B Pharmacy 5th Semester Pharmacology 1 Important Question Answer

B.Pharmacy 5th Semester Pharmacology Important Question Answer 

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Pharmacology 1 Important Question Answer  

Pharmacology Very Short Question Answers {2-Marks}  

1. Define inotropic agents with suitable example. 
Inotropic agents are drugs that influence the strength or force of heart muscle contraction. 

• Positive inotropes increase myocardial contractility (e.g., Digoxin). 

• Negative inotropes decrease myocardial contractility (e.g., Propranolol). 

 

2. Write mechanism of action and uses of statins. 
MOA: Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis. 
Uses: To lower LDL cholesterol and prevent cardiovascular diseases like myocardial infarction and stroke. 

 

3. Give example and uses of plasma volume expanders. 
Example: Dextran, Hetastarch. 
Uses: Treatment of hypovolemia, burns, hemorrhagic shock, and as adjunct in plasma replacement. 

 

4. Write mechanism of action and uses of streptokinase. 
MOA: Streptokinase forms a complex with plasminogen to convert it to plasmin, which degrades fibrin clots. 
Uses: Acute myocardial infarction, pulmonary embolism, and deep vein thrombosis. 

 

5. Write a short note on 5-HT antagonists. 
5-HT antagonists block serotonin (5-HT) receptors. 

• Examples: Ondansetron (5-HT₃ antagonist) used for nausea and vomiting; Cyproheptadine (5-HT₂ antagonist) used for allergy and serotonin syndrome. 

 

6. Write uses of prostaglandin analogues. 
Prostaglandin analogues are used in: 

• Glaucoma (Latanoprost), 

• Induction of labor (Misoprostol), 

• Gastric ulcer prevention, 

• Abortion (Carboprost). 

 

7. Enlist hormones regulating plasma calcium level. 

• Parathyroid hormone (PTH) 

• Calcitonin 

• Vitamin D (Calcitriol) 

 

8. How do thyroid hormones play a crucial role in metabolism? 
Thyroid hormones (T₃, T₄) increase basal metabolic rate, stimulate protein synthesis, regulate carbohydrate and lipid metabolism, and are essential for growth and development. 

 

9. What do you mean by Tocolytics? 
Tocolytics are drugs used to inhibit uterine contractions and delay premature labor. 
Example: Nifedipine, Terbutaline. 

 

10. Highlight the advantages of multiple point bioassay. 

• More accurate and reliable 

• Reduces biological variation 

• Requires fewer test animals 

• Graphical comparison with standard increases precision. 

 

11. Enlist antihypertensive drugs contraindicated during pregnancy. 

• ACE inhibitors (e.g., Enalapril) 

• ARBs (e.g., Losartan) 

• Direct renin inhibitors (e.g., Aliskiren) 

 

12. Define Haematinics with suitable example. 
Haematinics are agents used to treat anemia by increasing hemoglobin. 
Example: Iron, Folic acid, Vitamin B₁₂. 

 

13. Write about therapeutic indications for Atorvastatin. 
Used for: 

• Hypercholesterolemia 

• Prevention of cardiovascular events 

• Familial hyperlipidemia 

 

14. Define Plasma volume expanders with suitable examples. 
They are fluids used to restore blood volume. 
Examples: Dextran, Gelatin, Hetastarch, Human Albumin. 

 

15. Define Anabolic Steroids. 
Synthetic derivatives of testosterone that promote muscle growth and increase protein synthesis. 
Example: Nandrolone. 

 

16. Define Bioassay and enlist its limitations. 
Bioassay is the evaluation of drug potency using living systems. 
Limitations: Time-consuming, expensive, requires expertise, variable results. 

 

17. Write functions of Glucagon. 

• Increases blood glucose by glycogenolysis and gluconeogenesis 

• Stimulates lipolysis 

• Opposes insulin action 

 

18. Write physiological role of Substance P. 

• Acts as a neurotransmitter for pain 

• Causes vasodilation 

• Involved in inflammatory responses 

 

19. Write pharmacotherapy for thyroid storm. 

• Propylthiouracil or Methimazole (inhibit thyroid hormone synthesis) 

• Beta-blockers (e.g., Propranolol) 

• Glucocorticoids, Iodine, and supportive care. 

 

20. Define Gout and enlist at least two drugs for its management. 
Gout is a disorder of uric acid metabolism causing joint inflammation. 
Drugs: Colchicine, Allopurinol, NSAIDs. 

 

21. Discuss Starling’s Law. 
Starling’s law states that the force of heart contraction is directly proportional to the initial length of cardiac muscle fibers (end-diastolic volume). 

 

22. Enlist drugs acting on Renin-angiotensin system. 

• ACE inhibitors (Enalapril) 

• ARBs (Losartan) 

• Renin inhibitors (Aliskiren) 

 

23. Aspirin can be used as antiplatelet drug. Justify. 
Aspirin irreversibly inhibits COX-1, reducing thromboxane A₂ synthesis, thereby preventing platelet aggregation. 

 

24. Compare spironolactone and amiloride. 

Feature	Spironolactone	Amiloride
Class	Aldosterone antagonist	Sodium channel blocker
K⁺ sparing?	Yes	Yes
Use	Heart failure, hyperaldosteronism	Hypertension, edema

 

25. Define autacoids and classify them. 
Autacoids are locally acting biological factors. 
Classification: 

• Biogenic amines: Histamine, serotonin 

• Eicosanoids: Prostaglandins, leukotrienes 

• Peptides: Bradykinin, angiotensin 

 

26. How colchicine is effective in improving gout? 
Colchicine inhibits microtubule polymerization, reducing neutrophil migration and inflammation in gout. 

 

27. Classify hormones secreted from pituitary glands. 

• Anterior Pituitary: GH, ACTH, TSH, FSH, LH, Prolactin 

• Posterior Pituitary: ADH, Oxytocin 

 

28. Explain the hormonal control of insulin release. 

• Increased glucose → insulin release 

• Incretins (GLP-1, GIP) enhance secretion 

• Sympathetic stimulation inhibits; parasympathetic enhances insulin release. 

 

29. What do you understand by anabolic steroids? Give examples. 
Synthetic androgenic hormones that promote muscle growth. 
Examples: Nandrolone, Stanozolol. 

 

30. Summarize applications of bioassay. 

• Standardization of drugs 

• Quality control 

• Determination of potency 

• Evaluation of pharmacological action 

 

31. Define arrhythmia. What do you understand by re-entry? 
Arrhythmia is an abnormal heart rhythm. 
Re-entry refers to re-excitation of the same area of cardiac tissue, leading to arrhythmia. 

 

32. Write the mechanism of action of nitrates. 
Nitrates release nitric oxide, which activates guanylyl cyclase, increasing cGMP, causing vasodilation and reduced myocardial oxygen demand. 

 

33. Low molecular weight heparin is better than high molecular weight heparin. Justify. 
LMWH has better bioavailability, longer half-life, predictable response, and less risk of thrombocytopenia. 

 

34. How aspirin acts as antiplatelet? 
Aspirin irreversibly inhibits COX-1, preventing formation of thromboxane A₂, thus inhibiting platelet aggregation. 

 

35. Summarize the physiological and pathological role of prostaglandins on uterus and cardiovascular system. 

• Uterus: Stimulate contractions (labor, abortion) 

• CVS: Vasodilation (PGE₂), platelet aggregation modulation, and blood pressure regulation. 

 

36. Illustrate the mode of action of allopurinol as anti-gout drug. 
Allopurinol inhibits xanthine oxidase, reducing uric acid synthesis, thus lowering serum urate levels in gout. 

 

37. Enlist various endocrine glands and hormones secreted by each of them. 

• Pituitary: GH, ACTH 

• Thyroid: T₃, T₄, Calcitonin 

• Pancreas: Insulin, Glucagon 

• Adrenal: Cortisol, Adrenaline 

• Ovaries/Testes: Estrogen, Testosterone 

 

38. Explain the regulation of insulin secretion. 

• Triggered by high glucose 

• Enhanced by incretins (GLP-1) 

• Modulated by neural (vagal stimulation) and hormonal inputs 

 

39. Define Bioassay. Classify various types of bioassay. 
Bioassay is determination of drug potency using biological systems. 
Types: 

• End-point assay 

• Graded response assay 

• Quantal assay 

 

40. What are anabolic steroids? 
Synthetic hormones mimicking testosterone, used to promote protein synthesis and muscle growth. 
Examples: Nandrolone, Methandrostenolone. 

 

Pharmacology Short Question Answers {5-Marks} 

 

1. Classify anti-arrhythmic drugs and discuss the role of digitalis in arrhythmia. 

Classification of Anti-arrhythmic Drugs (Vaughan Williams classification): 

• Class I (Na⁺ channel blockers): 

• IA: Quinidine, Procainamide 

• IB: Lidocaine, Mexiletine 

• IC: Flecainide 

• Class II (β-blockers): Propranolol, Esmolol 

• Class III (K⁺ channel blockers): Amiodarone, Sotalol 

• Class IV (Ca²⁺ channel blockers): Verapamil, Diltiazem 

• Others: Adenosine, Digoxin, Magnesium sulfate 

Role of Digitalis (Digoxin) in Arrhythmia: 
Digoxin is a cardiac glycoside primarily used in the treatment of atrial arrhythmias such as atrial fibrillation and atrial flutter, especially in patients with concomitant heart failure. 

Mechanism of Action: 

• Digoxin inhibits the Na⁺/K⁺-ATPase pump → increases intracellular Na⁺ → decreases activity of Na⁺/Ca²⁺ exchanger → increased intracellular Ca²⁺ → enhances myocardial contractility (positive inotropy). 

• It increases vagal tone, which slows down the conduction through the AV node, making it useful in controlling ventricular rate in atrial arrhythmias. 

Therapeutic Use: 

• Atrial fibrillation 

• Atrial flutter 

• Congestive heart failure (as a secondary benefit) 

Adverse Effects: 

• Bradycardia 

• AV block 

• Ventricular arrhythmias 

• Digoxin toxicity (nausea, vision disturbances, arrhythmias) 

Precautions: 

• Requires monitoring of electrolyte levels, especially potassium 

• Narrow therapeutic index 

Conclusion: 
Digitalis remains valuable in the control of supraventricular arrhythmias, particularly in heart failure patients, due to its dual action on contractility and vagal stimulation. 

2. Classify anti-coagulants. Discuss mechanism of action and uses of heparin. 

Classification of Anticoagulants: 

1. Parenteral anticoagulants 

1. Heparin (Unfractionated) 

2. Low molecular weight heparin (Enoxaparin, Dalteparin) 

3. Direct thrombin inhibitors (Argatroban, Bivalirudin) 

2. Oral anticoagulants 

1. Vitamin K antagonists (Warfarin, Acenocoumarol) 

2. Direct oral anticoagulants (DOACs): 

1. Direct thrombin inhibitors: Dabigatran 

2. Factor Xa inhibitors: Rivaroxaban, Apixaban 

3. Fibrinolytics/Thrombolytics 

1. Streptokinase, Urokinase, Alteplase 

4. Antiplatelet agents 

1. Aspirin, Clopidogrel, Ticagrelor 

 

Mechanism of Action of Heparin: 
Heparin is an indirect anticoagulant that acts by activating antithrombin III, a natural inhibitor of several clotting factors. 

• The heparin–antithrombin III complex inactivates thrombin (factor IIa) and factor Xa, preventing the conversion of fibrinogen to fibrin, which is essential for clot formation. 

• Low molecular weight heparins (LMWHs) primarily inhibit factor Xa more than thrombin. 

