I'm a second mbbs student Today i have my final paper of pharmacology. The topic is want to revise is CVS Prepare flashcards to help me revise important topics in detail 2nd mbbs pharmacology
Reading File
Reading File
CVS pharmacology revision can be divided into these high-yield blocks:
-
Antihypertensives
Diuretics, ACE inhibitors, ARBs, beta-blockers, calcium-channel blockers, alpha-blockers, centrally acting drugs, vasodilators, hypertensive emergencies. -
Drugs for angina and ischemic heart disease
Nitrates, beta-blockers, calcium-channel blockers, ranolazine, ivabradine, drug choice in stable angina and acute coronary syndrome. -
Drugs for heart failure
ACE inhibitors/ARBs/ARNI, beta-blockers, diuretics, digoxin, mineralocorticoid antagonists, SGLT2 inhibitors, inotropes. -
Antiarrhythmic drugs
Vaughan-Williams classification, mechanisms, ECG effects, key adverse effects, adenosine, atropine, magnesium sulfate. -
Drugs affecting coagulation and thrombosis
Antiplatelets, anticoagulants, fibrinolytics, heparin antidotes, warfarin interactions, DOACs. -
Hypolipidemic drugs
Statins, fibrates, ezetimibe, PCSK9 inhibitors, adverse effects and monitoring. -
Shock and emergency cardiovascular drugs
Adrenaline, noradrenaline, dopamine, dobutamine, vasopressin, nitroprusside, acute pulmonary edema.
For an MBBS pharmacology paper, the most repeatedly tested areas are: antihypertensives, antianginals, heart-failure drugs, antiarrhythmics, antiplatelets/anticoagulants, and statins.
Which flashcard set should I prepare first?
- Complete rapid-revision deck - all CVS topics, exam-focused
- Antihypertensives + angina
- Heart failure + antiarrhythmics
- Anticoagulants + antiplatelets + thrombolytics
Make flashcards on antihypertensives and antianginal drugs
Finding Sources
Searching PubMed
hypertension AND pharmacotherapy
Searching the Web
WHO hypertension pharmacological treatment guideline antihypertensive medicines
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Searching PubMed
stable angina AND pharmacotherapy
CVS Pharmacology Flashcards: Antihypertensives and Antianginal Drugs
Use these actively: cover the answer, recall aloud, then check.
A. Antihypertensive Drugs
1. What are the major classes of antihypertensive drugs?
Answer:
- Diuretics
- ACE inhibitors
- Angiotensin receptor blockers (ARBs)
- Calcium-channel blockers (CCBs)
- Beta-blockers
- Alpha-1 blockers
- Central sympatholytics
- Direct vasodilators
- Direct renin inhibitor
2. What are the common first-line drug classes for uncomplicated hypertension?
Answer:
Thiazide/thiazide-like diuretic, ACE inhibitor or ARB, and long-acting dihydropyridine CCB.
WHO recommends these as initial pharmacological classes for most adults with hypertension in appropriate clinical settings, as summarized in the WHO hypertension guideline.
Thiazide/thiazide-like diuretic, ACE inhibitor or ARB, and long-acting dihydropyridine CCB.
WHO recommends these as initial pharmacological classes for most adults with hypertension in appropriate clinical settings, as summarized in the WHO hypertension guideline.
3. What is the basic principle of rational combination therapy in hypertension?
Answer:
Combine drugs with different mechanisms, usually:
Combine drugs with different mechanisms, usually:
- ACE inhibitor/ARB + thiazide
- ACE inhibitor/ARB + dihydropyridine CCB
Avoid ACE inhibitor + ARB together because of increased risk of hyperkalemia, hypotension, and renal impairment.
4. What is the mechanism of action of thiazide diuretics?
Answer:
They inhibit the Na+-Cl- cotransporter in the early distal convoluted tubule.
This causes natriuresis, reduced plasma volume initially, and reduced peripheral vascular resistance on long-term use.
They inhibit the Na+-Cl- cotransporter in the early distal convoluted tubule.
This causes natriuresis, reduced plasma volume initially, and reduced peripheral vascular resistance on long-term use.
