Learning
Objectives
Learning Objectives. Listed
below are learning objectives and lists of important drugs for each
contact hour in Medical Pharmacology. By the end of each contact hour,
students are expected to be able to answer each learning objective.
The drug lists summarize the essential drugs covered for each contact
hour. Questions on the progress exams will be designed to assess your
mastery of the learning objectives. Drugs shown in bold in the drug
lists are those included in the top 200 most commonly prescribed drugs
based upon the number of prescriptions dispensed. Please note that not all important and commonly used drugs are
necessarily "commonly prescribed" if, for example, they are
used primarily in a hospital setting (e.g. lidocaine, epinephrine, general
anesthetics), are sold over the counter (e.g. aspirin), or are highly
abused (cocaine).
Fall Semester 2007
(Last Modified on:
March 19, 2008
)
|
Basic Principles
Students will be introduced to:
- Course administrators.
- Recommended textbooks.
- Organization of the course.
- Exam and grading policies
- The course Web Site.
By the end of this session, you
should be able to:
- Define the terms: pharmacology,
drug, poison, pharmacodynamics and pharmacokinetics.
- Describe the two primary properties of a drug
receptor, and how a receptor differs from an inert binding site.
- Define the following drug properties: agonist,
antagonist, partial agonist, affinity, efficacy,
potency.
- Describe a typical dose-response curve for
a drug, and label the positions on the curve that are used to define drug
potency and efficacy.
- Describe several different signal transduction
mechanisms by which agonists exert their effects.
- Explain the difference between selectivity
and specificity of drug effect, and which is more commonly
observed.
- Describe what is meant by the term Therapeutic
Window.
- Describe and explain the effect(s) of competitive
and non-competitive antagonists on the dose-response curve for an agonist.
- Explain how a quantal dose-response curve
is constructed.
- Explain what is meant by additive and synergistic
drug effects.
- Define what "desensitization" means
& explain how it can occur.
- Define the terms ED50,
LD50, TD50
, and Therapeutic Index.
By the end of this session, you should be
able to:
- Describe how different dosage
forms alter the absorption, distribution and onset of action of drugs.
- Describe different dosage forms,
their correct names and special characteristics.
By the end of this session, you should be
able to:
- List the different parts of a prescription.
- List from memory the meaning of the
abbreviations: q.d., b.i.d., t.i.d., q.i.d, p.r.n, non.rep., q., p.o., p.c.,
a.c.
By the end of this session, you
should be able to:
- Explain what is meant by the term drug
disposition.
- Explain the which drug properties facilitate
absorption.
- Discuss which biological properties faciliate
absorption.
- Explain the mechanism of pH-dependent ion
trapping with respect to accumulation of drugs.
- Explain which chemical properties make a drug
more water soluble.
- Explain which chemical properties make a drug
more lipid soluble.
- Discuss protein binding and the effect of
concomitant administration of two protein-binding drugs on drug effect.
- Discuss the impact of drug distribution and
redistribution on drug action.
- Explain the basic principles by which drugs
are excreted from the body.
- Explain the principle of the chemical
defense hypothesis.
- Explain what is meant by the term drug
metabolism.
- List the major mechanisms responsible for
drug metabolism.
- Describe the major enzyme systems in the body
that are responsible for oxidation, reduction and/or hydrolysis of selective
pharmacological agents.
- Describe the basic principles of how drug
metabolism alters drug action.
- Define cytochrome p-450.
- Explain how drugs are chemically altered by
cytochrome p-450.
- Explain the rate limiting step in the general
non-specific pathway for drug metabolism in the liver.
- Discuss the difference between acute and chronic drug treatment with respect to
drug metabolism by the liver.
- Explain how drug-induced enzyme induction and inhibition can alter responses to drugs.
- Discuss the basic clinical interactions that
can result from changes in drug metabolism during co-administration of drugs.
DRUG LIST:
Cyt-P450 inhibitors:
cimetidine,
erythromycin,
ciprofloxacin,
fluoxetine
(Prozac ®), grapefruit
juice
Cyt-P450
inducers: rifampin,
barbiturates,
phenytoin,
carbamezepine,
St.
John's wort, (ethanol
in large amounts), thyroid
hormone
Cyt-P450 substrates:
warfarin,
theophylline,
oral
contraceptives
Cyt-P450
drug interactions: sulfa
drugs & phenobarbital, ethanol
& tolbutamide, phenobarbital
& warfarin, phenobarbital
& phenytoin
Other
metabolism related drug interactions:
ethanol
& disulfuram, MAO
inibitors & tyramine
By the end of this session,
you should be able to:
- Define the concepts of loading dose, maintenance dose, volume of distribution, clearance, elimination half-life.
- Calculate the initial volume of distribution given a loading dose and initial plasma drug concentration at time zero.
- Explain the difference between first-order and dose-dependent (zero-order) kinetics of drug elimination.
- List three examples of commonly used drugs that follow dose-dependent (zero-order) kinetics.
- Describe the concept of steady-state with regard to plasma drug concentrations.
- Explain the importance of different pharmacokinetic parameters on the duration of drug action.
- Calculate how long it will take to reach 90% of the steady state plasma drug level given a drug’s elimination half-life.
- Given a drugs half-life of elimination, calculate how long it will take for a plasma drug level to fall to 50%, 25% and 10% of its current value if drug administration is discontinued.
- Describe what is meant by a one-compartment and two-compartment model of drug distribution and elimination.
- Calculate a loading dose to achieve a target plasma drug level given the drug’s Vd.
- Given a drug’s elimination clearance, calculate the maintenance dose needed to achieve or maintain an average steady-state drug level (Css) using either a continuous infusion (mg/hr) or dose per time interval (e.g. 300 mg q.i.d.).
