Pharmacology

KURSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF PHARMACOLOGY
TEACHING INSTRUCTIONS
IN PHARMACOLOGY
Kursk - 2003
УДК:615 (072) =111
ББК: :52.81:81.2Англ я 7
It was printed according to the decision of editorial council of KSMU.
Teaching instructions in Pharmacology (teaching textbook, edited by

assistant of professor Tatarenkova I.A., professor Pokrovsky M.V.). – Kursk:
KSMU, 2003. – 96 p.
Reviewers:
professor, the head of the department of Clinical Pharmacology of
Kursk State Medical University N.G. Philippenko;
professor, the head of the department of Pharmacology of Pyatigorsk
State Pharmaceutical Academy M.N.Ivashev;
associate professor, head of the department of Foreigh Languages of
Pyatigorsk State Pharmaceutical Academy Yu.V.Usmansky.
Teaching textbook contains the most important items, questions for self-
control, problem tasks. Selected questions and tasks correspond to the present
educational plans. Such textbook allows the students to check and fix their
knowledge in pharmacology.
ISNB: 5-7487-0694-6 ББК: 52.81:81.2Англ я 7
© Коллектив авторов, КГМУ, 2003

1. INTRODUCTION:
Pharmacology is one of the fundamental sciences in the system of doctors

training which is connected with medical, biological and clinical disciplines. The
program has been worked out on the basis of the Standard Program for the higher
medical educational establishments, which was approved by the Educational Board
of the Public Health Ministry. It involves the history of the subject, basic trends of
drug interactions with biological systems. It gives the systematization of basic
drugs, principles of administering drugs and their dosages depending on the age,
food constituents. The program outlines some preventive measures for
pharmacotherapeutic complications.
2. AIMS AND TASKS OF PHARMACOLOGY:
The common tasks of Pharmacology teaching are the following:
- development of general understanding of basic up-to-date drug groups
action on the organism (their pharmacodynamics, pharmacokinetics, side effects,
toxicology, and comparative characteristics of individual drugs, indications and
contraindications for the use of drugs);
- revealing the general tendency of drug action on the physiologic systems of
different organization levels;
- revealing the main directions, trends and scientific ideas of pharmacology
development.
Teaching of pharmacology is carried out according to the requirements of
the clinic and is based on the knowledge of such subjects as organic chemistry,
inorganic chemistry, physiology, anatomy, Latin language,biochemistry,which the
students studied at the 1st and 2nd courses.
PURPOSES OF PHARMACOLOGY STUDYING:
In the result of Pharmacology studying a student must know the following:
- general knowledge of absorption, distribution, biotransformation and
excretion of drugs;
- modern assortment, classification and characteristics of the drugs
belonging to different pharmacological groups (their mechanism of action,
indications, contraindications, side effects);
- differences between important drugs of the same group (chemical
structure, pharmacokinetics and pharmacodynamics, basic side effects, routes of
drug administration, indications and contraindications);
- treatment principles and therapy remedies for the main emergent
conditions and drug poisoning;
- peculiarities of drug interaction within the group being studied, drug
interaction with other groups and with foods.
A STUDENT SHOULD BE ABLE:
- to be well-informed about the increasing number of drugs;
- to differ new drugs from existed ones;
- to compare the drugs and the prototypes within the group;
- to solve the problem of pharmacokinetic and pharmacodynamic
interactions in cases of simultaneous drug administration.
SUGGESTIONS FOR EFFECTIVE STUDY.
The study of pharmacology is not different from that of the other basic
medical sciences. For most students pharmacology may seem more relevant than
other subjects to the practice of clinical medicine. It has the advantage of coming
last in the curriculum of basic sciences. Nevertheless, the disadvantage of
pharmacology is the need to commit to memory an enormous number of names
and facts about numerous drugs and furthermore to relate these to each other and to
clinical medicine. Most students find it advantageous to learn a classification of
drugs that enables them to immediately place a drug into a category that
characterizes the likely pharmacology. In addition the main or original drug in each
category (the prototype drug) should be thoroughly studied. The close relatives
need merely to be known by name and with reference to their advantages over the
prototype drug.
Though it may be obvious, it is still worth repeating that a minimum
knowledge of prototype drugs consists of the following:
1. Chemistry. You should be able to recognize the structural formula. Are
there any structure-activity relationships (SARs)? What is the main ring structure?
steroid? quinolone? benzodiazepine? sympathetic amine? etc.
2. Mechanism of action. This usually consists of two parts: (1) molecular
and (2) cellular or physiologic. Mechanisms of action mainly explain
pharmacodynamics or effects on organ systems that are of most use in a clinical
knowledge of the drug. For example, does the drug lower blood pressure and, if so,
does it do so by vasodilation, negative inotropic effects on the heart, central
nervous system mechanisms, etc.?
3. Pharmacokinetics. This covers absorption, distribution, and elimination
of the drug. What is the usual route of administration of the drug? What is its half-
life, degree of protein binding, etc.? The dose of the drug is usually not asked in
modern examinations. However, the means by which dosage can increase or
decrease blood levels of drugs must be known. This is the essence of
pharmacokinetics. Concepts and formulas for determing half-life, volume of
distribution, and clearance must be understood and memorized.
4. Clinical use. You should know FDA indications plus medically accepted
uses.
5. Toxicity. This includes adverse reactions and serious toxicities, such as
nephritis, hepatitis, blood dyscrasia, etc. You should know important drug
interactions.
With respect to names of drugs, the generic name must be known even
though the trade name is often more commonly used. It is advantageous to
memorize certain endings because they give a clue as to the category in which a
drug belongs; there are many exceptions, but these endings do help memory. The
following are examples of endings of generic names:
Ending Drug class Examples
- ane Volatile general anesthetics Halothane, enflurane
- azepam Antianxiety drugs Diazepam, lorazepam
- azine Phenothiazine-like antipsychotic drugs Chlorpromazine, thioridazine
- bital Barbiturate sedative-hypnotic drugs Phenobarbital, secobarbital
- caine Local anesthetics Cocaine, procaine
- cillin Penicillins Nafcillin, piperacillin
- cycline Tetracycline-type antibiotics Doxycycline, methacycline
- mycin Aminoglycoside antibiotics Streptomycin, kanamycin
- olol Beta-adrenergic blockers Propranolol, metoprolol
- (o)pril Angiotensin-converting enzyme inhibitors Captopril, enalapril
- statin HMG-CoA reductase inhibitors Lovastatin, pravastatin
- zosin Postsynaptic alpha-receptor blockers Terazosin, prazosin
Recommended Literature
1. Jacob L.S. Pharmacology, 4/e. The Science of Review, TM, Williams &
Wilkins, 1996.
2. Tripathi K.D. Essentials of Medical Pharmacology, 4/e. New Delhi,
Jaypee Brothers, 1999.
3. Harvey R.A., Champe P.C. Lippincot’s Illustrated Reviews:
Pharmacology, 2/e. J.B.Lippincott Company, East Washington Square,
Philadelphia, Pennsylvania, 2001.
4. Katzung B.G. Basic and Clinical Pharmacology, 7/e. East Norwalk, CT,
Appleton & Lange, 1998.
5. Hardman J.G. et al: Goodman and Gilman’s the pharmacological basis of
therapeutics, 9/e, New York, 1996, McGraw-Hill.
6. Rosenfeld G.C., Loose-Mitchell D.S. Pharmacology. BRS, Williams and
Wilkins, 1998.
7. Chaudhuri S.K. Quintessence of Medical Pharmacology, 1/e, India, New
Central Book Agency LTD, 1997.
8. Rang H.P. et all (eds): Pharmacology, 4-e. Edinburgh, Churchill
Livingstone, 1999.
Lesson N 1
Topic: “ ENGLISH PRESCRIPTION. HARD, LIQUID
AND SOFT DRUG FORMS”.
Introduction: A prescription is a written order given by a physician to a

pharmacist. In addition to the name of the patient and that of the physician, the
prescription should contain the name or names of the drugs ordered and their
quantities, instructions to the pharmacist, and directions to the patient.
INITIAL LEVEL OF KNOWLEDGE:
For the material mastering it is necessary to revise the following:
- structure of the Latin prescription (from Latin language course).
Parts of prescription.
1. Superscription – This is simply Rx, the abbreviation for recipe, the
imperative of recipere, meaning “take thou”.
2. Inscription – This represents the ingredients and their amounts. If a
prescription contains several ingredients in a mixture, it is customary to write them
in the following order: (1) basis or principal ingredient, (2) adjuvant, which may
contribute to the action of the basis, and (3) corrective, which may eliminate some
undesirable property of the active drug or the vehicle, which is the substance used
for dilution.
3. Subscription – This contains directions for dispensing. Often it consists
only of M., the abbreviation for misce, meaning “mix”.
4. Signature – This is often abbreviated as Sig. And contains the directions
to the patient, such as “Take one teaspoonful three times a day before meals.” The
signature should indicate whether the medicine is intended for external application
and whether it has some special poisonous properties. Wherever possible,
instructions of a general nature, such as “take as directed”, should be avoided since
the patient may misunderstand verbal directions given by the physician.
In addition to the basic parts of a prescription, it should have the patients
name and the physician’s signature, followed by the abbreviation M.D.
General definitions:
Pharmacology: Pharmacology is the study of the interaction of chemicals
with living systems.
Medical Pharmacology: Medical pharmacology is the study of drugs used
for the diagnosis, prevention, and treatment of disease.
Drug is any substance or product that is used or intended to be used to
modify or explore physiological systems or pathological states for the benefit of
the recipient. Drugs are substances that act on living systems at the chemical
(molecular) level.
Medicine is any drug which has a definite form, dose level and is
therapeutically used for the treatment of disease in living subject.
Generic name (official) is the legal, noncommercial name for a drug.
Brand (trade) name is the commercial name for a drug, normally the
property of the drug manufacturer.
Chemical name is the chemical formula for a drug.
Pharmacodynamics: Pharmacodynamics refers to the action of a drug on
the body, including receptor interactions, dose-response phenomena, and
mechanisms of therapeutic and toxic action.
Pharmacokinetics: Pharmacokinetics refers to the action of the body on the
drug, including absorption, distribution, metabolism, and excretion. A drug may be
eliminated by metabolism or by excretion. Biodisposition is a term sometimes
used to describe the processes of metabolism and excretion.
Toxicology: Toxicology is the study of the untoward effects of chemical
agents on living systems. It is usually considered an area of pharmacology.
Chemotherapy: Chemotherapy is that subdivision of pharmacology which,
according to the definition first proposed by Paul Ehrlich, deals with drugs that are
capable of destroying invading organisms without destroying the host.
Pharmacotherapeutics is the application of drugs in the treatment of
disease.
Pharmacy is concerned with the preparation and dispending of drugs.
Pharmacopeia – authoritative list of drugs, formulas, preparations, and
information which sets a standard for drug manufacturing and dispensing.
Idiosyncrasy refers to an unusual drug response in an individual than in
most individuals.
Tolerance refers to decreased responsiveness to a drug as a consequence of
continued administration of a given dose of drug.
Tachyphylaxis refers to a rapid decrease in responsiveness after
administration of a drug.
Hyporeactivity refers to decreased intensity of drug’s effect for a given
dose, in comparison to effect seen in most individuals.
Hypersensitivity refers to allergic or other immunologic responses to drugs.
Drug addiction is a state of periodic or chronic intoxication produced by the
repeated consumption of certain drugs.
Drug dependence. Due to repeated administration, certain drugs may make
the individual both psychologically and physically dependent on them.
Antidote an agent that is given to counteract an unwanted effect of a drug.
Contraindications – factors in the patient’s condition which prevent the use
of a particular drug or treatment (which forbid the use of a particular drug).
Side effect is a toxic (harmful) effect which routinely results from the use of
a drug.
Aerosol – drug suspended in air particles.
Suppositories – cone-shaped objects containing medication which are
inserted into the rectum, vagina, or urethra, from which the medication is absorbed
into the bloodstream.
Mixtures – drugs dissolved or suspended in water.
Emulsions – mixture of two immiscible liquids (e.g. oil and water) by
means of an emulsifying agent (e.g. gum acacia).
Syrups – concentrated solution of sugar containing flavoring, coloring and
therapeutically active substances.
Elixirs – sweetened, flavored hydroalcoholic solution containing drug or
without any drug (for use as a vehicle).
Tinctures – alcoholic or hydroalcoholic solution of vegetable drugs.
Capsules – shells of gelatin containing drug.
Ampoules – containing single dose of injection solution.
Vials – rubber-capped bottles containing a number of doses.
WORK AT THE LABORATORY STUDY:
Task N 1. Prescribe 20 tablets of nitroglycerine. Each tablet contains 0.0005
g for sublingual administration. Use one tablet in acute attacks of angina pectoris.
Task N 2. Prescribe 20 capsules containing 250 mg of Tetracycline. Use one
capsule two times a day.
Task N 3. Prescribe 5 ampules of 0.05% Strophanthin solution for injections.
Each ampule contains 1 ml of solution.
Task N 4. Prescribe 30.0 g of 2 % Ketoconazole cream. Apply 1-2 times
daily, continuing for a few days after lesions have healed.
Task N 5. Prescribe 20.0 ml of Orciprenaline aerosol. Use 1-2 puffs if
necessary after not less than 30 minutes to max.
Lesson N 2
Topic: “PHARMACOKINETICS”.
Introduction: Medical pharmacology is the science of chemicals (drugs) that
interact with the human body. These interactions are divided into two classes:
- pharmacodynamics, the effects of the drug on the body, and
- pharmacokinetics, the way the body affects the drug with time (i.e.
absorption, distribution, metabolism and excretion).
The knowledge of general points of pharmacokinetic and pharmacodynamic
processes is necessary to assess a drug during studying private pharmacology.
- Peculiarities in the biochemical processes for newborn infants and elderly
people.
- Basic ways of the xenobiotics biotransformation (biochemistry).
- Osmotic and oncotic pressure; pK, pH, mechanisms of drug transport
through the membranes (biophysics).
OBJECTIVES (AIMS OF INDEPENDENT WORK):
Define the following terms:
- Absorption
- Area under the curve (AUC)
- Bioavailability
- Clearance
- Distribution
- Drug
- Elimination
- Enzyme induction
- Excretion
- First-pass effect
- Half-life (t ½)
- Metabolism
- Microsomal mixed-function oxidase system
- Permeation
- Phase I and phase II biotransformation
- pKa and acid dissociation constant Ka
- Slow acetylators
- Volume of distribution
- Weak acid, weak base
- Zero-order, first-order elimination.
YOU SHOULD BE ABLE TO:
- Predict the relative ease of permeation of a weak acid or base from
knowledge of its pKa and the pH of medium.
- List and discuss the common routes of drug administration and excretion.
- Draw graphs of the blood level versus time for drugs subject to zero-order
elimination and for drugs subject to first-order elimination.
- Compute the half-life of a drug from its clearance and volume of
distribution.
- Calculate loading and maintenance dosage regimens for oral or intravenous
administration of a drug when the minimum therapeutic concentration, clearance,
and volume of distribution are known.
- List the major phase I and phase II metabolic reactions.
- Describe the mechanism of hepatic enzyme induction.
- List 3 drugs that inhibit the metabolism of other drugs.
- List 3 drugs for which there are well-defined genetically determined
differences in metabolism.
- Discuss the effects of smoking, liver disease, and kidney disease on drug
elimination.
- Describe the pathways by which acetaminophen is metabolized (1) to
harmless products if taken in normal doses and (2) to hepatotoxic products if taken
in excess.
Wilkins, 1996. - P. 1-7.
Jaypee Brothers, 1999. - P. 1-35.
Philadelphia, Pennsylvania, 2001. - P. 1-15, 23-25.
Questions for self-assessment:
1. Define pharmacokinetics (PK).
2. Define absorption.
3. What does the rate and efficacy of absorption depend on?
4. How does the dosage affect drug absorption? How is this influence
called?
5. In what way does the pH of a drug affect its charge?
6. How does charge affect a drug’s ability to permeate a cell membrane?
7. Define bioavailability.
8. What is the bioavailability of an intravenously injected drug?
9. What is the bioavailability of any drug that is not intravascularly
injected?
10. What factors affect bioavailability?
11. What is first-pass metabolism?
12. What are the routes of drug administration?
13. Factors governing choice of route.
14. Name the 4 types of alimentary routes of administration and state the
advantages of each.
15. Name the 4 parenteral routes of administration and state the advantages
of each. Do the parenteral routes bypass the alimentary tract?
16. What category of drugs is commonly administered by inhalation?
17. How are inhaled drugs administered?
18. When is topical administration used?
19. When is transdermal administration used?
20. Define distribution. Clinical distribution (Vd). Clearance (Cl).
21. By what three biochemical mechanisms are drugs absorbed into cells?
22. What does distribution depend upon?
23. Why does the body biotransform drug?
24. Principles of drug metabolism (biotransformation).
25. What are the two general sets of modifications that occur in
biotransformation?
26. What happens in a phase I reaction? What types of phase I reactions
occur?
27. What happens in phase II conjugation reactions? What substrates are
added in phase II conjugation reactions?
28. Where do phase I and phase II reactions occur?
29. What factors affect drug biotransformation?
30. Are the rates for drug biotransformation predictable? Define first-order
and zero-order kinetics.
31. What is excretion? Major routes of excretion.
32. Factors affecting drug excretion.
WORK AT THE PRACTICAL STUDY:
Task N 1. Comparative characteristics of routes of drug administration.
Route of administration Advantages Disadvantages
Oral
Sublingual
Rectal
Intravenous
Intramuscular
Inhalational
Task N 2. Drug X has a narrow therapeutic index: the minimum toxic

plasma concentration is 150 mg/L while the minimum therapeutic plasma
concentration is 100 mg/L. The half-life is 6 hours. It is essential to maintain the
plasma concentration above the minimum therapeutic level. What would be the
most appropriate dosing regimen?
Task N 3. The pharmacokinetics of theophylline include the following
average parameters: Vd =35 L; CL= 48 mL/min; half-life=8 hours. If an
intravenous infusion of theophylline is started, how long will it take to approach a
steady-state plasma level, ie, 93,75% of final steady-state?
Task N 4. Mr. Jones is admitted to General Hospital with pneumonia due to
gram-negative bacteria. The antibiotic tobramycin is ordered. The CL and V d of
tobramycin in Mr Jones are 80 mL/min and 40 L, respectively. What maintenance
dosage must be administered intravenously every 6 hours to eventually obtain
average steady-state plasma concentrations of 4 mg/L?
Lesson N 3
Topic: “PHARMACODYNAMICS”.
- Bases of the organs and systems neurohumoral regulation.
- Notion about receptors and histohematic barriers (physiology)
- Role of c-AMP in the biochemical processes regulation (biochemistry).
OBJECTIVES (AIM OF INDEPENDENT WORK):
- Chemical antagonist
- Competitive antagonist
- Coupling protein
- Drug efficacy
- Drug potency
- ED50, TD50, LD50
- Effector
- Effector mechanism
- Graded dose-response curve
- Irreversible antagonist
- Partial agonist
- Physiologic antagonist
- Special carrier
- Receptor
- Receptor agonist
- Termination of action
- Specify whether an antagonist is competitive or irreversible on the basis of
its effect on the dose-response curve of the agonist.
- Compare the efficacy and potency of drugs on the basis of their dose-
response curves.
- Predict the effect of a partial agonist on a system in the presence and in the
absence of a full agonist.
- Name an important inert binding-site protein in blood.
- Predict the effect of adding drug B when a barely subtoxic dose of drug A
is present if drug A and drug B both binds to the same inert binding site.
- Give examples of partial agonists, competitive and irreversible antagonists,
and physiologic and chemical antagonists.
- Name the coupling and effector proteins that are activated by the beta
adrenoceptor.
- Name 4 methods by which drug-receptor signals bring about effects.
1. Define pharmacodynamics (PD).
2. Mechanisms of drug-receptor interactions (transmembrane, ligand-gated
ion channels, intracellular, second messenger system).
3. What are second messenger systems? Name the best-known second
messenger systems and enzyme that produces each of them.
4. What is an agonist?
5. What is a full agonist?
6. What are partial agonists?
7. What are antagonists?
8. What does a competitive antagonist do?
9. How can a competitive antagonist be overcome?
10. What does a noncompetitive antagonist do?
11. How will such noncompetitive antagonists affect the maximum
efficacy of a drug?
12. Pharmacokinetic and pharmacodynamic interactions. Examples.
13. Enhancement of drug effects. What types is the synergism divided
into?
14. Relation between drug dose and clinical response.
15. Define efficacy and potency. What is the difference between them?
16. What is EC50?
17. What factors are involved in determining an appropriate drug dose for
a patient?
18. What is volume of distribution (Vd)? How is Vd calculated?
19. What is the significance of a large Vd?
20. What is a maintenance dose? What is the equation for calculating a
maintenance dose?
21. What is a loading dose? What is the equation for calculating a loading
dose?
22. What is the steady-state plasma concentration?
23. What factors will dosing frequency affect?
24. Plasma half-life. How many half-lives are required to reach steady-
state concentration?
25. What is clearance?
26. What is an excretion rate?
27. What is a therapeutic index? Determination of therapeutic index.
Margin of safety.
28. Factors modifying drug action (quantitative and qualitative).
29. Methods of prolonging the duration of action of a drug.
30. Types of adverse effects.
31. Tolerance, tachyphylaxis, idiosyncrasy, hyporeactivity, hyperreactivity,
hyposensitivity, hypersensitivity, cumulation. Define them.
Wilkins, 1996. - P. 7-13.
Philadelphia, Pennsylvania, 2001. - P. 17-22.
Task N 1. Compare efficacy and potency of drugs A, B and C (Look at the
figure).
Biological effect
Log drug concentration
Task N 2. In the absence of other drugs, pindolol causes an increase in heart
rate by activating beta receptors. However, in the presence of highly effective beta
stimulants, pindolol causes a dose-dependent, reversible decrease in heart rate. Is
pindolol a noncompetitive antagonist, physiologic antagonist, chemical antagonist,
partial agonist or spare receptor agonist?
Task N 3. Two drugs, A and B, have the same mechanism of action. Drug A
in a dose of 5 mg produces the same magnitude of effect as drug B in a dose of 500
mg. Compare efficacy and potency of these drugs.
AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY

Introduction: The autonomic nervous system (ANS) regulates functions that
are not under conscious control, such as BP, HR and intestinal motility. The
sympathetic nervous system prepares you for “flight or fright” situations. The
parasympathetic nervous system is also known as the rest and digest system. These
two systems oppose each other’s actions. Remember that both systems are working
at all times; however, which system predominates over an organ will depend on the
situation.
Lesson N 4
Topic: “STRUCTURE OF THE PERIPHERAL EFFERENT NERVOUS
SYSTEM”.
- Major subdivisions of nervous system.
- Physiologic action of the sympathetic and parasympathetic nervous
systems.
- Localization of cholinergic and adrenergic fibers (physiology).
- Anatomic differences between sympathetic and parasympathetic nerves.
- Neurotransmitters in the ANS.
- Cholinergic transmission.
- Adrenergic transmission.
- Structure of eye (anatomy, physiology).
- Adrenergic
- Adrenoceptor
- Autonomic effector cells
- Autonomic ganglion
- Baroreceptor reflex
- Cholinergic
- Cholinoceptor
- Dopaminergic
- Parasympathetic
- Postsynaptic receptor
- Presynaptic receptor
- Sympathetic
- Describe the steps in the synthesis and the termination of action of the
major autonomic transmitters.
- Describe the organ system effects of stimulation of the parasympathetic
and sympathetic systems.
- Predict the effects of inhibitors of acetylcholine on the function of the
major organ systems.
- Name the major types of receptors found on autonomic effector tissues.
Topic: “CHOLINERGIC (PARASYMPATHETIC) AGONISTS.

