ACVCP cheat sheet

Bioavailability (F) = (AUC_oral × Dose_IV) / (AUC_IV × Dose_oral); IV dose defines F = 1.0 by convention.

Volume of distribution Vd = Dose / C0 (extrapolated plasma concentration at time zero); large Vd indicates extensive tissue distribution.

Clearance CL = (Dose × F) / AUC; total CL = hepatic CL + renal CL, and half-life t½ = (0.693 × Vd) / CL.

Steady state is reached in ~4–5 half-lives; loading dose = (Vd × target concentration) / F, maintenance rate = CL × target concentration.

First-order kinetics: a constant fraction is eliminated per unit time; zero-order (saturation) kinetics: a constant amount is eliminated per unit time regardless of concentration.

Weak-acid drugs are more lipid-soluble and better absorbed in acidic gastric pH; weak bases are trapped (ionized) in acidic compartments - ion trapping affects milk and urine pH manipulation.

Cytochrome P450 (CYP) enzymes mediate most phase I oxidative hepatic metabolism; glucuronidation (phase II) is deficient in cats, prolonging elimination of many drugs.

P-glycoprotein at the blood-brain barrier limits CNS entry of drugs like ivermectin; MDR1/ABCB1 mutation in Collies permits neurotoxicity at label doses.

Drug half-life determines dosing interval; therapeutic index = toxic dose / effective dose, and narrow-index drugs (digoxin, warfarin) warrant monitoring.

NSAIDs act by inhibiting cyclooxygenase (COX); COX-1 is constitutive (gastroprotection, renal perfusion) and COX-2 is induced at inflammation - COX-2 selectivity reduces but does not eliminate GI and renal risk.

Aminoglycosides are concentration-dependent, bactericidal, and nephro/ototoxic; once-daily dosing exploits the post-antibiotic effect while limiting accumulation.

Beta-lactams (penicillins, cephalosporins) are time-dependent killers; efficacy correlates with time above MIC, favoring frequent or extended-infusion dosing.

Fluoroquinolones are concentration-dependent and bactericidal via DNA gyrase inhibition; avoid in growing animals (cartilage) and reserve for susceptible organisms.

Glucocorticoid potency parallels anti-inflammatory effect; abrupt withdrawal after prolonged use risks iatrogenic hypoadrenocorticism from HPA-axis suppression - taper.

Insulin therapy in diabetic dogs/cats: cats often achieve remission with early tight control; dogs generally require lifelong insulin, and handling/rolling of suspension matters.

Antiepileptic monitoring: phenobarbital therapeutic range ~15–45 µg/mL in dogs; check trough levels and monitor liver enzymes and sedation.

Antimicrobial stewardship: culture and susceptibility before therapy when feasible, use the narrowest effective spectrum, and observe species-specific prohibitions (e.g., enrofloxacin retinal toxicity in cats at high doses).

Thyroid therapy: levothyroxine for canine hypothyroidism is dosed to effect (monitor T4 ~4–6 h post-pill); methimazole or radioiodine treats feline hyperthyroidism.