Special pharmacology

1. Classification of general anesthetics, their general physical-chemical characteristics and principles of action?

General anesthetics bring about a reversible loss of pain sensation and consciousness. Depth of anesthesia appropriate
for the conduct of surgical procedure can be achieved a variety of drugs, either one or a combination
General anesthetics can be classified/ administered:
1. Intravenous: causes rapid loss of consciousness and induction is pleasant. produce little muscular relaxation
and frequently do not reduce reflexes adequately. they have little analgesic activity hence they are seldomly
used alone
a. Short acting (15 min): ketamine
b. Medium acting (20-30 min): Thiopentalum natrium
c. Long acting: Natrii oxybuiras
2. Inhalation: Depth of anesthetics can change rapidly by altering the inhaled concentration, and because of
their rapid elimination, they do not contribute to post-operative respiratory depression
a. Gases: Nitrous oxide, cyclopropane
b. Volatile Liquids: Trichloro Ethylene, Phthorothanum
General anesthetics stimulate GABA receptors and inhibit cholinergic and glutamic neurons.

2. Consecution of general anesthetics action on different parts of central nervous system?

Stages of anesthesia based on depth of anesthesia:

 Stage I: Analgesia – amnesia is common N2O falls in this category when it is used for conscious sedation
 Stage II: Delirium – excitement phase – this stage begins with unconsciousness
 Stage III: Surgical anesthesia – tis stage begins with unconsciousness
 Stage IV: respiratory paralysis

Sites that are most sensitive to general anesthetics are: dorsal lamina of spinal cord, reticular activating system,
hippocampus and relay circuits between thalamus and cortex

Site of action of anesthesia:

1. General Anesthetics – CNS – inhalation, depresses CNS leads to loss of consciousness

2. Regional anesthesia – Spinal- injected into subarachnoid space of spinal cord at 2nd lumbar vertebra level
3. Conduction Block – spine - injection into spine near a nerve trunk, absence of sensation
4. Local anesthesia – Local area, infiltration into tissue or an application of topical or local anesthetic on surface of
skin or mucous membrane

3. Possible complications on the different stages of inhalation anesthesia, its preventive measures and help?

The mechanism of action of anesthetics increase the threshold for the firing of the CNS neurons. The potency of most
inhaled anesthetics is proportionate to their lipid solubility. Possible mechanism of action includes effects on ion
channels (potassium, sodium and calcium) by interaction with membrane lipids or proteins and effects on central
neurotransmitter mechanism

Pharmacodynamics of inhaled anesthetics:

 Pulmonary effects:
o Increase tidal volume, increase respiratory rate (except NO)
o All volatile anesthetics are respiratory depressants
o Increase apneic threshold and decrease the ventilary response to hypoxia
o Can produce have Broncho-dilatory effect
o Depress the muco-ciliary function with resultant pooling of mucus
  Cardiovascular effect
 Metabolism
 Toxicity

4. Inhale anesthetics, their pharmacodynamics and using, comparative characteristics.

Intravenous anesthetics are mainly used for rapid induction of anesthesia which is then maintained by an inhalational
agent. They also serve to reduce the amount of maintenance anesthetics.

IV anesthetics exert their action through potentiation of GABA receptor activity. This increase chloride ion conductance
resulting in inhibitory post synaptic currents and ultimately inhibition of neural activity.

5. Non-inhale anesthetics, its pharmacodynamics, comparative characteristics, prescription for using.

6. Pharmacodynamics, using and Dicain toxicology.

It’s a local anesthetic used parenterally or topically at 0.25-0.5% concentration. Local anesthetics reversibly block
impulse conduction in restricted area of the body where it is applied. All local anesthetics posses varying degree of water
solubility. Lipid solubility helps in migration of active drug into the neural fiber and water solubility is essential to get the
drug to site of action from site of administration.

Pharmacodynamics:

Action on CNS: local anesthetics stimulate the CNS to produce restlessness, tremor, mental confusion, convulsion. In
toxic doses it causes respiratory depression, coma and death.

Action on CVS: local anesthetics are myocardial depressants and decrease heart rate and amplitude of myocardial
contraction, they also decrease blood pressure

Pharmacokinetics: local anesthetics are readily absorbed through the mucus membranes and damaged skin. They are
weak bases and at tissue pH diffuse through the connective tissue and cellular membranes to reach the nerve fibers
where ionization can occur. Local anesthetics are metabolized in the liver and in some cases in the kidney. They are
protein bound inside the body and their action can be prolonged by adding adrenaline 1 in 20000.

Side effects: CNS side effects include dizziness, mental confusion, tremors, twitching, convulsion and respiratory
depression. CVS toxicity include hypotension, cardiac arrythmias and brady cardia

7. Pharmacodynamics and using of Anaesthesin and Novocain.

Novocain/procaine is a local anesthetic that is used parenterally at 0.5-2% injection. For spinal cord use 2-3mL at 5%
solution introduced into the subarachnoid space at level above the 1st lumbar.

8. Pharmacodynamics, mechanism of action and using of Xycain and Trimecain.

Xycain/ lidocaine is two times stronger in activity than Novocain with the same toxicity.

Usage:

 Infiltrative: 0.25-0.5% solutions

 Conductive: 0.5-2% solutions
 Peridural: 0.5% solution
 Spinal cord: 5% solution
 Terminal: 4-10% solution

Xycain/ Lidocaine eliminates cardiac arrythmias of ventricular origin i.e. extra systolic, fibrillation of ventricles in acute
myocardial infarction, in these cases xycain/ Lidocain is administered intravenously slowly in a 0.2% solution
9. Acute poisoning by local anesthetic drugs, its prophylactic and help.

Symptoms: decreasing arterial pressure, cardiac arrest, depression of CNS and breathing seizures,

Treatment: vasoconstrictive drugs (noradrenaline, adrenaline), antiseizure drugs (sibazone, thiopental sodium),
Cardiotonic (strophantin)

Prophylaxis: use the least possible volume and the most possible dilution of local anesthetics

10. Drugs which irritates skin and mucous membranes: character and mechanism of action, using.

11. Astringents, slime, absorptive drugs, mechanism of action, using.

12. Anticholinesterase drugs: pharmacodynamics, mechanism of action and using, side effects?

It’s an indirect cholinergic stimulant that works by inhibiting the action of acetylcholine esterase which hydrolyses
acetylcholine, this prolongs the life time of acetylcholine, that’s why these drugs are more mild. Their action can be
reversible or irreversible. Hence these drugs produce an accumulation of acetylcholine in various cholinergic sites.

reversible anticholinesterases have a structural resemblance to acetylcholine, are capable of combining with anionic
and esteratic sites of cholinesterase as well as with acetylcholine receptor e.g. NEOSTIGMINE is a drug of choice in the
treatment of myasthenia gravis, a chronic disease characterized by muscular weakness and rapid fatiguability of the
skeletal muscles due to impaired neuromuscular transmission. The defect may be presynaptic or postsynaptic

13. M-cholinomimetic drugs: pharmacodynamics, mechanism of action and using?

M-Cholinomimetic drugs mimic (direct acting) acetylcholine and muscarine and bind to M-choline receptors and
stimulate them eliciting a response. M1-in CNS autonomic ganglion, M2- in myocardium, M3- in glands, M4- in smooth
muscles, M5 – in non-innervated tissue.

Pharmacodynamics:

Cardiovascular system: Acetylcholine decreases the contractility (negative inotropy) and decreases the conduction
velocity (negative dromotropy) of the atria. It depresses the sinoauricular node, decreases the heart rate (negative
chronotropy)

Effect on smooth muscles: Acetylcholine causes increase in tone, amplitude of contractions, peristalsis and secretory
activity of the gastrointestinal tract. It causes contraction of smooth muscles of gall bladder and relaxation of sphincters
of gastrointestinal and biliary tract. Acetylcholine causes bronchoconstriction and increase in bronchial secretion and
can precipitate the bronchial asthma.

Effect on secretions: Acetylcholine increases the salivary, sweat, lacrimal, nasopharyngeal, gastric and bronchial
secretions. All these secretory effects are blocked by atropine and enhanced by cholinesterase inhibitors e.g.
physostigmine.

Effect on eye: After intraconjunctival instillation, acetylcholine causes miosis, due to contraction of circular muscles of
the iris and fall in intraocular tension

14. M-cholinoblocker drugs: pharmacodynamics, mechanism of action and using, side effects?

Anticholinergic or cholinergic blocking agents are the agents which block the action of acetylcholine at the
postganglionic parasympathetic nerve endings. They are also termed as antimuscarinic or muscarinic blockers and
atropine is the classical antagonist which blocks the effect of acetylcholine on muscarinic receptors. The nicotinic
antagonists also block certain actions of acetylcholine and are termed as ganglion blocking agents

M-Cholinblockers/ M-cholinergic antagonists e.g. atropine sulfas which is used for mydriasis, antispasmoic (GI and
Bladder)
Pharmacological Actions Pharmacological actions of atropine are due to equal blockade of M1, M2 and M3 muscarinic
receptors

Effect on cardiovascular system: Atropine initially decrease the heart rate due to stimulation of vagal centre followed by
tachycardia due to peripheral vagal block on SA node. It also shortens effective refractory period of AV node and
facilitates AV conduction. In therapeutic doses, atropine completely blocks the peripheral vasodilatation and decrease in
blood pressure produced by cholinergic agents

Effect on central nervous system: In therapeutic doses, atropine causes stimulation of medullary vagal nuclei and higher
cerebral centres and may produce bradycardia and increase in rate & depth of respiration. By depressing vestibular
excitation, it has antimotion sickness property

Effect on gastrointestinal system: Atropine decreases the tone and motility of all parts of gastrointestinal tract.

Effect on other smooth muscles: Atropine relaxes the smooth muscles of bronchi and bronchioles which results in
widening of the airways. It is effective in relieving bronchospasm produced by cholinergic agents.

Effect on secretions: Atropine reduces the various body secretions e.g. sweat, salivary, bronchial and lacrimal

15. N-cholinomimetic agents: pharmacodynamics, mechanism of action and using?

N-Cholimimetic: mimic aceylcholine and nicotine and interact with N-cholinergic receptors to stimulate them. N2 is in
neuromuscular junction/ somatic muscle synapse N1 in ganglia

Nicotinic Actions

Effect on autonomic ganglia: It can cause stimulation of sympathetic and parasympathetic ganglia and stimulation of
adrenal medulla, which leads to rise in arterial blood pressure due to peripheral vasoconstriction.

Effect on myoneural junction: Acetylcholine cause stimulation of skeletal muscles and in larger concentration at the
myoneural junction can produce paralysis of skeletal muscles.

Effect on CNS: Acetylcholine when injected parenterally does not cross blood brain barrier being a quarternary
ammonium compound and does not have any central action

16. Ganglion/N blockers: localization and mechanism of action, indication and contra-indication for using, complications.

17. Myorelaxants: pharmacodynamics, mechanism of action, indication for using?

Skeletal muscle relaxants act peripherally at the neuromuscular junction or centrally in the cerebrospinal axis to reduce
muscle tone.

CENTRALLY ACTING MUSCLE RELAXANTS

These agents reduce skeletal muscle tone by a selective action on cerebrospinal axis without affecting consciousness.
Mephenesin was the first drug used as muscle relaxant but due to its serious side effects e.g. haemolysis, hypotension
and thrombophlebitis, it is not clinically used now.

18. Myorelaxants: drugs, possible complications and antagonists. Pharmacogenomics of Dithyline (succinylcholine)?

SUCCINYLCHOLINE It is a quaternary ammonium compound with a structure similar to acetylcholine used as a adjuvant
to general anesthesia (specially in major surgical procedures e.g. abdominal and thoracic surgery, orthopedic
procedures, intubation etc.). and Succinylcholine is used for surgical procedure of brief duration (endotracheal),
Succinylcholine is used to avoid convulsion and coma from electroconvulsive therapy and in the treatment of tetanus
and emergency of epilepsy (status epilepticus)

19. Pharmacodynamics, mechanism of action and using of adrenaline, side effects?

Pharmacodynamics:

Heart (Beta 1 receptors’): increase heart rate, increase force of myocardial contraction and output

Blood vessels: constrict blood vessels of skin and mucous membrane (alpha 1, 2 receptors) and dlate blood vessles to
muscles (beta 2 receptors)

GIT: cause relaxation of smooth muscles of GIT and reduces motility

Respiratory system (Beta 2): bronchodilation

Eye: mydriasis (pupil dilation), intraocular tension is reduced due to less aqueous humour production

Adverse Effects: Restlessness, anxiety, tremor, headache. Both adrenaline and noradrenaline cause sudden increase in
blood pressure, precipitating sub-arachnoid hemorrhage and occasionally hemiplegia, and ventricular arrhythmias. May
produce anginal pain in patients with ischemic heart disease.

Therapeutic uses: allergic reaction, bronchial asthma, stimulate cardiac arrest,

20. Pharmacodynamics, mechanism of action and using of ephedrine, side effects?

21. Comparative pharmacological characteristic of nor-adrenaline, adrenaline, mesatone, isoproterenol and Salbutamol?

Adrenaline It is an adrenomimetic which stimulates a1, a2 and B1, B2 adrenoreceptors, Administration: Cardiac
arrest, for example, during surgical general anesthesia, electric trauma,shock (anaphylactic shock)
Nor-adrenaline Is an adrenomimetic of direct action which stimulates 1-, 2- and 1-adrenoreceptors,
administration: in cases of acute decreasing of blood pressure, shock and collapse conditions,
surgeries, traumas
Mesatone Is a synthetic a1-adrenomimetic drug of direct action, Administration: acute hypotensive conditions,
prophylaxis of decreasing of blood pressure, nose drops in case of rhinitis
Isoproterenol is a synthetic catecholamine, which is a strong stimulant of β1- і β2-adrenoreceptors,
Administration: bradycardia, atrio-ventricular blockade, bronchial spasm
Salbutamol selective b2-adrenomimetic of direct action, Administration: inhalations during attacks of bronchial
asthma and bronchial spasms of any etiology

22. Using of adrenomimetic drugs in medical practice?

The sympathomimetic or adrenergic or adrenomimetic drugs mimic the effects of adrenergic sympathetic nerve
stimulation. These are the important group of therapeutic agents which may be used to maintain blood pressure and in
certain cases of severe bronchial asthma

23. a-adrenoblockers: pharmacodynamics, mechanism of action and using, side effects? 24. B-adrenoblockers:
pharmacodynamics, mechanism of action and using, side effects? 25. Sympatolytics: drugs, pharmacodynamics,
mechanism of action and using, side effects?

