TOPICAL ROUTE

Drugs may be used for local applications in the form of dusting powder, lotion, paste,
ointments, plasters etc.

Drugs are commonly applied on skin, eye, nose, ear, throat, rectum, and vagina.

Merits/Advantages

• Easiest route of drug administration

• Prolonged effect of drug

Demerits/Disadvantages

• Watery soluble drug sometimes absorbed in blood which may lead to an undesirable
toxic effect.
• Drugs for corneal application may penetrate and produce irritation, e.g. cocaine

ORAL ROUTE
Drugs are administered in the form of tablets, capsule, and liquid orals with the help of fluids
i.e. water or milk.

Advantages

• Oldest and safest route

• Most convenient
• Most economical
• Self-medication is possible
• Withdrawal of drug is possible

Disadvantages

• Onset of action is slow

• Bio-availability is not 100%
• Required high dose
• Accuracy of dose is not possible
• Not suitable for uncooperative and unconscious patients
• Irritant and unpalatable drug cannot be administered
• Not suitable in emergency cases

PARANTERAL ROUTE

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 A. INJECTIONS: Drugs are administered by injection which takes the drug directly into
the tissue fluid or blood without having to cross the intestinal mucosa.
Advantages
• Onset of action is very quick
• Bioavaibility is 100%
• Low dose are effective
• Accuracy of dose is possible.
• Suitable for uncooperative and unconscious patients
• Irritant and unpalatable drugs can be given by this route.
• Suitable for emergency case

Disadvantages

• Risky route
• Inconvenient
• Costly route
• Self- medication is not possible
• Withdrawal of drug is not possible
• Aseptic technique is to be followed to avoid possibility of infection

FACTORS MODIFYING DRUG ABSORPTION

A) Physical state: Drugs in the form of liquids are well absorbed than solids.
B) Particle size: Smaller the particle size better is the absorption.
C) Concentration: Higher concentrated form of drugs are quickly absorbed than dilute
solutions
D) Solubility: Lipid soluble drugs are easily absorbed in compared to water soluble drugs.
E) Absorbing surface: Drugs can be better absorbed from the small intestine than from
the stomach because of large surface area.
F) PH of drug: Acidic drugs are better absorbed from the stomach, e.g. salicylates. Basic
drugs are better absorbed from the intestine, e.g. ephedrine
G) Ionization: Unionized drugs are lipid soluble and are well absorbed than ionized drugs
H) Formulation: Diluents used in the formulation of drugs may sometimes interfere with
absorption, e.g. calcium and magnesium reduce the absorption of tetracycline when
used as a diluents.
I) Diseases: Disease of guts like malabsorption, diarrhea reduced the absorption of drug.
J) Presence of other agents: Vitamin C enhance the absorption of iron, Liquid paraffin
reduces the absorption of fat soluble vitamins A, D, E, K.

Factors modifying drug effects.

The various factors which modify the response to a drug are as follows:

➢ Age
➢ Sex

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 ➢ Route of administration
➢ Time of administration
➢ Pathological state
➢ Genetic factors
➢ Cumulation
➢ Tolerance
➢ Tachyphylaxis
➢ Drug Interaction

➢ Age: Children are hyper reactive to certain drugs. The reasons are immaturity of renal
functions or poor development of enzymes needed for inactivation. So, a lesser dose
must be given for children than for adults. The dose for children can be calculated by
making use of the following formulae:

a. Young’s formula: Age x Adult dose

Age + 12

b. Dilling’s formula: Age x Adult dose

20
➢ Sex: Women are more susceptible to the effects of certain drugs e.g. morphine produces
more excitation in women than in men.
➢ Route of administration: Route of drug administration may modify the drug response,
e.g. Intravenous dose of a drug is less than subcutaneous dose.
➢ Time of administration: Drugs which produce nausea, vomiting and irritation should
be taken after meal. But anthelmintic should be taken in empty stomach.
➢ Pathological state: The effect of a drug may be modified in pathological conditions
e.g. hyperthyroid individuals require a large dose of morphine.
➢ Genetic factors: The effects of a drug may vary due to genetic factors like inherited
enzyme deficiencies e.g. primaquine produces hemolysis in individuals with a
deficiency of Glucose-6- phosphate dehydrogenase.
➢ Cumulation: Drugs like digitalis are excreted slowly. So repeated administration leads
to accumulation in the body so as to produce toxicity. This phenomenon is called as
cumulation.
➢ Tolerance: It is the unusual resistance to normal therapeutic dose of a drug. So a large
dose is required to produce an effect.
➢ Tachyphylaxis: It is an acute type of tolerance. It occurs on repeated administration of
the drug at short intervals.
➢ Drug Interaction: The effects of a drug may be altered by the prior or simultaneous
administration of another drug. The effects produced by drug combinations can be
classified as:

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 i. Additive effect: Here, the total pharmacological response produced by two
drugs is equal to the sum of the individual effects. E.g. the effects of ephedrine
and aminophylline in bronchial asthma.
ii. Synergism: The total effect produced by two drugs is greater than the sum of
individual of individual effects e.g. ammonium chloride synergizes the effect of
mercurial diuretics.
iii. Antagonism: Two drugs act on the same physiological system and produce
opposite effects. E.g. antagonism of acetylcholine by atropine at muscarinic
receptors.

SEDATIVES AND HYPNOTICS

Sedative: these are the drugs which reduce excitement without producing sleep.

Hypnotics: are the drugs which produces sleep resembling natural sleep.

Small doses of Hypnotic produces sedative effect and large doses of sedative produces hypnotic
effect.

CLASSIFICATION:

1. Barbiturates Phenobarbitone
Pentobarbitone
Secobarbitone

Thiopentone

2. Benzodiazepenes Diazepam
Nitrazepam
Alprazolam

3. Non-benzodiazepenes Zoplicone

Zolpidem

Barbiturates:

Barbiturates are the derivative of barbituric acid act as general depressant. They are not prefers
now a days as sedatives and hypnotics because of development of relatively safer
benzodiazepines.

PHARMACOLOGICAL ACTIONS:

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 ▪ C.N.S: Barbiturates produces C.N.S depression such that from mild sedation to even
coma.
▪ Sleep: barbiturates induces sleep resemble natural sleep but there is hangover effect
after awakening.
▪ C.V.S: they depress cardiac activity and in higher dose cause fall in B.P.
▪ Respiratory system: in higher dose they depress respiratory Centre in brain and may
produces death.
▪ Kidneys : large dose decrease urinary output due to decrease in glomerular filtration
and release of ADH (anti diuretics hormone)
▪ Liver: large dose may produce hepatic dysfunction.

ADVERSE EFFECTS

• Intolerance like nausea, headache and diarrhoea.

• Foetal respiratory depression
• Dependence and withdrawal symptoms.

USES

• As a sedative and hypnotics

• Potentiation of analgesics like salicylates
• Pre-anaesthetic medication
• Anticonvulsant (specially long acting barbiturates)

Narcotic analgesics are drugs that relieve pain, can cause numbness (lack of sensation) and induce a
state of unconsciousness. They work by binding to opioid receptors, which are present in the central
and peripheral nervous system.

CLASSIFICATION:

1. Natural opium Alkaloids Morphine

Codeine
Papaverine

2. Semisynthetic derivatives of Heroin

opium alkaloids
Dihydromorphine

Apomorphine

3. Synthetic substitutes of Pethidine

opium alkaloids
Methadone

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MORPHINE
Morphine is a natural opium alkaloids obtain from the unripe capsule of the poppy plant,
papaver somniferum.

