🎯 What You'll Learn
- ✓ Mechanism of acetaminophen toxicity?
- ✓ Antidote for acetaminophen overdose?
- ✓ Aspirin mechanism?
- ✓ Aspirin overdose acid-base picture?
- ✓ ACE inhibitor side effects?
Mechanism, class effects, and the adverse reactions Step 1 keeps asking about, organised by system rather than alphabetically. High-yield in the literal sense: the drugs that actually recur on the exam.
Hepatic CYP2E1 oxidizes APAP → toxic NAPQI metabolite. Glutathione normally detoxifies; in overdose glutathione is depleted → centrilobular hepatic necrosis.
N-acetylcysteine — replenishes glutathione.
Irreversible COX-1 / COX-2 inhibitor → ↓ thromboxane A₂ in platelets (antithrombotic) + ↓ prostaglandins (analgesic, antipyretic, anti-inflammatory).
Mixed: respiratory alkalosis (early — direct medullary stimulation) + anion-gap metabolic acidosis (later — uncoupled oxidative phosphorylation).
Cough (↑ bradykinin), angioedema, hyperkalemia, creatinine bump, teratogenic.
Block AT1 receptor instead of ACE → no bradykinin increase → no cough, less angioedema. Same K+/Cr risks.
Severe bradycardia, AV block, decompensated heart failure, severe asthma (esp. non-selective).
β₁-selective: metoprolol, atenolol, esmolol, bisoprolol ('A through M = β1-selective except carvedilol/labetalol').
HMG-CoA reductase inhibitor → ↓ cholesterol synthesis. Side: myopathy/rhabdomyolysis (esp. + fibrate), hepatotoxicity.
Inhibits vitamin K epoxide reductase → ↓ active vitamin K → ↓ synthesis of factors II, VII, IX, X (1972) and proteins C, S.
Vitamin K (slow, hours-days); fresh frozen plasma or 4-factor PCC for urgent reversal.
Activates antithrombin III → inactivates thrombin (IIa) and factor Xa. Monitor with aPTT.
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