What are the mechanism of action, administration technique, and contraindications of Adenosine?

Activates A1 receptors on the AV node, opening Gi-coupled K+ channels (hyperpolarization) and inhibiting Ca2+ influx to transiently block AV nodal conduction. First-line for stable regular narrow-complex SVT; given via rapid IV push with immediate saline flush. Contraindicated in asthma and pre-excited AF (WPW).

What are the nephron site of action, molecular mechanism, and electrolyte abnormalities of Furosemide (Lasix) and Bumetanide?

Loop diuretics that inhibit the Na+/K+/2Cl- (NKCC2) cotransporter in the thick ascending limb of the loop of Henle. Cause hypokalemia, hypomagnesemia, hypocalcemia (increased Ca2+ excretion), hyperuricemia, metabolic contraction alkalosis, and ototoxicity.

What are the mechanism of action and hemodynamic profile of Ranolazine (Ranexa) in chronic stable angina?

Inhibits the late phase of the inward sodium current (INa) in ischemic cardiomyocytes, reducing intracellular Na+ and Ca2+ overload during diastole to improve myocardial relaxation. Does not significantly alter heart rate or blood pressure; can prolong QT interval.

What are the hemodynamic mechanisms and specific heart failure indications of Hydralazine plus Isosorbide Dinitrate (BiDil)?

Hydralazine increases cGMP in arterial smooth muscle (afterload reduction); isosorbide dinitrate releases NO/cGMP in venous smooth muscle (preload reduction). Reduces mortality in self-identified Black patients with NYHA class III–IV HFrEF on optimal therapy (or patients intolerant to ACEI/ARB/ARNI).

What are the mechanism of action, clinical indications, and cardiopulmonary contraindications of Mannitol?

Osmotic diuretic filtered at the glomerulus but not reabsorbed, increasing tubular osmolarity in the proximal tubule and descending loop of Henle. Used for elevated intracranial or intraocular pressure. Contraindicated in acute decompensated heart failure/pulmonary edema and anuria.

What is the mechanism of action of the PCSK9 inhibitors Evolocumab (Repatha) and Alirocumab (Praluent)?

Monoclonal antibodies that inhibit PCSK9 (proprotein convertase subtilisin/kexin type 9), preventing lysosomal degradation of hepatic LDL receptors and dramatically lowering LDL cholesterol by 50–60%.

How do Prazosin, Terazosin, and Doxazosin differ from Tamsulosin in alpha-1 adrenergic receptor subtype selectivity and clinical effects?

Prazosin/terazosin/doxazosin non-selectively block alpha-1A and alpha-1B receptors, treating both BPH and hypertension (and PTSD nightmares for prazosin), but cause first-dose orthostatic hypotension. Tamsulosin selectively blocks prostatic alpha-1A/1D receptors, minimizing orthostasis while causing floppy iris syndrome and retrograde ejaculation.

What are the Vaughan Williams class, mechanism of action, and structural heart disease contraindication (CAST trial) for Flecainide and Propafenone?

Class IC antiarrhythmics that strongly block fast inward Na+ channels with slow dissociation ('pill-in-the-pocket' for paroxysmal A-fib). Contraindicated in patients with structural heart disease or prior myocardial infarction due to proarrhythmic mortality risk.

What are the pharmacological class, mechanism of action, and classic adverse effects of Lisinopril and Enalapril?

Class: ACE Inhibitors. MOA: Inhibit angiotensin-converting enzyme, decreasing Angiotensin II and aldosterone while increasing bradykinin. Adverse effects: Dry cough, angioedema, hyperkalemia, teratogenicity, acute creatinine rise in bilateral renal artery stenosis.

What is the dual mechanism of action of Digoxin (inotropy versus vagomimetic effect), and what factors precipitate digoxin toxicity?