PHARMACOLOGICAL ACTIONS.

❖ Analgesia: Morphine relieves severe pain like visceral pain and pain of trauma.
❖ C.N.S: Morphine produces euphoria (a condition of physical and mental good health)
in the presence of pain, but in the absence of pain, it produces dysphoria. And in
increased dose it produce sleep.
❖ Respiration: Morphine produces depression of respiration by directly depressing the
respiratory center in the brain

❖ Pupils: Morphine produces constriction of the pupil (miosis) and higher dosage it
characterized by pin point pupil.
❖ Emetic action: In small doses, morphine produce vomiting due to stimulation of CTZ
(chemo receptor trigger zone) but in higher dose it depress the vomiting center and
hence there is no vomiting in poisoning.
❖ Antitussive effect: Morphine suppresses cough by depressing the cough center.
❖ ADH secretion: Morphine produces release of ADH. This results in decrease of urine
output.
❖ CVS effect: Normal dose of morphine produce no effect on heart or circulation but
hypotension may be produced at toxic dose.

ADVERSE EFFECTS
• Acute morphine poisoning: It cause due to accidental overdose and suicidal intention,
characterized by respiratory depression, pin point pupil, hypotension, hypothermia,
cyanosis, coma and death.
• Intolerance like tremor, delirium and skin rashes
• Drug dependence.

USES

• As an analgesic for relief of severe pain.

• For the treatment of diarrhoea.
• As an Antitussive
• As pre-anaesthetic medication.

SALICYLATES
PHARMACOLOGICAL ACTIONS :

1) Analgesic: aspirin is a good analgesic and effective only in dull achieving pain of low
intensity.

2) Antipyretics: In fever salicylate bring down the temperature to normal level. But in normal
individual there is a no change in temperature

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3) Respiration: salicylate stimulate respiration indirectly and directly and increase respiration
rate and volume and may lead respiratory alkalosis.

4) G.I.T: aspirin causes gastric irritation and produces pain, nausea, vomitting, salicylates also
causes gastric ulceration and haemorrhage.

5) Anti-inflammatory action: at higher dose of 4-6gm/day aspirin act as anti-inflammatory

agents and suppressed the sign of swelling erythema and pain.

6) Kidneys: in low dose it depresses uric acid excretion where as in high dose it enhance uric
acid excretion.

7) C.V.S: No effects at normal dose, toxic doses produce paralysis of vasomotor centers.

8) Blood: salicylate lower erythrocytic sedimentation rate (ESR). They also increases
Prothrombin level of plasma prolong bleeding time.

9) Endocrines: salicylate stimulates the release of adrenaline, adrenal medulla ACTH. They
interference with the binding of thyroxine depresses the secretion of thyroid stimulating
hormones.

10) Local action: salicylate having antiseptic, fungi statics and karatolytic affects

PHARMACOKINETICS
It will absorbed orally and distributed through out the body.it can cross blood brain barrier and
placenta. They are metabolized in liver and excreted through urine.

ADVERSE EFFECTS:

• SALICYLISM: higher dose causes salicylism characterized by nausea,

vomiting, dizziness, hyperventilation, drowsiness, confusion, deafness, tremors,
convulsions, coma, death due to respiratory failure and C.V collapse
• GIT disturbance: nausea, vomiting , diarrhea, ulceration, perforation, and
haemorrhage
• Prolong use can cause hepatotoxicity, intolerance leading to skin rashes

USES:
• As an analgesic and antipyretic
• As an anti rheumatic
• For local application as keratolytic , fungistatic and antiseptic

Drug addiction is a state in which an individual is incapable of maintaining normal physical

and mental functions without the presence of drug.

Characteristic of drug dependence are:

• An overpowering desire to take the drug
• A tendency to obtain the drug by any means.

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 • A tendency to increase the dose physical and psychological dependence on the body
• Harmful effect to the individual and society.

Examples:

• opium alkaloids:
Ex: morphine, heroin, pethidine
• cannabis indica
Ex:cocaine
• others:
Ex: lysergic acid diethyl amine, barbiturates, alcohol etc

DRUG ABUSE
Drug abuse refers to the use of drug for the purposes other than approved medicinal and social
use.
Ex: narcotics like morphine, pethidine, barbiturates

DRUG HABITUATION
Drug habituation is a condition which occurs due to repeated administration of drug . It is
characterize by:

• Desire to take the drug.

• No tendency to increase the dose.
• Only psychic but not physical dependence on the drug
• A harmful effect if only to the individual and not to the society

Local anaesthetics are drugs which block conduction of impulses in nerves, when applied
locally and produce loss of sensation of pain from localized area.

CLASSIFICATION

1) Injections
• Low potency
Ex: procaine, chlorprocaine.
• Intermediate potency
Ex: Lignocaine, prilocaine
• High potency
Ex: tetracaine, bupivacaine, dibucaine
2) Surface anaesthetics
Ex: cocaine, lignocaine, tetracaine

MECHANISM OF ACTION/PHARMACODYNAMIC
Local anaesthetics prevent the generation and conduction of impulses in the nerve by blocking
voltage dependent sodium channels which prevents depolarization.

PHARMACOLOGICAL ACTIONS

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 1. Effect on sensations: Local anaesthetics block the sensation of pain, temperature,
touch, and pressure
2. Effect on C.N.S.: Local anaesthetics produce stimulation of CNS which causes
euphoria, restlessness and tremors
3. Effect on CNS: All local anaesthetics produces vasodilation, except cocaine

ADVERSE EFFECTS: Restlessness, Tremors, Hypotension, Dermatitis, Vasodilation,

Euphoria

USES
• Surface anaesthesia: for pain due to burns, ulcers.
• Infiltration anaesthesia : to anaesthetize nerve ending by subcutaneous in
filtration
• Nerve block anaesthesia: anaesthetize nerve when injected dose to specific
nerve.
• Spinal anaesthesia: use in the case of spinal surgery.
Oral Contraceptives
Contraceptive drugs are substances which prevent conception. Most oral contraceptives in
use are a combination of an estrogen and progesterone. Rarely only progesterone can be used.
Oral contraceptive prevents conception by:

• Somehow inhibiting ovulation.

• Making the endometrium unsuitable for implantation of ovum.
• Changing the character of cervical mucus- this reduces sperm motility.

The usual estrogen in this combination is Ethinyl Oestradiol and the commonest progesterone
is norethisterone or levonorgestrel.

Only progesterone containing pills can also be used but they are less effective contraceptive
as compared to combination pills.

Different preparations of oral contraceptives contain:-

1. Progestogen only
Norethisterone 350μmgs
Levonnorgestrel 30 μmgs
2. Combined preparations
Ethinyloestradiol : 20-35 μmgs + Norethisterone 500-1000 μmgs
Ethinyloestradiol : 30-50 μmgs + Levonnorgestrel 50-200 μmgs
Ethinyloestradiol : 30-50 μmgs + Norgestrel 300-500 μmgs

Most of the oral contraceptives are taken for 21 days, starting on the fifth day of the
normal cycle. This is followed by a seven days interval, during which withdrawal
bleeding occurs, before starting the next course.