 

Uses of Heparin: 

• Treatment and prevention of deep vein thrombosis (DVT) 

• Pulmonary embolism 

• Unstable angina, myocardial infarction 

• Used during cardiopulmonary bypass and dialysis 

• To prevent clotting in catheters and blood samples 

 

Adverse Effects: 

• Bleeding 

• Heparin-induced thrombocytopenia (HIT) 

• Osteoporosis (long-term use) 

• Hypersensitivity reactions 

 

Conclusion: 
Heparin is a fast-acting anticoagulant crucial for the acute management of thromboembolic disorders and is carefully monitored due to its potential bleeding risk. 

3. Classify diuretics and describe pharmacology of loop diuretics. 

Classification of Diuretics: 

1. High ceiling (loop) diuretics: Furosemide, Torsemide, Bumetanide 

2. Thiazide diuretics: Hydrochlorothiazide, Chlorthalidone 

3. Potassium-sparing diuretics: 

1. Aldosterone antagonists: Spironolactone, Eplerenone 

2. ENaC blockers: Amiloride, Triamterene 

4. Carbonic anhydrase inhibitors: Acetazolamide 

5. Osmotic diuretics: Mannitol 

6. ADH antagonists: Conivaptan, Tolvaptan 

 

Pharmacology of Loop Diuretics: 

Mechanism of Action: 
Loop diuretics act on the thick ascending limb of the loop of Henle. 

• They inhibit the Na⁺-K⁺-2Cl⁻ symporter, which blocks the reabsorption of Na⁺, Cl⁻, and K⁺. 

• This leads to increased excretion of Na⁺, K⁺, Cl⁻, and water, along with Ca²⁺ and Mg²⁺, making them powerful diuretics. 

 

Pharmacokinetics: 

• Administered orally or IV 

• Rapid onset (especially IV) 

• Short duration of action 

• Metabolized in liver, excreted by kidneys 

 

Therapeutic Uses: 

• Acute pulmonary edema 

• Congestive heart failure (CHF) 

• Hypertension (in patients with renal impairment) 

• Edema due to liver cirrhosis or nephrotic syndrome 

• Hypercalcemia (promotes calcium excretion) 

 

Adverse Effects: 

• Hypokalemia, hyponatremia 

• Hypocalcemia, hypomagnesemia 

• Ototoxicity (hearing loss, tinnitus) 

• Hyperuricemia (may cause gout) 

• Dehydration and hypotension 

 

Conclusion: 
Loop diuretics are the most potent class of diuretics, essential in emergency and volume-overloaded conditions. However, due to significant electrolyte imbalances, monitoring is required during therapy. 

4. Classify H receptor antagonists and give a comparative note on first-generation and second-generation antihistamines. 

Classification of Histamine (H) Receptor Antagonists: 

1. H₁ Receptor Antagonists (Antihistamines): 

1. First-generation: Diphenhydramine, Chlorpheniramine, Hydroxyzine 

2. Second-generation: Loratadine, Cetirizine, Fexofenadine 

2. H₂ Receptor Antagonists: 

1. Ranitidine, Famotidine, Cimetidine 

3. H₃ and H₄ Antagonists: 

1. Still under research and not widely used clinically. 

 

Comparison of First-Generation and Second-Generation H₁ Antihistamines: 

Feature	First-Generation	Second-Generation
Lipophilicity	High	Low
Blood-Brain Barrier	Cross easily	Poor penetration
Sedation	Causes sedation	Non-sedating or mild
Duration of action	Shorter (4–6 hours)	Longer (12–24 hours)
Anticholinergic action	Present	Minimal or absent
Use in allergy	Effective in acute allergy	Effective in chronic allergy

 

Therapeutic Uses: 

• First-generation: Allergic rhinitis, urticaria, motion sickness, nausea, insomnia 

• Second-generation: Seasonal allergic rhinitis, chronic urticaria 

 

Adverse Effects: 

• First-generation: Drowsiness, dry mouth, dizziness, blurred vision 

• Second-generation: Rare CNS side effects, minimal sedation 

 

Conclusion: 
First-generation antihistamines are sedative and anticholinergic, suitable for short-term or acute allergic conditions. Second-generation drugs are preferred for long-term use due to better safety and minimal CNS effects. 

5. Outline pharmacology of glucocorticoids. 

Glucocorticoids are steroid hormones synthesized by the adrenal cortex. They play a crucial role in metabolism, immune regulation, and stress response. Synthetic glucocorticoids are widely used for their anti-inflammatory and immunosuppressive properties. 

 

Mechanism of Action: 
Glucocorticoids bind to intracellular glucocorticoid receptors, forming a receptor–steroid complex that enters the nucleus and modulates gene transcription. 

• This results in decreased production of inflammatory mediators like prostaglandins, leukotrienes, cytokines, and histamine. 

• They suppress the activation of T cells, B cells, and macrophages, reducing immune responses. 

 

Pharmacological Actions: 

1. Anti-inflammatory: Inhibit phospholipase A2, reduce prostaglandin and leukotriene synthesis. 

2. Immunosuppressive: Suppress immune cell proliferation and function. 

3. Metabolic effects: 

1. Increase gluconeogenesis → hyperglycemia 

2. Protein breakdown → muscle wasting 

3. Fat redistribution → “moon face,” “buffalo hump” 

4. Cardiovascular: Enhance vascular responsiveness to catecholamines 

5. CNS: Mood elevation or psychosis 

6. GI tract: Increase gastric acid secretion 

7. Bone: Promote bone resorption → osteoporosis 

 

Therapeutic Uses: 

• Autoimmune diseases (e.g., rheumatoid arthritis, lupus) 

• Bronchial asthma 

• Allergic conditions 

• Inflammatory bowel disease 

• Replacement therapy in adrenal insufficiency (e.g., Addison’s disease) 

• Organ transplantation (to prevent rejection) 

 

Adverse Effects: 

• Cushingoid features (weight gain, central obesity) 

• Hyperglycemia 

• Osteoporosis 

• Peptic ulcers 

• Hypertension 

• Increased infection risk 

• Growth retardation in children 

 

Examples: Hydrocortisone, Prednisolone, Dexamethasone, Betamethasone 

 

Conclusion: 
Glucocorticoids are potent drugs with diverse pharmacological actions. Their benefits must be balanced against serious side effects, especially with long-term use. 

6. Describe the principles and applications of bioassay. 

Bioassay is a method of determining the potency and concentration of a drug by testing its biological effect on living organisms or tissues. It is especially useful when chemical or physical assays are not feasible. 

 

Principles of Bioassay: 

1. Biological Response-Based Measurement: 
   The assay depends on comparing the pharmacological response of the test sample with that of a standard preparation. 

2. Dose-Response Relationship: 
   The effect of the drug is directly proportional to the dose administered, within a certain range. 

3. Use of Standard and Test Sample: 
   Both the standard and the unknown (test) are tested under identical conditions for a reliable comparison. 

4. Minimization of Biological Variation: 
   Multiple-point assays and statistical analysis are used to reduce errors due to natural variability. 

 

Types of Bioassay: 

• Quantal Bioassay: Based on all-or-none response (e.g., death, convulsions). 

• Graded Response Bioassay: Based on variable magnitude of response (e.g., muscle contraction). 

• End Point Bioassay: The minimum dose required to produce a specific effect. 

• Matching and Bracketing Assay: Response of unknown is matched or bracketed between known doses of standard drug. 

 

Applications of Bioassay: 

• Standardization of biological products such as insulin, oxytocin, digitalis, etc. 

• Quality control of drugs where chemical methods are inadequate. 

• Comparative potency testing of different batches or sources. 

• Pharmacological research for new drug discovery. 

• Toxicological studies in safety evaluation. 

 

Limitations: 

• Time-consuming and expensive 

• Requires animal facilities and ethical clearance 

• High biological variability 

 

Conclusion: 
Bioassay remains an essential technique in pharmacology, especially for biological drugs where precise measurement of biological activity is crucial. 

7. Discuss pharmacology of oral contraceptives. 

Oral contraceptives (OCs) are medications used to prevent pregnancy by interfering with the normal process of ovulation, fertilization, and implantation. They are primarily made up of estrogens and progestins, or progestin alone. 

 

Types of Oral Contraceptives: 

1. Combined oral contraceptives (COCs): 

1. Contain both estrogen (usually ethinylestradiol) and progestin (e.g., levonorgestrel). 

2. Can be monophasic, biphasic, or triphasic. 

2. Progestin-only pills (POPs): 

1. Contain only progestin. 

2. Suitable for lactating women or those with estrogen contraindications. 

 

Mechanism of Action: 

• Inhibition of ovulation: Estrogen suppresses FSH, and progestin suppresses LH surge. 

• Thickening of cervical mucus: Progestin makes it hostile to sperm penetration. 

• Endometrial changes: Prevent implantation by making the endometrium unsuitable. 

 

Pharmacokinetics: 

• Taken orally, absorbed in the GI tract 

• Undergo hepatic metabolism 

• Excreted in urine and bile 

 

Therapeutic Uses: 

• Contraception 

• Menstrual disorders (e.g., dysmenorrhea, menorrhagia) 

• Polycystic ovarian syndrome (PCOS) 

• Acne and hirsutism 

• Endometriosis 

 

Adverse Effects: 

• Nausea, vomiting 

• Weight gain, breast tenderness 

• Headache, mood changes 

• Thromboembolism (in smokers and older women) 

• Hypertension 

• Breakthrough bleeding 

 

Contraindications: 

• History of thromboembolism 

• Breast or endometrial cancer 

• Liver disease 

• Smokers over age 35 

 

Conclusion: 
Oral contraceptives are highly effective and reversible methods of birth control, with added non-contraceptive benefits. Proper patient selection and counseling are crucial to minimize risks. 

8. Write a note on hormones regulating plasma calcium levels. 

Plasma calcium levels are tightly regulated within a narrow range (8.5–10.5 mg/dL) to maintain neuromuscular function, blood coagulation, and bone metabolism. Three key hormones are primarily involved in this regulation: 

 

1. Parathyroid Hormone (PTH): 

• Secreted by parathyroid glands in response to low serum calcium. 

• Actions: 

• Increases bone resorption by stimulating osteoclasts → raises serum calcium. 

• Enhances renal calcium reabsorption and decreases phosphate reabsorption. 

• Stimulates activation of vitamin D (calcitriol) in kidneys, enhancing calcium absorption from the gut. 

 

2. Calcitriol (1,25-dihydroxy vitamin D₃): 

• Active form of vitamin D, synthesized in kidneys under the influence of PTH. 

• Actions: 

• Increases intestinal absorption of calcium and phosphate. 

• Promotes bone mineralization at normal levels but can cause resorption at high levels. 

• Enhances renal reabsorption of calcium. 

 

3. Calcitonin: 

• Secreted by parafollicular (C cells) of the thyroid gland in response to high calcium levels. 

• Actions: 

• Inhibits osteoclastic bone resorption, reducing calcium release from bone. 

• Slightly increases renal excretion of calcium. 

• Overall lowers plasma calcium. 

 

Regulatory Balance: 

• PTH and calcitriol act to raise calcium levels, while calcitonin acts to reduce it. 

• This hormonal interplay ensures that calcium levels are maintained within physiological limits. 

 

Conclusion: 
PTH, calcitriol, and calcitonin act in a coordinated feedback system to regulate calcium homeostasis, essential for muscle contraction, nerve conduction, and bone health. 

9. Write pharmacology of NSAIDs. 

Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are a class of drugs that provide analgesic, antipyretic, and anti-inflammatory effects by inhibiting prostaglandin synthesis. They are among the most commonly used medications globally. 

 

Mechanism of Action: 

NSAIDs inhibit the enzyme cyclooxygenase (COX), which exists in two isoforms: 

• COX-1: Constitutive enzyme, responsible for protective prostaglandins in GI tract, kidneys, and platelets. 

• COX-2: Inducible enzyme, primarily involved in inflammation and pain. 
  Some NSAIDs are non-selective (e.g., ibuprofen), while others are COX-2 selective (e.g., celecoxib). 