Adrenoreceptor agonists (adrenoblockers) are classified into:

I. Direct acting Adrenoblockers

1. a-adrenoblocker - blocks a- receptors hence preventing its stimulation by a catecholamine, hence it acts of the
post neuron cell i.e. the effector: Prazosinum, Doxazosinum, Pyrroxanum
2. B-blockers- blocks b- receptors hence preventing its stimulation by a catecholamine, hence it acts of the post
neuron cell i.e. the effector:
a. Non selesctive B-adrenoblockers: Propranololum
b. Selectivs B-adrenoblocker: Atenololum, Metoprololum, Timololum, Nadololum
3. B + a – adrenoblockers: Labetatolum, Carvediolum
II. Indirect acting Adrenoblockers (sympatholytics)- sympatholytics act on the adrenergic neuron to either
interfere in neurotransmitter release or after the uptake of neurotransmitter into the adrenergic nerve:
Reserpinum

Therapeutic use Adverse rxn

a-blockers management of pheochromocytoma and also to treat
peripheral vasospastic conditions e.g. Raynaud’s
disease and shock syndrome.
B-blockers ischemic heart disease, arterial hypertension, cardiac
tachyarrhythmia, acute myocardium infarction.
palpitation, nasal stuffiness, postural
hypotension, retention of fluid, diarrhea,
inhibition of ejaculation and impotence.

Sympatholytics Treatment of hypertension swelling of nose mucous membrane with

complication of nose breathing,
bradycardia
26. Comparative pharmacological characteristic of narcotic analgesic drugs?

Analgesics: drugs that provide pain relief by heightening the threshold level in the body without hampering
consciousness or varying other sensory modalities

27. Narcotic and non-narcotic analgesic drugs mechanism of analgesic action, specialties of using fighting different types
of pain?

Classification of analgesics

Narcotic/ opioid Non-narcotic NSAID

Acts on CNS Acts on peripheral nerves to reduce Anti-inflammatory drugs which
e.g. morphine, codeine, pethidine pain alleviate pain by reducing local
no ceiling effect e.g. Paracetamol inflammatory response by reducing
the release of prostaglandins
e.g. Ibuprofen
has ceiling effect – increase in dose
does not increase analgesia but
increase side effects
Opioid receptor subtypes
µ Analgesia, depression of breathing, euphoria, addiction development, sedative side effect, depression of
content moving through GI tract, miosis (constriction of pupils)
Kappa Sedative effect, psychotomimetic action
Delta Analgesia, euphoria, behavior changes
Sigma Mania, increase in breathing frequency, hallucination, Mydriasis (enlargement of pupil)

28. Morphine: pharmacokinetics, pharmacodynamics, mechanism of action and using?

Drugs obtained from morphine are known as opioids or narcotic analgesics. Morphine and other opioids exert their
pharmacological actions by acting on different receptors namely mu (µ), kappa (κ) and delta (δ).

Analgesic, respiratory, depression as well as euphoria produced by morphine result mainly from action at mu receptors.

Pharmacological Actions

Effect on CNS: The main action of morphine is CNS depression which further results in analgesia, depression of
respiratory centre, cough centre and sleep. In addition, it causes euphoria or dysphoria and dependence.

Analgesia: Morphine produces analgesia by elevation of pain threshold, thereby reducing the perception of pain. It also
altered psychic reaction to pain which may be associated with feeling of well being e.g. euphoria. It also produces
lethargy and sleep, morphine relieves all types of pain

Action on eye: Morphine causes constriction of pupil (miosis) due to action on oculomotor nerve nucleus

Other smooth muscle: Morphine causes bronchoconstriction which is due to histamine release and may be dangerous in
patients suffering from bronchial asthma. Morphine also cause flushing and itching of skin due to histamine release

Chemoreceptor trigger zone (CTZ): Morphine stimulates CTZ and produces nausea and vomiting

Pharmacokinetics: Morphine orally is less effective and absorption is very slow. It has variable and high first pass
metabolism when given by subcutaneous route, its analgesic effect starts within 10 minutes which persists for 4 to 5
hours and by IV route, it produces immediate action. In plasma, it binds to plasma proteins (approx. 30%). In liver it is
metabolized by conjugation to glucuronic acid to form active and inactive products, which are excreted in urine. It is also
excreted though bile and in the feces.

29. Non-narcotic analgesics: drugs, their pharmacodynamics, using and side effects?

Non-steroidal antiinflammatory drugs (NSAIDs) are also known as nonopioid analgesics. They relieve pain without
interacting with opioid receptors and do not depress CNS and have no drug dependence or drug abuse property and
possess antipyretic activity also. They act primarily on peripheral pain mechanisms and also in CNS to raise pain
threshold.

Trauma: stimulates the enzyme phospholipase A2 which metabolizes phospholipids into Arachidonic acids. Arachidonic
acids are acted upon a number of enzymes such as cyclo-oxygenase 2 COX 2 forming Endoperoxides which are
converted into prostaglandins. Prostaglandins cause inflammation and stimulation of free nerve endings resulting in pain
transmission. Non-Opioids / Non-steroidal anti-inflammatory drugs (NSAIDS): e.g. Ibuprofen or Paracetamol act to
block the action of COX2 providing relief from mild to medium severity pain

Indications for administration of non-narcotic analgesics:

Headache, toothache, radiculitis, neuritis, neuralgias, myositis, myalgia, arthritis, arthralgia, pain, connected with pelvic
organs (dysmenorrheal)
30. Ethyl alcohol, pharmacodynamics and using in medical practice?

Ethanol is a drug with sedative, hypnotic and antianxiety actions. Its use is not regulated and abuse (alcoholism)
represents a complex social medical disorder with devastating effects. Ethyl alcohol has a narcotic type of action and
antiseptic properties. Antiseptic action is connected with denaturation of microbial cell proteins. Locally ethanol is used
to clean the hands of the surgeon and operation field. Ethyl alcohol resorptive action is connected with influence at all
organs and systems. The influence on CNS has 3 stages: excitation, Narcosis, paralysis. Ethanol stimulates and then
oppresses the respiratory and vascular moving centers, causes fist tachycardia then bradycardia, increases the blood
pressure then decreases the blood pressure. Activated saliva and stomach glands. In high concertation decreases
stomach motility.

31. Anti-epileptic drugs: classification, pharmacodynamics, mechanism of action, using and side effects?

Epilepsy is a neurological disorder characterized by short, recurrent and periodic attacks of motor, sensory or
psychological malfunction. It is associated with paroxysmal abnormal electrical discharge in the brain.

General effects of antiseizure drugs is to suppress repetitive action of potentials in epileptic foci in the brain. Different
mechanisms are involved in achieving this effect.

At therapeutic concentrations, Dipheninum, Carbamazepinum block voltage gated sodium channels in neural
membranes. This action results in prolongation of the inactivated state of Na+ channel and the refractory period of the
neuron.

Benzodiazepines interact with specific receptors on the GABA receptor-chloride ion channel macro molecular complex.

Classification of antiepileptic drugs:

1. Agents for treating generalized tonic-clonic conditions e.g. phenobarbitalum

2. Agents for treatment of slight tonic-clonic conditions e.g. Natrii valproas
3. Agents for treatment of myoclonic seizures e.g. Diazepamum

32. Pharmacodynamics and using anty-parkinsonic agents, side effects?

Parkinsonism is an extrapyramidal motor disorder, characterized by akinesia, rigidity and tremor with secondary
manifestations such as excessive salivation, seborrhoea, mood changes (especially depression) and in certain patients,
liver damage has been reported.

In parkinsonism, there is a degeneration of dopaminergic nerve endings of the basal ganglion (neurons in substantia
nigra and the nigrostriatal tract), which results in deficiency of dopamine and cholinergic overactivity. This imbalance
between the dopamine deficiency and overactivity of cholinergic system gives rise to this motor disorder. Thus, the
rational approach to the therapy of parkinsonism would be either to increase the central dopaminergic activity or to
decrease the central cholinergic activity.

Classification of anti-Parkinson’s drugs:

I. Drugs activating the dopaminergic system:

a. Precursor of dopamine: Levadopum, Nacom
b. Dopaminomimetics: Bromoniphinum
c. Inhibitors of MAO: Selegellinum
II. Drugs inhibiting the glutamatergic system: Amantadinum
III. Drugs inhibiting cholinergic influences: Cyclodolum

33. Neuroleptics: classification, pharmacy-dynamics, mechanism of action, using and side effects?

Neuroleptic drugs (AKA anti-schizophrenic drugs) are a group of sedative medicines with potent anti-psychotic activity
(they can remove delirium, hallucinations, psychomotor anxiety). They also influence the vegetative nervous system
functions (BP, temperature) and after long term using cause parkinsonism (Extrapyramidal disorders).

Classification of neuroleptic drugs:

1. phenothiazine derivatives: Amanozine

2. Butyrophenone derivatives: Haloperidol
3. Thioxanthene derivatives: Benzamides
4. Benzodiazepine Derivatives: Clozapine

Older antipsychotic drugs mainly interact with Dopamine (D2) receptors. New antipsychotic agents have higher affinity
for other receptors e.g. Alpha adrenoceptor blocking action correlates well with an antipsychotic effect.

Clozapine is a drug with significant D4 and %-Hydroxytryptamine (5-HT2) receptor blocking actions, has affinity for D2
receptors. Most of the newer atypical drugs e.g. sertindolum have affinity for 5-HT2A receptors, though they may also
interact with D2 and other receptors.

Lithium inhibits a recycling of neural membrane phosphoinositides involved in the generation of inositol trisphosphate
(IP3) and diacylglycerol (DAG). These secondary messengers are important in amine neurotransmission including that
mediated by central adrenoceptors and muscarinic receptors. Competition between lithium and natrium sites may lead
to altered neuronal functions.

34. Tranquilizers: drugs, pharmacodynamics, mechanism of action, using and side effects.

35. Benzodiazepines derivative as sedative, anti-convulsive drugs, its pharmacodynamics and using.

36. Sedative agents: drugs, their pharmacodynamics, mechanism of action, using and side effects.

37. Psychostimulators: drugs, their pharmacodynamics, mechanism of action, using and side effects.

38. Analeptics: drugs, their pharmacodynamics, mechanism of action, using and side effects?

39. Antidepressants: drugs, their pharmacodynamics, mechanism of action, using and side effects.
40. Adaptogens: drugs, pharmacodynamics and using.

41. Cardiac and extracardiac action of cardiac glycosides (steroid cardiotonic drugs)?

Extra cardiac action:

 Digitalis (cardiac glycoside) produces diuresis in cardiac heart failure patients CHF, it increases the secretion of
sodium and water by the kidney which may be due to decrease in the venous pressure bringing about shifting of
edema fluid into the circulation and also improves the renal circulation
 Digitalis can produce nausea and vomiting which is probably due to chemoreceptor trigger zone CTZ stimulation
 Digitalis has mild vasoconstriction action increasing the peripheral resistance, but in CHF patient’s peripheral
resistance decrease due to withdrawal of reflex sympathetic over reactivity. Venous tone improves in normal as
well as CHF patients. It has no effect on coronary circulation

Cardiac pharmacological action:

 Contractibility: Digitalis (cardiac glycoside) increases the force of myocardial contraction with out causing an
increase in oxygen consumption which is why its used in CHF patients.
 Cardiac output: digitalis increases the cardiac output in CHF patients by increasing the force of myocardial
contractions
 Heart rate: in CHF patients the heart rate decreases due to stimulation of Vagus nerve. The vagal action can be
blocked by Atropine but after a full digitilising dose the effect can not be blocked by atropine due to its direct
cardiac action
 SA node: digitalis sensitivities the SA node to normal vagal impulse resulting in bradycardia
 Automaticity: digitalis increases the ability of the purkinje cell and ventricular muscle to initiate impulse
 Conduction: conduction through AV node is depressed whereas conduction is slightly increased in the auricle
and ventricles.

42. Mechanism of cardiac action of glycosides and its using?

Digitalis (cardiac glycoside) acts by interfering with the sodium and potassium transport across the cell membrane and
by increasing the amount of coupling calcium i.e. making more calcium available for excitation contraction coupling.

Cardiac glycosides inhibit Na+ K+ ATPase by competing with potassium. Inhibition of the Na+ K+ ATPase leads to increase
in intracellular sodium and decrease in potassium.

Calcium also forms a link between the electrical events in the membrane and contractile proteins. Digitalis makes more
calcium available for excitation – contraction coupling and increasing cardiac contractibility

Digitalis also exerts some indirect action on heart mainly by increase in vagal activity which ultimately influences activity
of AV node, SA node and auricles

43. Cardiac action of glycosides, changes of ECG under the influence of heart glycosides?

ECG: Digitalis in Therapeutic doses causes inversion of T wave, sagging of S-T segment and shortening of Q-T interval
(shortening of systole). In Toxic Dose it causes prolongation of P-R interval (Slowing of AV conduction), atrial
arrhythmias (atrial tachycardia and atrial fibrillation) with AV block and ventricular arrhythmias

44. Pharmacokinetics and using of cardiac glycosides?

Among the cardiac glycosides, digitoxin is absorbed rapidly and completely from the GI tract with oral absorption of
approximately 90-100% with plasma protein binding of approx. 95% with plasma half life of 5-7 days. It enters the liver
cells where it is metabolized to epidisitoigenin and is excreted in bile and urine

45. Main point of therapeutic action of glycosides in treatment of congestive heart failure?
Digitalis (cardiac glycoside) increases stroke volume and cardiac output, hence about a more complete emptying of the
ventricles during systole. This reduces the pulmonary congestion and edema and decrease in systemic venous pressure.
The cardiac glycoside primarily corrects systolic dysfunction.