CARDIOVASCULAR DRUGS

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30 - CARDIAC GLYCOSIDES

Cardiac glycosides are the group of chemically related drugs which having specific action on
the heart. Cardiac glycosides are used for the treatment of congestive heart failure. Cardiac
glycoside mainly obtained from:

1. Digitalis: containing cardiac glycoside digitoxin and gitoxin

2. Stropanthus: Containing cardiac glycosides G-stropanthus and A-stropanthus
3. Squills: Containing cardiac glycoside proscillaridine
4. Toad: only the animal source containing cardiac glycoside bufotoxin.

Cardiac glycoside containing sugar (glycone) and non sugar (aglycone) portion. Aglycone
portion is responsible for the pharmacological action on the heart. The sugar portion helps in
the permeability of cardiac glycosides on the myocardium.

DIGITALIS

Pharmacological action of digitalis

A) Cardiac actions
1. Cardiac contractility: Digitalis increases the force of systolic contraction of the heart
muscle. Also it decreases the duration of systole. So in limited time, the heart contracts
powerfully leading to complete ventricular emptying.
2. Heart rate: In individual with congestive cardiac failure (CCF), digitalis reduce the
heart rate. Small dosage of digitalis produce a decrease in heart rate by stimulation of
the vagus nerve.
3. Blood pressure: The effect depends on the initial state of the circulation. If it is low, it
is returned to normal and it is not raised beyond normal.
4. Cardiac size: Digitalis decreases the size of both normal and failing heart, which
causes reduce in cardiac output.
5. Cardiac output: Digitalis decreases cardiac output in normal heart and this effect is
due to reduction in size. In failing heart, digitalis increases cardiac output. This effect
is produced due to return of heart to normal size, increased force of contraction and
complete cardiac emptying.
6. Conduction system: Digitalis depresses the conduction system directly. Also, the
refractory is increased and the conduction rate is slowed.

B) Extra cardiac actions

1. Kidney: The first prominent manifestation of the effect of digitalis in edema is dieresis.
This is due to:
• Decrease in venous pressure which shifts the edema fluid into circulation.
• Direct renal action, inhibiting the reabsorption of sodium.
2. Gastrointestinal tract: In toxic doses, digitalis produces nausea, vomiting and
diarrhoea

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Pharmacokinetics
Digitalis is adequately absorbed from the intestine. Subcutaneous or intramuscular injection is
unreliable and it may produce local irritation, swelling and abscess. In blood, it is bound to
plasma albumin. High concentration is found in the heart. It is eliminated very slowly through
the kidney. So it is likely to produce cumulative toxicity.

Adverse effect
1. Gastrointestinal tract: Digitalis produce nausea, vomiting and diarrhoea.
2. Cardiac toxicity: Digitalis produces all types of cardiac arrhythmias like atrial
tachycardia, atrial fluter, atrial fibrillation, ventricular tachycardia, ventricular flutter
and ventricular fibrillation.
3. Blood coagulation: Digitalis increases the coagulabilty of blood.
4. Vision: Digitalis produces visual defects like blurred vision and colour defects.
5. Neurological symptoms: They are headache, fatigue, drowsiness and mental
symptoms.

Uses: For the treatment of congestive heart failure, to control arrhythmias

31 - ANTI-ARRHYTHMATIC DRUGS
Cardiac arrhythmia is a disease characterized by disturbance in cardiac rhythm caused due
to effective impulse formation or defective impulse conduction. Anti-arrhythmic are the drugs
used to correct cardiac arrhythmias.

Classification
1. Myocardial depressants: Ex:- Quinidine, Procainamide, Lignocaine, phenytoin
2. Sympathetic blockers: Ex:- Propranolol
3. Calcium channel blockers: Ex:- Verapamil
4. Miscellaneous: Ex:- Potassium, Amiodorone

QUINIDINE
Quinidine is a natural alkaloid obtain from cinchona bark.

Pharmacological actions

A. Cardiac effects
1. Depolarisation: Quinidine slows the rate of depolarization. This is produced by
depressing the entry of sodium ions into the cell. So quinidine prolongs the
depolarization-repolarisation cycle.
2. Impulse formation: Quinidine slows the production of impulse from the SA node.

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 3. Excitability: Quinidine decreases the excitability of cardiac muscle. So AV impulse
becomes ineffective.
4. Refractory period: Quinidine increases the refractory period. During refractory
period the heart does not respond to weak and premature stimuli.
5. Conduction velocity: Quinidine slows the rate of conduction in the heart muscle.
This along with decrease excitability and increased refractory period brings down
the heart rate
6. Cardiac contractility: Cardiac contractility is decreased by decreasing the entry of
calcium into cardiac muscle cells.
B. Extra cardiac effects
1. Quinidine produces a fall in blood pressure on oral or Parentral administration.
2. Quinidine produces a relaxant effect on skeletal muscles.
3. Quinidine also having Antimalarial, antipyretics and oxytocic actions.

Pharmacokinetics
Quinidine is well absorbed from GIT tract and also after intramuscular injection. In plasma it
is partially bound to albumin. It is metabolized in the liver and excreted through urine.

Adverse effects
1. GIT effects: Nausea, vomiting and diarrhoea
2. Cinchonism: Characterised by giddiness, light-headedness, tinnitus, impaired hearing
and blurred vision.
3. Cerebral: Convulsions due to effects on CNS
4. Hypotension

Uses: Treatment of cardiac arrhythmias.

32 - ANTI-ANGINAL DRUGS (Vasodilators)

Angina pectoris is a condition in which there is a compressing type of pain occurs in the chest.
Angina pectoris may occurs due to occlusion of coronary vessels due to thrombosis or due to
anaemic conditions. The coronary vasodilators are useful in the treatment of angina pectoris.

Classification of anti-anginal drugs

(Coronary vasodilators)

1. Nitrites and nitrates: Ex:- Amyl nitrite, Glyceryl trinitrate, Isosorbide dinitrate
2. Beta adrenergic blockers: Ex:- Propranolol
3. Calcium channel blockers: Ex:- Verapamil, Nifidipine, Diltiazem
4. Potassium channel openers: ex:- Nicorandil

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Nitrites and nitrates

Pharmacological actions
1. Blood vessels: These compounds produce direct relaxant effect on arteries, veins and
capillaries. All blood vessels are not equally affected. Vasodilatation is marked in
coronary, cerebral and Cutaneous vessels.
2. Smooth muscles: Nitrites and nitrates produce relaxation of smooth muscles like
intestine, biliary tract, ureter and uterus.
3. Eye: These drugs dilate intraocular blood vessels. So intraocular pressure may be
increased.
4. Methemoglobin formation: Nitrites convert hemoglobin to methemoglobin.
Methemoglobin combines with cyanides to form non-toxic cyanmethemoglobin. So
nitrites are useful in the treatment of cyanide poisoning.

Adverse effects: Headache, flushing of face, hypotension.

Uses: Treatment of angina pectoris.

33 - ANTI-HYPERTENSIVE DRUGS
Hypertension is blood pressure elevated enough to perfuse tissues and organs. Elevated
systemic blood pressure is usually defined as a systolic reading greater than or equal to 140
mm Hg and a diastolic reading greater than or equal to 90 mm Hg (≥140/90).

Hypertension is the most common cardiovascular disorder. Hypertensions are of two types:

1. Primary (or essential) hypertension, in which no specific cause can be identified,

constitutes more than 90% of all cases of systemic hypertension.
2. Secondary hypertension, resulting from an identifiable cause, such as renal disease or
adrenal hyper functions.