 

Pharmacological Actions: 

1. Anti-inflammatory: Reduce prostaglandins at inflammation sites. 

2. Analgesic: Decrease pain by inhibiting prostaglandins that sensitize nociceptors. 

3. Antipyretic: Lower elevated body temperature by acting on the hypothalamus. 

4. Antiplatelet (aspirin): Inhibits thromboxane A₂ → decreased platelet aggregation. 

 

Examples of NSAIDs: 

• Non-selective: Aspirin, Ibuprofen, Naproxen, Diclofenac 

• COX-2 selective: Celecoxib, Etoricoxib 

• Salicylates: Aspirin 

• Others: Indomethacin, Ketorolac 

 

Therapeutic Uses: 

• Mild to moderate pain (headache, musculoskeletal pain) 

• Fever 

• Inflammatory conditions (rheumatoid arthritis, osteoarthritis) 

• Dysmenorrhea 

• Post-operative pain 

 

Adverse Effects: 

• Gastrointestinal: Ulcers, gastritis, bleeding (especially COX-1 inhibitors) 

• Renal: Sodium retention, renal impairment 

• Cardiovascular: Hypertension, thrombotic events (COX-2 inhibitors) 

• Hypersensitivity: Skin rashes, bronchospasm 

 

Conclusion: 
NSAIDs are versatile and effective, but their use should be cautious, especially in patients with GI, renal, or cardiovascular risks. COX-2 selective agents may reduce GI toxicity but increase cardiovascular risks. 

10. Write pharmacology of thyroid hormone inhibitors. 

Thyroid hormone inhibitors, also called antithyroid drugs, are used in the management of hyperthyroidism (excess thyroid hormone production), including Graves’ disease and thyroid storm. They work by suppressing the synthesis or release of thyroid hormones or by destroying thyroid tissue. 

 

Classification: 

1. Thioamides: 

1. Propylthiouracil (PTU) 

2. Methimazole 

3. Carbimazole (converted to methimazole in the body) 

2. Iodides: 

1. Potassium iodide, Lugol’s iodine 

3. Radioactive iodine: 

1. Iodine-131 

4. Others (Adjuvants): 

1. β-blockers (e.g., propranolol) – for symptomatic relief 

2. Glucocorticoids – in thyroid storm 

 

Mechanism of Action: 

1. Thioamides (PTU, Methimazole): 

1. Inhibit thyroid peroxidase enzyme, blocking iodination of tyrosine and coupling reactions, thereby reducing T₃ and T₄ synthesis. 

2. PTU additionally inhibits peripheral conversion of T₄ to T₃. 

2. Iodides: 

1. In high doses, inhibit thyroid hormone release and organification (Wolff–Chaikoff effect). Used pre-operatively. 

3. Radioactive Iodine (I-131): 

1. Selectively taken up by thyroid → emits β-rays → destroys thyroid tissue. Used in non-pregnant adults with Graves’ disease. 

 

Therapeutic Uses: 

• Graves' disease 

• Toxic multinodular goiter 

• Pre-operative preparation for thyroidectomy 

• Thyroid storm (PTU + supportive therapy) 

• Radioiodine ablation in selected cases 

 

Adverse Effects: 

• Skin rash, fever 

• Agranulocytosis (rare but serious) 

• Hepatotoxicity (especially with PTU) 

• Arthralgia 

• Hypothyroidism with overuse 

• GI upset 

 

Conclusion: 
Thyroid hormone inhibitors are central to hyperthyroidism treatment, either for temporary control or long-term remission. Monitoring thyroid levels and adverse effects is crucial during therapy. 

11. Write pharmacology of drugs acting on uterus. 

Drugs acting on the uterus are classified into uterotonics (stimulate uterine contractions) and tocolytics (inhibit uterine contractions). These drugs are mainly used in obstetric and gynecological conditions, especially during labor, abortion, and preterm labor management. 

 

1. Uterotonics (Oxytocics): 

These drugs increase frequency, intensity, and tone of uterine contractions. 

A. Oxytocin: 

• Mechanism: Binds to oxytocin receptors on uterine smooth muscle, increasing intracellular Ca²⁺, leading to contractions. 

• Uses: Induction and augmentation of labor, postpartum hemorrhage (PPH), uterine inertia. 

B. Ergot Alkaloids (e.g., Methylergometrine): 

• Mechanism: Stimulate α-adrenergic and serotonin receptors, causing sustained uterine contraction. 

• Uses: PPH, following delivery of placenta (not used to induce labor). 

C. Prostaglandins (e.g., Misoprostol, Carboprost, Dinoprostone): 

• Mechanism: Increase uterine tone via EP receptors. 

• Uses: Medical abortion, cervical ripening, PPH. 

 

2. Tocolytics (Uterine Relaxants): 

These drugs inhibit uterine contractions and are used to delay preterm labor. 

A. β₂-agonists (e.g., Ritodrine, Terbutaline): 

• Stimulate β₂ receptors → uterine relaxation 

B. Calcium channel blockers (e.g., Nifedipine): 

• Inhibit Ca²⁺ entry into uterine muscle cells 

C. Magnesium sulfate: 

• Competes with calcium → inhibits uterine activity 

D. NSAIDs (e.g., Indomethacin): 

• Inhibit prostaglandin synthesis 

 

Adverse Effects: 

• Oxytocin: Uterine rupture, water intoxication 

• Ergometrine: Hypertension, nausea 

• Tocolytics: Tachycardia, hypotension, pulmonary edema (β₂-agonists) 

 

Conclusion: 
Drugs acting on the uterus are critical in labor management, abortion, and PPH control. Proper drug selection and monitoring is essential to ensure maternal and fetal safety. 

2. Classify antihypertensive drugs and write a detailed note on calcium channel blockers. 

 

Classification of Antihypertensive Drugs: 

1. Diuretics: 

1. Thiazides (e.g., Hydrochlorothiazide) 

2. Loop diuretics (e.g., Furosemide) 

3. Potassium-sparing (e.g., Spironolactone) 

2. Sympatholytics: 

1. β-blockers (e.g., Propranolol, Atenolol) 

2. α-blockers (e.g., Prazosin) 

3. Centrally acting (e.g., Clonidine, Methyldopa) 

3. Calcium Channel Blockers (CCBs): 

1. Dihydropyridines (e.g., Amlodipine, Nifedipine) 

2. Non-dihydropyridines (e.g., Verapamil, Diltiazem) 

4. RAAS Inhibitors: 

1. ACE inhibitors (e.g., Enalapril) 

2. ARBs (e.g., Losartan) 

3. Direct renin inhibitors (e.g., Aliskiren) 

5. Vasodilators: 

1. Hydralazine, Minoxidil, Sodium nitroprusside 

 

Calcium Channel Blockers (CCBs): 

Mechanism of Action: 
CCBs inhibit L-type calcium channels in vascular smooth muscle and cardiac muscle → reduce intracellular calcium → vasodilation and reduced myocardial contractility. 

 

Types: 

1. Dihydropyridines (e.g., Amlodipine): 

1. Act mainly on vascular smooth muscle → potent vasodilators 

2. Minimal cardiac depressant effect 

2. Non-dihydropyridines (e.g., Verapamil, Diltiazem): 

1. Act on both heart and blood vessels 

2. Reduce heart rate and contractility 

 

Pharmacological Actions: 

• Reduce systemic vascular resistance (afterload) 

• Decrease myocardial oxygen demand 

• Non-DHPs slow AV conduction → useful in arrhythmias 

 

Therapeutic Uses: 

• Hypertension (especially in elderly and Black patients) 

• Angina pectoris 

• Cardiac arrhythmias (non-DHPs) 

• Raynaud’s phenomenon 

• Subarachnoid hemorrhage (Nimodipine) 

 

Adverse Effects: 

• Dihydropyridines: Headache, flushing, peripheral edema, reflex tachycardia 

• Non-DHPs: Bradycardia, AV block, constipation (Verapamil) 

 

Conclusion: 
CCBs are effective antihypertensives with added benefit in angina and arrhythmias. Choice of agent depends on patient profile and comorbidities. 

13. Write pharmacology of coagulants. 

Coagulants are drugs that promote blood clotting and are used in the treatment or prevention of bleeding disorders. These agents either replace missing clotting factors or enhance the body’s natural coagulation mechanisms. 

 

Classification of Coagulants: 

1. Vitamin K and its analogs: 

1. Phytomenadione (Vitamin K1) 

2. Menadione (Vitamin K3) 

2. Fibrinogen and clotting factors: 

1. Fresh frozen plasma (FFP) 

2. Cryoprecipitate 

3. Factor VIII, IX concentrates 

3. Antifibrinolytic agents: 

1. Tranexamic acid 

2. Aminocaproic acid 

4. Local hemostatics (styptics): 

1. Thrombin, fibrin sealants 

2. Adrenaline (topical) 

 

Pharmacology: 

1. Vitamin K: 

• Mechanism: Essential for the hepatic synthesis of clotting factors II, VII, IX, and X. 

• Uses: 

• Warfarin overdose 

• Newborn prophylaxis 

• Vitamin K deficiency due to liver disease or malabsorption 

2. Clotting Factors: 

• Mechanism: Replace deficient coagulation factors in hemophilia or liver disease. 

• Uses: 

• Hemophilia A (Factor VIII), Hemophilia B (Factor IX) 

• Massive transfusion 

• DIC (Disseminated Intravascular Coagulation) 

3. Antifibrinolytics (e.g., Tranexamic Acid): 

• Mechanism: Inhibit plasminogen activation → prevent fibrin degradation. 

• Uses: 

• Menorrhagia 

• Dental surgery in hemophiliacs 

• Postoperative bleeding 

4. Local Hemostatics: 

• Applied topically to control capillary bleeding. Useful in surgeries and dental procedures. 

 

Adverse Effects: 

• Vitamin K: Hypersensitivity reactions (especially IV), hemolysis in newborns (K3) 

• Clotting factors: Anaphylaxis, antibody formation 

• Tranexamic acid: Thrombosis, nausea 

 

Conclusion: 
Coagulants are vital in bleeding disorders and surgical settings. Selection depends on the underlying cause—whether it is due to clotting factor deficiency, excessive fibrinolysis, or local bleeding. 

14. Write a note on drugs used in therapy of shock. 

Shock is a life-threatening condition where there is inadequate tissue perfusion and oxygenation, leading to cellular and organ dysfunction. Management includes restoring blood flow, correcting underlying causes, and using pharmacological agents to support circulation. 

 

Types of Shock and Drug Therapy: 

1. Hypovolemic Shock (e.g., hemorrhage, dehydration): 

1. Primary treatment: Fluid resuscitation (Normal saline, Ringer’s lactate) 

2. Drugs: Vasopressors (only after fluid resuscitation) 

1. Dopamine (high dose), Norepinephrine 

2. Cardiogenic Shock (e.g., myocardial infarction, heart failure): 

1. Drugs: 

1. Inotropes: Dobutamine (↑ cardiac contractility) 

2. Dopamine (moderate doses) 

3. Diuretics if pulmonary edema present 

4. Vasodilators (e.g., Nitroglycerin) with caution 

3. Septic Shock (due to infection): 

1. Drugs: 

1. Broad-spectrum antibiotics 

2. Vasopressors: Norepinephrine (first-line), Vasopressin (second-line) 

3. Hydrocortisone (if refractory shock) 

4. Fluids: Crystalloids, colloids 

4. Anaphylactic Shock: 

1. Drugs: 

1. Epinephrine IM (first-line) 

2. Antihistamines (e.g., Diphenhydramine) 

3. Corticosteroids (e.g., Hydrocortisone) 

4. Bronchodilators (e.g., Salbutamol) 

5. Neurogenic Shock: 

1. Drugs: 

1. Vasopressors (Phenylephrine, Norepinephrine) 

2. Atropine (if bradycardia present) 

3. Fluids for volume expansion 

 

Supportive Therapy: 

• Oxygen supplementation 

• Mechanical ventilation (if needed) 

• Monitoring of BP, urine output, lactate levels 

 

Conclusion: 
Drug therapy in shock is type-specific and supportive. Timely use of fluids, vasopressors, inotropes, and corticosteroids can be life-saving, along with addressing the underlying cause. 