Inhibits sarcolemmal Na+/K+-ATPase -> increases intracellular Na+ -> decreases NCX Ca2+ extrusion -> increases SR Ca2+ and contractility; also increases vagal tone at the AV node. Toxicity (nausea, yellow-green halos, bidirectional VT) is precipitated by hypokalemia, renal failure, verapamil, amiodarone, and quinidine.

What are the mechanism of action, clinical uses, and withdrawal rebound phenomenon of Clonidine and Guanfacine?

Central alpha-2 adrenergic agonists that decrease sympathetic outflow from the CNS. Used for resistant hypertension, ADHD, and opioid/autonomic withdrawal. Abrupt discontinuation of clonidine causes life-threatening rebound hypertensive crisis.

What is the antianginal mechanism of sublingual Nitroglycerin, and why are phosphodiesterase-5 (PDE-5) inhibitors strictly contraindicated?

Converted in vascular smooth muscle to nitric oxide (NO), activating guanylyl cyclase to increase cGMP and preferentially dilate veins (decreasing preload and myocardial wall stress/O2 demand). Co-administration with sildenafil/tadalafil within 24–48 hours causes fatal refractory hypotension.

What are the site of action, mechanism, and urinary calcium effect of Hydrochlorothiazide (HCTZ) and Chlorthalidone?

Thiazide/thiazide-like diuretics that inhibit the Na+/Cl- (NCC) cotransporter in the early distal convoluted tubule. Unlike loop diuretics, thiazides increase renal calcium reabsorption (causing hypercalcemia and reducing calcium nephrolithiasis).

What are the high-intensity dosing regimens, mechanism of action, and adverse effects of Atorvastatin (Lipitor) and Rosuvastatin (Crestor)?

High-intensity statins (Atorvastatin 40–80 mg, Rosuvastatin 20–40 mg lower LDL-C by >=50%). Competitively inhibit HMG-CoA reductase, upregulating hepatic LDL receptors. Adverse effects: Myopathy/rhabdomyolysis (check CK), hepatotoxicity (AST/ALT), and new-onset diabetes.

What are the mechanism of action, clinical indication, and mandatory washout rule for Sacubitril/Valsartan (Entresto)?

Class: Angiotensin Receptor-Neprilysin Inhibitor (ARNI). MOA: Valsartan blocks AT1 receptors; sacubitril inhibits neprilysin (increasing natriuretic peptides BNP/ANP). Indication: HFrEF. Mandatory 36-hour washout when switching from an ACE inhibitor to prevent severe angioedema.

What are the Vaughan Williams class, electrophysiologic effect, and primary cardiac indication of intravenous Lidocaine?

Class IB antiarrhythmic that blocks inactivated Na+ channels with rapid kinetics, preferentially acting on ischemic/depolarized ventricular tissue and shortening action potential duration. Used for acute ventricular arrhythmias (especially post-MI).

What are the receptor blockade profile and primary clinical indications of Carvedilol (Coreg)?

Non-selective beta-1/beta-2 blocker with alpha-1 adrenergic blocking activity (causing vasodilation) and antioxidant properties. Indications: HFrEF (reduces mortality), post-MI left ventricular dysfunction, and hypertension.

What are the mechanism of action, acid-base effect, and clinical indications of Acetazolamide?

Carbonic anhydrase inhibitor acting in the proximal convoluted tubule to decrease NaHCO3 reabsorption. Causes normal anion gap (hyperchloremic) metabolic acidosis (Type 2 RTA). Indications: Acute angle-closure glaucoma, idiopathic intracranial hypertension, and altitude sickness.

What are the Vaughan Williams class, mechanism of action, and classic autoimmune adverse effect of Procainamide?

Class IA antiarrhythmic (moderate Na+ channel blockade + K+ channel blockade; prolongs QRS and QT). Causes reversible drug-induced lupus erythematosus (anti-histone antibodies positive) and agranulocytosis.

What is the mechanism of action of Ezetimibe (Zetia), and what is its clinical role in lipid lowering?

Selectively inhibits the NPC1L1 sterol transporter at the brush border of the small intestine, decreasing dietary and biliary cholesterol absorption. Lowers LDL-C by ~18–25% when added to statin therapy.