The drug used for the treatment of hypertension is known as anti-hypertensive drugs.

Classification of anti-hypertensive drugs

1. ACE inhibitors: Ex:- Captopril, Enalapril, Lisinopril, Ramipril
2. Angiotensin antagonist: Ex:- Candesartan, losartan, Telmisartan, Valsartan

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 3. Calcium channel blockers: Ex:- Diltiazem, Verapamil, Amlodipine, Felodipine,
Nicardipine
4. Diuretics: Ex:- Chlorothiazide, Hydrochlorthiazide, Frusemide, Amiloride,
Spironalactone
5. Beta adrenergic blockers: Ex:- Propranolol, Metoprolol, Atenolol
6. Alpha adrenergic blockers: Ex:- Prazocin, Terazocin, Phentolamine
7. Central Sympatholytics: Ex:- Clonidine, Methyldopa
8. Vasodilators: Ex:- Diazoxide, Hydralazine, Minoxidil, Nitroprusside

Angiotensin Converting Enzymes (ACE) Inhibitors: ACE inhibitors prevents the

conversion of Angiotensin I to Angiotensin II, responsible for vasoconstrictions and increased
B.P. ACE inhibitors effective in all types of hypertension.

Calcium Channel Blockers: The contractility of cardiac and vascular smooth muscles is
dependent on extra cellular calcium concentration. The calcium channel blockers interfere with
the entry of calcium into myocardial and vascular smooth muscles to produce dilation of
arterioles to reduce blood pressure.

Diuretics: Diuretics enhance salt and water excretion and helps in reducing blood pressure.
Thiazide diuretics (Chlorothiazide, Hydrochlorthiazide) are the first line drugs in mild to
moderate hypertension. And they also potentiate the effect of other antihypertensive drugs.

34 - DRUGS USED IN ATHEROSCLEROSIS (Lipid Lowering Agents)

Atherosclerosis is a disease characterized by narrowing of blood vessels. Atherosclerosis is

associated with increase level of plasma lipids like cholesterol and triglycerides.

Classification
1. Drugs lowering triglyceride: Ex:- Clofibrate, Gemfibrozil
2. Drugs lowering cholesterol: Ex:- Cholestyramine, Dextrothyroxine, Probucol
3. Drugs lowering triglyceride and cholesterol: Ex:- Nicotinic acid

CLOFIBRATE
Clofibrate lower the plasma level of triglyceride by two ways:

1. Inhibiting synthesis of cholesterol in liver

2. Inhibiting the transfer of triglyceride from liver to plasma.

Clofibrate orally administered and well absorbed from GIT, metabolized in liver and excreted
through urine.

Adverse effects: Nausea, vomiting, diarrhoea, allergy and fluid retention

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Uses: Management of atherosclerosis.

It is defined as the treatment of specific infections with chemical agents. In the broadest
sense, it includes therapy with antibiotics and also conditions where infection is not involved
e.g. malignancy

A chemotherapeutic agent may be:

1. Bacteriostatic if it inhibits the growth of bacteria.

2. Bactericidal if it destroys and kills the bacteria

Antibiotics: are the chemical substances or drugs obtained from one type of micro-organisms
and effective against another type of micro-organisms in a very small concentration.
Antibiotic is a general term for antimicrobial.

Antibiotics are of 3 types:

1. Natural Antibiotics: Those antibiotics which are directly derived from one type of
micro-organisms and used against another type of micro-organisms. E.g. Penicillin G,
Penicillin V, Tetracycline.
2. Semi-Synthetic Antibiotics: Those antibiotics which are derived from micro-organisms
and then modified in laboratory for their better antimicrobial action. E.g. Ampicillin,
Amoxicillin, Cephalosporins.
3. Synthetic Antibiotics: Those antibiotics which are totally prepared in laboratory. E.g.
Fluoroquinolones (Ciprofloxacin, Norfloxacin, Ofloxacin, Levofloxacin)

An antibiotic is said to be:

a. Broad spectrum, if it is effective against both gram+ve and gram-ve micro-

organisms.
b. Narrow spectrum, if it is effective only against small group of micro-organisms
(gram+ve or gram-ve).
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Q.1. Classify Anti-Microbial agents with examples

Ans. Classification of Anti-Microbial agents:

I. Based on chemical nature:

1. Sulphonamides Sulphamethoxazole

Sulphadiazine

2. Cephalosporins Cephalexin
Cefuroxime
Cefixime

3. Penicillins Ampicillin

Amoxicillin
Cloxacillin

4. Tetracyclines Oxytetracycline
Doxycycline

5. Aminoglycosides Gentamicin

Amikacin

6. Macrolides Erythromycin
Roxithromycin
Azithromycin
Clarithromycin

7. Polyenes Nystatin
Amphotericin-B

8. Polypeptide Antibiotics Bacitracin

Colistin
Polymyxin-B

9. Quinolones Ciprofloxacin
Norfloxacin
Ofloxacin
Levofloxacin

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 10. Imidazole derivatives Micanozole
Clotrimazole
Ketoconazole

Fluconazole

II. Based on Mechanism of Action:

1. Cell wall synthesis inhibitors Penicillin

Cephalosporins

Vancomycin

2. Inhibition of protein synthesis Tetracyclines

Macrolides

3. Inhibition of DNA gyrase enzyme Fluroquinolones

4. Interfere with DNA function Rifampin

Metronidazole

5. Interference with DNA synthesis Acyclovir

Zidovudine

Idoxuridine

6. Inhibiting the function of cell membrane Polymyxin

Novobiocin

Q.2. Classify Sulphonamides with examples. Add a note on Sulphonamides. Write the
Pharmacological/ Mechanism of action of sulphonamides.

Ans. Sulphonamides are antimicrobial agents which contain a sulfonamido (SO2 NH2) group.
They are derivatives of the parent compound, para amino benzene sulphonamide.

Classification:

I. SULPHONAMIDES FOR SYSTEMIC INFECTION

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 a. Short acting Sulfadiazne

Sulfadimidine

Sulfamethizole

b. Intermediate acting Sulfamethoxazole

Sulfamoxole

c. Long acting Sulfomethoxine

Sulfodimethoxine

II. SULPHONAMIDES FOR BOWEL Sulfasalazine

DISEASES

Mechanism of Action:

• Sulphonamides have a structural similarity to para amino benzoic acid (PABA)

• Folic acid is required for growth and development of certain bacteria.
• These bacteria take PABA from surrounding media and prepare folic acid.
• Sulphonamides inhibit the enzyme folic acid synthetase, which is useful in the
conversion of PABA to folic acid.
• When sulphonamides are administered, bacteria cannot distinguish or identify
between PABA and para amino benzene sulphonamides, because of their chemical
resemblance.
• They take up sulphonamide in place of PABA and they cannot convert it in to folic
acid.
• So, for lack of folic acid, bacteria die.

Adverse effects:

• Allergic reactions like fever, skin rashes.

• Crystalluria
• Agranulocytosis and thrombocytopenia.

Therapeutic uses:

• Acute bacillary dysentery

• Ulcerative colitis
• Urinary tract infections
• Meningitis

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Q.3. Discuss in detail about β-lactam Antibiotics. Add a note on penicillins or
cephalosporins. Write the mechanism of action of Penicillins or Cephalosporins.

