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USMLE Step 1 Pharmacology: Mechanisms, Toxicities and Antidotes (University)

20 cards · 9 topics · by Quizcard team · 0 hearts · Updated 2026-11-03

Pharmacokinetics — Volume of DistributionPharmacokinetics — Half-life & ClearancePharmacokinetics — DosingPharmacokinetics — Order of KineticsPharmacodynamics — Agonists & AntagonistsPharmacodynamics — Potency & EfficacyPharmacodynamics — Therapeutic IndexAutonomic DrugsCardiovascular Drugs
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Pharmacokinetics — Volume of Distribution

What is the formula for volume of distribution (Vd), and what does a low vs. high Vd imply about a drug?

Answer: Vd = (amount of drug in the body) / (plasma drug concentration). Low Vd (~4–8 L, plasma volume): drug stays in blood (large, charged, highly protein-bound, e.g. warfarin). High Vd (>body water, e.g. >42 L): drug sequesters in tissues (lipophilic, e.g. digoxin, TCAs).

Explanation

Worked example: 100 mg drug given IV, measured plasma concentration = 2 mg/L → Vd = 100 mg / 2 mg/L = 50 L.

Pharmacokinetics — Half-life & Clearance

What is the formula for drug half-life (t1/2)?

Answer: t1/2 = 0.7 × Vd / CL

Explanation

0.7 ≈ ln(2). Example: Vd = 50 L, CL = 3.5 L/hr → t1/2 = 0.7 × 50 / 3.5 = 10 hr.

How many half-lives does it take to reach steady state after starting a drug, or to eliminate a drug after stopping it?

Answer: About 4–5 half-lives in each direction.

Explanation

After 4-5 half-lives, plasma concentration is ~94–97% of the way to steady state (or eliminated).

What is the formula for clearance (CL)?

Answer: CL = rate of drug elimination / plasma drug concentration = 0.7 × Vd / t1/2

Explanation

Reflects the body's overall ability to eliminate drug (renal + hepatic). Example: Vd = 50 L, t1/2 = 10 hr → CL = 0.7 × 50 / 10 = 3.5 L/hr.

Pharmacokinetics — Dosing

What is the formula for loading dose, and does it change in renal/hepatic disease?

Answer: Loading dose = Cp × Vd / F. It does NOT need adjustment in renal or hepatic disease because it depends only on Vd and target concentration, not clearance.

Explanation

Cp = target plasma concentration, F = bioavailability (F=1 for IV). Example: Cp = 10 mg/L, Vd = 50 L, F = 1 → LD = 500 mg.

What is the formula for maintenance dose, and does it change in renal/hepatic disease?

Answer: Maintenance dose = Cp × CL × τ / F. It MUST be adjusted (lowered) when clearance is decreased, as in renal or hepatic failure.

Explanation

τ = dosing interval. Example: Cp = 10 mg/L, CL = 5 L/hr, τ = 1 hr, F = 1 → MD = 50 mg/hr.

Pharmacokinetics — Order of Kinetics

Distinguish zero-order from first-order elimination kinetics.

Answer: Zero-order: a constant AMOUNT of drug is eliminated per unit time (rate independent of concentration) → linear decline in plasma level. First-order: a constant FRACTION/PERCENTAGE of drug is eliminated per unit time (rate proportional to concentration) → exponential decline. Most drugs follow first-order kinetics.

Which drugs classically exhibit zero-order elimination kinetics?

Answer: Phenytoin, Ethanol, Aspirin (at high/toxic doses) — mnemonic "PEA".

Explanation

At toxic doses these drugs saturate their metabolic enzymes, switching from first-order to zero-order kinetics.

Pharmacodynamics — Agonists & Antagonists

On a dose-response curve, how do competitive and noncompetitive antagonists differ in their effect on an agonist?

Answer: Competitive (surmountable) antagonist: shifts the curve right, same Emax achievable with higher agonist dose (decreased potency). Noncompetitive (insurmountable) antagonist: decreases Emax, no rightward shift (decreased efficacy).

What is a partial agonist, and how does it behave when given together with a full agonist?

Answer: A partial agonist binds the receptor but produces a submaximal response even at full receptor occupancy. Given with a full agonist, it competes for the receptor and acts as a net antagonist, lowering the overall effect.

Pharmacodynamics — Potency & Efficacy

Define potency and efficacy, and how do they appear on a dose-response curve?

Answer: Potency = amount of drug needed to produce a given effect (reflected by EC50 — lower EC50 = more potent, curve shifted left). Efficacy = the maximal effect a drug can produce (Emax), regardless of dose or potency.

Pharmacodynamics — Therapeutic Index

What is the formula for therapeutic index (TI), and which drugs classically have a low TI?

Answer: TI = TD50 / ED50 (toxic dose in 50% of population ÷ effective dose in 50%). A higher TI = safer drug. Classic low-TI (narrow therapeutic window) drugs: warfarin, digoxin, lithium, theophylline.

Explanation

On a graph, a low-TI drug has its toxicity curve close to (overlapping) its efficacy curve.

Autonomic Drugs

What is bethanechol, and what is it used for?

Answer: A direct muscarinic (cholinergic) agonist resistant to acetylcholinesterase that does not cross the BBB; used for postoperative/neurogenic ileus and urinary retention.

What is the mechanism and clinical use of atropine?

Answer: Muscarinic acetylcholine receptor antagonist. Used to treat bradycardia and as part of treatment for organophosphate (cholinesterase inhibitor) poisoning.

Describe the classic anticholinergic toxidrome.

Answer: "Red as a beet (flushed), dry as a bone (dry mouth/skin), blind as a bat (mydriasis/cycloplegia), mad as a hatter (confusion/agitation), hot as a hare (hyperthermia)" plus tachycardia and urinary retention.

Why is phenoxybenzamine given preoperatively in pheochromocytoma?

Answer: It is an irreversible nonselective alpha-blocker that prevents a hypertensive crisis from catecholamine release during tumor manipulation/surgery.

Why are nonselective beta-blockers used cautiously in asthmatics and diabetics?

Answer: Beta-2 blockade causes bronchoconstriction (dangerous in asthma/COPD) and masks the tachycardia/tremor warning signs of hypoglycemia in diabetics.

Cardiovascular Drugs

What is the mechanism of digoxin, and what is its signature toxicity and antidote?

Answer: Inhibits the Na+/K+-ATPase → increased intracellular Na+ → decreased Na+/Ca2+ exchanger activity → increased intracellular Ca2+ → positive inotropy; also increases vagal tone. Toxicity: hyperkalemia (marker of acute toxicity), arrhythmias, GI upset, yellow-green visual changes. Antidote: digoxin immune Fab.

Summarize the 4 classes of antiarrhythmics by mechanism.

Answer: Class I: Na+ channel blockers (IA quinidine, IB lidocaine, IC flecainide). Class II: beta-blockers. Class III: K+ channel blockers, prolong QT (amiodarone, sotalol). Class IV: Ca2+ channel blockers (verapamil, diltiazem).

What is the signature toxicity profile of amiodarone?

Answer: Pulmonary fibrosis, hepatotoxicity, hypo- or hyperthyroidism (contains iodine), corneal microdeposits, blue-gray skin discoloration, bradycardia/heart block.

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