What are the mechanism of action, heart failure indication criteria, and visual adverse effect of Ivabradine (Corlanor)?

Selectively inhibits the hyperpolarization-activated cyclic nucleotide-gated 'funny' channel (If) in the SA node, slowing heart rate without affecting contractility or BP. Indicated in HFrEF (EF =70 bpm on maximal beta-blocker. Adverse effect: Phosphenes (luminous visual phenomena).

How do Spironolactone and Eplerenone compare in mechanism of action, heart failure mortality benefit, and endocrine adverse effects?

Mineralocorticoid receptor antagonists (K+-sparing diuretics) that competitively block aldosterone in the cortical collecting tubule; reduce mortality in HFrEF. Spironolactone is non-selective and causes gynecomastia/antiandrogenic effects; eplerenone is selective and avoids gynecomastia.

What is the mechanism of action of Losartan and Valsartan, and what is their key clinical advantage over ACE inhibitors?

Class: Angiotensin II Receptor Blockers (ARBs). MOA: Selectively block AT1 receptors, preventing angiotensin II-mediated vasoconstriction and aldosterone secretion. Advantage: Because ARBs do not inhibit ACE (kininase II), they do not impair bradykinin degradation and have a much lower incidence of dry cough and angioedema (though rare angioedema can still occur, so caution is warranted in patients with prior ACE-inhibitor angioedema).

How does Amlodipine (Norvasc) compare with Diltiazem and Verapamil in dihydropyridine versus non-dihydropyridine calcium channel blockade?

Amlodipine (dihydropyridine CCB) selectively blocks L-type Ca2+ channels in vascular smooth muscle, producing arterial vasodilation (side effects: peripheral ankle edema, flushing, headache; minimal AV nodal conduction effect). Verapamil and diltiazem (non-dihydropyridine CCBs) inhibit L-type Ca2+ channels in the SA/AV nodes and myocardium, slowing conduction and contractility (used for SVT and atrial fibrillation rate control; contraindicated in HFrEF, high-grade AV block, and pre-excited AF).

How do Metoprolol Succinate and Metoprolol Tartrate compare in receptor selectivity and heart failure mortality evidence?

Cardioselective beta-1 adrenergic blocker (at low-to-moderate doses). Only extended-release metoprolol succinate (along with carvedilol and bisoprolol) carries proven mortality reduction in chronic HFrEF.

Which antihypertensive medications are first-line during pregnancy, and which classes are strictly contraindicated?

Safe antihypertensives in pregnancy: Labetalol (alpha-1/beta blocker), Nifedipine extended-release (DHP CCB), and Methyldopa (central alpha-2 agonist prodrug; can cause positive direct Coombs test/hemolytic anemia). ACEIs, ARBs, and direct renin inhibitors are strictly contraindicated.

What are the mechanism of action, primary lipid effect, and statin interaction profile of Fenofibrate and Gemfibrozil?

Fibrates activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha), upregulating lipoprotein lipase (LPL) and ApoA-I/A-II to reduce serum triglycerides by 35–50%. Gemfibrozil inhibits OATP1B1 and hepatic glucuronidation of statins, markedly increasing statin blood levels and rhabdomyolysis risk (fenofibrate is preferred if fibrate-statin combination therapy is necessary).

What is the mechanism of action of Amiloride and Triamterene, and why is Amiloride specifically indicated for lithium-induced nephrogenic diabetes insipidus?

Potassium-sparing diuretics that directly block epithelial sodium channels (ENaC) in the cortical collecting tubule. Amiloride is the drug of choice for lithium-induced nephrogenic diabetes insipidus because it blocks lithium entry into principal cells via ENaC.

What are the cardiovascular and renal protective mechanisms of Empagliflozin and Dapagliflozin beyond glycemic control?