- Explain why Cl and Vd are considered “primary” pharmacokinetic parameters, while half-life (t1/2) is not.
DRUG LIST:
phenytoin,
aspirin,
ethyl alcohol
By the end of this session, you
should be able to:
- Define pharmacogenomics.
- Explain the different ways that genetics plays a role in drug metabolism/response (e.g. for succinylcholine).
- Explain the relationship between Glucose-6-Phosphate dehydrogenase deficiency & drug induced hemolytic anemia by primaquine & other drugs.
- Explain the relationship between “acetylator phenotype” and the incidence of side effects when patients are treated with isoniazid, procainamide, sulfa drugs or dapsone.
- Describe how mutations can alter patient response to 5-fluorouracil treatment.
- Describe how an understanding of the genomics of chronic myelogenous leukemia (CML) resulted in the identification of a new drug target to treat CML.
DRUG LIST:primaquine, isoniazid,
succinylcholine,
imatinib
(Gleevac ®), 5-Fluorouracil
By the end of this session, you
should be able to:
- Explain the role of drug metabolism
in drug interactions.
- Describe the process of enzyme induction.
- Describe the process of enzyme inhibition.
- List the major isozymes of cytochrome P-450
(CYP) with respect to drug metabolism in humans.
DRUG LIST:cimetidine,
warfarin,
rifampin
Inflammation
By the end of this session, you
should be able to:
- Define the general principles of immunosuppression.
- Name seven immunosuppressants and, for each,
describe the mechanism of action, clinical uses and toxicities.
- Describe the mechanisms of action, clinical
uses and toxicities of antibodies used as immunosuppressants.
- Describe the general principles of immunostimulants
and their indications.
- Describe the different types of allergic reactions
to drugs.
DRUG LIST: prednisone, cyclosporine, tacrolimus, sirolimus
(rapamycin), azathioprine, cyclophosphamide, antithymocyte
globulin, Rho(D)
immune globulin, muromonab-CD3, infliximab, daclizumab, etanercept, thalidomide, mycophenolate
mofetil, aldesleukin,
interferons (alpha, beta & gamma), methotrexate.
By the end of this session, you
should be able to:
- Explain the origin
and definition of eicosanoids.
- Describe the physiologic
and pathophysiologic roles of COX-1 and COX-2.
- Discuss the different
types of eicosanoid receptors.
- Explain the role of
eicosanoids in:
a. Smooth
muscle function
b. Gastric acid secretion
c. Platelet function
d. Renal function
-
Describe
the role of eicosanoids in:
a. Inflammation
b. Pain
c. Fever
- Describe the lipoxygenase
pathway of arachidonic acid metabolism.
- Discuss the biologic
role of PAF.
DRUG LIST: Selective
COX-2 inhibitors: Celecoxib
(Celebrex ®). Nonselective COX inhibitors: aspirin,
ibuprofen,
naproxen,
nabumetone,
diclofenac.
Analgesic & Antipyretic: acetaminophen.
Glucocorticoids:
beclomethasone,
dexamethasone Prostaglandins: alprostadil,
dinoprostone,
misoprostol,
latonoprost, PGI2 / prostacyclin; thromboxane. Leukotriene inhibitors: montelukast, zafirlukast,
zileuton.
Recently
removed from market: rofecoxib
(Vioxx ®)
By the end of this session, you
should be able to:
- Explain how histamine
is formed and describe the locations of its synthesis, storage and catabolism.
- Explain the difference
between H1 and H2 receptors and their physiologic/pathophysiologic function
in:
a) the cardiovascular system; b) the pulmonary system; c) non-vascular smooth
muscle; d) sensory nerve endings; e) gastric glands
- Describe the "triple
response of Lewis" and the mechanism(s) underlying each response.
- Describe the primary
therapeutic uses, pharmacokinetic properties, and side effects of H1 and
H2 antagonists and the antidegranulating drugs.
DRUG LIST:histamine.
H2 agonist: betazole.
H1 antagonists: bromopheniramine,
chlorpheniramine,
diphenydramine,
fexofenadine,
loratidine,
hydroxyzine.
Antigranulating drugs: cromolyn
sodium, nedocromil
sodium. H2 blockers: cimetidine,
famotidine,
nizatidine,
ranitidine.
By the end of this session, you
should be able to:
- Describe the mechanism
of action of selective and non-selective COX inhibitors (NSAIDs).
- Explain the special
properties of aspirin.
- Describe the dose-dependent
signs and symptoms of aspirin toxicity.
- Explain the mechanism
of action of acetaminophen and describe the symptoms of acetaminophen toxicity.
- Explain the use of
prostaglandins and prostaglandin analogs in the treatment of diseases such
as glaucoma & pulmonary hypertension.
- Explain the use of
NSAIDs and disease modifying drugs in the treatment of arthritis.
- Explain the use of
lipoxygenase inhibitors and leukotriene antagonists in the treatment of
asthma.
- Discuss the role of
omega-3 and omega-6 polyunsaturates (fish oil) in the formation of lipid
mediators.
DRUG LIST: NSAIDs & steroids
(see above), acetaminophen
(Rx for overdose: N-acetylcysteine).Disease-modifying
antirheumatics: gold
salts, azathioprine,
chloroquine,
penicillamine, methotrexate,
TNF-alpha blocking antibodies (adalimumab,
infliximab
& etanercept).
Rx of gout: colchicine,
allopurinol,
probenicid,
sulfinpyrazone.
By the end of this session, you
should be able to:
- Explain the physiologic regulation of the
hypothalamic-pituitary adrenal axis.
- List the natural and synthetic adrenocoritical
steroids, their actions, therapeutic uses, and adverse effects.