The dosing schedule is dependent on the desired speed of action and urgency. The maintenance dose is the amount
required to maintain the therapeutic effect and is equal to the amount eliminated a day. Dosing can be IV or oral

46. Symptoms and principles of treatment of intoxication by glycosides, its prophylactic?

Adverse effects: it includes anorexia, vomiting, headache, visual disturbance, cardiac arrythmias.

Treatment of digitalis induced arrhythmias

Tachyarrhythmias: infuse KCl 20mmol/L intravenously or orally depending upon the case

Supraventricular arrhythmias: can be treated by beta blockers e.g. Propranolol 10-40mg every 6 hours orally or 0.5-1mg
IV

Ventricular arrhythmias: Lignocaine (1-2mg/kg IV)

AV block and Bradycardia: treated by Atropine (0.6-1.2mg IM)

47. Non-glycosides (non-steroid) cardiotonic drugs, their pharmacodynamics, mechanism of action, using and side
effects?

Non-steroid cardiotonic drugs include: Amrinonum, Milrinonum

Amrinone: it’s a relatively selective inhibitor of cyclic GMP, Cyclic AMP-PDE. It causes vasodilation with a consequent
decrease in systemic vascular resistance. It increases both the force of contraction and velocity of relaxation of cardiac
muscle. It is administered IV 0.75 mg/kg/min. Side effects include nausea, abdominal pain, diarrhea, fever,
thrombocytopenia and hepatotoxicity

48. Pharmacological characteristics and using of clofeline (clonidine) and methyldopa?

Both Clonidine and methyldopa are antihypertensive agents that are centrally acting sympathetic inhibitors

Clonidine: is a Beta adrenoceptor blocking antihypertensive drug, It stimulates presynaptic, α2 receptors in vasomotor
centre of brain causing decreased sympathetic outflow which results in fall of blood pressure and bradycardia. It is
indicated in hypertension of all grades except pheochromocytoma, glaucoma and migraine.

Methyldopa: It is α-methyl analogue of DOPA, the precursor of dopamine and noradrenaline. It is converted to alpha
methyl noradrenaline which stimulates central alpha2 adrenergic receptors in brain thereby decreasing sympathetic
outflow. It decreases peripheral resistance more than heart rate or cardiac output. It is indicated in mild to moderate
hypertension

49. Pharmacokinetics, mechanism of action and using of anaprilin (Propranolol), side effects?

Anaprilin/ propranolol is a non-selective Beta blocker. It is rapidly distributed in the body because it is lipid soluble. It can
readily cross blood brain barrier (BBB).

Therapeutic uses:

 Hypertension: Propranolol is antihypertensive. Propranolol suppresses the activation of heart by blocking the β1
receptor.
 Glaucoma: Timolol and other ocular βblockers are used to treat glaucoma. Propranolol is effective in diminishing
intraocular pressure in glaucoma. This occurs by decreasing the secretion of aqueous humor by ciliary
epithelium. Used in chronic cases only
 Hyperthyroidism: Propranolol blocks the peripheral conversion of thyroxine to triiodothyronine.
  Angina pectoris: Propranolol decreases O2 requirement and work of heart muscle and therefore is effective in
reducing the chest pain on exertion which occurs in angina
 Myocardial infarction: It blocks the action of circulating catecholamines which would increase the oxygen
demand in already ischemic heart muscle thereby limiting the infarct size

Side effects: brady cardia, bronchial asthma, cardiac failure, cardiogenic shock, hypoglycemia

50. Pharmacodynamics, mechanism of action, using of nifedipine?

Nifedipine: It causes coronary vasodilatation and increases coronary blood flow. It reduces the total peripheral vascular
resistance and systolic and diastolic blood pressure is reduced. It causes reflex tachycardia. It is indicated in vasospastic
angina, chronic stable angina, hypertension, hypertensive emergency, hy

Nifedipine is a calcium channel blocking antianginal drug.

51. Myotropic hypotensive drugs (natrium nitroprusside, magnium sulphate, appresin): pharmacodynamics, mechanism
of action, using?

They are all antihypertensive which are peripheral vasodilators

Sodium nitroprusside: is an antihypertensive drug that exerts its effect by direct vasodilation. Its given IV infusion 0.1-
0.3mg/min

Classification of antihypertensive drugs according to clinical applications:

I: agents affecting the renin angiotensin system:

1. ACE inhibitors
2. Angiotensin 2 antagonists

II: Sympatholytic drugs:

1. Central acting adrenergic drugs: Clonidine, Methyldopa

2. Central and peripheral acting:
a. Sympatholytic: Reserpine
b. Ganglioblockers: Benzohexonium
c. Beta blockers: Propranolol

III: Peripheral vasodilators:

1. Direct vasodilators: Magnesium sulfate, sodium nitroprusside

2. Calcium channel blockers: Nifedipine
3. Alpha Blockers: Prazosin
4. Diuretics: Hydrochlorthiazidum

52. Inhibitors of angiotensin-converting enzyme: mechanism of action, using, side effects.

53. Pharmacological characteristics and using of nitroglycerin?

Glyceryl trinitrate (GTN) releases nitrite ion (NO2–.

) which is further metabolised to NO by enzymatic step involving reaction with tissue sulphydryl (–SH) groups in vascular
smooth muscles. NO released by GTN activates soluble, cytosolic form of guanylyl cyclase in vascular smooth muscles by
interacting with haem group in the enzyme. This converts GTP to cGMP. cGMP dephosphorylates myosin light chain
kinase and prevent myosin interaction with actin leading to relaxation.

54. Antianginal drugs: classification, pharmacokinetics, mechanism of action, using?

Ischemic heart disease is compromised of angina pectoris and infarction of the myocardium which are pathological
states associated with the coronary insufficiency.

Angina pectoris is the strangling chest pain that occurs when coronary blood flow is inadequate to supply the oxygen
demands of the myocardium.

To restore the balance between the myocardium oxygen demand and supply, some techniques maybe used:

1. increasing the coronary blood flow

2. reduction of cardiac oxygen demand (by decreasing cardiac work)
3. stimulation of the tolerance of the heart to hypoxia

Classification of antianginal drugs:

I: Vasodilators:

1. Nitrates and Nitrites: nitroglycerine, long acting nitrates include isobride dinitrate
2. Spasmolytic: papaverine hydrochloride, No-spa
3. Reflectory-acting drugs: Validolum

II: Drugs affecting the adrenoreceptors:

1. Beta adrenoblockers: Propranolol

2. Ant adrenergic drugs: Cordarone

IV: Ca2+ channel blockers: Nifedipine

V: drugs which increase myocardium tolerance to hypoxia:

1. Trimetazidine
2. Vitamins A, B, E, P
3. Anabolic: Retabolile

55. Pharmacological characteristic and using of quinidine and novocainamide (procainamide)?

Procainamide: It has got quinidine like cardiac property. It depresses the excitability of both atria and ventricles.
Contractility and conductivity are also depressed. It has got minimal vagolytic action. It deceases the rate of rise of
action potential and prolongs the effective refractory period. It’s a sodium channel blocker

It is indicated in ventricular arrhythmia, ventricular premature depolarization and paroxysmal ventricular tachycardia,
supra-ventricular tachycardia and atrial arrhythmia.

Quinidine: Its sodium channel blocking property results in an increased threshold for excitability and decreased
automaticity. As a consequence of its potassium channel blocking properties, it prolongs action potential in most cardiac
cells.

56. Pharmacological characteristic and using of xycaine, anapriline, aethmosine and verapamil as antiarrhythmic drugs.

57. Pharmacology of amiodarone: mechanism of action, using, side effects.

58. Anti-coughing and expectoration drugs, pharmacodynamics, mechanism of action, using.

59. Mechanism of action and using of vomiting and anti-vomiting drugs?

Emetic (vomit causing) drugs are divided into:

  Drugs of central action: aponorphini hydrochloridum acting on the hemoreceptor trigger zone connecting to the
emetic center through the fasciculus Solitarius
 Drugs of peripheral action:
o Expectonrantive plant drugs pf themopsidis
o Solution of ammonia caustricum

Antiemetics (inhibit vomiting) – usually drugs that control activity in the chemoreceptor trigger zone

 Droperidol: asopemine receptor blocker

 Metoclopramide: a dopamine and 5 HT3 receptor agonist
 Ondansetron: inhibits 5 HT3 (seraotnin) receptors
 Dronabinol: a cannabinoid

Vomiting is induced when something toxic might be ingested and prevented when patient is unconscious or something
highly alkaline/ acidic was ingested to protect the esophagus.

Emetic drugs stimulate dopamine receptors

Antiemetic drugs block dopamine receptors

60. Specialties of action on stomach secretion of H2-histamine receptors blockers, M1-cholinoblockers, blockers of Na+-
K-ATP, cholinergic and adhesive drugs, using for treatment of ulcer disease?

These are agents used in the treatment of peptic ulcers as they prevent gastric secretions.

Na-K ATP: they block the proton pump hence H+ doesn’t get inside the gastric lumen therefore HCl can’t be formed. Its
most effective for treatment of peptic ulcers. Drugs end with -zole e.g. Omeprazole. NSAIM cause peptic ulcers as they
block prostaglandins

H-2 Histamine receptor blockers: The H2 antagonists in clinical use are analogs of histamine that competitively inhibit
the interaction of histamine with H2 receptors and are highly selective. They inhibit gastric acid secretion elicited by
histamine and other H2 agonists in a dose dependent manner. E.g. Ranitidine

Note, H1 histamine are for allergic reactions

Selective M1 Blockers:

61. Antacid drugs: mechanism of action, using, side effects?

Ant acids are basic compounds that neutralize acid in gastric lumen, they have no effect on gastric secretion. They are
classified into:

 Systemic antacids: e.g. sodium carbonate, they are soluble compounds and can be absorbed by stomach lumen,
side effect may lead to alkalosis and worsen edema due to increased Na+ load
 Non-systemic antacids: they are insoluble and poorly absorbed compounds. E.g. magnesium carbonate which
has a laxative effect, aluminum hydroxide which has a constipating effect and calcium carbonate which if used
for long periods can cause hypercalcemia, hypercalciuria and the formation of calcium stones in the kidneys

62. Classification of cholagogue agents, mechanism of action, using?

Cholagogue is a medicinal agent that promotes the purging of bile from the system, purging it downwards.

Choleretic drugs: stimulate bile secretion, they are divided into:

 Drug consist of bile acids: Allocholum, Cholenzyme

 Synthetic Drugs – oxaphenamidum
 Plant drugs: Cholosasum
Cholecinetic drugs: stimulate tone of bile bladder causing to relax i.e. relaxes the smooth muscle cells e.g. Magnesii
Sulfas

63. Drugs that are used during acute and chronic pancreatitis, their pharmacodynamics, mechanism of action?

Drugs decreasing pancreatic secretion are proteolysis inhibitors which decrease pancreas enzyme activity ins the case of
acute pancreatitis or pancreas cancer. Proteolysis inhibitors (Contry Calum, Gordex, Pentripinum, Trasilolum) inactivates
trypsin circulating in the blood, remove toxemia, block quinines, protect pancreas from destruction and inhibit
fibrinolysis

64. Hepatoprotectors: drugs, mechanism of action, using?

Hepatoprotectors increase the stability of hepatocytes.

Hepatoprotctor drugs include:

 Essenciale, Silimarinum, Hepabene, Thiatriozolinum, Antralum are antioxidants

 Acidum Lipoicum: increase energy metabolism of hepatocytes

65. Laxative drugs, mechanism of action, using?

Laxatives are drugs that promote evacuation of bowels, they are classified into:

1. Bulk Forming agents: e.g. methyl cellulose – these drugs act to increase the volume of stool by absorbing
water and as a result softening the stool
2. Osmotic laxative: magnesium or sodium salts (sulphates), glycerol suppositories – these solutes are not
absorbed in intestine. They retain water osmotically in bowel lumen and distend the bowel there by
increasing peristalsis indirectly. Should be used while drinking a lot of water
3. Stool softener: liquid paraffin, docusate sodium – docusate acts by its detergent action which reduces the
surface tension
4. Stimulant laxatives: castor oil – these drugs exert their laxative action by increasing motility of colon. They
mainly alter absorptive and secretory activity by inhibiting Na+/K+ ATPase in mucosal cells leading to water
and electrolyte accumulation in lumen

66. Diuretics drugs, mechanism of action, using?

Diuretics are the agents which increase the rate of urine formation by the kidneys or which cause a net loss of sodium
and water in urine i.e. the diuretics increase the urine output of ions and fluids from the kidneys. They are prescribed for
management of hypertension, congestive heart failure, nephrotic edema.

Diuretics exert their action by influencing uropoiesis which includes filtration, reabsorption and secretion. Significant
increase in Diuresis is reached only by inhibition of reabsorption.

67. Urgent diuretics: pharmacodynamics, mechanism of action, using , side effects?

Diuretics are the agents which increase the rate of urine formation by the kidneys, or which cause a net loss of sodium
and water in urine, i.e. the diuretics increase the urine output of ions and fluids from the kidneys.

Almost all diuretics exert their action at the luminal surface of the renal tubule cells. Their mechanism of action includes
interaction with specific membrane transport proteins like thiazides, furosemide etc., osmotic effects which prevent the
water permeable segments of the nephron from absorbing water like mannitol, and specific interaction with enzyme like
carbonic anhydrase inhibitors i.e. acetazolamide, and hormone receptors in renal epithelial cells like spironolactone.

Therapeutic Uses

1. Edema: Thiazides are useful adjunctive therapy in controlling the edema associated with CHF and cirrhosis.
2. Hypertension: They are widely used in the treatment of hypertension with or without edema and often serve as the
first drug of choice.

3. Diabetes insipidus: They reduce urine volume in both pituitary and renal diabetes insipidus. They are especially
valuable for the latter in which ADH is ineffective. Hydrochlorothiazide

Adverse Reactions Abnormalities of fluid and electrolyte imbalance are the most common forms of clinical toxicity,
overdose may result in rapid reduction of blood volume, dizziness, orthostatic hypotension, headache, hypokalemia.
Gastrointestinal symptoms of nausea, vomiting, diarrhea is common with ethacrynic acid

68. Agents for Gout treatment: mechanism of action and using?

Gout results from hyperuricemia i.e. increased serum uric acid levels. Normal serum uric acid level is 1-5 mg/dl. Uric acid
is formed in the metabolism of purine. When the blood levels of uric acid are high, it precipitates in joints, cartilage,
kidney and subcutaneous tissues and leads to various signs and symptoms.