SGLT2 inhibitors reduce proximal tubular Na+ and glucose reabsorption, restoring tubuloglomerular feedback (afferent arteriolar vasoconstriction -> decreased intraglomerular pressure/hyperfiltration) and reducing preload/afterload. Proven to reduce hospitalizations and mortality in HFrEF, HFpEF, and proteinuric CKD regardless of diabetes status.

What are the Vaughan Williams class, multi-channel mechanism, and baseline/follow-up monitoring requirements for Amiodarone?

Class III antiarrhythmic (predominantly blocks K+ channels to prolong action potential duration/ERP, with Class I, II, and IV activity). Despite QT prolongation, low risk of Torsades. Requires monitoring of PFTs (pulmonary fibrosis), TFTs (hypo-/hyperthyroidism), LFTs, and slit-lamp/vision exams.

What are the Vaughan Williams class, mechanism of action, and principal proarrhythmic risk of Sotalol and Dofetilide?

Class III potassium channel (IKr) blockers (sotalol also has non-selective beta-blocking activity). Prolong phase 3 repolarization and QTc interval; carry a high risk of Torsades de Pointes, especially with hypokalemia, hypomagnesemia, or renal impairment.

What is the mechanism of action of Sodium Nitroprusside, and how does cyanide toxicity present and get treated?

Short-acting parenteral vasodilator that releases nitric oxide to dilate both arteries and veins rapidly in hypertensive emergencies. Prolonged infusion (>24–48h) or renal/hepatic dysfunction leads to cyanide/thiocyanate toxicity (altered mental status, lactic acidosis); treated with hydroxocobalamin or sodium thiosulfate.

Top 200 Drugs: Cardiovascular, Renal & Lipid-Lowering Agents (Brand, Generic, Class & MOA)

High-yield Top 200 prescribed cardiovascular, renal, antiarrhythmic, and lipid-lowering medications: brand and generic names, pharmacological classes, mechanisms of action, clinical indications, and adverse effects.

Level: basic
Languages: en → en
Cards: 32
Markdown: Top 200 Drugs: Cardiovascular, Renal & Lipid-Lowering Agents (Brand, Generic, Class & MOA) (.md)

Flashcards (32)