ANTICHOLINESTERASE AGENTS”.
Introduction: The major therapeutic uses of the cholinomimetics are for
diseases of the eye (glaucoma, accommodative esotropia), the gastrointestinal and
urinary tracts (postoperative atonia, neurogenic bladder), and the neuromuscular
junction (myasthenia gravis, curare-induced neuromuscular paralysis).
Cholinesterase inhibitors are occasionally used in the treatment of atropine
overdosage.
- Acetylcholine synthesis and inactivation (biochemistry).
- Physiologic effects of stimulation of M (muscarinic) and N (nicotinic)
receptors (physiology).
- Peculiarities of the tertiary and quaternary amines transport through blood-
brain barrier (general pharmacology).
OBJECTIVES:
- Parasympathomimetic
- Cholinomimetic alkaloids
- Direct-acting cholinomimetics
- Indirect-acting cholinomimetics
- Choline esters
- Short- and long-acting cholinesterase inhibitors
- Nicotinic agonists
- Muscarinic agonists
- Organophosphates
- Organophosphate aging
- Cholinergic crisis
- Myasthenic crisis
- List the locations and types of acetylcholine receptors in the major organ
systems (CNS, eyes, heart, vessels, bronchi, gut, genitourinary tract, skeletal
muscle, exocrine glands).
- Describe the effects of acetylcholine on the major organs.
- Relate the different pharmacokinetic properties of the various choline
esters and cholinomimetic alkaloids to their chemical properties.
- List the major clinical uses of cholinomimetic agonists.
- Describe the pharmacodynamic differences between direct- and indirect-
acting cholinomimetic agents.
- List the major signs and symptoms of (1) acute nicotine toxicity and (2)
organophosphate insecticide poisoning.
Main drugs for studying: Acetylcholine, Methacholine, Bethanechol,
Carbachol, Pilocarpine, Physostigmine, Neostigmine, Pyridostigmine,
Ambenonium, Edrophonium, Demecarium, Echothiophate, Malathion, Parathion.
Wilkins, 1996. - P. 19-22, 35-38.
Jaypee Brothers, 1999. - P. 77-82, 83-102.
1. What are cholinergic agonists?
2. What are the 2 major families of cholinergic receptors?
3. What do pharmacologic subtypes of muscarinic receptors exist?
4. Identify the 2 types of nicotinic receptors.
5. Where are cholinergic receptors located in the body?
6. Pharmacologic (physiologic) actions of acetylcholine (Ach).
7. What receptors does Ach activate?
8. What are the clinical indications of Ach? Why?
9. What are the adverse reactions of Ach?
10. Classification of cholinergic drugs (direct-, indirect-acting).
11. Mechanism of action of direct- and indirect-acting drugs.
12. Indications (clinical uses) for cholinergic agonists.
13. Cholinergic drugs used for treatment of open-angle glaucoma.
14. Side (adverse) effects of cholinergic agonists.
15. Can physostigmine enter the CNS? Does neostigmine enter the CNS?
16. Why are physostigmine, neostigmine, edrophonium, and
pyridostigmine considered to be reversible?
17. Myasthenia gravis. Treatment by cholinergic drugs.
18. Clinical use for edrophonium.
19. Reversal of organophosphate effects.
20. What are organophosphates (indirect-acting irreversible) used for
today?
21. Manifestations (symptoms) of organophosphate intoxication.
22. Treatment of organophosphate poisoning.
23. Contraindications to use of cholinergic agonists.
Task N 1. Properties of choline esters.
Choline ester Susceptibility to Cholinesterase Muscarinic action Nicotinic action
Acetylcholine
Methacholine
Carbachol
Bethanechol
Task N 2. Uses and duration of action of cholinesterase inhibitors used in

therapeutics.
Drug Uses Duration of action
Edrophonium
Neostigmine
Pyridostigmine
Physostigmine
Ambenonium
Demecarium
Echothiophate
Lesson N 5
Topic: “ANTICHOLINERGIC DRUGS (PARASYMPATHETIC
ANTAGONISTS)”.
Introduction: Muscarinic receptor-blocking drugs are used for the treatment

of Parkinson’s disease, motion sickness, peptic ulcer, asthma, cholinergic
poisoning, for the ophthalmoscopic examination and in preanesthetic medication.
The major remaining therapeutic application of ganglion-blocking drugs is for
short-term blood pressure control. Neuromuscular blocking agents are used during
surgical procedures and in intensive care units to cause paralysis. They are also
used as an adjunct to general anesthesia.
- Localization of M- and peripheral N-cholinoceptors.
- Effects of M- and N-cholinoceptors blockade (physiology).
- Notion about bronchial asthma, peptic ulcer and hypertension
(pathophysiology).
OBJECTIVES:
- Anti-motion-sickness agent
- Antimuscarinic delirium
- Atropine fever
- Atropine flush
- Cholinesterase regenerator
- Cycloplegia
- Depolarizing blockade
- Miotic
- Mydriatic
- Nondepolarizing blockade
- Parasympatholytic
- Describe the effects of atropine on the major organ systems (CNS, eyes,
heart, vessels, bronchi, gut, genitourinary tract, exocrine glands, skeletal muscle).
- List the signs, symptoms, and treatment of atropine poisoning.
- List the major clinical indications and contraindications for the use of
muscarinic antagonists.
- Describe the autonomic effects of the ganglion-blocking nicotinic
antagonists.
- List one antimuscarinic agent promoted for each of the following special
uses: mydriasis and cycloplegia, parkinsonism, peptic ulcer, and asthma.
Main drugs for studying: Atropine, Scopolamine (Hyoscine), Pirenzepine,
Homatropine, Cyclopentolate, Tropicamide, Dicyclomine, Benztropine,
Trihexyphenydyl, Glycopyrrolate, Propantheline, Ipratropium; Hexamethonium,
Mecamylamine, Trimethaphan; Tubocurarine, Metocurine, Gallamine,
Alcuronium, Pancuronium, Vecuronium, Atracurium, Decamethonium,
Succinylcholine (Suxamethonium), Benzoquinonium.
Wilkins, 1996. - P. 38-44.
1. What are cholinergic antagonists?
2. Classification of antimuscarinic drugs (mark tertiary and quaternary
compounds).
3. Classification of antinicotinic drugs (ganglionic blockers and
neuromuscular blocking agents).
4. Mechanism of action of antimuscarinic drugs.
5. Mechanism of action of ganglionic blockers.
6. Mechanism of action of neuromuscular blocking agents (non-
depolarizing and depolarizing).
7. What agents can be used to counteract the effects of atropine?
8. Does atropine cross the BBB (blood-brain barrier)?
9. Pharmacologic effects of atropine (peripheral and central).
10. Pecularities of scopolamine’s action in the comparison with atropine.
11. Effects of antimuscarinic drugs on the eye. Onset of mydriais
development, duration of these action.
12. Therapeutic uses of atropine and related drugs.
13. Why atropine is used in anesthesiology?
14. What intoxications are treated by atropine?
15. Contraindications to usage of atropine.
16. Pharmacokinetic properties of atropine. Duration of action.
17. Side effects of atropine.
18. Atropine intoxication. Symptoms and treatment.
19. Reversal of non-depolarizing blocking agents.
20. Therapeutic uses of neuromuscular blocking agents.
21. Adverse effects of neuromuscular blockers (NMBs).
22. Sequence of paralysis.
23. Peculiarities of quaternary NMBs transport through GIT mucous,
placenta and BBB.
24. What is the danger of succinylcholine?
25. Mechanism of action of ganglionic blockers.
26. Pharmacological effects of ganglionic blockade (sympathetic and
parasympathetic).
27. Peculiarities of ganglionic blockers transport through GIT mucous,
placenta and BBB.
28. Duration of action of ganglionic blockers.
29. Therapeutic usage of ganglionic blockers.
30. Side effects and contraindications to ganglionic blockers.
31. Alkaloid nicotine. Characterize the changes of HR and BP in smokers.
Mechanism of pressor action of nicotine and tachycardia development.
32. Mechanism of anginal attacks under smoking.
33. Action of tobacco smoking on TXA2 and prostacycline synthesis.
Mechanism of atherosclerosis development.
34. Action of nicotine on respiratory system.
Task N 1. Comparative characteristic of antimuscarinic drugs.
Drug Pharmacokinetic peculiarities Indications Side effects
Atropine
Hyoscine
Pirenzepine
Ipratropium
Cyclopentolate
Task N 2. Relative autonomic tone and effects of ganglion blockade.

Organ Dominant tone Effect of ganglion blockade (Side effects)
1. Heart
2. Blood vessels
3. Iris
4. Ciliary muscle
5. Intestines
6. Bladder
7. Male sexual function
8. Salivary glands
9. Sweat glands
Task N 3. Comparative characteristic of neuromuscular blocking agents.

Drug Group Indications (therapeutic Duration of Side
uses) action effects
Succinylcholine
Tubocurarine
Gallamine
Pancuronium
Atracurium
Rocuronium
Lesson N 6
Topic: “ADRENERGIC AGONISTS (SYMPATHOMIMETICS)”.
Introduction: The sympathetic nervous system is an important regulator of

the activities of organs such as the heart and peripheral vasculature, especially in
responses to stress. The effects of the studied drugs depend on their receptor
affinity (alpha or beta), and the compensatory reflexes evoked by their direct
actions. An understanding of the pharmacology of these agents is thus a logical
extension of what we know about the physiologic role of the catecholamines.
Sympathomimetic drugs are very potent and can have profound effects on a variety
of organ systems, particularly the heart and peripheral circulation.
- Steps in biosynthesis of CAs. Fate of CAs (biochemistry).
- Localization and effects of stimulation of 1and adrenoceptors
(physiology).
OBJECTIVES:
- Anorexiant
- Catecholamine (CA)
- Decongestant
- Direct, indirect agonist
- Mydriatic
- Selective alpha agonist, beta agonist
- Sympathomimetic
- Reuptake inhibitor
- List the tissues that contain significant numbers of - or 2 –
receptors.
- List the tissues that contain significant numbers of - or  –
receptors.
- Describe the major organ system effects of a pure alpha agonist, a pure
beta agonist, and a mixed alpha and beta agonist, and give examples of each type
of drug.
- List the major clinical applications of the adrenoceptor agonists.
Main drugs for studying: Adrenaline (Epinephrine), Noradrenaline
(Norepinephrine), Isoproterenol (Isoprenaline), Dopamine, Dobutamine,
Ephedrine, Salbutamol (Albuterol), Orciprenaline (Metaproterenol), Terbutaline,
Ritodrine, Phenylephrine, Methoxamine, Metaraminol, Prenalterol,
Xylomethazoline, Fenfluramine, Mazindol, Amphetamine.
Wilkins, 1996. - P. 22-30.
Philadelphia, Pennsylvania, 2001. - P. 55-69, 474.
1. Steps of noradrenaline synthesis in adrenergic nerve endings.
2. Ways of noradrenaline inactivation.
3. Distribution of α1 -receptors.
4. Distribution of α2-receptors.
5. Distribution of β1 -receptors.
6. Distribution of β2-receptors.
7. Classification of adrenergic agonists according to mode of action (direct,
indirect). Explain it.
8. Classification of adrenergic agonists according to receptor selectivity.
9. Classification of adrenergic agonists according to chemical structure.
Structure of catecholamines.
10. Classification of adrenergic agonists according to therapeutic utility.
11. Structure-activity relationship of adrenergic drugs.
12. Therapeutic uses of adrenaline, noradrenaline, isoprenaline, dopamine,
dobutamine, phenylephrine.
13. Adverse effects of -adrenergic agonists.
14. Adverse effects of -adrenergic agonists.
15. Physiologic (pharmacologic) responses when  -receptors are
stimulated.
16. Physiologic (pharmacologic) responses when -receptors are
stimulated.
17. What receptors does dopamine act on?
18. Biphasic action of adrenaline.
19. To what does the term “epinephrine reversal” refer?
20. How does norepinephrine reduce heart rate (HR)?
21. Route of noradrenaline administration.
22. Contraindications to adrenergic agonists administration.
23. Differences between orciprenaline and isoprenaline in action on
bronchi and heart.
24. Pharmacological effects of ephedrine.
25. Therapeutic uses of ephedrine.
26. Therapeutic uses of orciprenaline, terbutaline, salbutamol.
Task N 1. Comparative characteristic of adrenergic agonists.
Drug Effect on adrenoceptors Indications (therapeutic uses)
Noradrenaline
Isoprenaline
Salbutamol
Ephedrine
Dobutamine
Phenylephrine
Lesson N 7
Topic: “ANTI-ADRENERGIC DRUGS (SYMPATHETIC
ANTAGONISTS)”.
Introduction: Since catecholamines play a role in a variety of important

physiologic responses, drugs that block adrenoceptors have obvious pharmacologic
applications. Beta-receptor-blocking drugs have been found useful in a wide
variety of clinical conditions – hypertension, ischemic heart disease, cardiac
arrhythmias, glaucoma.
- Structure of the sympathetic nervous system.
- Effects of adrenoceptors blockade.
- Regulation of vascular tone (physiology).
- Role of the sympathetic tone increasing in the cardiovascular pathology
(pathophysiology).
OBJECTIVES:
- Competitive blocker
- Covalently bound inhibitor
- Epinephrine reversal
- Intrinsic sympathomimetic activity (ISA)
- Irreversible blocker
- Open-angle glaucoma
- Orthostatic hypotension
- Pheochromocytoma
- Raynaud’s phenomenon
- Describe the effects of phentolamine on hemodynamic responses to
epinephrine and norepinephrine.
- Compare the effects of propranolol, metoprolol, and pindolol.
- Compare the pharmacokinetics of propranolol, atenolol, esmolol, and
nadolol.
- Describe the clinical indications and toxicities of typical alpha- and beta-
blockers.
Main drugs for studying: Phentolamine, Prazosin, Terazosin, Doxazosin,
Phenoxybenzamine, Ergotamine, Ergotoxine, Propranolol, Sotalol, Nadolol,
Timolol, Pindolol, Oxprenolol, Alprenolol, Labetalol, Dilevalol, Metoprolol,
Atenolol, Acebutolol, Esmolol, Betaxolol; Reserpine, Bretylium, Guanethidine;
Methyldopa, Clonidine, Guanfacine.
Wilkins, 1996. - P. 30-35.
Jaypee Brothers, 1999. - P. 133- 147.
Philadelphia, Pennsylvania, 2001. - P. 71-79, 425-428.
1. What are adrenergic antagonists?
2. Classification of -blockers.
3. Mechanism of action of -blockers.
4. Physiologic (pharmacologic) effects of -blockade and -blockade.
5. Clinical uses of -blockers.
6. Adverse effects of -blockers.
7. Phenoxybenzamine. How does this drug work? Pharmacological effects.
Duration of action. Therapeutic use. Adverse effects.
8. Phentolamine. Mechanism of action. Clinical uses. Route of
administration. Adverse effects.
9. Classification of -blockers.
10. Pharmacologic actions of non-selective -blockers.
11. What are the advantages of -selectivity?
12. Haemodynamical effects of blockers.
13. Clinical indications for -blockers.
14. Adverse effects of -blockers.
15. Are there any advantages to using -blockers with ISA (intrinsic
sympathomimetic activity)? What are these drugs used for?
16. Why are these drugs (with ISA) considered to be partial agonists?
17. Labetalol. Mechanism of action. Clinical use. Adverse effects.
18. Name centrally acting sympatholytics.
19. Mechanism of antiadrenergic action of clonidine and methyldopa.
20. Pharmacological effects of clonidine.
21. Therapeutic uses of clonidine. Side effects.
22. Methyldopa. Therapeutic uses. Side effects.
23. Name adrenergic neuron blockers.
24. Mechanism of reserpine and bretylium actions.
25. Reserpine, bretylium. Therapeutic uses. Side effects.
26. How is hypotensive action of sympatholytics changed in simultaneous
usage with TCAD (tricyclic antidepressants) and why?
Task N 1. Comparative characteristic of anti-adrenergic drugs.
Drug Mechanism of action Pharmacological effects Indications
Phentolamine
Prazosine
Propranolol
Metoprolol
Nadolol
Reserpine
Clonidine
Lesson N 8
Topic: FINAL LESSON N 1 “DRUGS AFFECTING ON NEUROHUMORAL
TRANSMISSION”.
Prepare lessons NN 4-7 according to the following scheme for each

pharmacological group or subgroup:
1. Classification.
2. Mechanism of action.
3. Pharmacological (physiological) effects.
4. Therapeutic uses (indications).
5. Side (adverse) effects.
6. Contraindications.
7. Symptoms and management (treatment) of organophosphate, atropine
poisoning and intoxication by neuromuscular blocking agents.
CENTRAL NERVOUS SYSTEM PHARMACOLOGY

Introduction: Certain general depressants of the CNS are used to relieve
anxiety, to sedate or to induce sleep (hypnosis). The magnitude of their effects is
dose-dependent. Besides their sedative, hypnotic and anxiolytic properties, as a
class they are characterized as being anticonvulsants, CNS muscle relaxants and
anesthetics; and by their activity to develop physical dependence.
Lesson N 9
Topic: “GENERAL ANESTHETICS”.
Introduction: Narcosis (anesthesia) as the method of the organism protection

from aggression (superstrong and continuous irritant) is widely used during
operative treatment and diagnostic investigations in surgery, obstetric-
gynecological practice, stomatology and other fields of medicine as well as with
the therapeutic aim (for tetanus, myocardial infarction, eclampsia and so on).
General anesthetics are drugs, which produce:
- analgesia;
- unconsciousness;
- amnesia;
- loss of sensory and ANS reflexes;
- skeletal muscular relaxation in the subjects.
For material mastering it is necessary to know the following:
- the peculiarities of lipophilic, ionizic and neutral molecules transport
through the membranes (general pharmacology);
- the mechanisms of synaptic transmission of excitation (physiology);
- the notion about general anesthesia (general surgery).
- Amnesia
- Balanced anesthesia
- Inhalation anesthesia
- Minimal alveolar anesthetic concentration (MAC)
- Analgesia
- General anesthesia
- Intravenous anesthesia
- Stages of anesthesia
- Identify the main inhalation and intravenous anesthetic agents and describe
their pharmacodynamic properties.
- Describe the relationship between the blood:gas partition coefficient of an
inhalation anesthetic and the speed of onset (and offset) of anesthesia with it.
- Describe how changes in pulmonary ventilation and blood flow can
influence the speed of onset (and offset) of inhalation anesthesia.
- Describe the pharmacokinetics of the commonly used intravenous
anesthetics.
Main drugs for studying: Nitrous oxide, Halothane, Enflurane, Isoflurane,
Methoxyflurane,Thiopentone sodium, Propofol, Etomidate, Methohexitone sod.,
Diazepam, Lorazepam, Midazolam, Ketamine, Innovar.
Wilkins, 1996 – P. 49-50, 83, 87-95.
1. Characteristics of anesthesia stages: symptoms and functional changes of
CNS.
2. Theories of narcosis.
3. Classification of general anesthetics.
4. Mechanism of anesthetic action in different stages.
5. Advantages and disadvantages of inhalation and intravenous anesthesia.
6. Complications during and after anesthesia.
7. Aims of preanesthetic medication. Drugs used in preanesthetic
medication.
8. Pharmacological effects of general anesthetics (the influence on
breathing, cardiovascular system, autonomic nervous system, frequency of reflexo-
complications).
9. Notion about MAC and blood-gas partition coefficient.
10. Peculiarities of some drugs action.
11. Overdosage, preventive measures and rendering of assistance when
being poisoned.
12. What is induction of anesthesia?
13. Factors that influence the rate of induction: solubility, pulmonary
ventilation, partial pressure, alveolar blood flow, and arteriovenous concentration
gradient.
14. What is recovery?
15. What does recovery depend upon?
16. Pharmacokinetics of inhalation anesthetics
17. How does solubility affect the rate of induction?
18. How does pulmonary ventilation affect the rate of induction?
19. How does partial pressure affect the rate of induction?
20. How does alveolar blood flow affect the rate of induction?
21. How does arteriovenous concentration gradient affect the rate of
induction?
22. What factors is tissue anesthetic uptake influenced by?
23. Physicochemical theories of anesthesia (lipid and protein).
24. Balanced anesthesia. Neuroleptanesthesia. Dissociative anesthesia.
25. Why is nitrous oxide called “laughing gas”?
26. Halothane. Cardiovascular effects. Clinical indications. Metabolism.
Toxic effects.
27. What is malignant hyperthermia?
28. Enflurane. Clinical indications. Cardiovascular effects. Metabolism,
toxic effects.
29. Isoflurane. Clinical indications, metabolism, cardiovascular effects,
toxic effects.
30. Desflurane. Clinical indications, metabolism, cardiovascular effects,
toxic effects.
31. Sevoflurane. Metabolism, cardiovascular effects, toxic effects.
32. Methoxyflurane. Side effects.
33. Nitrous oxide. Clinical indications. Route of administration.
Cardiovascular effects. Contraindications to the use of N2O.
34. What special considerations should be taken into account during the
recovery phase (for N2O)? Toxic effects.
35. Thiopental. Clinical indication, mechanism of action, pharmacological
effects, side effects.
36. Benzodiazepines (diazepam, lorazepam, midazolam). Mechanism of
action.
37. Why is midazolam used as a preanesthetic medication?
38. Why is midazolam the preferred benzodiazepine for induction and
maintenance of anesthesia?
39. What are the side effects of benzodiazepines (BDZs)?
40. Propofol. Pharmacological characteristics. Side effects.
41. Ketamine. Clinical indications. Cardiovascular effects, side effects.
How does it act?
Task N 1. Comparative characteristic of general anesthetics. Fill in the chart:
Drugs Onset Duration Effects Analgesic Miorelaxant Irritant Recovery
(min) of action on activity activity stage
(min) CVS (min)
Halothane
Nitrous
oxide
Ether
Ketamine
Thiopentone
sodium
Propofol
Task N 2. Premedication anesthesia. Fill in the chart:

Drugs Pharmacological effects Aim (purpose)
Morphine
Barbiturates
Benzodiazepines
Atropine
H2 – blockers (Ranitidine)
Neuroleptics (Droperidol)
Lesson N 10
Topic: “SEDATIVE-HYPNOTICS. ANTIEPILEPTIC DRUGS.
ANTIPARKINSONIAN DRUGS”.
Introduction: Assignment of a particular compound to the sedative-hypnotic

class of drugs indicates that its major therapeutic use is to cause sedation (with
concomitant relief of anxiety) or to encourage sleep. These clinical uses are of such
magnitude that sedative-hypnotics are among the most freguently prescribed drugs
worldwide.
Approximately 1% of the population has epilepsy, the second most common
neurologic disorder after stroke. In most cases of epilepsy the choice of medication
depends on the empirical seizure classification.
The normally high concentration of dopamine in the basal ganglia of the
brain is reduced in parkinsonism, and pharmacologic attempts to restore
dopaminergic activity with levodopa and dopamine agonists have been successful
in alleviating many of the clinical features of the disorder.
- physiological role of the sleep, sleep structure (physiology);
- notion about sleep disturbances, types of insomnias (pathophysiology);
- pathogenetic factors of epilepsy;
- pathogenetic mechanisms and biochemical bases of parkinsonism
(pathophysiology).
OBJECTIVES:
- Sedation
- Hypnosis
- REM sleep
- Tolerance
- Physical dependence
- Anxiolytic
- Psychologic dependence
- Absence (petit mal) seizures
- Generalized tonic-clonic (grand mal) seizures
- Infantile spasms
- Myoclonic jerking
- Partial and generalized seizures
- Status epilepticus
- Dopaminergic-cholinergic balance
- Dyskinesia
- Levodopa adjunct
- Movement disorder
- On-off phenomena
- Identify the major chemical classes of sedative-hypnotics.
- Describe the sequence of CNS effects of a typical sedative-hypnotic over
the entire dose range.
- Describe the pharmacodynamics of benzodiazepines, including interactions
with neuronal membrane receptors.
- Compare the pharmacokinetics of commonly used benzodiazepines and
barbiturates and understand how differences between them apply to clinical use.
- Describe the clinical uses of sedative-hypnotics.
- List the major drugs for partial and generalized tonic-clonic seizures and
describe their main adverse effects.
- List the major drugs for absence seizures and describe their main toxic
effects.
- Describe the pharmacokinetic factors that must be considered in designing
a dosage regimen for antiepileptic drugs.
- Describe the mechanisms by which levodopa, bromocriptine, amantadine,
and muscarinic blockers alleviate parkinsonism.
- Describe the therapeutic and toxic effects of the antiparkinsonism agents.
- List the chemical agents and drugs that cause parkinsonian symptoms.
Main drugs for studying: Phenobarbitone, Butobarbitone, Secobarbitone,
Pentobarbitone, Thiopentone, Hexobarbitone, Methohexitone, Diazepam,
Flurazepam, Nitrazepam, Flunitrazepam, Temazepam, Triazolam, Midazolam,
Chlordiazepoxide, Oxazepam, Lorazepam, Alprazolam, Clonazepam, Flumazenil;
Phenytoin, Carbamazepine, Ethosuximide, Valproic acid, Gabapentin,
Lamotrigine, Felbamate, Vigabatrin; Levodopa (L-dopa), Bromocriptine, Lisuride,
Pergolide, Carbidopa, Benserazide, Amantadine, Selegiline (Deprenyl),
Trihexyphenidyl (Benzhexol), Procyclidine, Biperiden.
Wilkins, 1996. – Р. 50-59.
Philadelphia, Pennsylvania, 2001. - P. 81-93, 94-97, 143-150, 443-446.
1. Classification of sedative-hypnotics.
2. Phases of sleep (REM and NREM sleep).
3. Barbiturates. Mechanism of action. Pharmacological effects. Clinical
uses. Toxic effects.
4. Metabolism of barbiturates. Mechanism of tolerance development.
5. Symptoms of barbiturate intoxication, preventive measures and rendering
of assistance when being poisoned.
6. Withdrawal syndrome of barbiturates.
7. What are the hangover effects of barbiturates?
8. Barbiturate interactions.
9. Why are benzodiazepines (BDZs) preferred as sedative-hypnotics?
10. Mechanism of action of BDZs.
11. Pharmacological effects, therapeutic uses, adverse effects of BDZs.
12. Metabolism, routes of administration.
13. BDZs interactions. BDZs antagonist.
14. What is a seizure?
15. Types of seizures (partial, generalized tonic-clonic, status epilepticus,
absence, febrile, myoclonic).
16. Therapeutic classification of anticonvulsant drugs.
17. Phenytoin. Mechanism of action. Therapeutic uses of phenytoin.
Describe metabolism and absorption of this drug. Toxic effects. Drug interactions.
18. Carbamazepine. Mechanism of action, absorption, metabolism of this
drug, adverse effects, carbamazepine’s interactions.
19. Phenobarbital. Mechanism of action, therapeutic uses, absorption,
metabolism, adverse effects.
20. Primidone. Mechanism of action, therapeutic uses, metabolism, adverse
effects.
21. Valproic acid. Mechanism of action, indications, route of administration,
metabolism, side effects.
22. Ethosuximide, mechanism of action, therapeutic uses, absorption and
metabolism, side effects.
23. Benzodiazepines that are used for antiepileptic purposes.
24. Newer antiepileptic drugs (Gabapentin, Lamotrigine). Mechanism of
action, therapeutic uses, metabolism, toxic effects.
25. What is Parkinson’s disease? Pathogenesis of this disease. Clinical
features.
26. What is the treatment strategy (pharmacological approaches).
27. Classification of drugs for Parkinson’s disease treatment.
28. L-dopa. Mechanism of action. Pharmacokinetics. Adverse effects.
29. What are disadvantages of using L-dopa alone? Combinations of L-dopa.
30. What are the «on-off» phenomena?
31. Carbidopa. Mechanism of action. Efficacy of levodopa/carbidopa
treatment.
32. Bromocriptine. Therapeutic uses. Adverse effects.
33. Pergolide. Mechanism of action. Indications. Adverse effects.
34. Selegiline. Mechanism of action. Therapeutic uses.
35. Amantadine. Mechanism of action, indications, toxic effects.
36. Anticholinergic agents, their therapeutic efficacy and adverse effects.
37. Treatment of drug-induced parkinsonism.
Task N 1. Characteristics of sedative-hypnotics. Fill in the chart:
Drug Mechanism of action Indications Adverse effects
Phenobarbitone
Thiopentone
Diazepam
Lorazepam
Task N 2. Characteristics of antiparkinsonian drugs.
Drugs Mechanism Effect on Effect on Effect on
tremor rigidity bradykynesia
of action
L-dopa
Bromocriptine
Selegiline
Trihexyphenidyl
Task N 3. Characteristics of antiepileptic drug.
Drug Chemical Mechanism of action Indications Side
structure effects
Phenobarbitone
Phenytoin
Carbamazepine
Valproic acid
Ethosuximide
Clonazepam
Lesson N 11
Topic:”ANTIPSYCHOTIC DRUGS. ANTIDEPRESSANTS.
LITHIUM SALTS”.
Introduction: Antipsychotics (neuroleptics) are used mainly for treating
schizophrenia but are effective in some other phychoses and agitated states. The
physician whose practice often or sometimes requires prescribing drugs for long-
term management of psychotic disorders does not need to know all of the drugs but
should become familiar with the effects – including the adverse effects – of one or
two drugs in each class.
Depression is one of the most common psychiatric disorders. At any given
moment, about 5-6% of the population is depressed (point prevalence) and an
estimated 10% of people may become depressed during their lives (lifetime
prevalence).
- notion about physiological basis of psychological activity (physiology);
- notion about psychosis and neurosis (pathophysiology).
OBJECTIVES:
- Bipolar disorder
- Extrapyramidal reaction
- Neuroleptic
- Tardive dyskinesia
- Neuroleptic malignant syndrome
- Endogenous depression
- Tricyclic antidepressant
- Bipolar affective disorder
- Describe the dopamine hypothesis of schizophrenia.
- List the major dopaminergic tracts in the CNS.
- Describe the behavioral effects of antipsychotic drugs on normal and
schizophrenic individuals.
- List the adverse effects of the major antipsychotic drugs.
- Describe the pharmacokinetics and pharmacodynamics of lithium.
- Describe the probable mechanisms and the major pharmacodynamic
properties of tricyclic antidepressants.
- List the toxic effects that occur during chronic therapy with tricyclic
antidepressants.
- Describe the therapeutic use and toxic effects of MAO inhibitors.
- Identify new generation antidepressants and their distinctive properties.
- Identify the major drug interactions associated with the use of
antidepressant drugs.
Main drugs for studying: Chlorpromazine, Triflupromazine, Fluphenazine,
Trifluoperazine, Thioproperazine, Thioridazine, Thiothixene, Haloperidol,
Droperidol, Promethazine, Risperidone, Pimozide, Sulpiride, Clozapine,
Molindone, Chlorprothixene, Flupenthixol; Isocarboxazid, Tranylcypromine,
Phenelzine; Imipramine, Amitriptyline, Nortriptyline, Desipramine, Trimipramine,
Clomipramine, Doxepin, Dothiepin, Mianserin, Amoxapine, Maprotiline,
Trazodone, Fluoxetine, Bupropion, Lithium carbonate.
Wilkins, 1996. – Р. 59-62, 65-69.
1. The nature of schizophrenia, positive and negative symptoms. Theories
of schizophrenia (Dopamine theory).
2. Dopamine receptors and dopaminergic pathways. Mechanism of action
of antipsychotics.
3. Classification of phenothiazines according to the type of side-chain
attached to the N-atom of the phenothiazine ring (aliphatic, piperidine, piperazine).
4. Do antipsychotic agents differ in potency?
5. Pharmacokinetic aspects of phenothiazines (metabolism, onset of action).
6. Pharmacological effects of antipsychotics.
7. Unwanted effects of the traditional antipsychotics. Degree of each type
of side effect.
8. Side effects of thioridazine.
9. What is tardive dyskinesia?
10. What is neuroleptic malignant syndrome? Therapy for it.
11. Name atypical antipsychotic drugs. Why are these drugs considered
“atypical”?
12. Mechanism of action, clinical uses, side effects of atypical
antipsychotics.
13. The nature of affective disorders. The “Monoamine theory” of
depression.
14. Types of antidepressant drugs.
15. Mechanism of action of MAOI, TCADs, SSRIs.
16. Tricyclic antidepressant drugs. Mechanism of action, clinical
indications, toxicity.
17. Selective 5-HT uptake inhibitors. Metabolism, administration, side
effects (“serotonin syndrome”).
18. Monoamine oxidase inhibitors (MAOI). Types of MAO.
Pharmacokinetics, clinical indications, adverse effects. Drug interactions.
19. “Atypical” antidepressant drugs. Why are these drugs considered
atypical?
20. Clinical effectiveness of antidepressant treatments.
21. What is mania? Name the mood stabilizers.
22. Lithium salts. Pharmacological effects and mechanism of action.
23. Pharmacokinetic aspects, toxicity and contraindications of lithium
salts.
24. Symptoms and treatment of lithium toxicity.
Task N 1. Characteristics of antipsychotic drugs.
Drug Receptor affinity Main side effects
D D2 - H1 mACh 5- EPS Seda- Hypoten Hypothermia Gynecomastia
adr HT2 tion -sion
Chlorpromazin
e
Thioridazine
Haloperidol
Flupenthixol
Sulpiride
Clozapine
Risperidone
Lesson N 12
Topic: “CNS-STIMULANTS. ANTIANXIETY (ANXIOLYTIC) DRUGS.
ALCOHOLS.”
Introduction: Ethyl alcohol (ethanol) is a sedative-hypnotic consumed as a

social drug. Alcohol abuse (alcoholism) is a complex disorder whose natural
history and basic causes are not well defined. It is a major medical and public
health problem in many societies. Ethanol and many other alcohols with
potentially toxic effects are used in industry, some in enormous quantities. Thus,
ethanol, methanol and ethylene glycol toxicity occur with sufficient frequency.
- physical and chemical properties of ethanol (organic chemistry).
- pharmacological characteristics of benzodiazepines (from previous
classes).
OBJECTIVES:
- Alcoholism
- Psychological and physical dependence
- Tolerance, cross-tolerance
- Wernicke-Korsakoff syndrome
- Acute ethanol intoxication
- Alcohol withdrawal syndrome
- Fetal alcohol syndrome
- Describe the pharmacodynamics and pharmacokinetics of acute ethanol
ingestion.
- List the toxic effects of chronic ethanol ingestion.
- Outline the treatment of (a) ethanol overdosage and (b) the alcohol
withdrawal syndrome.
- Describe the toxicity and treatment of acute poisoning with (a) methanol
and (b) ethylene glycol.
Main drugs for studying: Diazepam, Chlordiazepoxide, Oxazepam,
Lorazepam, Alprazolam, Meprobamate, Buspirone, Propranolol; Doxapram,
Nikethamide, Amphetamine, Methylphenidate, Cocaine, Methylxanthines
(Caffeine, Theophylline), Piracetam; Ethyl Alcohol (Ethanol), Methyl Alcohol
(Methanol), Disulfiram.
Wilkins, 1996. - P. 62-77, 69-70.
Jaypee Brothers, 1999. - P. 358-365, 414-417, 430-431, 477-482.
1. Pharmacokinetics of ethanol (oxidation rate in the body, role of
alcoholdehydrogenase in alcohol metabolism, elimination route).
2. Alcohol action on CNS.
3. Alcohol action on CVS in chronic intoxication (influence on lipid
metabolism, blood pressure, coronary vessels, myocardium metabolism and
contractile function, thromboxane A2 and prostacycline production and aggregant
action of thrombocytes).
4. Alcohol action on GIT in chronic intoxication.
5. Alcohol action on kidney and liver in chronic intoxication.
6. Teratogenic action of alcohol.
7. Indications to alcohol usage in medical practice.
8. Disturbances of drug’s pharmacokinetics and pharmacodynamics in
patients suffering alcohol intoxication.
9. Symptoms of acute alcohol intoxication, preventive measures and
rendering of assistance when being poisoned.
10. Therapy of alcoholism (drugs used and mechanism of their action).
11. Classification of CNS-stimulants.
12. Pharmacological effects of methylxanthines. Pharmacokinetics.
13. Therapeutic uses for methylxanthines.
14. Adverse effects of methylxanthines.
15. Amphetamines. Pharmacological effects and uses.
16. Analeptics. The role of analeptics in therapeutics.
17. Cerebroactive drugs (Piracetam, Pyritinol, Dihydroergotoxine).
Mechanism of action. Indications.
18. Names of antianxiety drugs.
19. Mechanism of their action.
20. Therapeutic uses.
21. Pharmacokinetics.
22. Pharmacological effects.
23. Side effects.
24. “Day tranquilizers”. Pharmacological properties.
Task N 1. Toxicological characteristic of ethanol in dependence of
intoxication stage (with concentration indication).
Task N 2. Formulate the principles of alcoholism treatment (with indication of
mechanisms of drug’s action).
Task N 3. Fill in the following chart:
Drug Group Mechanism of action on Pharmacological Indications
CNS effects
Theophylline
Amphetamine
Piracetam
Temazepam
Lesson N 13
Topic: “NARCOTIC ANALGESICS. OPIOID ANTAGONISTS”.
Introduction: Management of pain is essential to good medical practice and

requires careful consideration of proper dose, type of drug, and the disease being
treated. There are many situations in which analgesia must be provided before a
definitive diagnosis can be reached. Indeed, in some acute situations relief of pain
may actually facilitate history taking and physical examination and thus speed the
diagnostic process. Use of these drugs in acute situations may be contrasted to their
use in chronic pain management, where other factors must be considered –
particularly tolerance and physical dependence.
- mechanisms of nociceptive reception formation (physiology);
- notion about pain shock (pathophysiology);
- drug dependence (general pharmacology).
OBJECTIVES:
- Opiate, opioid
- Opiopeptin
- Agonist, antagonist
- Mixed agonist-antagonist
- Tolerance
- Psychological dependence
- Physical dependence
- Cross-tolerance
- List the receptors affected by opioid analgesics and the endogenous opioid
peptides.
- Rank the major opioid analgesic agonists in terms of the relative intensity of
their action at receptors.
- Identify the drugs that are opioid receptor antagonists and those that have
mixed agonist-antagonist activity.
- Describe the main pharmacodynamic and pharmacokinetic properties of
agonist opioid analgesics and list their clinical uses.
- List the main toxic effects of acute and chronic use of opioid analgesics.
- Describe the clinical uses of the opioid receptor antagonists.
Main drugs for studying: Morphine, Codeine, Ethylmorphine, Pholcodeine,
Pethidine (Meperidine), Fentanyl, Methadone, Dextropropoxyphene, Alfentanil,
Sulfentanil, Nalorphine, Pentazocine, Nalbuphine, Buprenorphine, Butorphanol,
Naloxone, Naltrexone.
Wilkins, 1996. – Р. 70-77.
2. Tripathi K.D. Essentials of Medical Pharmacology, 4/e. New Delhi, Jaypee
Brothers, 1999. - P. 432-449.
3. Harvey R.A., Champe P.C. Lippincot’s Illustrated Reviews: Pharmacology,
2/e. J.B.Lippincott Company, East Washington Square, Philadelphia,
Pennsylvania, 2001. - P. 133-142.
1. Note the sources of narcotic analgesics.
2. Name the major opioid alkaloids.
3. Classification of opioid analgesics (according opioid receptor selectivity).
4. Pharmacological effects of morphine.
5. Mechanism of analgesic action of morphine.
6. Name the indications (therapeutic uses) of morphine.
7. Uses of morphine and its congeners.
8. Side effects of morphine.
9. Precautions and contraindications to morphine usage.
10. Drug interactions of morphine and other opioids.
11. Symptoms of morphine intoxication and management (treatment).
12. Preventive measures of dependence development to morphine.
13. Onset of action and duration of action after intramuscular (subcutaneous)
morphine administration.
14. Pharmacokinetics of morphine.
15. Peculiarities of pentazocine action in comparison with morphine.
16. Peculiarities of meperidine action in comparison with morphine.
17. Peculiarities of fentanyl analgesic action.
18. Point narcotic analgesic used in neuroleptanalgesia.
19. Name the drugs used for treatment of colics.
20. Pure opioid antagonists. Mechanism of their action. Uses.
Task N 1. Differences between Morphine and Codeine.
Features Morphine Codeine
1. Efficacy
2. Analgesic effect
3. Dependence liability
4. High dose (action on CNS)
5. Uses
Task N 2. Differences between Morphine and Pethidine.
Features Morphine Pethidine
1. Source
2. Analgesic effect
3. Cough suppression
4. Constipation
5. Duration of action
6. Pupil
7. Urine retention
8. Use in labor pain
9. Dependence liability
10.Hypnotic effect
11.Local anesthetic effect
12.Atropine-like side effects
Task N 3. Functional effects associated with the main types of opioid
receptor.
  
Analgesia
Supraspinal
Spinal
Peripheral
Respiratory depression
Pupil constriction
Reduced GI motility
Euphoria
Dysphoria
Sedation
Physical dependence
Task N 4. Selectivity of opioid drugs for receptor subtypes.
  
