1. What is the mechanism of action of warfarin and how does it differ from heparin? Explain the implications for monitoring and reversal of anticoagulation. - Warfarin is a vitamin K antagonist that inhibits the synthesis of clotting factors II, VII, IX and X in the liver. Heparin is an indirect thrombin inhibitor that binds to antithrombin III and enhances its activity. Warfarin has a delayed onset and offset of action, whereas heparin has an immediate effect. Warfarin requires regular monitoring of the international normalized ratio (INR) to adjust the dose and prevent bleeding or thrombosis. Heparin requires monitoring of the activated partial thromboplastin time (aPTT) or anti-Xa levels. Warfarin can be reversed with vitamin K or prothrombin complex concentrate (PCC). Heparin can be reversed with protamine sulfate. 2. What are the main adverse effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)? How can they be prevented or managed? - The main adverse effects of ACE inhibitors and ARBs are hypotension, hyperkalemia, renal impairment and cough (more common with ACE inhibitors). They can be prevented or managed by adjusting the dose, monitoring blood pressure, electrolytes and renal function, avoiding potassium supplements or potassium-sparing diuretics, and switching to an ARB if cough is intolerable. 3. What are the indications and contraindications for the use of beta-blockers in cardiovascular diseases? Give examples of selective and non-selective beta-blockers and their pharmacokinetic properties. - Beta-blockers are indicated for the treatment of hypertension, angina, myocardial infarction, heart failure, arrhythmias, and prevention of migraine. They are contraindicated in patients with asthma, severe bradycardia, heart block, cardiogenic shock, or peripheral vascular disease. Selective beta-blockers (e.g., atenolol, metoprolol) block beta-1 receptors in the heart and have less effect on beta-2 receptors in the lungs and blood vessels. Non-selective beta-blockers (e.g., propranolol, nadolol) block both beta-1 and beta-2 receptors and have more potential for bronchoconstriction and vasoconstriction. Beta-blockers differ in their lipid solubility, which affects their ability to cross the blood-brain barrier and cause central nervous system effects (e.g., sedation, depression). Lipid-soluble beta-blockers (e.g., propranolol) have more CNS effects