Pharmacology Ticket Ques.

2022

*Note:- This Tickets is prepared on the basis of ticket received by Students. So Be Careful and Best of
Luck.

Ticket 1
1. M-cholinomimetics, N-cholinomimetics. The localization of M, N-cholinoreceptors, drugs
stimulating them. Mechanism of action and pharmacological effects, indications and contraindications
for their use. Symptoms of muscarinic poisoning and first aid measures.
Ans: M-cholinomimetics.
Localization of M-cholinergic receptors- M-cholinergic receptors are located in the postsynaptic
membrane of cells of effector organs at the endings of postganglionic cholinergic (parasympathetic) fibers.
There are:
a. m1-cholinergic receptors (in the autonomic ganglia and in the central nervous system),
b. m2-cholinergic receptors (the main subtype of m-cholinergic receptors in the heart),
c. m3-cholinergic receptors (in smooth muscles, most exocrine glands),
d. m4-cholinergic receptors (in the heart, the wall of the pulmonary alveoli, CNS)
e. m5-cholinergic receptors (in the central nervous system, in the salivary glands, the iris, in
mononuclear blood cells).
Drugs that stimulate them- Pilocarpine hydrochloride, Aceclidine, muscarine,
carbachol, bethanchol,acetyl acetylcholine ,methacholine
The mechanism of action is a direct stimulating effect on m-cholinergic receptors.
Pilocarpine :
directly stimulates cholinergic receptors, acting on a subtype of muscarinic receptor (M3) found on the iris
sphincter muscle, causing the muscle to contract and produce miosis.
hydrochloride;
primary site of action is the distal tubule of the nephron where it selectively blocks sodium transport,
thereby inhibiting sodium-potassium exchange..
Pharmacological effects:
1. Eye: contraction of the m.constrictorpupillae, constriction of the pupil (miosis), opening of the angle of
the anterior chamber of the eye, improved outflow of fluid into the Schlemm canal, contraction of the ciliary
muscle and improved outflow of intraocular fluid through the trabecular meshwork, increased lens curvature
(near focus)
2. Bladder: detrusor contraction, decreased bladder capacity.
3. Uterus: in humans, it is not sensitive to M-agonists.
4. Respiratory system: contraction of the muscles of the bronchial tree, increased secretion of the bronchial
glands
5. CNS: parkinson-like effects.
Indications for use-
Pilocarpine is widely used in ophthalmic practice to lower intraocular pressure in glaucoma, as well as to
improve eye trophism in case of thrombosis of the central retinal vein, acute obstruction of the retinal artery,
optic nerve atrophy, and vitreous hemorrhages.
Aceclidine is a drug that prevents and eliminates atony of the bladder, especially with an increase in the
amount of urine associated with neurogenic disorders of the bladder, with atony of the muscles of the
gastrointestinal tract. Aceclidine solutions are used to narrow the pupil and reduce intraocular pressure in
glaucoma.
Contraindications to the use of certain drugs-
PILOCARPING Hypersensitivity, iritis, cyclitis, iridocyclitis, keratitis, condition after ophthalmic
operations and other eye diseases, in which pupil constriction undesirable.
ACECLIDIN in bronchial asthma, severe heart disease, angina pectoris, bleeding from the gastrointestinal
tract, epilepsy, hyperkinesis, during pregnancy, as well as in inflammatory processes in the abdominal
cavity before surgery.
Symptoms of muscarine poisoning- profuse salivation, profuse sweat, flushing of the face, nausea,
vomiting, abdominal pain, diarrhea. The pupils are constricted, vision is unclear due to spasm of
accommodation. With the progression of poisoning, there may be observed: heart rhythm disturbances, a
significant decrease in blood pressure up to collapse.
Relief measures- The antidote therapy is atropine sulfate, which is injected under the skin in the form of 1
ml of a 0.1% solution repeatedly (at intervals of 10 minutes), up to 3 times (if indicated). In severe cases, the
drug may be given slowly intravenously. If the poison gets inside, the stomach is washed with a suspension
of activated charcoal, a 0.1% solution of potassium permanganate. In case of circulatory disorders, camphor,
cordiamine, caffeine-sodium benzoate are injected under the skin.

● N-Cholinomimetics.

Localization of N-cholinergic receptors: neuronal ganglia ANS, medulla adrenal glands, CNS neurons
Drugs that stimulate them:Nicotine, cytisine, anabasine hydrochloride, pilocarpine,
hydrochloride ,muscarine ,carbachol ,bethanchol,acetyl acetylcholine ,methacholine
Mechanism of action: have a two-phase effect on n-cholinergic receptor.
a. The first phase (excitation) is characterized by depolarization of the membranes of ganglionic
neurons,
b. The second (depression) is due to competitive antagonism with acetylcholine.
Mechanisms of action;
Pilocarpine :
directly stimulates cholinergic receptors, acting on a subtype of muscarinic receptor (M3) found on
the iris sphincter muscle, causing the muscle to contract and produce miosis.
hydrochloride;
primary site of action is the distal tubule of the nephron where it selectively blocks sodium
transport, thereby inhibiting sodium-potassium exchange
Pharmacological effects:
1) stimulation of autonomic ganglia (sympathetic more than parasympathetic)
2) Cardiovascular system: tachycardia, peripheral and coronary vasospasm, hypertension
3) Gastrointestinal tract, urinary system: inhibition of activity
4) Chemocarotid zone: stimulation of respiration
5) CNS: low doses: psychostimulation, high doses - vomiting, tremor, convulsions, coma.
Indications for use: smoking cessation relief, reflex respiration arrest(during operations, injuries, etc.),
shock and collaptoid states (pressor effect), respiratory and circulatory depression in patients with
infectious diseases.
Contraindications for use: atherosclerosis, pronounced increase in blood pressure, erosive and ulcerative
lesions of the gastrointestinal tract in the acute phase, bleeding from large vessels, pulmonary edema,
pregnancy.
Toxicology of nicotine and tobacco smoke products.
In acute nicotine poisoning, hypersalivation, nausea, vomiting, and diarrhea are noted. Bradycardia is
replaced by tachycardia. Blood pressure is elevated, shortness of breath turns into respiratory depression.
The pupils are first constricted, then dilated. Help is mainly aimed at maintaining breathing, since death
occurs from paralysis of the respiratory center. Chronic nicotine poisoning is usually associated with
tobacco smoking. Symptoms of chronic poisoning are quite diverse. Typical inflammatory processes of the
mucous membranes of the respiratory tract. There is hypersalivation.

2. Local anesthetics. Classification according to chemical structure. The mechanism of anesthetic

action. The use of drugs for different types of anesthesia. Factors that prolong the anesthetic effect.
Comparative characteristics of drugs with procaine. Causes of idiosyncrasy to procaine.
Ans: Mechanism of anesthetic action.
The mechanism is expressed in the blocking of nerve conduction. They reduce the permeability of the cell
membrane for Na + leads to membrane depolarization. They displace Ca2+ from receptors located on the
inner surface of the membrane. By changing the action potential in the membranes of nerve cells, local
anesthetics do not lead to a pronounced change in the resting potential. Small nerve fibers are more sensitive
to the action of anesthetics than large ones. At the same time, non-myelinated fibers are more easily blocked
than myelinated ones.
The use of drugs for different types of anesthesia.
1. For surface anesthesia: cocaine, dicaine, lidocaine.
2. For infiltration anesthesia: novocaine, trimecaine, lidocaine
4. For conduction anesthesia: novocaine, trimecaine, lidocaine
5. For spinal anesthesia: trimekain
Factors prolonging the anesthetic effect.
To reduce the systemic action, toxic effect and prolong the effect of local anesthetics, they are used in
combination with vasoconstrictors (adrenaline). They slow down the absorption of a local anesthetic. Add 1
ml of adrenaline per 100 ml of anesthetic solution. In addition to adrenaline, a 0.02% solution of
noradrenaline is used in the ratio.
Comparative characteristics of drugs with novocaine.
Lidocaine has a more pronounced intensity and duration of action (3-5 hours), does not have a toxic
effect on respiratory function. The anesthetic effect is 4 times greater than that of novocaine, the toxicity
is 2 times higher.

Sovkain-the anesthetic effect is 20 times greater than novocaine, the toxicity is 30 times greater.
Trimekain- Anesthetic efficacy and duration of the drug is three times higher than novocaine, but it is 1.5
times more toxic.
Causes of idiosyncrasy to novocaine: Idiosyncrasy is based on congenital increased reactivity and
sensitivity to certain stimuli or a reaction that occurs in the body as a result of repeated weak effects of
certain substances.

3. The subject of Pharmacology and its position in the system of medical education. The
importance of Pharmacology for medical education. Characteristics of the main stages of
Pharmacology development. The role of Hippocrates, Galen, Avicenna, and Paracelsus in the
development of medicinal science.
Ans: Pharmacology is the science of the interaction of chemical compounds with living organisms. pharmacology mainly
studies medicines used for the treatment and prevention of various diseases and pathological conditions. One of the most
important tasks of pharmacology is to find new effective and safe medicines. The range of pharmacological studies is very
wide. It includes the study of the effect of substances on biological systems of varying complexity - from the whole
organism to individual cells, subcellular formations, receptors and enzymes. Changes in the functioning of the biological
system caused by chemicals serve as a manifestation of their biological action (activity). Pharmacology studies medicines
used in medicine for the treatment and prevention, as well as diagnostics in patients (and animals) of various diseases and
pathological processes, that is, in essence, pharmacology is the science of medicines used in medicine for various
purposes.
The history of the use of medicinal substances in medicine dates back to ancient times. For a long time,
people with diseases instinctively sought to alleviate their suffering by resorting to one therapy or another.
They drew medicines from the plant world, and as they gained experience, they began to use substances of
animal and mineral origin. The search for remedies was empirical, that is, on the basis of personal
experience, and attention was paid primarily to such remedies that attracted ancient man with their shape,
color, smell, taste, and strong physiological effect. Some books containing information about herbal
preparations, as well as preparations prepared on the basis of metals,
means of animal origin for about 3000 years. The medicines first described in the Ayurveda (books of life)
were later to some extent replaced by chemicals or even modified by the alchemists.
The first systematization of the existing experience in the treatment of patients with drugs was made in the
4th century BC, when the ancient Greek physician and thinker Hippocrates brought together medical
observations and made an attempt to give them a philosophical justification. Since Hippocrates was not a
supporter of the widespread use of drugs, he recommended only the logically justified use of simple and
effective remedies.
Pharmacology was further developed in the works of Galen, the largest representative of Roman medicine in
the 2nd century AD. Unlike Hippocrates, who believed that medicines were given in nature in finished form,
Galen introduced into practice the extraction of useful principles from natural materials, most often from
plants. Such drugs are still called galenic.
Science received further development about drugs in the writings of Avicenna (X century AD). The scientist
left a wonderful work "The Canon of Medical Art" in 5 books, and the second book of the "Canon" is
devoted to the study of simple medicines from the point of view of a practical doctor.
XYI century, in the Renaissance, the greatest thinker Paracelsus (Theophrastus Hohenheim) opposed the
teachings of Hippocrates-Galen. This physician was the founder of iatrochemistry. He gave rise to the
chemical branch of pharmacology.

Ticket 2
1. Anticholinesterase drugs. Classification of drugs by mechanism of action. Pharmacological effect.
Indications and contraindications for their use. Symptoms of poisoning with drugs of the
organophosphorus compounds group and first aid measures.
ANS: Classification of drugs according to the mechanism of action.
a. Reversible drugs - Physostigmine salicylate Prozerin Galantamine hydrobromide
b. Irreversible drugs - Armin
Drugs name; galantamine, Physostigmine, neostigmine ,rivastigmine,donepenzil.
Mechanism of Action:
neostigmine;
Inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to
acetylcholinesterase at sites of cholinergic transmission
Donepezil binds and reversibly inactivates the cholinesterases, thus inhibiting hydrolysis of acetylcholine.
This increases acetylcholine concentrations at cholinergic synapses.
Pharmacological effects:
1) CNS: low doses - diffuse EEG activation, psychostimulation, high doses - generalized convulsions,
coma, respiratory arrest.
2) Eye, GI tract, MPS, respiration: effects of parasympathetic stimulation (miosis, lachrymation, salivation,
intestinal spasms, vomiting, diarrhea, frequent urination, bronchospasm, hypersecretion)
3) CCC: medium doses - moderate bradycardia and a decrease in cardiac output, high doses - bradycardia, a
decrease in blood pressure
4) Skin – increased perspiration
5) Skeletal muscles - fasciculations, weakness, depolarization block, paralysis.
Indications for use: myasthenic syndrome, postoperative intestinal atony, atonic constipation, bladder
emptying disorders after gynecological operations and childbirth, elimination of the effect of non-
depolarizing curariform drugs, peripheral striated muscle paralysis, poliomyelitis, encephalitis, weakness of
labor activity, optic nerve atrophy, for constriction of the pupil and a decrease in intraocular pressure in
open-angle glaucoma.
Contraindications for use: mechanical obstruction of the intestines or urinary tract, bronchial asthma,
hypersensitivity to anticholinesterase drugs, epilepsy, angina pectoris, atherosclerosis.
Symptoms of poisoning with drugs of the FOS group:
Excitation of M-cholinergic receptors (miosis, salivation, sweating, vomiting, diarrhea). The greatest threat
is bronchospasm with pulmonary edema.
Help measures.
First of all, FOS should be removed from the injection sites. If it is the skin or mucous membranes, they
must be thoroughly washed with a 3-5% solution of sodium bicarbonate. When substances enter the
digestive tract, the stomach is washed, adsorbents and laxatives are given, and high siphon enemas are
prescribed.

2. Drugs belonging to the group of enveloping agents. Mechanism of action, indications for use.
Adsorbents, the essence of their action, indications for use. Modem enterosorbents.
Ans: Magnesia white (basic magnesium carbonate);
aluminum hydroxide; Vikair; Liquiriton; Sucralfate; Phosphalugel; Almagel.
1.Mechanism of action, indications for use.
Mechanism of action: They line the mucous membranes with a thick colloidal film, protecting sensitive
receptors from irritation.
Indications: acute inflammatory diseases of the gastrointestinal tract (gastritis, enteritis, enterocolitis,
colitis); acute poisoning with alkaloids, heavy metals (tannin is used to bind and precipitate these poisons);
peptic ulcer, chronic gastritis and duodenitis; chemical burns of the mucosa.
2. Adsorbing agents, the essence of their action, indications for use.Insoluble indifferent powders with a
high adsorption capacity, binding various substances on their surface, reducing their absorption,
mechanically protecting the mucous membrane and the endings of the sensory nerves located in it. The most
commonly used adsorbents are activated charcoal and white clay. With flatulence (to absorb gases), diseases
of the gastrointestinal tract and acute poisoning, activated charcoal is prescribed inside. In diseases of the
skin and mucous membranes, talc, white clay, magnesium oxide, zinc oxide, etc. are applied externally.
3. Modern enterosorbents.
Activated carbon-has a high surface activity and high sorption capacity. Reduces absorption from the
gastrointestinal tract of toxic substances, salts of heavy metals, alkaloids and glycosides, medicinal
substances, contributing to their excretion from the body. It adsorbs gases on its surface. Indications:
Dyspepsia, intoxication with dysentery, salmonellosis, food poisoning, flatulence, drug poisoning.
Enterosgel-detoxifying action when taken orally, has sorption and detoxification properties. In the lumen of
the gastrointestinal tract, the drug binds and removes endogenous and exogenous toxic substances of various
nature from the body. Indications: acute and chronic intoxication, poisoning with poisons and potent
substances, intestinal infections, food and drug allergies.
Smekta-stabilizes the mucous barrier, increases the amount of mucus, improves its gastroprotective
properties. Indications: acute and chronic diarrhea, infectious diarrhea, symptomatic treatment of heartburn,
bloating, dyspepsia.

