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Chapter 5 of 8

Anti-infectives

Aminoglycosides such as gentamicin act via concentration-dependent killing and are limited by nephrotoxicity and ototoxicity, both of which can be reduced by once-daily dosing. Vancomycin infusion reactions, termed red man syndrome, result from histamine release during rapid infusion, producing flushing and pruritus rather than a true IgE-mediated allergy; slowing the infusion prevents the reaction. The cross-reactivity risk between penicillins and cephalosporins has historically been quoted as around 10%, but modern estimates place the actual rate closer to 1-2%, particularly with first-generation cephalosporins sharing a similar R1 side chain, and even lower with third- and fourth-generation agents.

Antivirals for herpesviruses center on acyclovir, which is activated by viral thymidine kinase to its triphosphate form and acts as a DNA chain terminator, primarily against HSV and VZV, with nephrotoxicity if patients are not adequately hydrated. Ganciclovir is the CMV-specific counterpart, much more potent against CMV but considerably more myelosuppressive. The four first-line anti-tuberculosis drugs each carry distinct toxicities: isoniazid causes hepatotoxicity and peripheral neuropathy from vitamin B6 depletion, so B6 (pyridoxine) supplementation is given prophylactically; rifampin is a potent CYP450 inducer (reducing levels of many drugs including oral contraceptives and warfarin) and produces benign orange discoloration of body fluids; ethambutol's signature toxicity is optic neuritis with red-green color blindness; and pyrazinamide causes both hepatotoxicity and hyperuricemia that can precipitate gout.

All chapters
  1. 1Analgesics, Anti-inflammatories & Gout Therapy
  2. 2Anticoagulation & Antithrombotic Therapy
  3. 3Cardiovascular Drugs
  4. 4Endocrine & Metabolic Drugs
  5. 5Anti-infectives
  6. 6CNS, Autonomic & Neuromuscular Pharmacology
  7. 7Anesthesia, Pain Management & Local Anesthetics
  8. 8Chemotherapy, Biologics & Specialty Drugs

Drill it

Reading is not remembering. These come from the Usmle Step 1 High Yield Pharmacology deck:

Q

Mechanism of acetaminophen toxicity?

Hepatic CYP2E1 oxidizes APAP → toxic NAPQI metabolite. Glutathione normally detoxifies; in overdose glutathione is depleted → centrilobular hepatic necrosis.

Q

Antidote for acetaminophen overdose?

N-acetylcysteine — replenishes glutathione.

Q

Aspirin mechanism?

Irreversible COX-1 / COX-2 inhibitor → ↓ thromboxane A₂ in platelets (antithrombotic) + ↓ prostaglandins (analgesic, antipyretic, anti-inflammatory).

Q

Aspirin overdose acid-base picture?

Mixed: respiratory alkalosis (early — direct medullary stimulation) + anion-gap metabolic acidosis (later — uncoupled oxidative phosphorylation).