- Describe the glucocorticoid and mineralcorticoid
effects of adrenocortical steroids.
- List the adrenocortical antagonists and discuss
their mechanism of action, uses, and adverse effects.
DRUG LIST: prednisone,
hydrocortisone, dexamethasone,
fludrocortisone,
methylprednisone,
mifepristone
(RU-486),
metyrapone
.
By the end of this session, you
should be able to:
- Describe the unique features of dematopharmacology.
- Describe the principles of percutaneous absorption.
- List the indications for topical uses of corticosteroids.
- List the indications for the topical use of
retinoids.
- Explain how photochemotherapy works.
- Explain the clinical case and the pharmacology of the drugs used to treat the patient's condition (see case in handout).
- List two antipruritic agents and their clinical profile.
- List three trichogenic and antitrichogenic agents and their clinical profile.
DRUG LIST: Antiinflammatory Steroid: triamcinolone
acetonide; Acne Preparations: adapalene, azelaic acid, benzoyl peroxide, tretinoin, isotretinoin (Accutane); Drugs for Psoriasis: alefacept, calcipotriene, efalizumab, etanercept, tazarotene; Anti-pruritics: doxepin, pramozine; Treatment of Alopecia: finasteride (Propecia), minoxidil (Rogaine); Rx of Excessive Hair Growth in Women: eflornithine; Rx of T cell lymphoma: denileukin
diffitox, bexarotene
EXAM - Basic Principles & Inflammation
Block
Antibacterial Drugs
By the end of this session, you should be able to:
-
Define the terms: antibiotics,
selective toxicity, therapeutic index,
bacteriostatic and bactericidal.
-
Explain the host determinants
in relation to selection of an antimicrobial drug for therapy.
-
Define MIC and MBC values.
-
Describe the methodology for
sensitivity assays.
-
Define bacterial resistance
and list the mechanisms involved in acquiring bacterial resistance.
-
Explain the mechanisms involved
in transfer of drug resistance to bacterial cells.
-
Describe the basic principles
of combination therapy with antimicrobial drugs.
-
Describe the terms of synergism
and antagonism by giving examples.
-
Discuss the classification of
antimicrobial drugs based upon the mechanism of action.
-
Explain the modes of action
of various antimicrobial drugs.
By the end of this session, you should be able
to:
- Describe the structural relationship of the penicillin molecule with antimicrobial activity.
- Explain the mechanism of action of b-lactam antibiotics.
- Describe the pharmacokinetic properties of penicillins.
- Discuss primary therapeutic indications for penicillin G.
- Describe the repository penicillins.
- Explain the major side effects of penicillins.
- Describe the indications for broad-spectrum penicillins.
- List the penicillinase-resistant penicillins.
- List the combinations of inhibitors of b-lactamase with penicillins.
- Describe the antimicrobial activity of monobactams and carbapenems.
- Explain the pharmacological basis for combining imipenem with cilastatin.
DRUG LIST: penicillin
G, penicillin
V, methicillin,
oxacillin,
cloxacillin,
nafcillin,
ampicillin,
amoxicillin,
carbenicillin,
indanyl
carbenicillin ,
ticarcillin, piperacillin,
mezlocillin, meropenem,
imipenem,
aztreonam. Beta-lactamase inhibitors: clavulanic acid, sulbactam & tazobactam.
By the end of this session, you should be able
to:
- Describe the structural differences between
penicillins and cephalosporins.
- Explain the mechanism of action of cephalosporins.
- Describe the four generations of cephalosporins
with specific examples and the differences in their antimicrobial spectrum
and pharmacokinetic properties.
- Describe the adverse effects due to cephalosporins.
- Explain the terms superinfection
and cross-hypersensitivity.
- Discuss the mechanism of action of vancomycin.
- Describe the pharmacokinetic properties of vancomycin.
- Describe the main therapeutic indications and
toxicities of vancomycin.
DRUG LIST: cephalexin,
cefazolin,
cefoxitin,
cefaclor,
cefprozil
(Cefzil ®), cefotaxime,
ceftriaxone,
ceftazidime,
cefepime,
vancomycin
| Chloramphenicol/Tetracyclines/Fluoroquinolones |
 |
Dr. Agrawal |
By the end of this session, you should be able
to:
- Explain the mechanism of action and the mode of bacterial resistance of each class of antibiotics.
- Discuss and compare the pharmacokinetics.
- Describe the therapeutic indications for each class of antibiotics.
- List the various toxicities associated with each class of antibiotics.
- Explain the drug interaction of tetracyclines and antacid, and tetracyclines and penicillins.
- List the advantages of newer fluoroquinolones over older fluoroquinolones.
- Describe the adverse effects of ciprofloxacin, including contraindications in children and pregnant women.
DRUG LIST: chloramphenicol,
tetracyclines
(tetracycline, doxycycline,
minocycline), fluoroquinolones
(ciprofloxacin, levofloxacin).
By the end of this session, you should be able
to:
- Discuss the mechanism of action of sulfonamides
and explain the synergistic inhibition due to sequential blockade with cotrimoxazole.
- Classify sulfonamides giving an example for
each group.
- Describe the pharmacokinetic properties of sulfonamides
and discuss the principles for use of combination of sulfonamides to avoid
crystalluria.
- Describe the major therapeutic indications of
sulfonamides alone, and in combination with trimethoprim (cotrimoxazole).
- Describe the major adverse effects associated
with the use of sulfonamides.
DRUG LIST: sulfamethoxazole,
trimethoprim
(Bactrim ®, Cotrim ®, cotrimoxazole).
By the end of this session, you should be able
to:
- Explain the mechanism of action of metronidazole,
mupirocin and nitrofurantoin.