Ans. β-lactam antibiotics are the antibiotics having β-lactam ring.

There are two major groups of β-lactam antibiotics

a. Penicillins
b. Cephalosporins.

Penicillins are the first antibiotic used clinically in 1941.Originally discovered from
penicillium notatum by Alexander Fleming in 1928. Now penicillium chrysogenum is
used.

Classification of penicillins.

I. Natural penicillins Penicillin G (Benzyl penicillin)

Penicillin V(Phenoxy methyl penicillin)

II. Semisynthetic penicillins

1. Acid resistant Potassium phenoxymethyl penicillin

Potassium phenoxyethyl penicillin

2. Penicillinase resistant Methicillin

Cloxacillin

Dicloxacillin

3. Broad spectrum penicillins Amoxicillin

Ampicillin

Mechanism of action:

It is a bactericidal drug. It acts by inhibiting the synthesis of bacterial cell wall. This action is
produced by inhibiting the synthesis of peptidoglycans (which provide stability to cell wall).

Penicillins bind with target proteins in bacterial cell membrane

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 Interfere with the synthesis of peptidoglycans

No synthesis of peptidoglycans

Bacterial cell wall becomes weak, the cell swells and bursts

Bacterial cell dies

Adverse effects:

1. Intolerance which includes allergic and anaphylactic reactions. Allergy may occur in
the form of skin rashes, renal disturbances and anaemia. Anaphylaxis may occur in
the form of cardiovascular collapse, bronchospasm and angiodema.
2. Miscellaneous like nausea and vomiting.

Therapeutic uses:

• Respiratory tract infections (RTI)

• Orodental infections.
• Skin and soft tissue infection (SSTI)
• Gynaecological infections.

Cephalosporins:

Cephalosporins are derived from cephalosporium acremonium. They have a structural

resemblance to 6-APA nucleus of penicillins.

Classification:

1st generation Cephalexin, Cefadroxil, Cefazolin

2nd generation Cefuroxime, Cefoxitin, Cefaclor

3rd generation Cefixime, Cefpodoxime, Ceftriaxone, Cefotaxime

4th generation Cefepime,

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Mechanism of Action: Same as that of Penicillin (Refer mechanism of action of penicillin)

Adverse effects:

• Skin rashes, fever and serum sickness (a hypersensitivity reaction occurring several
days after administration of an anti-serum or certain drug therapy).
• Easinophilia, neutropenia and splenomegaly.
• Azotemia (excess of urea in the blood) and anaphylactic reaction.
• Renal damage.

Therapeutic uses:

• Infections resistant to penicillins.

• Patients allergic to penicillins.
• UTI

Q.4. Add a note on Tetracyclines.

Ans. Tetracyclines are broad spectrum antibiotics. They are effective against gram-positive
organisms, gram negative organisms, actinomyces, and rickettsia and Chlamydia organisms.

Tetracyclines are Bacteriostatic. They act by following mechanism:

• It binds to 30 s ribosomal unit which inhibits protein synthesis.

• Chelation of cations like calcium and magnesium.
• Interference with phosphorylation of glucose.

Adverse effects:

1. Intolerance like skin rashes and photosensitivity.

2. GI disturbances like nausea, vomiting and diarrhoea.
3. Teeth and bones: it interferes with calcification in bones and teeth. Administration
during pregnancy cause deposition of tetracycline in foetal bones and may reduce the
growth of foetus and also produces yellow staining of teeth.
4. Renal disturbances like proteinuria, aminoaciduria and glycosuria.

Therapeutic uses:

• In cholera
• Pneumonia
• Bacillary infections.
• UTI
• Veneral diseases (gonorrhoea, syphyllis)
• Acne vulgaris
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 • In the treatment of dysentery.

Q.5. Classify Anti-Neoplastic (Anti-cancer or Anti-tumour) drugs with examples. Write

the pharmacology of Alkylating agents. Write the pharmacological actions of
cyclophosphamide.

Ans. These are the drugs used in the treatment of cancer.

Classification:

I. ALKYLATING AGENTS

a. Nitrogen Mustards Cyclophosphamide

Chlorambucil

Melphalan

b. Alkyl sulfonates Busulfan

II. ANTIMETABOLITES

a. Folic acid antagonist Methotrexate

b. Purine antagonist 6-mercaptopurine

Azathioprine

c. Pyrimidine antagonist 5-fluorouracil

Fluoro-uracil

III. RADIOACTIVE ISOTOPES Radioiodine

Radiophosphorous

IV. ANTIBIOTICS Actinomycin-D

Rubidomycin

Mitomycin

V. HORMONES Androgens

Estrogens

Progestins

Corticosteroids

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 VI. MISCELLANEOUS Vincristine, Vinblastine

Mechanism of action of Alkylating agents / Cyclophosphamide.

They act by the mechanism known as alkylation; in which negatively charged components of
cell (Nucleoprotein) combine with the positively charged components of alkylating agents
(e.g. methyl, ethyl i.e. alkyl radicals). This results in loss of cell proliferation and cell death.

Pharmacological actions:

1. Cytotoxic effect: These drugs affect rapidly growing cells and produce the following
effects:
a. Bone marrow depression leading to leucopenia, anaemia and thrombocytopenia.
b. Damage of intestinal mucosa leading to ulceration, perforation and haemorrhage.
c. Damage of hair follicles causing alopecia.
d. Damage of gonads causing inhibition of spermatogenesis in males and
amenorrhoea (absence or stoppage of menstruation) in females.
2. Emetic effect: The alkylating agents produce nausea and vomiting.
3. Immunosuppressant effect: They suppress the immune response by blocking antibody
production.
4. Radiomimetic effect: Similar to radioactive isotopes, the alkylating agents produce
the following effects:
a. Intestinal ulceration and bone marrow depression
b. Foetal abnormalities and genetic changes.
c. Inhibition of antibody production.
So, the alkylating agents are also called as ‘radiomimetic agents.’

Therapeutic uses:

1. Hodgkin’s disease (a disease characterised by painless enlargement of lymph nodes

beginning in the cervical region with the enlargement of liver and spleen).
2. Chronic leukaemia.
3. Bronchogenic (originating in the bronchus) and ovarian carcinoma.

Q.6.Add a note on Antimetabolites / Write the mechanism of action of Methotrexate.

Ans. Antimetabolites

A metabolite is a chemical substance which takes part in cellular metabolic reactions. An

antimetabolite blocks a metabolic reaction, due to its structural similarity to the metabolite.

Methotrexate: It is a folic acid antagonist.

Mechanism of action:

In a cell, folic acid is converted to tetrahydrofolic acid (THF) by the enzyme folate reductase.

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Methotrexate competes with folic acid for the enzyme, folate reductase.

So, folic acid is not converted to THF. In the absence of THF, synthesis of DNA does not
occur. So cell division and growth is inhibited.

Therapeutic uses:

• Acute lymphatic leukaemia

• Acute myeloid leukaemia
• Choriocarcinoma (A highly malignant tumour arising from the chorionic cells). The
outermost membrane of the foetus.
• Breast cancer

Q.7. Mention the drugs used in the treatment of Tuberculosis / Classify Anti-tubercular
drugs with examples. Write the mechanism of action of INH and Rifampicin. Add a
note on multi drug therapy.

Ans. Tuberculosis is an infectious disease caused by bacillus Mycobacterium tuberculosis. It

is generally transmitted from one person to another by inhalation; by droplet infection usually
affect the lungs.