Drugs used for gout can be divided into two groups:

 Drugs for acute attack of gout: NSAIDs – (have strong anti-inflammatory action), colchicine (0.25mg/day),
corticosteroids.
 Drugs for chronic gout/hyperuricemia: Can be uric acid synthesis inhibitors (allopurinol – 200-800mg/day - It
inhibits the terminal steps in uric acid biosynthesis by inhibiting enzyme xanthine oxidase) and uricosurics
(increase renal excretion of uric acids) e.g. probenecid and sulfinpyrazone, furosemide

69. Pharmacology of drugs that strengthen birth activity?

The contractile activity and tone of myometrium are regulated by neurohormonal mechanisms. The myometrium
contains M-Cholinergic alpha and Beta 2 adrenoceptors. The stimulation of M-cholinoceptors and alpha adrenoceptors
leads to the stimulation of the myometrium tone and contractions and the excitation of Beta 2 adrenoceptors causes its
relaxation.

In addition, there are some biologically active substances which exert significant stimulating influence upon the
myometrium contractile ability. There is female gonadal hormone- estrogens, in posterior pituitary hormone – oxytocin
and some prostaglandins. There are also some endogenous substances which inhibit the myometrium contractile ability
e.g. progesterone.

Drugs which influence upon the tone and contractile ability the myometrium are divided into the following groups:

I: Drugs which exert influence upon the myometrium rhythmical contractile activity

1. Drugs which stimulate the myometrium rhythmical contractile activity and relaxing the uterus cervix – Dinoprost
(prostaglandin F2a), Dinoprostrone (prostaglandin E2)
2. Drugs which in low doses stimulate the uterine rhythmical contractile activity and in high doses increase the
myometrium tone – oxytocin
3. Drugs which increase the uterine rhythmical contractile activity – castor oil
4. Drugs which decrease the uterine contractile ability
a. Beta 2 – adrenomimetic – Salbutamol
b. General anesthetic – Natrii oxybutyrus
c. Miscellaneous drugs – progesterone

II: Drugs which increase myometrium tone:

1. Drugs of plant origin (Ergot alkaloids) – Ergotal

2. Synthetic drugs – cotarnini chloridum

III: Drugs which decrease the cervix tone: atropine sulfas, Drotaverini hydrochloridum (No-Spa)
70. Pharmacological properties and usage of medical agents of Secale cornutum and other drugs that provoke tonic
contraction of myometrium?

Secale cornutum is a plant of Ergot origin. Ergot alkaloids and cotarnine are used mainly for the arresting of uterine
atomic hemorrhage. The principle of their action is a stable increase of the myometrium tone which leads to the
mechanical compression of small uterine vessels.

71. Pharmacology of drugs that are used for treatment of hypo- and hyper chromic anemias?

Drugs that influence hemopoiesis are divided into:

1. drugs which influence erythropoiesis

2. drugs which influence leucopoiesis

Anaemia is the decrease in number of red blood cells or hemoglobin content caused by blood loss, deficient
erythropoiesis, excessive hemolysis, or combination of these changes. Iron deficiency anaemia is probably the most
common nutritional deficiency in the world.

Classification of drugs that stimulate erythropoiesis

1. drugs used for treatment of hypochromic (iron deficiency) anemias:

a. drugs for peroral introduction:
i. mono drugs which contain iron i.e. iron sulfate, iron gluconate, iron lactate
ii. combined drugs (iron with copper, ascorbic acid and folic acid) i.e. Ascofer, Tothema
b. Drugs for the parenteral introduction i.e. ferrum-lek, Fercoven

Adverse reaction of Iron supplements include nausea, vomiting, constipation and diarrhea (iron sulfate), staining of
teeth and metallic taste in tongue. Iron depo in body are spleen, liver and bone marrow. Antidote for iron overdose is
desferroxamine. Iron supplement are given for a long period as the body can only absorb a certain amount of iron a day
limited by transport proteins.

2. Drugs used for treatment of hyperchromic anemias:

a. For treatment of megaloblastic anemia – cyanocobalamin, folic acid
b. For treatment of macrocytic anemia – folic acid
c. Drugs used for the treatment of anemias in chronic renal failure, recombinant human erythropoeitins
e.g. Epoetin alfa, Epoetin Beta, Epoetin Omega

Drugs which inhibit erythropoiesis – Natrium phosphate with radioactive 32P

Fe2+ consisted drugs are used to form hemoglobin and in depo tissues Fe2+ is stored in complex with apoferritin as
ferritin. Iron may be used to form hemoglobin in erythrocytes, other hemin (myoglobin) non-hemin enzymes
(Cytochrome C oxidase) and others.

When there is a deficit in Cyanobalaminum (synthetic vitamin B12), the disturbances of the bone marrow function take
place and erythrocytes transform to megaloblasts. Impairment of tongue mucous, improves the immune status.

Acidum folicum takes purine, pyrimidine, nucleic acids, amino acid synthesis, in erythropoiesis, in regeneration in
leucopoiesis, thrombocytopoiesis, immune system activity. Erythropoetinum is a glycoprotein stimulating proliferation,
differentiation of erythropoit cell in the bone marrow. Eythropoetinum normalizes hemopoiesis and blood film.

72. Pharmacology of drugs that stimulate leukopoiesis?

Leucopoiesis stimulators

1. Myeloid growth factors: Lenograstim, Molgramostim

 2. Non-specific agents which stimulate nucleic acid synthesis: Leucogenum, Natrium Nucleinate

Leucopoiesis Inhibitors: used for transplants, autoimmune disease diseases

1. Glucocorticoids: Prednisolone
2. Cancer therapeutic drugs:
a. Alkylates agents: cyclophosphamide
b. Anti-metabolites: Methotrexate
c. Miscellaneous: Asparaginase

Erythropoiesis inhibitors Natrii phosphas marked with radioactive P32 decrease erythrocyte and thrombocytes content
and is used in polycythemia (erythremia). Derivatives of nickelic acids and pyrimidines stimulate leukopoiesis, wound
healing, posses anti inflammatory action, methyl uracilum has cardiotonic effect.

73. Mechanisms of action and usage of medical agents that depress aggregation of blood plates?

Classification of drugs that are used for the treatment of thrombosis based on mechanism of action:

 Agents which decrease blood coagulation (anticoagulants):

1. Coagulants of direct action: Heparinum, Natrii Citras
2. Anticoagulants of indirect action: Phenylinum
 Agents which increase the activity of fibrinolytic system (Fibrinolytics):
1. Fibrinolytics of direct action: Fibrinolysinum
2. Fibrinolytics of indirect action: Streptoliasum
 Agents which reduce thrombocyte aggregation (antiaggregant, antiplatelets): acidum acetylsalicylicum
(aspirin)

Antiaggregant: platelet aggregation is the most effective defense mechanism against the leakage of blood during
circulation. The antiaggregant must remove thromboxane A2 ADP action, increase level of cAMP in thrombocytes,
decrease Ca2+ concentration, block thrombocyte membrane glycoproteins IIb/IIIa. These drugs used for prophylactic of
myocardial infarction, instable angina, for prophylactics of insult of thrombosis.

Agents which reduce the thrombocyte aggregation includes:

1. Agents which inhibit the thromboxane system activity: Acetylsalicylic acid

2. Agents which increase the activity of prostacyclin system: Carbacycline
3. Agents inhibiting binding of fibrinogen to thrombocyte glycoprotein receptors: Clopidogrel
4. Miscellaneous agents: dipyridamole

74. Pharmacological characteristics and usage of hemostatic?

Drugs which are used to arrest hemorrhages (hemostatic), classification by mechanism of action:

1. Agents which increase blood coagulation:

a. Coagulants with direct action: Fibrinogen, Thrombin, Calcium chloride, Calcium gluconate
b. Coagulants with indirect action: Herba Millefolli
2. Agents which decrease the activity of the fibrinolytic system (fibrinolysis inhibitors): amino carbonic acid
3. Drugs which stimulate platelet aggregation: Thrombane, serotonin
4. Heparin antagonists: Protamine Sulfate
5. Drugs which decrease the permeability of the capillary wall: adroxonum, Ascorutinum

75. Pharmacodynamics, mechanisms of action and usage of heparin?

Heparin binds to antithrombin III and induces a conformational change that accelerates the interaction of antithrombin
III with coagulative factors. Heparin also catalyzes the inhibition of conversion prothrombin to thrombin, fibrinogen to
fibrin. It gives negative charge to vessels and brakes aggregation to adhesion. Low molecular weight heparins depresses
activated Stuart-Prauers factor more than prothrombin and act longer.

Heparin is well absorbed after subcutaneous administration and is not effective orally, and metabolized mainly in liver. It
is not secreted in milk and does not cross placental barrier.

HEPARIN ANTAGONISTS The agents like protamine sulfate react with the strongly acidic groups of heparin and can
abolish its anticoagulant activity. Approximately 1 mg of protamine sulfate neutralizes 80 to 100 units of heparin. It is
used only in severe bleeding or when heparin action needs to be terminated rapidly e.g. after cardiac or vascular
surgery.

76. Pharmacological properties of anti-coagulative drugs of indirect action, their usage, antagonists, prophylactic of
complications?

ORAL ANTICOAGULANTS: They act by interfering with synthesis of vitamin K dependent clotting factors in liver. They act
as competitive antagonists of vitamin K and reduce plasma levels of clotting factors in a dose dependent manner. They
act by interfering with regeneration of active form of vitamin K. Factor VII levels are reduced first followed by factor IX, X
and II.

77. Mechanism of fibrinolytic action of streptokinase. Principles of action of Contrikal and aminocapronic acid?

Streptokinase is a fibrinolytic drug. It acts by forming a complex with circulating plasminogen that binds loosely to fibrin
and it converts plasminogen to plasmin. It has no intrinsic activity. It is given by parenteral route and has a short plasma
half life.

78. Drugs of a forward share of a pituitary body, their pharmacodynamics, usage?

The pituitary gland is situated in sella turcica or hypophyseal fossa of the sphenoid bone attached to the brain by a stalk
which is continuous with the part of brain i.e. hypothalamus and there is a communication between the hypothalamus
and the pituitary gland by means of nerve fibres and a complex of blood vessels. Pituitary gland consists of three parts –
anterior lobe or adenohypophysis, posterior lobe or neurohypophysis and middle lobe or pars intermedia. The anterior
lobe secretes various trophic hormones, the posterior lobe is responsible for the secretion of oxytocin and antidiuretic
hormone (vasopressin) and middle lobe secretes melanocyte-stimulating hormone (MSH) which may affect the synthesis

Anterior lobe of pituitary is the master gland of the endocrine system as a whole because it produces peptide trophic
hormones which affect the other ductless/endocrine glands. The anterior lobe secretes the following hormones:f
melanin.

1. Growth hormone or somatotrophic hormone (GH & STH).

2. Thyroid stimulating hormone (TSH) or thyrotrophic hormone.
3. Adrenocorticotrophic hormone (ACTH).
4. Follicle stimulating hormone (FSH).
5. Luteinising hormone (LH) or interstitial cell stimulating hormone (ICSH).
6. Lactogenic hormone or prolactin

Endocrine drugs include: natural hormone analogues, synthetic substitutes of natural hormones, drugs which stimulate
the synthesis of natural hormones and antagonists of hormones. These drugs are used in the case of
hypo/hypersecretion of hormones.

Classification of endocrine drugs by chemical structure:

Peptides: preparations of hormones of hypothalamus, pituitary and parathyroid glands, pancreatic hormones,
calcitonin. The mechanism of action is associated with the interaction with specific receptors located on the cell
membranes that lead to activation of adenyl cyclase and phospholipidase C and as a consequence of this, the
accumulation of secondary intracellular mediators – cAMP, cGMP, Ca2+ inositol, 1,4,5-triphosphate (ITP), diacylglycerol.
As a result of this the kinetics of various biochemical processes and level of the cell and whole organ activity are
changed. Some proteins (insulin) change the permeability of cellular membranes to other endogenous substances.

Amino acid derivatives: thyroid hormone preparations.

The mechanism of action of these hormones is associated
with their penetration into the cell and binding to the
specific receptors in the nucleus, that leads to the
activation of protein synthesis.

Steroid hormones: adrenal and gonadal hormone

preparations. These substances penetrate into the cells,
bind to cytoplasmic receptors and are transported into the
nucleus where they activate DNA< RNA that leads to the
stimulation of protein synthesis

Anterior pituitary Hormone drugs: corticotropine, somatotropine, FSH, LH (Gonadotrophic hormones), Thyroid
stimulating hormone, somatostatin, prolactin

79. Drugs of a back share of a pituitary body, their pharmacodynamics, usage?

The posterior lobe secretes two hormones namely oxytocin and antidiuretic hormone (ADH or vasopressin).

Oxytocin is an octapeptide synthesized in hypothalamus and transported down the axons into the posterior lobe of
pituitary. It promotes contraction of the uterine muscle. It also causes contraction of the myoepithelial cells of the
lactating breast and squeezing milk into the large ducts situated behind the nipple of the mammary gland. Oxytocin
takes part in the onset of parturition, expulsion of the foetus and placenta. It also facilitates the transport of sperm in
the female genital tract. Oxytocin is used in induction of labour, in postpartum haemorrhage, abortion and in breast
engorgement. It is used by IM/IV route (PITOCIN, 2-5 IU/ml inj).

80. Pharmacological properties and usage of hormonal drugs of a thyroid gland?

Thyroid gland secretes two important hormones, thyroxine (T4) and triiodothyronine (T3). The third hormone, calcitonin
secreted from interstitial cells is physiologically different and is responsible for the regulation of calcium metabolism.
Thyroid hormones exert their effect by binding to nuclear receptors in target organs. Both the thyroid hormones are
well absorbed after oral administration. They are conjugated with sulfuric acid in liver and excreted in bile.