- Describe the pharmacokinetic properties of metronidazole,
mupirocin and nitrofurantoin..
- Describe the major therapeutic indications for
use of these 3 drugs against anaerobic bacterial infections and their use
as an antiparasitic agents.
- Describe the major toxicities of these drugs
(including the disulfiram-like reaction with metronidazole due to alcohol).
DRUG LIST: metronidazole,
mupirocin,
nitrofurantoin
By the end of this session, you should be able
to:
- Discuss the mechanism of action of aminoglycosides.
- Describe the pharmacokinetic properties of aminoglycosides.
Explain the importance of peak and trough levels of aminoglycosides.
- Discuss the need of and the method of dose adjustment
for aminoglycosides in patients with compromised renal function.
- Explain the mechanism of acquired drug resistance
due to aminoglycosides and compare the relative ease development of resistance
to streptomycin, gentamicin, tobramycin and amikacin.
- Describe the therapeutic indications of aminoglycosides.
- Explain the rational basis for combination therapy
with an aminoglycoside and a penicillin, cephalosporin, or vancomycin.
- Discuss the main three toxicities of aminoglycosides
and precautions taken to limit them.
DRUG LIST: streptomycin,
neomycin,
gentamicin,
tobramycin,
amikacin,
netilmicin.
By the end of this session, you should be able
to:
- Describe the mechanism of action of macrolides,
clindamycin and streptogramins.
- Explain the pharmacokinetic properties of erythromycin
and compare with clarithromycin, azithromycin and clindamycin.
- Describe the primary therapeutic indications
for each class of antibiotics.
- Describe the major drug interactions of macrolides
due to inhibition of cytochrome P450 enzymes.
- Discuss the major side effects of each class
of antibiotics.
DRUG LIST: erythromycin,
clarithromycin
(Biaxin ®), azithromycin
(Zithromax ®), clindamycin,
Streptogramins
(quinupristin/dalfopristin)
By the end of this session, you should be able
to:
- Generate hypotheses in relation to a patients
illness.
- Predict the infecting organisms and list the
antibiotics that can be used to treat the infection.
- Define cross-hypersensitivity and
cite examples of drugs that exhibit this behavior.
- List the drugs used for prophylaxis against
subacute bacterial endocorditis involving upper respiratory tract procedures
and genitourinary/gastrointestinal procedures.
- Discuss the drugs which are effective against
penicillin-resistant organisms.
- Learn to calculate the dose of gentamicin based
on the body weight of the patient.
- Explain the adjustment of doses of gentamicin
in patients with compromised renal function.
- Describe the common feature of nosocomial infections
in the ICU.
Antifungals
By the end of this session, you should be able to:
-
List the various antifungal
drugs useful in the treatment of fungal infections.
-
Discuss the mechanism of action
of these drugs.
-
Describe the pharmacokinetic
properties of the various antifungal drugs.
-
Describe the liposomal preparations
of amphotericin B.
-
Describe the major therapeutic
indications of these drugs.
-
Describe the important adverse
effects of the various antifungal drugs.
-
Discuss the drug interactions
of griseofulvin and warfarin; ketoconazole and warfarin.
EXAM - Antibacterial & Antifungal Drugs
Antiparasitics
By the end of this session, you should be able to:
-
List the drugs of choice and
alternate drugs available for treatment of diseases due to various helminths.
-
List the opportunistic infections
commonly occurring in patients with AIDS and the drugs used for their treatment.
-
Describe the mechanism of action
of ivermectin, mebendazole, praziquantel, pentamidine, trimetrexate and
atovaquone.
-
List the broad spectrum anthelmintic
drugs and their spectrum of activity.
-
Learn the drug of choice for
treatment of asymptomatic, mild to moderate intestinal disease, severe intestinal
disease and hepatic abscess due to E. histolytica.
DRUG LIST: atovaquone, mebendazole, thiabendazole, albendazole, pyrantel
pamoate, ivermectin, diethylcarbamazine, nifurtimox, suramin, pentamidine, praziquantel, trimetrexate
Antivirals
By the end of this session, you should be able to:
- Classify antiviral
drugs based upon their site of inhibition in the viral replication cycle.
- Explain their mechanisms
of action.
- Describe their major
therapeutic indications.
- Compare their pharmacokinetic
properties.
- List their adverse
side effect and potential drug interactions.
- Explain the factors
that regulate antiviral drug resistance.
DRUG LIST: amantadine, rimantadine, zanamivir, oseltamivir, idoxuridine, trifluridine, vidarabine, acyclovir, valacyclovir, ganciclovir, valganciclovir, foscarnet, ribavirin, interferon
alpha
By the end of this session, you should be able to:
-
Describe how treatment
of HIV has dramatically changed the prognosis of this previously fatal disease.
-
List the drugs
(antiretrovirals) used for treatment of HIV-1 infection by:
a. Classification
b. Toxicities
-
Explain the rationale
for combination of nucleoside analogue reverse transcriptase inhibitors
(NRTIs), nonnucleoside transcriptase inhibitors (NNRTIs), and protease inhibitors
(PIs).
-
Explain the
following concepts needed for the understanding of the clinical decision
making process when treating HIV-infected patients:
a. Viral replication and suppression
b. Viral drug-resistance
c. Adherence to treatment
d. Immune reconstitution
e. Complications of treatment
-
Describe the current
guidelines for the treatment of HIV-infected patients.
-
Explain why the
guidelines change
DRUG LIST:HAART,
zidovudine
(azt), didanosine
(ddi), lamivudine
(3tc), stavudine
(d4t), abacavir,
nevirapine,
delavirdine,
efavirenz,
indinavir, nelfinavir,
ritonavir
/ lopinavir,
amprenavir,
enfuvirtide
EXAM - Antivirals & Antiparasitics
Cancer Chemotherapy / Neoplasia
By the end of this session, you
should be able to:
- Explain the role of chemotherapy in the management
of patients with cancer.