Anti-tubercular drugs are the agents which are used to treat tuberculosis.

Classification:

Anti TB drugs are classified on the basis of efficacy, activity and risk of adverse effects. They
are of two types:

I. First line Anti TB drugs: These drugs are more active, more efficacious and have
less adverse effects. Examples:
• Ethambutol
• Isoniazid
• Pyrazinamide
• Rifampicin
• Streptomycin
II. Second line Anti TB drugs: These drugs are less active, low effective and have
more adverse effects. The second line drugs are only used to treat disease that is
resistant to first line therapy or Multi Drug Resistant (MDR) tuberculosis.
Examples:
• Amikacin
• Kanamicin
• Ciprofloxacin
• Levofloxacin
• Moxifloxacin
• Clofazimine
• Cycloserine
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Isoniazid (Isonicotinic acid hydrazide, INH): It is the most effective drug. It is bactericidal
and can kill the intracellular bacteria.

Mechanism of Action: It inhibits the synthesis of mycolic acid which is the essential component
of mycobacterium cell wall.

Adverse effects:

• Intolerance like fever, malaise or jaundice

• Peripheral neuritis due to pyridoxine deficiency is an important toxicity
• CNS effects like convulsions
• Epigastric distress, dryness of mouth and urinary retention.

Rifampicin: It is a bactericidal for mycobacteria. It is obtained from Streptomyces

mediterranei.

MOA: It inhibits DNA dependent RNA polymerase which is responsible for RNA synthesis.
So, Rifampicin inhibits RNA synthesis.

Adverse effects:

• Nephritis
• Orange colourization of urine, sweat and tears
• Thrombocytopenia, leucopenia
• Nausea, vomiting

Multiple-drug therapy

It means taking several different drugs at the same time. This is the first choice of treatment for
active TB. The standard treatment is to take isoniazid, rifampicin and pyrizanamide for 2
months. Treatment is then continued for at least 4 months with fewer medicines. Treatment
with several medicines makes it more likely that all TB-causing bacteria will be killed.

The standard treatment for TB using a combination of four medicines is very effective. It takes
at least 6 months of treatment for a cure. It could take longer if doses are missed. It can also
take longer if disease does not respond well to the medicine.

Q.8. Classify Anti-emetics. Write the pharmacology of metoclopramide / prokinetics.

Ans. Anti-emetics are the agents which are used to control vomiting.

Classification:

1. Anticholinergics Hyoscine

Dicyclomine

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 2. Antihistamines Cyclizine

Meclizine

3. Prokinetics Metaclopramide

Domperidone

4. 5-HT3 antagonist Granisetron

Ondensetron

5. Neuroleptics Chlorpromazine

Perchlorperazine

Prokinetics: These are the drugs which promote gastrointestinal motility and quicken gastric
emptying.

Metaclopramide: It is chemically related to procainamide. The anti-emetic action is due to

both central and peripheral effects. The central action is due to blockade of dopaminergic
receptors. The peripheral action is due to increased gastric emptying and increased peristaltic
movement.

Uses: In post-operative vomiting, vomiting during induction of anaesthesia and in hiccough.

Q.9.Classify Anti-histamines with example and add a note on triple response of histamine

Ans. Anti-histamines are the drugs which antagonize the actions of histamine liberated in the
body.

Classification:

1. First generation or highly sedative Diphenhydramine HCL

Chlorpheniramine maleate

2. Second generation or moderately Cetrizine

sedative
Loratidine

Pheniramine

Astemizole

3. Third generation or Non-sedative Levocetrizine

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Triple response of Histamines:

On intradermal injection, histamine produces a ‘triple response’ which consists of:

i) Local redness (flush) due to dilatation of capillaries and venoules.

ii) Local arteriolar dilatation (flare)
iii) Local oedema (wheal) due to escape of fluid from the capillaries.

Q.10. Add a note on Cotrimoxazole.

Ans. Cotrimoxazole:

It is a combination of Sulphamethoxazole with Trimethoprim.

This combination has a synergistic action, Sulphamethoxazole 400 mg + Trimethoprim 80 mg

is combined together which act against sulphonamide resistant strains.

Mechanism of Action of Sulphamethoxazole:

• Sulphonamides have a structural similarity to para amino benzoic acid (PABA)

• Folic acid is required for growth and development of certain bacteria.
• These bacteria take PABA from surrounding media and prepare folic acid.
• Sulphonamides inhibit the enzyme folic acid synthetase, which is useful in the
conversion of PABA to folic acid.
• When sulphonamides are administered, bacteria cannot distinguish or identify between
PABA and para amino benzene sulphonamides, because of their chemical resemblance.
• They take up sulphonamide in place of PABA and they cannot convert it in to folic
acid.
• So, for lack of folic acid, bacteria die.

Mechanism of action of Trimethoprim:

In a cell, folic acid is converted to tetra hydro folic acid (THF) by the enzyme folate reductase.
Trimethoprim competes with folic acid for the enzyme folate reductase.

So, folic acid is not converted to THF. In the absence of THF, synthesis of DNA does not occur.
So, cell division and cell growth is inhibited.

Adverse effects:

• Nausea, vomiting and skin rashes.

• Anaemia, leucopenia and thrombocytopenia.
• Glossitis and Crystalluria.

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Therapeutic uses:

• Urinary tract infection.

• Respiratory infections, gonorrhoea and typhoid fever.

Q.11.Mention the names of two drugs used in the treatment of each of the following
diseases.

DISEASES DRUGS

GOUT PROBENECID

ASPIRIN

EPILEPSY / CONVULSIONS PHENYTOIN

SODIUM VALPROATE

CARBAMAZEPINE

AMOEBIASIS / AMOEBIC DYSENTRY METRONIDAZOLE

TINIDAZOLE

DILOXANIDE FUROATE

HELMINTHIASIS ALBENDAZOLE

MEBENDAZOLE

PIPERAZINE CITRATE

MALARIA CHLOROQUINE

QUININE

MEPACRYINE

DIABETES / HYPOGLYCAEMIA METFORMIN

PHENFORMIN

GLIBENCLAMIDE

BRONCHIAL ASTHMA SALBUTAMOL

AMINOPHYLLINE

IPRATROPIUM BROMIDE

BLOOD SUBSTITUTES OXYGLOBIN

DEXTRAN HAEMOGLOBIN

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PLASMA EXPANDERS DEXTRAN

ALBUMIN HUMAN

PEPTIC ULCER /ANTI-ULCER / PROTON OMEPRAZOLE

PUMP INHIBITORS
PANTAPRAZOLE

RABEPRAZOLE

PARKINSONISM LEVODOPA

CARBIDOPA

HYPERTHYROIDISM / ANTI-THYROID PROPYL THIO URACIL

DRUGS
METHIMAZOLE

SYPHILLIS PENICILLIN

DOXYCYCLINE

CEFTRIAXONE

AZITHROMYCIN

AIDS / HIV • ZIDOVUDINE

• STAVUDINE
• ABACAVIR
HYPERLIPEDEMIA • ATORVASTATIN
ANTIHYPERLIPEDEMIC • ROSUVASTATIN
• CLOFIBRATE
• FENOFIBRATE
DIURETICS • ACETAZOLAMIDE
• METHAZOLAMIDE
CARBONIC ANHYDRASE INHIBITORS
• DICHLORPHENAMIDE
DEPRESSION / ANTI DEPRESSANTS ISOCARBOXAZID
PHENELZINE
MONOAMINE OXIDASE INHIBITORS
SELEGILINE
(MAO INHIBITORS)

ANTI-HYPERTENSIVES CAPTOPRIL
ENALAPRIL
ACE INHIBITORS
RAMIPRIL
URINARY TRACT INFECTION NORFLOXACIN
LEVOFLOXACIN
SPARFLOXACIN
MYASTHENIA GRAVIS PYRIDOSTIGMINE
PREDNISOLONE

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 LEPROSY / ANTI LEPROTIC DAPSONE

Q.12. Give the examples of drugs causing following toxicity.