Thyroid hormones and drugs and inhibitors: alpha-Thyroxine, Triiodothyronine hydrochloride, Lugol solution,
Radioactive Iodine.

The various preparation used are:

Thyroxine (l-thyroxine sodium) (ELTROXIN) 50-300 µg/day

Liothyronine sodium 20-60 µg/day (TETROXIN)

Thyroglobulin (PROLOID) 32.5-195 mg/day

Therapeutic Uses of Thyroid Hormones

 Infant hypothyroidism (cretinism).

 Adult hypothyroidism (myxoedema).
 Myxoedema coma: It is an emergency. Liothyronine 100 µg IV can be used and maintained by thyroxine 500 µg
IV
 In the treatment of non-toxic goitre.
 Papillary thyroid carcinoma: It is often responsive to TSH.

Adverse reactions include palpitation, angina, tremors, thyrotoxicosis, allergic reactions, headache, tachycardia,
diarrhoea, sweating, restlessness, loss of weight and muscle weakness.

81. Antithyroid agents: drugs, mechanism of action and usage?

These are used to inhibit the functional activity of hypersecretive thyroid gland. The hypersecretion leads to the
development of thyrotoxicosis. The antithyroid agents acts by interfering with the synthesis and release of thyroid
hormones.

Drugs Inhibiting Hormone Synthesis The thioamides which include propyl thiouracil and methimazole are the major
drugs for the treatment of thyrotoxicosis. In India carbimazole is most commonly used drug. They bind to thyroid
peroxidase and prevent the oxidation of iodide and iodotyrosyl residue which subsequently inhibits the formation of
tyrosine residue in thyroglobulin and coupling of iodotyrosine residues to T3 and T4.

82. Comparative characteristic of drugs of insulin, usage?

Insulin (MW 5,800) a polypeptide hormone secreted from β-cells of islets of Langerhans in pancreas. It’s formed from
proteolysis of proinsulin to give rise to two peptide chains (A with 21 amino acid residues and B with 30) which are
interconnected by disulphide bond.

Insulin acts by binding to insulin receptors on cell membrane. The insulin receptor complex is internalized. By
phosphorylation and dephosphorylation reactions there is stimulation or inhibition of enzymes involved in metabolic
actions of insulin. Second messengers like phosphatidyl inositol glycan and DAG also mediate the action of insulin on
metabolic enzymes.
In diabetes mellitus, there is either insulin deficiency or insulin resistance in peripheral tissues which lead to
hyperglycemia and glycosuria. Insulin corrects the various abnormalities of carbohydrate metabolism by its action on
various tissues.

Insulin preparations:

 Rapid acting: insulin zinc suspension, Proinsulin injection

 Intermediate acting: Semilente insulin suspension
 Prolonged acting: Ultralente insulin Zinc suspension

Insulin is not given orally. After IV or SC injection, it circulates as free, monomer in blood and has a short plasma half life.
Insulin is degraded mainly in liver, muscle and kidney.

Adverse Reactions: The most frequent and serious adverse reaction is hypoglycemia. It can occur in any diabetic patient
due to heavy dose of insulin, failure to eat or missing a meal, performing extensive exercise or by consuming alcohol.
The hypoglycemia caused by insulin is characterized by neuroglucopenic symptoms that include confusion, dizziness,
behavioural changes, visual disturbances, fatigue, muscle incoordination and may be fall in blood pressure

83. Peroral antidiabetic agents, mechanism of action, indication to usage, side effects?

ORAL ANTIDIABETIC AGENTS: These are the agents which are effective orally and lower the elevated blood glucose
levels.

SULFONYLUREAS: These drugs stimulate insulin secretion from pancreatic β-cells (so called ‘sulfonylurea receptors’)
which cause depolarisation by reducing conductance of ATP sensitive K+ channels. They lower down the blood sugar
level in type II diabetics and non-diabetic individuals. They also decrease the elevated plasma free fatty acid levels. They
also sensitize the target tissues to action of insulin by increasing the number of insulin receptors. Sulfonylureas inhibit
neoglucogenesis and glycogenolysis. Sulfonylureas are rapidly absorbed from the gastrointestinal tract after oral
administration and are more than 90 percent bound to plasma proteins and excreted unchanged in urine. E.g. Copamide

BIGUANIDES: They lower the blood sugar levels in all types of diabetes mellitus but like sulfonylureas they do not lower
the blood sugar level in normal individuals. They act by increasing peripheral anaerobic glycolysis (stimulate peripheral
utilization of glucose), inhibit absorption of carbohydrate in the gut and suppress hepatic gluconeogenesis. E.g.
Metformin

α-GLUCOSIDASE INHIBITORS: e.g. ACARBOSE It is a pseudo-tetra saccharide derived from the fermentation process of
the fungus Actinoplanes utahensis. It acts by competitively inhibiting pancreatic alpha amylase and intestinal alpha
glucosidase hydrolase enzymes. Thus, it delays carbohydrate digestion, prolongs digestion time and reduces the rate of
glucose absorption thereby lowering postprandial hyperglycemia. Given orally less than 2% is absorbed as the oral drug.
It is metabolised in the GI tract primarily by intestinal bacteria and to a lesser degree by digestive enzymes.

THIAZOLIDINEDIONES: e.g. ROSIGLITAZONE, a member of the thiazolidinedione class of antidiabetic agents, improves
glycemic control by improving insulin sensitivity. The oral bioavailability of rosiglitazone is 99%. Peak plasma
concentrations are observed about one hour after dosing. Rosiglitazone plasma concentration increases in a dose-
proportional manner over the therapeutic dose range

84. Glucocorticoid drugs: the basic sides of their pharmacodynamics, which are used in medical practice. The indications
to usage? NOTE: Glucocorticoids are antagonists of insulin

Secretion of adrenocortical steroids is controlled by the pituitary release of corticotrophin (ACTH). The adrenal gland has
two main parts, adrenal medulla, which is responsible for the release of catecholamines and adrenal cortex which
secretes glucocorticoids, mineralocorticoids and sex hormones.

The glucocorticoids and mineralocorticoids are synthesized in the adrenal cortex from cholesterol.
Pharmacological Actions

Metabolic effects: Glucocorticoids promote glycogen deposition in liver by stimulating glycogen synthetase activity and
increasing glucose production from protein. They also inhibit peripheral utilization of glucose and increase glucose
release from liver. It produces resistance to insulin. Glucocorticoids also cause breakdown of protein and amino acid
mobilization from peripheral tissues. They stimulate the conversion into glucose (neoglucogenesis) in the liver.
Glucocorticoids inhibit the uptake of glucose by fat cells, resulting in increased lipolysis. The increased insulin secretion
in response to hyperglycaemia also stimulates lipogenesis and ultimately increase in fat deposition. The catabolic effect
on bone can cause osteoporosis in Cushing’s syndrome.

Anti-inflammatory and immunosuppressive effects: Glucocorticoids suppress all types of inflammation,

hypersensitization and allergic reactions. They suppress the edema, capillary dilatation, migration of leukocytes, capillary
permeability in the inflamed area. Glucocorticoids inhibit the functions of leukocytes and tissues macrophages. They
also stabilize lysosomal membranes, thereby reducing the concentration of proteolytic enzymes at the site of
inflammation. Glucocorticoids also inhibit the production of plasminogen activator by neutrophils. They also influence
the inflammatory response by reducing the prostaglandin and leukotriene synthesis that results from activation of
enzyme phospholipase A2.

Mechanism of Action: Most of the established pharmacological effects of glucocorticoids are mediated by cytoplasmic
glucocorticoid receptors. After binding to the receptor, the steroid-receptor complex binds to chromatin and stimulate
the formation of mRNA. The mRNA stimulates the synthesis of enzymes which produce various pharmacological actions.

Therapeutic Uses of Glucocorticoids: Glucocorticoids are used in the following physiological and clinical conditions:

1. Adrenocortical insufficiency:
• Acute: Hydrocortisone/dexamethasone IV inj.
• Chronic: Addison’s disease; congenital adrenal hyperplasia (genetic disorder due to deficiency of
steroidogenic enzymes).
2. Rheumatology:

a. Intraarticular injection: Rheumatoid arthritis, osteoarthritis, gouty arthritis, joint sequelae of fractures and
dislocations.

b. Periarticular/soft tissue injection: Scapulohumeral periarthritis, periarthritis of hip, bursitis, tendinitis,

synovitis, tenosynovitis, tarsalgia, metatarsalgia, epicondylitis, Dupuytren’s contracture, Peyronie’s disease,
cystic tumors of aponeurosis or tendon (ganglia).

3. Severe allergic reactions such as urticaria, serum sickness, anaphylaxis.

4. Bronchial asthma, in acute and severe chronic asthma, aspiration pneumonia and pulmonary edema.
5. Autoimmune haemolytic anaemia, thrombocytopenia etc.
6. Ear disorders
7. Dermatology: Topical steroids are useful in keloids, hypertrophic scars, other localised hypertrophic, infiltrated,
inflammatory lesions of lichen planus, psoriatic plaques, granuloma annulare and lichen simplex chronicus;
discoid lupus erythematosus, necrobiosis lipoidica diabeticorum and alopecia areata.
8. Neurology: Lumbago, sciatica, cervicobrachial neuralgia and other painful radiculopathies; selected cases of
inflammatory disorders such as tuberculous meningitis and multiple sclerosis.
9. GIT: Ulcerative colitis, Crohn’s disease etc.
10. Malignant diseases: Corticoids are used in combination with other therapy in the treatment of Hodgkin’s
disease, acute lymphatic leukemia and other lymphomas.
11. Miscellaneous uses: Corticoids in higher dose can be given along with other immunosuppressants in certain
organ transplantation cases to prevent rejection reaction.
85. Complication of therapy by glucocorticoid drugs. Preventive measures?

Glucocorticoids are antagonists of insulin and may cause development of Diabetes mellitus.

Hypocalcemia, hypertension and osteoporosis

Redistribution of fat i.e. moon face

86. Glucocorticoid drugs as antiallergic agents, mechanism of their action and usage?

Glucocorticoids easily penetrate through cell membranes and interact within the cell with specific receptors changing
the activity of many enzymes. This results in changes of the synthesis and metabolism of nucleic acids and proteins. The
main action is directed on carbohydrate and protein metabolism and less on water salt. The action upon carbohydrate
metabolism is manifested by decrease of utilization of glucose from the blood and by decrease of its synthesis in the
liver, that results in increase of blood glucose amount (hyperglycemia) and appearance of glucose in urine (glucosuria)
so glucocorticoids are antagonists of insulin and may cause the development of diabetes mellitus. They also stimulate
formation of glucose from amino acids that leads to reduction of protein synthesis and to increase in nitrogen excretion
with the urine (i.e. -ve nitrogen balance). The inhibitor of protein synthesis is accompanied by inhibition of regeneration
(a decrease in healing of wounds and ulcers) and proliferative (immunosuppressant effect – reducing the amount of
lymphocytes and formation of antibodies) processes. The influence upon lipid metabolism is manifested by mobilization
of tissue lipids, an increase of amounts of ketoacids (ketoacidosis) and by redistribution of fat (accumulation in the neck,
shoulder, face (moon face)). The influence upon the water salt balance is manifested by delay pf sodium ions and water
due to stimulation of their reabsorption in the kidneys, by an increase of potassium excretion in the urine, inhibition of
calcium absorption in the intestine and by stimulation of its excretion by the kidneys. The consequences of these effects
are arterial hypertension, hypocalcemia and osteoporosis. They exert significant anti-inflammatory action associated
with inhibition of synthesis of prostaglandins, oxi acids and leukotrienes which control migration of leukocytes to the
focus of inflammation. This is accompanied by stabilization of lysosomal membrane, a decrease in proteases discharge,
constriction of small vessels, decrease permeability of capillaries and exudation of plasma.

Better to take glucocorticoids in the morning as the body makes hormones in the morning

87. Withdrawal at usage of glucocorticoid drugs, mechanism of its appearance, preventive measures and treatment?

Withdrawal – returning of the original symptoms (some times stronger) if discontinued due to renal insufficiency. Hence
must decrease dose of glucocorticoids until kidney can secrete enough on its own, this could take a year.

88. Pharmacodynamics and usage of drugs with mineralocorticoid activity?

89. Pharmacodynamics and usage of estrogenic and hestagenic drugs?

Estrogen: Estradiol, Antiestrogen: Clomiphene, Tamoxifen

Progesterone: progesterone, Anti-progestin: Mifepristone

Androgens: Testosterone, Antiandrogens: Danzol, Flutamide,

ESTROGENS: Estrogens are produced mainly by the ovary and the placenta and the synthesis of estrogens takes place
from cholesterol. Estradiol is the major secretory product of ovary. Estrogens are required for normal maturation of the
female. They stimulate the development of secondary sexual characters e.g. stimulate stromal development, ductal
growth in the breast, growth of axillary and pubic hair and alter the distribution of body fat to produce typical female
body contours. Estrogens are anabolic but weaker than testosterone. Estrogens also cause retention of nitrogen, sodium
and fluid in tissues. Estrogens also protect from osteoporosis in postmenopausal women, which occur as a result of
estrogen deficiency.

Estrogens also play a role in stimulation of the proliferative or preovulatory phase of endometrium and vasodilatation of
endometrial capillaries.

Pharmacological Actions: Estrogens act by interacting with the specific estradiol receptors in the cytoplasm of the target
cells and mediate the transcription of the relevant mRNA by attaching itself to the appropriate gene.

Therapeutic Uses: The most common use of estrogen are as oral/parenteral contraceptive and for hormone
replacement therapy.

 Primary hypogonadism: Estrogens have been used for replacement therapy in estrogen deficient patients
(treatment of amenorrhoea).
 in post menopausal hormonal therapy:
o Estrogen have been used in prevention and treatment of osteoporosis.
o Improve the general physical, mental and also sexual activity.
o Maintain calcium balance.
o Decreases the risk of cardiovascular (coronary artery) disease.
 Transdermal estradiol is equally effective:
o In atrophic vaginitis.
o In atrophic urethritis.
o For the treatment of vaginal complaints such as dyspareunia, dryness and itching.
o Pre and postoperative therapy in postmenopausal women undergoing vaginal surgery.
o Infertility due to cervical hostility.
o As a diagnostic aid in case of doubtful atrophic cervical smear.