Morphine
Pentazocine
Nalbuphine
Buprenorphine
Naloxone
Lesson N 14
Topic: Final lesson N 2 “DRUGS ACTING ON THE CNS”.
pharmacological group:
1. Classification.
7. Symptoms and management (treatment) of barbiturates, benzodiazepines,
lithium salts, narcotic analgesics intoxications.
Lesson N 15
Topic: “NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS)
DRUGS FOR ARTHRITIDES AND GOUT”.
Introduction: These drugs have analgesic, antipyretic and, at higher doses,

anti-inflammatory actions. They are extensively used and almost a quarter of
patients consulting their general practitioners have some form of ‘rheumatic’
complaint. These patients are frequently prescribed NSAIDS and additional
millions of aspirin, paracetamol and ibuprofen tablets are bought over the counter
for the self-treatment of headaches, dental pain, various musculoskeletal disorders,
etc. They are not effective in the treatment of visceral pain (e.g. myocardial
infarction, renal colic, acute abdomen), which requires opioid analgesics.
However, NSAIDs are effective in certain types of severe pain (e.g. bone cancer).
Aspirin has important antiplatelet activity.
For the material mastering it is necessary to know the following:
- What is inflammation? (pathophysiology)
- How does the body mediate the inflammation?
- Physiologic actions of prostaglandins.
- What is an eicosanoid?
- What is arachidonic acid?
- What are the two major enzymes that use arachidonic acid as a substrate?
- What is uric acid? Disturbances in purine metabolism (biochemistry).
- What is gout? What are the common clinical signs and symptoms of gout?
OBJECTIVES:
- Antipyretic
- Cyclooxygenase inhibitor
- NSAIDs
- Prostaglandin
- Uricosuric
- Xanthine oxidase inhibitor
- Describe the effects of aspirin on prostaglandin synthesis.
- List the toxic effects of aspirin.
- Contrast the actions of aspirin and the newer NSAIDs.
- Describe the mechanisms of action of 3 different drug groups used in gout.
- Describe the effects and the major toxicity of acetaminophen.
Main drugs for studying: Aspirin, Salicylamide, Benorylate, Diflunisal,
Phenylbutazone, Indomethacin, Sulindac, Ibuprofen, Naproxen, Ketoprofen,
Fenoprofen, Flurbiprofen, Mephenamic acid, Enfenamic acid, Diclofenac,
Tolmetin, Piroxicam, Tenoxicam, Ketorolac, Paracetamol (Acetaminophen),
Metamizol, Propiphenazone, Nefopam; Colchicine, Probenecid, Sulfinpyrazone,
Allopurinol.
Wilkins, 1996. - P. 193-208, 208-213.
Brothers, 1999. - P. 450-476.
Pennsylvania, 2001. - P. 401-417, 466-469.
1. Classification of non-steroidal anti-inflammatory drugs (NSAIDs).
2. Pharmacological effects of NSAIDs.
3. Mechanism of analgesic, anti-inflammatory and antipyretic actions.
4. How does aspirin differ in its action from the other NSAIDs?
5. Therapeutic uses of NSAIDs.
6. How are NSAIDs metabolized?
7. Describe the adverse effects of NSAIDs.
8. Symptoms of salicylism and treatment for salicylate toxicity.
9. Acetaminophen (paracetamol). Pharmacological effects. Indications.
10. Can acetaminophen be administered to gout patients who are taking
probenecid?
11. Metabolism of acetaminophen. Side effects. Toxic dose.
12. Why does acetaminophen cause hepatotoxicity?
13. Treatment of acetaminophen intoxication.
14. Antirheumatic drugs. Classification. Clinical indications.
15. Mechanism of action of gold salts. Adverse effects.
16. Mechanism of action of penicillamine. Adverse effects.
17. Mechanism of action of hydroxychloroquine. Adverse effects.
18. Mechanism of action of methotrexate. Adverse effects.
19. Treatment strategy of gout (for an acute attack and a chronic case).
20. Can aspirin be used in the treatment of gout?
21. Indomethacin. Mechanism of action. Therapeutic uses. Adverse effects.
22. Phenylbutasone. Mechanism of action. Therapeutic uses. Adverse
effects.
23. Colchicine. Mechanism of action. Therapeutic uses. Route of
administration. Adverse effects. Contraindications.
24. Uricosuric agents. Name them. Mechanism of action. Therapeutic uses.
Route of administration.
25. Adverse effects of probenecid and sulfinpyrasone.
26. Allopurinol. Mechanism of action.
27. Therapeutic uses. Route of administration. Adverse effects.
28. Can you combine allopurinol with other antigout drugs?
29. Are allopurinol, probenecid and sulfinpyrasone indicated in the treatment
of acute attacks?
Task N 1. Differences between narcotic and non-narcotic analgesics.
Features Narcotic analgesic Non-narcotic analgesic
1. Site of action
2. Types of pain relieved
3. Nature and addiction liability
4. Mode of action
5. Route of administration
6. Role in inflammation
7. Therapeutic index
Lesson N 16
Topic: “DRUGS USED TO TREAT ASTHMA AND COUGH”.
Introduction: Drugs of this group (antitussives, expectorants, agents used for

the treatment of bronchial asthma) are widely used in complex pharmacotherapy of
acute and chronic diseases of respiratory system. Asthma affects over 5-10% of the
population in industrialized countries. Some chest physicians consider that the
increase in morbidity may be result of the currently available therapy not being
used optimally.
- What is asthma?
- Causes of airway obstruction in asthma.
- Clinical manifestations of asthma.
- Regulation of the musculature, blood vessels and glands of the airways
(efferent, afferent pathways).
- Pharmacological characteristic of M-cholinoceptor blockers, adrenergic
agonists, xanthines, and narcotic analgesics (from previous pharmacology classes).
OBJECTIVES:
- Beta2-selective sympathomimetic
- Bronchial hyperreactivity
- Extrinsic asthma
- IgE-mediated disease
- Immunologic model for asthma
- Intrinsic asthma
- Leukotrienes
- Mast cell degranulation
- Mediators of bronchoconstriction
- Phosphodiesterase
- Tachyphylaxis
- List the major classes of drugs used in asthma.
- Describe the mechanisms of action of these drug groups.
- List the major adverse effects of the most important asthma drugs.
Main drugs for studying: Sodium and Potassium citrate or acetate, Terpin
hydrate, Ammonium chloride or carbonate, Potassium iodide, Ipecacuanha,
Bromhexine, Acetyl cysteine; Codeine, Noscapine, Dextromethorphan,
Chlorpheniramine, Diphenhydramine, Promethazine; Orciprenaline, Terbutaline,
Salbutamol, Ephedrine, Adrenaline, Isoprenaline, Theophylline, Aminophylline,
Ipratropium bromide, Sodium cromoglycate, Nedocromil, Ketotifen,
Hydrocortisone, Prednisolone, Beclomethasone dipropionate, Budesonide,
Flunisolide; Zileuton, Zafirlukast.
Wilkins, 1996. - P. 182-184.
Brothers, 1999. - P. 222-238, 178-184.
Pennsylvania, 2001. - P. 419-425, 450-451, 470.
1. Classification of drugs used for treatment bronchial asthma.
2. Sympathomimetic agents. Mechanism of action. Their clinical role. Route
of administration.
3. Adverse effects of inhaled bronchodilators.
4. Corticosteroids. How do they they work in treating asthma?
5. When are corticosteroids used in asthma management?
6. Adverse effects of inhaled corticosteroids.
7. Adverse effects of systemic corticosteroids such as prednisone.
8. Ipratropium. Mechanism of action. Clinical uses. Side effects.
9. Leukotriene inhibitors. Mechanism of action. Route of administration.
10. Clinical role of these drugs. Adverse effects.
11. Methylxanthines. Mechanism of action.
12. Which drugs decrease and which drugs increase theophylline plasma
levels?
13. What are possible complications with theophylline overdose?
14. Cromolyn sodium and nedocromil. Mechanism of action. Therapeutic
uses. Side effects.
15. What is status asthmaticus? Treatment of this state.
16. Antitussives (Cough suppressants). Classification (central, peripheral).
17. Mechanism of action of directly acting expectorants (mucokinetics).
18. Mechanism of action of potassium iodide (reflexly acting mucokinetics).
19. Mechanism of action of mucolytics (Bromhexine, acetylcysteine).
20. Differences of opioid antitussives from nonopioids.
21. Antihistamines. Name them.
23. Therapeutic uses.
24. Side effects.
25. Possible future strategies for asthma therapy.
Task N 1. Comparative characteristics of drugs affecting the respiratory
system.
Drug Pharmacological Mechanism Clinical Side
group of uses effects
action
Codeine
Dextromethorphan
Benzonatate
Potassium iodide
Acetylcysteine
Bromhexine
Albuterol
Cromolyn-sodium
Ipratropium
bromide
Task N 2. Strategy of the asthma treatment.
Form of asthma Drugs
Acute (or status asthmaticus)
Chronic:
- Mild
- Moderate
- Severe
Lesson N 17
Topic: “DRUGS USED TO TREAT GASTROINTESTINAL DISORDERS”
Introduction: An estimated 10% of adults in the western world will suffer an

episode of peptic ulcer disease during their life-time. Although the mortality rate of
this condition is low, the recurrence rate is high and the socioeconomic cost is
great.
- Pathogenesis of peptic ulcer disease.
- What factors do control gastric acid secretion by parietal cells? (gastrin,
acetylcholine, histamine).
- The innervation and the hormones of the GIT (gastrointestinal tract).
- The reflex mechanism of vomiting (vomiting center, chemoreceptor trigger
zone in the area postrema).
- Pharmacological characteristic of M-cholinoceptor blockers, neuroleptics,
M-cholinomimetics.
OBJECTIVES:
- Acid-peptic disease
- Zollinger-Ellison syndrome
- List the major drugs for the peptic ulcer treatment.
- Contrast the actions of cimetidine and the newer H2-receptor antagonists.
- Describe the mechanisms of action of antacids, anticholinergics, and proton
pump inhibitors and mucosal protective agents.
- List the main side effects of drugs used for peptic ulcer.
Main drugs for studying: Sodium bicarbonate, Magnesium hydroxide,
Magnesium carbonate, Magnesium trisilicate, Aluminium hydroxide gel, Calcium
carbonate; Cimetidine, Ranitidine, Famotidine, Nizatidine, Roxatidine, Loxatidine,
Atropine, Propantheline, Oxyphenonium, Pirenzepine, Omeprazole, Misoprostol,
Enprostil, Rioprostil, Sucralfate, Colloidal bismuth subcitrate, Carbenoxolone
sodium, Metoclopramide.
Wilkins, 1996. - P. 184-186, 187-188.
Brothers, 1999. - P. 628-670.
Pennsylvania, 2001. - P. 235-245.
1. Classification of drugs used for peptic ulcer treatment.
2. Antacids (systemic and nonsystemic). Mechanism of action. Side effects
of each. Combinations of them.
3. H2-receptor blockers. How effective are they in reducing gastric acid
secretion?
4. Mechanism of action of H2-receptor antagonists.
5. Side effects of H2-receptor antagonists.
6. Anticholinergic drugs. Mechanism of action. Pharmacological effects. Side
effects.
7. Proton pump inhibitors. Mechanism of action.
8. Therapeutic uses. How effective are they? Potential side effects.
9. Mucosal protective agents. Sucralfate. Mechanism of action.
10. Can sucralfate be taken with H2-receptor blockers or proton pump
inhibitors?
11. Bismuth. Mechanism of action. Therapeutic actions.
12. Misoprostol. Mechanism of action. Clinical indications. Major side
effects.
13. Prokinetic drugs (Cisapride. Metoclopramide). Mechanism of action.
Adverse effects.
14. Antiemetic drugs. Classification.
15. Clinical indications to antiemetic drugs.
16. Laxatives. Classification.
17. Indications. Contraindications to laxatives.
18. Stimulants laxatives. Name them. Mechanism of action. Side effects.
19. Bulking agents. Name them. How do these drugs work?
20. Stool softeners. Name them. How do they work?
Task N 1. Characteristics of antacids.
Antacids Metabolic Rebound Diarrhea Constipation Milk-alkali
alkalosis activity syndrome
NaHCO3
CaCO3
Al(OH)3
Mg(OH)2
Task N 2. Compare the drugs acting on GIT:
Drug Type of action on GIT Mechanism of action Indications Side effects

Pirenzepine
Cimetidine
Omeprazole
Sucralfate
Lesson N 18
Topic:”LOCAL ANAESTHETICS”.
Introduction: Local anesthetics have several types of clinical applications, and

their suitability for these varies with their pharmacological properties. Some of
these applications are (1) infiltration and block anesthesia, (2) surface anesthesia,
(3) spinal anesthesia, (4) epidural and caudal anesthesia, and (5) intravenous
anesthesia.
- mechanism of depolarization formation during excitation of nerve cell
receptors (physiology);
- peculiarities of transport of tertiary amines, lipophilic, ionized and neutral
molecules through membranes (general pharmacology).
OBJECTIVES:
- Describe the mechanism of blockade of the nerve impulse by local
anesthetics.
- Discuss the relation between pH, pKa, and onset or intensity of blockade.
- List the factors that determine the susceptibility of nerve fibers to blockade.
- List the major toxic effects of the local anesthetics.
- Explain use-dependent blockade.
Main drugs for studying: Procaine, Chlorprocaine, Mepivacaine, Lidocaine,
Tetracaine, Bupivacaine, Dibucaine (Cinchocaine), Cocaine, Benzocaine,
Butylaminobenzoate (Butamben), Benoxinate, Cyclomethycaine, Oxethazaine.
Wilkins, 1996. - P. 83-87.
Brothers, 1999. - P. 160-172.
Pennsylvania, 2001. - P. 117-118.
1. Properties of ideal local anesthetic.
2. Types of local anesthesia.
3. Classification of local anesthetics (LAs).
4. Two types of LAs: ester and amides. How does the metabolism of the ester
and amide anesthetics differ?
5. Mechanism of action of LAs. Which nerve fibers are most sensitive to
LAs?
6. Pharmacokinetics of LAs.
7. Pharmacological effects of lidocaine, procaine and cocaine.
8. Clinical indications for LAs.
9. How is the duration of action of local anesthetics increased?
10. Side effects of LAs.
11. Symptoms and treatment of cocaine intoxication.
Task N 1. Comparison of procaine and cocaine.
Features Procaine Cocaine
1. Nature
2. Power and toxicity
4. Addiction
5. Effect on eye
6. Action on CNS
7. Effect on CVS
8. Antiarrhythmic effect on heart
Task N 2. Comparison of procaine and lignocaine.
Features Procaine Lignocaine
1. Chemical structure
3. Penetration
4. Onset
Task N 3. Properties of local anesthetics.

Drug Onset Duration Tissue penetration Main side effects
Cocaine
Procaine
Lignocaine (lidocaine)
Amethocaine (tetracaine)
Bupivacaine
Prilocaine
Task N 4. Methods of administration, uses and adverse effects of local

anesthetics (LAs).
Method Uses Drugs Notes and adverse effects
Surface anaesthesia
Infiltration anaesthesia
Intravenous regional anaesthesia
Nerve-block anaesthesia
Spinal anaesthesia
Epidural anaesthesia
Lesson N 19
Topic: “ANTIHYPERLIPIDEMIC DRUGS”.
Introduction: Atherosclerosis is the leading cause of death in the USA and
other Western countries. LDL are linked to accelerated atherogenesis.
Atherosclerotic disease of both coronary and peripheral arteries appears to be a
dynamic process. An understanding of the biology of the lipoproteins and the
pathophysiology of the various hyperlipidemic states is essential to the rational
choice of treatment regimens.
- What is a lipoprotein?
- Name the major lipoproteins.
- What causes hyperlipidemias?
- Classification of hyperlipoproteinaemias (primary, secondary).
- The relationship between atherosclerosis/thrombosis and LDL-cholesterol
concentration in the plasma.
- What is HMG Co A reductase? (biochemistry, pathophysiology).
OBJECTIVES:
- Lipoproteins
- Chylomicrons
- FFA, HMG-Co A, ACAT, LCAT, LPL
- HDL, LDL, IDL, VLDL
- Hyperlipoproteinemia
- Hyperlipemia
- Describe the dietary management of hyperlipoproteinemia.
- Describe the mechanism of action and toxic effects of nicotinic acid,
lovastatin, clofibrate, and bile acid-binding resins. Describe probucol.
Main drugs for studying: Cholestyramine, Colestipol, Clofibrate,
Gemfibrozil, Bezafibrate, Lovastatin, Simvastatin, Pravastatin, Nicotinic acid,
Probucol.
Wilkins, 1996. - P. 132-136.
Brothers, 1999. - P. 616-627.
Pennsylvania, 2001. - P. 207-215, 449.
1. What are the treatment options?
2. Major groups of antihyperlipidemic drugs.
3. Bile acid-binding resins (cholestyramine and colestipol). Their mechanism
of action and adverse effects.
4. HMG Co A reductase inhibitors. Name them. Route of administration.
Mechanism of action.
5. What is the role of reductase inhibitors on hyperlipidemia? Adverse
effects.
6. What other drugs should generally not be prescribed to a patient taking
HMG Co A reductase inhibitors?
7. Fibric acid derivates. Name them. Route of administration.
8. Mechanism of action of fibrates. For what are these drugs used?
9. Adverse effects of clofibrate. Are these drugs safe to use in pregnancy?
10. Nicotinic acid (Niacin). Mechanism of action. Clinical use. Adverse
effects.
Task N 1. Summary of actions of lipid-lowering drugs.
Drugs LDL HDL Triglycerides
Cholestyramine
Gemfibrozil
Clofibrate
HMG CoA reductase inhibitors
Nicotinic acid
Probucol
DRUGS ACTING ON CARDIOVASCULAR SYSTEM (CVS).
Introduction: Congestive cardiac failure, cardiac arrhythmias, angina pectoris
and hypertension are the major diseases of the CVS. They are the major causes of
death and disability throughout the world.
Drugs used for the treatment of cardiovascular diseases include chemical
agents, which act primarily on the heart and blood vessels as well as those acting
mainly on other systems e.g. diuretics. Also a large number of drugs (autonomic
drugs) influence the cardiovascular functions although they exert their main
actions on other systems of the body. All such drugs have been discussed
elsewhere. Only drugs acting primarily on heart and blood vessels will be covered
in this section.
Lesson N 20
Topic: “DRUGS USED TO TREAT CONGESTIVE HEART FAILURE”.
Introduction: Congestive heart failure (CHF) occurs when the cardiac output
is inadequate to provide the oxygen needed by the body. Traditional therapy of
CHF is an increase in cardiac contractility and prevention of salt and water
retention.
- Properties of cardiac muscle; basic rates (indices) of the cardiac function;
mechanisms of the heart work regulation (physiology).
- Define congestive heart failure (CHF).
- What are the most common causes of CHF (high-output, low-output)?
- Name symptoms of CHF (left-sided & right-sided heart failure).
- Describe the compensatory physiologic mechanisms that occur in heart
failure.
- Notion about polarity of drugs (organic chemistry).
- Cumulation, peculiarities of the polar and non-polar compounds transport
through biological membranes (general pharmacology).
OBJECTIVES:
- Atrioventricular node
- Afterload
- Congestive heart failure
- ECG deflections: P, QRS, T waves
- ECG intervals: PR, QT, QRS duration; ST segments
- Premature ventricular beats
- Preload
- Sinus node
- Sodium pump (Na+, K+–ATPase)
- Sodium-calcium exchange
- Ventricular tachycardia
- Describe the process of excitation-contraction coupling in cardiac muscle.
- Describe the strategies and list the major drug groups used in the treatment
of congestive heart failure.
- Describe the probable mechanism of action of digitalis.
- Describe the nature and mechanism of the toxic effects of digitalis on the
heart.
- List some positive inotropic drugs that have been investigated as digitalis
substitutes.
Main drugs for studying: Digoxin, Digitoxin, Strophanthin, Ouabain,
Dobutamine, Amrinone, Milrinone, Furosemide, Hydrochlorothiazide,
Hydralazine, Nitroprusside sodium, Captopril, Enalapril.
Wilkins, 1996. - P. 101-106.
Brothers, 1999. - P. 483-502.
Pennsylvania, 2001. - P. 151-161.
1. Name three major pharmacological approaches for the treatment of CHF.
2. What are the pharmacological options for treating patients who have CHF?
3. Cardiac glycosides. Classification.
4. Describe the mechanism of action.
5. Chemical structure (sugar & non-sugar parts). Functions of the parts.
6. How does digoxin differ from digitoxin with respect to the absorption,
route of administration, half-life, and % plasma bound protein, and metabolism?
7. Where do cardiac glycosides originate?
8. Pharmacological effects of cardiac glycosides (cardiac, extracardiac).
9. What are the clinical indications for the administration of digoxin?
10. What is the therapeutic index of cardiac glycosides?
11. Digitalization. Types of digitalization (slow, rapid).
12. What is the action of digitalis on normal heart?
13. State the contraindications to using these drugs.
14. What major electrolyte imbalance can predispose to digoxin toxicity?
15. Describe the potential ECG findings that occur with digitalis toxicity.
16. How digitalis causes cardiac arrhythmia?
17. How can you detect hypokalaemia?
18. Symptoms of digoxin toxicity. How do you treat digoxin toxicity?
19. Are there any drug interactions?
20. -adrenergic agonists (Dobutamine, Dopamine). Mechanism of action.
Clinical uses.
21. Why adrenaline (isoprenaline) is not used as cardiotonic drug?
22. Vasodilators for the treatment of CHF (Nitrates, Hydralazine, ACE-
inhibitors). Pharmacological effects. Why are they used for the treatment of CHF?
23. Diuretics. Give examples of them. How do diuretics work in the
treatment of CHF?
24. ACE-inhibitors. Name them. Why are ACE-inhibitors used in the
management of CHF?
25. -adrenergic blockers. When should physicians employ -adrenergic
blockers?
Task N 1. Comparison of digoxin and digitoxin.
Points Digoxin Digitoxin
Source
Structure
Lipid solubility
Plasma protein binding capacity
Plasma half-life
Metabolism
Route of administration
Therapeutic utility
Task N 2 Pharmacological effects of therapeutic and toxic doses of Digitalis

glycosides.
Stages SV (stroke MV RV HR Diuresis QRS P-Q T
volume) (minute (residual (heart
volume) volume) rate)
Therapeutic
Toxic
Task N 3. Vasodilators for use in chronic CHF.

Arteriodilators Combined Arteriolo- and Venodilators Venodilators
(reduction of (reduction of preload and afterload) (reduction of preload)
afterload)
Lesson N 21
Topic: “ANTIARRHYTHMIC DRUGS”.
Introduction: Cardiac arrhythmias are a frequent problem in clinical practice,
occurring in up to 25% of patients treated with digitalis, 50% of anesthetized
patients, and over 80% of patients with acute myocardial infarction. Arrhythmias
may require treatment because too rapid, too slow, or asynchronous contractions
reduce cardiac output. More importantly, some arrhythmias can precipitate more
serious or even lethal rhythm disturbances – e.g, early premature ventricular
depolarization can precipitate ventricular fibrillation. The aim of therapy of the
arrhythmias is to reduce ectopic pacemaker activity and modify critically impaired
conduction.
- Conductive heart system (anatomy).
- Basic regulation mechanisms of the rhythmic cardiac activity (physiology).
- Autonomic control of the heart (sympathetic and parasympathetic system).
- What is arrhythmia? Types of arrhythmias (pathophysiology).
- How do arrhythmias form (re-entry, enhanced automaticity, triggered
automaticity)?
- What are two types of cardiac tissue?
- Describe the stages of a fast response cardiac action potential (phase 1,
phase 2, phase 3, and phase 4).
- How does a slow response cardiac action potential differ from a fast
response action potential?
- Types of supraventricular arrhythmias.
- Types of ventricular arrhythmias.
- Pharmacological properties of beta-blockers, atropine, cardiac glycosides,
phenytoin, lidocaine (pharmacology).
OBJECTIVES:
- Abnormal automaticity
- Action potential
- Atrial, ventricular fibrillation
- Calcium channel blockers
- Conduction velocity, time
- Group I, II, III, and IV drugs
- Local anesthetics
- Reentrant arrhythmia
- Refractory period
- Sodium channel blockers
- Supraventricular tachycardia
- Ventricular tachycardia
- Describe the distinguishing features of the 4 major groups of antiarrhythmic
drugs and adenosine.
- List 2 or 3 of the most important drugs in each of the 4 groups.
- List the major toxicities of the drugs in the preceding item.
- Explain how hyperkalemia, or an antiarrhythmic drug can cause an
arrhythmia.
Main drugs for studying: Qunidine, Procainamide, Disopyramide,
Lidocaine, Phenytoin, Mexiletine, Tocainide, Flecainide, Encainide, Propafenone,
Propranolol, Esmolol, Metoprolol, Bretylium, Amiodarone, Verapamil, Diltiazem,
Digoxin, Adenosine, Potassium.
Wilkins, 1996. - P. 106-117.
Brothers, 1999. - P. 503-519.
Pennsylvania, 2001. - P. 163-174.
1. What are the four classes of antiarrhythmic drugs?
2. Class I antiarrhythmics – Sodium channel blockers. How are Class I drugs
subdivided?
3. Class IA. Which drugs are considered to be Class IA antiarrhythmics?
4. Quinidine. How does quinidine work?
5. Clinical indications for administration of quinidine. Its effects on ECG.
6. How is this drug administered? Where is it metabolized? Adverse effects:
noncardiac (cinchonism) and cardiac (Torsade de pointes). Are there drug
interactions?
7. Procainamide. Therapeutic indications.
8. Describe the metabolite of procainamide. How is procainamide
administered? Adverse effects of this drug.
9. Disopyramide. Mechanism of action.
10. How is disopyramide administered? Clinical uses. Describe the
metabolism of this drug. What adverse effects should you watch for?
11. Which drugs are considered to be Class IB antiarrhythmics?
12. Lidocaine (Lignocaine). What ion channels does lidocaine affect? When
do you use this drug?
13. How is lidocaine administered? Describe the metabolism of lidocaine.
What are the ECG effects? Are there side effects to monitor during administration?
14. Tocainide. Therapeutic indications. How is it administered? What are
this drug’s adverse effects?
15. Mexiletine. Clinical use. How is mexiletine administered? What
toxicities are important to remember when using mexiletine?
16. Phenytoin. How is this drug classified? Route of administration. State
the therapeutic indications. Adverse effects.
17. State the drugs considered being Class IC antiarrhythmics.
18. Flecainide. How does this drug work? When is flecainide used? What
toxicities are associated with flecainide?
19. Propafenone. Mechanism of action. Clinical uses. Adverse effects.
20. Moricizine. Mechanism of action. Clinical uses. Adverse effects.
21. Class II antiarrhythmics – -blockers. State the names of drugs. At
which part of action potential do these drugs work?
22. Sotalol. Mechanism of action. Clinical use.
23. Esmolol. When is this drug used?
24. Class III antiarrhythmics – Potassium channel blockers. Name them.
25. Bretylium. Mechanism of action. Clinical use. Adverse effects.
26. Amiodarone. Mechanism of action. Clinical uses. How is amiodarone
administered? Adverse effects of amiodarone.
27. Class IV antiarrhythmics – Calcium channel blockers. Which drugs
belong to this group?
28. How do they work? What types of arrhythmia are treated with calcium
channel blockers?
29. Major side effects of calcium channel blockers.
30. Other antiarrhythmic agents. Digoxin. How does this drug work? How
does digoxin serve as an antiarrhythmic?
31. How is digoxin used therapeutically? What are toxicities to watch for?
32. Adenosine. How does adenosine work? Describe adenosine’s clinical
role. What are the adverse effects?
33. How can you detect hypokalemia?
Task N 1. Comparison between electrophysiological actions of antiarrythmic
drugs.
Drugs Automaticity Excitability Conduction Effective refractory Contractility
velocity period
SA Ectopic AV Muscle AV Purkinji Muscle
node Foci node tissue node tissue
Quinidine
Lignocaine
Propranolo
l
Bretylium
Verapamil
Task N 2. Comparative characteristic of antiarrhythmic drugs.

