Practice pharmacology Cardio exam - Dr Matt Cheesman - 2009PHM 2023 (1).docx

1. (a) Name the two different drug classes (and ONE example drug) that are used to treat hypertension by interacting with α or β receptors. (2 MARKS) (b) Use diagrams, if you wish, to show their mechanism of action. (4 MARKS) 2. The renin-angiotensin-aldosterone system (RAAS) pathway can be interven...

1. (a) Name the two different drug classes (and ONE example drug) that are used to treat hypertension by interacting with α or β receptors. (2 MARKS) (b) Use diagrams, if you wish, to show their mechanism of action. (4 MARKS) 2. The renin-angiotensin-aldosterone system (RAAS) pathway can be intervened with using numerous different cardiovascular drugs. (a) Name the drug classes that can affect the RAAS, and the cardiovascular conditions in which they are used for treatment. (b) Name specific drugs from each of these drug classes. (c) Describe or draw the mechanisms of action of the drugs and include in your answer how they affect the RAAS. 3. (a) Using the diagram below, show how indapamide acts to promote diuresis. What is the pharmacological outcome in terms of ion concentrations in blood and urine? (6 MARKS) (b) Describe the “ceiling effect” that occurs with the use of thiazide and thiazide-like drugs. (2 MARKS) 4. How does aldosterone cause the reabsorption of Na+ into the blood, and the loss of K+ in the urine? Draw a diagram showing this mechanism and indicate where this process can be blocked by two different classes of potassium-sparing diuretics. (6 MARKS). Also, name the drugs from these drug classes. (2 MARKS) 5. The following questions relate to drugs that increase blood flow. Name the different drug classes, and specific drug names from those classes, which increase cyclic GMP (cGMP) inside smooth muscle cells which ultimately leads to the dilation of blood vessels. (5 MARKS) For each drug, describe the molecular mechanism of action which causes this vasodilation. (8 MARKS) How does treatment with these drugs affect the cardiovascular system? (3 MARKS) 6. Complete the following Table on the third-line antianginal drugs. Drug Mechanism of action Extra task ivabradine Name TWO (2) adverse effects: blocks the carnitine palmitoyltransferase enzyme in cardiac cells. the cells then use glucose instead of fatty acids. less O2 consumed, less demand on heart. Discuss the importance of a cytochrome P450 in the use of this drug: nicorandil Why do some patients experience headaches and dizziness when taking this drug? 7. The following questions refer to drugs that are used to treat dyslipidaemia. Name all of the cholesterol-lowering drug classes that cause increases in the expression of hepatic LDL receptors. (3 MARKS) What are the drug names from these classes? (2 MARKS) What are their drug mechanisms that ultimately lead to the overexpression of liver LDL receptors? Use diagrams, if you wish, to show your answers. (6 MARKS) 8. Discuss the progression of statin-induced muscle toxicity that can lead ultimately to rhabdomyolysis. (5 MARKS) 9. Discuss the importance of cytochrome P450 enzymes in possible drug interactions with the statin drugs. (4 MARKS) 10. What are the different types of heparins? Discuss the differences between these different drug classes in terms of their pharmacological mechanisms of action. (5 MARKS) 11. To which class of drugs do bivalirudin and dabigatran belong? Draw a diagram showing the differences in binding of these drugs to their target. (4 MARKS) 12. Name TWO (2) drugs that bind to the target indicated on the following diagram: (2 MARKS) 13. Which drug inhibits the vitamin K oxidoreductase enzyme? Describe how this drug works and its pharmacological outcomes. (4 MARKS) 14. When drugs are administered to patients to lyse a blood clot, this is known as “lysis therapy” or “thrombolytic therapy”. What are the names of THREE of these drugs, and how do they work pharmacologically? (4 MARKS) 15. Draw a diagram showing how platelet attachment to damaged endothelium, and aggregation to each other. (5 MARKS) Once activated, what do the platelets now start producing in high amounts? (1 MARK) 16. What role does aspirin play in platelet aggregation? (2 MARKS) 17. Draw the pathway by which ADP causes platelet aggregation. Which drugs would you use to interfere with this process? Is binding of these drugs to their target permanent or reversible? (4 MARKS) 18. Show how the drugs abciximab, tirofiban and eptifibatide interfere with platelet aggregation. What class of drugs do they belong to? (3 MARKS) 19. Describe the mechanism of action of digoxin which leads to an increased concentration of Ca2+ inside cardiac smooth muscle cells. (3 MARKS) Some more practice pharmacology MCQs 1. Which of the following increases the expression of apoA1 and apoA5? [1 MARK] ezetimibe gemfibrozil pravastatin niacin colestipol 2. Which of the following is stimulated by the nitric oxide (NO) that is liberated from nitrate drugs? [1 MARK] cyclic GMP cyclic AMP guanyl cyclase myosin light chain phosphatase actin 3. Which of the following is a non-modifiable risk factor for hypertension? [1 MARK] BMI and waist circumference cholesterol level physical activity familial hypercholesterolaemia salt intake 4. Which of the following drugs slows down sympathetic outflow from the central nervous system? [1 MARK] prazosin mannitol ramipril irbesartan clonidine 5. Which of the following drugs stops the production of thrombin? [1 MARK] bivalirudin rivaroxaban unfractionated heparins phytomenadione cholestyramine 6. To which drug class does aspirin belong? [1 MARK] Heparin blockers Antiplatelets Antifibrinolytics Thrombolytics Vitamin K antagonists 7. Which of the following drugs lowers triglyceride (TG) levels by agonism of the PPARα receptors? [1 MARK] Atorvastatin Cholestyramine Ezetimibe Gemfibrozil Niacin Note: Don’t forget to study all of your workshop questions as well, and review all lectures, since this practice exam does not cover everything on the pharmacology.