#	Front (Term / Question)	Back (Definition / Answer)
1	What are the mechanism of action, administration technique, and contraindications of Adenosine?	Activates A1 receptors on the AV node, opening Gi-coupled K+ channels (hyperpolarization) and inhibiting Ca2+ influx to transiently block AV nodal conduction. First-line for stable regular narrow-complex SVT; given via rapid IV push with immediate saline flush. Contraindicated in asthma and pre-excited AF (WPW).
2	What are the nephron site of action, molecular mechanism, and electrolyte abnormalities of Furosemide (Lasix) and Bumetanide?	Loop diuretics that inhibit the Na+/K+/2Cl- (NKCC2) cotransporter in the thick ascending limb of the loop of Henle. Cause hypokalemia, hypomagnesemia, hypocalcemia (increased Ca2+ excretion), hyperuricemia, metabolic contraction alkalosis, and ototoxicity.
3	What are the mechanism of action and hemodynamic profile of Ranolazine (Ranexa) in chronic stable angina?	Inhibits the late phase of the inward sodium current (INa) in ischemic cardiomyocytes, reducing intracellular Na+ and Ca2+ overload during diastole to improve myocardial relaxation. Does not significantly alter heart rate or blood pressure; can prolong QT interval.
4	What are the hemodynamic mechanisms and specific heart failure indications of Hydralazine plus Isosorbide Dinitrate (BiDil)?	Hydralazine increases cGMP in arterial smooth muscle (afterload reduction); isosorbide dinitrate releases NO/cGMP in venous smooth muscle (preload reduction). Reduces mortality in self-identified Black patients with NYHA class III–IV HFrEF on optimal therapy (or patients intolerant to ACEI/ARB/ARNI).
5	What are the mechanism of action, clinical indications, and cardiopulmonary contraindications of Mannitol?	Osmotic diuretic filtered at the glomerulus but not reabsorbed, increasing tubular osmolarity in the proximal tubule and descending loop of Henle. Used for elevated intracranial or intraocular pressure. Contraindicated in acute decompensated heart failure/pulmonary edema and anuria.
6	What is the mechanism of action of the PCSK9 inhibitors Evolocumab (Repatha) and Alirocumab (Praluent)?	Monoclonal antibodies that inhibit PCSK9 (proprotein convertase subtilisin/kexin type 9), preventing lysosomal degradation of hepatic LDL receptors and dramatically lowering LDL cholesterol by 50–60%.
7	How do Prazosin, Terazosin, and Doxazosin differ from Tamsulosin in alpha-1 adrenergic receptor subtype selectivity and clinical effects?	Prazosin/terazosin/doxazosin non-selectively block alpha-1A and alpha-1B receptors, treating both BPH and hypertension (and PTSD nightmares for prazosin), but cause first-dose orthostatic hypotension. Tamsulosin selectively blocks prostatic alpha-1A/1D receptors, minimizing orthostasis while causing floppy iris syndrome and retrograde ejaculation.
8	What are the Vaughan Williams class, mechanism of action, and structural heart disease contraindication (CAST trial) for Flecainide and Propafenone?	Class IC antiarrhythmics that strongly block fast inward Na+ channels with slow dissociation ('pill-in-the-pocket' for paroxysmal A-fib). Contraindicated in patients with structural heart disease or prior myocardial infarction due to proarrhythmic mortality risk.
9	What are the pharmacological class, mechanism of action, and classic adverse effects of Lisinopril and Enalapril?	Class: ACE Inhibitors. MOA: Inhibit angiotensin-converting enzyme, decreasing Angiotensin II and aldosterone while increasing bradykinin. Adverse effects: Dry cough, angioedema, hyperkalemia, teratogenicity, acute creatinine rise in bilateral renal artery stenosis.
10	What is the dual mechanism of action of Digoxin (inotropy versus vagomimetic effect), and what factors precipitate digoxin toxicity?	Inhibits sarcolemmal Na+/K+-ATPase -> increases intracellular Na+ -> decreases NCX Ca2+ extrusion -> increases SR Ca2+ and contractility; also increases vagal tone at the AV node. Toxicity (nausea, yellow-green halos, bidirectional VT) is precipitated by hypokalemia, renal failure, verapamil, amiodarone, and quinidine.
11	What are the mechanism of action, clinical uses, and withdrawal rebound phenomenon of Clonidine and Guanfacine?	Central alpha-2 adrenergic agonists that decrease sympathetic outflow from the CNS. Used for resistant hypertension, ADHD, and opioid/autonomic withdrawal. Abrupt discontinuation of clonidine causes life-threatening rebound hypertensive crisis.