3. Peculiarities of drugs absorption and action while enteral administration (sublingual, in the
stomach, rectal). The effect time of development, the influence of the stomach environment pH on the
absorption of drugs-acids and drugs-bases.
Ans: 1.Ingestion (oral route)
When characterizing the absorption of drugs from the digestive tract, it must be taken into account that the
gastric mucosa has a large thickness, a small absorption surface, high electrical resistance, and is covered
with mucus. The intestinal epithelium is thin, with low electrical resistance, and forms a significant suction
surface. Medicines, even in the form of ions, are absorbed faster from the intestines. The effect occurs in 15-
40 minutes, the dose is 2-3 times higher than with parenteral administration. In some cases, medicines
intended for local action in the intestinal lumen are prescribed orally.
2. Sublingual (resorption under the tongue)
Resorption in the oral cavity ensures the rapid flow of drugs into the system of the superior vena cava,
while there is no action of digestive juices and liver enzymes. Only drugs with high lipid solubility are
taken sublingually - nitroglycerin for the relief of an angina attack, antihypertensive drugs - clonidine,
nifedipine for hypertensive crisis, steroid hormones - methyltestosterone, pregnine, anabolic drugs.
3. Rectal route
The rectal route is necessary when it is impossible to take drugs inside. From the rectum, 50% of the dose
is absorbed into the system of the inferior vena cava, bypassing the liver, and 50% enters the portal vein
and is partially inactivated in the liver.
The onset of the effect. Absorption of drugs when taken orally begins after 15-30 minutes. The effect of
sublingual administration occurs by the end of the first minute. The therapeutic effect in the rectal route of
administration develops after 5–15 minutes.
an increase in the pH value of the mediumthe dissociation of acids increases and that of bases decreases.

Ticket 3
1. M-cholinoblockers(drugs) of central and peripheral actions. Mechanism of action and
pharmacological effects of atropine and other M-cholinoblockers in comparison with it. Indications
and contraindications for use. Symptoms of atropine poisoning and first aidmeasures.
Ans: Mechanism of action:blockage of M-Chr. A classic example is atropine: it blocks all types of
muscarinic receptors, relieves the tonic effect of the central nervous system on internal organs, competitive
blockage by atropine is removed with an increase in the concentration of ACh or muscarinic agonists,
prevents the formation of IF3 in M 1 - and M 3 -Xr or reduces the level of cAMP in M2-Chr.
Drugs name; galantamine, Physostigmine, neostigmine ,rivastigmine,donepenzil.
Mechanism of Action:
neostigmine; Inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to
acetylcholinesterase at sites of cholinergic transmission
Donepezil binds and reversibly inactivates the cholinesterases, thus inhibiting hydrolysis of acetylcholine.
This increases acetylcholine concentrations at cholinergic synapses.
Pharmacological effects of atropine:
1) Skin: blockage of sweating, dry skin, possibly hyperpyrexia, flushing
2) Vision: cycloplegia, mydriasis, difficulty in outflow of fluid (increased intraocular pressure), decreased
lachrymation.
3) Gastrointestinal tract: hyposalivation, decreased tone and motility of the gastrointestinal tract, vagal
secretion of the stomach, pancreas, intestines, bile.
4) Respiratory system: bronchial dilatation, decreased secretion of bronchial glands.
Other M-anticholinergics in comparison with it: If atropine has a stronger effect on the heart, bronchi, and the
digestive tract, then scopolamine affects the eyes and the secretion of a number of excretory glands. Scopolamine has a
shorter effect than atropine.
In terms of CNS effects, scopolamine differs significantly from atropine. At therapeutic doses, scopolamine
usually causes sedation, drowsiness, and sleep. It does not affect the CNS. It differs from atropine in a more
pronounced bronchodilator effect. In terms of effect on the eye, it is much weaker than atropine.
Indications for use: peptic ulcer of the stomach and duodenum, spastic conditions of the gastrointestinal
tract, biliary tract, ureters, irritable bowel syndrome, urological disorders: MP hyperkinesia with cystitis,
hypersalivation and increased secretion of bronchial mucus during anesthesia, reflex bradycardia and
arrhythmia during anesthesia, poisoning with inhibitors ACCE, muscarine (atropine)
Contraindications for use: glaucoma, heart disease, gastrointestinal obstruction, ulcerative colitis.
Symptoms of atropine poisoning: Suppression cholinergic effects and the effect of the substance on the
central nervous system. There is dryness of the mucous membrane of the oral cavity, nasopharynx, which is
accompanied by a violation of swallowing, speech. The skin becomes dry. Body temperature rises. Pupils
are wide, photophobia is typical.
Help measures:Treatment consists in removing unabsorbed atropine from the gastrointestinal tract,
accelerating the excretion of the substance from the body (forced diuresis, hemosorption) and the use of
physiological antagonists (for example, anticholinesterase agents that penetrate well into the central nervous
system) . With severe arousal, diazepam (sibazon) is prescribed, sometimes short-acting barbiturates. In case
of excessive tachycardia. it is advisable to use β-blockers. Decrease in body temperature is achieved by
external cooling.

2. Ethyl alcohol. Pharmacokinetic features (oxidation rate, energy potential, elimination).

Pharmacodynamic effects (influence on the cerebral cortex, CNS, pulse transmission, microsomal
liver apparatus, analgesic effect, genetic apparatus). Indications for use for medical purposes.
Symptoms of acute ethanol poisoning and first aid measures.
Ans: When taken orally, it is rapidly absorbed mainly in the small intestine and about 20% in the stomach.
The rate of absorption depends on the nature of the contents of the gastrointestinal tract and the intensity of
peristalsis. Especially quickly resorptive action occurs on an empty stomach. Fats and carbohydrates delay
its absorption. 90% metabolized to CO2and water. In the liver, alcohol is oxidized (at a rate of 10 ml / h),
while energy is released (7.1 kcal / g). With prolonged use - the induction of liver enzymes, in which the
rate of alcohol inactivation increases. Unchanged, it is excreted by the lungs, kidneys and sweat glands.
Pharmacodynamic effects (influence on the cerebral cortex, central nervous system, impulse
transmission, liver microsomal apparatus, analgesic effect, genetic apparatus).
The resorptive action is aimed at the central nervous system - an inhibitory effect, which increases with an
increase in the concentration of ethyl alcohol in the blood and brain tissues. 3 stages:
1) The stage of excitement - euphoria, increased mood, the person is overly sociable. Behavior, self-control
suffer, inadequate assessment of the environment; performance is reduced.
2) Stage of anesthesia: analgesia, drowsiness occur, consciousness is disturbed. Spinal reflexes are
suppressed. There comes the stage of anesthesia, which, however, is short-lived and 3) Agonal: complete
paralysis of the central nervous system.
Central effect on the central nervous system: influence on thermoregulation - increased heat transfer
(expansion of skin vessels - inhibition of the vasomotor center). Therefore, in the cold, ethyl alcohol
contributes to hypothermia.
Diuretic effect - the production of antidiuretic hormone of the posterior pituitary gland decreases). Effect on
the digestive system: enhances the secretory activity of the salivary and gastric glands. An increase in the
secretion of the gastric glands with direct exposure to alcohol is associated with the release of humoral
substances (gastrin, histamine). Alcohol enhances the secretion of HCl. In response to an irritating effect on
the mucous membrane, the glands of the stomach produce a large amount of mucus. The motility of the
stomach also changes. In high concentrations, it causes pyloric spasm and reduces gastric motility.

Indications for use in medical purposes.

Sometimes - as an anti-shock agent (given its analgesic effect), rarely - as a hypnotic or sedative. In some
cases, the appointment of ethyl alcohol (in low concentrations) for malnourished patients is indicated -
energy value. However, it should be borne in mind that ethyl alcohol is not a nutrient. It is used as an
antiseptic for the treatment of surgeons' hands, instruments, surfaces, a drying agent, for the preparation of
tinctures, warming compresses. As an antidote for methanol poisoning.
Symptoms of acute ethanol poisoning and measures to help.
Symptoms:• Emotional lability; Violation of redness of the face; Nausea and vomiting;
Coma superficial: no speech contact, loss of consciousness, decreased pupillary reflexes,
oppressed pain sensitivity, decrease or increase in muscle tone
and
tendon reflexes; floating movements of the eyeballs, the pupils are usually constricted, with
increase in respiratory disorders expand,
Deep: complete loss of pain sensitivity, absence or sharp decline corneal, pupillary, tendon reflexes, muscle
atony, decrease in body temperature, tachypnea, acrocyanosis, tachycardia, a sharp decrease in blood
pressure, dilated pupils.
Relief measures: Ensure adequate ventilation of the lungs. Spend a toilet of the oral cavity, clean the upper
respiratory tract. To reduce the secretion of the salivary and bronchial glands, atropine is administered.
Administer oxygen inhalation. If necessary - IVL. Enter analeptics (to stimulate the respiratory and
vasomotor centers) - corazole, cordiamine, caffeine. The stomach is washed, forced diuresis is carried out.
Correction of the acid-base state (sodium bicarbonate is administered intravenously). In a serious condition
of the patient - hemodialysis.

Ticket 4
1. ß-blockers. Drugs classification, mechanism of action, main pharmacological effects. Indications
and contraindications for use. Side effects.
Ans: Classification of drugs
Non-selective. They act equally on both types of β-adrenergic receptors (propranolol).
Selective. They act to a greater extent on β1-adrenergic receptors (metoprolol, atenolol, etc.).
Mechanism of action: consists in preventing the cardiotoxic effect of catecholamines, reducing heart rate,
myocardial contractility and blood pressure, which leads to a decrease in myocardial oxygen demand.
Improvement in perfusion of ischemic myocardial regions with the use of β-blockers is also due to diastole
lengthening and "reverse coronary steal" due to an increase in vascular resistance in non-ischemic areas of
the myocardium.
propranolol. It competes with sympathomimetic neurotransmitters for binding to receptors, which inhibits
sympathetic stimulation of the heart
Metoprolol is a cardioselective beta-1-adrenergic receptor inhibitor that competitively blocks beta1-
receptors with minimal or no effects on beta-2 receptors at oral doses of less than 100 mg in adults.
Pharmacological effects
β1-blockers
1) decrease in the automatism of the sinus node, decrease in heart rate, slowing down of AV conduction,
decrease in myocardial contractility and excitability, decrease in cardiac output, decrease in myocardial
oxygen demand
2) suppression of the stimulating effect of catecholamines on the heart during physical and psycho-
emotional stress.
3) hypotensive effect
4) normalization of the heart rate in supraventricular tachycardia and atrial fibrillation
5) limiting the zone of myocardial ischemia in myocardial infarction
β1, β2-blockers
1) reduce heart rate, myocardial contractility, reduce blood pressure
2) reduce myocardial oxygen demand (by reducing contractility), stabilize lysosomal membranes and
increase the resistance of cardiomyocytes to ischemia
3) reduce the activity of ectopic foci of excitation in the heart
4) reduce the production of renin in the kidneys
Indications and contraindications for use.
β1-blockers.
Indications: arterial hypertension, prevention of angina attacks, cardiac arrhythmias, secondary prevention
after myocardial infarction, hyperkinetic cardiac syndrome (including with hyperthyroidism), prevention of
migraine attacks
Contraindications: AV blockade II and III degree, sinoatrial blockade, bradycardia (heart rate less than 50
beats / min, arterial hypotension, chronic heart failure stage II B-III, acute heart failure, cardiogenic shock,
metabolic acidosis, severe peripheral circulatory disorders , hypersensitivity to drugs.

β1, β2-blockers.
Indications: arterial hypertension, exertional angina, unstable angina, sinus tachycardia (including with
hyperthyroidism), supraventricular tachycardia, supraventricular and ventricular extrasystole, essential
tremor, migraine prevention, symptomatic therapy for thyrotoxicosis, fear syndrome.
Contraindications: AV blockade II and III degree, sinoatrial blockade, bradycardia (heart rate less than 55
beats / min), arterial hypotension, chronic heart failure stage II B-III, acute heart failure, bronchial asthma
and other obstructive respiratory diseases, vasomotor rhinitis.
Side effects
1) Digestive system: dry mouth, nausea, vomiting, diarrhea, constipation; in some cases - liver dysfunction
2) CNS and peripheral nervous system: weakness, fatigue, dizziness, headache, muscle cramps, feeling
cold and paresthesia in the extremities, depression, sleep disturbances, nightmares
3) Eye: hypolacrimation, conjunctivitis
4) Endocrine system: hypoglycemic conditions in patients with diabetes mellitus
5) Respiratory system: symptoms of bronchial obstruction may appear in susceptible patients
6) Allergic reactions: skin rash, itching

2. Antitussive drugs. Classification by mechanism of action. Mucolytic drugs, the mechanism of

expectorant action of these drugs. Peculiarities of particular drugs. Expectorants of direct and reflex
types of action.
Ans: Codeine- opium alkaloid, direct inhibition of the neurons of the cough center. Weak analgesic effect -
associated with the transformation in the body into morphine.
В therapeutic doses practically does not depress the respiratory center. With prolonged use - addiction and
drug dependence.
Ethylmorphine hydrochloride- has a pronounced inhibitory effect on the cough center. It is used to calm
the painful unproductive cough in lung diseases, bronchitis, tracheitis.
Glaucine -selectively inhibits the activity of cough center neurons. Does not depress the respiratory center.
Does not cause addiction, drug dependence.
Libekin-blocks the peripheral links of the cough reflex due to: local anesthetic action, reduces the irritability
of peripheral cough receptors of the respiratory tract; bronchodilatory action - suppression of stretch
receptors involved in the cough reflex; a slight decrease in the activity of the respiratory center (without
respiratory depression).
3) Expectorants of direct and reflex type of action.
a) reflex action They have a moderate irritating effect on the receptors of the gastric mucosa and reflexively
increase the activity of the ciliated epithelium of the respiratory tract, stimulate the peristaltic contractions of
the bronchioles, promoting the promotion of sputum from the lower to the upper respiratory tract and its
removal. This effect is usually combined with an increase in the secretion of the bronchial glands and a
slight decrease in the viscosity of the sputum, which also facilitates its separation. Some drugs have a direct
effect in part - essential oils are excreted through the respiratory tract and cause increased secretion and
sputum thinning. Apply: infusions and extracts of thermopsis herb, decoction of istod root, preparations of
licorice root, marshmallow root, 6)
direct acting expectorantsThese include sodium iodide, potassium iodide,
ammonium chloride, sodium bicarbonate. The drugs are secreted by the mucous membrane of the
respiratory tract, stimulate the secretion of bronchial glands and cause liquefaction (hydration) of sputum;
reduce its viscosity, they also slightly increase the motor activity of the ciliated epithelium of the respiratory
tract.
4) Mucolytic drugs, the mechanism of expectorant action of these drugs.
The mechanism is aimed at stimulating the serous cells of the glands of the bronchial mucosa and activating
the hydrolase. The action can be mediated by a thinning effect on the mucous membranes, facilitate the
removal of viscous secrets and exudates in inflammatory diseases of the respiratory tract. Acetylcysteine
(ACC, Mukosolvin, Mukobene), carbocysteine (Mukodin, Mukosol), bromhexine (Solvin, Bizolvon) are
used , Ambroxol (Ambrobene, Ambrohexal, Lazolvan).

3. The concept of bioavailability of drugs. The influence of dosage form on bioavailability. Period of
preliminaly and its dependence on the Association of drug with blood plasma proteins.
Ans: The parameter that characterizes the absorption of drugs is bioavailability. Bioavailability shows how
much of the administered dose of the drug entered the systemic circulation and characterizes the rate at
which this occurs. Factors affecting bioavailability:
1. Dose of medicinal substance.
2. The route of administration of the drug substance (with the intravenous route of administration,
bioavailability
100%).
3. Chemical structure (some drugs are destroyed by the acidic contents of the stomach, so they are not
administered orally, for example, penicillin, insulin).
4. The state of the gastrointestinal tract (accelerated peristalsis disrupts absorption, therefore,
bioavailability is reduced).
With intravenous administration, the bioavailability of the drug is 100%. (However, the bioavailability can
be reduced by the introduction of another drug). If the substance is administered by other routes (eg, orally),
then its bioavailability is reduced, as a result of its incomplete absorption and metabolism, which this drug
undergoes as a result of the first pass.
Elimination half periodexpresses the relationship between the volume of distribution and the clearance of a
substance and depends on both of these parameters. The half-life of the drug (t1 / 2) depends on both the
volume of its distribution (Vd) and the clearance of the drug (Cl). Changes in drug binding to proteins can
affect both the volume of distribution and clearance of the drug, sometimes in completely opposite
directions.
The volume of distribution is the conditional volume of liquid necessary for the uniform distribution of the
drug in it, which is found in therapeutic concentration in the blood plasma.
If the volume of distribution is less than 0.5 l / kg, the drug is located mainly in the blood plasma and in the
extracellular fluid, if more, the drug is distributed throughout the aqueous phase and in low-vascularized
tissues.
If the volume of distribution is more than 1 l / kg, the substance is mainly found in lipids, muscles and other
tissues. In this case, the use of hemosorption in case of poisoning is useless.