5. Name thiazide and thiazide-like diuretics.
Answer:
- Hydrochlorothiazide
- Chlorthalidone
- Indapamide
6. List important adverse effects of thiazides.
Answer:
HyperGLUC mnemonic:
HyperGLUC mnemonic:
- Hyperglycemia
- Hyperuricemia
- Hyperlipidemia
- Hypercalcemia
- Hypokalemic metabolic alkalosis
- Hyponatremia
- Erectile dysfunction
- Sulfonamide hypersensitivity
7. Which diuretic is especially useful in hypertension with recurrent calcium stones?
Answer:
Thiazide, because it decreases urinary calcium excretion.
Thiazide, because it decreases urinary calcium excretion.
8. What is the antihypertensive role of loop diuretics?
Answer:
They are not routine first-line drugs for uncomplicated hypertension. They are useful when hypertension coexists with:
They are not routine first-line drugs for uncomplicated hypertension. They are useful when hypertension coexists with:
- Heart failure with edema
- Chronic kidney disease
- Reduced GFR
- Pulmonary edema
9. Which diuretic causes hyperkalemia and gynecomastia?
Answer:
Spironolactone.
It is an aldosterone antagonist and potassium-sparing diuretic.
Spironolactone.
It is an aldosterone antagonist and potassium-sparing diuretic.
10. What are the important uses of spironolactone in CVS pharmacology?
Answer:
- Resistant hypertension
- Hyperaldosteronism
- Heart failure with reduced ejection fraction
- Cirrhosis with ascites
11. What is the mechanism of ACE inhibitors?
Answer:
They inhibit ACE, causing:
They inhibit ACE, causing:
- Decreased angiotensin II
- Decreased aldosterone
- Decreased vasoconstriction
- Increased bradykinin
Net effect: reduced preload, afterload, and blood pressure.
12. Name common ACE inhibitors.
Answer:
- Captopril
- Enalapril
- Lisinopril
- Ramipril
- Perindopril
- Fosinopril
13. What are the adverse effects of ACE inhibitors?
Answer:
- Dry cough
- Angioedema
- Hyperkalemia
- First-dose hypotension
- Acute kidney injury in bilateral renal artery stenosis
- Fetotoxicity
14. Why do ACE inhibitors cause dry cough and angioedema?
Answer:
They inhibit degradation of bradykinin, leading to bradykinin accumulation.
They inhibit degradation of bradykinin, leading to bradykinin accumulation.
15. What are the contraindications to ACE inhibitors?
Answer:
- Pregnancy
- Previous ACE inhibitor-induced angioedema
- Bilateral renal artery stenosis
- Significant hyperkalemia
Use cautiously in renal impairment and volume depletion.
16. What is the mechanism of ARBs?
Answer:
ARBs selectively block AT1 receptors for angiotensin II.
They reduce vasoconstriction, aldosterone secretion, and sympathetic activation.
ARBs selectively block AT1 receptors for angiotensin II.
They reduce vasoconstriction, aldosterone secretion, and sympathetic activation.
17. Name common ARBs.
Answer:
- Losartan
- Valsartan
- Telmisartan
- Candesartan
- Olmesartan
18. What is the major advantage of ARBs over ACE inhibitors?
Answer:
ARBs usually do not cause dry cough, because they do not increase bradykinin significantly.
ARBs usually do not cause dry cough, because they do not increase bradykinin significantly.
19. Which ARB has a uricosuric effect?
Answer:
Losartan.
It may be preferred in a hypertensive patient with hyperuricemia or gout, if otherwise suitable.
Losartan.
It may be preferred in a hypertensive patient with hyperuricemia or gout, if otherwise suitable.
20. What is the mechanism of action of calcium-channel blockers?
Answer:
They block L-type calcium channels.
They block L-type calcium channels.
- In blood vessels: vasodilation
- In heart: reduced contractility, conduction, and heart rate depending on the drug
21. Classify calcium-channel blockers.
Answer:
Dihydropyridines:
Dihydropyridines:
- Amlodipine
- Nifedipine
- Felodipine
- Nicardipine
Non-dihydropyridines:
- Verapamil
- Diltiazem
22. What are the main differences between dihydropyridine and non-dihydropyridine CCBs?
Answer:
| Feature | Dihydropyridines | Verapamil/Diltiazem |
|---|---|---|
| Main action | Vascular smooth muscle | Heart plus vessels |
| Heart rate | Reflex tachycardia possible | Bradycardia |
| Contractility | Minimal decrease | Decreased |
| AV conduction | Little effect | Decreased |
| Main use | Hypertension, angina | Angina, supraventricular tachyarrhythmias |
23. What are adverse effects of dihydropyridine CCBs?
Answer:
- Headache
- Flushing
- Dizziness
- Ankle edema
- Reflex tachycardia, especially short-acting nifedipine
- Gingival hyperplasia
24. What is a characteristic adverse effect of verapamil?
Answer:
Constipation.