15. Discuss the detailed pharmacology of digoxin. 

Digoxin is a cardiac glycoside derived from the plant Digitalis lanata. It is used primarily in the treatment of congestive heart failure (CHF) and certain cardiac arrhythmias, particularly atrial fibrillation. 

 

Mechanism of Action: 

Digoxin inhibits the Na⁺/K⁺-ATPase pump in cardiac myocytes → 
⬇ Na⁺ efflux → ⬆ intracellular Na⁺ → inhibits Na⁺/Ca²⁺ exchanger → ⬆ intracellular Ca²⁺ → 
⬆ myocardial contractility (positive inotropic effect). 

Additionally, it increases vagal tone → slows AV node conduction → useful in supraventricular arrhythmias. 

 

Pharmacological Actions: 

1. Positive inotropic effect: Increases force of cardiac contraction 

2. Negative chronotropic effect: Slows heart rate via vagal stimulation 

3. Negative dromotropic effect: Slows AV nodal conduction 

4. Diuretic effect (indirect): Due to improved cardiac output 

 

Pharmacokinetics: 

• Route: Oral or IV 

• Bioavailability: ~60–80% orally 

• Half-life: ~36–48 hours 

• Excretion: Mainly renal (dose adjustment in renal impairment) 

 

Therapeutic Uses: 

• Congestive heart failure (especially with reduced ejection fraction) 

• Atrial fibrillation and atrial flutter (to control ventricular rate) 

• Paroxysmal supraventricular tachycardia (PSVT) 

 

Adverse Effects: 

• GI: Nausea, vomiting, anorexia 

• Cardiac: Bradycardia, AV block, ventricular arrhythmias 

• CNS: Confusion, fatigue, visual disturbances (yellow vision = xanthopsia) 

• Toxicity: Enhanced by hypokalemia, hypomagnesemia, or renal impairment 

 

Drug Interactions: 

• Diuretics: Cause hypokalemia → ⬆ digoxin toxicity 

• Quinidine, Verapamil: ⬆ digoxin levels 

• Antacids: Decrease digoxin absorption 

 

Conclusion: 
Digoxin improves cardiac efficiency and slows ventricular rate in atrial arrhythmias. However, due to its narrow therapeutic index, careful dose monitoring and electrolyte balance are essential during therapy. 

16. Classify antihyperlipidemic drugs. Explain mechanism and side effects of statins. 

 

Classification of Antihyperlipidemic Drugs: 

1. HMG-CoA Reductase Inhibitors (Statins): 

1. Atorvastatin, Simvastatin, Rosuvastatin, Lovastatin 

2. Fibric Acid Derivatives (Fibrates): 

1. Gemfibrozil, Fenofibrate 

3. Bile Acid Sequestrants: 

1. Cholestyramine, Colestipol 

4. Cholesterol Absorption Inhibitors: 

1. Ezetimibe 

5. Niacin (Nicotinic Acid): 

1. Vitamin B₃ 

6. PCSK9 Inhibitors: 

1. Alirocumab, Evolocumab 

7. Omega-3 Fatty Acids: 

1. Eicosapentaenoic acid (EPA), Docosahexaenoic acid (DHA) 

 

Mechanism of Action of Statins: 

• Statins competitively inhibit the enzyme HMG-CoA reductase, which is the rate-limiting step in cholesterol biosynthesis. 

• ↓ Cholesterol synthesis → ↑ LDL receptors on hepatocytes → ↑ uptake of LDL from blood → ↓ LDL cholesterol levels. 

• Also slightly ↓ triglycerides and ↑ HDL. 

 

Therapeutic Effects: 

• Primarily reduce LDL cholesterol 

• Modest reduction in triglycerides 

• Slight increase in HDL 

• Useful in primary and secondary prevention of cardiovascular events 

 

Adverse Effects of Statins: 

1. Hepatotoxicity: 

1. ↑ Liver enzymes (monitor ALT, AST) 

2. Contraindicated in active liver disease 

2. Myopathy: 

1. Muscle pain, tenderness 

2. Risk of rhabdomyolysis, especially with drug interactions (e.g., with fibrates, macrolides) 

3. Gastrointestinal disturbances: 

1. Nausea, abdominal pain, constipation 

4. CNS effects (rare): 

1. Memory loss, headache 

 

Conclusion: 
Statins are the first-line therapy for hypercholesterolemia due to their potent LDL-lowering effect and proven cardiovascular benefit. Regular monitoring of liver enzymes and muscle symptoms is essential during therapy. 

17. Describe physiological and pathophysiological roles of prostaglandins. 

 

What are Prostaglandins? 

Prostaglandins (PGs) are lipid-derived autacoids, synthesized from arachidonic acid via the cyclooxygenase (COX) pathway. They are short-lived, locally acting mediators with diverse physiological and pathophysiological functions. 

 

Physiological Roles of Prostaglandins: 

1. Gastrointestinal Tract: 

1. PGE₂ and PGI₂ protect the gastric mucosa by promoting mucus and bicarbonate secretion, and reducing acid secretion. 

2. Kidneys: 

1. PGE₂ and PGI₂ maintain renal blood flow and glomerular filtration rate, especially during stress. 

3. Cardiovascular System: 

1. PGI₂ (prostacyclin) causes vasodilation and inhibits platelet aggregation. 

2. TXA₂ (thromboxane A₂) causes vasoconstriction and promotes platelet aggregation. 

4. Reproductive System: 

1. PGF₂α and PGE₂ stimulate uterine contractions. 

2. Important in labor and menstruation. 

5. Respiratory System: 

1. PGE₂ and PGI₂ cause bronchodilation; 

2. PGF₂α causes bronchoconstriction. 

6. Central Nervous System: 

1. PGE₂ mediates fever (pyrogenic response) and pain sensitization. 

 

Pathophysiological Roles of Prostaglandins: 

1. Inflammation: 

1. PGE₂ and PGI₂ are major mediators → vasodilation, increased vascular permeability, and edema. 

2. Pain and Fever: 

1. PGE₂ sensitizes pain receptors and elevates body temperature by acting on the hypothalamus. 

3. Dysmenorrhea: 

1. Excessive PGF₂α causes uterine cramps and pain. 

4. Asthma and Bronchoconstriction: 

1. Overproduction of PGD₂ and PGF₂α contributes to bronchospasm. 

5. Gastrointestinal Ulcers: 

1. NSAIDs inhibit protective prostaglandins → increased risk of gastric ulcers. 

6. Thrombosis: 

1. Imbalance between PGI₂ (anti-thrombotic) and TXA₂ (pro-thrombotic) may promote thrombotic events. 

 

Conclusion: 
Prostaglandins are critical local mediators with roles in homeostasis and disease. Their diverse actions make them targets for drugs like NSAIDs, prostanoid analogues, and COX inhibitors in managing inflammation, pain, labor, ulcers, and thrombosis. 

18. Write pharmacological action, adverse drug reaction, uses and interaction of aspirin. 

 

Pharmacological Actions of Aspirin (Acetylsalicylic Acid): 

1. Analgesic: 

1. Inhibits prostaglandin synthesis (mainly PGE₂) → reduces mild to moderate pain. 

2. Antipyretic: 

1. Lowers fever by acting on hypothalamic thermoregulatory center. 

3. Anti-inflammatory: 

1. At high doses, inhibits COX enzymes → reduces inflammation in rheumatic and autoimmune diseases. 

4. Antiplatelet: 

1. Irreversible inhibition of COX-1 in platelets → ↓ thromboxane A₂ → inhibits platelet aggregation. 

5. Uricosuric: 

1. At high doses only (low doses may decrease uric acid excretion). 

 

Adverse Drug Reactions (ADRs): 

1. Gastrointestinal: 

1. Gastric irritation, peptic ulcers, GI bleeding (due to ↓ protective prostaglandins). 

2. Bleeding tendency: 

1. Prolonged bleeding time due to platelet inhibition. 

3. Hypersensitivity reactions: 

1. Urticaria, asthma, rhinitis (esp. in aspirin-sensitive individuals). 

4. Reye’s Syndrome: 

1. In children with viral infections → hepatic failure, encephalopathy (avoid in <12 years). 

5. Salicylism (toxicity): 

1. Tinnitus, dizziness, vomiting, metabolic acidosis. 

 

Therapeutic Uses: 

• Mild to moderate pain (e.g., headache, toothache) 

• Fever (not preferred in children) 

• Rheumatoid arthritis, osteoarthritis 

• Antiplatelet agent: 

• Myocardial infarction, stroke prevention 

• Post-angioplasty or stenting 

• Anti-inflammatory: 

• Pericarditis, Kawasaki disease 

 

Drug Interactions: 

• Warfarin/Heparin: ↑ risk of bleeding 

• Methotrexate: ↓ renal clearance → ↑ toxicity 

• Uricosuric drugs (e.g., Probenecid): ↓ effectiveness 

• Other NSAIDs: Compete for COX enzymes → ↓ cardioprotective effect of aspirin 

 

Conclusion: 
Aspirin is a versatile NSAID with analgesic, antipyretic, anti-inflammatory, and cardioprotective antiplatelet effects, but its gastrointestinal and bleeding risks must be considered, especially in long-term use. 

19. Classify antihyperglycemic drugs. Discuss mode of action of sulfonylurea. 

 

Classification of Antihyperglycemic (Antidiabetic) Drugs: 

A. Insulin and Insulin Analogs 

• Rapid-acting: Insulin lispro, aspart 

• Short-acting: Regular insulin 

• Intermediate: NPH insulin 

• Long-acting: Glargine, detemir 

B. Oral Hypoglycemic Agents 

1. Insulin Secretagogues: 

1. Sulfonylureas: Glibenclamide, Glipizide, Gliclazide 

2. Meglitinides: Repaglinide, Nateglinide 

2. Insulin Sensitizers: 

1. Biguanides: Metformin 

2. Thiazolidinediones: Pioglitazone 

3. α-Glucosidase Inhibitors: 

1. Acarbose, Miglitol 

4. DPP-4 Inhibitors (Gliptins): 

1. Sitagliptin, Vildagliptin 

5. GLP-1 Receptor Agonists: 

1. Exenatide, Liraglutide 

6. SGLT2 Inhibitors: 

1. Dapagliflozin, Canagliflozin 

 

Mode of Action of Sulfonylureas: 

• Primary Action: Stimulate insulin release from pancreatic β-cells. 

• Mechanism: 

• Bind to sulfonylurea receptor (SUR1) component of ATP-sensitive K⁺ channels on β-cell membrane. 

• Channel closes → membrane depolarization → Ca²⁺ influx → insulin exocytosis. 

• Requires functioning β-cells (only effective in type 2 diabetes mellitus). 

 

Examples of Sulfonylureas: 

• 1st Generation: Tolbutamide, Chlorpropamide 

• 2nd Generation: Glibenclamide, Gliclazide, Glipizide (more potent and fewer side effects) 

 

Adverse Effects: 

• Hypoglycemia: Especially in elderly or renal/hepatic impairment 

• Weight gain 

• GI upset: Nausea, bloating 

• Allergic reactions: Skin rash 

• Disulfiram-like reaction with alcohol (rare) 

 

Conclusion: 
Sulfonylureas are effective and widely used oral antidiabetic agents for type 2 diabetes. Proper dosing and patient selection are key to avoid hypoglycemia and weight gain. 