Ticket 5
1. α-blockers. Drugs classification, mechanism of action, main pharmacological effects. Indications
and contraindications for use.
Ans: Classification of drugs:
a) α1-blockers - doxazosin, prazosin, tamsulosin (α1A - antagonist)
b) α2-blockers - iohimbine
c) α1- and α2-blockers - phentolamine, dihydroergotamine.
Mechanism of action:
α-Adrenoblockers block the activation of postsynaptic α1-adrenergic receptors by circulating and neuronal-
released catecholamines. This leads to dilatation of resistive vessels and a decrease in peripheral resistance.
There is no significant change in cardiac output, due to concomitant venous dilatation (decreased venous
return) and simultaneous slight reflex activation of the sympathetic nervous system by vasodilation.
Doxazosin works by relaxing blood vessels so that blood passes through them more easily. This helps to
lower blood pressure. Doxazosin is also used to treat benign (noncancerous) enlargement of the prostate
(benign prostatic hyperplasia
iohimbine; Blocks presynaptic α2 adrenergic receptors. This effect can increase sympathetic outflow and
potentiate the release of norepinephrine from nerve endings, leading to activation of α1 and β1 receptors
in the heart and peripheral vasculature, with a consequent rise in blood pressure.
Main pharmacological effects:
1) decrease in total peripheral vascular resistance and decrease in blood pressure, decrease in afterload on
the heart
2) expansion of peripheral veins, reduction of preload on the heart
3) improvement of systemic and intracardiac hemodynamics in patients with chronic heart failure
4) decrease in pressure in the pulmonary circulation
5) improvement of the blood lipid profile (reduction of total cholesterol due to LDL and increase in HDL
levels)
6) increased tissue sensitivity to insulin
Indications: arterial hypertension, chronic heart failure (as part of combination therapy)
Contraindications: arterial hypotension, chronic heart failure against the background of constrictive
pericarditis, cardiac tamponade, heart defects with reduced filling pressure of the left ventricle, pregnancy,
lactation, children under 12 years of age, hypersensitivity to prazosin.

2.
Ticket 6
1. Adrenomimetics. Classification of drugs by the mechanism of action. Mechanisms of action of drugs
of different groups, pharmacological effects of drugs that affect different types of adrenoreceptors
(except epinephrine). Indications and contraindications to the use of various drugs.
Ans: Classification of drugs according to the mechanism of action.
. direct action (epinephrine, norepinephrine, phenylephrine, isadrine, etc.);
. indirect action (neofedrin).
Mechanisms of action of drugs of different groups,
Adrenomimetics of direct action bind to adrenergic receptors, while indirect adrenergic agonists increase the
release of norepinephrine or inhibit its reuptake. Differences between drug effects direct and indirect action
become especially pronounced if the stocks of endogenous norepinephrine changed - exposure to certain
antihypertensive drugs, inhibitors.
MAO. In these cases, only direct adrenomimetics should be used.
Drugs name; methoxamine, phenylephrine ,oxymetazoline,dobutamine,
Mechanisms of action;
Dobutamine is a synthetic catecholamine that acts on alpha-1, beta-1 and beta-2 adrenergic receptors. In
the heart, the stimulation of these receptors produces a relatively strong, additive inotropic effect and a
relatively weak chronotropic effect
Pharmacological effects of drugs that affect different types of adrenergic receptors (except adrenaline).

● α1-agonists :
1) increased total peripheral vascular resistance and blood pressure,
2) reflex bradycardia (increased vagal tone in response to hypertension),
3) vasoconstrictor effect when applied topically,
4) mydriasis, lowering intraocular pressure in open-angle glaucoma.
● β1-adrenergic agonists:
1) positive inotropic effect (increase in heart rate).
2) decreased ventricular filling pressure,
3) increased coronary blood flow, improved myocardial oxygen supply,
4) increased renal perfusion and increased excretion of sodium and water (by increasing CO)
● β2-agonists:
1) prevention and relief of bronchospasm, reduced resistance in the airways, increased lung capacity,
2) prevention of the release of histamine, a slowly reacting substance from mast cells and neutrophil
chemotaxis factors,
3) a positive chrono- and inotropic effect on the myocardium,
4) expansion of the coronary arteries,
5) a decrease in the tone and contractile activity of the myometrium.
● α, β-agonists:
1) an increase in the frequency and force of heart contractions, UO and IOC,
facilitation of AV conduction, increased automatism,
2) increased myocardial oxygen demand,
3) vasoconstriction of the abdominal organs, skin, mucous membranes, to a lesser extent - skeletal muscles,
4) increased peripheral vascular resistance (in high doses) and blood pressure (mainly systolic ),
5) relaxation of the SMC of the bronchi,
Indications for use and contraindications for use:
α-agonists.
Indications: reduction of swelling of the mucous membrane of the nasopharynx, conjunctiva with colds
and allergic diseases, increased blood pressure during collapse and arterial hypotension due to a decrease
in vascular tone Contraindications: arterial hypertension, severe atherosclerosis, tendency to spasms of
coronary vessels β1-agonists.
Indications: AHF and CHF (with decompensation as a temporary adjuvant against the background of
traditional therapy), low IOC as a side effect of mechanical ventilation, a diagnostic tool for IHD
Contraindications: idiopathic hypertrophic subaortic stenosis, hypersensitivity to β2-agonists.
Indications: long-term regular treatment of reversible airway obstruction in bronchial asthma and COPD, to
prevent symptoms at night and / or daytime caused by reversible airway obstruction, prevention and relief of
bronchospasm in all forms of bronchial asthma, bronchial obstructive syndrome in children, threatening
preterm labor with contractile activity of the uterus; childbirth before 37-38 weeks of gestation, isthmic-
cervical insufficiency, decrease in fetal heart rate depending on uterine contractions during periods of
cervical dilatation and expulsion
Contraindications: hypersensitivity to drugs, the threat of miscarriage in the I and II trimesters of
pregnancy, premature detachment of the placenta, bleeding or toxicosis in the III trimester of pregnancy,
children under 2 years of age
α and β-
agonists.Indications:
a) systemic application: anaphylactic shock and some other immediate allergic reactions, relief of bronchial
asthma attacks, insulin overdose b) topical application: stopping bleeding, prolonging the action of local
anesthetics, for lowering intraocular pressure in open-angle glaucoma (danger of arrhythmias).

2. Antidepressants. Classification of drugs by mechanism of action. Possible mechanisms of

antidepressant effect of drugs of different groups. Tactics of prescribing MAO inhibitors. Side effects
of particular drugs.
Ans: Means of indiscriminate neuronal capture:By inhibiting the reuptake of neuronal monoamines,
mainly norepinephrine and serotonin, they reduce or eliminate anxiety, agitation, and the actual depressive
manifestations.
Selective action: Serotonin:The mechanism is associated with an increase in serotonergic activity in the
central nervous system, as a result of inhibition of the reuptake of serotonin by brain neurons. Less
anticholinergic effect, a slight effect on adrenergic-histamine receptors.
Norepinephrine:blocks the reuptake of monoamines, but significantly more strongly inhibits the reuptake
of norepinephrine by presynaptic nerve endings compared to the reuptake of serotonin.
MAO inhibitors:when MAO-A is inhibited, as a result of which the content of noradrenaline and serotonin
increases in the brain tissues. Non-selective-irreversibly block MAO-A and MAO-B, selective-reversibly
block MAO-A
3) Tactics of prescribing MAO inhibitors.
Treatment begins with an average therapeutic daily dose, if necessary, increasing it after 7-10 days until the
appearance of a therapeutic or side effect.
All antidepressants with a stimulating effect are prescribed in the first half of the day, i. up to 15 hours, in
2-3 doses. Drugs with a sedative effect are prescribed in 3 doses, most of the daily dose falls on the second
half of the day.
When using drugs from the group of MAO inhibitors, it is necessary to follow a special diet: it is forbidden
to eat cheese, smoked meats, legumes, bananas, beer, wine, lactic acid products, fish. They cannot be used
in combination with many other, especially adrenomimetic, drugs.
4) Side effects of individual drugs.
Prozac-diarrhea, nausea, vomiting, dysphagia, convulsions, ataxia, dizziness, fatigue
(drowsiness, asthenia), violation of the process of concentration and thinking,
manic
reaction, mydriasis, blurred vision, dry mouth, increased sweating, itching, skin
rash, urticaria, photosensitivity
Amitriptylinedry mouth, urinary retention, constipation, intestinal obstruction, blurred vision,
accommodative paresis, increased intraocular pressure,reinforced sweating. achycardia, orthostatic
hypotension, arrhythmia, stomatitis, taste disturbance,darkening of the tongue. skin rash,itching,
agranulocytosis, leukopenia,eosinophilia thrombocytopenia
Maprotilin-Orthostatic hypotension, tachycardia, convulsions, ataxia, feeling hot, blurred vision,
disturbances of accommodation, impaired coordination of movements and handwriting, hair loss, increased
appetite, aggressiveness, impaired memory and concentration, increased depression.

3. Basic mechanisms of absorption. Influence of physical and chemical properties of drugs on drug
transport (ionization, molecular weight, lipid solubility, etc.).
Ans: Absorption is the process by which drugs enter the bloodstream from the site of administration.
There are 4 main mechanisms of absorption: diffusion, filtration, active transport, pinocytosis.
Passive diffusion occurs through the cell membrane. Absorption occurs until the concentration of the drug
on both sides of the biomembrane is equal. Passive diffusion of substances proceeds without energy
expenditure along the concentration gradient.
Facilitated diffusion is the transport of drugs through biological membranes with the participation of
molecules of specific carriers. In this case, the transfer of the drug is also carried out along the
concentration gradient, but the transfer rate is much higher.
Filtration is carried out through the pores of cell membranes. This mechanism of passive absorption
proceeds without energy expenditure and is carried out along a concentration gradient. characteristic of
hydrophilic substances.
Active transport is carried out with the participation of specific transport systems of cell membranes. Unlike
passive diffusion and filtration, active transport is an energy-consuming process and can be carried out
against a concentration gradient.
Pinocytosis (corpuscular absorption or pensorption) is also a type of absorption with energy expenditure,
the implementation of which is possible against a concentration gradient. In this case, the capture of the
drug substance and invagination of the cell membrane with the formation of a vacuole occurs, which goes
to the opposite side of the cell, where exocytosis occurs with the release of the drug compound.
Chemical structure, physicochemical and physical properties of medicines. Effective interaction of a
substance with a receptor requires such a structure of the drug that provides the closest contact with the
receptor. The strength of intermolecular bonds depends on the degree of convergence of a substance with a
receptor. For the interaction of a substance with a receptor, their spatial correspondence, i.e.,
complementarity, is especially important. This is confirmed by differences in the activity of stereoisomers. If
a substance has several functionally active groups, then the distance between them must be taken into
account. Many quantitative and qualitative characteristics of the action of a substance also depend on such
physical and physico-chemical properties as solubility in water and lipids; for powdered compounds, the
degree of their grinding is very important.
Ticket 7
1. Adrenomimetics. Localization of adrenoreceptors of different types. Drugs classification by their
effect on different types of adrenoreceptors. Pharmacological effects of the drugs influencing the
different types of adrenoreceptors. Pharmacological effects of epinephrine, indications and
contraindications for its use.
Ans: Localization of adrenoreceptors of different types: α1-adrenergic receptors are localized
postsynaptically, α2-adrenergic receptors - presynaptically and outside synapses. β1-adrenergic receptors
(for example, in the heart), β2-adrenergic receptors (in the bronchi, vessels, uterus) and β3-adrenergic
receptors (in adipose tissue)
Drugs name; methoxamine, phenylephrine ,oxymetazoline,dobutamine,
Mechanisms of action;
Dobutamine is a synthetic catecholamine that acts on alpha-1, beta-1 and beta-2 adrenergic receptors. In
the heart, the stimulation of these receptors produces a relatively strong, additive inotropic effect and a
relatively weak chronotropic effect
Classification of drugs according to the effect on different types of adrenergic receptors.
I. Direct adrenomimetics:
1) Non-selective - Adrenaline hydrochloride, Norepinephrine hydrochloride
2) α-agonists:
a) α 1-agonists Mezaton, Gutron
b) α 2-agonists central: Clonidine, Guanfacine,
Methyldopa peripheral: Xylometazoline,
Naphazoline
3) β-adrenergic agonists:
a) β 1-agonists: Dobutamine, Dopexamine
b) β 1,2-adrenergic agonists: Isadrin, Orciprenaline sulfate
c) β 2-adrenergic agonists: Salbutamol, Fenoterol, Hexoprenaline
II. Sympathomimetics: Ephedrine hydrochloride
Pharmacological effects of adrenaline:
1) an increase in the frequency and strength of heart contractions, IOC, facilitation of AV conduction, an
increase in automatism,
2) an increase in myocardial oxygen demand,
3) vasoconstriction of the abdominal organs, skin, mucous membranes, to a lesser extent - skeletal muscles,
4) an increase BP (mainly systolic),
5) relaxation of bronchial SMCs,
Indications for use: in anaphylactic shock and some other allergic reactions of immediate type; as a
bronchodilator for the relief of asthma attacks; with hypoglycemic coma caused by antidiabetic agents
(insulin, etc.); to eliminate the atrioventricular block, as well as in case of cardiac arrest (administered
intracardially); pupil dilation and open-angle glaucoma. Adrenaline is added to anesthetic solutions.
Vasoconstriction in the injection area of adrenaline enhances local anesthesia and reduces the resorptive and
possible toxic effects of anesthetics.
Contraindications for use:
1) When administered intravenously, adrenaline can cause cardiac arrhythmias, in the form of ventricular
fibrillation.
2) Slight restlessness, tremor, agitation.
3) With the introduction of adrenaline, pulmonary edema may occur.