12	What is the antianginal mechanism of sublingual Nitroglycerin, and why are phosphodiesterase-5 (PDE-5) inhibitors strictly contraindicated?	Converted in vascular smooth muscle to nitric oxide (NO), activating guanylyl cyclase to increase cGMP and preferentially dilate veins (decreasing preload and myocardial wall stress/O2 demand). Co-administration with sildenafil/tadalafil within 24–48 hours causes fatal refractory hypotension.
13	What are the site of action, mechanism, and urinary calcium effect of Hydrochlorothiazide (HCTZ) and Chlorthalidone?	Thiazide/thiazide-like diuretics that inhibit the Na+/Cl- (NCC) cotransporter in the early distal convoluted tubule. Unlike loop diuretics, thiazides increase renal calcium reabsorption (causing hypercalcemia and reducing calcium nephrolithiasis).
14	What are the high-intensity dosing regimens, mechanism of action, and adverse effects of Atorvastatin (Lipitor) and Rosuvastatin (Crestor)?	High-intensity statins (Atorvastatin 40–80 mg, Rosuvastatin 20–40 mg lower LDL-C by >=50%). Competitively inhibit HMG-CoA reductase, upregulating hepatic LDL receptors. Adverse effects: Myopathy/rhabdomyolysis (check CK), hepatotoxicity (AST/ALT), and new-onset diabetes.
15	What are the mechanism of action, clinical indication, and mandatory washout rule for Sacubitril/Valsartan (Entresto)?	Class: Angiotensin Receptor-Neprilysin Inhibitor (ARNI). MOA: Valsartan blocks AT1 receptors; sacubitril inhibits neprilysin (increasing natriuretic peptides BNP/ANP). Indication: HFrEF. Mandatory 36-hour washout when switching from an ACE inhibitor to prevent severe angioedema.
16	What are the Vaughan Williams class, electrophysiologic effect, and primary cardiac indication of intravenous Lidocaine?	Class IB antiarrhythmic that blocks inactivated Na+ channels with rapid kinetics, preferentially acting on ischemic/depolarized ventricular tissue and shortening action potential duration. Used for acute ventricular arrhythmias (especially post-MI).
17	What are the receptor blockade profile and primary clinical indications of Carvedilol (Coreg)?	Non-selective beta-1/beta-2 blocker with alpha-1 adrenergic blocking activity (causing vasodilation) and antioxidant properties. Indications: HFrEF (reduces mortality), post-MI left ventricular dysfunction, and hypertension.
18	What are the mechanism of action, acid-base effect, and clinical indications of Acetazolamide?	Carbonic anhydrase inhibitor acting in the proximal convoluted tubule to decrease NaHCO3 reabsorption. Causes normal anion gap (hyperchloremic) metabolic acidosis (Type 2 RTA). Indications: Acute angle-closure glaucoma, idiopathic intracranial hypertension, and altitude sickness.
19	What are the Vaughan Williams class, mechanism of action, and classic autoimmune adverse effect of Procainamide?	Class IA antiarrhythmic (moderate Na+ channel blockade + K+ channel blockade; prolongs QRS and QT). Causes reversible drug-induced lupus erythematosus (anti-histone antibodies positive) and agranulocytosis.
20	What is the mechanism of action of Ezetimibe (Zetia), and what is its clinical role in lipid lowering?	Selectively inhibits the NPC1L1 sterol transporter at the brush border of the small intestine, decreasing dietary and biliary cholesterol absorption. Lowers LDL-C by ~18–25% when added to statin therapy.
21	What are the mechanism of action, heart failure indication criteria, and visual adverse effect of Ivabradine (Corlanor)?	Selectively inhibits the hyperpolarization-activated cyclic nucleotide-gated 'funny' channel (If) in the SA node, slowing heart rate without affecting contractility or BP. Indicated in HFrEF (EF <=35%) in sinus rhythm with resting HR >=70 bpm on maximal beta-blocker. Adverse effect: Phosphenes (luminous visual phenomena).
22	How do Spironolactone and Eplerenone compare in mechanism of action, heart failure mortality benefit, and endocrine adverse effects?	Mineralocorticoid receptor antagonists (K+-sparing diuretics) that competitively block aldosterone in the cortical collecting tubule; reduce mortality in HFrEF. Spironolactone is non-selective and causes gynecomastia/antiandrogenic effects; eplerenone is selective and avoids gynecomastia.