It can also cause bradycardia, AV block, hypotension, and worsening heart failure.
Constipation.
It can also cause bradycardia, AV block, hypotension, and worsening heart failure.
25. Why should verapamil or diltiazem generally not be combined with beta-blockers?
Answer:
Both depress SA-node activity, AV-node conduction, and myocardial contractility. Combination can cause:
Both depress SA-node activity, AV-node conduction, and myocardial contractility. Combination can cause:
- Severe bradycardia
- AV block
- Heart failure
26. What is the mechanism of beta-blockers in hypertension?
Answer:
They lower blood pressure by:
They lower blood pressure by:
- Decreasing heart rate and cardiac output
- Decreasing renin release from juxtaglomerular cells via beta-1 blockade
- Reducing sympathetic activity
27. Name common beta-blockers used in CVS disorders.
Answer:
- Metoprolol
- Atenolol
- Bisoprolol
- Propranolol
- Carvedilol
- Labetalol
- Nebivolol
- Esmolol
28. Which beta-blockers have alpha-1 blocking action?
Answer:
- Labetalol
- Carvedilol
This produces additional vasodilation.
29. What are major adverse effects of beta-blockers?
Answer:
- Bradycardia
- AV block
- Fatigue
- Cold extremities
- Sleep disturbances/nightmares
- Sexual dysfunction
- Masking of hypoglycemia
- Bronchospasm with nonselective drugs
- Rebound tachycardia, angina, or hypertension if stopped abruptly
30. What are contraindications or major cautions for beta-blockers?
Answer:
- Bradycardia
- Second- or third-degree AV block
- Acute decompensated heart failure
- Severe asthma, especially for nonselective beta-blockers
- Vasospastic angina
31. Which antihypertensive is preferred in pregnancy?
Answer:
Commonly used drugs include:
Commonly used drugs include:
- Labetalol
- Nifedipine
- Methyldopa
- Hydralazine, especially IV use in severe hypertension
Avoid ACE inhibitors, ARBs, and direct renin inhibitors in pregnancy.
32. What is the mechanism of methyldopa?
Answer:
It is converted in the CNS to alpha-methylnoradrenaline, a central alpha-2 agonist. This reduces sympathetic outflow and lowers blood pressure.
It is converted in the CNS to alpha-methylnoradrenaline, a central alpha-2 agonist. This reduces sympathetic outflow and lowers blood pressure.
33. What are important adverse effects of methyldopa?
Answer:
- Sedation
- Depression
- Dry mouth
- Postural hypotension
- Coombs-positive hemolytic anemia
- Hepatotoxicity
- Hyperprolactinemia
34. What is the mechanism and important adverse effect of clonidine?
Answer:
Mechanism: central alpha-2 agonist that reduces sympathetic outflow.
Adverse effects: sedation, dry mouth, bradycardia, depression.
Abrupt withdrawal can cause rebound hypertension.
Mechanism: central alpha-2 agonist that reduces sympathetic outflow.
Adverse effects: sedation, dry mouth, bradycardia, depression.
Abrupt withdrawal can cause rebound hypertension.
35. What is the mechanism of prazosin?
Answer:
It selectively blocks peripheral alpha-1 receptors, causing arteriolar and venous dilation.
It selectively blocks peripheral alpha-1 receptors, causing arteriolar and venous dilation.
36. What is the classic adverse effect of prazosin?
Answer:
First-dose syncope, due to marked postural hypotension.
Start with a low bedtime dose.
First-dose syncope, due to marked postural hypotension.
Start with a low bedtime dose.
37. What are the additional uses of alpha-1 blockers?
Answer:
They improve urinary symptoms in benign prostatic hyperplasia by relaxing smooth muscle in the prostate and bladder neck.
They improve urinary symptoms in benign prostatic hyperplasia by relaxing smooth muscle in the prostate and bladder neck.
38. What is the mechanism of hydralazine?
Answer:
A direct arteriolar vasodilator. It decreases systemic vascular resistance and afterload.
A direct arteriolar vasodilator. It decreases systemic vascular resistance and afterload.