Drug Mechanism of antiarrhythmic action Therapeutic uses (indications)
Phenytoin
Procainamide
Amiodarone
Verapamil
Lesson N 22
Topic: “ANTIANGINAL DRUGS”.
Introduction: The coronary arteries supply blood to the heart. With increasing
age atheromatous plaques progressively narrow the arteries, and the obstruction to
blood flow may eventually become so severe that when exercise increases the
oxygen consumption of the heart, not enough blood can pass through the arteries to
supply it. The ischaemic muscle then produces the characteristic symptoms of
angina pectoris, probably because waste products released during muscle
contraction accumulate in the poorly perfused tissue.
The basic aim of drug treatment in angina is to reduce the work of the heart
and hence its oxygen demand.
- Physiological factors that regulate coronary blood flow (physiology);
- Metabolic and physiologic effects of c-AMP, adenosine, c-GMP; role of
adenylatcyclase, guanylatcyclase and adenosindesaminase in the metabolism
(biochemistry).
- Consequences of coronary atherosclerosis (angina, myocardial infarction).
- Myocardial oxygen consumption and coronary blood flow
(pathophysiology).
- Pharmacological properties of beta-blockers, Ca2+–channel blockers
(pharmacology).
OBJECTIVES:
- Angina of effort
- Classic angina
- Atherosclerotic angina
- Vasospastic angina
- Variant angina
- Prinzmetal’s angina
- Coronary vasodilator
- Peripheral vasodilator
- “Monday disease”
- Nitrate tolerance
- Tachyphylaxis
- Unstable angina
- Preload
- Afterload
- List the major determinants of cardiac oxygen consumption.
- List the strategies for relief of anginal pain.
- Contrast the therapeutic and adverse effects of nitrates, beta-blockers, and
calcium channel blockers when used for angina.
- Contrast the effects of medical therapy and surgical therapy of angina.
Main drugs for studying: Glyceryl trinitrate (Nitroglycerin), Isosorbide
dinitrate, Amylnitrite, Nifedipine, Verapamil, Diltiazem, Propranolol, Metoprolol.
Wilkins, 1996. - P. 117-121.
Brothers, 1999. - P. 520-538.
1. What is the definition of angina pectoris?
2. Identify the 3 types of angina. Which type accounts for most angina cases?
3. What is the treatment strategy for angina?
4. What is myocardial oxygen demand dependent upon?
5. Classes of drugs used to treat angina.
6. Why is aspirin useful in treating angina?
7. Nitrates. Classification and their routes of administration.
8. How do nitrates relieve angina? What is the principal physiologic effect of
low doses of nitroglycerin? What happens at higher doses of nitrates?
9. Pharmacokineics of nitroglycerin.
10. Therapeutic uses of nitroglycerin.
11. Does tolerance develop to nitrates? What are the toxicities of nitrates
due to vasodilation? What is nitrate syncope?
12. Calcium channel blockers. Name them. Mechanism of action.
Therapeutic uses. What are the special traits of verapamil?
13. What is the site of action for nifedipine?
14. What are the special traits of diltiazem?
15. How can Ca2+ channel blockers be administered?
16. List the possible toxic effects of the calcium channel blockers.
17. -blockers. What is the role of -blockers in angina?
18. What are the contraindications to the use of these drugs?
19. How do you decide which -blocker to use? Can these drugs be used in
combination?
Task N 1.Comparison between calcium slow channel blockers.
Verapamil Nifedipine Diltiazem
Chemistry
Coronary vasodilatation
Peripheral vasodilatation
Myocardial contractility
Heart rate
Blood pressure
SA and AV nodal function
Antiarrhythmic property
Adverse effects
Task N 2. Characteristic of nitrate’s drug forms.

Name of drug Drug form Duration of action
Short-acting:
Intermediate-acting:
Long-acting:
Task N 3. Side effects of antianginal drugs.

Hypotensio Left Decreased Gastrointestin Bronchoconstricti
n, flushing, ventricula heart rate, al symptoms on
headache r atrioventricul
dysfunctio ar block
n
Beta-
blockers
Nitrates
Diltiazem
Nifedipin
e
Verapami
l
Lesson N 23
Topic: “DIURETICS”.
Introduction: Diuretics are used to reduce oedema in congestive heart failure,
some renal diseases, and hepatic cirrhosis. Some diuretics, notably the thiazides,
are widely used in the treatment of hypertension, but their long-term hypotensive
action is not related to their diuretic properties.
- The structure of the nephron (anatomy).
- Regulation mechanism of diuresis (physiology).
- Pharmacodynamics of theophylline and cardiac glycosides (pharmacology).
OBJECTIVES:
- Bicarbonate diuretic
- Hyperchloremic metabolic acidosis
- Hypokalemic metabolic alkalosis
- Nephrogenic diabetes insipidus
- Potassium-sparing diuretic
- Uricosuric diuretic
- List 5 major types of diuretics and relate them to their sites of action.
- Describe 2 drugs that reduce potassium loss during a sodium diuresis.
- List the major applications and the toxicities of thiazides, loop diuretics, and
potassium-sparing diuretics.
Main drugs for studying: Acetazolamide, Mannitol, Furosemide, Ethacrynic
acid, Hydrochlorothiazide, Indapamide, Spironolactone, Triamterene, Amiloride.
Wilkins, 1996. - P. 143-153.
Brothers, 1999. - P. 556-574.
Pennsylvania, 2001. - P. 223-233.
1. What are diuretics?
2. How do diuretics work?
3. What are their principal sites of action?
4. Name the five major classes of diuretics.
5. Carbonic anhydrase inhibitors. Name them. What is the function of
carbonic anhydrase?
6. How does a carbonic anhydrase inhibitor produce diuresis? How efficient
is the diuresis produced by a carbonic anhydrase inhibitor?
7. Acetazolamide. Route of administration. Clinical uses. Drug’s adverse
effects. Mountain sickness.
8. Name the loop diuretics. Mechanism of action and site of action of these
drugs.
9. Why are the loop diuretics also called “high ceiling diuretics”? Why are
they the most efficacious diuretics?
10. How do loop diuretics affect Ca2+ metabolism? Clinical uses of loop
diuretics. Route of administration. Adverse effects. Forced diuresis.
11. Name the thiazide diuretics. Where do they work? How do they work?
How effective are thiazides?
12. Clinical uses and side effects of thiazides. How do thiazides affect Ca2+
levels?
13. Osmotic diuretics. What are the most commonly used osmotic diuretics?
Mechanism of action and clinical uses of these drugs. Route of administration.
14. What are the toxicities associated with osmotic diuretics?
15. Name the potassium-sparing diuretics. Mechanism of action and efficacy
of these drugs.
16. How does spironolactone work? Clinical indications for the use of
spironolactone.
17. Are there any problems associated with administration of
spironolactone? How does spironolactone differ from triamterene and amiloride?
18. What are the adverse effects of potassium-sparing drugs? Why does
spironolactone cause gynecomastia and impotence?
Task N1. Changes in urinary electrolyte patterns in response to diuretic drugs.
Agents Urinary Electrolyte Patterns
NaCl NaHCO3 K+
Carbonic anhydrase inhibitors
Loop agents
Thiazides
K+-sparing agents
Task N 2. Compare Thiazides and Frusemide.

Features Thiazide Frusemide
1. Site of action
2. Onset of action
4. Potency
5. Use
6. Antihypertensive effect
7. Ototoxicity
8. In diabetes insipidus
9. Oedema of chronic renal failure
Lesson N 24
Topic: “ANTIHYPERTENSIVE DRUGS”.
Introduction: High blood pressure is associated with decreased life expectancy

and increased risk of stroke, coronary heart disease and other end-organ disease
(e.g. retinopathy, renal failure). Lowering the blood pressure of patients with a
diastolic blood pressure of above 90 mmHg and systolic BP greater than 140
mmHg decreases mortality and morbidity. In some patients with mild
hypertension, weight reduction, if appropriate, reduced alcohol consumption and
moderate reduction in salt consumption may be sufficient, but usually drug
treatment is required.
- Control of vascular smooth muscle tone (regulation of Ca 2+, the role of the
renin-angiotensin system).
- Define hypertension. How can hypertension be categorized?
(pathophysiology).
- Causes of hypertension (etiology). Potential complications of hypertension.
- Hydraulic equation for blood pressure (BP).
- Pharmacodynamics and pharmacokinetics of ganglionic blockers,
antiadrenergic drugs, diuretics, Ca2+ channel blockers.
OBJECTIVES:
- Baroreceptor reflex
- Calcium channel blockade
- Catecholamine pump
- End-organ damage
- Essential hypertension
- False transmitter
- Malignant hypertension
- Orthostatic hypotension
- Postganglionic neuron blocker
- Rebound hypertension
- Reflex tachycardia
- Reuptake of transmitter
- Stepped care
- Sympatholytic, sympathoplegic
- Transmitter vesicle
- Vasomotor center
- List the 4 major groups of antihypertensive drugs and give examples of
drugs in each group.
- Describe the homeostatic responses to each of the 4 major types of
antihypertensive drugs.
- List the major sites of action of sympathoplegic drugs and give examples of
drugs that act at each site.
- List the major toxicities of the prototype antihypertensive agents.
- Describe the reasons for the low incidence of detection of hypertension and
the inadequate compliance of patients with treatment regimes once hypertension is
diagnosed.
Main drugs for studying: Hydrochlorothiazide, Furosemide, Methyldopa,
Clonidine, Guanabenz, Trimethaphan, Hexamethonium, Mecamylamine,
Guanethidine, Guanadrel, Reserpine, Prazosin, Terazosin, Propranolol, Metoprolol,
Atenolol, Labetalol, Hydralazine, Minoxidil, Verapamil, Nifedipine, Nitroprusside,
Captopril, Saralasin, Enalapril, Lisinopril.
Wilkins, 1996. - P. 121-131,186-187.
Brothers, 1998. - P. 539-555.
Pennsylvania, 2001. - P. 179-191.
1. Approaches to the treatment of hypertension.
2. What are the major classes of drugs used to treat hypertension?
3. Sympatholytic agents. Centrally acting: Methyldopa, Clonidine, and
Guanfacine. Mechanism of action, pharmacological effects, route of
administration. Clinical indications. Potential toxicities. What drug interactions
should the physician be concerned about?
4. Name -blockers, which are used as antihypertensives. How do they
work? Pharmacological effects of these drugs. Clinical uses. Adverse effects.
5. -blockers. Classification. Mechanism of antihypertensive action. Clinical
uses. Adverse effects. Contraindications.
6. Ganglionic blockers. Name them. Clinical use. Adverse effects.
7. Postganglionic adrenergic neuronal blockers (reserpine, guanethidne).
Mechanism of action. Clinical role in hypertension. Side effects.
8. Diuretics. What types of diuretics are chosen most frequently to control
hypertension? How are diuretics used therapeutically?
9. Adverse effects of diuretics.
10. Vasodilators. Hydralazine, Minoxidil, Sodium nitroprusside, Diazoxide.
Mechanism of action. Clinical uses. Route of administration. Adverse effects.
11. Calcium channel blockers. Name them. Mechanism of action.
12. Clinical indications. Adverse effects.
13. ACE inhibitors. Which physiologic system are ACE inhibitors effective
against? Explain this system.
14. Name ACE inhibitors. How do they work? Therapeutic uses.
15. Describe the absorption of captopril. How is captopril eliminated?
16. Adverse effects of ACE inhibitors. Should ACE inhibitors be
administered to pregnant women?
17. What drug interactions should the physician monitor while administering
ACE inhibitors?
18. Angiotensin II receptor antagonists: Losartan and Valsartan. Mechanism
of action of these drugs. Route of administration.
19. How are these drugs used clinically? Adverse effects. Contraindication.
20. What is malignant hypertension? How is this condition treated?
Task N 1. Comparative characteristics of antihypertensive drugs.
Drugs Mode of action Therapeutic uses Adverse effects
Thiazide diuretics
Propranolol
Captopril
Nifedipine
Prazosin
Lesson N 25
Topic: “ ANTICOAGULANT, FIBRINOLYTIC, AND ANTIPLATELET
DRUGS”.
Introduction: Bleeding and thrombosis are altered states of hemostasis.

Impaired hemostasis results in spontaneous bleeding; stimulated hemostasis results
in thrombus formation. The drugs used to arrest bleeding and to inhibit thrombosis
are the subjects of this lesson.
- Define the term thrombus.
- What causes a thrombus?
- What are the two major pathways of coagulation cascade, and what activates
each?
- What is the function of the fibrinolytic system?
- What is the role of plasmin in the fibrinolytic system?
- Notion about platelet aggregation inductors (thromboxane A2 etc.) and
inhibitors (PG etc.).
- Thromboembolism (pathophysiology).
- Action of the aspirin, dipyridamole, propranolol, verapamil, nitroglycerine,
clonidine, sodium nitroprusside, papaverine, xanthines on the blood coagulation
(pharmacology).
OBJECTIVES:
- Clotting cascade
- Coumarin derivates
- Embolism
- Extrinsic pathway
- Intrinsic pathway
- Thrombosis
- Vitamin K-dependent factors
- Compare the oral anticoagulants with heparin in terms of their
pharmacokinetics, mechanisms, and toxicities.
- Compare the 4 thrombolytic preparations.
- Compare the antiplatelet drugs.
- List 3 different drugs used to treat disorders of excessive bleeding.
Main drugs for studying: Heparin, Warfarin, Streptokinase, Tissue
plasminogen activator (tPA, alteplase), Urokinase, Aspirin, Dipyridamole,
Sulfinpyrazone, Phytonadione (vitamin K1), Aminocaproic acid, Tranexamic acid.
Wilkins, 1996. - P. 131-132,179-182.
Brothers, 1999. - P. 595-615.
Pennsylvania, 2001. - P. 193-204, 446-448.
1. Classification of anticoagulants.
2. Heparin. Does heparin exist normally within the body? How does heparin
work? What are heparin’s indications? What are the limitations of heparin? Route
of administration.
3. What measure is used to monitor the actions of heparin – prothrombin
time (PT) or activated partial thromboplastin time (a PTT)?
4. Is heparin safe to use in pregnant women?
5. What adverse effects should you watch for when administering heparin?
6. How do you counteract the effects of heparin?
7. What are the contraindications to the administration of heparin?
8. Warfarin. How is warfarin different from heparin? What is warfarin’s
mechanism of action? Describe warfarin’s onset of action. When would you use
this drug? Can you use this drug in pregnant women? What drugs potentiate the
actions of warfarin? What is the principal toxicity of warfarin? How do you reverse
the actions of warfarin?
9. Fibrinolytics. Name them. Do fibrinolytics distinguish between beneficial
hemostatic plugs and unwanted thrombi? How are all fibrinolytics administered?
10. Streptokinase. How does it work? Therapeutic uses. What are the
toxicities of streptokinase?
11. Urokinase. How does it work? Therapeutic use. Adverse effects.
12. Tissue plasminogen activator (TPA). What is the major advantage of
TPA over other thrombolytics? What are the indications for this agent? State its
adverse effects. How do you reverse the actions of streptokinase, urokinase, and
TPA?
13. Antiplatelet drugs. What is the action of the antiplatelet drugs?
14. Aspirin. Mechanism of action. What is aspirin’s role in anticoagulating a
patient?
15. State aspirin’s adverse effects.
16. Ticlopidine. Mechanism of action. Uses, adverse effects of this drug.
17. Dipyridamole. Mechanism of action, its uses and adverse effects.
18. Sulfinpyrasone. Mechanism of action, its uses. State the adverse effects.
Task N 1. Drugs affecting blood.
Group of drugs Names of drugs Mechanism of action Clinical use Side effects
Anticoagulant
Antiplatelet
Fibrinolytics
Antifibrinolytics
Task N 2. Comparative aspects of heparin and oral anticoagulants.

Heparin Warfarin
2. Onset of action
4. Activity
5. Mechanism of action
6. Antagonist
7. Lab. Control
8. Use
Topic:“AGENTS USED TO TREAT ANEMIA”.

