREE RIBOSOMES
“Toxic to Cell”  GOLGI APPARATUS
 Antibodies produced by the Immune system  LYSOSOMES
response bind to antigens on the pt own cell CELL PROPERTIES
surfaces  ENDOCYTOSIS- incorporation of material into the cell
*Ex. ABO incompatibility o PINOCYTOSIS- cell-drinking
3. SERUM SICKNESS o PHAGOCYTOSIS- cell-eating
 Immune system reacts to medicines that  EXOCYTOSIS- secretion of substances out of the cell
contains protein HOMEOSTASIS
*Ex. Vaccines, Antiserum PASSIVE TRANSPORT
4. DELAYED ALLERGIC REACTION  DIFFUSION- higher to lower concentration
“Cell-mediated)  OSMOSIS- lower to higher solutes
 Takes 2-3 days o ISOTONIC
 Cell-mediated response (CD4 & HELPER T o HYPERTONIC- higher solutes
CELLS- recognize antigen) o HYPOTONIC-lower solutes
*Ex. Tuberculin test, contact dermatitis  FACILITATED DIFFUSION- w/ carrier
*HAPTENS- incomplete antigen ACTIVE TRANSPORT- requires energy
CELL CYCLE
DRUG-INDUCED TISSUE & ORGAN DAMAGE 1. GO PHASE- resting phase
1. DERMATOLOGICAL REACTIONS: 2. G1 PHASE- synthesize substances for DNA formation
 RASHES 3. S PHASE- actual synthesis of DNA
 HIVES (burning & itching) 4. G2 PHASE- produce substances for mitotic spindles
2. MUCOUS MEMBRANES: 5. M PHASE- cell division. Mitosis
 STOMATITIS
3. SUPERINFECTIONS (Suprainfection)
 New infection occurring in pt w/ preexisting
CHAPTER 8- Anti-infective Agents
infection
4. BLOOD DYSCRASIA/BONE MARROW DEPRESSION
 CHAPTER 9- Antibiotics
5. TOXICITY
6. ALTERATION IN GLUCOSE METABOLISM ANTIBIOTIC- inhibit bacteria
7. ELECTROLYTE IMBALANCES BACTERIOSTATIC- prevent growth of bacteria
8. SENSORY EFFECTS BACTERICIDAL- kill bacteria
9. NEUROLOGIC EFFECTS BACTERIA:
10. TERATOGENICITY  GRAM-POSITIVE- respi & soft tissues infections
 GRAM-NEGATIVE- GU & GI infections
CHAPTER 5- Dosage Calculations  SYNERGY- given in combination
1. AMINOGLYCOSIDES
PART 2- CHEMOTHERAPEUTIC AGENTS a. Treat serious infection caused by gram-
CHAPTER 7- Introduction to Cell negative aerobic bacilli
b. Bactericidal
Physiology c. Ex. Amikacin, Gentamicin, Kanamycin,
Neomucin, Streptomycin
The Cell 2. CEPHALOSPORINS
1. CELL NUCLEUS a. 1960
 RIBOSOMES- sites of protein synthesis b. Similar to penicillin
2. CELL MEMBRANE c. Has 4 generations (Peck, HENPeCK,
 LIPOPROTEIN HENPeCKS, for gram+ & -)
 d. Bactericidal & bacteriostatic b. PROTEASE INHIBITORS- blocks protease
e. Nephrotoxicity (essential for maturation of infectious virus)
f. Ex. Cephalexin activity
3. FLUROQUINOLONES c. NUCLEOSIDES- inhibits cell protein synthesis
a. New class with broad spectrum d. FUSION INHIBITORS- new class of drugs,
b. Ex. Ciprofloxacin, Levofloxacin, Ofloxacin prevents fusion of virus w/ human cell
4. MACROLIDES membrane
a. Interfere w/ protein synthesis 4. DRUGS USED FOR HEPA B
b. Bactericidal/ bacteriostatic a. Ex. Adefovir,Entecavir
c. Ex. Erythromycin, Azithromycin 5. LOCALLY ACTIVE ANTIVIRAL AGENTS
5. LINCOSAMIDES a. Given locally to treat viral infection
a. Similar to the macrolides but are more toxic b. Ex. Aldara, Herplex, Abreva
b. Ex. Clindamycin, Lincomycin
6. MONOBACTAM ANTIBIOTICS CHAPTER 11- Antifungal Agents
a. Gram-negative inhibitor
b. Ex. Azactam
MYCOSIS- infection caused by fungus
7. PENICILLINS & PENISILLINASE-RESISTANT
ERGOSTEROL- found in cell wall of fungi
ANTIBIOTICS
1. SYSTEMIC ANTIFUNGALS
a. Alexand Fleming
a. EX. Amphotericin B, Caspofungin,
b. w/ tetracyclines, the effectiveness will
Micafungin, Nystatin
decrease