39. What are adverse effects of hydralazine?
Answer:
- Reflex tachycardia
- Fluid retention
- Headache
- Flushing
- Drug-induced lupus-like syndrome, especially with high doses and slow acetylators
40. What is the mechanism of minoxidil?
Answer:
It opens ATP-sensitive potassium channels in arteriolar smooth muscle, causing hyperpolarization and powerful arteriolar vasodilation.
It opens ATP-sensitive potassium channels in arteriolar smooth muscle, causing hyperpolarization and powerful arteriolar vasodilation.
41. What are important adverse effects and uses of minoxidil?
Answer:
Adverse effects:
Adverse effects:
- Reflex tachycardia
- Fluid retention
- Hypertrichosis
- Pericardial effusion
Uses: severe resistant hypertension; topical formulation for androgenetic alopecia.
42. What is sodium nitroprusside and what is its use?
Answer:
A rapidly acting IV vasodilator that releases nitric oxide and dilates both arteries and veins.
Used in hypertensive emergencies and acute LV failure under close monitoring.
A rapidly acting IV vasodilator that releases nitric oxide and dilates both arteries and veins.
Used in hypertensive emergencies and acute LV failure under close monitoring.
43. What is the serious toxicity of sodium nitroprusside?
Answer:
Cyanide toxicity, particularly with prolonged infusion, high doses, or renal/hepatic impairment. It can cause severe metabolic acidosis and neurological/cardiovascular toxicity.
Cyanide toxicity, particularly with prolonged infusion, high doses, or renal/hepatic impairment. It can cause severe metabolic acidosis and neurological/cardiovascular toxicity.
44. What is a hypertensive emergency?
Answer:
Severe hypertension with acute target-organ damage, for example:
Severe hypertension with acute target-organ damage, for example:
- Encephalopathy
- Pulmonary edema
- Acute kidney injury
- Aortic dissection
- Acute coronary syndrome
- Eclampsia
It needs carefully titrated IV therapy, not abrupt uncontrolled BP reduction.
B. Antianginal Drugs
45. What is the fundamental mechanism behind angina?
Answer:
Angina occurs due to imbalance between myocardial oxygen demand and myocardial oxygen supply.
Angina occurs due to imbalance between myocardial oxygen demand and myocardial oxygen supply.
46. What factors increase myocardial oxygen demand?
Answer:
- Increased heart rate
- Increased contractility
- Increased wall stress/preload
- Increased afterload
Remember: HR, contractility, preload, afterload.
47. What are the principal antianginal drug groups?
Answer:
- Organic nitrates
- Beta-blockers
- Calcium-channel blockers
- Ivabradine
- Ranolazine
- Nicorandil, where available
48. What is the mechanism of action of nitrates?
Answer:
Nitrates release nitric oxide (NO) in vascular smooth muscle.
NO activates guanylyl cyclase, increases cGMP, and causes vascular smooth-muscle relaxation.
Nitrates release nitric oxide (NO) in vascular smooth muscle.
NO activates guanylyl cyclase, increases cGMP, and causes vascular smooth-muscle relaxation.
49. What is the major hemodynamic effect of nitroglycerin?
Answer:
Predominant venodilation.
This reduces venous return, preload, left ventricular wall stress, and myocardial oxygen demand.
Predominant venodilation.
This reduces venous return, preload, left ventricular wall stress, and myocardial oxygen demand.
50. How do nitrates relieve angina?
Answer:
- Decrease preload and myocardial oxygen demand
- Dilate large epicardial coronary arteries
- Relieve coronary vasospasm
- Improve subendocardial perfusion through reduced LV end-diastolic pressure
51. Name important nitrate preparations.
Answer:
- Glyceryl trinitrate/nitroglycerin
- Isosorbide dinitrate
- Isosorbide mononitrate
- Amyl nitrite, rarely used
52. Which nitrate is used for rapid relief of an acute anginal attack?
Answer:
Sublingual nitroglycerin (glyceryl trinitrate).
Sublingual nitroglycerin (glyceryl trinitrate).
53. What are major adverse effects of nitrates?
Answer:
- Throbbing headache
- Flushing
- Postural hypotension
- Dizziness/syncope
- Reflex tachycardia
- Methemoglobinemia, rarely
- Tolerance with continuous use
54. Why should nitrates not be combined with sildenafil or other PDE-5 inhibitors?
Answer:
Both increase the NO-cGMP vasodilator pathway, which may cause profound, potentially fatal hypotension.