- Define anemia. Types of anemia.
- Name the major categories of anemia.
- Iron turnover and balance.
- What is the function of vitamin B12?
- What is the physiologic function of folic acid?
OBJECTIVES:
- Colony-stimulating factor
- Erythropoietin
- Hemolytic anemia
- Hypochromic anemia
- Intrinsic factor
- Megaloblastic anemia
- Pernicious anemia
- Transferrin
- Describe the normal mechanism of regulation of iron stored in the body.
- List the major forms of iron used in the therapy of anemias.
- List the anemias for which iron supplementation is indicated and those for
which it is contraindicated.
- Describe the acute and chronic toxicity of iron.
- Describe the clinical applications of vitamin B12 and folic acid.
- Describe the major hazard involved in the use of folic acid as sole therapy
for megaloblastic anemia.
Main drugs for studying: Ferrous sulfate, Ferrous gluconate, Ferrous
fumarate, Iron dextran, Cyanocobalamin, Pteroylglutamic acid, Erythropoietin,
Filgrastim, Sargramostin.
Wilkins, 1996. - P. 157-167.
Brothers, 1999. - P. 580-594.
Pennsylvania, 2001. – P. 204-206.
1. Iron. What type of anemia is caused by iron deficiency? What are the
major causes of iron deficiency?
2. How is iron distributed in the body?
3. What are the reasons for administering iron?
4. What form of iron is administered?
5. What are the toxicities of iron?
6. How do you treat acute iron intoxication?
7. How do you manage chronic iron intoxication?
8. Cyanocobalamin (vitamin B12). What is necessary for the absorption of
vitamin B12? Is vitamin B12 stored within the body?
9. What are the three most common causes of B12 deficiency? What
symptoms are caused by vitamin B12 deficiency?
10. Therapeutic use of vitamin B12. Route of administration. Toxicity.
11. Folic acid. Clinical indications. Is folate stored in the body as much as
vitamin B12 is?
12. What are the most common causes of folate deficiency?
13. How is folic acid administered?
14. What is the toxicity of folic acid?
15. Erythropoietin. When do you use it? What is its toxicity?
Lesson N 26
Topic: Final lesson N 3 “DRUGS WHICH INFLUENCE ON THE
EXECUTIVE ORGANS”.
pharmacological group:
1. Classification.
7. Symptoms and management (treatment) of heparin, warfarin, nitrates,
quinidine and digitalis intoxications.
Lesson N 27
Topic: “SULFONAMIDES AND TRIMETOPRIM. BETA-LACTAM
ANTIBIOTICS (PENICILLINS, CEFALOSPORINS) ”.
Introduction: The sulphonamides were the first drugs found to be effective in
the treatment of systemic infections. However, they are now of little importance
because of the development of more effective agents those are less toxic. Also,
many organisms have developed resistance to sulphonamides. Their principal use
alone is in the treatment of urinary tract infections caused by sensitive Gram-
positive or Gram-negative organisms.
Penicillins and cephalosporins are large groups of drugs that share features of
chemistry, mechanism of action, pharmacologic and clinical effects, and
immunologic characteristics. These drugs are referred to as beta-lactam drugs or
cell wall inhibitors. Cephalosporins have traditionally been divided into three
major groups or “generations”, depending mainly on microbiologic spectrum of
activity. All cephalosporins are inactive against enterococci and methicillin-
resistant staphylococci.
- notion about antibiosis, antibiotics, methods of the bacterial sensitivity
determination to antibiotics;
- notion about chemotherapy, infectious diseases and agents of them
(microbiology).
- role of folic acid, PABA, methemoglobinreductase and glucoso-6-
phosphatedehydrogenase (biochemistry).
OBJECTIVES:
- Antimicrobial chemoprophylaxis
- Antimicrobial synergism and antagonism
- Empiric (presumptive) therapy
- Susceptibility testing
- Dihydropteroate synthetase
- Dihydrofolate reductase
- Selective toxicity
- Bacteriostatic
- Bactericidal
- Bacterial resistance
- Beta-lactam ring structure
- Penicillin-binding proteins
- Peptidoglycan chains
- Beta-lactamase enzyme activity
- Hypersensitivity reactions
- Superinfection
- Describe 4 different mechanisms of action of antimicrobial drugs.
- Classify the major antimicrobial drug groups in terms of their mechanism of
action.
- List 4 different mechanisms by which microorganisms become resistant to
drugs.
- Identify the major mechanisms responsible for resistance to the
antimicrobial drugs commonly used in clinical settings.
- Describe the mechanisms of action of sulfonamides and trimethoprimon
bacterial folic acid synthesis.
- Describe the mechanisms of resistance to sulfonamides and trimethoprim.
- List the major clinical uses of sulfonamides and trimethoprim, singly and in
combination.
- Indicate the major pharmacokinetic features of sulfonamides and
trimethoprim.
- Describe the adverse effects of sulfonamides and trimethoprim.
- Describe the mechanism of antibacterial action of beta-lactam antibiotics.
- Describe the mechanisms underlying the resistance of bacteria to beta-
lactam antibiotics.
- Identify the important drugs in each subclass of penicillins and describe their
antibacterial activity and clinical uses.
- Identify the 3 subclasses of cephalosporins and describe their antibacterial
activities and clinical uses.
- List the major adverse effects of the penicillins and the cephalosporins.
- Identify the important features of aztreonam and imipenem.
Main drugs for studying: Penicillin V, Penicillin G, Methicillin, Nafcillin,
Oxacillin, Dicloxacillin, Ampicillin, Carbenicillin, Amoxicillin, Ticarcillin,
Azlocillin, Cephalothin, Cefazolin, Cephradine, Cephrapirin, Cefamandole,
Cefoclor, Cefoxitin, Cefuroxime, Cefoperazone, Cefotaxime, Ceftazidime,
Moxalactam, Sulfisoxazole, Sulfamethoxazole, Sulfacetamide, Sulfasalazine,
Mafenide, Sulfadiazine, Trimethoprim, Pyrimethamine.
Wilkins, 1996. - P. 281-294.
Brothers, 1999. - P. 671-693, 700-717.
Pennsylvania, 2001. - P. 239-309.
1. Critical factors that determine the selection of an antimicrobial drug.
2. Classes of antimicrobial agents according to their mechanisms of action.
3. Which drugs are bactericidal?
4. Which drugs are considered bacteriostatic?
5. Basic mechanisms by which microorganisms can become resistant to
antibiotics. Give an example of each.
6. Describe the structure of a sulfonamide compound.
7. How do sulphonamides (SAs) work?
8. Name the sulfonamides (according to duration of action).
9. Are sulfonamides bactericidal?
10. Antimicrobial spectrum of sulfonamides.
11. Routes of sulfonamides administration and absorption for these drugs.
12. Do sulfonamides enter the CNS?
13. How are sulfonamides used clinically?
14. How are sulfonamides metabolized?
15. What toxicities should you watch for when prescribing SAs to your
patients?
16. Should pregnant women be given SAs?
17. How does resistance to SAs occur?
18. How does trimetoprim work?
19. Co-trimoxazole. Clinical uses. Can this drug be used for chancroid,
shigellosis, typhoid fever (due to Salmonella typhi), and nocardiosis?
20. Adverse effects of co-trimoxazole.
21. Mechanism of action of penicillins.
22. Do penicillins enter the CNS?
23. Structural features of -lactam antibiotics. Structure-activity
relationship.
24. How are the penicillins classified?
25. Name natural penicillins and their routes of administration.
26. What can natural penicillins be used for?
27. Describe the absorption of penicillins. Time of administration.
28. Routes of excretion of penicillins.
29. What are the most common adverse effects seen with patients who are
medicated with all penicillins?
30. Name penicillinase-resistant penicillins (antistaphylococcal penicillins)
and their routes of administration.
31. When do you use penicillinase-resistant penicillins?
32. Toxicity of antistaphyloccal penicillins.
33. Name antipseudomonal penicillins and their routes of administration.
34. Are these drugs inactivated by penicillinase?
35. What is their antimicrobial spectrum?
36. Toxicity with ticarcillin and carbenicillin.
37. Name extended-spectrum penicillins.
38. What organisms can ampicillin and amoxicillin be used against?
39. Are these drugs inactivated by -lactamase?
40. Toxicity of ampicillin.
41. With what other agents are these two drugs often combined?
42. lactamase inhibitors.
43. Mechanism of action of cephalosporins.
44. How are cephalosporins subdivided?
45. How do the characteristics of cephalosporins change from first to third
generation agents?
46. Which organisms are first-generation cephalosporins active against?
47. Name first-generation cephalosporins and routes of drug administration
for each.
48. Name second-generation cephalosporins and state the route of
administration of each.
49. What infections can be treated with second-generation cephalosporins?
50. Name third-generation cephalosporins and their routes of administration.
51. Against what organisms to these agents exert action?
52. What are all cephalosporins inactive against?
53. What are the adverse effects of the cephalosporins?
54. Mechanism of action of the monobactams (aztreonam)?
55. Clinical indications for aztreonam.
56. Adverse effects of aztreonam.
57. Carbapenems (Imipenem). Antibacterial spectrum of this drug.
58. Imipenem’s adverse effects.
59. Vancomycin. Mechanism of action.
60. Antibacterial spectrum, route of administration and adverse effects of
vancomycin.
61. Bacitracin. Antimicrobial spectrum, mechanism of action, usual route of
administration, adverse reactions.
62. Cycloserine. Mechanism of action, clinical indications and its toxicities.
Task N 1. Compare the antimicrobial drugs:
Drug Drug’s Pharmacological Antimicrobial Mechanism of
form group spectrum antimicrobial action
Methicillin
Cefalotin
Vancomycin
Aztreonam
Sulfadimethoxin
Lesson N 28
Topic: “PROTEIN SYNTHESIS INHIBITORS (Tetracyclines, Macrolides,
Polypeptides, Aminoglycosides). QUINOLONES ”.
Introduction: The aminoglycosides are valuable drugs in the treatment of

severe infections, but are likely to produce nephrotoxic and ototoxic effects. The
tetracyclines are wide-spectrum antibiotics, but increasing bacterial resistance has
reduced their usefulness. Macrolides have a similar antibacterial spectrum to
benzylpenicillin. Chloramphenicol is effective against a wide range of organisms,
but serious side effects (e.g. aplastic anaemia) restrict its use. Important properties
of the quinolones are their good penetration into tissues and cells, their
effectiveness when given orally, and their relatively low toxicity.
- material of the previous class on Pharmacology.
OBJECTIVES:
- Broad-spectrum agent
- Aminoacyl-tRNA
- Gray baby syndrome
- Peptidyltransferase
- Superinfection
- 30S ribosomal subunit
- Ototoxicity
- DNA gyrase
- Describe the mechanisms of action of chloramphenicol and tetracyclines.
- Describe the mechanisms responsible for clinical bacterial resistance.
- List the major clinical uses of these drugs.
- Describe the pharmacokinetic features of these agents that are relevant to
their clinical use.
- List the main toxic effects of these drugs.
- Describe the probable mechanism of action of aminoglycoside antibiotics
and the mechanism by which bacterial resistance to this class of drugs occurs.
- List the major clinical applications of aminoglycosides and describe their
main toxic effects.
- Describe the pharmacokinetics of this drug class, with special reference to
the importance of renal clearance and its relationship to toxicity.
- Describe the mechanism of action, clinical uses, and major toxic effects of
polymyxins.
- Describe the mechanisms of antibacterial action of clindamycin,
erythromycin, fluoroquinolones, and vancomycin.
- Describe the clinical uses of clindamycin, erythromycin, fluoroquinolones,
and vancomycin; the significant features of their biodisposition; and their main
toxic effects.
Main drugs for studying: Chloramphenicol, Tetracycline, Demeclocycline,
Doxycycline, Minocycline, Gentamicin, Tobramycin, Amikacin, Netilmicin,
Streptomycin, Neomycin, Kanamycin, Spectinomycin, Polymyxin B, Colistin
(polymyxin E), Erythromycin, Azithromycin, Lincomycin, Clindamycin,
Vancomycin, Ciprofloxacin, Norfloxacin, Nalidixic acid, Cinoxacin.
Wilkins, 1996. - P. 294-304.
Brothers, 1999. - P. 693-699, 718-751.
Pennsylvania, 2001. - P. 311-329, 456.
1. How do protein synthesis inhibitors work?
2. Why don’t protein synthesis inhibitors work on eukaryotic cells?
3. Which antibiotics work on the bacterial 30S ribosomal subunit?
4. Which antibiotics work on the bacterial 50S ribosomal subunit?
5. Name aminoglycosides.
6. What is the mechanism of action of aminoglycosides?
7. Pharmacokinetics of aminoglycosides.
8. Routes of these drugs administration.
9. Therapeutic uses of aminoglycosides.
10. Are there any toxicities with the aminoglycosides?
11. Name tetracyclines.
12. Mechanism of action of the tetracyclines.
13. What is the antimicrobial spectrum of the tetracyclines?
14. How are the tetracyclines administered?
15. Adverse effects of tetracycline administration.
16. Contraindications to the use of tetracyclines.
17. Mechanism of action of chloramphenicol.
18. What is chloramphenicol effective against?
19. Are there adverse reactions of chloramphenicol?
20. Name macrolides.
21. How do macrolides work?
22. What are the clinical indications of macrolides?
23. Difference between erythromycin’s antibacterial activity and that of
clarythromycin and azythromycin.
24. Routes of administration of macrolides.
25. Adverse effects associated with the macrolides.
26. Lincosamides (lincomycin, clindamycin).
27. Mechanism of action of lincomycin, clinical uses, side effects, routes of
administration.
28. Spectinomycin. Mechanism of action, clinical uses, route of
administration, side effects.
29. Why do the quinolones (Nalidixic acid, Cinoxacin) have limited use?
30. Name fluoroquinolones.
31. What are the advantages of fluoroquinolones over quinolones?
32. Mechanism of action of fluoroquinolones.
33. Distribution of the fluoroquinolones.
34. What is the antimicrobial activity of the fluoroquinolones?
35. Major uses of fluoroquinolones.
36. Adverse effects of fluoroquinolones.
37. Can fluoroquinolones be used in children?
38. Routes of drug administration of fluoroquinolones.
39. Possible new antibacterial drugs.
Task N 1. Characteristics of protein synthesis inhibitors. Fill in the chart.
Drug Antimicrobial spectrum Mechanism of action Indications Side effects
Doxycycline
Streptomycin
Erythromycin
Polymyxine
Ciprofloxacin
[M.B.1][M.B.2][M.B.3][M.B.4][M.B.5][M.B.6]
Lesson N 29
Topic: “ANTIFUNGAL DRUGS”.
Introduction: Fungal infections (mycoses) may be superficial (affecting skin,

nails, scalp or mucous membrane) or systemic (affecting deeper tissues and
organs).
The need for better antifungal drugs has been made more pressing by the
greatly increased incidence of local and disseminated fungal infections in
immunodeficient patients (acquired immunodeficiency syndrome (AIDS) patients,
corticosteroids, anticancer drugs).
- structure of a fungus;
- notion about pathogenic fungi (biology);
- basic notions about synthesis and role of the sterols in the functions of organ
cells (biochemistry).
OBJECTIVES:
- Describe the probable mechanisms of action of griseofulvin and the
antifungal agents for systemic infections.
- Describe the clinical uses and pharmacokinetics of amphotericin B,
flucytosine, fluconazole, griseofulvin, and ketoconazole.
- Indicate the major toxic effects of systemic antifungal drugs and
griseofulvin.
- Identify the main topical antifungal agents.
Main drugs for studying: Amphotericin B, Flucytosine, Fluconazole,
Ketoconazole, Griseofulvin, Nystatin, Miconazole, Clotrimazole, Tolnaftate.
Wilkins, 1996. - P. 304-309.
Brothers, 1999. - P. 770-780.
Pennsylvania, 2001. - P. 337-343.
1. Name drugs used for systemic and subcutaneous mycoses.
2. Amphotericin B. Mechanism of action. Does amphotericin B bind to
cholesterol?
3. Does amphotericin B enter the CNS? Pharmacokinetics. Route of
administration. Antifungal spectrum. Clinical role. Adverse effects.
4. Flucytosine. When is it used? Mechanism of action. Antifungal spectrum.
How is flucytosine usually administered? Pharmacokinetics of flucytosine.
Toxicities of this drug.
5. Ketoconazole. Mechanism of action. Antifungal spectrum. How is this
drug administered? Pharmacokinetics. Major toxicities. Can ketoconazole and
amphotericin B be used together?
6. Fluconazole. What are the major advantages of fluconazole over
ketoconazole? Therapeutic uses. Side effects.
7. Itraconazole. Therapeutic uses. Adverse effects.
8. Name drugs used to treat superficial mycotic infections.
9. Griseofulvin. Mechanism of action. Antifungal spectrum of this drug.
Pharmacokinetics. State the drug’s adverse effects.
10. Nystatin. Its structure, route of administration. Therapeutic uses.
11. Miconazole, clotrimazole and econazole. Route of administration for
these drugs. Indications for use. What are pharmacological properties of these
drugs?
12. Potential new antifungal therapies.
Task N 1. Outline of the uses of antifungal drugs.
Disease Drugs used
Systemic infections
Systemic candidiasis
Cryptococcosis (meningitis)
Systemic aspergillosis
Blastomycosis
Histoplasmosis
Coccidiomycosis
Disseminated sporotrichosis
Superficial infections
Dermatomycosis
Candidiasis
Skin
Mouth (thrush)
Vagina
Chronic mucocutaneous candidiasis
Topic: “ANTIVIRAL DRUGS”.
Introduction: Viruses are intracellular parasites that lack independent

metabolism and can replicate only within living host cells. Since their replication
cycle is so intimately connected with the metabolic processes of the host cell, it has
proved extremely difficult to produce drugs that are selectively toxic to viruses.
For this reason, vaccines have been the main method for controlling viral
infections (e.g. poliomyelitis, rabies, yellow fever, measles, mumps, rubella).
Some effective antiviral drugs have been produced and although they are of limited
use, they have transformed the treatment of several diseases, notably those caused
by herpes virus infections.
- Define virus.
- Structural components of a virus particle.
- Examples of pathogenic viruses (DNA and RNA viruses).
- What is viral uncoating?
- Steps in viral replication.
- What pathogens are included in the herpes virus family?
- Define acquired immunodeficiency syndrome (AIDS).
- How does HIV differ from other viruses?
OBJECTIVES:
- Identify the main steps in viral replication.
- Describe the mechanisms of antiviral actions of purine and pyrimidine
antimetabolites (idoxuridine, vidarabine, acyclovir, and azidothymidine),
amantadine, and the interferons.
- Describe the clinical uses of the antimetabolites, amantadine, and the
interferons and list the toxic effects of drugs that are used systemically.
- Identify the newer antiviral drugs dideoxyinosine, disoxaril, foscarnet,
ganciclovir, and ribavirin.
Main drugs for studying: Idoxuridine, Trifluorothymidine, Cytarabine,
Acyclovir, Vidarabine, Azidothymidine, Dideoxyinosine, Ganciclovir, Ribavirin,
Amantadine, Rimantadine, Immune globulin, Interferon.
Wilkins, 1996. - P. 315-319, 321-323.
Brothers, 1999. - P. 781-788.
Pennsylvania, 2001. - P. 363-371, 457-463.
1. Can all viruses be pharmacologically treated?
2. Name drugs used to treat herpes virus infection.
3. Acyclovir. Mechanism of action. Therapeutic uses. Route of
administration. Metabolism. Adverse effects.
4. Ganciclovir. Mechanism of action. Clinical indications. Pharmacokinetics.
Adverse effects.
5. Idoxuridine. Mechanism of action. Clinical uses. Route of administration.
Adverse effects.
6. Trifluridine. Therapeutic use.
7. Vidarabine. Mechanism of action. Clinical use. Route of administration.
Metabolism. Adverse effects.
8. Foscarnet. Mechanism of action. Route of administration. Clinical use.
Metabolism. Adverse effects.
9. Which drugs are used in the treatment of respiratory viruses?
10. Amantadine and Rimantadine. Mechanism of action. Therapeutic use.
Route of administration. Metabolism. Adverse effects.
11. Ribavirin. Mechanism of action. Therapeutic uses. Route of
administration. Adverse effects. Should this drug be used in pregnant women?
12. Interferons. Therapeutic uses. Adverse effects.
13. Drugs used to treat HIV infection and AIDS.
14. Reverse transcriptase inhibitors (Zidovudine, Didanosine, Zalcitabine,
Stavudine). Mechanism of action of these drugs. Side effects.
15. Protease inhibitors (Saquinavir, Ritonavir, Indinavir, Nelfinavir).
Mechanism of action. Side effects.
16. Possible future developments in antiviral therapy.
Task N 1. Comparative characteristic of antiviral drugs.
Drug Mechanism of action Therapeutic uses Adverse effects
Acyclovir
Vidarabine
Amantadine
Zidovudine
Saquinavir
Topic: “DRUGS USED TO TREAT TUBERCULOSIS AND LEPROSY”.
Introduction: The incidence of tuberculosis has been increasing because the

disease can occur in patients with AIDS and in the homeless.
- Which organism causes TB?
- Which organism causes leprosy?
- Basic properties of Mycobacterium tuberculosis (microbiology).
- Principles of chemotherapy, mechanism and spectrum of rifampin’s and
streptomycin’s antimicrobial action, their adverse effect (pharmacology).
OBJECTIVES:
- Describe the special problems of chemotherapy for mycobacterial infections.
- Describe the pharmacodynamic and pharmacokinetic properties of the first-
line drugs used in tuberculosis (isoniazid, ethambutol, pyrazinamide and rifampin).
- identify the second-line drugs used in tuberculosis and describe their
limitations.
- identify the drugs used in leprosy and describe their toxic effects.
Main drugs for studying: Isoniazid, Ethionamide, Pyrazinamide, Rifampin,
Ethambutol, Streptomycin, Aminosalicylic acid, Cycloserine, Capreomycin,
Dapsone, Clofazimine, Amithiozone.
Wilkins, 1996. – Р. 309-314.
Brothers, 1999. - P. 752-769.
3. Harvey R.A., Champe P.C.: Lippincot’s Illustrated Reviews:
1. What makes tuberculosis (TB) difficult to treat? Why is TB treated with
multiple drugs?
2. First-line pharmacological treatment options for tuberculosis.
3. Isoniazid. How does this drug work? Route of administration. Distribution,
metabolism. State isoniazid’s adverse effects. When is isoniazid given alone? Can
you use isoniazid in pregnant women?
4. Rifampin. Mechanism of action. Pharmacokinetics (absorption,
distribution, metabolism). Therapeutic uses. Adverse effects.
5. Pyrazinamide. When is this drug used? Absorption and distribution of this
drug. Adverse effects.
6. Ethambutol. Absorption and distribution of the drug. Is this drug
bacteriostatic or bactericidal? Adverse effects.
7. Streptomycin. What is the classification of this drug? What is its
mechanism of action? Adverse effects.
8. Treatment strategy for the initial treatment of active TB.
9. Name second-line agents used in the treatment of TB. Why are these drugs
second-line agents?
10. What are the pharmacological treatment options for leprosy?
11. Dapsone. How does dapsone work? Route of administration. Metabolism
of this drug. How is it used? Adverse effects.
12. Clofazimine. Mechanism of action. When is clofazimine used? Adverse
effects.
Task N 1. Characteristic of antitubercular drugs.
Drug Mechanism of action Adverse effects Prevention of adverse effects
Isoniazid
Ethambutol
Pyrazinamide
Streptomycin
Rifampin
Lesson N 30
Topic: “ DRUGS ACTING ON PARASITES”.
Introduction: Only a few parasitic diseases are common in Great Britain (e.g.
threadworms, giardiasis); but in tropical and subtropical areas, where abundant
water and high temperatures provide an optimal environment for the larvae and
intermediate vector hosts (e.g. mosquitoes), parasitic diseases are common and
widespread. Overcrowding, malnutrition and lack of sanitation facilitate the spread
of disease and as many 1000 million people may be infected with parasites. Drugs
play an important role in the treatment and control of parasitic diseases.
ANTIPROTOZOAL DRUGS.
- What are the protozoa?
- Which organism causes malaria?
- Which plasmodium species infect humans?
- What is the vector of transmission?
- Notion about infection carrier (transmitting agent) and agents (stimuli) of
infectious diseases: malaria, amebiasis, lambliasis (giardiasis), toxoplasmosis,
leishmaniasis, trichomoniasis, balantidiasis.
OBJECTIVES:
- Amebicides
- Schizonticide
- Hypnozoite
- Gametocide
- Sporonticide
- List the major groups of antiprotozoal drugs.
- Describe the main pharmacodynamic and pharmacokinetic properties of the
antimalarial drugs (chloroquine, quinine, primaquine, and the antifolate agents).
- Describe the main pharmacodynamic and pharmacokinetic properties of the
amebicides (diloxanide, emetine, iodoquinol, and metronidazole). List other
clinical applications of nitroimidazoles.
- Identify the main trypanosomicidal drugs and list their toxic effects.
Main drugs for studying: Quinine, Mefloquine, Chloroquine, Primaquine,
Pyrimethamine, Emetine, Diloxanide furoate, Metronidazole, Sodium
stibogluconate, Pentamidine, Suramin.
Wilkins, 1996. – Р. 315.
Brothers, 1999. - P. 789-815.
Pennsylvania, 2001. - P. 345-357.
1. How are antimalarial drugs differentiated?
2. What are the five stages in the Plasmodium life cycle?
3. Which Plasmodium species have a dormant hepatic (hypnozoite) stage that
causes recurrent infections and relapses?
4. Classification of antimalarial drugs.
5. Chloroquine. Mechanism of action. Route of administration. How is
chloroquine distributed and metabolized? Major clinical uses. Adverse effects.
6. Quinine. Mechanism of action. Route of administration. How is quinine
metabolized? Clinical uses. Adverse effects. What is a rare complication that can
occur in patients who have been sensitized to quinine?
7. Mefloquine. How does this drug work? Route of administration. How is
mefloquine distributed and metabolized? Clinical use, its adverse effects.
8. Pyrimethamine. Mechanism of action. Route of administration. How is
this drug metabolized? Clinical use. Adverse effects.
9. Fansidar. Clinical use.
10. Chloroguanide. Mechanism of action. Route of administration. How is it
metabolized? Clinical use. Adverse effects.
11. Primaquine. Mechanism of action. Route of administration. How is the
drug metabolized? Clinical use. Is primaquine effective in treating acute attacks?
Adverse effects of primaquine.
12. Toxoplasmosis. Treatment of choice.
13. Leishmaniasis. Drug of choice for the treatment of both mucocutaneous
and visceral leishmaniasis. How does this drug work? Route of administration.
How is this drug metabolized? Adverse effects.
14. What are alternative agents for the treatment of leishmaniasis?
15. What drugs are used to treat trichomoniasis?
16. What drugs are used to treat trypanosomiasis?
17. Melarsoprol (Mel B). Mechanism of action. Route of administration.
How is it distributed and metabolized? Clinical use. Adverse effects.
Contraindications.
18. Pentamidine. How does this drug work? Route of administration,
distribution, metabolism. Major clinical uses for pentamidine. List the adverse
effects.
19. Nifurtimox. How does this drug work? Route of administration,
metabolism. Clinical use. Adverse effects.
20. Suramin. How does this drug work? Route of administration. Clinical
uses. Adverse effects.
21. Amebiasis. Drugs for treatment of amebiasis.
22. Metronidazole. Mechanism of action. Route of administration.
Distribution, metabolism. Clinical uses. Adverse effects. Is metronidazole safe for
pregnant women?
23. Diloxanide furoate. Route of administration. Metabolism. Clinical use.
Adverse effects. Contraindications.
24. Emetine and dehydroemetine. Mechanism of action. Distribution,
metabolism. Clinical use. Adverse effects.
25. New approaches to antiprotozoal therapy.
Task N 1. Drugs used for treatment and chemoprophylaxis of malaria.
Infections Drugs for the treatment of Drugs for
the clinical attack chemoprophylaxis
All plasmodial infections except
chloroquine-resistant P.falciparum
Infection with chloroquine-resistant
P.falciparum
Task N 2. Give drugs used:

- To prevent transmission;
- To effect radical cure;
- To treat the acute attack;
- For chemoprophylaxis.
Task N 3. Fill in the chart:
Drug Pharmacotherapeutic activity
Emetine
Metronidazole
Leishmaniasis
Trypanosomiasis
Fansidar
Topic: “ANTHELMINTIC DRUGS”.