ADVERSE EFFECTS / TOXICITY DRUGS

CRYSTALURIA SULPHONAMIDES

PERIPHRAL NEUROPATHY THALIDOMIDE

HYPOTHYROIDISM

BONE MARROW DEPRESSION ANTI CANCER DRUGS, INDOMETHACIN

OTOTOXICITY AMINOGLYCOSIDE

ANTIBIOTICS (KANAMYCIN,STREPTOMYCIN)

CROSS RESISTANCE MELPHALAN,

ADRIAMYCIN, ACTINOMYCIN

CINCHONISM QUININE / QUINIDINE

NEPHROTOXICITY PENICILLINS, THIAZIDE DIURETICS, NSAIDS

HYPERACIDITY AND GASTRIC ULCERS NSAIDS , ASPIRIN

GREY BABY SYNDROME CHLORAMPHENICOL

Drugs acting on ANS

The autonomic nervous system (vegetative, visceral or involuntary nervous system) is

widely distributed throughout the body.

It controls tissues (e.g. smooth muscles, heart and glands) which are not under our
control. It consists of two divisions:

1. The sympathetic
2. The parasympathetic

The sympathetic and parasympathetic mostly exhibit mutual antagonism.

The parasympathetic is mainly concerned with the vegetative functions e.g. motility and
secretions of gastrointestinal tract. This system is essential for the normal existence of the
organism.

The sympathetic is concerned with preparing the organism for emergency (fight or flight).
Unlike parasympathetic, the sympathetic is not essential for normal existence.

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 Both the sympathetic and parasympathetic essentially consists of:

o A preganglionic nerve
o A ganglion (a collection of nerve cells)
o A postganglionic nerve
o An effector organ

1. Parasympathetic system:
• The transmitter in preganglionic parasympathetic nerve is acetylcholine (Ach)
which is liberated at the ganglion.
• Again, acetylcholine is the transmitter in postganglionic parasympathetic nerve. It
is liberated at the postganglionic parasympathetic nerve ending.

2. Sympathetic system:
• Similar to preganglionic parasympathetic nerves, acetylcholine is the transmitter
in preganglionic sympathetic nerves also.
• But in postganglionic sympathetic nerves, nor-adrenaline is the transmitter. It is
liberated at the postganglionic nerve ending.

Cholinergic receptors:

The receptors for acetylcholine are classified as:

i) Muscarinic receptors
ii) Nicotinic receptors

Muscarinic receptors: They are present at postganglionic parasympathetic nerve ending.

There are 3 subtypes of muscarinic receptors:

Receptors Location Function Blockers

M1 Gastric glands, CNS Gastric acid secretion Pirenzepine and

and GI motility. telenzepine

M2 Heart They produce a methoctramine

decrease in the rate
and force of heart

M3 Smooth muscles and Contraction of smooth Darifenacin

exocrine glands muscles, secretions of
exocrine glands.

Nicotinic receptors: They are:

Receptors Location Function Blockers

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 Nn Both sympathetic Stimulation of both Pentamethonium or
and parasympathetic these ganglia hexamethonium
ganglia

Nm Neuromuscular Contraction of d-tubocurarine

junction skeletal muscle

Cholinergic drugs (parasympathomimetics)

These are drugs which produce actions similar to that of Ach, either by directly interacting
with cholinergic receptors or by increasing availability of Ach at these sites.

Classification:

1. Esters of choline Acetylcholine

Methacholine

Carbachol

2. Cholinomimetic alkaloids Pilocarpine

Arecholine

Muscarine

3. Anticholinestrases

a. Reversible Physostigmine

Neostigmine

Pyridostigmine

b. Irreversible
Parathion

Malathion

Pharmacology of Acetylcholine:

The actions of Ach are generally classified in to two types:

1. Muscarinic actions:
a) Heart: It decreases heart rate and may produce cardiac arrest.
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 b) Blood vessels: It dilates a variety of blood vessels (like those of skin, mucous
membrane and coronary arteries) and produces a fall in blood pressure.
c) Smooth muscles: It produces contraction of smooth muscles like those of g.i.t,
bronchi, urinary bladder and uterus.
d) Secretions: It increases gastric, intestinal, pancreatic, bronchial, lachrymal and
salivary secretions.
e) Eye: Instillation in to the eye has no effect. But injection of Ach in the carotid
artery produces
▪ Miosis (constriction of the pupil)
▪ Decrease in intraocular tension
▪ Spasm of accommodation (vision is fixed for short distance)
2. Nicotinic actions:
a) Stimulation of sympathetic and parasympathetic ganglia
b) Contraction of skeletal muscle.

Uses: Acetylcholine is not used for any therapeutic effect. It is used only for experimental
purposes.

Cholinergic blocking drugs (Anticholinergics, parasympatholytics)

These are the drugs which bind with the cholinergic receptors and blocks the actions of
Ach. These drugs in therapeutic doses block only muscarinic actions of acetylcholine. So,
they are also called as antimuscarinic drugs.

Classification:

1. Natural alkaloids Atropine

Scopolamine (Hyoscine)

2. Semi-synthetic derivatives Homatropine

Ipratropium bromide

3. Synthetic derivatives Tropicamide

Cyclopentolate

Dicyclomine

Pharmacology of anticholinergics (Atropine):

1. Smooth muscles:
i) Gastrointestinal tract: Atropine reduces tone and motility of GIT.

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 ii) Urinary tract: Atropine reduces normal as well as drug induced ureteral
peristalsis. It reduces tone of bladder muscles and tend to produce urinary
retention.
iii) Bronchi: It relaxes the bronchial smooth muscles.
iv) Biliary tract: It produces an anti-spasmodic action.
2. Secretions: Atropine decreases all secretions under cholinergic influences. It
decreases secretions of nose, pharynx and bronchi and also salivary secretion.
3. Eye: Atropine produces:
▪ Mydriasis (dilatation of pupil)
▪ Cycloplegia (eye is fixed for distant vision)
▪ Increase in intraocular tension.
4. Cardiovascular system:
▪ The effect on heart depends on dose. Smaller doses produces central slowing.
Larger doses produce acceleration due to peripheral vagal paralysis.
▪ Atropine by itself has no effect on blood vessels or blood pressure. But it
counters vasodilatation and hypotension produced by parasympathomimetic
agents.
5. C.N.S: Therapeutic dose has no effect with toxic dose, it produces central excitation.

Adverse effects:

• Dry mouth, difficulty in speech and swallowing

• Dry skin and increase in body temperature
• Urinary urgency and difficulty in Micturition
• Excitement, restlessness and motor in-coordination.

Uses:

• In peptic ulcer to decrease the secretion of acid

• In colic of the g.i.t
• As a biliary antispasmodic
• In organophosphorous poisoning
• As pre-anaesthetic medication.