b. AZOLES- newer drugs that treats systemic
c. Ex. Amoxicillin, Ampicillin
fungal infections
8. SULFONAMIDES
i. Ex. Ketoconazole, Fluconazole
a. Inhibit folic acid synthesis
2. TOPICAL ANTIFUNGAL
b. Not used much any more
a. DERMATOPHYTES- causative agent
c. Competitively block para-aminobenzoic acid
b. Causes tinea infections: ringworm, athlete’s
(gram + & -)
foot, jock itch
d. Teratogenic
c. Ex. Gentian violet, Butenafine, Butoconazole
e. Ex. Sulfadiazine, Cotrimoxazole
9. TRTRACYLCINES
a. Semisynthetic CHAPTER 12- Antiprotozoal Agents
b. Inhibiting protein synthesis
c. Composed of four rings PROTOZOA- thrives in tropical area
d. Ex. Tetracycline, Minocycline 1. MALARIA
10. ANTIMYCOBACTERIAL ANTIBIOTICS a. ANOPHELES MOSQUITO- PLASMODIUM
a. Acid-fast bacteria i. FALCIPARUM- most dangerous
b. Ex.Rifampicin, Isoniazid, Ethambutol ii. VIVAX- mild, seldom
11. LEPROSTATIC DRUGS iii. MALARIAE- endemic
a. Ex. Dapsone iv. OVALE- rarely seen
b. LIFE CYCLE
i. GAMETOCYTES
CHAPTER 10- Antiviral Agents ii. SPOROZOITES
iii. TROPHOZOITES
VIRUSES
iv. MEROZOITES
INTERFERONS- signals other cell of virus invasion
c. ANTIMALARIALS
1. AGENTS FOR INFLUENZA A & RESPI VIRUSES
i. Ex. Quinine, Chloroquine,
a. Prevent shedding of viral protein coat &
Mefloquine, Primaquine
entry of viruses
ii. Interrupts plasmodial reproduction
b. Ex. Amantadine, Ribavirin, Rimatidine,
of protein synthesis in RBC stage
Zanamivir
iii. Risk fo cardiac toxicity & convulsions
2. AGENTS FOR HERPES & CYTOMEGALOVIRUS
2. AMEBIASIS
a. Inhibit viral DNA replication
a. ENTAMOEBA HISTOLYTICA
b. Ex. Acyclovir, Cidofovir, Foscarnet
b. CYST-TROPHOZOITE
3. AGENTS FOR HIV & AIDS
c. Can cause death
a. REVERSE TRANSCRIPTASE INHIBITORS- blocks
3. LEISHMANIASIS
RNA & DNA, prevent transfer of information
a. SAND FLIES- PROMASTIGOTE- AMASTIGOTE
4. TRYPANOSOMIASIS
 a. TRYPANOSOMA a. In combination therapy
i. AFRICAN SLEEPING SICKNESS b. Inhibit DNA production that depend on
ii. CHAGAS’ DISEASE metabolites
5. TRICHOMONIASIS c. Ex. Methotrexate, Pentostatin, Capecitabine
a. TRICHOMONAS VAGINALIS 3. ANTINEOPLASTIC ANTIBIOTICS
b. Cause vaginitis a. Not selective
6. GIARDIASIS b. Toxic to human cells
a. GIARDIA LAMBLIA c. Toxic to rapidly multiplying cells (GI, skin,
7. PNEUMOCYSTIS CARINII PNEUMONIA marrow)
a. Most common opportunistic infection in pts d. Interfere w/ DNA synthesis by inserting
w/ AIDS themselves between base pairs in the CAN
OTHER ANTIPROTOZOAL AGENTS chain & causing a mutant DNA molecule
 Ex. Metronidazole, Pentamidine e. Ex. Doxorubicin, Bleomycin, Dactinomycin
4. MITOTIC INHIBITORS
CHAPTER 13- Anthelmintic Agents a. Kill cells as the process of mitosis begins
b. Interfere w/ the ability of a cell to divide
c. Ex. Vincristine, Vinblastine, VInorelvbine
INTESTINE-INVADING WORMS
5. HORMONES & HORMONE MODULATORS
 NEMATODES, PINWORMS, WHIPWORMS,
a. Cancer in the breast tissue, ovaries, uterus,
THREADWORMS, ASCARIS, HOOKWORMS,
prostate & testes
PLATUHELMINTS: CESTODES
b. Used to block the release of gonadotropic
TISSUE-INVADING WORM INFECTION
hormones
1. TRICHINOSIS
c. Ex. Tamoxifen, Anastrazole, Estramustine
a. TRICINELLA SPIRALIS
2. FILARIASIS
a. ELEPHANTIASIS PART 3- DRUGS ACTING ON THE
3. SCHISTOSOMIASIS IMMUNE SYSTEM
a. SNAIL
ANTIHELMINTIC CHAPTER 15- Introduction to the
 Ex. Mebendazole, Praziquantel, Albendazole Immune Response & Inflammation
CHAPTER 14- Antineoplastic Agents BODY DEFENSES
1. BARRIER DEFENSES