- What is a helminth?
- Types of helminthes (biology).
- Names of helminthiasis, notion about dehelminthization.
OBJECTIVES:
- Identify the drugs of choice for treatment of common infections caused by
nematodes, trematodes, and cestodes.
- Describe the mechanisms of action (if known), important pharmacokinetic
features, and major toxic effects of these drugs.
Main drugs for studying: Pyrantel pamoate, Mebendazole, Thiabendazole,
Diethylcarbamazine, Ivermectin, Praziquantel, Niclosamide.
Wilkins, 1996. - P. 314.
2. Tripathi K.D.: Essentials of Medical Pharmacology, 4/e. New Delhi, Jaypee
Brothers, 1999. - P. 816-824.
Pennsylvania, 2001. - P. 359-362.
1. Name drugs used predominantly in the treatment of nematodes.
2. Name drugs used predominantly in the treatment of cestodes and
trematodes.
3. Mebendazole. What infections are treated with mebendazole? Mechanism
of action, route of administration. Is mebendazole safe for pregnant women?
Adverse effects of mebendazole.
4. Thiabendazole. Mechanism of action, route of administration. Therapeutic
use. Adverse effects of this drug.
5. Albendazole. How does it work? Clinical use. Adverse effects of
albendazole.
6. Pyrantel pamoate. How does it work? Drug’s therapeutic use. Adverse
effects.
7. Diethyl carbamazine. Its mechanism of action. Clinical indications.
Adverse effects.
8. Ivermectin. How does it work? Does ivermectin affect human GABA
receptors? Therapeutic use. Adverse effects.
9. Praziquantel. Mechanism of action. Therapeutic use. Route of
administration. How is it metabolized? Adverse effects.
10. Niclosamide. Mechanism of action. Therapeutic uses. Adverse effects.
Task N 1. Drugs used in helminth infections.
Helminthes Drugs used
Threadworm (pinworm) (Enterobius vermicularis)
Strongyloides stercoralis
Common roundworm (Ascaris lumbricoides)
Other roundworms (filariae)
Wuchereria bancrofti, Loa loa
Onchocerca volvulus
Guinea-worm (Dracunculus medinensis)
Trichiniasis (Trichinella spiralis)
Tapeworm (Taenia saginata, Taenia solium)
Cysticercosis (infection with larval T.solium)
Hydatid disease (Echinococcus granulosus)
Hookworm (Ankylostoma duodenale, Necator americanus)
Whipworm (Trichuris trichiura)
Blood flukes (Schistosoma species)
Cutaneous larva migrans (Ankylostoma caninum)
Visceral larva migrans (Toxacara canis)
Lesson N 31
Topic: Final lesson N 4 “Anti-infective drugs”.
pharmacological group or subgroup:
1. Classification.
3. Antimicrobial spectrum.
4. Pharmacokinetics.
Lesson N 32
Topic: “HORMONES” (Part 1).
HYPOTHALAMIC AND PITUITARY HORMONES.
Introduction: Neuroendocrine control of metabolism, growth, and certain

aspects of reproduction is mediated by a combination of neural and endocrine
systems located in the hypothalamus and pituitary gland. Therapeutic preparations
of pituitary and hypothalamic peptide hormones are usually synthetic; a few are
purified from human sources. Their applications lie in three areas:
(1) as replacement therapy for hormone deficiency states; (2) as drug therapy
for a variety of disorders using pharmacologic doses to elicit a hormonal effect that
is not present at physiologic blood levels; and (3) as diagnostic tools for
performing stimulation tests to diagnose hypo- or hyperfunctional endocrine states.
- What hormones are secreted from the hypothalamus: hormones that affect
growth; hormones that affect gonadal function; hormones that affect corticosteroid
release; hormones that regulate other endocrine organs?
- Physiological role of these hormones (physiology).
- Which two hormones are synthesized in the hypothalamus but are not
secreted from there?
- What hormones are synthesized and secreted from the anterior lobe of the
pituitary (adenohypophysis)?
- What are the physiological actions of these hormones? (GH, ACTH, TSH,
FSH, LH, prolactin)?
- Which two hormones are released from the posterior pituitary
(neurohypophysis)?
- Physiologic actions of oxytocin.
- Vasopressin (ADH). Physiological action.
OBJECTIVES:
- Releasing hormone
- Target gland
- List or describe the major hypothalamic releasing hormones.
- List or describe the major anterior pituitary hormones and their effects.
- List or describe the major posterior pituitary hormones and their effects.
Main drugs for studying: Somatropin, Bromocriptine, Chorionic
gonadotropin, Corticotropin, Gonadorelin acetate and hydrochloride (GnRH),
Leuprolide, Menotropins, Octreotide, Oxytocin, Pergolide, Sermorelin (GHRH),
Thyrotropin (TSH), Urofollitropin, Vasopressin.
Wilkins, 1996. – Р. 219-223,230-234, 241-247.
Brothers, 1999. - P. 239-283, 326-331.
Pennsylvania, 2001. - P. 247-261, 452-454.
THYROID AND ANTITHYROID DRUGS

Introduction: Thyroid hormones (thyroxine and triiodothyronine) are essential
for growth and development and for regulation of energy metabolism. Thyroid
preparations are used for the replacement treatment of hypothyroidism.
- Regulation of thyroid hormones synthesis, storage and secretion;
- Basic structure of the thyroid gland;
- How are T3 and T4 formed and transported within the body?
- Abnormalities of thyroid function.
OBJECTIVES:
- Graves’ disease
- Hypothyroidism
- Iodide organification
- Iodide trapping
- Myxedema
- T 3, T4
- Thyrotoxicosis
- List the principal drugs used in the treatment of hypothyroidism.
- List the principal drugs used in the treatment of hyperthyroidism.
- Describe the major toxicities of thyroxine and the antithyroid drugs.
Main drugs for studying: Propylthiouracil, iodide salts, 131I (radioactive
iodine), Methimazole, Levothyroxine sodium (T4), Liothyronine sodium (T3).
1. Name three major hormones secreted by the thyroid gland.
2. What are the symptoms of hypothyroidism? What diseases and conditions
commonly cause hypothyroidism?
3. What are the treatment options for hypothyroidism?
4. Levothyroxine sodium, liothyronine sodium. Clinical uses, adverse effects.
5. What are the symptoms of hyperthyroidism? What is the most common
cause?
6. What are the treatment options of hyperthyroidism?
7. Treatment of myxedema coma.
8. Propylthiouracil and methimazole. Mechanism of action, route of
administration, adverse effects.
9. Iodide (Iodine salts). Why are iodides given in hyperthyroidism? In what
clinical situations do you use iodides?
10. Adverse effects of iodides.
11. Ionic inhibitors (Perchlorate and thiocyanate). Mechanism of action,
clinical uses.
12. Radioactive iodine (131I). Why is it used? In whom do you use it?
Adverse effects. Contraindications.
13. Thyroid storm. What is the reason of it? How do you manage a patient
who has thyroid storm?
INSULINS AND ORAL HYPOGLYCEMIC DRUGS

Introduction: The insulin-dependent group (type 1) represents about 9% of
the diabetic population in the USA. Most type II diabetes do not require exogenous
insulin for survival, but many need exogenous supplementation of their
endogenous secretion to achieve optimum health. It is estimated that as many as
20% of type II diabetics in the USA (2-2.5 million people) are presently taking
insulin.
- control of blood glucose.
OBJECTIVES:
- A or alpha cell
- B or beta cell
- C-peptide
- Insulin-dependent and non-insulin-dependent diabetes mellitus (IDDM and
NIDDM)
- Insulin-resistant diabetes
- Oral hypoglycemic agent
- List the sources of insulin in clinical use.
- List the principal types of insulin preparations with different durations of
action.
- Describe the effects of insulin on the liver, on muscle, and on adipose tissue.
- Describe the major hazards of insulin therapy.
- Describe the mechanisms of action of the 2 major classes of oral
hypoglycemic agents.
- Describe the use of glucagon in diabetes.
Main drugs for studying: Tolbutamide, Tolazamide, Acetohexamide,
Chlorpropamide, Glyburide, Glipizide, Phenformin, Metformin, Acarbose; Insulin
injection USP (regular, crystalline zinc), Insulin zinc suspension USP (prompt,
semilente), Isophane insulin suspension USP (NPH insulin), Insulin zinc
suspension USP (lente), Protamine zinc insulin suspension USP (PZI), Insulin zinc
suspension extended USP (ultralente).
1. What is the general treatment strategy for insulin-dependent diabetes
(Type 1)?
2. What is the general treatment strategy for non-insulin-dependent diabetes
(Type 2)?
3. How does insulin work?
4. Pharmacological effects of insulin (liver, muscle, adipose tissue).
5. Types of insulin preparations used clinically.
6. Which types of insulin are used for management of hyperglycemic
emergencies?
7. What are the sources of insulin?
8. What does determine the onset, peak, and duration of action of a particular
type of insulin preparations?
9. Route of insulin administration. Dosage (international units).
10. Adverse effects of insulin use.
11. Insulin interactions with other drugs.
12. Major classes of oral hypoglycemic agents. Can these classes be used in
combination to achieve glycemic control?
13. Sulfonylureas. Name them. Mechanism of action, adverse effects.
Pharmacokinetics. Contraindications to use.
14. What drugs do potentiate the effects of sulfonylureas?
15. What drugs do reduce the effects of sulfonylureas?
16. Name the biguanides. Mechanism of their action.
17. Does metformin cause a hypoglycemia? Contraindications and adverse
effects of metformin.
18. -glucosidase inhibitor (acarbose). Mechanism of action. Its advantage
over other oral hypoglycemic agents. Adverse effects.
19. Thiazolidinedione derivates (Troglitazone). Mechanism of action,
metabolism, adverse effects.
Task N 1. Fill the chart “Insulin: Types and activity” in:
Pharmacokinetic type Species Type Activity (hours)
Peak Duration
Rapid acting:
Insulin injection USP (regular, crystalline zinc)
Insulin zinc suspension USP (prompt, semilente)
Intermediate acting:
Isophane insulin suspension USP (NPH insulin)
Insulin zinc suspension USP (lente)
Long acting:
Protamine zinc insulin suspension USP (PZI)
Insulin zinc suspension extended USP (ultralente)
Task N 2. Characteristics of hormones.

Drug Group Mechanism of action Therapeutic uses
Levothyroxine sodium
Propylthiouracil
Potassium iodide
Radioactive iodine
Lesson N 33
Topic:”HORMONES” (Part 2).
GONADAL HORMONES and INHIBITORS
Introduction: Androgens are used mainly for replacement therapy in castrated

males or in males who are hypogonadal due to either pituitary or testicular disease.
Anabolic steroids have relatively little androgenic activity and are used to try and
increase protein synthesis after major surgery and in chronic debilitating disease.
Oestrogens are used for replacement therapy in primary hypogonadism and in
postmenopausal women to prevent hot flushes, atrophic vaginitis and osteoporosis.
They are also used in a number of menstrual disorders (e.g. spasmodic
dysmenorrhoea), and in combination with progestogens, as contraceptives.
Progestogens are used mainly for hormonal contraception. Sex hormones and
antagonists are used in the treatment of certain cancers.
- Neurohormonal control of the female reproductive system;
- Neurohormonal control of the male reproductive system;
- The behavioral effects of sex hormones.
OBJECTIVES:
- Anabolic steroid
- Antiestrogen
- Combination, sequential, progestin-only contraceptives
- Oral contraceptive
- Ovulation-inducing agent
- Describe the hormonal changes that occur during the menstrual cycle.
- List the benefits and hazards of oral contraceptives.
- Describe the status of pharmacologic contraception in the male.
- List the benefits and hazards of postmenopausal estrogen therapy.
- Describe the use of sex hormones in the treatment of cancer in women and
men.
- List or describe the toxic effects of anabolic steroids used to build muscle
mass.
Main drugs for studying: Estradiol, Ethinyl estradiol, Diethylstilbestrol,
Mestranol, Estradiol cypionate, Quinestrol, Tamoxifen, Clomiphene, Progesterone,
Norethindrone, Norgestrel, Danazol, Mifepristone, Testosterone,
Methyltestosterone, Fluoxymesterone, Nandrolone, Cyproterone, Flutamide,
Finasteride, Danazol.
Wilkins, 1996. – Р. 223-230, 234-241, 268-270.
Brothers, 1999. - P. 284-325, 332-341.
Pennsylvania, 2001. - P. 263-277, 454-455, 476-477.
1. What are the three major categories of sex steroids?
2. What are estrogen’s most important physiologic effects?
3. Give examples of estrogens that are currently used clinically.
4. What are the clinical uses of estrogens?
5. What is the route of administration?
6. What are the potential toxic effects of estrogen replacement?
7. Name absolute contraindications to estrogen replacement therapy.
8. Name estrogen inhibitors.
9. Tamoxifen. Clomiphene. Therapeutic uses, adverse effects.
10. What are the physiologic effects of progesterone?
11. Give examples of synthetic progestins.
12. What are the therapeutic uses of progestins?
13. How can progestins be administered?
14. Adverse effects of progestins.
15. Progestin inhibitors. Mifepriston, therapeutic uses, adverse effects.
16. Gonadotrophins. Names, therapeutic uses.
17. Danazol. Therapeutic uses, adverse effects.
18. What are the physiologic effects of the androgens?
19. Give examples of synthetic androgens.
20. What are the clinical uses of synthetic androgens?
21. Describe the toxicities of synthetic androgen treatment.
22. Contraindication to androgen use.
23. Androgen antagonists. Classification. Therapeutic uses.
24. Oral contraceptives. What are the three different kinds of oral
contraceptives currently available?
25. How do oral contraceptives work?
26. What are the adverse effects of combination oral contraceptives?
27. What are the most common side effects of progestin-only
contraceptives?
28. What are the absolute contraindications for combination oral
contraceptives?
29. Drug interactions of oral contraceptives.
30. Anabolic steroids. Pharmacological effects. Clinical uses. Adverse
effects.
CORTICOSTEROIDS and INHIBITORS

Introduction: The natural adrenocortical hormones are steroid molecules
produced and released by the adrenal cortex. Both natural and synthetic
corticosteroids are used for diagnosis and treatment of disorders of adrenal
function. They are also used – more often and in much larger quantities – for
treatment of a variety of inflammatory and immunologic disorders. Antagonists of
the synthesis or action of ACTH and the adrenocortical steroids are important in
the treatment of several tumors.
- physiological role of the hormones in metabolic processes (physiology);
- pathophysiology of the adrenal medulla and gonadal glands;
- notion about rheumatism and other systemic diseases of connective tissue,
leukemia, hormon-dependent tumors.
OBJECTIVES:
- Addison’s disease
- Adrenal androgens, adrenal estrogens
- Circadian rhythm of secretion
- Cushing’s syndrome
- Glucocorticoid
- Mineralocorticoid
- Describe the major naturally occurring glucocorticosteroid and its actions.
- List or describe several synthetic glucocorticoids and their differences from
the naturally occurring hormones.
- List or describe the actions of the major naturally occurring
mineralocorticoid and one synthetic agent in this group.
- List the indications for the use of corticosteroids in adrenal and nonadrenal
disorders.
- List or describe the toxic effects of the glucocorticoids when given
chronically.
Main drugs for studying: Betamethasone, Cortisone, Dexamethasone,
Hydrocortisone, Prednisolone, Triamcinolone, Fludrocortisone,
Aminoglutethimide, Metyrapone, Spironolactone, Mifepristone, Ketoconazole.
1. What are the two major groups of corticosteroids?
2. Describe the functions of the two major pharmacological groups of
corticosteroids.
3. How are corticosteroids administered?
4. How do glucocorticoids work?
5. What are the major physiologic effects of glucocorticoids?
6. Name the major synthetically produced glucocorticoids?
7. What are the therapeutic uses of synthetic glucocorticoids?
8. What are the adverse effects of glucocorticoids?
9. Why corticosteroid should not be withdrawn suddenly after prolong use?
10. What precautions should be taken on prolong corticosteroid therapy?
11. Name mineralocortocoids.
12. Function of mineralocorticoids.
13. Fludrocortisone. Therapeutic uses, adverse effects.
14. Adrenocorticosteroid antagonists (aminoglutethimide, metyrapone).
Mechanism of action, therapeutic uses, side effects.
Task N1. Make a characteristic of mineralocorticoids, glucocorticoids,
gonadal hormones, and anabolic steroids.
Drug Pharmacological group Indications Side effects
Dexamethasone
Fludrocortissone
Mifepristone
Ethinylestradiol
Norethindrone
Methyltestosterone
Cyproterone
Task N 2. Determine the group of drugs (A, B). Indicate (point out) the names of drugs from
each group.
Effects A B
Anti-inflammatory and desensitizing ++++
Na+ and water retention, K+ excretion +++ +
Increasing of blood sugar level + +++
Inhibition protein catabolism + +++
Neutrophilia, lymphocytopenia, eosinopenia +
DRUGS THAT AFFECT CALCIUM HOMEOSTASIS

Introduction: Calcium and phosphate, the major mineral constituents of
bone, are also two of the most important minerals for general cellular function.
Bone serves as the principal structural support for the body and provides the space
for hematopoiesis. Thus, abnormalities in bone mineral homeostasis can lead not
only to a wide variety of cellular dysfunction (e.g. tetany, coma, muscle weakness)
but also to disturbances in structural support of the body (e.g. osteoporosis with
fractures) and loss of hematopoietic capacity (e.g. infantile osteopetrosis).
Main drugs for studying: Calcitonin, Calcifediol, Cholecalciferol,
Ergocalciferol, Calcitriol, Gallium nitrate, Plicamycin (Mithramycin), Calcium
carbonate, Calcium gluconate, Calcium lactate, Etidronate.
1. What are the pharmacologic treatment options available for hypocalcemia?
2. Name calcium salt preparations.
3. What are the adverse effects of calcium supplementation?
4. Name vitamin D agents currently available.
5. How does vitamin D work?
6. Clinical indications for the use of vitamin D supplements?
7. Side effects of vitamin D agents.
8. Pharmacologic treatment options those are available to treat
hypercalcemia.
9. Name biphosphonates.
10. How do these drugs work? Route of administration.
11. When are biphosphonates used?
12. Adverse effects of biphosphonates.
13. Calcitonin. Physiologic actions. When is it used? What type of calcitonin
is used?
14. Adverse effects of calcitonin.
15. Gallium nitrate. How does it work? Indication for use. Adverse effects.
16. Plicamycin. How does it work? What are adverse effects?
17. How do glucocorticoids decrease plasma calcium levels?
18. What conditions respond best to glucocorticoid (prednisone) therapy?
19. What is the role of thiazide diuretics and loop diuretics in the treatment
in hypercalcemia?
Lesson N 34
Topic: “ ANTICANCER (ANTINEOPLASTIC) DRUGS”.
Introduction: The aim of treatment in patients with cancer is cure, or if this is

not possible, effective palliation. Many cancers present as localized tumour
masses, but surgery or radiotherapy often fail to eradicate the disease, which
eventually becomes widespread. For this reason, there is a trend to incorporate
systemic treatment with local treatment at the time of diagnosis.
- The special characteristics of cancer cells (biology);
- The notion about malignant tumor (pathophysiology);
- The stages of the cell cycle.
OBJECTIVES:
- Releasing hormone
- Target gland
- Pulse therapy
- Rescue therapy
- Describe the relevance of cell cycle kinetics to the mode of action and
clinical use of anticancer drugs.
- Identify the major subclasses of anticancer drugs and describe the
mechanisms of action of the main drugs in each subclass.
- Identify the drugs of choice for the more important neoplastic diseases and
describe their pharmacokinetics and their toxic effects.
- Understand the strategies of combination chemotherapy.
Main drugs for studying: Cyclophosphamide, Carmustine, Busulfan,
Cisplatin, Dacarbazine, Procarbazine, Methotrexate, Mercaptopurine, Fluorouracil,
Vinblastine, Vincristine, Etoposide, Doxorubicin, Bleomycin, Dactinomycin,
Mitomycin, Cytarabine, Prednisone.
Wilkins, 1996. – Р. 253-268, 270-274.
Brothers, 1999. - P. 825-839.
Pennsylvania, 2001. - P. 373-399, 463-466.
1. What are the cell-specific (CCS) antineoplastic agents?
2. What are the cell-nonspecific (CCNS) antineoplastic agents?
3. What are the options for treating cancer in addition to chemotherapy?
4. Classification of antineoplastic agents.
5. How does resistance develop to chemotherapeutic drugs?
6. Major classes of alkylating agents.
7. Nitrogen mustards: Mechlorethamine, Cyclophosphamide, Melphalan.
Mechanism of action. Clinical uses. Route of administration. Adverse effects.
8. Nitrosoureas: Lomustine and Carmustine. Mechanism of action.
Solubility. Clinical uses. Adverse effects.
9. Miscellaneous alkylating agents: Cisplatin, Carboplatin, Busulfan,
Dacarbazine, Procarbazine. Mechanism of action, clinical uses, adverse effects.
10. Antibiotics (Dactinomycin, Doxorubicin, Daunorubicin, Bleomycin,
Mitomycin, Plicamycin). Mechanism of action. Clinical uses, route of
administration. Adverse effects.
11. Antimetabolites (Methotrexate, 6-Mercaptopurine, Cytarabine, 5-
Fluorou-racil, Hydroxyurea). Mechanism of action. Clinical uses. Adverse effects.
12. What is the “leucovorin rescue”?
13. Hormones and related agents: Flutamide, Tamoxifen, Leuprolide,
Glucocorticoids. Mechanism of action, clinical uses, adverse effects.
14. Plant alkaloids (Vinblastine, Vincristine). Mechanism of action, clinical
uses, route of administration, adverse effects.
15. Schedule of treatment. Principles of combined therapy.
16. Techniques for dealing with emesis and myelosuppression.
Task N 1.Make short characteristics of anticancer drugs and fill the following
chart in:
Drug Mechanism of action Therapeutic uses Drug forms
Cyclophosphamide
Methotrexate
Doxorubicin
Procarbazine
Carmustine
Task N 2. Analyze the following drug’s combinations:

Vinblastin+Bleomycin+Cisplatin;
Cyclophosphamide+Methotrexate+Fluorouracil;
Cyclophosphamide+Oncovin (vincristine)+Prednisone.
Task N 3. This drug is an antimetabolite that inhibits dihydrofolate reductase
and is used in certain leukemias and lymphomas. Its myelosuppressant and
gastrointestinal effects can be reduced by “leucovorin rescue”. Name this drug.
Task N 4. This drug is an antimetabolite that is used in acute myelogenous
leukemia. It is phosphorylated to form a nucleotide inhibitor of DNA polymerases.
Its major toxic effect is myelosuppression.
Lesson N 35
Topic: “ANTISEPTICS AND DISINFECTANTS. VITAMINS”.
Introduction: There are many drugs that are useful in decreasing the bacterial
flora when applied directly to the skin, infected wounds, instruments, or excreta.
These locally effective drugs have a low enough therapeutic index to make them
unsuited as systemic chemotherapeutic agents. Antiseptics are drugs that are
applied to living tissues for the purpose of killing bacteria or inhibiting their
growth. Disinfectants are bactericidal drugs that are applied to nonliving materials.
Vitamins should be used in medicine in (1) individuals with a poor dietary
history (e.g. vegetarians, pregnant or lactating women, infants), (2) deficiency
diseases (e.g. alcoholism, pernicious anemia, chronic pancreatitis), (3) special
disease states (e.g. hypoparathyroidism, carcinoid syndrome) or (4) hereditary
vitamin dependency states.
- role of vitamins in metabolic processes (biochemistry);
- symptoms and pathogenesis of avitaminosis, hypo- and hypervitaminosis
(hygiene, pathophysiology).
OBJECTIVES:
- Antiseptic
- Sterilization
- Disinfectant
- Identify the compounds used as antiseptics and disinfectants.
- Describe the advantages and disadvantages of the most commonly used
antiseptics and disinfectants.
Main drugs for studying: Ethanol, Folmaldehyde, Acetic acid, Iodine,
Chlorine, Silver nitrate, Mercury bichloride, Hexachlorophene, Benzalkonium
chloride, Chlorhexidine, Cetylpyridinium chloride.
Brothers, 1999. - P. 876-889, 862-871.