20. Describe the pharmacology of oxytocin. 

 

Introduction: 

Oxytocin is a nonapeptide hormone synthesized in the hypothalamus and secreted by the posterior pituitary gland. It plays a vital role in labor, lactation, and uterine contractions, and is used therapeutically as an oxytocic agent. 

 

Mechanism of Action: 

Oxytocin binds to oxytocin receptors (G-protein coupled receptors) on uterine smooth muscle, increasing intracellular calcium via phospholipase C activation. This causes: 

• Rhythmic uterine contractions 

• Milk ejection from mammary glands (via myoepithelial contraction) 

 

Pharmacological Actions: 

1. On Uterus: 

1. Stimulates rhythmic contractions of uterus. 

2. Increases frequency and intensity during labor. 

3. Estrogen increases oxytocin receptor sensitivity. 

2. On Breast: 

1. Causes milk ejection during lactation by contracting myoepithelial cells. 

3. On Cardiovascular System (in high doses): 

1. Mild vasodilation → transient hypotension 

2. Antidiuretic action (similar to vasopressin) 

 

Pharmacokinetics: 

• Route: IV (for labor induction), IM (for postpartum hemorrhage) 

• Onset: Immediate (IV), a few minutes (IM) 

• Half-life: 3–5 minutes 

• Metabolism: Liver and kidney 

 

Therapeutic Uses: 

• Induction of labor (when continuation of pregnancy is risky) 

• Augmentation of labor in cases of uterine inertia 

• Prevention and treatment of postpartum hemorrhage 

• Management of incomplete abortion 

• Stimulation of milk ejection (rare) 

 

Adverse Effects: 

• Uterine hyperstimulation → uterine rupture 

• Fetal distress due to decreased uteroplacental blood flow 

• Water intoxication (in high doses) due to ADH-like effect 

• Hypotension, tachycardia 

 

Contraindications: 

• Cephalopelvic disproportion 

• Fetal distress not requiring delivery 

• Hyperactive uterus 

• Previous uterine surgery (risk of rupture) 

 

Conclusion: 
Oxytocin is a key uterotonic agent used in obstetric practice to facilitate labor and control postpartum bleeding. Its use must be monitored carefully to avoid complications for both mother and fetus. 

21. Discuss bioassay of insulin. 

 

Introduction to Bioassay: 

A bioassay is a method to determine the biological activity or potency of a substance by observing its effect on a living organism or tissue. It is essential for biologically active compounds like insulin, whose exact chemical assay is difficult due to complexity and sensitivity. 

 

Principle of Insulin Bioassay: 

The hypoglycemic effect of insulin is used as the basis of its bioassay. Insulin lowers blood glucose by promoting glucose uptake in muscle and fat and suppressing hepatic glucose output. The extent of blood glucose reduction is used to estimate its potency. 

 

Methods for Bioassay of Insulin: 

1. Rabbit Hypoglycemic Method (Official Method): 

Procedure: 

• Fasted rabbits are divided into 3 groups: 

• Test sample group (unknown insulin) 

• Standard insulin group 

• Control group 

• Each rabbit is injected intravenously or subcutaneously with a known dose. 

• Blood samples are drawn at fixed intervals (e.g., 1–2 hours). 

• Blood glucose levels are estimated using glucose oxidase method. 

• Hypoglycemic response is plotted and compared with standard. 

Calculation: 

• The potency of test insulin is determined by comparing glucose reduction to that of the standard. 

 

2. Mouse Convulsion Method (Alternative Method): 

• Based on insulin-induced hypoglycemia causing convulsions in fasted mice. 

• The time taken for the onset of convulsions is inversely proportional to insulin dose. 

 

Applications of Insulin Bioassay: 

• Standardization of insulin preparations 

• Quality control during manufacturing 

• Determination of potency in various insulin formulations 

 

Limitations: 

• Ethical concerns with animal use 

• Inter-individual variation in response 

• Requires strict fasting and handling conditions 

• Slower and less reproducible than chemical assays 

 

Conclusion: 
Bioassay of insulin, especially the rabbit hypoglycemic method, is a classical and reliable technique to estimate the biological potency of insulin. Despite limitations, it remains valuable in biological standardization and regulatory testing of insulin formulations. 

22. Classify antihyperlipidemic drugs and discuss the pharmacology of HMG-CoA reductase inhibitors. 

 

Classification of Antihyperlipidemic Drugs: 

1. HMG-CoA Reductase Inhibitors (Statins): 

1. Atorvastatin, Simvastatin, Rosuvastatin, Lovastatin 

2. Fibric Acid Derivatives (Fibrates): 

1. Gemfibrozil, Fenofibrate 

3. Bile Acid Sequestrants: 

1. Cholestyramine, Colestipol 

4. Cholesterol Absorption Inhibitor: 

1. Ezetimibe 

5. Niacin (Nicotinic Acid): 

1. Extended-release formulations preferred 

6. PCSK9 Inhibitors (Monoclonal antibodies): 

1. Alirocumab, Evolocumab 

7. Omega-3 Fatty Acids: 

1. EPA, DHA (used in hypertriglyceridemia) 

 

Pharmacology of HMG-CoA Reductase Inhibitors (Statins): 

Mechanism of Action: 

• Statins competitively inhibit the enzyme HMG-CoA reductase, the rate-limiting step in hepatic cholesterol synthesis. 

• This leads to: 

• ↓ hepatic cholesterol levels 

• ↑ expression of LDL receptors on hepatocytes 

• ↑ clearance of LDL from blood 

• ↓ plasma LDL, total cholesterol, and triglycerides 

• Slight ↑ HDL cholesterol 

 

Pharmacokinetics: 

• Oral administration 

• Extensive first-pass metabolism (mainly hepatic) 

• CYP450 metabolism (especially CYP3A4 for simvastatin, atorvastatin) 

• Excretion: Bile > urine 

 

Therapeutic Uses: 

• Primary and secondary prevention of cardiovascular diseases 

• Familial hypercholesterolemia 

• Post-myocardial infarction 

• Stroke prevention 

 

Adverse Effects: 

• Hepatotoxicity: Elevated liver enzymes (monitor LFTs) 

• Myopathy and Rhabdomyolysis: Muscle pain, CK elevation 

• GI disturbances: Dyspepsia, flatulence 

• CNS effects (rare): Memory loss 

• New-onset diabetes mellitus (rare) 

 

Drug Interactions: 

• Increased toxicity with fibrates, niacin 

• Interactions with CYP3A4 inhibitors (e.g., erythromycin, grapefruit juice) 

• Should not be combined with gemfibrozil 

 

Conclusion: 
Statins are the most effective LDL-lowering agents and form the cornerstone of dyslipidemia management. Their cardiovascular benefits outweigh their side effects, but require monitoring of liver and muscle function. 

23. What are hematinics? Discuss the pharmacological actions and uses of iron. 

 

Definition of Hematinics: 

Hematinics are agents that are used to increase hemoglobin levels and promote the formation of blood components, especially red blood cells. They are primarily used in the treatment of anemia, particularly iron deficiency anemia. 

 

Examples of Hematinics: 

• Iron (Ferrous sulfate, Ferric hydroxide polymaltose complex) 

• Vitamin B₁₂ (Cyanocobalamin) 

• Folic acid 

 

Pharmacology of Iron: 

A. Pharmacological Actions: 

Iron is an essential component of: 

• Hemoglobin: Carries oxygen in RBCs 

• Myoglobin: Oxygen store in muscles 

• Enzymes: Cytochromes, catalase, peroxidase 

It helps in: 

• Oxygen transport and storage 

• Electron transfer in oxidative metabolism 

• DNA synthesis and cell proliferation 

 

B. Absorption and Metabolism: 

• Absorbed mainly in the duodenum and proximal jejunum 

• Better absorbed in ferrous (Fe²⁺) form than ferric (Fe³⁺) 

• Vitamin C enhances absorption 

• Stored in the liver as ferritin and hemosiderin 

 

Therapeutic Uses of Iron: 

1. Iron deficiency anemia (due to chronic blood loss, pregnancy, malnutrition) 

2. Prophylaxis in pregnancy and lactation 

3. During rapid growth (infants, adolescents) 

4. Post-surgical recovery and in chronic diseases 

 

Available Forms: 

• Oral: Ferrous sulfate, Ferrous gluconate, Ferrous fumarate 

• Parenteral: Iron dextran, Iron sucrose, Ferric carboxymaltose (for patients intolerant or unresponsive to oral iron) 

 

Adverse Effects: 

Oral Iron: 

• Nausea, epigastric pain 

• Constipation or diarrhea 

• Black stools 

Parenteral Iron: 

• Pain at injection site 

• Hypersensitivity reactions 

• Iron overload (hemochromatosis with repeated use) 

 

Conclusion: 
Iron is a key hematinic for the prevention and treatment of iron deficiency anemia. Oral iron is preferred for most cases, but parenteral forms are used when oral therapy fails or is contraindicated. 

24. Illustrate the mode of action, uses and adverse reactions of warfarin sodium. 

 

Introduction: 

Warfarin sodium is an oral anticoagulant belonging to the class of vitamin K antagonists. It is widely used to prevent and treat thromboembolic disorders. 

 

Mechanism of Action: 

• Warfarin inhibits the vitamin K epoxide reductase (VKOR) enzyme in the liver. 

• This prevents the conversion of inactive vitamin K epoxide to active vitamin K hydroquinone. 

• As a result, the γ-carboxylation (activation) of vitamin K–dependent clotting factors is inhibited, specifically: 

• Clotting factors II, VII, IX, and X 

• Anticoagulant proteins C and S 

• This leads to production of non-functional clotting factors, reducing blood coagulation. 

 

Therapeutic Uses: 

1. Prevention and treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) 

2. Prophylaxis in atrial fibrillation (to prevent stroke) 

3. Post-cardiac valve replacement (mechanical valves) 

4. Prophylaxis of thromboembolism in hypercoagulable states 

 

Adverse Reactions: 

1. Bleeding: 

1. Most common and serious effect 

2. Includes epistaxis, GI bleeding, intracranial hemorrhage 

2. Skin Necrosis: 

1. Rare, due to protein C deficiency 

3. Teratogenicity: 

1. Contraindicated in pregnancy (causes fetal warfarin syndrome) 

4. Purple toe syndrome: 

1. Cholesterol emboli in extremities 

5. Drug interactions: 

1. Potentiated by: Aspirin, antibiotics, cimetidine (↑ bleeding risk) 

2. Reduced by: Barbiturates, phenytoin, rifampin (↓ effectiveness) 

 

Monitoring and Reversal: 

• Monitoring: INR (International Normalized Ratio) 

• Target INR: 2.0–3.0 (except mechanical valves: 2.5–3.5) 

• Reversal of warfarin effect: 

• Vitamin K (oral or IV) 

• Fresh frozen plasma (FFP) or prothrombin complex concentrates (PCCs) in emergencies 

 

Conclusion: 
Warfarin is a potent oral anticoagulant with proven benefit in thromboembolic conditions, but it has a narrow therapeutic index and requires careful monitoring to avoid serious bleeding complications. 

25. Demonstrate arachidonic acid pathway. Explain the physiological and pathological roles of prostaglandins. 

 

Arachidonic Acid Pathway: 

Arachidonic acid (AA) is a polyunsaturated fatty acid present in membrane phospholipids. Upon cell activation (by trauma, cytokines, etc.), phospholipase A₂ is stimulated, which releases arachidonic acid from membrane phospholipids. 