- Describe the prospects for "cure",
or long term survival in cases of advanced cancer.
- Describe the various limitations to effective
drug treatment.
- Define and explain the terms: selective
toxicity, mass doubling time and growth fraction.
- Explain the concept of "total cell kill"
in cancer patients.
- Define the optimal dosage schedules in cancer
patients.
- Explain the term cell cycle specificity and be able to classify the various anticancer agents based on this parameter.
- Describe the principles of combination chemotherapy
in the treatment of cancer.
- Explain the mechanisms for resistance to anticancer
drugs.
By the end of this session, you
should be able to:
- Describe the mechanism of action and therapeutic
indications of various anticancer drugs (see below).
- Describe the common toxic effects for each
major class of anticancer drugs (alkylating agents, antimetabolites, natural
products and miscellaneous agents) (see drug list below).
- Learn the relative differences in toxicity
of drugs within each major class.
- Explain the bioactivation pathways required
for the action of cyclophosphamide.
- Describe the intracellular activation of different
antimetabolites.
- Explain the use of antidotes in high dose
methotrexate therapy.
- List the specific toxic effects of commonly
used anticancer drugs.
- Describe the cumulative dose dependent toxicity
of anthracyclines.
- Describe the preferred drug combinations that
have major activity against specific types of cancer.
- Explain the concept of adjuvant chemotherapy,
and learn the regimens used in breast adenocarcinoma and osteogenic sarcoma.
DRUG LIST:
| Alkylating agents: |
busulfan, cyclophosphamide, dacarbazine, mechlorethamine, melphalan, nitrosoureas |
| Antimetabolites: |
cytosine
arabinoside or Cytarabine, 5-fluorouracil, 6-mercaptopurine, methotrexate, thioguanine |
| Natural products: |
dactinomycin
(actinomycin D), bleomycin, daunorubicin,
camptothecins (irinotecan, topotecan), doxorubicin, etoposide, paclitaxel, vinblastine, vincristine |
| Miscellaneous agents: |
cisplatin, imatinib, procarbazine |
By the end of this session, you
should be able to:
- Describe the chemical structural requirements
for carcinogenicity of polycyclic aromatic hydrocarbons (PA).
- Explain the mechanism of activation of PAHs
for their carcinogenic effects.
- Describe the mechanism of activation of aromatic
amines, azo dyes and nitrosoamines for their carcinogenic potential.
- Explain the mechanism of chemical carcinogenesis
involving three stages and learn the various agents that can modify their
processes.
- Learn the increased risk of developing lung
cancer with smoking.
- Describe the important chemical carcinogenic
constituents in the side stream smoke.
By the end of this session, you
should be able to:
- Explain the concept of neoadjuvant and adjuvant
chemotherapy.
- Explain the rationale of high dose therapy
at short intervals.
- Learn the basic principle of the combination
chemotherapy.
- Describe the role of G-CSF in chemotherapy.
- Explain the role of allopurinol in chemotherapy.
- Describe the rationale for using docetoxal
and/or trastuzumab (herceptin ®) in breast cancer.
- Describe the role of rituximab (rituxan ®)
in the treatment of large cell lymphoma.
DRUG LIST: allopurinol, G-CSF(filgrastim ®), trastuzumab (Herceptin ®), rituximab, tamoxifen
Heme Block
By the
end of this session, you should be able to:
- Describe the causes
of different anemias.
- Explain the type
of anemia expected as a result of deficiencies of iron, erythropoietin,
Vitamin B12 and folic acid.
- Discuss the nature,
production, and effects of erythropoietin.
- Describe the primary
sites of action of erythropoietin.
- Explain the approved
indications for treatment of anemia by erythropoietin, iron, folic acid
and Vitamin B12.
- Describe the absorption
of iron by the intestines.
- Explain the treatment
for iron toxicity or overdose.
- Explain the mechanistic
reason why folic acid alone is contraindicated in the treatment of pernicious
anemia.
- Discuss the mechanismss
by which drugs interfere with the effects of folic acid
- Define atrovorum
factor.
DRUG
LIST: erythropoietin, ferrous sulfate, deferoxamine, folic acid, Vitamin
B12, iron
dextran
By the
end of this session, you should be able to:
- Define the terms: anticoagulant, thrombolytic, antiplatelet agent.
- Describe the general
stages of the clotting process.
- Describe the role
of the major clotting factors in the coagulation scheme.
- Describe the different
tests that are used to assess the effects of anticoagulant therapy.
- Describe the indications
and contraindications for anticoagulant therapy.
- Describe the mechanism
of action of heparin and coumadin.
- Explain the procedures
for treatment of overdosing with heparin and coumadin.
- Describe the mechanisms
by which other drugs can modify the effect of anticoagulants.
- Describe the mechanism
by which aspirin and dipyridamole act as antiplatelet agents.
- Describe the indications
for use of thrombolytic agents, and their side effects.
DRUG
LIST: warfarin, heparin, enoxaparin
(LMW heparin), vitamin
K, protamine
sulfate, aspirin, streptokinase, clopidogrel
By the
end of this session, you should be able to:
- List common drugs used
to inhibit the primary hemostatic system.
- Explain the role of
glycoprotein IIb/IIa and the effects of drugs that interact with this receptor
complex.
- List common drugs used
to inhibit secondary hemostatis.
- Explain the the pharmacologic
treatment of deep venous thrombosis.
- List the indications
for thrombolytic therapy.
- Explain the anticoagulant
managment of coronary artery disease.
- List common factor
replacement products.
