ABCP Diplomate cheat sheet

Bioavailability (F) = fraction of dose reaching systemic circulation intact; IV F = 1 by definition.

Volume of distribution Vd = dose / plasma concentration at time zero; large Vd (>1 L/kg) implies extensive tissue binding.

Clearance CL = dose rate / steady-state concentration; at steady state, dosing rate = CL x Css.

Half-life t1/2 = 0.693 x Vd / CL; steady state is reached in ~4-5 half-lives regardless of dose.

Zero-order elimination: constant amount removed per unit time, so t1/2 lengthens as concentration rises (e.g., ethanol, phenytoin at high levels).

First-order elimination: constant fraction removed per unit time; t1/2 is independent of concentration.

Loading dose = (Vd x target concentration) / F; maintenance dose = (CL x target concentration x dosing interval) / F.

Therapeutic index = TD50 / ED50; a narrow index requires therapeutic drug monitoring (e.g., digoxin, lithium, warfarin).

Cytochrome P450 inducers (rifampin, carbamazepine, phenytoin, St. John's wort) lower substrate levels; inhibitors (ketoconazole, ritonavir, grapefruit) raise them.

Beta-1 selective blockers (metoprolol, atenolol) reduce bronchospasm risk relative to nonselective agents but selectivity is dose-dependent.

ACE inhibitors cause cough and hyperkalemia via bradykinin accumulation and reduced aldosterone; ARBs avoid the cough.

Aminoglycosides are concentration-dependent killers with nephro/ototoxicity; extended-interval dosing exploits peak-to-MIC ratio.

Vancomycin requires AUC-guided (or trough) monitoring; nephrotoxicity risk rises with concurrent piperacillin-tazobactam or loop diuretics.

Warfarin effect is monitored by INR; heparin by aPTT or anti-Xa; direct oral anticoagulants generally need no routine coagulation monitoring.

Opioids plus benzodiazepines carry additive respiratory depression; naloxone reverses opioid effect but has a shorter half-life than many opioids.

Anticholinergic burden (diphenhydramine, oxybutynin, tricyclics) worsens cognition and urinary retention, especially in older adults.

NSAIDs cause GI ulceration via COX-1 inhibition and acute kidney injury via reduced afferent prostaglandin vasodilation; risk rises with ACE inhibitors plus diuretics (triple whammy).

Serotonin syndrome is suggested by the triad of mental status change, autonomic instability, and neuromuscular excitation (clonus, hyperreflexia) after serotonergic combinations.