Both increase the NO-cGMP vasodilator pathway, which may cause profound, potentially fatal hypotension.
55. How can nitrate tolerance be prevented?
Answer:
Provide a daily nitrate-free interval of approximately 8-12 hours, often overnight.
Provide a daily nitrate-free interval of approximately 8-12 hours, often overnight.
56. What is the role of beta-blockers in chronic stable angina?
Answer:
They reduce heart rate, contractility, and blood pressure. This lowers myocardial oxygen demand and improves exercise tolerance.
They reduce heart rate, contractility, and blood pressure. This lowers myocardial oxygen demand and improves exercise tolerance.
57. Why are beta-blockers avoided in vasospastic/Prinzmetal angina?
Answer:
Especially nonselective beta-blockers may worsen coronary vasospasm by allowing unopposed alpha-mediated vasoconstriction.
CCBs and nitrates are preferred.
Especially nonselective beta-blockers may worsen coronary vasospasm by allowing unopposed alpha-mediated vasoconstriction.
CCBs and nitrates are preferred.
58. Which CCBs are useful in stable angina?
Answer:
- Amlodipine
- Nifedipine
- Diltiazem
- Verapamil
They reduce afterload and improve coronary blood flow. Verapamil/diltiazem additionally reduce HR and contractility.
59. Which drugs are preferred for vasospastic (Prinzmetal) angina?
Answer:
Calcium-channel blockers and nitrates.
They relieve and prevent coronary vasospasm.
Calcium-channel blockers and nitrates.
They relieve and prevent coronary vasospasm.
60. What is ivabradine's mechanism of action?
Answer:
It selectively inhibits the If funny current in the SA node.
This lowers heart rate without directly reducing myocardial contractility.
It selectively inhibits the If funny current in the SA node.
This lowers heart rate without directly reducing myocardial contractility.
61. What are important adverse effects of ivabradine?
Answer:
- Bradycardia
- Atrial fibrillation
- Luminous visual phenomena/phosphenes
- Hypertension
62. What is the mechanism of ranolazine?
Answer:
It inhibits the late inward sodium current in cardiac cells. This reduces intracellular sodium and calcium overload, improving diastolic relaxation and reducing ischemia.
It inhibits the late inward sodium current in cardiac cells. This reduces intracellular sodium and calcium overload, improving diastolic relaxation and reducing ischemia.
63. What are the key clinical features of ranolazine?
Answer:
It is used as an add-on drug in chronic stable angina.
It has minimal effect on heart rate and blood pressure, but may prolong the QT interval.
It is used as an add-on drug in chronic stable angina.
It has minimal effect on heart rate and blood pressure, but may prolong the QT interval.
64. What is the mechanism of nicorandil?
Answer:
It has dual action:
It has dual action:
- Potassium-channel opening causing arterial dilation
- Nitrate-like NO-mediated venodilation
It reduces both afterload and preload.
65. Compare the preferred pharmacological approach in stable angina and vasospastic angina.
Answer:
| Condition | Preferred drugs | Drugs to avoid/caution |
|---|---|---|
| Chronic stable angina | Beta-blocker or CCB; nitrates for relief/prevention | Avoid harmful combinations causing bradycardia |
| Vasospastic angina | CCB + nitrates | Beta-blockers, particularly nonselective agents |
| Acute anginal episode | Sublingual nitroglycerin | Nitrates with PDE-5 inhibitors |
Last-Minute Exam Pearls
- ACE inhibitors: cough, angioedema, hyperkalemia, fetotoxicity.
- ARBs: no cough, but still cause hyperkalemia and are contraindicated in pregnancy.
- Thiazides: hyperuricemia, hyperglycemia, hypercalcemia, hypokalemia.
- Spironolactone: hyperkalemia and gynecomastia.
- Verapamil: constipation, bradycardia, AV block.
- Prazosin: first-dose syncope.
- Clonidine: rebound hypertension on abrupt withdrawal.
- Hydralazine: lupus-like syndrome.
- Minoxidil: hypertrichosis and fluid retention.
- Nitrates + sildenafil: severe hypotension.
- Beta-blockers: useful in stable angina, avoid in vasospastic angina.
- CCBs + nitrates: key drugs for Prinzmetal angina.
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