2. Antiparkinsonian drugs. Classification by mechanism of action. The possibility of using central and
peripheral muscle relaxants (drugs) in case of parkinsonism. Side effects of particular drugs and their
contraindications.
Ans: Central anticholinergics:
Tropacin-reduces the excitability of peripheral m-cholinergic systems and causes relaxation of smooth
muscles. Indications: treatment of parkinsonism, Parkinson's disease, striatal hyperkinesis, spastic paresis
and paralysis. Contraindications: glaucoma, Side effects: Dry mouth, dilated pupils, dyspepsia, tachycardia,
headache, dizziness.
Also use benztropine mesylate-central anticholinergic. Cyclodol- Blocks central n-cholinergic and
peripheral m-cholinergic receptors. Indications: Parkinsonism, Parkinson's and Little's disease; spastic
paralysis. Side effects: Dry mouth, drowsiness, dizziness, nervousness, delirium, hallucinations, blurred
vision, increased intraocular pressure, constipation, urinary retention, tachycardia, skin rash, purulent
parotitis (with prolonged use). Contraindications: Hypersensitivity, glaucoma (especially angle-closure),
gastrointestinal obstruction, atrial fibrillation, prostate adenoma, pregnancy.
3) Side effects of individual drugs and contraindications for use.
Levodopa: Side effects:Nausea, anorexia, vomiting, epigastric pain, constipation, dysphagia, hypotension,
weakness, dizziness, agitation, insomnia, tachycardia, polyuria. Contraindications: Glaucoma, psychosis,
liver, kidney, cardiovascular, endocrine system disorders, blood diseases, pregnancy, lactation , decreased
visual acuity, allergic reactions, cramps in the calf muscles; rarely - orthostatic hypotension, collapse.
Contraindications: Hypersensitivity, preeclampsia, diseases of the cardiovascular system, arterial hypo- or
hypertension, diseases of the valvular apparatus of the heart, pronounced rhythm disturbance, liver failure.
Midantan: Side effects:convulsions, headache, dizziness, irritability, insomnia, tremor, mental disorders,
visual hallucinations, heart failure, tachycardia, dry mouth, nausea, dyspepsia, polyuria, nocturia, the
appearance of a bluish coloration of the skin of the upper and lower extremities, decreased visual acuity.
Contraindications: Hypersensitivity, epilepsy, thyrotoxicosis, glaucoma, liver and kidney failure, pregnancy

3. Elimination routes of drugs (examples). Changes in drug elimination depending on dose,

age,solubility, polarity, degree of ionization and protein binding, liver, kidney, and cardiovascular
diseases.
Ans: Medicinal substances and their metabolites are excreted from the body:
- with urine - glomerular filtration, active tubular secretion - most drugs in free form.
- with bile - active transport, passive diffusion, pinocytosis - digitoxin, penicillins, tetracyclines,
streptomycin, quinine, strychnine.
- through the intestine - passive diffusion, bile secretion without recycling - doxycycline, ionized organic
acids.
- with saliva - passive diffusion and active transport - penicillins, sulfonamides, salicylates, ethanol.
- through the lungs - passive diffusion - drugs for inhalation anesthesia, iodides, camphor, ethanol, essential
oils.
- with sweat - passive diffusion - some sulfonamides.
- with milk - passive diffusion and active transport - indirect anticoagulants, antibiotics, lithium salts.
Elimination is the removal of a drug from the body by both biotransformation and excretion.
Biotransformation of drugs can occur in the liver, intestinal wall, kidneys and other organs.
Drugs can affect the rate of biotransformation in the liver, inhibiting it (indomethacin, chlorpromazine) or
accelerating it (phenobarbital).
The biotransformation of drugs is affected by hepatic blood flow. If drugs (acetylsalicylic acid) are able to
quickly inactivate, then in acute hepatitis, when the blood flow rate is not reduced, their biotransformation
does not change. It decreases during the cirrhotic process, with depletion of blood flow.
Excretion - the removal of a xenobiotic from the body can be carried out by the liver, kidneys, intestines,
lungs, glands and external secretion. The most important are the liver and kidneys.
The liver excretes both unchanged compounds and metabolites formed in it with bile. At the same time,
most substances are not absorbed back and are excreted by the intestines.
Excretion of drugs by the kidneys consists of their filtration, secretion and reabsorption. Filtration of drugs
in the glomeruli is passive. The molecular weight of substances should not be more than 5-10 thousand, they
should not be associated with blood plasma proteins. Secretion is an active process, independent of the
binding of drugs to plasma proteins. Reabsorption of glucose, amino acids, cations and anions is active,
while fat-soluble substances are passively reabsorbed. In young children (up to 3 years), these processes are
carried out more slowly than in older children.
Filtration is the main mechanism for excretion by the kidneys of drugs that are not bound to plasma proteins.
In renal insufficiency, adjustment of the dosing regimen is carried out by calculating the clearance of
endogenous creatinine. Clearance is the hypothetical volume of blood plasma that is completely cleared of
the drug per unit of time. Normal clearance of endogenous creatinine is 80-120 ml/min.

Ticket 8
1. Anti-anginal drugs. Classification of antianginal drugs (except nitrates) by chemical structure and
mechanisms of anti-ischemic action. Pharmacological effects of particular groups of drugs, Principles
of ischemic heart disease therapy.
Ans: Calcium channel blockers:
Verapamil– Action: block of L-calcium channels, as a result of which conductivity decreases and the
effective refractory period in the sinoatrial and atrioventricular nodes increases (antiarrhythmic action). A
decrease in the supply of calcium ions to myocardial cells leads to a decrease in the use of phosphate bond
energy for the mechanical work of the heart.
. Application: supraventricular tachyarrhythmias and extrasystoles. ischemic heart disease.
Side effects: Hypotension, increased heart failure, atrioventricular blockade, nausea, vomiting, dizziness,
allergic reactions.
Fenigidin(nifedipine): Blocks calcium channels mainly in the vessels - causes a pronounced expansion of
the coronary vessels, and also reduces blood pressure and afterload. This leads to an increase in oxygen
delivery, as well as a decrease in the need for it.
Application: as an antianginal and antihypertensive agent.
Side effects - reflex tachycardia, edema.
Potassium channel activators:
Pinacidil:causes expansion of coronary and peripheral vessels. Reduces
afterload on the heart. Increases heart rate. Side effects: swelling, headache,
palpitations, tachycardia. Application: with vasospastic angina pectoris, with arterial hypertension. With
mild attacks of angina pectoris - validol.
Two main principles of pharmacological correction of coronary artery disease:
1. Expansion of the coronary vessels and thus an increase in oxygen delivery.
2. Decrease in the work of the heart muscle and thus a decrease in myocardial oxygen demand.
Antianginal therapy:
- Beta-blockers (cardioselective BBs: metoprolol, bisoprolol, carvedilol, nebivolol. The criterion for the
adequacy of the dosage is ↓ heart rate at rest). Reduce the likelihood of VS, re-MI, increase the life
expectancy of patients with PICS. Improve prognosis if CAD is complicated by HF
- Inhibitors of If channels of the sinus node (ivabradin). Used for contraindications to the appointment of BB
- Long-acting calcium antagonists (non-dihydropyridines can be an alternative to BB.

2. Indirect anticoagulants , mechanism , indications for use , control of their action Antagonists of
direct and indirect anticoagulants.
Ans:

3. The concept of cumulation , types ( examples ) . Addiction and tachyphylaxis ( examples ) ; possible
causes of these manifestations and principles of overcoming.
Ans: Cumulation(cumulatio accumulation, increase) - strengthening the action of drugs and poisons with
their repeated administration in the same doses.
Distinguish between material and functional cumulation.
under materialimply the accumulation of the active substance in the body, which is confirmed by direct
measurement of its concentration in the blood and tissues. Material cumulation, as a rule, is characteristic of
substances that are slowly metabolized and not completely eliminated from the body. Material cumulation
often occurs when taking a number of cardiac glycosides (for example, digitoxin), alkaloids (atropine,
strychnine), long-acting hypnotics (phenobarbital), indirect anticoagulants (syncumara, etc.), salts of heavy
metals (for example, mercury).
Functional cumulationis more characteristic of substances that affect the activity of the central nervous
system, and, as a rule, indicates a high sensitivity of the body to such substances. A classic example of
functional cumulation is a mental disorder and personality change in chronic alcoholism and drug addiction.
Functional cumulation is also possible when taking antidepressants from the group of MAO inhibitors,
irreversible anticholinesterase agents (phosphacol), etc.
Drug addiction- weakening of the effects of drugs with their repeated use. Rapid addiction to drugs (after 2-
4 injections) is referred to as "tachyphylaxis". Addiction to drugs can be pharmacokinetic and (or)
pharmacodynamic in nature. The basis of the pharmacokinetic mechanisms for the development of addiction
is a decrease in the concentration of drugs in the region of receptors sensitive to them due to changes in the
pharmacokinetics of drugs (drugs from the group of barbituric acid derivatives, benzodiazepine tranquilizers
and some other drugs) with repeated administration. With the pharmacodynamic type of addiction to drugs,
their concentration in the region of the corresponding specific receptors does not change, but there is a
decrease in the sensitivity of organs and tissues to drugs. The reasons for this kind of adaptive response of
the organism to drugs are a decrease in the density of specific receptors, a decrease in their sensitivity to
drugs, and a change in the process of conjugation of the function of receptors of their intracellular mediators
and effector molecular systems. Pharmacodynamic mechanisms are typical for addiction to narcotic
analgesics, adrenomimetics, sympathomimetics, adrenoblocking agents, etc. Quite often, addiction to drugs
develops both as a result of changes in their pharmacokinetics and as a result of a decrease in the body's
sensitivity to them. a decrease in their sensitivity to drugs and a change in the process of conjugation of the
function of the receptors of their intracellular mediators and effector molecular systems. Pharmacodynamic
mechanisms are typical for addiction to narcotic analgesics, adrenomimetics, sympathomimetics,
adrenoblocking agents, etc. Quite often, addiction to drugs develops both as a result of changes in their
pharmacokinetics and as a result of a decrease in the body's sensitivity to them. a decrease in their sensitivity
to drugs and a change in the process of conjugation of the function of the receptors of their intracellular
mediators and effector molecular systems. Pharmacodynamic mechanisms are typical for addiction to
narcotic analgesics, adrenomimetics, sympathomimetics, adrenoblocking agents, etc. Quite often, addiction
to drugs develops both as a result of changes in their pharmacokinetics and as a result of a decrease in the
body's sensitivity to them.
For the prevention of complications, the most important is the correct selection of doses of drugs, the choice
of the optimal scheme for their administration, careful monitoring of the dynamics of functional changes in
the body.

Ticket 9
1. Neuroleptics. Classification according to chemical structure. Pharmacological effects of
chlorpromazine and its mechanisms of action. Indications for the use of drugs of the group, side
effects, contraindications.
Ans: Classification by chemical structure.
A. "Typical" antipsychotics
Phenothiazine derivatives- Aminazine Triftazine Fluorphenazine
Thioxanthene derivatives- Chlorprothixene
Butyrophenone derivatives- Haloperidol
B. "Atypical" antipsychotics
Benzamides- Sulpiride
Derivatives of benzodiazepine-Clozapine
Mechanisms of action;
clozapine exerts its effects involves the blocking of 5-HT2A/5-HT2C serotonin receptors and the D1-4
dopamine receptors, with the highest affinity for the D4 dopamine receptor.
Chlorprothixene blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain;
depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular
activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and
emesis
Pharmacological effects
antipsychotic effect - due to blockade of D2 receptors of the central nervous system
sedative (calming) effect - due to the blockade of adrenoreceptors of the reticular formation of the brain
stem
antiemetic effect - due to the blockade of D2 receptors of the vomiting center
Mechanisms of action of chlorpromazine.
The mechanism of the antipsychotic action of chlorpromazine is associated with the blocking of
postsynaptic mesolimbic dopaminergic receptors in the brain. Aminazine has a hypothermic effect with a
weak effect on cholinergic receptors. It reduces or eliminates the increase in blood pressure and other
effects caused by adrenaline and other adrenomimetics.
Indications for the use of group drugs
В psychiatric practice is used for various types of psychomotor agitation and psychotic conditions in
patients suffering from schizophrenia, manic arousal in manic-depressive psychosis and other mental
illnesses of various origins, accompanied by fear, anxiety, agitation, insomnia, mood disorders in
psychopathy, in psychotic disorders in patients with epilepsy and organic diseases of the central nervous
system, to alleviate the state of withdrawal from alcoholism and substance abuse.
Side effects
The development of a variety of extrapyramidal disorders:
acute dystonia - spastic contractions of the skeletal muscles of the face, opisthotonus, dysphagia,
laryngospasm, etc.
parkinsonian syndrome - bradykinesia, skeletal muscle rigidity, tremor, monotonous speech akathisia -
uncontrolled motor restlessness, restlessness
Contraindications. contraindicated in liver damage (cirrhosis, hepatitis, hemolytic jaundice, etc.), kidney
(nephritis), dysfunction of hematopoietic organs, myxedema, progressive systemic diseases of the brain and
spinal cord, decompensated heart defects, thromboembolic disease, as well as patients in the late stages of
bronchiectasis. Relative contraindications are cholelithiasis, urolithiasis, acute pyelitis, rheumatism,
rheumatic heart disease. In case of peptic ulcer of the stomach and duodenum, chlorpromazine should not be
administered orally (administered intramuscularly).

2. Drugs that affect appetite. Drugs of different mechanisms of action that stimulate appetite (the
essence of their action). Anorexigenic agents (classification by chemical structure, mechanisms of
appetite reduction, side effects, contraindications to use).
Ans: Gastrin-binds to specific gastrin receptors in the stomach, increased adenylate cyclase activity in the
parietal cells of the stomach - an increase in the secretion of gastric juice, especially hydrochloric acid.
Increases the secretion of pepsin by the main cells of the stomach, increases the secretion of mucus in the
stomach, providing protection to the mucous membrane.
Histamine-stimulates the secretion of the gastric glands due to interaction with H2 receptors. To exclude
side effects associated with the excitation of H1 receptors, it is used together with H1 blockers
(diphenhydramine, diprazine).
2) Drugs of different groups that reduce gastric secretion.
Histamine H blockers2-receptorsCimetidine, ranitidine, famotidine, H blockers +To+-
ATPaseOmeprazole (Omez, Losek), lansoprazole
M-anticholinergics
a) non-selective M-cholinergic blockers Atropine, metacin, platifillin
b) selective M-cholinergic blockers Pirenzepine (Gastrocepin)
3) Characteristics of antacids (speed of onset of effect, duration of action, effectiveness).
Antacids neutralize hydrochloric acid, have a short-term effect (30-60 minutes), are used to relieve pain and
heartburn during an exacerbation of peptic ulcer. The rate of onset of the antacid effect is determined by the
rate of dissolution of the drugs. An antacid taken one hour after a meal stays longer in the stomach and has
the longest lasting effect.

Speed offensive Duration

A drug
effect actions

sodium bicarbonate High short-term

calcium carbonate High Medium

Magnesium hydroxide High Medium

Magnesium trisilicate Low long

aluminum hydroxide Low long

4) Indications for the use of drugs that affect the secretion of the stomach.
Antisecretory: -Peptic ulcer of the stomach and duodenum (including those caused by NSAIDs),
hyperacidity of gastric juice (reflux esophagitis, gastritis, duodenitis), pancreatitis, tumor of the secreting
cells of the stomach (Zollinger-Ellison syndrome) - peptic ulcer of the stomach and duodenum; reflux
esophagitis; erosive and ulcerative lesions of the stomach and duodenum associated with the use of
NSAIDs; stress ulcers; Zollinger-Ellison syndrome.

3. Phenomena observed in the pharmacodynamic interaction of drugs (increased effect, varieties of

antagonism), examples. Problems of combined pharmacotherapy.
Ans: Pharmacological interactions are divided into pharmacokinetic and pharmacodynamic interactions.
Pharmacodynamic interaction.The main "targets" of the action of medicinal substances are specific
receptors, enzymes, ion channels, transport systems.
1. Interaction of medicinal substances at the level of specific receptors
Naltrexone blocks opioid receptors, so morphine does not cause euphoria against the background of
naltrexone. Naltrexone is used in the treatment of morphinism.
Interaction is possible when substances affect different receptors. So, the M-anticholinergic ipratropium and
the beta-agonist salbutamol are able to relax the smooth muscles of the bronchi and act as synergists as
bronchodilators.
2. Interaction of medicinal substances at the level of enzymes. Organophosphorus compounds (OPs)
covalently bind cholinesterases, in particular acetylcholinesterase. In the first hours of OPC poisoning,
cholinesterase reactivators - trimedoxime (dipiroxime) and isonitrosine - can be effective.
3. Interaction of drugs at the level of ion channels
The activator of K + channels, diazoxide, acting on arterioles, causes hyperpolarization of the muscle fiber
membrane; against the background of hyperpolarization, voltage-dependent Ca2+ channels do not open.
Nifedipine is a blocker of voltage-dependent Ca2+ channels. Both drugs dilate mainly arterial vessels.
Nifedipine enhances the vasodilating effect of diazoxide.
4. Interaction of medicinal substances at the level of transport systems.
Against the background of the action of tricyclic antidepressants (imipramine, amitriptyline), the
hypotensive effect of guanethidine is significantly weakened, since tricyclic antidepressants disrupt the
neuronal uptake of guanethidine. Special variants of drug interactions.
Acetylcholine usually lowers blood pressure, but in large doses, against the background of the action of
atropine, it increases blood pressure (a nicotine-like effect of acetylcholine is manifested).
Adrenaline usually increases blood pressure, but against the background of the action of phentolamine, it
lowers blood pressure (the vasodilating effect of adrenaline associated with the activation of beta-adrenergic
receptors is manifested).
Reserpine has a sedative effect and lowers blood pressure. Against the background of the action of MAO
inhibitors, reserpine causes excitation of the central nervous system and increases blood pressure.
Problems of combined pharmacotherapy.The choice of a combination of drugs is one of the most difficult
elements of pharmacotherapy. Currently, competent combined pharmacotherapy is impossible without
taking into account the achievements of clinical pharmacology in studying the mechanisms of drug
interaction.

