Source / episode info

• **Episode:**398
• **Title:**Divine Intervention Episode 398 – Some Pharmacology Scenarios For Step 2/3
• **Published:**2022-06-27
• Source:Episode page

One-liner

Episode 398 emphasizes high-yield basic science pathophysiology for board exams, covering the mechanisms of coronary vasospasm (cocaine/meth), right-sided endocarditis (IVDU), drug-induced flushing reactions (Vanco, nitrates, CCBs), and critical pharmacology traps regarding QT prolongation and TCA toxicity.

High-yield summary

• Coronary Vasospasm: Acute chest pain with ST elevation in V1-V4 despite minimal coronary stenosis is highly suggestive of vasospasm (e.g., Prinzmetal's angina), often triggered by stimulants (cocaine, methamphetamine) or drugs (triptans, nitrates).
• Right-Sided Endocarditis: In IV drug users, the first site of infection is typically the tricuspid valve. The murmur heard at the left lower sternal border that increases with inspiration suggests right-sided heart pathology. Always obtain blood cultures before administering antibiotics.
• Drug-Induced Flushing/Vasodilation: Common causes include Vancomycin (histamine release), Nitrates, Calcium Channel Blockers (especially dihydropyridines), and Acinocandins. These agents cause systemic vasodilation, leading to flushing.
• TCA Toxicity: Tricyclic antidepressants block sodium channels, causing a characteristic widening of the QRS complex. They also have anti-_1 (causing orthostatic hypotension) and anti-muscarinic effects.
• QT Prolongation: This is often due to blockade of potassium or sodium ion channels by various drugs (e.g., macrolides, fluoroquinolones, certain antipsychotics like ziprasidone).

Learning objectives

• Differentiate the pathophysiology and clinical presentation of coronary vasospasm versus fixed atherosclerotic stenosis.
• Identify the classic signs, risk factors, and initial management steps for right-sided endocarditis in IV drug users.
• Recognize multiple causes of systemic flushing (e.g., histamine release, PDE activity) and their associated medications.
• Understand the mechanism by which TCAs prolong QRS duration (Na+ channel blockade) versus QT interval prolongation (K+/Na+ channel blockade).
• Apply knowledge of anti-infective agents, specifically recognizing the cell wall synthesis targets of acinocandins.

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