23	What is the mechanism of action of Losartan and Valsartan, and what is their key clinical advantage over ACE inhibitors?	Class: Angiotensin II Receptor Blockers (ARBs). MOA: Selectively block AT1 receptors, preventing angiotensin II-mediated vasoconstriction and aldosterone secretion. Advantage: Because ARBs do not inhibit ACE (kininase II), they do not impair bradykinin degradation and have a much lower incidence of dry cough and angioedema (though rare angioedema can still occur, so caution is warranted in patients with prior ACE-inhibitor angioedema).
24	How does Amlodipine (Norvasc) compare with Diltiazem and Verapamil in dihydropyridine versus non-dihydropyridine calcium channel blockade?	Amlodipine (dihydropyridine CCB) selectively blocks L-type Ca2+ channels in vascular smooth muscle, producing arterial vasodilation (side effects: peripheral ankle edema, flushing, headache; minimal AV nodal conduction effect). Verapamil and diltiazem (non-dihydropyridine CCBs) inhibit L-type Ca2+ channels in the SA/AV nodes and myocardium, slowing conduction and contractility (used for SVT and atrial fibrillation rate control; contraindicated in HFrEF, high-grade AV block, and pre-excited AF).
25	How do Metoprolol Succinate and Metoprolol Tartrate compare in receptor selectivity and heart failure mortality evidence?	Cardioselective beta-1 adrenergic blocker (at low-to-moderate doses). Only extended-release metoprolol succinate (along with carvedilol and bisoprolol) carries proven mortality reduction in chronic HFrEF.
26	Which antihypertensive medications are first-line during pregnancy, and which classes are strictly contraindicated?	Safe antihypertensives in pregnancy: Labetalol (alpha-1/beta blocker), Nifedipine extended-release (DHP CCB), and Methyldopa (central alpha-2 agonist prodrug; can cause positive direct Coombs test/hemolytic anemia). ACEIs, ARBs, and direct renin inhibitors are strictly contraindicated.
27	What are the mechanism of action, primary lipid effect, and statin interaction profile of Fenofibrate and Gemfibrozil?	Fibrates activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha), upregulating lipoprotein lipase (LPL) and ApoA-I/A-II to reduce serum triglycerides by 35–50%. Gemfibrozil inhibits OATP1B1 and hepatic glucuronidation of statins, markedly increasing statin blood levels and rhabdomyolysis risk (fenofibrate is preferred if fibrate-statin combination therapy is necessary).
28	What is the mechanism of action of Amiloride and Triamterene, and why is Amiloride specifically indicated for lithium-induced nephrogenic diabetes insipidus?	Potassium-sparing diuretics that directly block epithelial sodium channels (ENaC) in the cortical collecting tubule. Amiloride is the drug of choice for lithium-induced nephrogenic diabetes insipidus because it blocks lithium entry into principal cells via ENaC.
29	What are the cardiovascular and renal protective mechanisms of Empagliflozin and Dapagliflozin beyond glycemic control?	SGLT2 inhibitors reduce proximal tubular Na+ and glucose reabsorption, restoring tubuloglomerular feedback (afferent arteriolar vasoconstriction -> decreased intraglomerular pressure/hyperfiltration) and reducing preload/afterload. Proven to reduce hospitalizations and mortality in HFrEF, HFpEF, and proteinuric CKD regardless of diabetes status.
30	What are the Vaughan Williams class, multi-channel mechanism, and baseline/follow-up monitoring requirements for Amiodarone?	Class III antiarrhythmic (predominantly blocks K+ channels to prolong action potential duration/ERP, with Class I, II, and IV activity). Despite QT prolongation, low risk of Torsades. Requires monitoring of PFTs (pulmonary fibrosis), TFTs (hypo-/hyperthyroidism), LFTs, and slit-lamp/vision exams.
31	What are the Vaughan Williams class, mechanism of action, and principal proarrhythmic risk of Sotalol and Dofetilide?	Class III potassium channel (IKr) blockers (sotalol also has non-selective beta-blocking activity). Prolong phase 3 repolarization and QTc interval; carry a high risk of Torsades de Pointes, especially with hypokalemia, hypomagnesemia, or renal impairment.
32	What is the mechanism of action of Sodium Nitroprusside, and how does cyanide toxicity present and get treated?	Short-acting parenteral vasodilator that releases nitric oxide to dilate both arteries and veins rapidly in hypertensive emergencies. Prolonged infusion (>24–48h) or renal/hepatic dysfunction leads to cyanide/thiocyanate toxicity (altered mental status, lactic acidosis); treated with hydroxocobalamin or sodium thiosulfate.