Ticket 10
1.Antibiotics. Classification of penicillin group drugs. Mechanism, spectrum and nature of
antimicrobial action of penicillins. Pharmacokinetic features of natural and semi-
synthetic penicillins (duration of action, spectrum of antimicrobial activity, resistance to β-lactamases,
frequency and methods of administration, dosage). Indications and contraindications for use, side
effects.
Ans: The spectrum of antimicrobial activity of various generations of penicillins:
HRC 1st generationhas a high antibacterial activity, but the spectrum of action is limited. Active against
Gram + cocci (stapholococci, strepto-, pneumococci), sensitive to listeria, most corynebacteria. Gram-cocci
(meningo-, gonococci), diphtheria bacillus, anthrax fell, clostridia, spirochetes, actinomycetes.
PC 2 generationeffective (in addition to the previous spectrum of action) against bacteria producing
penicillinase (anti-staphylococcal activity).
PC 3a wide range of Gram + and Gram-bacteria: Salmonella, Shigella, some strains of Proteus, Escherichia
coli, Friedlander's bacillus, influenza bacillus. Carbencillin is also effective against all types of Proteus and
Pseudomonas aeruginosa.
PC 4act on gram + (staphylococcus, streptococcus, pneumococcus) and gram- (gonococcus,
meningococcus, E. coli, salmonella, shigella) microorganisms. They are a combination of 2 and 3
generations (Ampioxum = Ampicillin + oxacillin), due to the content of oxacillin, it is active against
penicillinase-forming staphylococci. As well as combinations of PC3pok. and inhibition of β-lactamase
(Unasyn, Amoxiclav).
Preparations 5th generationbroad spectrum of action, active against Gram and Pseudomonas aeruginosa.
Not resistant to penicillinases other than Tazocin.
Mechanism of bactericidal action of penicillins:
According to the mechanism of action, penicillins are bactericidal drugs. Their action is based on the
inhibition of the synthesis of cell wall components and their
spatial location. Penicillins disrupt the synthesis of peptidoglycan, a biopolymer, which is the main
component of the bacterial cell wall. Penicillin inhibitor. peptidoglycan transpeptidase and endogenous
inhibitor (active murein hydrolase and cleaves peptidoglycan) The type of development of resistance to
these drugs is penicillin (slow). Its development is based on the production of β-lactamase enzymes that
destroy β-lactams (plasmid mechanism).
The use of penicillinindicated for sepsis, in all sulfanilamide-resistant cases of relevant infections, with
extensive and deeply localized infectious processes, after injuries with involvement in the process and
infection of large musculoskeletal arrays, in the postoperative period for the prevention of purulent
complications, with infected burns of the third and fourth degree, with soft tissue injuries, chest injuries,
purulent meningitis, brain abscesses, erysipelas, gonorrhea and its sulfanilamide-resistant forms, syphilis,
severe furunculosis, sycosis, and various inflammations of the eye and ear.

2. Hormonal drugs. Principles of glucocorticosteroid therapy. Glucocorticoid drugs, therapy

principles of treatment using these drugs. Mechanisms of anti-inflammatory and anti-allergic effects.
Influence of glucocorticosteroid drugs on metabolic processes, hematopoiesis,
CNS, immunogenesis system, etc. Indications and contraindications for use, side effects.
Ans: The main principle of glucocorticosteroid therapy is to achieve maximum effect with minimum doses.
It is very important that in each case the dose of glucocorticosteroid drugs is optimal. The choice of a dose
exceeding the optimal one quickly leads to the development of side effects. If the dose is chosen below the
optimal, the duration of treatment increases, and the pathological process is not stopped. The choice of the
optimal dose of glucocorticosteroid hormones in each clinical situation is a medical art that can be mastered
in the process of working with patients and scientific literature. Given the possibility of developing severe
complications of pharmacotherapy, glucocorticoids are prescribed only for strict indications. The choice of
the most adequate drug is made taking into account the individual reaction, if the patient has taken the drug
before, and concomitant diseases. The criteria for establishing the minimum effective or optimal dose of
glucocorticosteroids and the duration of treatment are the nature and dynamics of the pathological process
in a particular patient. They include hydrocortisone, prednisolone, dexamethasone.
The anti-inflammatory effect of glucocorticoids is associated with their effect on the formation of
inflammatory mediators, on the vascular component, as well as on the cells involved in inflammation.
Under the influence of glucocorticoids, small vessels narrow and fluid exudation decreases. The
accumulation of leukocytes in the area of inflammation is reduced, the activity of macrophages and
fibroblasts is reduced. The immunosuppressive effect of glucocorticoids is associated with the suppression
of the activity of T- and B-lymphocytes, a decrease in the production of a number of interleukins and other
cytokines, as well as the complement content in blood plasma, a decrease in the level of circulating
lymphocytes and macrophages, as well as with a depressing effect on the migration-inhibiting factor
(MIF) . Glucocorticoids (hydrocortisone, etc.) have a pronounced and diverse effect on metabolism. On the
part of carbohydrate metabolism, this is manifested by an increase in blood glucose, which is associated
with more intense gluconeogenesis in the liver. Possible glycosuria. The effect on fat metabolism is
manifested by the redistribution of fat. With the systematic use of glucocorticoids, significant amounts of
fat accumulate on the face (moon face), dorsal part of the neck, and shoulders. When using glucocorticoid
preparations, hematopoiesis changes. A decrease in the number of eosinophils and lymphocytes in the
blood is characteristic. At the same time, the content of erythrocytes, reticulocytes and neutrophils
increases. With the systematic use of glucocorticoids, significant amounts of fat accumulate on the face
(moon face), dorsal part of the neck, and shoulders. When using glucocorticoid preparations, hematopoiesis
changes. A decrease in the number of eosinophils and lymphocytes in the blood is characteristic. At the
same time, the content of erythrocytes, reticulocytes and neutrophils increases. With the systematic use of
glucocorticoids, significant amounts of fat accumulate on the face (moon face), dorsal part of the neck, and
shoulders. When using glucocorticoid preparations, hematopoiesis changes. A decrease in the number of
eosinophils and lymphocytes in the blood is characteristic. At the same time, the content of erythrocytes,
reticulocytes and neutrophils increases.
A direct indication for the use of glucocorticoids is acute and chronic adrenal insufficiency. However, they
are most widely used as anti-inflammatory and antiallergic agents. Due to these properties, glucocorticoids
are successfully used for collagenosis, rheumatism, inflammatory skin diseases (eczema, etc.), allergic
conditions (for example, with bronchial asthma, hay fever), and some eye diseases (iritis, keratitis). They
are also prescribed in the treatment of acute leukemia. Often in medical practice, glucocorticoids are used
for shock. The immunosuppressive effect may be useful for suppressing immune responses during organ
and tissue transplantation.
Glucocorticosteroids can cause a delay in the tissues of excess amounts of water, the development of edema,
and an increase in blood pressure. There may be a significant increase in blood sugar, a violation of the
distribution of fat. The process of regeneration slows down, ulceration of the mucous membrane of the
gastrointestinal tract, osteoporosis are possible. Decreased resistance to infections. Mental disorders,
menstrual irregularities were noted.

3. The concept of dose. Classification of doses by effect and frequency of administration. Latitude of
therapeutic effect of drugs (examples), significance.
Ans: Dose - the amount of a drug introduced into the body that causes a pharmacological effect, expressed
by weight, volume, or in units of biological activity.
Classification of doses by effect
Therapeutic- Therapeutic dose - causes physiological changes in the body, has a therapeutic effect.
Minimum (min.) - gives the minimum therapeutic manifestations (threshold dose). Average (med.) - a
standard dose that gives a pronounced therapeutic effect in most animals. Maximum (max.) - the highest
dose, DVR, DIC, the limit of the therapeutic effect of the drug.
toxic- Poisoning dose - causes signs of poisoning, leads to the appearance of toxic effects
Lethal- Lethal dose - from the action of which death occurs. DL5– (min.) – causes the death of 10% of
animals; DL50- (media) - causes the death of 50% of animals; DL100 - (abs.) - causes the death of 100% of
animals.
Classification of doses according to the frequency of administration Single- 1) Full - dose for a single dose.
2) Fractional - reduced full dose, divided into separate portions. 3) Shock - a dose exceeding the next 2
times.

Daily- The amount of the drug (dose) used by the patient per day / day. Course - The dose of the drug
substance required for the entire course of treatment. Cyclic - Dose of the drug, prescribed intermittently
(Diacarb - 3 days of taking the drug, the next 3 days - a break).
Breadth of therapeutic action- the range between the mintherapeutic (acting) and mintoxic dose of the drug.
The more STD of the drug, the easier it is to dose the drug, the safer it is. STD is a sign of drug safety. Ether
FDA = 140-200mg%. STD of chloroform = 40-55mg%.
 Ticket 11
1. Antihypertensive drugs. Classification of antihypertensive drugs of the neurotropic type of action.
Mechanisms of the antihypertensive effect of drugs of different groups, pharmacological effects. Side
effects of drugs. Sedative and diuretic drugs for the treatment of hypertension.
Ans:
1. Clonidine, its hypotensive effect is associated with stimulating effects on postsynaptic a2-adrenergic
receptors and imidazoline I1-receptors of neurons of the nuclei of the solitary tract in the rostral
ventrolateral part of the medulla oblongata, which leads to inhibition of the neurons of the vasomotor center
of the medulla oblongata and a decrease in the tone of sympathetic innervation, activation of neurons of the
centers of the vagus nerves and decrease in renin production. The result is a decrease in the tone of vascular
smooth muscles and a decrease in the work of the heart - blood pressure decreases. It has a pronounced
hypotensive effect, has a sedative effect, reduces heart rate and intraocular pressure.
2. Side effects - with a sudden cessation of taking the product, a hypertensive crisis may develop. Dry
mouth, weakness, drowsiness, at high doses - constipation, orthostatic collapse.
3. Benzohexonium, as a result of inhibition of the sympathetic ganglia, vasodilation occurs, pre- and
afterload decreases. The pressure is dropping. In addition, n-cholinergic receptors of the chromaffin cells of
the adrenal medulla are blocked, as a result, the secretion of adrenaline and norepinephrine into the blood
decreases. This also helps to reduce pressure. It causes a decrease in the secretion of glands and a decrease
in the functions of the gastrointestinal tract and the elimination of bronchial spasms under the action of
Benzohexonium causes the use of the drug for the treatment of peptic ulcer, some forms of bronchial
asthma, hyperhidrosis.
4. Side effects: general weakness, dizziness, palpitations. Large doses can cause orthostatic collapse,
severe mydriasis, dry mouth, bladder atony.
5. Reserpine, the mechanism of hypotensive action is a violation of the deposition of norepinephrine in
vesicles, resulting in a decrease in the content of NA in varicose thickenings, which leads to a block of
efferent impulses at the level of peripheral adrenergic endings. This leads to a decrease in the work of the
heart and the tone of peripheral vessels. It also, having a central hypotensive effect, slows down cardiac
activity, causes hypothermia (reduces body temperature) and somewhat slows down metabolic processes,
increases gastric secretion.
Side effects - bradycardia; increased secretory and motor activity of the gastrointestinal tract; miosis;
drowsiness; general weakness; depressive states; extrapyramidal disorders.
4.A. Prazosin, the mechanism of hypotensive action is associated with a block, mainly, of postsynaptic
alpha1-adrenoreceptors, due to which presynaptic alpha2-adrenoreceptors function and the negative
feedback mechanism is preserved and increased release of NA does not occur; there is a decrease in the tone
of resistive vessels, a decrease in venous return and, consequently, the work of the heart.
Side effects - headache; heartbeat; drowsiness; orthostatic hypotension; dizziness; water retention in tissues.
4.B. Anaprilin,the hypotensive effect is associated with a decrease in the minute volume of blood,
sympathetic stimulation of peripheral vessels, a decrease in the activity of the renin-angiotensin system, the
sensitivity of baroreceptors of the aortic arch and the effect on the central nervous system. The hypotensive
effect stabilizes by the end of the 2nd week of the course appointment. The drug enhances spontaneous and
uterotonic-induced uterine contractions. Reduces bleeding during childbirth and in the postoperative period.
Reduces intraocular pressure and reduces the secretion of aqueous humor. The tone of the bronchi due to
the blockade of beta-2 adrenoreceptors increases.
Side effects - nausea, vomiting, diarrhea, dizziness, worsening sleep, general weakness, bradycardia,
hypotension, symptoms of circulatory failure, bronchospasm, impotence.
4.B. Labetalol, as a result of interaction with α- and β-adrenergic receptors, labetalol causes vasodilation
and a decrease in peripheral vascular resistance, leading to a decrease in systemic blood pressure without a
significant decrease in cardiac output and the development of reflex tachycardia. The drug does not
significantly affect the amount of cardiac output and heart rate
. Side effects: dizziness, headache, nausea, constipation or diarrhea, fatigue, skin itching.
Diureticsreduce both systolic and diastolic pressure, slightly affect cardiac output. These include:
Hydrochlorothiazide, Indapamide, Furosemide, Ethacrynic acid, Spironolactone. Sedatives - valerian,
motherwort, elenium.

2. Antiplatelet agents and agents that affect fibrinolysis. Main antiplatelet agents, the essence of their
mechanisms of action, indications for use. Classification of agents that affect fibrinolysis, mechanisms
of action, indications for use.
Ans: The most common antiplatelet agent in practice is acetylsalicylic acid (aspirin). It is an inhibitor of
cyclooxygenase, as a result of which the synthesis of cyclic endoperoxides and their metabolites
thromboxane and prostacyclin is disrupted. In recent years, substances acting on platelet glycoprotein
receptors (GP IIb/IIIa) have attracted much attention. These receptors play a critical role in platelet
aggregation. Drugs that affect their activity are divided into 2 groups. The first is competitive or non-
competitive blockers of glycoprotein receptors (abciximab, tirofiban, etc.). The second group is represented
by drugs that prevent the activating effect of ADP on platelets and the expression of their glycoprotein
receptors (ticlopidine, clopidogrel). In both cases, binding to glycoprotein receptors of fibrinogen and a
number of other factors does not occur or decreases, which underlies the antiaggregant action of these
substances. Dipyridamole (curantil) has some antiplatelet activity, inhibits phosphodiesterase and
significantly increases the content of cAMP in platelets, it potentiates the action of adenosine, which inhibits
platelet aggregation and has a vasodilating effect.
Indications for useASA are CHD, the presence of several risk factors for CHD, silent myocardial ischemia,
unstable angina pectoris, myocardial infarction, valvular mitral heart disease and atrial fibrillation, mitral
valve prolapse (prophylaxis of thromboembolism), recurrent pulmonary embolism, pulmonary infarction,
acute thrombophlebitis. Drugs that affect platelet glycoprotein receptors are used in surgical interventions
on coronary vessels for angina pectoris, myocardial infarction.
1. The first group includes substances that directly affect blood plasma, a clot of fibrin threads. The
representative of the drugs of the first group is fibrinolysin, urokinase
2. In the second group there are fibrinolysis activators. when introduced into the body, they activate the
endogenous fibrinolytic blood system-streptokinase
Streptokinase interacts with profibrinolysin; the resulting complex acquires proteolytic activity and
stimulates the transition of profibrinolysin (plasminogen) to fibrinolysin (plasmin) both in the thrombus and
in the blood plasma. Fibrinolysin dissolves fibrin. Effective in fresh thrombosis. As a result of the
conversion of circulating profibrinolysin into fibrinolysin, urokinase can cause systemic fibrinolysis. The
latter is due to the fact that fibrinolysin is a non-selectively acting protease capable of metabolizing many
protein compounds found in blood plasma. This leads to a decrease in plasma levels of fibrinogen, a2-
antifibrinolysin, a number of blood coagulation factors (V, VIII).
They are usually used to dissolve blood clots in the coronary vessels with myocardial infarction, pulmonary
embolism, deep vein thrombosis, acute blood clots in the arteries of different localization.

3. Main types of resorptive action of drugs (examples).

Ans: The action of a substance that develops after its absorption, entry into the general circulation and then
into the tissues is called resorptive.
The resorptive action develops after the absorption of the drug into the blood and its distribution along with
it in peripheral tissues (peripheral action) or in the central nervous system (central action).

Resorptive action can be direct and indirect.