Pathways of Arachidonic Acid Metabolism: 

1. Cyclooxygenase (COX) Pathway: 

1. COX-1 and COX-2 convert AA into: 

1. Prostaglandins (PGD₂, PGE₂, PGF₂α) 

2. Prostacyclin (PGI₂) 

3. Thromboxane A₂ (TXA₂) 

2. Lipoxygenase (LOX) Pathway: 

1. Produces: 

1. Leukotrienes (LTB₄, LTC₄, LTD₄, LTE₄) 

2. Lipoxins 

3. Cytochrome P450 Epoxygenase Pathway: 

1. Generates epoxyeicosatrienoic acids (EETs) and HETEs 

 

Physiological Roles of Prostaglandins: 

1. Gastrointestinal Tract: 

1. PGE₂ and PGI₂ protect gastric mucosa by stimulating mucus and bicarbonate secretion and inhibiting acid secretion. 

2. Renal Function: 

1. Maintain renal blood flow and GFR (PGE₂, PGI₂). 

3. Reproductive System: 

1. PGF₂α and PGE₂ induce uterine contraction (labor, menstruation). 

4. Vascular System: 

1. PGI₂ causes vasodilation and inhibits platelet aggregation. 

2. TXA₂ causes vasoconstriction and promotes platelet aggregation. 

5. Respiratory Tract: 

1. PGE₂ and PGI₂ cause bronchodilation. 

2. PGF₂α causes bronchoconstriction. 

6. Central Nervous System: 

1. PGE₂ mediates fever and pain perception. 

 

Pathological Roles of Prostaglandins: 

1. Inflammation: 

1. PGE₂ and PGI₂ mediate vasodilation, increase capillary permeability, and contribute to pain and edema. 

2. Fever: 

1. PGE₂ raises the hypothalamic set point for temperature, causing fever. 

3. Pain Sensitization: 

1. PGE₂ sensitizes nociceptors, enhancing pain response to other mediators like bradykinin. 

4. Dysmenorrhea: 

1. Excess PGF₂α causes intense uterine contractions and pain. 

5. Asthma: 

1. Certain prostaglandins and leukotrienes contribute to bronchospasm and airway inflammation. 

6. Thrombosis: 

1. Imbalance between PGI₂ and TXA₂ can lead to abnormal clotting or bleeding tendencies. 

 

Conclusion: 
The arachidonic acid pathway produces multiple mediators including prostaglandins, which play essential physiological roles (homeostasis, reproduction) and contribute to pathological states (inflammation, pain, thrombosis). Drugs like NSAIDs and corticosteroids target this pathway to provide therapeutic benefits. 

26. Classify various types of diabetes. Explain the mode of action, adverse reactions, interactions and uses of insulin. 

 

Classification of Diabetes Mellitus: 

1. Type 1 Diabetes Mellitus (T1DM): 

1. Autoimmune destruction of pancreatic β-cells → absolute insulin deficiency 

2. Common in children and adolescents 

2. Type 2 Diabetes Mellitus (T2DM): 

1. Insulin resistance + relative insulin deficiency 

2. Common in adults; associated with obesity and lifestyle factors 

3. Gestational Diabetes Mellitus (GDM): 

1. Diabetes diagnosed during pregnancy 

4. Secondary Diabetes: 

1. Due to pancreatic disorders, endocrine diseases (Cushing’s), drugs (glucocorticoids, thiazides), genetic defects 

 

Insulin: 

Insulin is a polypeptide hormone secreted by β-cells of the pancreas and is essential for glucose metabolism. 

 

Mode of Action: 

• Insulin binds to insulin receptors (tyrosine kinase receptors) on target cells (liver, muscle, adipose tissue). 

• Activates receptor autophosphorylation → intracellular signaling via PI3K and MAPK pathways. 

• Promotes: 

• Glucose uptake via GLUT4 in muscle/adipose tissue 

• Glycogenesis in liver/muscle 

• Lipogenesis and protein synthesis 

• Inhibits: 

• Gluconeogenesis, glycogenolysis, lipolysis, ketogenesis 

 

Adverse Reactions: 

1. Hypoglycemia: 

1. Symptoms: Sweating, tremors, confusion, coma 

2. Most common and serious side effect 

2. Weight gain 

3. Allergic reactions: 

1. Local redness, swelling (rare) 

4. Lipodystrophy: 

1. Lipoatrophy or lipohypertrophy at injection sites 

5. Insulin resistance (long-term use) 

 

Drug Interactions: 

• Increased hypoglycemic effect with: 

• Sulfonylureas, MAO inhibitors, alcohol, β-blockers 

• Decreased effect with: 

• Corticosteroids, thiazides, sympathomimetics, oral contraceptives 

 

Therapeutic Uses: 

• Type 1 DM (lifelong requirement) 

• Type 2 DM (when uncontrolled by oral drugs) 

• Diabetic ketoacidosis (DKA) 

• Gestational diabetes (when oral agents not suitable) 

• Hyperkalemia (with glucose to shift K⁺ intracellularly) 

• Perioperative glycemic control in surgery or infections 

 

Conclusion: 

Insulin is the backbone of diabetes treatment, particularly in Type 1 diabetes and uncontrolled Type 2 diabetes. Despite risks like hypoglycemia, it remains essential for metabolic control and preventing long-term complications. 

 

 

Pharmacology Long Question Answers {10-Marks} 

1. Illustrate pharmacology of anti-hypertensive drugs and design drug therapy for management of hypertension during pregnancy. 

 

Introduction: 

Hypertension (HTN) is defined as persistently elevated arterial blood pressure. Antihypertensive drugs aim to reduce blood pressure and prevent complications like stroke, MI, and kidney failure. The choice of therapy depends on severity, comorbidities, and patient profile (e.g., pregnancy). 

 

Classification of Antihypertensive Drugs: 

1. Diuretics 

1. Thiazides: Hydrochlorothiazide 

2. Loop: Furosemide 

3. K⁺-sparing: Spironolactone 

2. Sympatholytics 

1. Central: Clonidine, Methyldopa 

2. Beta-blockers: Atenolol, Metoprolol 

3. Alpha-blockers: Prazosin 

3. Calcium Channel Blockers (CCBs) 

1. Dihydropyridines: Amlodipine 

2. Non-dihydropyridines: Verapamil, Diltiazem 

4. RAAS Inhibitors 

1. ACE inhibitors: Enalapril, Ramipril 

2. ARBs: Losartan, Telmisartan 

3. Direct renin inhibitors: Aliskiren 

5. Vasodilators 

1. Hydralazine, Minoxidil, Sodium nitroprusside (IV emergency use) 

 

Pharmacology Overview: 

• Diuretics: Decrease plasma volume and peripheral resistance 

• Beta-blockers: Reduce cardiac output and inhibit renin release 

• CCBs: Inhibit Ca²⁺ influx in vascular smooth muscle → vasodilation 

• ACE inhibitors/ARBs: Block angiotensin II → vasodilation, ↓ aldosterone 

• Centrally acting drugs: ↓ sympathetic tone 

• Vasodilators: Directly relax vascular smooth muscle 

 

Hypertension in Pregnancy: 

Hypertension during pregnancy may include gestational HTN, pre-eclampsia, or chronic HTN. Untreated HTN can lead to eclampsia, placental abruption, and fetal growth restriction. 

 

Safe Antihypertensive Drugs in Pregnancy: 

1. Methyldopa 

1. Central α₂ agonist; reduces sympathetic outflow 

2. First-line; safe throughout pregnancy 

2. Labetalol 

1. Combined α and β-blocker; effective and safe 

3. Nifedipine 

1. Calcium channel blocker; used in acute and chronic HTN 

4. Hydralazine 

1. Used in hypertensive emergencies in pregnancy (IV form) 

 

Drugs Contraindicated in Pregnancy: 

• ACE inhibitors and ARBs: Risk of fetal renal damage, oligohydramnios, and congenital anomalies 

• Direct renin inhibitors (Aliskiren): Teratogenic 

• Diuretics: May reduce uteroplacental perfusion 

 

Drug Therapy Example (Pre-eclampsia): 

• Mild cases: Methyldopa or Labetalol orally 

• Severe cases: Hydralazine IV ± Magnesium sulfate (to prevent seizures) 

• Monitoring: Blood pressure, fetal well-being, and urine protein 

 

Conclusion: 
Antihypertensive therapy aims to prevent maternal and fetal complications. Drug selection in pregnancy should balance efficacy and safety, with methyldopa, labetalol, and nifedipine as preferred options. 

2. Classify NSAIDs and explain pharmacology of aspirin. 
(10 Marks | 400–450 words) 

 

Introduction: 

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are a diverse group of drugs that exhibit analgesic, antipyretic, and anti-inflammatory activities. They primarily act by inhibiting cyclooxygenase (COX) enzymes involved in prostaglandin synthesis. Aspirin is the prototype NSAID with additional antiplatelet action. 

 

Classification of NSAIDs: 

A. Based on COX Selectivity: 

1. Non-selective COX inhibitors: 

1. Aspirin, Ibuprofen, Diclofenac, Indomethacin, Naproxen 

2. Preferential COX-2 inhibitors: 

1. Nimesulide, Meloxicam 

3. Selective COX-2 inhibitors (Coxibs): 

1. Celecoxib, Etoricoxib 

B. Based on Duration of Action: 

• Short-acting: Ibuprofen 

• Long-acting: Piroxicam, Naproxen 

 

Pharmacology of Aspirin: 

1. Mechanism of Action: 

• Aspirin irreversibly inhibits COX-1 and COX-2 enzymes by acetylating serine residues. 

• Inhibition of COX leads to ↓ synthesis of prostaglandins and thromboxanes: 

• ↓ PGE₂ → ↓ inflammation, fever, and pain 

• ↓ TXA₂ → ↓ platelet aggregation 

 

2. Pharmacological Actions: 

• Analgesic: Relief of mild to moderate pain by decreasing PGE₂ sensitization of nociceptors. 

• Antipyretic: Acts on hypothalamic thermoregulatory center to dissipate heat via vasodilation and sweating. 

• Anti-inflammatory: Reduces vasodilation, capillary permeability, and edema in inflamed tissues. 

• Antiplatelet: At low doses (75–150 mg), selectively inhibits platelet COX-1 → ↓ TXA₂ → used to prevent MI and stroke. 

 

3. Pharmacokinetics: 

• Rapid absorption orally 

• Hydrolyzed to salicylate 

• Metabolized in the liver; excreted by kidneys 

• Dose-dependent kinetics 

 

4. Therapeutic Uses: 

• Analgesic: Headache, musculoskeletal pain 

• Antipyretic: Fever (not preferred in children) 

• Anti-inflammatory: Rheumatoid arthritis, osteoarthritis 

• Antiplatelet: Prevention of myocardial infarction, stroke, post-angioplasty 

 

5. Adverse Effects: 

• GI Irritation, Ulcers, Bleeding (due to inhibition of protective PGE₂) 

• Prolonged bleeding time (irreversible platelet inhibition) 

• Hypersensitivity: Bronchospasm, urticaria (especially in asthmatics) 

• Reye’s Syndrome in children with viral infections 

• Salicylism: Tinnitus, dizziness, metabolic acidosis (at toxic doses) 

 

6. Drug Interactions: 

• ↑ Bleeding with warfarin or heparin 

• ↓ Effectiveness of uricosuric drugs 

• Additive GI toxicity with other NSAIDs or corticosteroids 

 

Conclusion: 

Aspirin is a widely used NSAID with unique antiplatelet properties. While effective, it requires cautious use due to GI and bleeding risks, especially with long-term therapy. Selective COX-2 inhibitors are preferred when GI protection is needed. 

3. Explain pharmacology of oral hypoglycemic agents. 
(10 Marks | 400–450 words) 

 

Introduction: 

Oral hypoglycemic agents are drugs used to lower blood glucose levels in patients with Type 2 Diabetes Mellitus (T2DM). These agents act through various mechanisms such as stimulating insulin secretion, improving insulin sensitivity, delaying glucose absorption, or promoting glucose excretion. 