1. Differences between antiseptics and disinfectants.
2. Requirements to antiseptics and disinfectants.
3. Classification of antiseptics and disinfectants.
5. Phenol. Properties and uses.
6. Potassium permanganate. Clinical uses.
7. Hydrogen peroxide. Pharmacological properties and uses.
8. Iodine. Pharmacological actions.
9. Chlorhexidine. Uses.
10. Chlorine-containing compounds. Name them.
11. Ethanol. Pharmacological effects.
12. Formaldehyde. Action and uses.
13. Silver compounds. Actions, uses.
14. Gentian violet. Effects, uses.
Task N 1. Characteristic of vitamins.
Drug Names of Basic Action on Indications
coenzymes, in which treatment and biochemical
vitamins are prophylactic processes, organs
involved effect and tissues
Thiamine
bromide
Pyridoxine
Cyancobalamin
Riboflavin
Folic acid
Retinol acetas
Tocoferol
acetas
Ascorbic acid
Lesson N 36
Topic: “POISONS AND ANTIDOTES. DRUG INTERACTIONS. ”
Introduction: Humans live in a chemical enviroment. Estimates indicate that

more than 60,000 chemicals are in common use and about 500 new chemicals are
said to enter the commercial market annually. In the biochemical area the
toxicologist is primarily concerned with adverse effects in humans resulting from
exposure to drugs and other chemicals as well as the demonstration of safety or
hazard associated with their use. Thousands of cases of acute poisoning occur each
year. Most of the deaths are due to intentional suicidal overdose with a drug or
toxic substance.
- previous pharmacology studied course.
OBJECTIVES:
- Hemodialysis
- Hemoperfusion
- Specific antidote
- Universal antidote
List or describe the following:
- The most common causes of death in poisonings caused by sedative-
hypnotics, narcotics, cocaine, digitalis, and tricyclic antidepressants.
- Specific antidotes for heroin and other narcotics, acetaminophen, methanol
and ethylene glycol, and parathion.
- The emergency treatment (before laboratory results are available) of a
comatose patient.
- The contraindications to the use of emesis for treatment of a patient who has
ingested a toxin.
Main drugs for studying: Acetylcysteine, Atropine, Deferoxamine, Ethanol,
N-Acetylpenicillamine, Calcium disodium edetate (CaEDTA), Dimercaprol
(BAL), Penicillamine, Naloxone, Physostigmine, Pralidoxime (2-PAM).
Wilkins, 1996. - P. 337-344.
Brothers, 1999. - P. 872-875.

Task N 1. Fill in the chart “Poisons and their antidotes”:
Poison Symptoms of intoxication Antidot
Barbiturates
N-acetylcysteine
Methanol
Dry mouth, urinary retention, constipation, blurred vision,
fever, delirium
Flumazenil
Pin-point pupil
Topic: “DRUG INTERACTIONS”.
Introduction: When several drugs are administered concurrently, they may

influence each other favorably or unfavorably. The adverse drug interactions may
be of great clinical importance when the margin of safety of the drugs is small.
OBJECTIVES:
- Antagonism
- Enzyme induction
- Pharmacokinetic interaction
- Pharmacodynamic interaction
- Potentiation
- Synergism
- Describe the mechanisms of the acute interaction between alcohol and
barbiturates and between alcohol and disulfiram.
- Describe the mechanism of the interaction between barbiturates and
warfarin.
- Describe the interaction between quinidine and digoxin.
Wilkins, 1996. - P. 329-333.
Task N 1. Analyze the following combinations:
Aspirin + Anticoagulant
Tetracycline + Antacids
MAO-inhibitors + Sympathomimetics
Digitalis + Thiazides
Frusemide + Aminoglycosides
Benzodiazepines + Alcohol
Probenecid + Penicillin
Probenecid + Aspirin
Morphine + Phenothiazines
Examination questions
1. Pharmacology as a field of medicine. General pharmacological principles.
Routes of drug administration. Factors governing choice of route.
2. Absorption, distribution. Pharmacokinetic parameters (bioavailability,
volume of distribution, clearance).
3. Biotransformation (metabolism). First-pass (presystemic) metabolism).
4. Excretion. Kinetics of excretion.
5. Pharmacodynamics. Principles of drug action. Mechanisms of drug action.
Combined effect of drugs.
6. Drug dosage.
7. Factors modifying drug action.
8. Adverse drug effects.
9. Parasympathomimetic drugs and Anticholinesterase agents. Classification.
Pharmacologic effects. Therapeutic uses. Adverse effects. Reversal of
cholinesterase inhibition.
10. Parasympathetic antagonists. Classification. Pharmacologic effects.
Therapeutic uses. Adverse effects. Contraindications.
11. Ganglionic stimulators and blockers. Preparations. Pharmacologic effects.
Therapeutic uses. Adverse effects. Toxicological characteristic of nicotin.
12. Neuromuscular blocking agents. Classification. Mechanism of action.
Therapeutic uses. Adverse effects. Reversal of neuromuscular blockade.
13. Sympathomimetic (adrenergic) agents (Epinephrine and Norepinephrine).
Sympathetic nervous system (Functions, location of adrenergic receptors,
neurotransmitters). Pharmacologic effects. Mechanism of action. Therapeutic uses.
Adverse effects.
14. Adrenergic agents (except Epinephrine and Norepinephrine).
Classification. Mechanism of action. Pharmacologic effects. Therapeutic uses.
Adverse effects.
15. Sympathetic antagonists. Classification. Alpha- adrenergic blocking
agents. Pharmacologic effects. Mechanism of action. Therapeutic uses. Adverse
effects.
16. Sympathetic antagonists. Classification. Beta- adrenergic blocking agents.
Pharmacologic effects. Mechanism of action. Therapeutic uses. Adverse effects.
17. Sympathetic antagonists (Agents that inhibit the actions of adrenergic
nerves). Preparations. Pharmacological effects. Mechanism of action. Therapeutic
18. General anesthetics. Classification. Theories of narcosis.
Pharmacokinetics and pharmacologic effects of inhalation and IV anesthetics.
Therapeutic uses. Adverse effects.
19. General anesthetics. Classification. Pharmacologic effects of intravenous
anesthetics. Therapeutic uses. Adverse effects.
20. Sedative-Hypnotics. Classification. Mechanism of action. Pharmacologic
effects. Therapeutic uses. Adverse effects.
21. Agents used in the treatment of seizures (Antiepileptics). Classification.
Mechanism of action. Therapeutic uses. Adverse effects.
22. Agents used in the treatment of Parkinsonian Disorders. Classification.
Mechanism of action. Pharmacologic effects. Adverse effects.
23. Antipsychotic agents. Classification. Pharmacologic effects. Therapeutic
24. Mood-Altering drugs /Antidepressants and Lithium salts/. Classification.
25. Agents used in the treatment of anxiety. Classification. Pharmacologic
26. CNS-stimulants. Preparations. Pharmacologic effects. Therapeutic uses.
Adverse effects.
27. Narcotic analgesics. Classification. Morphine.Pharmacokinetics and
pharmacologic effects. Mechanism of action. Therapeutic uses. Adverse effects.
Drugs used in the treatment of narcotic toxicity.
28. Synthetic narcotic analgesics. Preparations. Mechanism of action.
Pharmacologic effects. Therapeutic uses. Adverse effects.
29. Non-narcotic analgesics. Classification. Mechanism of anti-inflammatory
and analgesic action. Pharmacologic effects. Therapeutic uses. Adverse effects.
30. Drugs used in the treatment of Gout. Classification. Mechanism of action.
31. Disease-modifying antirheumatic drugs. Classification. Therapeutic uses.
Adverse effects.
32. Local anesthetics. Types of local anesthesia. Classification. Mechanism of
action. Therapeutic uses. Adverse effects.
33. Drugs used in the treatment of hyperlipidemia. Classification. Mechanism
of action. Therapeutic uses. Adverse effects.
34. Drugs used in the treatment of congestive heart failure. Classification.
Cardiac glycosides. Pharmacologic effects. Mechanism of action. Therapeutic
35. Drugs used in the treatment of arrhythmia. Classification. Mechanism of
action. Pharmacologic effects. Therapeutic uses. Adverse effects.
36. Drugs used in the treatment of angina pectoris. Classification. Mechanism
of action. Pharmacologic effects. Therapeutic uses. Adverse effects.
37. Drugs used in the treatment of hypertension. Classification.
Pharmacologic effects. Mechanism of action. Therapeutic uses. Adverse effects.
38. Drugs that interfere with the renin-angiotensin system. Preparations.
39. Diuretic agents. Classification. Mechanism of action. Therapeutic uses.
Adverse effects.
40. Anticoagulants. Classification. Mechanism of action. Therapeutic uses.
Adverse effects. Reversal of anticoagulant effects.
41. Antithrombotic and thrombolytic drugs. Preparations. Mechanism of
42. Agents used in the treatment of anemia. Preparations. Pharmacokinetics of
iron. Pharmacological effects. Therapeutic uses.
43. Hormones. Pituitary hormones. Physiologic role and effects. Classification
(preparations). Therapeutic uses. Adverse effects.
44. Thyroid and parathyroid hormones. Antithyroid agents. Preparations.
Pharmacologic effects. Therapeutic uses.
45. Hormones /Glucocorticoids/. Preparations. Pharmacologic effects.
46. Insulin. Metabolic effects of insulin deficiency. Mechanism of action.
Preparations. Therapeutic uses. Adverse effects.
47. Hormones /Mineralocorticoids/. Pharmacologic effects. Therapeutic uses.
Adverse effects.
48. Oral hypoglycemic agents. Preparations. Mechanism of action.
Pharmacologic effects. Therapeutic uses. Adverse effects.
49. Hormones /Estrogens.Antiestrogens/. Preparations. Pharmacologic effects.
50. Hormones /Progestines, Antiprogestines/. Preparations. Therapeutic uses.
Adverse effects.
51. Hormonal contraceptives. Types of oral contraceptives. Mechanism of
their action. Therapeutic uses. Adverse effects. Contraindications.
52. Hormones /Androgens.Antiandrogens/. Preparations. Pharmacologic
53. Sulfonamides and Trimethoprim. Classification. Mechanism of action.
54. Antibiotics /Penicillins/. Classification. Mechanism of action.
Pharmacokinetics. Therapeutic uses. Adverse effects.
55. Antibiotics /Aminoglycosides/. Classification. Mechanism of action.
56. Antibiotics /Tetracyclines/. Classification. Mechanism of action.
57. Antibiotics /Cephalosporins/. Classification. Mechanism of action.
58. Quinolones. Preparations. Mechanism of action. Pharmacologic effects.
59. Antibiotics /Erythromycin, Clindamycin, Vancomycin/. Antimicrobial
spectrum. Mechanism of action. Therapeutic uses. Adverse effects.
60. Antibiotics /Polypeptides/. Preparations. Mechanism of action.
61. Cancer chemotherapy. Classification. Mechanism of action. Therapeutic
uses. Adverse effects. Drug combinations and toxicity.
62. Drugs for peptic ulcer. Classification. Mechanism of action.
Pharmacological effects. Therapeutic uses. Adverse effects.
63. Emetics and antiemetics. Drugs for constipation and diarrhea. Laxatives.
Classifications. Mechanism of action. Therapeutic uses. Adverse effects.
64. Pharmacological control of asthma. Classification. Mechanism of action.
Adverse effects.
65. Antitussive drugs. Classification. Mechanism of action. Pharmacologic
66. Agents used for treatment of fungus infections. Classification. Mechanism
67. Agents used for treatment of tuberculosis. Principles of treatment this
disease. Classification. Mechanism of action. Adverse effects.
68. Agents used for treatment of leprosy. Preparations. Mechanism of action.
Pharmacological effects. Adverse effects.
69. Anthelmintics. Classification. Mechanism of action. Therapeutic uses.
Adverse effects.
70. Agents used for treatment of protozoal infections and malaria.
Classification. Mechanism of action. Therapeutic uses. Adverse effects.
71. Agents used for treatment of viral infections. Classification. Mechanism of
72. Vitamins. Classification. Physiological functions. Therapeutic uses.
Adverse reactions.
73. Drugs affecting Calcium balance. Preparations. Pharmacologic effects.
74. Oxytocin and drugs acting on the uterus. Classification. Pharmacologic
75. Principles of drug interactions. Pharmacokinetic and pharmacodynamic
interactions.
76. Ethyl and methyl alcohols. Pharmacologic effects. Pharmacokinetics.
Toxicological characteristic of alcohol and methanol. Treatment of ethanol and
methanol intoxication.
77. Antiseptics, disinfectants and ectoparasiticides. Classification. Mechanism
CONTENTS
Introduction. Aims and tasks of Pharmacology 3

Lesson N English prescription. Hard, liquid and soft drug forms 5
1.
Lesson N Pharmacokinetics 7
2.
Lesson N Pharmacodynamics 10
3.
Lesson N Cholinergic agonists. Anticholinesterase agents. 13
4.
Lesson N Anti-cholinergic drugs (parasympathetic antagonists) 16
5.
Lesson N Adrenergic agonists (sympathomimetics) 19
6.
Lesson N Anti-adrenergic drugs (sympathetic antagonists) 20
7.
Lesson N Final lesson N 1“Drugs affecting on neurohumoral 22
8. transmission”
Lesson N General anesthetics. 23
9.
Lesson Sedative-hypnotics. Antiepileptic drugs. Antiparkinsonian drugs. 26
N10
Lesson Antipsychotic drugs. Antidepressants. Lithium salts. 29
N11
Lesson CNS-stimulants. Antianxiety (anxiolytic) drugs. Alcohols. 31
N12
Lesson Narcotic analgesics. Opioid antagonists. 33
N13
Lesson Final lesson N 2 “Drugs acting on the CNS” 35
N14
Lesson Non-steroidal anti-inflammatory drugs (NSAIDS) 36
N15
Lesson Drugs used to treat asthma and cough. 38
N16
Lesson Drugs used to treat gastrointestinal disorders. 40
N17
Lesson Local anaesthetics. 42
N18
Lesson Antihyperlipidemic drugs. 43
N19
Lesson Drugs used to treat congestive heart failure. 45
N20
Lesson Antiarrhythmic drugs. 47
N21
Lesson Antianginal drugs. 50
N22
Lesson Diuretics 52
N23
Lesson Antihypertensive drugs 54
N24
Lesson Anticoagulant, fibrinolytic and antiplatelet drugs. Agents used to
N25 56
treat anemia
Lesson Final lesson N3 “Drugs which influence on the executive 60
N26 organs”
Lesson Sulfonamides and Trimetoprim. Beta-lactam antibiotics 60
N27
Lesson Protein synthesis inhibitors (Tetracyclines, Macrolides,
N28 Polypeptides, Aminoglycosides). Quinolones 64
Lesson Antifungal drugs. Antiviral drugs. Drugs used to treat
N29 tuberculosis and leprosy 66
Lesson Drugs acting on parasites: Antiprotozoal and Anthelmintic drugs 70
N30
Lesson Final lesson N 4 “Anti-infective drugs” 74
N31
Lesson Hormones:hypothalamic and pituitary hormones; thyroid and
N32 Parathyroid drugs; insulins and oral hypoglycemic drugs 74
Lesson Hormones:gonadal hormones and inhibitors; corticosteroids and
N33 inhibitors. Drugs that affect calcium homeostasis 78
Lesson Anticancer (antineoplastic) drugs 82
N34
Lesson Antiseptics and disinfectants. Vitamins. 84
N35
Lesson Poisons and antidotes. Drug interactions 85
N36
Examination questions 88
NOTES
Издательство Курского государственного медицинского университета
305041, г. Курск, ул. К. Маркса, 3.
Лицензия ЛР № 020862 от 30.04.99 г.

Тираж 160 экз.
Отпечатано в типографии КГМУ.

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Заказ № 612.

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KURSK STATE MEDICAL UNIVERSITY

It was printed according to the decision of editorial council of KSMU.

Teaching instructions in Pharmacology (teaching textbook, edited by

ISNB: 5-7487-0694-6 ББК: 52.81:81.2Англ я 7

© Коллектив авторов, КГМУ, 2003

Pharmacology is one of the fundamental sciences in the system of doctors

Introduction: A prescription is a written order given by a physician to a

Task N 2. Drug X has a narrow therapeutic index: the minimum toxic

AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY

Topic: “CHOLINERGIC (PARASYMPATHETIC) AGONISTS.

Task N 2. Uses and duration of action of cholinesterase inhibitors used in

Introduction: Muscarinic receptor-blocking drugs are used for the treatment

Task N 2. Relative autonomic tone and effects of ganglion blockade.

Task N 3. Comparative characteristic of neuromuscular blocking agents.

Introduction: The sympathetic nervous system is an important regulator of

Introduction: Since catecholamines play a role in a variety of important

Prepare lessons NN 4-7 according to the following scheme for each

CENTRAL NERVOUS SYSTEM PHARMACOLOGY

Introduction: Narcosis (anesthesia) as the method of the organism protection

Task N 2. Premedication anesthesia. Fill in the chart:

Introduction: Assignment of a particular compound to the sedative-hypnotic

Introduction: Ethyl alcohol (ethanol) is a sedative-hypnotic consumed as a

Introduction: Management of pain is essential to good medical practice and

Introduction: These drugs have analgesic, antipyretic and, at higher doses,

Introduction: Drugs of this group (antitussives, expectorants, agents used for

Introduction: An estimated 10% of adults in the western world will suffer an

Task N 2. Compare the drugs acting on GIT:

Drug Type of action on GIT Mechanism of action Indications Side effects

Introduction: Local anesthetics have several types of clinical applications, and

Task N 3. Properties of local anesthetics.

Task N 4. Methods of administration, uses and adverse effects of local

Task N 2 Pharmacological effects of therapeutic and toxic doses of Digitalis

Task N 3. Vasodilators for use in chronic CHF.

Task N 2. Comparative characteristic of antiarrhythmic drugs.

Task N 2. Characteristic of nitrate’s drug forms.

Task N 3. Side effects of antianginal drugs.

Task N 2. Compare Thiazides and Frusemide.

Introduction: High blood pressure is associated with decreased life expectancy

Introduction: Bleeding and thrombosis are altered states of hemostasis.

Task N 2. Comparative aspects of heparin and oral anticoagulants.

Topic:“AGENTS USED TO TREAT ANEMIA”.

INITIAL LEVEL OF KNOWLEDGE:

Introduction: The aminoglycosides are valuable drugs in the treatment of

Introduction: Fungal infections (mycoses) may be superficial (affecting skin,

Topic: “ANTIVIRAL DRUGS”.

Introduction: Viruses are intracellular parasites that lack independent

Topic: “DRUGS USED TO TREAT TUBERCULOSIS AND LEPROSY”.

Introduction: The incidence of tuberculosis has been increasing because the

Task N 2. Give drugs used:

Topic: “ANTHELMINTIC DRUGS”.

Introduction: Neuroendocrine control of metabolism, growth, and certain

THYROID AND ANTITHYROID DRUGS

INSULINS AND ORAL HYPOGLYCEMIC DRUGS

Task N 2. Characteristics of hormones.

Introduction: Androgens are used mainly for replacement therapy in castrated

CORTICOSTEROIDS and INHIBITORS

DRUGS THAT AFFECT CALCIUM HOMEOSTASIS

Introduction: The aim of treatment in patients with cancer is cure, or if this is

Task N 2. Analyze the following drug’s combinations:

Questions for self-assessment:

Introduction: Humans live in a chemical enviroment. Estimates indicate that

WORK AT THE PRACTICAL STUDY:

Topic: “DRUG INTERACTIONS”.