1. Direct (primary) action - a change in the function of organs by drugs as a result of action on the cells of
these organs (increased heart rate by cardiac glycosides due to blockade of Na +, K + - ATP-ase of muscle
cells of the myocardium; increased urination during the action of diuretics on the reabsorption of ions and
water in the renal tubules ).
Indirect (secondary) action - a change in the function of organs and cells by drugs as a result of action on
other organs and cells functionally related to the former (cardiac glycosides have a diuretic effect, as they
increase heart contractions, improve blood flow in the kidneys, increase filtration and urine formation). A
special case of indirect action is reflex action.
 Ticket 13
1. Drugs used for the treatment of circulatory insufficiency. Cardiac glycosides. Classification by
source of processing and degree of polarity. Effect of cardiac glycosides on myocardial function and
hemodynamics. Indications and contraindications. Features of adonis preparations. Symptoms of
cardiac glycoside intoxication and first aid.
Ans: Classification by sources of receipt
• digitalis purple (Digitalis purpurea; Fig. 14.1) - digitoxin;
• woolly foxglove (Digitalis lanata) - digoxin, celanide (lanatoside C, isolanide);
• strophanthus Kombe (Strophanthus Kombé) - strophanthin K1;
• lily of the valley (Convallaria) - corglicon;
• Adonis (Adonis vernalis) - infusion of Adonis herb.
Classification by degree of polarity.
1. Polar or hydrophilic (they contain four or five hydroxyl groups in the aglycone molecule): - strophanthin
K - leaf lily of the valley glycoside (korglikon)
2. Relatively polar or hydrophilic-lipophilic (they contain two or three hydroxyl groups in the aglycone
molecule): - digoxin - lanatoside C (celanide)
Effect of cardiac glycosides on myocardial function and hemodynamics.
1) positive inotropic effect (increased heart contractions)
2) shortening of systole
3) diastole lengthening
4) the size of the heart is approaching the norm (i.e., decreasing)
5) stroke volume (SV) and minute volume (MOV) increases
6) negative chronotropic effect (decrease in heart rate).
Indications
1) acute and chronic heart failure
2) atrial fibrillation
3) paroxysmal supraventricular tachycardia
Contraindications.
1) incomplete atrioventricular block
2) severe bradycardia
3) abrupt organic changes in the heart and blood vessels (acute infectious myocarditis, endocarditis, severe
cardiosclerosis).
4) thyrotoxicosis and atrial extrasystole (relative contraindication: atrial fibrillation may develop).
5) administered with caution in hypokalemia and hypercalcemia (overly enhanced response).
Features of Adonis preparations.
According to their action, Adonis preparations belong to the group of digitalis glycosides - strophanthus and
have a pronounced cardiotonic effect: they slow down the rhythm of heart contractions, lengthen diastole
and increase systole, moderately reduce intracardiac conduction (in this case, adonis preparations act weaker
than foxglove), increase the stroke volume of the heart.
Adonis preparations have a more pronounced diuretic effect compared to other glycosides, which is
associated with the influence of cymarin. A characteristic feature of spring adonis preparations is their
calming effect on the central nervous system. Symptoms of intoxication with cardiac glycosides.
a) the occurrence of arrhythmias (bradycardia, ventricular extrasystole of the bi- and trigemenia type,
supraventricular and ventricular tachycardia, atrial fibrillation, ventricular fibrillation)
b) changes in the function of the central nervous system: increased tone of the vagus nerve
damage to the ophthalmic nerves (xanthopsia - impaired color vision, photophobia, impaired visual fields),
radiculitis, mental disorders (insomnia, apathy, fatigue)
c) changes in the function of the gastrointestinal tract (nausea, vomiting, anorexia, abdominal pain)
Relief measures.
1. Cancel the preparation of cardiac glycoside and other drugs that increase the level of cardiac glycosides
in the blood and sensitivity to them.
2. Prescribe physical antagonists: activated carbon or other sorbents.
Hypocalistia correction: potassium chloride and / or potassium and magnesium asparaginate (panangin or
asparkam).
2. Emetics and antiemetics. Classification of emetics by the mechanism of action, their use in medical
practice. Antiemetics of different groups, mechanisms of action and application, depending on the
genesis of the vomiting act.
К Ans: substances that excite the vomiting center reflexively include thermopsis and ipecac drugs, but they
are not used to induce vomiting. When administered enterally, they stimulate the stomach receptors and, in
large doses, reflexively induce vomiting. When the active ingredients of these drugs (thermopsin, emetine)
are absorbed, they also have a direct stimulating effect on the chemoreceptors of the trigger zone. Copper
sulfate and zinc sulfate, which irritate the gastric mucosa, have only a peripheral effect. Vomiting during
their enteral administration has a reflex character and is not eliminated when the starting zone is destroyed.
Emetics are of very limited use. Sometimes in acute poisoning, if gastric lavage is difficult for some reason,
apomorphine is prescribed (it is injected under the skin). Besides,

depending on the origin of vomiting, one or another antiemetic should be prescribed. So, with sea and air
sickness, vomiting is associated with excessive excitation of the vestibular apparatus, from where the
impulses come from with the participation of the cerebellum. Persons with increased excitability of the
vestibular apparatus are recommended to take preventive medications containing scopolamine. One of the
most common remedies for motion sickness is Aeron tablets. Metoclopramide, a benzamide derivative, is an
active antiemetic that depresses the trigger zone. Its central effects, including antiemetic, are due to the fact
that it blocks dopamine D2 receptors, and in high doses, serotonin 5-HT3 receptors. Metoclopramide is
much more active than chlorpromazine and acts more selectively.

3. Phenomena observed in the pharmacodynamic interaction of drugs (increased effect, varieties of

antagonism), examples. Problems of combined pharmacotherapy.
Ans: Pharmacological interactions are divided into pharmacokinetic and pharmacodynamic interactions.
Pharmacodynamic interaction.The main "targets" of the action of medicinal substances are specific
receptors, enzymes, ion channels, transport systems.
1. Interaction of medicinal substances at the level of specific receptors
Naltrexone blocks opioid receptors, so morphine does not cause euphoria against the background of
naltrexone. Naltrexone is used in the treatment of morphinism.
Interaction is possible when substances affect different receptors. So, the M-anticholinergic ipratropium and
the beta-agonist salbutamol are able to relax the smooth muscles of the bronchi and act as synergists as
bronchodilators.
2. Interaction of medicinal substances at the level of enzymes. Organophosphorus compounds (OPs)
covalently bind cholinesterases, in particular acetylcholinesterase. In the first hours of OPC poisoning,
cholinesterase reactivators - trimedoxime (dipiroxime) and isonitrosine - can be effective.
3. Interaction of drugs at the level of ion channels
The activator of K + channels, diazoxide, acting on arterioles, causes hyperpolarization of the muscle fiber
membrane; against the background of hyperpolarization, voltage-dependent Ca2+ channels do not open.
Nifedipine is a blocker of voltage-dependent Ca2+ channels. Both drugs dilate mainly arterial vessels.
Nifedipine enhances the vasodilating effect of diazoxide.
4. Interaction of medicinal substances at the level of transport systems.
Against the background of the action of tricyclic antidepressants (imipramine, amitriptyline), the
hypotensive effect of guanethidine is significantly weakened, since tricyclic antidepressants disrupt the
neuronal uptake of guanethidine. Special variants of drug interactions.
Acetylcholine usually lowers blood pressure, but in large doses, against the background of the action of
atropine, it increases blood pressure (a nicotine-like effect of acetylcholine is manifested).
Adrenaline usually increases blood pressure, but against the background of the action of phentolamine, it
lowers blood pressure (the vasodilating effect of adrenaline associated with the activation of beta-adrenergic
receptors is manifested).
Reserpine has a sedative effect and lowers blood pressure. Against the background of the action of MAO
inhibitors, reserpine causes excitation of the central nervous system and increases blood pressure.
Problems of combined pharmacotherapy.The choice of a combination of drugs is one of the most difficult
elements of pharmacotherapy. Currently, competent combined pharmacotherapy is impossible without
taking into account the achievements of clinical pharmacology in studying the mechanisms of drug
interaction.

Ticket 14
1. Drugs used for the treatment of circulatory insufficiency. Pharmacological characteristics
(mechanisms, effects, indications and contraindications) of non-glycosidic inotropic stimulants.
Ans: With prolonged use, non-glycoside cardiotonic drugs increase mortality. In this regard, at present, a
group of cardiotonic agents of a non-glycoside structure is used as an ambulance (short-term) for acute
(decompensated) heart failure.
1. Means that increase the content of cAMP and Ca2 + ions in cardiomyocytes:
A. Means that stimulate β 1-adrenergic receptors: Dopamine, Dobutamine
B. Phosphodiesterase inhibitors: Amrinone, Milrinone
2. Drugs that increase the sensitivity of myofibrils to calcium ions:Levosimendan
1.A.The cardiotonic action of Dopamine is associated with stimulation of the β1-adrenergic receptors of the
heart. At the same time, adenylate cyclase is activated, which leads to an increase in the content of cAMP in
cardiomyocytes and, accordingly, the concentration of calcium ions increases. As a result, the force of heart
contractions increases. Indications for use: shock of various etiologies; acute cardiac and vascular
insufficiency, "low cardiac output" syndrome associated with surgery, especially with cardiac surgery.
Contraindications for use: pheochromocytoma, with arrhythmia in combination with MAO (monoamine
oxidase) inhibitors, with Cyclopropane and halogen-containing anesthetics.
1.B. Amrinonhas a positive inotropic and vasodilating effect; in patients with congestive heart failure
increases cardiac output, reduces pressure in the pulmonary artery and reduces peripheral vascular
resistance. Indications for use: for short-term therapy of acute congestive heart failure. Side effects:
hypotension, tachycardia, supraventricular and ventricular arrhythmias, impaired renal function,
thrombocytopenia, as well as headache, gastrointestinal disorders, fever. Contraindications: with
obstructive myopathy, heart valve damage, as well as with hypovolemia, supraventricular arrhythmia, aortic
aneurysm, acute arterial hypotension, acute kidney failure, thrombocytopenia.
2. Levosimendanincreases the sensitivity of contractile proteins to calcium by binding to myocardial
troponin C in the calcium-dependent phase. Increases the strength of heart contractions, but does not affect
the relaxation of the ventricles. It has a vasodilating effect on arteries and veins. Levosimendan is a
selective phosphodiesterase III inhibitor in vitro. Due to the presence of a positive inotropic and
vasodilating effect in heart failure, it increases the strength of heart contractions and reduces both preload
and afterload.
Indications:short-term treatment of acute decompensation of severe CHF.
Side effects: a significant decrease in blood pressure, extrasystole, atrial fibrillation, tachycardia, ventricular
tachycardia, atrial flutter, myocardial ischemia, dizziness, headache, nausea, vomiting, hemoglobin,
hematocrit.
Contraindications: hypersensitivity, mechanical obstruction preventing filling and / or ejection of blood
from the ventricles, severe renal, hepatic insufficiency, severe arterial hypotension, severe tachycardia,
history of ventricular tachycardia of the "pirouette" type, uncorrected hypokalemia or hypovolemia, lactation
period, age up to 18 years.

2. Drugs that regulate the activity of the pancreas. Characteristics of replacement therapy drugs
prescribed for a decrease in the secretory function of the pancreas, indications for use. Drugs
prescribed for the treatment of acute pancreatitis, the principle of action of these drugs.
Ans: Means that regulate the function of the pancreas:-
1. Diagnostic tools - secretin, cholecystokinin.
2. Means that enhance secretion - hydrochloric acid diluted.
3. Means of substitution therapy - pancreatin, panzinorm, festal.
4. Drugs that inhibit secretion - M-cholinergic blockers, antacids.
5. Inhibitors of proteolytic enzymes - aprotinin.
With a decrease in secretory function, pancreatin is prescribed (powder from the dried pancreas of slaughter
cattle), it is an enzyme preparation containing trypsin and amylase, used for chronic pancreatitis,
enterocolitis. Sometimes m-anticholinergics are used (for acute pancreatitis).
Proteolysis inhibitors (pantrypin, ingitral, contrykal,) inhibit the activity of trypsin, chymotrypsin, kallekrin
and reduce the fibrinolytic activity of the blood. Antispasmodics (papaverine, no-shpa) lower the tone and
contractile activity of the smooth muscles of the internal organs and blood vessels.

3. The concept of drug dependence, its varieties; drugs that cause drug dependence. Prevention of
iatrogenic drug dependence. The concept of toxicomania.
Ans: Under drug addictionunderstand a mental and (sometimes) physical condition characterized by
behavioral and other responses that always include an urgent need for constant or periodic intake of certain
drugs in order to experience its effect on the psyche or avoid unpleasant symptoms that occur without taking
this drug.
• Psychological dependence syndrome - a condition of the body characterized by a pathological need to take
a psychotropic substance in order to avoid mental disorders or discomfort that occurs when the use is
stopped. This syndrome proceeds without the phenomena of abstinence.
• Syndrome of physical dependence - a condition characterized by the development of abstinence when you
stop taking drugs or after the introduction of its antagonists. It is characteristic, first of all, for drugs that
have a narcotic effect.
Painkillers, tranquilizers, and even antihypertensive drugs often cause tolerance and physical dependence.
iatrogenicsThese are all diseases and injuries that occur in patients and healthcare workers as a result of the
provision of any type of medical care.
Prevention. Compliance with medical principles by health workers. deontology. To prevent iatrogeny, it is
necessary to carry out systematic educational work with all personnel who communicate with patients.
Drug addiction and substance abuse- diseases resulting from the systematic abuse of various chemicals and
characterized by the following main features: a change in tolerance (endurance) to a chemical, a pathological
addiction to intoxication (pathological craving), a change in the picture of intoxication (drug intoxication),
the occurrence of an abstinence syndrome (a symptom complex of somatovegetative, neurological and
mental disorders upon discontinuation of the intake of a substance). The most important sign is a
pathological addiction, without which it is impossible to diagnose drug addiction or substance abuse.
Substance abuse is a disease that occurs as a result of the abuse of substances that are not classified as drugs.
All substances capable of causing pathological addiction are designated as psychoactive drugs. Substance
abuse caused by the abuse of volatile substances (inhalants). Inhalants inhibit the activity of the cerebral
cortex and stem structures, causing hypoxia. They quickly penetrate the lung tissue (all fat-soluble), blood
into the brain. The effect of exposure begins within a few seconds after inhalation. Toxic damage to organs
is caused by metabolites of volatile substances, and not by the original forms. With regular use, the face
becomes swollen, acquires an earthy color. Adolescents lag behind in development, lose their thinking
abilities up to the development of dementia. The effect of exposure begins within a few seconds after
inhalation. Toxic damage to organs is caused by metabolites of volatile substances, and not by the original
forms. With regular use, the face becomes swollen, acquires an earthy color. Adolescents lag behind in
development, lose their thinking abilities up to the development of dementia. The effect of exposure begins
within a few seconds after inhalation. Toxic damage to organs is caused by metabolites of volatile
substances, and not by the original forms. With regular use, the face becomes swollen, acquires an earthy
color. Adolescents lag behind in development, lose their thinking abilities up to the development of
dementia.

Ticket 15
1. Antianginal drugs. Classification of nitrates by duration of action, indicating the dosage form.
Nitroglycerin (the mechanism of antianginal action). Indications and contraindications for use, side
effects.
Ans: Nitrates can be classified according to duration of action:
1. Preparations of short duration of action (up to 1 hour). Nitroglycerin under the tongue, various aerosols
of nitroglycerin and isosorbide dinitrate. Designed for quick relief of an anginal attack;
2. Preparations of moderately prolonged action (from 1 to 6 hours). Tablets of isosorbide dinitrate,
isosorbide-5-mononitrate, sustak, nitrong, nitrocor.
3. Significantly prolonged action preparations: special tablets or capsules of isosorbide dinitrate (kardiket,
isoket) and isosorbide-5-mononitrate (efox), patches with nitroglycerin for skin application. The action of
such tablets and capsules can last up to 15 hours, and patches - up to 24 hours.
Nitroglycerine- effective when applied sublingually.
The antianginal effect is due to three mechanisms:
1. Stimulates the formation of NO in the wall of blood vessels.
2. Stimulates the synthesis of prostacyclin in the vascular wall.
3. Stimulates α2-adrenergic receptors of the central nervous system and increases the effect of coronary
dilating impulses on the vasomotor center.
Reduces the penetration of calcium ions into the vessels and cardiomyocytes. Reduces blood pressure and
afterload on the heart. Relaxes the wall of the veins and reduces the preload on the heart. Expands coronary
vessels. Reduces stroke volume, end-diastolic pressure, improves blood supply to subendocardial layers of
the myocardium. Reduces the work of the heart and myocardial oxygen demand. Under the influence of
nitroglycerin, venous blood flow to the heart decreases, pressure in the PP, in the pulmonary artery system
decreases, and peripheral vascular resistance also decreases.
Side effects:headache, dizziness, lowering blood pressure, and in case of an overdose -
orthostatic collapse. Contraindications: cerebral hemorrhage, increased intracranial pressure, severe
hypotension, and angle-closure glaucoma with high intraocular pressure.