NEOPLASM- cancer a. SKIN- has keratin, acidic sweat, sebum
 ANAPLASIA- loss of ability b. MUCOUS MEMBRANES- works like flypaper
 AUTONOMY- growing w/o restrictions c. GASTRIC ACID
 METASTASIS- travel from place d. MAJOR HISTOCOMPATIBILITY COMPLEX-
 ANGIOGENESIS- generate blood vessels ability to distinguish between self-cells &
CAUSES OF CANCER foreign cells
2. CELLULAR DEFENSES
 Genetic predisposition
a. LEUKOCYTES- lymphocytes & myelocytes
 Viral infection
b. NEUTROPHILS- capable of diapedesis (to go
 Constant irritation
outside the bloodstream), active kaau.
 Stress
phagocytes
 Areas w/ carcinogenic c. BASOPHILS- histamine
TYPES OF CANCER d. EOSINOPHILS- histaminase
 CARCINOMAS- tumors in epithelial cells e. MONOCYTES/ MACROPHAGES- antigen
 SARCOMAS- tumor in mesenchyme presenter
ANTINEOPLASTIC DRUGS f. MAST CELLS- fixed basophils in respi & GI
1. ALKYLATING AGENTS tract. Prostaglandin
a. Non-cell cycle-specific CLINICAL PRESENTATION
b. Most useful in slow-growing cancers, resting  CALOR- heat
phase  TUMOR- swelling
c. Disrupts cell mechanisms that affect DNA
 RUBOR- redness
d. Ex. Busulfan, Carboplatin
 DOLOR- pain
e. Magka alopecia
PATHOPHYSIOLOGY INVOLVING THE IMMUNE SYSTEM
2. ANTIMETABOLITES
 1. NEOPLASMS IMMUNE SUPPRESSANTS
2. VIRAL INVASION OF CELLS 1. T & B CELL SUPPRESSORS
3. AUTOIMMUNE DISEASE- suppressor t cells don’t 2. INTERLEUKIN RECEPTOR ANTAGONIST
suppress, genetic predisposition to develop 3. MONOCLONAL ANTIBODIES
autoantibodies CHAPTER 18- Vaccines & Sera
4. TRANPLANT REJECTION- t cells are activated by the
presence of the foreign cells
ACTIVE IMMUNITY- body recognizes foreign protein &
produces antibodies
CHAPTER 16- Anti-inflammatory Agents PASSIVE IMMUNITY- antibodies are injected
1. IMMUNIZATION- exposure to weakened protein
SALICYLATES- popular anti-inflammatory agents 2. VACCINES- stimulate formation of antibodies
 ANTIPYRETIC- fever-blocking a. Stimulate active immunity
 ANALGESIC- pain-blocking 3. IMMUNE SERA & ANTITOXINS
NONSTEROIDAL ANTI-INFLAMMATORY DRUGS- strong anti- a. SERA-contain antibodies
inflammatory &analgesic effects b. ANTITOXIN- immune sera that have
ACETAMINOPHEN- antipyretic & analgesic but no antibodies that might be released by
inflammatory effects of salicylates/ NSAID invading pathogens
1. SALICYLATES c. Immune sera provide passive immunity
a. Oldest anti-inflammatory
b. Inhibits thromboxane A, a vasoconstrictor CHAPTER 19- Introduction to Nerves &
that increases platelet aggregation & clot
formation the Nervous System
c. Inhibits synthesis of prostaglandin
d. Ex. Aspirin, Balsalazide, Mesalamine, CNS- integration
Olsalazine, Salsalate PNS- bring info to cns
2. NONSTEROIDAL ANTI-INFLAMMATORY DRUGS AUTOMATIC NS-regulate automatic unconscious responses
a. Ex. Ibuprofen, Celecoxib, Diclofenac ASCENDING TRACT- sensory
3. RELATED DRUGS DESCENDING TRACT- response
a. ACETAMINOPHEN PHYSIOLOGY OF THE NERVOUS SYSTEM
i. For pain & fever. For children 1. NEURONS
ii. Ex. Acetaminophen,  TYPES: Unipolar, Bipolar, Multipolar
Aurothioglucose, Anakinra,  SOMA- cell body
Penicillamine  DENDRITES- branch-like covering of neuron
b. GOLD COMPOUND  AXON- elongated process
i. CHRYSOTHERAPY- gold salts  AFFERENT- sensory
ii. Inhibits phagocytosis. The release of  EFFERENT- motor
lysosomal enzymes is inhibited & 2. ACTION POTENTIAL
tissues destruction is decreased IMPULSES & STIMULUS
iii. For rheumatic inflammatory  AT REST- negative inside cell