- Describe how to medically
manage von Willebrand's disease.
- Describe how to use
laboratory tests to determine the level of anticoagulant therapy.
- Explain the difference
in onset of time required for anticoagulant action of heparin and coumadin.
EXAM - Cancer Chemotherapy (Neoplasia) & Heme Blocks
Autonomic
Pharmacology
By the end of this session, you
should be able to:
- Compare and contrast the anatomy of the sympathetic
and parasympathetic divisions of the autonomic nervous system (ANS).
- Review the concept of neurotransmitters,
cotransmitters, and end-organ receptor specificity.
- Define words containing the suffixes, -ergic,
-mimetic, -lytic and –ceptive
- Describe homeostasis, fight-or-flight, and
rest-and-repair with regard to ANS activity.
- Describe how the central nervous system controls
the activity of the ANS.
- List and compare/contrast the physiological
responses of end organs produced by activation of the sympathetic and parasympathetic
nervous systems.
- Explain what tone is, and apply knowledge
of predominant tone to the regulation of dually-innervated organs.
- Deduce the diverse physiological effects of
muscarinic receptor activation in the ANS
DRUG LIST: acetylcholine,
norepinephrine,
epinephrine
(adrenaline), dopamine
By the end of this session, you
should be able to:
- List the steps in the synthesis, release
and inactivation of acetylcholine.
- List the locations and the differences between
muscarinic and nicotinic receptors.
- Deduce the physiological effects of muscarinic
or nicotinic receptor activation: therapeutic and adverse effects.
- Compare the two major cholinesterases: acetylcholinesterase
and butyryl-cholinesterase as to anatomical locations, sites of synthesis,
and function.
- Explain anticholinesterases are reversible
or irreversible, and indicate which anticholinesterases are in each category.
- Describe the physiological effects of accumulated
acetylcholine at muscarinic and nicotinic receptors in the periphery and
the central nervous system.
- List the therapeutic uses for and adverse
side effects of anticholinesterases.
- Describe the use and mechanism of action of
pralidoxime, and explain why pralidoxime is not effective at reactivating
all AChE.
- Explain why anticholinesterase agents can
be used as insecticides and chemical warfare agents, and discuss antidotes
in case of poisoning.
DRUG LIST: acetylcholine,
pilocarpine,
bethanechol, nicotine,
succinylcholine,
physostigmine,
neostigmine,
edrophonium,
echothiophate,
pralidoxime
(2-PAM),,
pyridostigmine,
sarin,
soman,
VX
By the end of this session, you
should be able to:
- Explain the rationale for the therapeutic
use of antimuscarinics for bronchoconstriction, excessive salivation, motion
sickness, and mydriasis and cycloplegia.
- Explain the side effects of antimuscarinics,
including xerostomia, blurred vision, photophobia, tachycardia, difficulty
in micturition, hyperthermia, glaucoma, and mental confusion in the elderly.
- Explain why antimuscarinics are contraindicated
in glaucoma, obstructive disease of the gastrointestinal or urinary tract,
and intestinal atony.
- Compare the selectivity of antinicotinics
for ganglionic and neuromuscular receptors.
- Describe the pharmacological effects of antagonists
at ganglionic nicotinic receptor sites, and understand the role of predominant
tone. Explain the rationale for original uses in the treatment of hypertension,
and list adverse side effects (not covered in lecture).
- Contrast and compare the uses and limitations
of depolarizing and competitive antagonists at the neuromuscular junction
(not covered in lecture)
DRUG LIST: atropine,
scopolamine,
ipratropium,
d-tubocurarine,
trimethaphan
By the end of this session, you
should be able to:
- Explain the mechanism of action
of anticholinesterases.
- Describe the pharmacological
effects of anticholinesterases.
- Discuss the strategy for treatment
of anticholinesterase intoxication from Soman and Sarin.
- Describe the complementary
role of atropine and pralidoxime as antidotes against irreversible anticholinesterases.
- Explain the importance of
pyridostigmine pre-treatment in the threat of an exposure to Soman.
DRUG LIST: atropine,
2-PAM
(pralidoxime), pyridostigmine
(as
pretreatment before Soman),
By the end of this session, you
should be able to:
- Describe the anatomy of the sympathetic nervous
system.
- Explain the actions of the transmitters of
the autonomic nervous system.
- Describe the role and responses mediated by
adrenergic receptors.
- Describe how adrenergic hormones and receptors
regulate cardiovascular function.
DRUG LIST: tyramine,
ephedrine,
dextroamphetamine,
cocaine,
imipramine,
bretylium, reserpine,
guanethidine,
pargyline,
methyldopa,
octopamine
By the end of this session, you
should be able to:
- Describe the biosynthetic steps and regulation
of the biosynthesis of catecholamines.
- Describe the function of the adrenergic nerve
terminal.
- Describe how neuronally released norepinephrine
regulates vascular and cardiac function.
- Describe the actions of drugs which alter
adrenergic neuronal function.
- Describe the inactivation pathways for catecholamines.
DRUG LIST: norepinephrine,
epinephrine,
dopamine,
acetylcholine,
isoproterenol
By the end of this session, you
should be able to:
- Describe the actions of sympathomimetics with
respect to receptor subtype selectivity.
- Explain the actions of dobutamine, and
- in the treatment of cardiogenic shock and
essential hypertension.
DRUG LIST: dobutamine,
albuterol,
terbutaline,
phenylephrine,
clonidine
By the end of this session, you
should be able to:
- Describe the actions of adrenergic blocking
drugs with regard to receptor subtype and selectivity.
- Explain the use of alpha receptor blocking
drugs in the treatment of hypertension.
- Explain the use of beta receptor blocking
drugs in the treatment of hypertension and angina.