2. Anticoagulants. Classification by mechanism of action. Pharmacological effects of heparin, dosage,

frequency of administration.
Ans:
1. Direct-acting anticoagulants (substances that affect clotting factors directly in the blood) Heparin,
Fraxiparine, Enoxaparin, Lepirudin
2. Anticoagulants of indirect action (substances that inhibit the synthesis of blood coagulation factors -
prothrombin, etc. - in the liver) Neodicumarin, Sinkumar, Warfarin, Phenylin Heparin is regarded as a
cofactor of antithrombin III. In blood plasma, it activates the latter (and, obviously, antithrombin II),
accelerating its anticoagulant effect. In this case, a number of factors that activate blood coagulation are
neutralized. The transition of prothrombin to thrombin is disrupted. In addition, thrombin (IIa) is inhibited.
Since heparin is a direct-acting anticoagulant, it is active not only in the whole organism, but also in vitro. In
high doses, heparin inhibits platelet aggregation. In addition to the main anticoagulant effect, heparin has the
ability to lower blood lipids. Heparin is dosed in units of action - ED (1 mg = 130 ED).
Unlike heparin, its low molecular weight analogs do not have an inhibitory effect on thrombin. Due to the
fact that these drugs bind little to plasma proteins, their bioavailability is higher than that of heparin. They
are excreted from the body slowly. They act longer than heparin. The action of hirudin is shorter than that of
heparin.

3. The basic principles of recognition and therapy of poisoning. Antidotes for poisoning with heavy
metals; morphine; methyl alcohol; barbiturates; benzodiazepines, muscarine.
Ans: Heavy metal salts can form compounds with alkaloids, nitrogenous bases, tannins, dyes, enzymes,
cardiac glycosides,
с sodium salts of derivatives of barbituric acid and sulfanilamide preparations, halogen compounds, salts of
alkali and alkaline earth metals. Precipitation can be formed during exchange reactions between salts of
heavy metals. The property of tannins to form insoluble precipitates with alkaloids in the form of alkaloid
tanates is used to identify alkaloids.
a) chlorpromazine and ethanol: increased inhibitory effect of alcohol on the central nervous system up to
the development of a coma b) aminoglycosides with dithylin: increased muscle relaxation, delay
recovery of voluntary breathing. The ability of aminoglycosides to cause the development of hypokalemia,
against which the effect of dithylin is enhanced.
c) halothane and adrenaline: extrasystole, mainly ventricular, ventricular fibrillation and cardiac arrest are
possible. Myocardial sensitization to catecholamines.
d) sulfonamides with novocaine: weakening of the antimicrobial action of sulfonamides. Formation during
the hydrolysis of novocaine and anesthesin para-aminobenzoic acid, which is a factor in the growth of
bacteria.
e) cardiac glycosides with adrenomimetics, calcium chloride, powerful diuretics:
violation of the heart rhythm, increased toxic effect of cardiac glycosides. Summation of the hypokalemic
action of the drugs of both groups; a sharp decrease in the content of potassium ions in the myocardium.
e) glucocorticosteroids with aspirin: development of edema, increased damaging effect on the mucous
membrane of the gastrointestinal tract. Summing up the damaging effect on the mucous membrane of the
gastrointestinal tract and the effects on the electrolyte and water metabolism of both groups of drugs.
Ticket 16
1. Drugs for the treatment of circulatory failure. Pharmacological characteristics (mechanisms,
effects, indications and contraindications for use) of drugs needed for correction of cardiovascular
system neurohumoral regulation.
К Ans: beta-blockers, including those with the simultaneous ability to blockade of alpha-
adrenergic receptors, angiotensin-converting enzyme inhibitors. Means acting on the renin-angiotensin
system Angiotheisin-converting enzyme inhibitors - Captopril, Enalapril, Ramipril, Lisinopril, Kvinapril.

Mechanism of action of NAPFassociated with a decrease in the formation of angiotensin II and a decrease
in the inactivation of bradykinin, as a result of which the arterioles expand, the total peripheral resistance
and afterload decrease. The dilation of the veins leads to a decrease in preload, venous return, and
ventricular volume. An increase in the content of vasodilating kinins in tissues, in particular in the kidneys,
leads to an increase in filtration, the removal of excess sodium and water, a decrease in circulating blood
volume and venous return of blood to the heart. A decrease in aldosterone also leads to an increase in the
excretion of sodium and water. Thus, in the treatment of ACE inhibitors in patients with heart failure, the
pressure in the veins, the nature of the atrium and pulmonary artery, as well as the total peripheral resistance,
decreases. ejection fraction increases,
ACE inhibitors are powerful neurohumoral modulators:
- they inhibit the activation of the renin-angiotensin system, which is harmful to patients with heart failure.
In this case, the sympathoadrenal system is inhibited by the feedback mechanism.
- NAPF stimulate the formation of kinins, which indirectly stimulates the entry into the blood of
prostaglandins 1-2 and H-2, which have vasodilating, natriuretic, cardio- and cytoprotective properties, as
well as the release of endothelial relaxing factor from the cells of the vascular wall.
Contraindications:angioedema in history, pregnancy and lactation.
Beta blockers
1. Non-selective without their own sympathomimetic activity - Propranolol, Timolol, Nidolol, Sotalol,
Chloranool.
2. Cardioselective without their own sympathomimetic activity - Atenolol, Metoprolon, Betaxolol,
Bisoprolol, Esmolol, Talinolol.
3. Cardioselective with its own symnatomimetic activity - Acebutolol.
4. Cardioselective with vasodilating properties - Celiprolol, Bevandolol.
5. New different mechanism of action - Nebivalol, Flestolol,.
6. Alpha-beta-blockers - Labetalol, Carvedilol, Proxodolol.
An increase in the activity of angiotensin II through stimulation of ATI receptors in synapses leads to an
increase in the synthesis and flushing of norepinephrine from postsynaptic endings. In turn, norepinephrine
through beta-adrenergic receptors stimulates the production of renin.
contraindications to the use of beta-blockers are: bronchial asthma, bradycardia, arterial hypotension,
severe decompensated heart failure.

2. Choleretic agents. Classification of agents that stimulate the formation of bile. Indications for their
use, the time of administration, depending on the meal. Drugs that stimulate the contraction of the
gallbladder and contribute to the production of bile (cholespasmolytics). Hepatoprotectors, use.
Ans: Chronic inflammatory diseases of the liver and biliary tract, incl. chronic cholecystitis and cholangitis,
they are used for biliary dyskinesia, in the treatment of constipation, chronic hepatitis.
All choleretic drugs, regardless of the form of release, must be taken 20 to 30 minutes before meals.
Moreover, the total daily dosage is divided equally into 3-5 doses, depending on how many times a day a
person eats. It is recommended to take choleretic drugs before each meal. The preparations must be washed
down with a sufficient amount of water and be sure to eat something half an hour after taking. If a person
does not eat something after taking a choleretic drug, then he will experience nausea, diarrhea and general
well-being will worsen.
Cholespasmolytics (means that improve the outflow of bile by relaxing the muscles of the gallbladder and
biliary tract): Cholinolytics (M-cholinergic blockers-atropine, platifilin) Myotropic antispasmodics-
papaverine, no-shpa, drotaverine, bendazol. Substances of this group increase the resistance of the liver to
the effects of damaging factors, contribute to the restoration of its functions, increase its detoxification
capabilities. The hepatoprotective effect may be due to the normalization of metabolic processes in
hepatocytes, an increase in the activity of microsomal enzymes, and the restoration of cell membrane
functions. Hepatoprotectors are used for acute and chronic hepatitis, dystrophy and cirrhosis of the liver,
toxic liver damage, including those associated with alcoholism, intrahepatic cholestasis. Legalol, Silbinin
dihydrosuccinate sodium salt, ademetionine.

3. The concept of adverse drug reactions (ADR) of medicinal substances. Classification of the main
varieties of ADR.
Side effects of drugs - undesirable effects that occur when using drugs in therapeutic doses. Undesirable
effects caused by drugs in doses exceeding therapeutic ones are considered toxic.
According to the pathogenetic principle, the side effects of drugs can be classified as follows.
I. Side effects due to the chemical nature of drugs.
1. Side effects due to specific pharmacological effects of drugs:
a) due to action on the same type of receptors in different organs or on different types of receptors; b) due to
changes in the synthesis or biotransformation of endogenous mediator substances;
c) due to influence on humoral regulatory mechanisms (enzymatic, hormonal).
2. Side effects of a cytotoxic nature:
a) general cellular cytotoxic effect;
b) selective cytotoxic action.
3. Secondary side effects due to:
a) changes in the saprophytic microflora in the body;
b) mass destruction of pathogens of infectious and parasitic diseases.
4. Side effects due to the interaction of drugs with each other or with biologically active ingredients of
foods.
5. Side effects of an allergic nature.
6. Drug addiction.
7. Mutagenic, teratogenic and embryotoxic effects.
II. Side effects due to the peculiarities of the body's reaction to drugs.
1. Side effects associated with genetically predetermined characteristics of the organism: a) due to
fermentopathy; b) due to hereditary diseases with altered reactivity to drugs.
2. Side effects associated with the acquired features of the body:
a) due to changes in the body's sensitivity to drugs under certain physiological conditions (early childhood,
old age, pregnancy, lactation); b) in diseases of the organs involved in the elimination
medicines; c) in diseases accompanied by changes in sensitivity to drugs; d) due to the characteristics of the
patient's personality; e) caused by bad habits or exposure to harmful environmental factors (smoking,
alcoholism, etc.).

Ticket 17
1. Synthetic antibacterial drugs. Fluoroquinolones. Nitroimidazoles. Pharmacological characteristics
(nature, mechanism, spectrum of antimicrobial action, indications and contraindications for use, side
effects).
Ans: Fluoroquinolones- quinolone derivatives containing fluorine atoms in the structure.
Mechanism of action:By inhibiting two vital enzymes of the microbial cell - DNA gyrase and
topoisomerase-4, fluoroquinolones disrupt DNA synthesis, which leads to the death of bacteria. In addition,
antibacterial activity is due to the effect on the RNA of bacteria, the stability of their membranes, and the
effect on other vital processes of bacterial cells.
Action spectrum:they are active against a number of gram-positive aerobic bacteria, most gram-negative
strains, and are active against bacteria resistant to quinolones of the first generation. Fluoroquinolones III
and, especially, IV generations are highly active against pneumococci, more active than II generation drugs
against intracellular pathogens, fast-growing atypical mycobacteria, anaerobic bacteria (moxifloxacin).
Enterococci are sensitive to fluoroquinolones to varying degrees.
Indications:upper and lower respiratory tract infections, intestinal infections, anthrax, intra-abdominal
infections, pelvic infections, prostatitis, gonorrhea, skin, soft tissue, bone and joint infections, eye
infections, meningitis, sepsis, tuberculosis.
Adverse reactionsfor all quinolones, adverse reactions are common.
Allergic reactions, convulsions, tremor, paresthesia, blurred vision, dizziness,
headache, dyspepsia,
Contraindications: sinus bradycardia, sick sinus syndrome, sinoatrial blockade, severe arterial hypotension,
collapse, shock, hypothyroidism, hyperthyroidism.

2. Antiseptics and disinfectants. The concept of antiseptic and disinfectant action, factors affecting the
antiseptic activity of drugs. Classification of antiseptics by chemical structure, mechanisms of
antiseptic action of drugs of different groups. Indications for use in various fields of medicine.
Ans: Antiseptics and disinfectants should have a wide spectrum of action against bacteria, protozoa and
fungi, be characterized by a short latent period of action, high activity, including in the presence of
biological substrates. It is important that the preparations are chemically stable and affordable in terms of
their production and cost. Important requirements for antiseptics are the absence of a local negative (for
example, irritating) effect on tissues, minimal absorption
с places of their application, the absence of an allergenic effect and low toxicity. A common criterion for
evaluating the activity of antiseptics is the so-called phenol coefficient (the ratio of the concentrations of
phenol and the tested antiseptic, in which the substances have the same antimicrobial effect). The
mechanism of action of various antiseptics and disinfectants is not the same and may be associated with
protein denaturation, impaired plasma membrane permeability, and inhibition of enzymes important for the
life of microorganisms.
The bactericidal action of detergents is due to a violation of the structure of the cell membrane, denaturation
of proteins and inhibition of enzymes. Detergents are used to treat the surgeon's hands, sterilize instruments
and equipment.
An important group of antiseptics are nitrofuran derivatives. Nitrofurans have a wide spectrum of action.
They have a detrimental effect on gram-positive and gram-negative bacteria, protozoa. Furacilin is used
mainly externally for the treatment of wounds, skin, mucous membranes, for washing the serous and
articular cavities.
The group of phenol and its derivatives includes many well-known aromatic antiseptics. Phenol acts mainly
on vegetative forms of bacteria and fungi. Phenol solutions are used to disinfect tools and household items.
The group of dyes includes a number of compounds of various chemical structures. Brilliant green is the
most widely used. Gram-positive cocci are especially sensitive to dyes. Brilliant green is a highly active and
relatively fast acting antiseptic. In the presence of proteins, its effectiveness is reduced. It is used externally,
mainly for purulent skin lesions (pyoderma). Ethacridine lactate (rivanol) is colored yellow. His activity is
quite high, but the action develops slowly. It is used externally and for washing infected cavities (pleura,
peritoneum), bladder, uterus.
Halogen-containing antiseptics are represented by preparations containing chlorine and iodine. Of great
importance is the formation of hypochlorous acid, which is a strong oxidizing agent. One of the drugs that
split off chlorine is chloramine B, which has antiseptic and deodorizing properties. It is used to disinfect the
secretions of patients, household items, non-metallic instruments, as well as to treat hands and infected
wound surfaces. A significant number of antiseptics are represented by compounds (salts) of metals. The
mechanism of antimicrobial action of metal salts at low concentrations is associated with the blocking of
sulfhydryl groups of microbial enzymes. In high concentrations, depending on the nature of the metal and
the acid residue, the salt concentration, the degree of its dissociation and solubility can various local effects
occur: astringent, irritant, cauterizing (necrotizing). The group of oxidizing agents includes hydrogen
peroxide and potassium permanganate. The principle of action of both drugs is the release of oxygen. When
applied to tissues in the presence of proteins, hydrogen peroxide is decomposed under the influence of
catalases with the release of molecular oxygen. Potassium permanganate in the presence of organic
substances splits off atomic oxygen. The drug is used in solutions for rinsing, douching, irrigation of
wounds, treatment of burn surfaces, gastric lavage in case of poisoning with morphine, phosphorus, etc.
Antiseptics also include some compounds from the group of aldehydes and alcohols. One of the
representatives of aldehydes is formaldehyde solution. It has strong antimicrobial and deodorizing
properties. It is used as a disinfectant, as well as to treat the skin with sweating. A number of acids and
alkalis can be used as antiseptics. So, for washing the mucous membranes and rinsing the mouth, a solution
of boric acid is sometimes prescribed. It can also be used topically in ointments and powders. However, the
antimicrobial activity of boric acid is low.

3.The main types of drug therapy (examples). Principles of chemotherapy.