conditions  DEPOLARIZATION- sodium rush into cell,
change is charge
CHAPTER 17- Immune Modulators  ACTION POTENTIAL- sudden reversal of
membrane lasts less than a micro-second
IMMUNE STIMULANTS- used to energize exhausted immune  REPOLARIZATION- returns to resting
system membrane
IMMUNE SUPPRESSANTS- used to block the normal effects of 3. GLIAL CELLS
immune system  TYPES:
i. ASTROCYTE-
IMMUNE STIMULANTS: ii. MICROGLIAL
1. INTERFERONS- stimulate interferon receptor sites to iii. EPENDYMAL
produce antiviral proteins iv. OLIGODENDROCYTES
2. INTERLEUKINS- chemicals produce by T cells to v. SCHWANN CELLS
communicate between leukocytes. Activate cellular  NODES OF RANVIER
immunity & inhibit tumor growth 4. NERVE SYNAPSE
3. T & B CELL MODULATOR  Where communication occurs
5. NEUROTRANSMITTERS
  Stimulate postsynaptic cells by exciting/ a. CEREBRAL CORTEX- associated w/ higher
inhibiting them brain function such as though & ation
 SYNAPTIC VESSICLE- produce b. RIGHT SIDE OF THE BRAIN- artistic
neurotransmitters i. Largest part of human brain
 MONOAMINOXIDASE- degrades c. LEFT SIDE OF THE BRAIN- analytical
neurotransmitters d. ENGRAM- reverberating circuit of action
1. ACETYLCHOLINE- nerves & muscle(degrades potential that eventually becomes a long-
neurotransmitters term
2. NOREPINEPHRINE & EPINEPHRINE- catecholamines i. Responsible for short-term memory
(stimulants) in times of emergency(fight/fly) e. Substances affecting learning:
3. DOPAMINE- coordination of impulses & responses i. ADH-released during reaction to
4. GAMMA-AMINOBUTRIC ACID- prevent stress
overexcitability like seizure ii. OXYTOCIN
5. SEROTONIN- arousal & sleep
CENTRAL NERVOUS SYSTEM PART 4- DRUGS ACTING ON THE
 BLOOD BRAIN BARRIER
 CAROTIDS CENTRAL & PERIPHERAL NERVOUS
 VERTEBRALS SYSTEMS
 CIRCLE OF WILLIS CHAPTER 20- Anxiolytic & Hypnotic
 GANGLION- composed of nerves outside spinal &
brain cord Agents
ANATOMY OF THE BRAIN
1. HINDBRAIN ANXIOLYTICS- prevent feeling of tension/ fear
a. BRAINSTEM-pons & medulla oblongata SEDATIVES- calm patients
b. Control basic, vital functions like respiration, HYPNOTICS- cause sleep
bp, swallowing reflex, & RAS ANXIETY- feeling of tension, nervousness, apprehension that
c. CEREBELLUM- regulates posture, balance & usually involves unpleasant reactions to a stimulus,
voluntary muscle activity  whether actual/ unknown
2. MIDBRAIN  fast heart rate, rapid breathing, elevated blood
a. THALAMUS- sensation, cold, heat, pain, pressure
touch, muscle senses- SEDATION- loss of awareness
b. HYPOTHALAMUS- major sensor for activities. HYPNOSIS- extreme sedation results to cns depression
Temperature, water balance, appetite & 1. BENZODIAZEPAM
fluid balance. Produce hormones & store in a. Most frequently used anxiolytic drugs
the posterior pituitary gland b. Act in the limbic system & the RAS to make
3. LIMBIC SYSTEM GABA more effective, causing interference
a. 3 neurotransmitters: EPINEPHRINE, NOR- w/ neuron firing
EPINEPHRINE, & SEROTONIN. c. For anxiety disorders, alcohol withdrawal,
b. Expression of emotions- anger, pleasure, hyperexcitability and preoperative relief of
motivation, stress anxiety & tension
4. FOREBRAIN d. Ex. Diazepam
a. Made up of 2 cerebral hemisphere joined by 2. BARBITURATES
CORPUS CALLOSUM a. Once the sedative/ hypnotic drugs of choice
b. Speech & communication b. Inhibit neuronal impulse conduction in the
5. BASAL GANGLIA- extrapyramidal motor system ascending RAS