Adrenergic system

Adrenergic receptors: The receptors present at the postganglionic sympathetic nerve ending
are called ‘adrenergic receptors’. The adrenergic receptors are classified as:

1. Alpha receptors, the action on which is excitatory (except intestine)

2. Beta receptors, the action on which is inhibitory (except heart).

Alpha receptors are further classified as:

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 o Alpha1 receptors which are present in vascular smooth muscles. The effect occurs as
constriction.
o Alpha2 receptors which are present in presynaptic adrenergic nerve terminals. They
decrease the release of noradrenaline from adrenergic nerve endings.

Beta receptors are further classified in to:

o Beta1 receptors which are present in heart. The effect occurs as an increase in force
and rate of contraction.
o Beta2 receptors which are present in bronchi. The effect occurs as relaxation.

Noradrenaline acts only on alpha receptors.

Isoprenaline acts only on beta receptors.

Adrenaline acts on both alpha and beta receptors.

Adrenergic drugs (sympathomimetics)

These are the agents which produce an effect similar to the stimulation of postganglionic
sympathetic nerves. Most of these drugs have an intact or partially substituted amino group.
So, they are also called as sympathomimetic amines.

Classification: Based on the presence or absence of catechol nucleus (ortho dihydroxy

benzene), the adrenergic drugs are classified as:

1. Catecholamines Adrenaline

Noradrenaline

Dopamine

Isoprenaline

2. Non-catecholamines Ephedrine

Amphetamine

Methyl amphetamine

Phenylephrine

Catecholamines : are compounds which contain catechol nucleus. This group includes:

➢ Adrenaline, the hormone of adrenal medulla

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 ➢ Noradrenaline, the sympathetic neurohumoural transmitter
➢ Dopamine, a neurohumoral transmitter in CNS
➢ Isoprenaline, a synthetic compound.

Adrenaline (Epinephrine):

It is synthesized in the adrenal medulla. It is stored within the intracellular particles or

granules of adrenal medulla.

Pharmacological actions:

1. Heart: Adrenaline acts on beta receptors of heart and produces an increase in

i) Rate of contraction (positive ionotropic effect)
ii) Force of contraction (positive chronotropic effect)
iii) Cardiac output.
2. Blood vessels: Adrenaline constricts the blood vessels of skin and mucous membrane
(due to its effect on alpha receptors). But it dilates the blood vessels of skeletal
muscles (due to its effect on beta receptors).
3. Blood pressure: On intravenous administration, adrenaline produces biphasic effect
on BP:
• First, there is an initial rise in BP due to stimulation of alpha receptors
(vasoconstriction)
• Later, there is a fall in BP due to an effect on beta receptors (vasodilatation)
• If adrenaline is injected after the administration of ergotoxine (an alpha
receptor blocking agent), it produces only a fall in BP. This phenomenon is
called as Dale’s vasomotor reversal.
4. Smooth muscles:
i. Gastrointestinal tract: Adrenaline relaxes the smooth muscles of intestine and
decreases the motility.
ii. Bronchi: Adrenaline relaxes the bronchial smooth muscle and relieves the
spasm.
iii. Uterus: The effect depends on species and presence or absence of pregnancy.
But rat uterus is relaxed irrespective of these factors.
iv. Spleen: The splenic capsule is contracted releasing more erythrocytes into
circulation.
5. Eye: Adrenaline produces mydriasis and reduction in intraocular tension.
6. Metabolic effect: Adrenaline increases blood sugar level. It also increases the free
fatty acid level of plasma.

Adverse effects:

• Tachycardia (increased heart rate), palpitation

• Dyspnea and severe headache.
• Severe hypertension and rapid collapse
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 • Pupil dilatation.

Therapeutic uses:

a. Emergency uses:
o In the syncopal attacks of Stokes-Adams syndrome
o For resuscitation of failing heart
o In allergic disorders.
o As a bronchodilator, in bronchial asthma.
b. Non-emergency uses:
o To prolong the effects of local anaesthetics
o To control haemorrhage by producing vasoconstriction.

Differences between adrenaline and nor-adrenaline:

Adrenaline Nor-adrenaline

It acts on both alpha and beta receptors. It acts only on alpha receptors.

It relaxes the bronchial smooth muscle. It has no bronchodilator effect.

On heart it has positive ionotropic and It does not have cardiac effect.
positive chronotropic effect.

It has metabolic effects like It does not have any metabolic effects.
hyperglycaemia.

Adrenergic blocking drugs (sympathetic blocking agents, sympatholytics)

These are the drugs which antagonize the receptor action of adrenaline and related drugs.

Classification:

I. Alpha adrenergic blocking agents:

Non selective α1 and α2 blockers Phenoxybenzamine

Tolazolanine

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 Phentolamine

Ergotamine

Ergotoxine

α1 selective Prazocin

Tamsulosin

α2 selective Yohombine

II. Beta adrenergic blocking agents:

Non selective β1 and β2 blockers Propranolol

Timolol

Sotolol

Nodolol

Selective β1 (Cardioselective) Atenolol

Metaprolol

Acebutol

Selective β2 Butoxamine

Pharmacology of β blockers:

1. Heart: Propranolol decreases heart rate, force of contraction and cardiac output.
2. Blood pressure: They reduce blood pressure by acting on the heart and decreasing
cardiac output.
3. Bronchi: They increase bronchial resistance by blocking β2 receptors.
4. CNS: β blockers like propranolol have sedative and anticonvulsant effects.
5. Local anaesthetic: propranolol is a potent local anaesthetic as lidocaine, but is not
clinically used for this purpose because of its irritant property.
6. Metabolism: It blocks adrenergically induced lipolysis and glycogenolysis. It also
blocks the free fatty acid level of plasma produced by adrenaline.
7. Eye: On instillation in to eye they produces a decrease in intraocular pressure.

Adverse effects:

• Sudden hypotension

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 • Bradycardia
• Allergic reactions
• Nausea, vomiting, constipation and bronchospasm.

Therapeutic uses:

• Angina pectoris
• Cardiac arrhythmias
• Myocardial infarction
• Hypertension

Drugs acting on autonomic ganglia

Drugs acting on autonomic ganglia can be either:

a) Ganglionic stimulants or
b) Ganglionic blocker

Ganglionic stimulants: The agents which stimulate the ganglia are known as ganglionic
stimulants.

e.g. nicotine, lobeline etc.

Pharmacological actions of ganglionic stimulants:

i) Heart: They produces Bradycardia

ii) Eye: They produces miosis
iii) Intestine: They increases motility therefore diarrohea
iv) Glands: They increase glandular secretion.

Ganglionic blockers: These are the agents which block transmission in both sympathetic and
parasympathetic ganglia.

e.g. Pentamethonium, Mecamylamine, Trimethaphan etc.

Pharmacological actions of ganglionic blockers:

i) Heart: They produces tachycardia.

ii) Eye: They produces mydriasis
iii) Intestine: They decreases motility therefore constipation.
iv) Glands: They decrease glandular secretion.

Neuromuscular Blocking Agents

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 These are the agents which produce relaxation of skeletal muscles by inhibiting the
transmission of nerve impulse at neuromuscular junction.

Classification:

1. Competitive blockers d-tubocurarine

Pancuronium

2. Non-competitive blockers Succinylcholine

Decamethonium

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