DRUG LIST: Alpha
blockers: phenoxybenzamine,
phentolamine,
prazosin,
doxazosin,
yohimbine.
Beta blockers: propranolol,
metoprolol,
butoxamine**,
pindolol,
labetalol,
bisoprolol,
Other alpha blockers in top 200: terazosin,
tamsulosin.
Other top 200 beta blockers: atenolol,
timolol,
carvedilol
(alpha & beta blocker).
** Not available
for clinical use
By the end of this session, you
should be able to:
- Explain the effects of low dose and high dose
epinephrine on arterial blood pressure, and the mechanisms for these effects.
- Explain how the major difference in the effects
of norepinephrine and epinephrine on blood pressure.
- Explain the mechanism for the effect of acetylcholine
on arterial blood pressure.
- Explain the effect of isoproterenol, and mechanism
of isoproterenol's effect, on arterial blood pressure.
- Describe the effect of atropine on blood pressure,
and responses to vagal stimulation and i.v. injections of acetylcholine.
- Describe the mechanism of tyramine's effect
on arterial blood pressure.
- Compare and contrast the effect of cocaine
pretreatment on blood pressure responses to epinephrine, isoproterenol,
and tyramine.
- Explain the mechanism of action of phentolamine,
and how it alters the blood pressure response to i.v. injections of epinephrine
vs. norepinephrine.
- Explain the effect of angiotensin on alterial
blood pressure, and describe its mechanism of action.
DRUG LIST: epinephrine,
norepinephrine,
cocaine,
tyramine,
isoproterenol, phentolamine,
angiotensin.
By the end of this session, you
should be able to:
- Compare, contrast & explain the cardiovascular effects of epinephrine, norepinephrine, isoproterenol and tyramine.
- Be able to correctly identify an unknown autonomic
drug based upon its direct effects on arterial blood pressure, and how it
alters responses to vagal stimulation, carotid artery occlusion, acetylcholine,
epinephrine, norepinephrine and tyramine.
Cardiovascular Pharmacology
By the end of this session, you
should be able to:
- Explain the mechanism of action of binding
resins (chlestyramine, colestipol) in the treatment of hypercholesterolemia.
- Explain the mechanism of action of nicotinic
acid and fibric acid derivatives (gemfibrozil) in the treatment of hypercholesterolemia
and hypertriglyceridemia.
- Explain the mechanism of action of HMG-CoA
reductase inhibitors in the treatment of hypercholesterolemia.
- Describe the common side-effects related to
hypolipidemic drugs.
DRUG LIST: cholestyramine,
colestipol,
nicotinic
acid (niacin), gemfibrozil,
lovastatin,
atorvastatin, pravastatin
By the end of this session, you
should be able to:
- Explain how congestive heart failure results
in the activation of 3 different compensatory mechanisms.
- Explain how digoxin produces a positive inotropic
effect by inhibiting the Na/K pump.
- Describe the effect of CHF on the slope and
position of the Frank-Starling relationship, and how digoxin alters this
relationship.
- Discuss digoxin's use for controlling the
ventricular rate in patients with atrial tachyarrhythmias.
- Describe the cellular mechanisms by which
digoxin can produce serious cardiac arrhythmias (3rd degree AV
block, bigeminy, ventricular tachycardia).
- Explain how digoxin toxicity can be enhanced
by hypokalemia, hypercalcemia and drug interactions with antiarrhythmics
and diuretics.
- List some of the more common "non cardiac"
signs and symptoms of digoxin toxcitity (that serve as a "warning sign").
- Describe the steps that should be taken to
diagnose and treat digoxin toxicity.
DRUG LIST: digoxin,
digoxin
immune Fab (Digibind ®), digitoxin**
(** not available
in the US)
By the end of this session, you
should be able to:
- Explain how blood flow in coronary circulation
is regulated.
- Describe the pathophysiology of the various
forms of angina.
- Explain the actions and indications of various
antianginal drugs.
- Explain the actions of nitric oxide.
DRUG LIST: nitroglycerin,
isosorbide dinitrate, nifedipine,
verapamil,
diltiazem; Related drugs:
dipyridamole, papaverine,
sodium
nitrate, amyl
nitrite. Drug Interaction: sildenafil
(Viagra ®).
By the end of this session, you
should be able to:
- Define the concepts of preload, myocardial
contractility and afterload as determinants of left ventricular performance.
- Explain the difference between systolic
dysfunction and diastolic dysfunction in congestive heart
failure.
- Explain the beneficial actions of diuretics,
inotropic agents, vasodilators, ACE inhibitors and beta-adrenergic blockers
in congestive heart failure.
- Explain the rationale for using calcium channel
blockers and beta-adrenergic blockers in the treatment of diastolic
heart failure .
DRUG LIST:
hydrochlorothiazide,
furosemide,
torsemide,
dopamine,
dobutamine,
digoxin,
nitroglycerin,
isosorbide dinitrate, hydralazine,
captopril,
enalapril,
carvedilol,
propranolol,
metoprolol,
diltiazem, verapamil,
spironolactone
By the end of this session, you
should be able to:
- List the two cellular electrical abnormalities
that produce cardiac arrhythmias.
- Explain how myocardial ischemia produces conduction
disturbances.
- List the three requirements for reentrant
excitation.
- Describe the effects of vagal and sympathetic
stimulation on the PR interval and AV node ERP.
- Explain which major ionic currents regulate
automaticity in the SA node and Purkinje fiber system.
- Explain how vagal and sympathetic neurotransmitters
modulate automaticity.
- List two types of abnormal automaticity, and
describe the cellular derangements that produce them.
By the end of this session, you
should be able to:
- List the three primary indications for treatment
of cardiac arrhythmias.