ANATOMY OF THE SPINAL CORD
 31 pairs of spinal nerves CHAPTER 21- Antidepressants Agents
 DORSALROOT- sensory fiber
 MOTOR FIBER- ventral root AFFECT- refer to people’s feelings in response to their
FUNCTIONS OF THE CNS environment
1. SENSORY FUNCTIONS DEPRESSION- feelings of severe & long-lasting sadness,
2. MOTOR FUNCTIONS despair, hopelessness, disorganization. Little energy, sleep
a. PYRAMIDAL SYSTEM “Voluntary movement” disturbances, lack of appetite, limited libido, inability to
b. EXTRAPYRAMIDAL “Unconscoius” perform activities
3. INTELLECTUAL& EMOTIONAL 1. TRICYCLIC ANTIDEPRESSANTS (TCAs)
 a. Inhibit presynaptic reuptake of the CHAPTER 23- Antiepileptic Agents
neurotransmitters which lead to an
accumulation of these neurotransmitters in
EPILEPSY- sudden discharge of excessive electrical energy
the synaptic cleft
from nerve cells
b. Ex. Impiramine
SEIZURES- caused by these abnormal cells called primary
2. MONOAMINE OXIDASE INHIBITORS
seizures because no underlying cause can be identified.
a. Inhibit MAO
Leads to head injury, drug overdose, environmental
b. Tyramine- thyroxine- epinephrine &
exposure- secondary seizures
norepinephrine
GENERALIZED SEIZURE
3. SELECTIVE SEROTONIN REUPTAKE INHIBITORS
 Begin in one area of the brain & rapidly spread
a. Newest drugs that specifically block the
throughout both hemisphere of the baine
reuptake of 5HT, w/ little to no effect on NE.
 Loss of consciousness resulting from thes massive
b. Increase extracellular level of serotonin by
electrical activity
limiting its reabsorption into the presynaptic
1. TONIC-CLONIC SEZIRES- aura warning sign.
cell
Grand mal seizure
2. ABSENCE SEIZURE- petit mal seizure. Abrupt,
CHAPTER 22- Psychotherapeutic Agents brief periods of unconsciousness
3. MYOCLONIC- sporadic periods of muscle
SCHIZOPHRENIA- hallucinations, paranoia, delusions, speech contractions that last for several minutes
abnormalities 4. FFEBRILE- related to very high fever. Self-
MANIA- overactivity & excitement limited & don’t reappear
NARCOLEPSY- daytime sleepiness & sudden periods of loss of 5. STATUS EPILEPTICUS- most dangerous. Rapid
wakfulness reoccurring
ATTENTION-DEFICIT DISORDERS- inability to concentrate on PARTIAL SEIZURES
one activity for longer than a few minutes  FOCAL SEIZURES
1. ANTIPSYCHOTIC/ NEUROLEPTIC DRUG  Involve one area of the brain & don’t spread
a. Essentially dopamine receptor blockers 1. SIMPLE PARTIAL-single muscle movement
b. Used to treat disorders that involve thought 2. COMPLEX PARTIAL- complex sensory
processes changes
c. Known as neuroleptic & major tranquilizers
d. Types:
i. TYPICAL- primarily dopamine
CHAPTER 24- Antiparkinsonism Agents
receptor blockers CHAPTER 25- Muscle Relaxants
ii. ATYPICAL- bock both dopamine &
serotonin receptors
CHAPTER 26- Narcotics & Antimigraine
e. Common neurological effects: Agents
i. DYSTONIA- hiwi liog
ii. AKATHISIA- foot tapping
iii. PSEUDOPARKINSONISM- slow char
iv. TARDIVE DYSKINESIA- lips & tongue
2. ANTIMANIC
a. Mania- opposite of depression
b. Lithium salts
3. CENTRAL NERVOUS SYSTEM STIMULANTS
a. Calm hyperkinetic children & help them
focus on one activity for a longer period
b. Excite the arousal stimuli from the RAS
c. Increase release of catecholamines leading
to an increase stimulation of the
postsynaptic neurons
d. Ex. Dexedrine
e. Contraindication: anxiety, agitation, tension,
dardiac disease, history of drug dependence
including alcoholism