Jawaharlal Nehru Technological University Hyderabad B.Pharmacy III Year PHARMACOLOGY-II Previous Question Paper (August - 2022 - R17)

Hypertension is defined as a persistent elevation of arterial blood pressure where the systolic pressure is 140 mmHg or higher and/or the diastolic pressure is 90 mmHg or higher.

Anti-hypertensive drugs are classified based on their mechanism of action:

1. Diuretics: These reduce blood volume and peripheral resistance. Thiazides (e.g., Hydrochlorothiazide) inhibit Na+/Cl- symporters in the distal convoluted tubule. Loop diuretics (e.g., Furosemide) inhibit the Na+/K+/2Cl- cotransporter in the ascending limb of the loop of Henle.
2. Sympatholytics: These reduce sympathetic outflow. Centrally acting agents (e.g., Methyldopa, Clonidine) stimulate alpha-2 adrenergic receptors in the brainstem to decrease sympathetic tone. Beta-blockers (e.g., Propranolol, Atenolol) block beta-1 receptors in the heart to reduce cardiac output and inhibit renin release. Alpha-blockers (e.g., Prazosin) block alpha-1 receptors on vascular smooth muscle to cause vasodilation.
3. ACE Inhibitors: Drugs like Enalapril and Lisinopril inhibit the Angiotensin-Converting Enzyme, preventing the conversion of Angiotensin I to the potent vasoconstrictor Angiotensin II and reducing aldosterone secretion.
4. Angiotensin Receptor Blockers (ARBs): Agents like Losartan and Telmisartan selectively antagonize the AT1 receptors, thereby blocking the effects of Angiotensin II directly.
5. Calcium Channel Blockers (CCBs): Dihydropyridines (e.g., Amlodipine) block L-type calcium channels in vascular smooth muscle, causing profound vasodilation. Non-dihydropyridines (e.g., Verapamil, Diltiazem) act on both the heart and blood vessels to reduce heart rate and contractility.
6. Vasodilators: Direct-acting vasodilators like Hydralazine act directly on vascular smooth muscle to cause relaxation, often used in severe hypertension.

Congestive Heart Failure (CHF) is a pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or can do so only from an elevated filling pressure. It results from structural or functional impairment of ventricular filling or ejection of blood.

Drugs used in the treatment of CHF are classified based on their mechanism of action and clinical utility:

• Inotropic Agents: Digoxin (a cardiac glycoside) inhibits the Na+/K+-ATPase pump, increasing intracellular calcium and enhancing myocardial contractility.
• RAAS Inhibitors: ACE inhibitors (e.g., Enalapril, Ramipril) are first-line agents that reduce preload and afterload by inhibiting the formation of Angiotensin II. Angiotensin Receptor Blockers (ARBs) like Losartan are used for patients intolerant to ACE inhibitors.
• Beta-Blockers: Carvedilol, Metoprolol, and Bisoprolol are essential in chronic CHF to block the deleterious effects of chronic sympathetic nervous system activation, improving long-term survival and ventricular remodeling.
• Diuretics: Loop diuretics (e.g., Furosemide) are used to manage fluid overload and pulmonary congestion by promoting sodium and water excretion. Thiazides may be used in mild cases.
• Aldosterone Antagonists: Spironolactone and Eplerenone block the effects of aldosterone on the heart and kidneys, preventing fibrosis and reducing mortality.
• Vasodilators: Hydralazine (arterial dilator) and Isosorbide dinitrate (venodilator) are often used in combination, particularly in patients who cannot tolerate ACE inhibitors or ARBs.
• Neprilysin Inhibitors: Sacubitril, combined with Valsartan (ARNI), inhibits the breakdown of natriuretic peptides, promoting vasodilation and natriuresis.
• SGLT2 Inhibitors: Dapagliflozin and Empagliflozin have recently become standard therapy for heart failure with reduced ejection fraction, providing significant cardiovascular protection.