ANTIESTROGENS: Also known as estrogen antagonists or ovulation inducing agents. They act by binding to estrogen
receptors

90. Hormonal contraceptives: classification, features of dosing, side effects?

Hormonal contraceptives are hormonal agents that prevent pregnancy. They are divided into

I. Oral contraceptives

1. combination f estrogens and progestins:

1.1. Monphasic combination tablets: Logest, Mercilon

1.2. Biphasic combination tablets: Anteovin

1.3. Triphasic combination tablets: Trisiston

2. Agents containing micro doses of progestins: Microlut

3. Postcoital contraceptive (morning after): Postinor

II. Parenteral contraceptive: Depo-Provera

III. Implantable contraceptives: Norplant system

Adverse Effects The most common side effects are nausea, vomiting, headache, dizziness, fatigue, weight gain and
breast fullness. The other side effects which appear after sometime of therapy are acne, increased body hair,
pigmentation of cheeks, nose and forehead (chloasma). The other serious side effects include high blood pressure,
increased risk of myocardial infarction, thromboembolic diseases like thrombophlebitis, venous thrombosis, cerebral
thrombosis.
91. Pharmacology and usage of androgenic drugs and anabolic steroids?

Androgens are substances which cause development of secondary sex characters in males. The most important
androgen secreted by testes is testosterone. Testosterone is synthesized from the cholesterol in testes mainly, under
the influence of LH from pituitary. In peripheral tissues testosterone is partly converted into more active
dihydrotestosterone. Adrenal cortex also produces small quantities of weak androgens (androstenedione and
dehydroepiandrosterone) which are partially converted to testosterone in peripheral tissues. In females, ovaries also
secrete small quantities of testosterone. Follicle stimulating hormone is responsible for the growth of testes. It promotes
spermatogenesis. Along with LH, FSH plays an essential role in maintaining the normal testicular functions such as
development of male sex organs e.g. penis, scrotum; development of secondary sexual characters e.g. growth of facial
axilla, chest and pubic hair and change in voice; development of accessory sexual organs e.g. seminal vesicles, prostate
and epididymis and development of male skeletal musculature.

Classification of androgens, anabolic steroids and antiandrogens

I. Natural Testosterone (as propionate, cypionate Propionate 25-200 mg IM per day to bimonthly; undecanoate,
enanthate; NUVIR) undecanoate 40 mg OD-TDS

II. Synthetic Methyltestosterone 25 mg/day SL

III. Anabolic steroids Nandrolone (as decanoate, phenyl 10-100 mg IM once a wk to every 3 wks

IV. Antiandrogens Danazol (DANOGEN) 200-800 mg/day

TESTOSTERONE It is a natural androgen secreted by testis. The secretion is regulated by LH hormone secreted by
pituitary gland. It is responsible for development of sex organs and secondary sex characters in males at puberty. It leads
to growth of genitals, growth of hair (pubic, axillary, beard, moustache, body hair), thickening of skin, larynx grows and
voice deepens and also behavioral changes. It is also needed for normal spermatogenesis and maturation of
spermatozoa. It is also responsible for pubertal spurt of growth in boys leading to increased bony and skeletal muscles
growth.

NANDROLONE It is closely related to androgen testosterone having both lower androgenic and higher anabolic
properties. Adverse effects include virilism, edema and hypercalcaemia. It is used in debilitating illness, postmenopausal
osteoporosis, burn or major illness, postmenopausal metastatic mammary carcinoma, haemolytic, hypoplastic or
malignancy associated anaemias.

92. Effect of vitamins f group B on metabolism and usage of their drugs in medical practice?

Vitamin drugs are classified into:

 Water soluble: B complex and vitamin C – are rapidly excreted from the body in urine and cause less toxicity
 Fat soluble: A, D, E, K – are stored in the body and excessive administration can cause toxicity

Vitamin B1 thiamine – thymine antineurotic, Thiamine pyrophosphate is a coenzyme and the active form of vitamin B1.
It functions as coenzyme in decarboxylation of αketo acid and in hexose monophosphate shunt.

Deficiency symptoms: In severe vitamin B1 deficiency beriberi develops.

It is indicated in wet beriberi, dry beriberi, Wernicke’s encephalopathy, prophylaxis of thiamine deficiency, hyperemesis
gravidarum, Korsakoff’s syndrome, chronic alcoholics, multiple neuritis, toxic and confusional states, delirium tremens
and anorexia nervosa.

Dosage: Mild chronic deficiency: 10-25 mg daily; severe deficiency, 200-300 mg daily.

VITAMIN B2 (RIBOFLAVIN) It carries its physiological function in its active forms, flavin mononucleotide (FMN) and flavin
adenine dinucleotide. These coenzymes are involved in various biochemical reactions.
Deficiency symptoms: It is characterized by glossitis, dermatitis of trunk and extremities, angular stomatitis, cheilosis,
anaemia, neuropathy, cataract formation and vascularization of cornea.

It is indicated in arteriosclerosis, as adjunct in treatment of hypertension, diabetes and obesity.

VITAMIN B3 (NIACIN) Niacin was initially called pellagra preventing factor. It is converted to coenzymes, nicotinamide
adenine dinucleotide (NAD) or nicotinamide adenine dinucleotide phosphate (NADP). These coenzymes are bound to
hydrogenases, function as oxidants by accepting hydrogen and electrons from substrates and become reduced.
Deficiency symptoms: In niacin deficiency, pellagra develops. The main features of this condition are diarrhoea,
dermatitis and dementia. Nausea, vomiting, stomatitis, dizziness, depression, insomnia, headache develops. In severe
deficiency hallucinations and dementia occurs.

Adverse effects include flushing, activation of peptic ulcer, vomiting, diarrhoea, pruritus, skin rash and transient
headache.

It is indicated in pellagra, for prophylaxis, Hartnup disease, hyperlipoproteinaemia

Vitamin В5 (pantothenic acid, anti-dermatitis) - It is a component of coenzyme A which is essential in the metabolism of
carbohydrate, fat and protein.

Deficiency symptoms: Deficiency of panthothenic acid is unlikely in man because of its widespread distribution in food,
though it has been administered by mouth as a nutritional supplement as the calcium salt and usually in conjunction
with other vitamins of the B group. Dosage: 50 to 100 mg per day.

Vitamin В6 (pyridoxine, аnti-dermatitic) - It is involved as a coenzyme (pyridoxal phosphate) in metabolism of

tryptophan, in several metabolic transformations of amino acids including transamination, decarboxylation and
racemization.

Deficiency symptoms: Peripheral neuritis, seizures, stomatitis, anaemia, seborrhoea like lesions, mental confusion and
growth retardation.

It is indicated to prevent and treat isoniazid, hydralazine, penicillamine and cycloserine induced neurological
disturbances, mental symptoms in women on oral contraceptives, pyridoxine responsive anaemia and homocystinuria,
morning sickness and hyperemesis gravidarum, convulsions in infants and children.

Dosage: Adults: 100 mg daily. In suppression of lactation: 2 tablets thrice daily followed by one tablet daily

Vitamin В12 (cyanocobalamin, аnti-anemic): CYANOCOBALAMIN (METHYLCOBALAMIN) Methylcobalamin is the

coenzyme form of vitamin B12. It is neurologically active, most bioavailable and best utilized. Unlike cyanocobalamin, it
does not require any conversion after absorption by the body and is better retained by the liver and other tissues. It has
exhibited beneficial effects against brain aging, irregular sleep patterns. It supports immune function and promote
normal cell growth. It represents one of the best values in nutritional products, given its comparably low cost and its
wide range of potential benefits. Methyl B12 is the superior form of vitamin B12.

Deficiency symptoms are glossitis, GIT disturbances, megaloblastic anaemia, subacute combined degeneration of spinal
cord, peripheral neuritis, poor memory, mood changes and hallucinations.

Vitamin 9/ Folic acids: takes part in synthesis of purines, pyrimidines, nucleic acid synthesis of erythrocytes,
thrombocytes and leukocytes.

Deficiency symptoms: The characteristic feature of folic acid deficiency is megaloblastic anaemia. Deficiency also leads
to glossitis, enteritis, diarrhoea, general debility, weight loss and sterility.

It is indicated in folic acid deficiency states e.g. megaloblastic anaemia, tropical and nontropical sprue, alcoholism;
adjunctive therapy in nutritional anaemias and anaemias of pregnancy.
Dosage: Adults: Therapeutic: 5 to 20 mg daily in divided doses. Children: 5 to 10 mg daily in divided doses.

93. Pharmacodynamics, mechanism of action and usage of an ascorbic acid and Rutin?

Vitamin C – Antiscorbutic: It functions as a cofactor in number of amidation and hydroxylation reactions. The active
form of vitamin C is ascorbic acid itself. The main function of ascorbate is as a reducing agent in a number of different
reactions. Vitamin C has the potential to reduce cytochrome a and c of the respiratory chain as well as molecular
oxygen. The most important reaction requiring ascorbate as a cofactor is the hydroxylation of proline residues in
collagen. Vitamin C is, therefore, required for the maintenance of normal connective tissue as well as for wound healing
since synthesis of connective tissue is the first event in wound tissue remodeling. Vitamin C is also necessary for bone
remodeling due to the presence of collagen in the organic matrix of bones. It is also required for conversion of folic acid
to folinic acid, biosynthesis of adrenal steroids, catecholamines, oxytocin and ADH; metabolism of cyclic nucleotides and
prostaglandins.

Deficiency symptoms: In vitamin C deficiency scurvy develops. It is characterized by ecchymosis, petechiae, swollen and
bleeding gums, subperiosteal haemorrhage, bones are painful to touch, impaired wound healing, anaemia, loosening of
teeth and gingivitis.

It is indicated for treatment of scurvy, for prophylaxis of vitamin C deficiency, to acidify urine, anaemia of vitamin C
deficiency, as antioxidant to protect natural colour and flavour of many foods, dental caries and increased capillary
fragility.

Dosage: Adults: Prophylaxis : 50-500 mg daily. Pregnancy and lactation: 100-150 mg daily.

94. Biological significance of vitamin E, its usage in medical practice?

Vitamin E – Anti sterile is an antioxidant vitamin. It presumably prevents oxidation of coenzyme Q and inhibits
generation of peroxidation products from unsaturated fatty acids. Vitamin E is a family of eight compounds. four
tocopherols and four tocotrienols. Tocotrienols appear to affect a key enzyme in the liver (HMG CoA reductase), which
plays a key role in the synthesis of cholesterol. As such tocotrienols help maintain good cardiovascular health. Vitamin E
is an antioxidant and prevents the oxidation of LDL (the bad cholesterol). Vitamin E functions as anticoagulant, which
means it delays the clotting of the blood. It can help prevent thrombosis, the formation of blood clots in the arteries.

Deficiency symptoms: In vitamin E deficiency in experimental animals the manifestations are seen in several systems
including cardiovascular, reproductive and haematopoietic.

The clinical manifestations are axonal degeneration, gait disturbances, ophthalmoplegia, hyporeflexia and necrotizing
myopathy.

Adverse effects include nausea, fatigue, headache, blurred vision, diarrhoea.

It is indicated in premature infants exposed to high concentration of oxygen, correction of established vitamin E
deficiency, in patients at risk of developing vitamin E deficiency, nocturnal muscle cramps, intermittent claudication,
fibrocystic breast disease, coronary artery disease and as an antioxidant.

Dosage: Adults: – Nocturnal muscle cramps: 400 mg daily for 8 to 12 weeks. – Intermittent claudication: 400 mg daily for
12 to 18 weeks. – Fibrocystic breast disease: 600 mg daily for 2 to 6 months. Children: 200 mg daily

95. Drugs of vitamin A, their pharmacodynamics, usage and side effects, hypervitaminosis A?

Vitamin A: Antixerophthalmic,

Retinol stimulates oxidative reduction processes in cells, intensifies their proliferation and differentiation. Retinol
promotes the synthesis of visual purple – Rhodopsin. Retinol activates release of growth hormone, thyroid hormone.
Retinol activates the synthesis of immunoglobulins, antibodies, lysosome enzymes.
It is indicated in night blindness, vitamin A deficiency (in infants, in pregnancy, lactation, malabsorption syndrome), for
prophylaxis of vitamin A deficiency, acne, ichthyosis, psoriasis, xerophthalmia, Bitot’s spots (especially children).

Dosage: Severe deficiency with xerophthalmia: 50,000 IU per day for three days followed by 50,000 IU per day for two
weeks. Severe deficiency: 100,000 IU per day for three days followed by 50,000 IU per day for two weeks. Children:
5,000 to 10,000 IU per day for two weeks.

96. Drugs of vitamin D, their pharmacodynamics, usage and side effects, hypervitaminosis D?

The term vitamin D is used for a range of compounds which possess the property of preventing or curing rickets. They
include ergocalciferol (calciferol, vitamin D2), cholecalciferol (vitamin D3), dihydrotachysterol, alfacalcidol (1α-
hydroxycholecalciferol) and calcitriol (1,25-dihydroxycholecalciferol).

It plays an important role in calcium metabolism. It regulates calcium homeostasis and maintains normal levels of
plasma calcium and phosphate.

Deficiency symptoms: Rickets occurs in patients who are having deficiency of vitamin D. The bones are unusually soft
and due to stress and strain of weight bearing produce characteristic deformities.

It is indicated in prophylaxis and treatment of rickets, postmenopausal osteoporosis, Fanconi syndrome and
hypoparathyroidism.

Adverse effects include headache, weakness, nausea, vomiting, dry mouth, muscle pain, constipation, somnolence,
ectopic calcification, hypertension, nephrocalcinosis and weight loss.

97. Enzymes as medical agents: pharmacodynamics and usage?

98. Antiatherosclerotic agents: drugs, effect on metabolism of cholesterol and lipoproteins, on processes of oxidation of
lipids, usage?

99. Pharmacodynamics and usage of drugs of sodium and potassium. Combination of drugs of potassium with heart
glycosides and diuretics.

