Hematology · USMLE Step 1 and Step 2

Aspirin song

Aspirin - Mechanism, Uses & Toxicity, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

Aspirin

Full song on YouTube ↗Spotify ↗

Key points in this song10

Aspirin irreversibly inhibits COX-1 and COX-2 by acetylating a serine residue, blocking thromboxane A2 in platelets and prostacyclin in endothelium.
At low doses (81 mg), aspirin preferentially inhibits platelet COX-1, reducing TXA2 and producing an antiplatelet effect that lasts the platelet's lifetime (7–10 days).
At high doses, aspirin inhibits COX-2 in the endothelium, reducing prostacyclin (PGI2), which can paradoxically increase thrombotic risk.
Aspirin is the drug of choice for immediate use in acute MI and ischemic stroke; it reduces mortality when given within 24 hours of an acute coronary event.
Aspirin is contraindicated in children with viral illness due to risk of Reye syndrome (hepatic encephalopathy with mitochondrial dysfunction and microvesicular steatosis).
Salicylate toxicity initially causes respiratory alkalosis (direct stimulation of the medullary respiratory center), followed by an elevated anion gap metabolic acidosis.
Chronic aspirin use can cause peptic ulcer disease by reducing PGE2-mediated mucosal protection; co-prescribe a PPI in high-risk patients.
Aspirin hypersensitivity triad (Samter's triad): asthma, nasal polyps, and aspirin/NSAID-induced bronchospasm, mediated by shunting arachidonic acid toward leukotrienes.
Aspirin is used in Kawasaki disease (high-dose anti-inflammatory phase, then low-dose antiplatelet phase) and in pre-eclampsia prophylaxis starting at 12–16 weeks gestation in high-risk patients.
Uricosuric effect occurs at high doses; low doses decrease uric acid excretion and can precipitate gout — a classic USMLE dose-dependent distinction.