Pharma first

MCQ IN PHARMACOLOGY

Simply

• Lasmiditan = Ditan • Target: 5-HT1F • Use: acute migraine • No vasoconstriction → safe in heart disease • Side effects: dizziness, drowsiness

MCQs in Pharmacology 📕

📕Pharmacology Test Prep: 1500 USMLE-Style

📌Vasopressin-Receptor Antagonists (VRAs / Vaptans) 🔹 Mechanism of Action • Block the binding of Vasopressin (ADH) to its receptors (mainly V2 receptor in the kidney collecting ducts). • This prevents water reabsorption in the collecting ducts → increases excretion of free water (without significant Na⁺ or K⁺ loss). • This effect is called the Aquaretic effect (excretion of electrolyte-free water). 🔹 Clinical Uses 1. Hyponatremia (especially due to SIADH, heart failure, or liver cirrhosis). 2. Heart failure (to reduce fluid overload). 3. Sometimes in Cirrhosis with ascites. 🔹 Examples 💊 Tolvaptan (selective V2 antagonist). 💊 Conivaptan (blocks both V1a + V2 receptors). 🔹 Adverse Effects • Excessive thirst. • Dehydration. • Rapid increase in serum Na⁺ (risk of osmotic demyelination syndrome if corrected too fast). • Hepatotoxicity (especially with Tolvaptan).

Fenoldopam 💊 • Mechanism: Dopamine D1 receptor agonist → G-protein-coupled receptor → arterial vasodilation → decreases peripheral resistance. • Administration: Intravenous only. • Properties: Short-acting; allows tight control of BP in emergencies. • Additional benefit: Promotes renal vasodilation, preserves renal perfusion.

⭕️ Drugs that commonly cause postural (orthostatic) hypotension: 1. Alpha-1 Selective Adrenergic Blockers • Examples: Prazosin, Doxazosin, Terazosin • Mechanism: Block α1 receptors → arterial and venous dilation → drop in BP on standing. • Notes: “First-dose effect” common, higher risk in elderly. ⸻ 2. Vasodilators / Direct Arteriolar Dilators • Examples: Minoxidil, Hydralazine • Mechanism: Direct smooth muscle relaxation → decreased peripheral resistance → postural hypotension. • Notes: Often combined with a diuretic and beta-blocker to counter reflex tachycardia. ⸻ 3. Diuretics • Examples: Thiazides (Hydrochlorothiazide), Loop diuretics • Mechanism: Volume depletion → decreased venous return → postural BP drop. • Notes: Elderly patients are particularly sensitive. ⸻ 4. Nitrates • Examples: Nitroglycerin, Isosorbide dinitrate • Mechanism: Venous dilation → reduced preload → hypotension on standing.

⭕️Withdrawal Syndrome (after sudden stoppage of clonidine / central α₂-agonists): 🔹 Symptoms: • Headache • Nervousness, agitation • Tachycardia • Sweating • Tremors • Palpitations • Rebound Hypertension (dangerous rise in BP) ⸻ 🔹 Causes (pathophysiology): • α-receptor supersensitivity develops with chronic use • Sudden withdrawal → abrupt release of stored catecholamines (NE, EPI) • This causes excess sympathetic discharge → hypertensive crisis ⸻ 🔹 Treatment: • IV Sodium Nitroprusside → direct vasodilator, rapidly lowers BP • IV Labetalol → α- and β-blocker, controls both HR and BP

⭕️ main contraindications for beta blockers: Absolute Contraindications: • Severe bradycardia (HR too low) • 2nd or 3rd degree AV block (without pacemaker) • Sick sinus syndrome • Acute decompensated heart failure (can worsen low output) • Cardiogenic shock • Severe asthma or bronchospasm (non-selective β-blockers → bronchoconstriction) Relative Contraindications (use with caution): • COPD (selective β₁-blockers may be safer) • Peripheral vascular disease / Raynaud’s phenomenon (can worsen vasospasm) • Diabetes mellitus (masks hypoglycemia symptoms like tachycardia) • Depression (some β-blockers may worsen mood)

⭕️ Angiotensin Converting Enzyme Inhibitors ( Drug Interactions)  🔄 Drug Interactions 1. ACE Inhibitors + Potassium-sparing Diuretics: •Can cause dangerous hyperkalemia 2. ACE Inhibitors + Lithium: •ACE inhibitors reduce renal excretion of lithium → Increases lithium toxicity 3. ACE Inhibitors + NSAIDs: •NSAIDs reduce prostaglandin synthesis, leading to: •Sodium and water retention •Reduced antihypertensive effect of ACE inhibitors

📌Comparison of Diuretic Classes

📝: Verapamil is not used in systolic heart failure (HFrEF) because it is a negative inotrope — it reduces heart contractility, which can worsen an already weak heart.

📌Calcium channel blockers: Dihydropyridines (DHPs) Vs Non-Dihydropyridines (Non-DHPs) 💡 Key takeaway: • DHPs = “vessels” → mostly widen arteries, minimal heart effect. • Non-DHPs = “heart + vessels” → slow heart rate, reduce contractility, some vessel

Note 📝: 📌Some drugs, like Fibrates, act on PPAR-α → they lower triglycerides. 📌 Drugs like Thiazolidinediones (TZDs) act on PPAR-γ → they improve insulin sensitivity in type 2 diabetes.