 

Classification of Oral Hypoglycemic Agents: 

1. Insulin Secretagogues: 

1. Sulfonylureas: Glibenclamide, Glipizide, Gliclazide 

2. Meglitinides: Repaglinide, Nateglinide 

2. Insulin Sensitizers: 

1. Biguanides: Metformin 

2. Thiazolidinediones: Pioglitazone, Rosiglitazone 

3. Alpha-Glucosidase Inhibitors: 

1. Acarbose, Miglitol 

4. DPP-4 Inhibitors (Gliptins): 

1. Sitagliptin, Vildagliptin, Saxagliptin 

5. GLP-1 Receptor Agonists: 

1. Exenatide, Liraglutide (injectable) 

6. SGLT2 Inhibitors: 

1. Dapagliflozin, Canagliflozin, Empagliflozin 

 

Pharmacology of Major Classes: 

1. Sulfonylureas: 

• Mechanism: Stimulate insulin release from pancreatic β-cells by closing ATP-sensitive K⁺ channels. 

• Adverse Effects: Hypoglycemia, weight gain. 

2. Biguanides (Metformin): 

• Mechanism: Decreases hepatic glucose production, improves peripheral insulin sensitivity, and enhances glucose uptake. 

• Advantages: Does not cause hypoglycemia or weight gain. 

• Adverse Effects: GI upset, lactic acidosis (rare but serious). 

3. Thiazolidinediones (Pioglitazone): 

• Mechanism: Activate PPAR-γ receptors → increase insulin sensitivity in fat and muscle. 

• Adverse Effects: Fluid retention, weight gain, risk of heart failure. 

4. Alpha-Glucosidase Inhibitors: 

• Mechanism: Inhibit intestinal α-glucosidase enzyme → delay carbohydrate digestion and glucose absorption. 

• Adverse Effects: Flatulence, diarrhea, abdominal discomfort. 

5. DPP-4 Inhibitors: 

• Mechanism: Inhibit DPP-4 enzyme → prolong GLP-1 action → increase insulin secretion and decrease glucagon. 

• Adverse Effects: Nasopharyngitis, headache, rare pancreatitis. 

6. SGLT2 Inhibitors: 

• Mechanism: Inhibit SGLT2 in the proximal renal tubule → ↑ urinary glucose excretion. 

• Adverse Effects: Genital infections, dehydration, ketoacidosis. 

 

Combination Therapy: 

• Frequently used for synergistic effect and better glycemic control. 

• Example: Metformin + Sulfonylurea, or Metformin + DPP-4 Inhibitor 

 

Conclusion: 

Oral hypoglycemic agents offer multiple mechanisms to control hyperglycemia in T2DM. Drug selection depends on patient profile, comorbidities, risk of hypoglycemia, and cost. Metformin remains the first-line agent, while other drugs are added based on therapeutic response. 

4. Define Autacoids. Classify them and discuss the physiological role of histamine. 
(10 Marks | 400–450 words) 

 

Definition of Autacoids: 

Autacoids are locally acting biological mediators that are synthesized and released in response to stimuli and act near the site of synthesis to regulate various physiological functions. Their action is usually brief and localized, and they are metabolized quickly. 

 

Classification of Autacoids: 

1. Biogenic Amines: 

1. Histamine 

2. Serotonin (5-HT) 

2. Lipid-derived Autacoids: 

1. Prostaglandins (PGs) 

2. Thromboxanes (TXA₂) 

3. Leukotrienes (LTs) 

3. Peptides: 

1. Bradykinin 

2. Substance P 

3. Angiotensin 

4. Vasopressin 

4. Gaseous Autacoids: 

1. Nitric Oxide (NO) 

5. Cytokines (sometimes included): 

1. Interleukins 

2. Tumor Necrosis Factor-α (TNF-α) 

 

Histamine – Overview: 

Histamine is a biogenic amine derived from histidine and stored primarily in mast cells, basophils, and certain neurons. It plays a key role in inflammation, gastric secretion, neurotransmission, and allergic reactions. 

 

Histamine Receptors and Their Functions: 

Receptor	Location	Physiological Role
H₁	Smooth muscles, endothelium, brain	Vasodilation, bronchoconstriction, increased capillary permeability, itching
H₂	Gastric parietal cells, heart	↑ Gastric acid secretion, ↑ heart rate
H₃	CNS neurons	Modulates neurotransmitter release
H₄	Eosinophils, mast cells	Role in chemotaxis and immune modulation

 

Physiological Roles of Histamine: 

1. Inflammation and Allergy (H₁-mediated): 

• Causes vasodilation by releasing nitric oxide from endothelial cells. 

• Increases vascular permeability, leading to tissue swelling and redness. 

• Responsible for itching and pain in allergic reactions. 

• Mediates bronchoconstriction in asthma and allergic rhinitis. 

2. Gastric Secretion (H₂-mediated): 

• Stimulates HCl secretion from gastric parietal cells. 

• Acts synergistically with acetylcholine and gastrin. 

3. Neurotransmission (H₁ and H₃): 

• Modulates wakefulness, appetite, and cognitive functions. 

• H₃ receptors act as presynaptic autoreceptors controlling histamine release. 

4. Immunomodulation (H₄): 

• Involved in chemotaxis of immune cells, especially eosinophils and mast cells. 

 

Clinical Relevance: 

• Histamine release is central in anaphylaxis, urticaria, allergic rhinitis, peptic ulcer disease, etc. 

• Antihistamines (H₁ and H₂ blockers) are used to treat these conditions (e.g., loratadine, ranitidine). 

 

Conclusion: 

Autacoids like histamine are vital regulators of physiological and pathological processes. Histamine, acting via multiple receptors, contributes to allergy, inflammation, gastric secretion, and neurological modulation, making it a key therapeutic target. 

5. Write a detailed note on oral contraceptives. 
(10 Marks | 400–450 words) 

 

Introduction: 

Oral contraceptives (OCs) are hormonal preparations used to prevent pregnancy. They are among the most effective and widely used reversible contraceptive methods. OCs mainly contain estrogens and/or progestins, which act by inhibiting ovulation and creating an unfavorable environment for fertilization or implantation. 

 

Types of Oral Contraceptives: 

1. Combined Oral Contraceptives (COCs): 

Contain both: 

• Estrogen: Usually ethinylestradiol 

• Progestin: Norethindrone, Levonorgestrel, Desogestrel, Drospirenone 

Types based on dosing: 

• Monophasic: Fixed estrogen and progestin dose throughout cycle 

• Biphasic/Triphasic: Varying progestin doses to mimic natural cycle 

2. Progestin-only Pills (POPs or Mini-pills): 

• Contain only low-dose progestin (e.g., norethindrone) 

• Suitable for women who cannot tolerate estrogen (e.g., breastfeeding women, older age) 

3. Emergency Contraceptive Pills (ECPs): 

• High-dose levonorgestrel or ulipristal acetate 

• Used within 72–120 hours of unprotected intercourse 

 

Mechanism of Action: 

Combined Oral Contraceptives: 

• Inhibit ovulation by suppressing LH and FSH from anterior pituitary 

• Thicken cervical mucus → prevents sperm penetration 

• Alter endometrial lining → impairs implantation 

Progestin-only Pills: 

• Do not reliably inhibit ovulation 

• Act mainly by thickening cervical mucus and endometrial changes 

 

Benefits and Non-Contraceptive Uses: 

• Highly effective contraception (failure rate <1%) 

• Regulates menstrual cycle 

• Reduces dysmenorrhea, menorrhagia 

• Improves acne 

• Lowers risk of endometrial and ovarian cancers, benign breast disease 

• Treats PCOS, endometriosis 

 

Adverse Effects: 

• Nausea, vomiting, breast tenderness 

• Weight gain, mood changes 

• Breakthrough bleeding (especially with POPs) 

• Increased risk of thromboembolism, especially in smokers or over age 35 

• Rare: Hypertension, liver dysfunction 

 

Contraindications: 

• History of thromboembolism or stroke 

• Liver disease 

• Estrogen-dependent tumors 

• Pregnancy 

• Heavy smokers over 35 years 

 

Drug Interactions: 

• Rifampin, phenytoin, carbamazepine may reduce efficacy 

• Antibiotics may alter gut flora and affect estrogen recycling 

 

Conclusion: 

Oral contraceptives offer safe, effective, and reversible birth control. They also provide several non-contraceptive health benefits, though they require careful screening for contraindications. Patient counseling and compliance are crucial for long-term success. 

6. Explain in detail hemodynamic and electrophysiology of human heart. 
(10 Marks | 400–450 words) 

 

Introduction: 

The human heart is a muscular organ that pumps blood through a coordinated process involving electrical excitation (electrophysiology) and mechanical contraction (hemodynamics). Proper functioning of both aspects ensures efficient circulation, oxygen delivery, and removal of metabolic waste. 

 

I. Hemodynamics of the Heart: 

Hemodynamics refers to the dynamics of blood flow within the cardiovascular system, governed by pressure gradients, cardiac output, and resistance. 

Key Parameters: 

1. Cardiac Output (CO): 

1. CO = Heart Rate (HR) × Stroke Volume (SV) 

2. Normal: ~5 L/min 

3. Regulated by autonomic nervous system, preload, afterload, and contractility 

2. Stroke Volume (SV): 

1. Volume of blood ejected per beat (~70 mL) 

2. Influenced by preload (end-diastolic volume), afterload (arterial pressure), and myocardial contractility 

3. Blood Pressure (BP): 

1. Systolic/Diastolic (e.g., 120/80 mmHg) 

2. Maintained by baroreceptor reflex, renin-angiotensin system 

4. Frank-Starling Law: 

1. ↑ ventricular filling (preload) → ↑ stroke volume due to optimal actin-myosin overlap in cardiac muscle 

5. Vascular Resistance: 

1. Total Peripheral Resistance (TPR) affects afterload 

2. Controlled by arteriolar tone (sympathetic activity, hormones) 

 

II. Electrophysiology of the Heart: 

Electrophysiology refers to the generation and conduction of electrical impulses in the heart, which trigger its rhythmic contractions. 

Conduction System: 

1. Sinoatrial (SA) Node: 

1. Pacemaker of the heart (60–100 bpm) 

2. Initiates impulse → atrial contraction 

2. Atrioventricular (AV) Node: 

1. Delays impulse (~0.1 sec) → allows ventricular filling 

3. Bundle of His → Right and Left Bundle Branches → Purkinje Fibers: 

1. Rapid conduction system ensuring synchronized ventricular contraction 

 

Phases of Cardiac Action Potential: 

A. Ventricular Myocytes (Fast Response): 

1. Phase 0: Rapid depolarization (Na⁺ influx) 

2. Phase 1: Initial repolarization (K⁺ out) 

3. Phase 2: Plateau (Ca²⁺ influx balances K⁺ efflux) 

4. Phase 3: Repolarization (K⁺ out) 

5. Phase 4: Resting membrane potential 

B. SA/AV Nodes (Slow Response): 

1. Phase 0: Ca²⁺ influx (slow depolarization) 

2. Phase 3: K⁺ efflux (repolarization) 

3. Phase 4: Slow depolarization via funny current (If) 

 

ECG Correlation: 

• P wave: Atrial depolarization 

• QRS complex: Ventricular depolarization 

• T wave: Ventricular repolarization 

• PR interval: AV nodal delay 

• QT interval: Ventricular depolarization and repolarization 

 

Conclusion: 

The heart's efficient pumping relies on synchronized electrical impulses and coordinated hemodynamic forces. Abnormalities in either domain can lead to arrhythmias, heart failure, or hemodynamic shock. Understanding both systems is essential for diagnosing and treating cardiovascular diseases. 