100. Drugs of magnesium, their pharmacodynamics, mechanism of action and usage?

101. Drugs of calcium, pharmacodynamics and usage. Regulation of a calcium metabolism with various drugs.

102. Anti-inflammatory agents of steroid structure: drugs, mechanism of action, usage, side effects?

103. Anti-inflammatory agents of nonsteroidal structure: drugs, mechanism of action, usage, side effects?

Non-steroidal antiinflammatory drugs (NSAIDs) are also known as nonopioid analgesics. They relieve pain without
interacting with opioid receptors and do not depress CNS and have no drug dependence or drug abuse property and
possess antipyretic activity also. They act primarily on peripheral pain mechanisms and also in CNS to raise pain
threshold.

NSAIDs exert analgesic, antipyretic, anti-inflammatory (except paracetamol) and related effects. During pain, fever and
inflammation the arachidonic acid is liberated from the phospholipid fraction of the cell membrane which is then
converted to prostaglandins (PGs) via cyclooxygenase pathway (both COX-1 & COX-2). COX-1 is present in kidney,
stomach and blood vessels and COX-2 is present in activated leukocytes and other inflammatory cells.
104. Anti-allergic agents: classification, mechanism of action and usage, side effects?

The important autacoids/ local hormones include:

 Histamine,
 Hydroxytryptamine (5-HT, serotonin),
 Prostaglandins,
 Leukotrienes, and
 Kinins.

Histamine is a potent biogenic amine, occurs in tissues in almost all forms of life and released in a free state in response
to injury or to any antigenantibody reaction.

Histamine Receptors The present evidence indicates that histamine act on three types of receptors namely H1, H2 & H3.
The contraction of smooth muscle, increase in vascular permeability and mucus secretion are mediated by H1 receptors
and is associated with increase in intracellular cyclic GMP. These types of effects are competitively blocked by H1
receptor antagonists (antihistaminics) like mepyramine.
Antihistaminic action: The anti-histaminics blocks histamine effects at a variety of sites. They inhibit most responses of
smooth muscles to histamine. They antagonize the stimulant actions of histamine on various smooth muscles of the
respiratory system, gastrointestinal tract, the uterus and the blood vessels. They inhibit the hypertensive effect (in
rabbits & guinea pigs) and hypotensive effect (in cat & dog) produced by histamine. They also reduced the triple
response induced by histamine injection.

Adverse Reactions The most common side effect, common to all H1 antagonists other than terfenadine and astemizole
is sedation. Other untoward reactions include fatigue, dizziness, tinnitus, lassitude, blurred vision, diplopia, euphoria,
nervousness, tremor and insomnia. Side effects include loss of appetite, nausea, vomiting, epigastric distress,
constipation or diarrhoea. Side effects due to antimuscarinic actions of H1-antagonists include dryness of mouth,
bladder disturbances.
Therapeutic Uses H1 antagonists have a widespread value in the symptomatic treatment of various disorders.

1. Hypersensitivity reactions: To prevent allergic reactions or to treat their symptoms, in which histamine is the
primary mediator, the H1-antagonists are the drugs of choice and are often quite effective. They are used
primarily to treat allergic reactions produced by the release of histamine e.g., edematous states, pruritus,
allergic rhinitis and urticaria. They are generally more effective in acute conditions and are used only for
symptomatic relief.
2. Motion sickness: Drugs like promethazine, promethazine chlorotheophyllinate, diphenhydramine,
dimenhydrinate, cyclizine and meclizine have value in prophylaxis of motion sickness.
3. Antivertigo: Drugs line cyclizine, cinnarizine, dimenhydrinate, diphenhydramine are used in the treatment of
vertigo.
4. Antiparkinsonism: Based on anticholinergic property, some H1antagonists such as diphenhydramine can be
used in the early stages of treatment of parkinsonism.
5. Local anaesthetics: In patients allergic to procaine H1-antagonists, such as diphenhydramine and
tripelennamine have been used successfully as local anaesthetic.

105. Antiseptic agents from group of oxidizers and halogen containing: the mechanism of action, usage?

Classification of antiseptics:

 Inorganic antiseptics:
o Halogens:
 Chlorine containing: Chlorohexidine
 Iodine containing: Lugol solution
o Oxidisers: Hydrogen peroxide, potassium permanganate
o Heavy metallic salts:
 Silver compounds:
 Mercury salts: mercury dichloride
 Copper compounds: copper sulfate
 Zinc compounds: zinc oxide
 Acids and Alkalis: boric acids, benzoic acids, caustic ammonia
 Organic antiseptics:
o Aliphatic agents (aldehydes and alcohols): formaldehyde
o Phenol derivatives:
o Dyes
o Nitrofuran derivatives:
o Detergents:

The mechanism of chlorine preparations is associated with hypochlorite acid which decays into chlorine and oxygen.
Chlorine takes place of hydrogen in NH-groups of microorganisms. Chlorhexidine bi-gluconate has the properties of
detergents.

The mechanism of action of oxidizers (hydrogen peroxide solution or potassium permanganate) is associated with the
release of oxygen which oxidizes the microbial proteins. Hydrogen peroxide also mechanically clean wound

106. Biosynthetic Penicillin: drugs, antimicrobial spectrum, pharmacokinetics, usage, side effects?

Penicillin consists of thiazolidine ring fused with a beta lactam ring which is essential for its antibacterial activity. These
two rings forms a nucleus named as 6-aminopenicillanic acid.

Mechanism of Action The bacterial cell wall is a rigid outer layer that completely surrounds the cytoplasmic membrane.
Penicillin and other beta lactam antibiotics inhibit bacterial growth by interfering with a specific step in bacterial cell wall
synthesis.
Pharmacokinetics After oral administration, benzyl penicillin is destroyed by gastric acid. It is mainly absorbed from the
duodenum. It is absorbed in aqueous solution rapidly after intramuscular or subcutaneous administration. Penicillin is
widely distributed in the body after absorption and approximately 60% of plasma penicillin is bound to albumin. The
major portion is rapidly excreted by the kidney mainly by tubular secretion and small amounts appear in bile, saliva, and
milk

Adverse Effects The penicillins are nontoxic and remarkably safe drug. The hypersensitivity reaction leading to
anaphylaxis is only major problem which is seen in approximately 5 to 10% of the patients taking penicillin. The minor
adverse effects include nausea, vomiting, pain and inflammation at the site of injection after intramuscular
administration has been reported. After intrathecal administration (which is a contraindication) it may lead to
convulsions, arachnoiditis and encephalopathy. The major side effect is allergic reactions and anaphylaxis which is
characterized by skin rash, pruritus, serum sickness like syndrome, eosinophilia, angioneurotic edema, asthma,
haematuria, albuminuria, haemolytic anemia, granulocytopenia and anaphylaxis.

Therapeutic Uses Penicillin G is the drug of choice for the following categories of infection

 Dental Infection, Streptococcal infection, Staphylococcal infection, STD, Gonococcal infection, pneumococcal
infection

Penicillin is effective against gram positive and negative cocci and some gram positive bacilli. Among the cocci,
streptococci are highly sensitive. Gonococci, pneumococci and meningococci are sensitive to penicillin.

Among the bacilli, gram positive Bacillus anthracis, Corynebacterium diphtheriae, Clostridium species are highly
sensitive.

Among the spirochetes, Treponema pallidum is highly sensitive to penicillin.

Gram negative bacilli, fungi, protozoa, rickettsiae, chlamydiae, viruses and Mycobacterium tuberculosis are totally
insensitive to penicillin.

107. Features of an antimicrobial spectrum and usage of half synthetic Penicillin?

Classification of antibiotics:

1. Beta-Lactam antibiotics:
a. penicillin:
i. Native Penicillin:
1. Drugs of short acting: Benzyl penicillin
2. Drugs of long action: benzyl penicillin Novocain
3. Drugs of oral administration: Penicillin G, Penicillin V
ii. Semisynthetic penicillin:
1. Penicillinase resistant penicillin’s: Methicillin
2. Broad spectrum penicillin: Ampicillin
3. Antipseudomonal penicillin: Carbenicillin
b. Cephalosporins:
i. I generations:
ii. II generation:
iii. III generation:
iv. IV generation:
2. Macrolides and Azalides:
a. I generation:
b. II generation:
3. Aminoglycosides:
a. I generation: Streptomycin
 b. II generation:
c. III generation:
d. IV generation:
4. Tetracyclines:

Semisynthetic penicillins are produced by combining the specific side chains in place of benzyl side chain. They have
been produced to overcome the shortcomings of benzyl penicillin like poor bioavailability, susceptibility to penicillinase
and narrow spectrum of activity.

PHENOXYMETHYL PENICILLIN It has an antibacterial spectrum similar to benzyl penicillin but is less active. It is gastric
acid stable and effective on oral administration.

Adverse effects include urticaria, fever, rashes, angioedema, anaphylaxis, haemolytic anemia, neutropenia,
thrombocytopenia, coagulation disorders, diarrhoea etc.

It is used in tonsillitis, otitis media, erysipelas, prophylaxis of rheumatic fever and pneumococcal infections

108. Cephalosporin’s: classification, antimicrobial spectrum, usage, adverse reactions and complications.

109. Drugs of aminoglycosides group: antimicrobial spectrum, usage, adverse reactions?

Aminoglycosides are group of bactericidal antibiotics originally obtained from various Streptomyces species. All
aminoglycosides act by inhibiting protein synthesis of bacteria by directly combining with ribosomes. They penetrate the
outer cytoplasmic membrane and inhibit protein synthesis. Streptomycin combines with the bacterial 30S ribosomes
and inteferes with the mRNA-ribosome combination. Other aminoglycosides bind to additional sites on 50S subunit as
well as to 30S-50S interface.

All aminoglycosides are poorly absorbed after oral administration, are more active in alkaline pH and are excreted
unchanged by glomerular filtration. Since excretion is principally via the kidney, accumulation occurs in renal
impairment.

All the aminoglycosides produce cochlear and vestibular damage (ototoxicity) which is a dose and duration of treatment
related side effect. Another serious side effect is nephrotoxicity.

Aminoglycosides also reduce the acetylcholine release from the motor nerve endings and cause neuromuscular
blockade.

Aminoglycosides are used for intracellular bacteria like Chlamydia, mycoplasma, rickettsia

Never combine furosemide with aminoglycoside because it will cause deafness

110. Antibiotics from group of Tetracycline and Chloramphenicol: drugs, spectrum of antimicrobial action, usage, side
effects?

TETRACYCLINES

The tetracyclines are a group of drugs with a common basic chemical structure and pharmacological activity. The first
tetracycline, chlortetracycline was isolated from Streptomyces aureofaciens, then oxytetracycline was derived from
Streptomyces rimosus and then tetracycline was obtained by catalytic dehalogenation of chlortetracycline.

Mechanism of Action The tetracyclines are primarily bacteriostatic and are thought to exert their antimicrobial effect by
the inhibition of protein synthesis. The tetracyclines, including doxycycline, have a similar

Tetracyclines, Chloramphenicol and Chemotherapy of UTI

antimicrobial spectrum of activity against a wide range of gram positive and negative organisms. Cross-resistance of
these organisms to tetracyclines is common.
Antimicrobial Spectrum of Activity Tetracyclines has one of the widest spectrum amongst antimicrobials. The microbes
that are sensitive to tetracycline include Staph. aureus, Staph. epidermidis, Strep. pyogenes, Strep. viridans, Strep.
pneumoniae, Strep. faecalis (UTI), Listeria monocytogenes, Bacillus anthracis, Clostridium sp., Actinomyces sp., T.
pallidum, T. pertenue, Borrelia recurrentis, Fusobacterium fusiforme, Brucella sp. and bacteroides sp. Commonly
occurring gram negative organisms e.g. H. influenzae, H. ducreyi, Neisseria gonorrhoeae, V. cholerae, E. coli,
Enterobacter aerogenes, Shigella sp. are also highly sensitive. Atypical bacteria e.g. Chlamydia sp., Mycoplasma sp.,
Ureaplasma urealyticum as well as Rickettsia are extremely sensitive to tetracycline. Besides being highly effective
against a wide range of gram positive and negative organisms, tetracycline is effective against all bacteria responsible for
sexually transmitted diseases viz. syphilis, gonorrhoea, chancroid and nongonococcal urethritis. It is effective/synergistic
with specific drugs against even protozoa and fungi. Though effective against a number of anaerobes it can not be relied
upon as sole therapy of anaerobic infections. Tetracycline is not effective against viruses, Pseudomonas, Proteus and
Klebsiella.

Pharmacokinetics: The absorption of tetracycline administered orally is variable and depend upon the type of
tetracycline used. The tetracycline forms insoluble complexes i.e. chelation with calcium, magnesium, milk and antacids
reduce their absorption. Administration of iron also interferes with the absorption of tetracycline. Doxycycline is rapidly
and virtually completely absorbed after oral administration and its absorption is not affected by presence of food or
milk. The tetracyclines are widely distributed in the body and diffuse into various body fluids.

Adverse Effects: Because of virtually complete absorption of doxycycline and minocycline side effects pertaining to the
lower bowel, particularly diarrhea have been infrequent. The following side effects have been observed with the use of
tetracycline including doxycycline. Anorexia, nausea, vomiting, diarrhea, glossitis, dysphagia, maculopapular and
erythematous rashes and photosensitivity hence use sunscreen; hypersensitivity reactions including urticaria,
angioneurotic edema, anaphylaxis, anaphylactoid reactions. They also cause discoloration of deciduous teeth.

Therapeutic Use: Orodental infection, Respiratory tract infection, urinary tract infection, STD, Dermatological infections,
Ophthalmic infections and prophylaxis for Traveler’s diarrhea.

CHLORAMPHENICOL

It is a broad spectrum antibiotic originally derived from Streptomyces venezuelae and later on became the first
completely synthetic antibiotic. It is used as palmitate and sodium succinate salt in given dosage.

Dose: 250-500 mg QID oral, 1-2 g IM injection, 0.5-1.0% topical (eye ointment/ drops/applicap and ear drops).