Ans:
1. Symptomatic therapy is aimed at eliminating a specific symptom of the disease, for example, the
appointment of antitussives for bronchitis.
2. Etiotropic therapy - elimination of the cause of the disease, when medicinal substances destroy the
causative agent of the disease. For example, the treatment of infectious diseases with chemotherapeutic
agents.
3. Pathogenetic therapy - is aimed at eliminating the mechanism of the development of the disease. For
example, the use of painkillers for trauma, when the pain syndrome leads to the development of a life-
threatening shock.
4. Substitution therapy is the restoration in the body of a deficiency of natural substances formed in it
(hormones, enzymes, vitamins) and taking part in the regulation of physiological functions. For example, the
introduction of a hormonal drug in case of loss of function of the corresponding gland. Substitution therapy,
without eliminating the causes of the disease, can provide life support for many years. So, insulin
preparations do not affect the production of this hormone in the pancreas, but with constant administration
of it to a diabetic patient, they ensure a normal metabolism of carbohydrates in his body.
General principles of chemotherapy
- malignant cells must be sensitive to the drug used;
- the drug must reach the cancerous tumor (for example, it must cross the blood-brain barrier in brain
tumors); - if the drug acts only in one phase of the cell development cycle, then it should be
take so often that all tumor cells can be affected;
- all malignant cells must be destroyed before they become insensitive to chemotherapy; - the use of several
chemotherapy drugs at the same time is more effective than the use of one.

Principles for choosing chemotherapy drugs

- l-in must have sufficient efficacy against a tumor of this type;
- if several drugs of the same type are available, then preference is given to the one with fewer side effects;
- the medicine should be used in the most effective mode and dosage;
- it is preferable to combine drugs with different mechanisms of action;
the interval between chemotherapy courses should be as short as possible.

Ticket 18

1. Narcotic analgesics (drugs). Mechanisms of analgesic effect. Pharmacological effects of morphine

and other drugs of the group in comparison with it. Indications for the use of morphine and other
drugs of the group. Contraindications. Symptoms of acute morphine poisoning, first aid measures.
Morphinism (symptoms, therapy, prevention).
Ans: Mechanisms of the analgesic effect.
a) activation of the antinociceptive system and an increase in its inhibitory effects
on thenociceptive system
b) increased activity of adenylate cyclase→ cAMP formation → cAMP activation dependent protein
kinases→
1. in presynaptic endings: inactivation of calcium channels→ violationcalcium entry into presynaptic
endings→ excretion disorder
neurotransmitter→difficulty in transmitting impulses in the nociceptive system
2. on the postsynaptic membrane: inactivation of calcium channels and opening of potassium channels with
the release of potassium from neurons→ membrane hyperpolarization, declineneuron
excitability→difficulty in perceiving the pain signal in the nociceptive system
c) activation of opiate receptors in the limbic structures of the brain→ change emotional perception of pain
(pain is perceived as insignificant)
Pharmacological effects of morphine and other drugs of the group in comparison with it.
1) Analgesia. 2) Euphoria. 3) Sedative action. 4) Miosis. 5) Bradycardia 6) Respiratory depression.
Codeine - in therapeutic doses, its analgesic effect is approximately 10 times less effective than morphine.
Much more often, codeine is used as an antitussive. Codeine may be effective for acute non-infectious
diarrhea.
Fentanyl is 100 times more potent than morphine. However, fentanyl is more effective than morphine.
Fentanyl is stronger than morphine, depresses the center of respiration.
Indications for the use of morphine and other drugs of the group: acute pain with injuries,
burns, operations, chronic severe pain not associated with neoplastic diseases (i.e. with tumors), pain in
malignant neoplasms, acute period of myocardial infarction, shortness of breath (dyspnea) and acute
pulmonary edema, labor pain relief, pre-anesthetic period premedication, pain relief in the postoperative
period, renal and hepatic colic.
Contraindications. conditions accompanied by depression of the respiratory center, bronchial asthma,
trauma to the head and brain, accompanied by an increase in intracranial pressure, pregnancy, childbirth
(because the tone of the uterus decreases and labor is lengthened, there may be respiratory depression in the
newborn), children under two years of age (due to the high sensitivity of the respiratory center to opioids),
with caution in older people (due to slow metabolism of morphine)
Symptoms of acute morphine poisoning,
1. The first signs of poisoning - 20-30 minutes after ingestion of toxic doses of opioids: dizziness,
weakness, vomiting, drowsiness, euphoria, turning into stupor, a sharp symmetrical constriction of the
pupils, oliguria, hypothermia
2. Complete analgesia quickly sets in, sleep, then complete loss of consciousness (coma)
3. Breathing is rare (sometimes 2-4 breaths per minute), arrhythmic, often Cheyne-Stokes breathing,
accompanied by cyanosis, sometimes pulmonary edema due to hypoxia, collapse.
4. A sharp drop in blood pressure, convulsions are possible in children
Relief measures.
1. Measures to restore and maintain breathing: transfer of the patient to artificial respiration (ALV) Carrying
out antidote detoxification - the introduction of naloxone intravenously.
2. Symptomatic treatment: restoration of cardiovascular activity, etc.
Morphinism (symptoms, therapy, prevention)).
Abrupt discontinuation of the drug that caused drug dependence leads to symptoms of deprivation. Fear,
anxiety, longing, insomnia appear. There may be restlessness, aggressiveness and other symptoms. Many
physiological functions are impaired. Sometimes there is a collapse. In severe cases, withdrawal can be fatal.
The introduction of an opioid analgesic relieves the phenomena of deprivation.
Help for morphine withdrawal.
1. β-blockers (nadolol, sotalol)
2. antipsychotics (droperidol)
3. M-anticholinergics (atropine sulfate, dicycloverine, hyoscine butyl bromide)
drugs that promote detoxification of the body (hemodez, B vitamins, sodium sulfate).

2.

3. Transformation of medicinal substances in the organism. Stages and types of biotransformation.

Inductors and inhibitors of the liver microsomal apparatus, their influence on biotransformation of
drugs (examples).
Ans: Biotransformation (metabolism) is a change in the chemical structure of medicinal substances and
their physicochemical properties under the action of body enzymes. The main focus of this process is the
conversion of lipophilic substances, which are easily reabsorbed in the renal tubules, into hydrophilic polar
compounds, which are rapidly excreted by the kidneys. In the process of biotransformation, as a rule, there
is a decrease in the activity (toxicity) of the starting substances. There are two types of metabolic reactions
of medicinal substances - non-synthetic and synthetic.
Non-synthetic reactions, in turn, are:
- microsomal - catalyzed by enzymes of the endoplasmic reticulum;
- non-microsomal - catalyzed by enzymes of a different localization (oxidation, reduction and hydrolysis
reactions).
Biotransformation of lipophilic drugs mainly occurs under the influence of liver enzymes localized in the
membrane of the endoplasmic reticulum of hepatocytes. These enzymes are called microsomal because they
are associated with small subcellular fragments of the smooth
endoplasmic reticulum (microsomes), which are formed during the homogenization of liver tissue or tissues
of other organs. Known inducers of the synthesis of microsomal enzymes (phenobarbital, phenytoin,
griseofulvin, etc.) and inhibitors of microsomal enzymes (cimetidine, chloramphenicol, furazolidone, MAO
inhibitors). In this regard, against the background of the systematic use of phenobarbital or griseofulvin, the
effect of glucocorticoids, contraceptives for oral administration is weakened. Phenytoin increases the
possibility of toxic effects of paracetamol. MAO inhibitors prolong the action of barbiturates.
Synthetic reactions are based on the conjugation of drugs with endogenous compounds or chemical groups
(glucuronic acid, glutathione, sulfates, glycine, etc.). Drugs that enter the body undergo the following
transformations:
• suction;
• protein binding and blood transport;
• interaction with receptors;
• distribution in tissues;
• metabolism and excretion from the body.
The mechanism of the first stage (absorption) is determined by the physicochemical properties of the drug.
Hydrophobic compounds easily penetrate membranes by simple diffusion, while lipid-insoluble drugs
penetrate membranes by transmembrane transport involving different types of translocases. Some insoluble
large particles can enter the lymphatic system by pinocytosis. The next stages of drug metabolism in the
body are also determined by its chemical structure.

Ticket 19
1. Hypnotics. Classification of drugs in chemical structure Mechanisms soporific effect, effect on sleep
structure. Pharmacological effects and comparative characteristics of different groups of drugs.
Indications for use and the choice of sleeping pills in different types of insomnia. Symptoms of
poisoning by barbiturates, benzodiazepines and assistance measures.

2. Bronchodilators. Classification of mechanism of action. Possible use in bronhoallergozah

antihistamines. Corticosteroids in the treatment of asthma.
Ans: Antihistamines can suppress reactions to histamine release, such as edema, bronchospasm,
vasodilation, and abnormal mucus secretion. There are drugs of 1 and 2 generations, it is necessary to
carefully select the drug. With an exacerbation of bronchial asthma, the use of 1st generation antihistamines
is contraindicated due to the presence of a sedative effect and their ability to cause dry mucous membranes,
which prevents sputum discharge, and this process is already difficult during an asthma attack. 2nd
generation drugs - high specificity for histamine receptors, rapid onset and pronounced duration of action.
The sedative effect is less pronounced.
Antihistamines may be used as an adjuvant in situations where an asthma exacerbation is associated with
exposure to a particular allergen, or for prophylactic purposes if exposure to an allergen is expected.
Possible use: Zyrtec-has a powerful antihistamine effect, and suppresses allergic inflammation, Hismantal
is the only non-sedative drug approved for the treatment of children of any age
3. Glucocorticosteroids in the treatment of bronchial asthma.
Glucocorticoids (by mouth or IV) are prescribed for attacks that do not respond to intensive treatment with
bronchodilators, and also as maintenance treatment if other drugs do not reduce the frequency and severity
of exacerbations. Glucocorticosteroids affect the course of bronchial asthma:
- block the synthesis of bronchoconstrictor and pro-inflammatory substances;
- enhance the bronchodilatory effect of adrenomimetics, increasing the expression 2-adrenergic receptors
of the respiratory tract;
- contribute to the suppression of neurogenic inflammation;
- increase the synthesis of vasocortin, contributing to a decrease in vascular permeability at the level of
postcapillary venules;
- prevent the penetration of some cells, especially eosinophils, into the focus of inflammation, and
contribute to their apoptosis;
- contribute to the reduction of IgE production
Apply:Budesonide, flunisolide, beclomethasone dipropionate.

3. The concept of dose. Classification of dose effect and frequency of appointments. The breadth of
therapeutic action of drugs (examples), value.
Ans: Dose - the amount of a drug introduced into the body that causes a pharmacological effect, expressed
by weight, volume, or in units of biological activity.
Classification of doses by effect
Therapeutic- Therapeutic dose - causes physiological changes in the body, has a therapeutic effect.
Minimum (min.) - gives the minimum therapeutic manifestations (threshold dose). Average (med.) - a
standard dose that gives a pronounced therapeutic effect in most animals. Maximum (max.) - the highest
dose, DVR, DIC, the limit of the therapeutic effect of the drug.
toxic- Poisoning dose - causes signs of poisoning, leads to the appearance of toxic effects
Lethal- Lethal dose - from the action of which death occurs. DL5– (min.) – causes the death of 10% of
animals; DL50- (media) - causes the death of 50% of animals; DL100 - (abs.) - causes the death of 100% of
animals.
Classification of doses according to the frequency of administration Single- 1) Full - dose for a single dose.
2) Fractional - reduced full dose, divided into separate portions. 3) Shock - a dose exceeding the next 2
times.

Daily- The amount of the drug (dose) used by the patient per day / day. Course - The dose of the drug
substance required for the entire course of treatment. Cyclic - Dose of the drug, prescribed intermittently
(Diacarb - 3 days of taking the drug, the next 3 days - a break).
Breadth of therapeutic action- the range between the mintherapeutic (acting) and mintoxic dose of the drug.
The more STD of the drug, the easier it is to dose the drug, the safer it is. STD is a sign of drug safety. Ether
FDA = 140-200mg%. STD of chloroform = 40-55mg%.

Ticket 20
1.
2. Antiatherosclerotic (hypolipidemic) drugs. Classification of drugs by mechanism of action,
pharmacological effects, indications for use in various forms of hyperlipidemia. Angioprotectors,
essence of action, use.
Ans: Lipid-lowering drugs - substances that reduce the high content of lipids in the blood and tissues.
Note a marked decrease in the concentration of LDL and cholesterol in the blood serum, as well as a
moderate decrease in the content of VLDL and triglycerides. At the same time, a decrease in the activity of
this enzyme leads to a decrease in the synthesis of biologically active substances - isoprenoids, which
underlies the so-called "pleiotropic" effects of statins, namely, anti-inflammatory, antiproliferative, and the
ability to improve endothelial function. The effect develops slowly (1-2 months after the start of treatment)
and disappears after discontinuation of the drug, therefore, as a rule, long-term (lifelong) therapy is
necessary.
The narrowest indications for prescribing are characterized by bile acid sequestrants, which are
recommended exclusively for patients with type IIa HLP. Statins are indicated for patients with both types
IIa and IIc HLP. Nicotinic acid can be administered to patients with any type of HLP. Fibrates are intended
mainly for the correction of type IIa HLP and the extremely rare dysbetalipoproteinemia (type III HLP).
Angioprotectors- drugs that reduce vascular permeability, normalize metabolic processes in the vascular
wall and improve microcirculation. The main properties that angioprotectors exhibit: improvement of
microcirculation and the state of tissue metabolism; antispasmodic action, expanding the lumen of blood
vessels; a decrease in vascular permeability, that is, a decrease in tissue swelling; improvement of blood
properties, for example, fluidity, and normalization of blood clotting.
Indications for use.
1. Treatment of vascular lesions that occur in diabetes mellitus, rheumatological diseases, widespread
atherosclerosis.
2. Blockage of the vascular lumen. The cause of this condition may be the appearance of atherosclerotic
plaques or a change in the blood composition. 3. Violation of blood circulation in the peripheral channel. In
this case, angioprotectors are agents that increase the resistance of surrounding tissues to a lack of oxygen.
4. Consequences of cerebrovascular accident and ischemic heart disease
5. Damage to the venous bed. Angioprotectors in this situation are venotonic drugs, antithrombotic drugs
and vasodilators.

3. Phenomena observed in the pharmacodynamic interaction of drugs (increased effect, varieties of

antagonism), examples. Problems of combined pharmacotherapy.
Ans: Pharmacological interactions are divided into pharmacokinetic and pharmacodynamic interactions.
Pharmacodynamic interaction.The main "targets" of the action of medicinal substances are specific
receptors, enzymes, ion channels, transport systems.
1. Interaction of medicinal substances at the level of specific receptors
Naltrexone blocks opioid receptors, so morphine does not cause euphoria against the background of
naltrexone. Naltrexone is used in the treatment of morphinism.
Interaction is possible when substances affect different receptors. So, the M-anticholinergic ipratropium and
the beta-agonist salbutamol are able to relax the smooth muscles of the bronchi and act as synergists as
bronchodilators.
2. Interaction of medicinal substances at the level of enzymes. Organophosphorus compounds (OPs)
covalently bind cholinesterases, in particular acetylcholinesterase. In the first hours of OPC poisoning,
cholinesterase reactivators - trimedoxime (dipiroxime) and isonitrosine - can be effective.
3. Interaction of drugs at the level of ion channels
The activator of K + channels, diazoxide, acting on arterioles, causes hyperpolarization of the muscle fiber
membrane; against the background of hyperpolarization, voltage-dependent Ca2+ channels do not open.
Nifedipine is a blocker of voltage-dependent Ca2+ channels. Both drugs dilate mainly arterial vessels.
Nifedipine enhances the vasodilating effect of diazoxide.
4. Interaction of medicinal substances at the level of transport systems.
Against the background of the action of tricyclic antidepressants (imipramine, amitriptyline), the
hypotensive effect of guanethidine is significantly weakened, since tricyclic antidepressants disrupt the
neuronal uptake of guanethidine. Special variants of drug interactions.
Acetylcholine usually lowers blood pressure, but in large doses, against the background of the action of
atropine, it increases blood pressure (a nicotine-like effect of acetylcholine is manifested).
Adrenaline usually increases blood pressure, but against the background of the action of phentolamine, it
lowers blood pressure (the vasodilating effect of adrenaline associated with the activation of beta-adrenergic
receptors is manifested).
Reserpine has a sedative effect and lowers blood pressure. Against the background of the action of MAO
inhibitors, reserpine causes excitation of the central nervous system and increases blood pressure.
Problems of combined pharmacotherapy.The choice of a combination of drugs is one of the most difficult
elements of pharmacotherapy. Currently, competent combined pharmacotherapy is impossible without
taking into account the achievements of clinical pharmacology in studying the mechanisms of drug
interaction.