- List the primary channel or receptor mechanisms
by which Class I, II , III and IV antiarrhythmic drugs produce their effects.
- Recognize and categorize different antiarrhythmic
drugs by their mechanism of action.
- Explain how Class I drugs increase the ERP.
- Explain how Class I drugs abolish reentrant
arrhythmias.
- List the primary drugs used for acute and
chronic treatment of AV node reentry.
- Explain which drugs are useful for reducing
ventricular rate in patients with atrial tachyarrhythmias.
- Explain how Class Ia drugs can produce a dangerous
increase in ventricular rate when used alone to treat atrial tachyarrhythmias.
- Describe which drugs reduce the incidence
of sudden death and reinfaraction after an MI.
- Cite major side effects of major antiarrhythmic
drugs (listed below) that limit their clinical usefulness.
DRUG LIST: lidocaine,
quinidine,
procainamide,
propranolol,
atenolol,
metoprolol, sotalol,
verapamil,
diltiazem, amiodarone,
adenosine
By the end of this session, you
should be able to:
- List the primary risk factors for ischemic
heart disease.
- Explain the rational for the use of aspirin
and beta-blockers in the treatment of patients with a previous MI.
- Identify several basic rhythm disturbances
based upon a patient's ECG.
- Discuss the possible etiologies of different
rhythm disturbances in patients with a history of heart disease and multiple
drug therapies.
- Describe the majar therapeutic goals in treating
patients with chronic atrial fibrillation.
- Explain which drugs may be useful in the treatment
of chronic atrial fibrillation.
- Identify drugs of choice for treatment of
hemodynamically significant ventricular arrhythmias in the ICU.
- Discuss the common clinical symptoms associated
with an acute MI.
DRUG LIST: lidocaine,
procainamide,
amiodarone,
aspirin,
atenolol,
digoxin,
hydrochlorothiazide
Pulmonary Pharmacology
By the end of this session, you
should be able to:
- List the three major subtypes of drugs used in the treatment of asthma.
- Discuss the types of drugs used for the treatment of acute asthmatic bronchoconstriction.
- Discuss the types of drugs used for the treatment of chronic asthma.
- Describe the target sites for pharmacologic intervention in asthmatic patients.
- Explain the beneficial aspects of aerosol drug formulations vs. oral drug formulations.
- Describe the role of cyclic AMP, cyclic GMP, and leukotrienes in the regulation of bronchiolar smooth muscle and pulmonary vasculature.
- Describe the side effects and toxicity of theophylline.
DRUG LIST:
Bronchodilators
epinephrine
short acting b2-agonists: albuterol, terbutaline
long acting b2-agonists: formoterol, salmeterol
muscarinic blockers: ipatroprium
bromide,
xanthine derivatives: theophylline
Antiinflammatory Drugs
degranulation inhibitors:
cromolyn sodium, nedocromil
corticosteroids: beclamethasone,
budesonide, fluticasone, prednisolone
antiboides: omalizumab
Leukotriene Antagonists
receptor blocker: montelukast
5-lipoxygenase inhibitor: zileuton
By the end of this session, you should be able to:
-
List the first line antitubercular
drugs and explain their mechanism of action.
-
Define the various phases of
actively and slow growing Myobacterium tuberculosis and compare
the relative effectiveness of various drugs.
-
Describe the regimen recommended
for preventative therapy and for conventional chemotherapy.
-
Describe the pharmacokinetic
profile of isoniazid and rifampin.
-
Describe the adverse effects
of isoniazid, rifampin, ethambutol and pyrizinamide.
-
Explain the drug interactions
of rifampin with anticoagulants and other drugs such as oral contraceptives.
-
Discuss the use of rifabutin,
clarithromycin and azithromycin for treatment of Mycobacterium avium
complex.
-
List the drugs used in the treatment
of Hansens disease and describe their mechanism of action.
-
Describe the drugs use for reversing
the lepra reactions and the erythema nolosum leprosum reaction.
-
Explain the WHO regimen for
treatment of leprosy.
EXAM - ANS, Cardiovascular & Pulmonary Blocks
Renal Pharmacology
By the end of this session, you
should be able to:
- Explain how GFR is regulated.
- Describe how vasoactive agents influence GFR.
- Describe the steps involved in the formation
of prostaglandins, nitric oxide and angiotensin II.
- Describe how the kidney regulates the release
of renin.
- Discuss renal transport processes.
DRUG LIST: Prostaglandins ( PGE2 & PGI2, thromboxane
A2 ), angiotensin
II, bradykinin, saralasin;
ACE inhibitors: captopril, ramapril, fosinopril, benazepril, quinapril; ARBs: losartan, valsartan, irbesartan.
By the end of this session, you
should be able to:
- Describe the processes involved in the formation
of urine by the kidney.
- Describe the actions of the major classes
of diuretics on the formation of urine and the excretion of sodium, potassium
and other cations.
- Explain the therapeutic indications, efficacy
and side effectsof the major classes of diuretics.
- Discuss the use of diuretics in the treatment
of essential hypertension and congestive heart failure as well as in other
edema states.
DRUG LIST: acetazolamide, indapamide, chlorothiazide, hydrochlorothiazide, furosemide, ethacrynic
acid, torsemide, triamterene, amiloride, spironolactone.
By the end of this session, you
should be able to:
- Describe the impact and mechanisms involved
in essential hypertension.
- Explain actions of major classes of antihypertensive
drugs.
- List the stepwise and monotherapy regiments
for treatment of hypertension.
- Describe the use of drugs in the treatment
of a hypertensive emergency or crisis.
DRUG LIST: hydralazine, diazoxide, sodium
nitroprusside, minoxidil, enalapril, lisinopril
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