Chloramphenicol is a potent inhibitor of microbial protein synthesis. It acts by binding reversibly to the 50S submit of the
bacterial ribosome. It inhibits the peptidyl transferase step of protein synthesis. It is bacteriostatic broad-spectrum
antibiotic active against gram positive and negative organisms, Rickettsia, the Chlamydia of the psittacosis,
lymphogranuloma group and Mycoplasma pneumoniae. The other organisms sensitive to chloramphenicol are E. coli, K.
pneumoniae, Shigella, and certain strains of Brucella, Pasteurella, Proteus and Vibrio comma. It exerts bactericidal
against H. influenzae, Strep. pneumoniae and N. meningitidis.

Adverse Effects: Allergic reaction, Bone marrow depression, CNS toxicity, Gray baby syndrome

Therapeutic Uses Because of bone marrow toxicity of chloramphenicol, its use is restricted to the treatment of infection
caused by S. typhi and paratyphi (treatment of typhoid fever). Other indications in which chloramphenicol can be used
are H. influenzae meningitis, urinary tract infections, anaerobic infections caused by Bacteroides fragilis and locally in
eye and external ear infections.

111. Antibiotics of group macrolides: a spectrum of action, usage, side effects?

Macrolides, as their name indicates are characterized by a large or macrocyclic lactone ring with attached sugar
residue(s). example is Erythromycin.
ERYTHROMYCIN: was the first macrocyclic antibiotic which was isolated from Streptomyces erythreus. Erythromycin is
widely used antibiotic both in children as well as in adults. It acts by binding with 50S ribosomal subunit of bacteria and
inhibit protein synthesis.

It is a narrow spectrum antibiotic, low concentration are bacteriostatic, however high concentrations are bactericidal.
The spectrum of activity also depends on the concentration of drug at the desired site and sensitivity of the target
microorganisms. It is more active in alkaline medium.

Erythromycin is effective against gram positive and few gram negative organisms which mainly includes pneumococci,
streptococci, staphylococci, Neisseria and some strains of C. diphtheriae, H. influenzae, Rickettsiae and Treponema. It is
also effective against penicillin resistant staphylococci, Mycoplasma, Campylobacter, Legionella, Gardnerella vaginalis
are also highly sensitive.

Adverse effects include gastrointestinal side effects like nausea, epigastric pain are common. Diarrhoea occurs
occasionally. Skin rashes, hypersensitivity reaction, hepatotoxicity (hepatitis alongwith cholestatic jaundice, especially
with estolate ester), oral candidiasis, thrombophlebitis and fever have been reported.

Erythromycin is used as a substitute to penicillin in allergic patients for upper respiratory tract infections, e.g. tonsillitis,
pharyngitis and mastoiditis, pneumococcal infection and prophylaxis of rheumatic fever. It is drug of choice in treatment
of atypical pneumonia due to Mycoplasma pneumoniae, Legionnaire’s pneumonia and whooping cough. It is also useful
in wound and burn infections and severe impetigo not responding to topical antibiotics

112. Side effects and possible complications of an antibiotic therapy, their prophylactic and treatment.

113. Sulphonamides: classification, antimicrobial spectrum, mechanism of action?

SULFONAMIDES: Chemically, all sulfonamides may be considered to be derivatives of sulfanilamide

Classification:
 1. Sulfonamides that are well absorbed:
a. Short acting:
b. Long acting:
c. Ultra long acting: Sulfalenum
2. Sulfonamides which are not absorbed:
3. Sulfonamides for local action: Aethazolum
4. Combination of Sulfonamides: Biseptolum

114. Sulphonamides: rules of dosing, negative side effects and their preventive measures?
115. The antimicrobial agents from group of fluoroquinolones, their properties and usage?
Mechanism of action: they bind to some trace elements (iron, copper) of the microbial cells with the formation of
chelate complexes, that leads to the inactivation of the microbial enzyme system. The type depends on the drug
concentration: in low doses the drugs manifest the bacteriostatic effect, in high doses – the bactericidal ones

116. Antituberculous remedies: classification, mechanism and spectrum of action, side effects, principles of
chemotherapy of tuberculosis?

Tuberculosis is a chronic infectious disease caused by various species of mycobacteria. The important human
mycobacterium pathogens are Mycobacterium tuberculosis and Mycobacterium bovis.

Classification of anti-tuberculosis drugs:

1. Group A (most effective): Isoniazid (Tab. 0.3g), Rifampicin (capsule 0.15)

2. Group B (effective): Streptomycin (bottles with 0.5 gram)
3. Group C (less effective): Thioacetazone (150mg/day)

Mechanism of action:

ISONIAZID It is the most active drug used in the treatment of tuberculosis. It is a hydrazide of isonicotinic acid. It is a
bactericidal drug, effective against Mycobacterium tuberculosis and ineffective against atypical mycobacteria. Isoniazid
possibly exerts its action by inhibiting the synthesis of mycolic acid which is an essential component of mycobacterial cell
wall. It is also postulated that the ability of isoniazid to suppress the formation of DNA and RNA and also inhibition of
various oxidative mechanisms may be responsible for its action. Isoniazid is completely absorbed on oral administration
and penetrates all tissues of the body. Peak plasma levels are reached within one hour and persists for 24 hours. It
penetrates intracellularly and diffuses into macrophages and the necrotic centres. It is metabolized in liver by
acetylation and isoniazid metabolites and a small amount of unchanged drug is excreted mainly by kidney.

117. Antisyphilitic agents: drugs, pharmacodynamics, mechanism of action, usage?

118. Classification, mechanism of action and usage of anthelminthic drugs?

Anthelmintic agents are used to eradicate (either kill or expel) the infesting helminths.

Classification of antiprotozoal drugs:

1. Drugs used for the treatment of malaria:

1.1. Quinoline derivatives:
1.1.1. 4-Quinolines: Chingaminum, Chinini Sulfas
1.1.2. 8-aminoquinolines: Mellfoquinum, primaquinum
1.2. Pyrimidine derivatives: Chloridinum, Proguanilum
2. Anti-amebial drugs: Metronidazole
3. Drugs for treatment of lambliosis: Metronidazole
4. Drugs used for the treatment of Pneumocystis and Toxoplasmosis: Pentamidum
5. Drugs used for treatment of Trichomoniasis: Metronidazole
6. Drugs used for treatment of Trypanosomiasis: Pentamidum
7. Drugs used for the treatment of Leishmaniasis: Metronidazole
8. Drugs for the treatment of leprosy: Dapsonum

Mechanism of action of metronidazole: metronidazole has a 5 nitro group which are reduced by the organism’s
enzymes. The enzyme pyruvate ferrodoxine oxyreductase is found inly in anaerobic organism reduces metronidazole
and thereby activates the drug. Reduced metronidazole disrupts replication and transcription and inhibits DNA repair.

Antihelminth drugs Classification:

1. Drugs with wide spectrum of action: Mebendazole tablet 0.1g

2. Chemotherapy of cestodes: Niclosamide
3. Chemotherapy of nematodes: Levamisole tablet 0.015 g

Mechanism of action:

MEBENDAZOLE It is a synthetic benzimidazole having a wide spectrum of anthelmintic activity. After administration it is
poorly absorbed and approximately 90 percent of the drug is passed in faeces. Complete clearance of the parasites from
the GIT may take up to three days. Mebendazole binds to microtubular protein ‘β tubulin’ of parasite and inhibits its
polymerization, thus irreversibly impairing glucose uptake.

LEVAMISOLE It is a synthetic imidazothiazole derivative and is highly effective in eradicating ascariasis and
ancylostomiasis. It acts by stimulating ganglia of the worm which results in tonic paralysis, which are subsequently
eliminated from the intestines.

NICLOSAMIDE It is salicylamide derivative, act by inhibiting anaerobic phosphorylation of ADP by the mitochondria of
the parasite. It is devoid of any major toxicity except minor gastrointestinal disturbances. After breakfast 1 gram will be
chewed then another 1 gram chewed after another hour

119. Antifungal agents: classification, spectrum of action, usage, side effects?

Antifungal agents are used in the treatment of topical and systemic fungal infection. They can be classified as systemic
or topical antifungal agents and some are used both systemically as well as topically in the form of powder, ointment
and vaginal tablets.

Classification of antifungal drugs:

1. Antibiotics: Amphotericin-B (50-100 mg QID, 200 µg to 1.5 mg/kg daily or on alternate days IV infusion, 3%
topical (ear drops), Nystatin (5 lac U orally TDS, 1 lac U topical (ointment vaginal tablet)
2. Synthetic agents: Fluconazole (400 mg on 1st day, then 200-400 mg OD, for 28 days), Miconazole (3-15 mg/kg
with glucose & saline IV infusion, 1-2% topical (powder, lotion, vaginal gel, ointment & vaginal ovules))

NYSTATIN It is obtained from Streptomyces noursei. It has similar antifungal action as amphotericin but is highly toxic
and used topically only. It is effective against Candida, Histoplasma, Trichophyton, Blastomyces, Microsporum audouini
etc. It is indicated in Candida albicans especially oral moniliasis, monilial vaginitis, conjunctival, cutaneous and corneal
candidiasis.

AMPHOTERICIN B chemically it is an amphoteric polyene macrolide. It has a highly double bonded structure. The cell
membrane sterol ‘ergosterol’ is found in the cell membrane of fungi and the predominant sterol of bacteria and human
cell is cholesterol. This antifungal antibiotic binds to ergosterol which alters the permeability of the cells by forming
amphotericin-B associated pores in cell membrane, which allows the leakage of intracellular ions and macromolecules
which can lead to cell death. Amphotericin B has a wide spectrum of antifungal activity. It is active against Histoplasma
capsulatum, Cryptococcus neoformans, Candida albicans, Sporotrichum schenkii, Blastomyces brasiliensis, Coccidioides
immitis, Rhodotorula, Aspergillus etc. It is fungicidal at high and fungistatic at low concentration. It is poorly absorbed
from GIT and topically. After IV administration it is widely distributed in tissues. About 60% drug is metabolized in liver
and excretion occurs slowly both in urine and bile. Adverse effects include nausea, vomiting, headache, fever,
breathlessness, anaemia, thrombophlebitis on IV administration. On long term use, dose related nephrotoxicity and
anaemia occurs. It is used orally for intestinal candidiasis, topically for oral, vaginal and cutaneous candidiasis and
hospital treatment of progressive and potentially fatal systemic fungal infections. It is the gold standard of antifungal
therapy. Flucytosine has supraadditive action with amphotericin B if the fungi is sensitive to both. It is also potentiated
by rifampicin and minocycline.

MICONAZOLE It has broad spectrum antifungal and antibacterial activity and is effective against Cryptococcus,
Blastomyces, dermatophytes, Microsporum, Coccidioides and Candida. Used topically as ointment, lotion, gel, ear drop
and vaginal gel. Adverse effects include fever, chills, allergic reaction and even anaphylaxis. It is indicated in vulvovaginal
candidiasis, Trichomonas vaginitis, otomycosis, tinea and Pityriasis versicolor

FLUCONAZOLE It has broad range of antifungal activity. It is well absorbed orally (94%). It is primarily excreted
unchanged in urine. Fungicidal concentration is achieved in nail, saliva and vagina and also penetrates brain. Adverse
effects include nausea, vomiting, headache, abdominal pain, diarrhea and skin rash. It is indicated in mucosal
candidiasis, systemic candidiasis, crypttococcosis, prophylaxis of fungal infections following cytotoxic chemotherapy or
radiotherapy; maintenance to prevent relapse of cryptococcal meningitis in patients with AIDS; sporotrichosis,
histoplasmosis and vaginal candidiasis.

120. Anticancer agents: classification, spectrum of action, features of usage, and preventive measures of complications.

Cancer is a disease of cells characterized by a shift in the control mechanism which govern cell proliferation and
differentiation and the anticancer agents either kill cancer cells or modify their growth.

Classification of anticancer drugs:

METHOTREXATE It is a broad spectrum antineoplastic drug which act as an antimetabolite of folic acid. It acts by
inhibiting dihydrofolate reductase. It inhibits conversion of dihydrofolic acid to tetrahydrofolic which is essential for
purine synthesis and amino acid interconversions. It primarily affects DNA synthesis but also RNA and protein synthesis.
It has cell cycle specific action and kills cells in S phase. It is readily absorbed from gastrointestinal tract but larger doses
are absorbed incompletely, little drug is metabolised and it is excreted largely unchanged in urine.

Adverse effects include nausea, vomiting, diarrhoea, anaphylaxis, hepatic necrosis, fever, bone marrow depression,
osteoporosis, menstrual dysfunction, cirrhosis, pulmonary infiltrates and fibrosis, renal toxicity and depigmentation

It is indicated in lymphoblastic leukemia and choriocarcinoma, psoriasis, adjuvant therapy of non-metastatic

osteosarcoma and to reduce corticosteroid requirement in patients with severe steroid dependent asthma.

121. Pharmacotherapy in dentistry?

Antiseptics and disinfectants:

 Antiseptics: used on living surfaces

 Disinfectants: used for inanimate objects

Examples:

 Oxidizing agents: potassium permanganate, hydrogen peroxide

 Acids: 4% boric acids
 Biguanides: chlorohexidine
Astringents: precipitates proteins in superficial layer of cells and are used to diminish the excretion or exudation of
superficial cell. They are also used as local hemostatic and mummifying agents. E.g. tannic acids, zinc sulphates, zinc
chloride

Obtundents: diminish or eliminate dentine sensitivity to make excavation less painful, limited use due to anesthetic
availability e.g. phenol, benzyl alcohol.

Mummifying agents: to remove pulp for root canal treatment (pulp devitalization) e.g. paraformaldehyde

Bleaching agents: remove tooth pigmentation e.g. UV rays, hydrogen peroxide

Styptics/ local hemostatic: thrombin, adrenaline, fibrin

Disclosing agents: diagnostics acid to reveal dental plaque e.g. methylene blue, lugol solution

Tooth pastes: mechanical aids (abrasives), antiseptics and therapeutics agents e.g. sodium fluorides

Mouth washes: can have antihistamines, corticosteroids, antimicrobial agents (tetracyclines, nystatins),

 Pilocarpine: for dry mouth

 Allopurinol: for stomatitis
 Chlorohexidine gluconate: control of plaque
 Hexetidine: antimicrobial and antifungal

Dental caries: ammonia ions and flourides can decrease incidents of caries