7. Enlist antihypertensive drugs. Give pharmacology of nitrates. 
(10 Marks | 400–450 words) 

 

I. Antihypertensive Drugs – Classification: 

Antihypertensives are used to lower elevated blood pressure and prevent complications like stroke and heart disease. They are classified as follows: 

1. Diuretics 

• Thiazide diuretics: Hydrochlorothiazide, Chlorthalidone 

• Loop diuretics: Furosemide 

• K⁺-sparing diuretics: Spironolactone 

2. Sympatholytics 

• Centrally acting: Clonidine, Methyldopa 

• Beta-blockers: Propranolol, Atenolol, Metoprolol 

• Alpha-blockers: Prazosin, Terazosin 

3. Vasodilators 

• Direct vasodilators: Hydralazine, Minoxidil 

• Nitrates: Nitroglycerin, Isosorbide dinitrate (used more for angina) 

4. Calcium Channel Blockers (CCBs) 

• Dihydropyridines: Amlodipine, Nifedipine 

• Non-dihydropyridines: Verapamil, Diltiazem 

5. RAAS Inhibitors 

• ACE inhibitors: Enalapril, Ramipril 

• ARBs: Losartan, Telmisartan 

• Direct renin inhibitors: Aliskiren 

 

II. Pharmacology of Nitrates: 

Nitrates are organic compounds that act as vasodilators primarily used in angina pectoris and heart failure, though occasionally used in hypertensive emergencies. 

1. Common Nitrates: 

• Nitroglycerin (GTN) 

• Isosorbide mononitrate 

• Isosorbide dinitrate 

• Sodium nitroprusside (used IV in emergencies) 

 

2. Mechanism of Action: 

• Nitrates are prodrugs that release nitric oxide (NO) in vascular smooth muscle. 

• NO activates guanylyl cyclase, increasing cyclic GMP (cGMP) levels. 

• cGMP causes dephosphorylation of myosin light chains, leading to relaxation of smooth muscle. 

• Venodilation predominates → ↓ preload → ↓ myocardial oxygen demand. 

• At higher doses: Arterial dilation → ↓ afterload 

 

3. Pharmacological Actions: 

• Vasodilation: Reduces myocardial oxygen consumption 

• Coronary vasodilation: Enhances blood flow in ischemic areas 

• Relieves angina by improving oxygen supply/demand ratio 

• Reduces pulmonary congestion in acute heart failure 

• In IV form (nitroprusside), used in hypertensive crisis 

 

4. Therapeutic Uses: 

• Angina pectoris (stable, unstable, variant) 

• Acute myocardial infarction 

• Congestive heart failure (CHF) 

• Hypertensive emergencies (e.g., nitroprusside) 

• Pulmonary edema 

 

5. Adverse Effects: 

• Headache, flushing, dizziness (due to vasodilation) 

• Hypotension, reflex tachycardia 

• Tolerance develops with continuous use → nitrate-free interval needed 

• Cyanide toxicity (with nitroprusside) 

 

6. Drug Interactions: 

• Severe hypotension with phosphodiesterase-5 inhibitors (e.g., sildenafil) 

 

Conclusion: 

While nitrates are not first-line agents for chronic hypertension, nitroprusside is vital in hypertensive crises. Their primary use remains in angina and heart failure, owing to their potent vasodilatory and preload-reducing actions. 

8. Classify diuretics. Give mechanism, pharmacological actions, side effects, uses and limitations of furosemide. 
(10 Marks | 400–450 words) 

 

I. Classification of Diuretics: 

Diuretics are agents that promote the excretion of water and electrolytes, primarily sodium, through the kidneys. They are classified as follows: 

1. High-Ceiling (Loop) Diuretics: 

• Furosemide, Bumetanide, Torsemide 

2. Thiazide Diuretics: 

• Hydrochlorothiazide, Chlorthalidone 

3. Potassium-Sparing Diuretics: 

• Aldosterone antagonists: Spironolactone, Eplerenone 

• Sodium channel blockers: Amiloride, Triamterene 

4. Carbonic Anhydrase Inhibitors: 

• Acetazolamide 

5. Osmotic Diuretics: 

• Mannitol 

 

II. Furosemide: A Prototype Loop Diuretic 

 

1. Mechanism of Action: 

• Furosemide acts on the thick ascending limb of the loop of Henle, where it inhibits the Na⁺–K⁺–2Cl⁻ cotransporter (NKCC2). 

• This inhibition: 

• Prevents reabsorption of ~25% of filtered Na⁺ 

• Causes excretion of Na⁺, K⁺, Cl⁻, Mg²⁺, Ca²⁺, and water 

• Leads to strong diuretic action 

 

2. Pharmacological Actions: 

• Potent diuresis: Rapid and extensive water and electrolyte loss 

• Venodilation (IV use): Reduces preload, helpful in pulmonary edema 

• Increased urinary excretion of calcium and magnesium 

 

3. Therapeutic Uses: 

• Acute pulmonary edema (rapid venodilation and diuresis) 

• Congestive heart failure (CHF) 

• Chronic renal failure and nephrotic syndrome 

• Hypertension (when complicated by renal impairment) 

• Hypercalcemia (promotes calcium excretion) 

• Cerebral edema (with mannitol) 

 

4. Adverse Effects: 

• Hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia 

• Hyperuricemia → may precipitate gout 

• Ototoxicity (especially with aminoglycosides) 

• Hypovolemia, hypotension 

• Hyperglycemia (mild) 

• Allergic reactions (sulfonamide derivative) 

 

5. Limitations: 

• Short duration of action (~6 hours) 

• Tolerance with prolonged use 

• Not ideal for long-term BP control 

• Risk of electrolyte disturbances and dehydration 

 

Precautions & Interactions: 

• Monitor electrolytes and renal function regularly 

• Avoid with other ototoxic drugs 

• Combine with potassium-sparing diuretic to prevent hypokalemia 

 

Conclusion: 

Furosemide is a potent loop diuretic, ideal for acute fluid overload conditions like pulmonary edema and heart failure. However, its electrolyte-depleting effects and short action duration limit its long-term use in uncomplicated hypertension. 

9. What are various thyroid inhibitors? Explain pharmacology of thioamides. 
(10 Marks | 400–450 words) 

 

Introduction: 

Thyroid inhibitors are drugs used to reduce the synthesis or release of thyroid hormones and are primarily used to treat hyperthyroidism, including Graves’ disease and thyrotoxicosis. These drugs target various steps in thyroid hormone synthesis and function. 

 

I. Classification of Thyroid Inhibitors: 

A. Inhibitors of Thyroid Hormone Synthesis (Antithyroid drugs): 

1. Thioamides: 

1. Propylthiouracil (PTU) 

2. Methimazole 

3. Carbimazole (prodrug of methimazole) 

2. Iodide (high doses): 

1. Potassium iodide 

2. Lugol’s iodine 

B. Inhibitors of Hormone Release: 

• High-dose iodine preparations 

• Lithium (inhibits hormone release) 

C. Iodine Uptake Inhibitors: 

• Perchlorate, thiocyanate (rarely used due to toxicity) 

D. Radioactive Iodine (RAI): 

• Iodine-131 (¹³¹I): Destroys thyroid tissue (used in hyperthyroidism and thyroid cancer) 

 

II. Pharmacology of Thioamides: 

1. Mechanism of Action: 

• Thioamides inhibit thyroid peroxidase (TPO) enzyme, which catalyzes: 

• Oxidation of iodide to iodine 

• Iodination of tyrosine residues (organification) 

• Coupling of iodotyrosines (MIT + DIT → T₃/T₄) 

• Propylthiouracil (PTU) also inhibits peripheral conversion of T₄ to T₃. 

 

2. Pharmacokinetics: 

• Methimazole is more potent, longer-acting, and preferred due to once-daily dosing. 

• PTU has a shorter half-life and requires multiple daily doses but is preferred in pregnancy and thyroid storm. 

 

3. Therapeutic Uses: 

• Graves’ disease (autoimmune hyperthyroidism) 

• Preparation for thyroid surgery (to attain euthyroid state) 

• Thyroid storm (PTU preferred) 

• Adjunct to radioactive iodine therapy 

 

4. Adverse Effects: 

• Skin rashes, pruritus, arthralgia 

• Agranulocytosis (rare but serious; requires monitoring of WBCs) 

• Hepatotoxicity (more common with PTU) 

• Teratogenicity (methimazole not preferred in the first trimester) 

• Goiter (due to compensatory rise in TSH) 

 

5. Limitations: 

• Slow onset of action (weeks), as stored hormone must be depleted 

• Frequent relapses after discontinuation 

• Requires long-term monitoring 

 

Conclusion: 

Thioamides like methimazole and PTU remain the first-line medical therapy for hyperthyroidism, especially in mild to moderate cases. Though effective, their adverse effect profile and slow onset necessitate careful monitoring and patient counseling. In refractory cases, RAI or surgery may be preferred. 

10. Classify drugs for CHF. Describe the mechanism, pharmacological action, uses, and interactions of digitalis. 
(10 Marks | 400–450 words) 

 

Introduction: 

Congestive Heart Failure (CHF) is a clinical syndrome characterized by the heart’s inability to pump sufficient blood to meet the metabolic needs of the body. Pharmacotherapy in CHF aims to improve cardiac output, relieve symptoms, and prolong survival. 

 

I. Classification of Drugs for CHF: 

1. Positive Inotropic Agents: 

• Cardiac glycosides: Digoxin 

• Sympathomimetics: Dobutamine, Dopamine 

• Phosphodiesterase inhibitors: Milrinone 

2. Diuretics: 

• Loop diuretics (Furosemide) 

• Thiazides (Hydrochlorothiazide) 

• K⁺-sparing (Spironolactone) 

3. Vasodilators: 

• ACE inhibitors (Enalapril) 

• ARBs (Losartan) 

• Hydralazine + Nitrates 

4. Beta-Blockers (in compensated CHF): 

• Carvedilol, Metoprolol, Bisoprolol 

5. Aldosterone Antagonists: 

• Spironolactone, Eplerenone 

6. Newer Agents: 

• ARNI (Sacubitril + Valsartan) 

• SGLT2 inhibitors: Dapagliflozin 

 

II. Digitalis (Digoxin) – A Cardiac Glycoside 

 

1. Mechanism of Action: 

• Digoxin inhibits Na⁺/K⁺-ATPase in cardiac myocytes. 

• This increases intracellular Na⁺, reducing Na⁺/Ca²⁺ exchange. 

• Result: ↑ intracellular Ca²⁺ → enhanced myocardial contractility (positive inotropy) 

• Also increases vagal tone, reducing SA node firing and AV conduction. 

 

2. Pharmacological Actions: 

• Heart: 

• ↑ force of contraction (positive inotropy) 

• ↓ heart rate (negative chronotropy) 

• ↓ AV conduction (useful in atrial fibrillation) 

• Kidney: 

• ↑ renal perfusion (due to ↑ cardiac output) 

• ANS: 

• Enhances parasympathetic (vagal) activity 

 

3. Therapeutic Uses: 

• CHF (especially with atrial fibrillation) 

• Atrial flutter/fibrillation 

• Less effective in diastolic heart failure without systolic dysfunction 

 

4. Adverse Effects: 

• Gastrointestinal: Anorexia, nausea, vomiting 

• Cardiac: Arrhythmias (PVCs, AV block) 

• CNS: Visual disturbances (yellow vision, confusion) 

• Narrow therapeutic index 

 

5. Drug Interactions: 

• Potentiated by hypokalemia (e.g., with diuretics) → ↑ toxicity 

• Quinidine, verapamil, amiodarone increase digoxin levels 

• Antacids, cholestyramine decrease absorption 

 

6. Monitoring: 

• Serum digoxin levels (therapeutic: 0.8–2.0 ng/mL) 

• Serum electrolytes (especially K⁺, Mg²⁺) 

• Renal function 

 

Conclusion: 

Digoxin is a potent positive inotropic drug that plays a crucial role in CHF with atrial arrhythmias. Despite its usefulness, it requires careful dosing, monitoring, and awareness of interactions, due to its narrow therapeutic index. 

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