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Pharmacology curriculum 26 chapters
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197 concepts
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Everything the adaptive question bank can teach and test in Pharmacology, from foundations through advanced practice. Work through it in order, or start practising and let the questions find your level.
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A. Absorption and routes of administration
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Enteral, parenteral, topical, inhaled: what each route buys in onset and costs in control.
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Oral drug crosses gut wall and liver before circulation, so oral and IV doses of the same drug differ.
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Fraction of dose reaching systemic circulation intact; IV is 100% by definition and is the reference.
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Weak acids and bases cross membranes un-ionized; stomach vs small-bowel absorption follows pKa.
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Food changes rate vs extent; divalent cations chelate tetracyclines and quinolones into inactivity.
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Immediate, enteric-coated, and extended-release forms; why crushing an ER tablet dose-dumps.
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Sublingual, transdermal, rectal, and inhaled routes skip portal circulation.
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IV, IM, and subcutaneous absorption profiles; depot forms trade fast onset for long duration.
B. Distribution and protein binding
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Vd is an apparent volume, not an anatomic one; a large Vd means tissue-sequestered.
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Albumin carries acidic drugs, alpha-1-acid glycoprotein basic ones; only free drug acts.
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Displacement raises free fraction transiently; clearance usually restores balance.
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Lipophilicity and efflux transporters gate CNS entry; peripheral decarboxylase inhibitors exploit it.
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Small lipophilic unbound drug crosses; ion trapping concentrates weak bases in milk.
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Short clinical action from redistribution out of brain, not from elimination.
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Fat mass, lean mass, and total body water shift Vd in infancy, obesity, and old age.
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Loading dose is set by Vd; maintenance dose is set by clearance.
C. Metabolism and the cytochrome P450 system
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Oxidation, reduction, and hydrolysis add or unmask a functional group.
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Glucuronidation, sulfation, and acetylation build water-soluble conjugates for excretion.
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CYP3A4, 2D6, 2C9, 2C19, and 1A2 carry most clinically important interactions.
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Inhibition is fast and raises substrate exposure; azoles, macrolides, and grapefruit are the archetypes.
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Induction takes days to weeks and lowers exposure; rifampin, carbamazepine, St Johns wort.
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When metabolism creates the active drug, an inhibitor reduces effect instead of raising it.
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Poor, intermediate, and ultrarapid metabolizer phenotypes and the genes that define them.
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Zero-order metabolism turns a small dose change into a large level change.
D. Excretion, clearance and dosing intervals
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Glomerular filtration, active tubular secretion, and passive reabsorption act on different drug properties.
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Alkalinizing urine traps ionized weak acids and speeds their loss.
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Biliary excretion plus gut reactivation recycles drug and prolongs exposure.
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Clearance is volume of plasma cleared per unit time and sets the maintenance rate.
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Four to five half-lives to reach steady state, and the same to wash out.
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Renally cleared drugs accumulate when eGFR falls; the failure mode is silent toxicity.
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What a trough answers, what a peak answers, and when a level is uninterpretable.
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Narrow-index drugs have no margin between effect and harm, which is why they are monitored.
E. Pharmacodynamics — receptors and dose-response
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Ion channels, G-protein-coupled receptors, kinase-linked, and nuclear receptors differ in response speed.
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Full, partial, and inverse agonism; a partial agonist can act as an antagonist in a high-tone system.
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Competitive antagonism is surmountable; noncompetitive and physiologic antagonism are not.
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Binding tightly and producing an effect are separate properties.
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Potency vs efficacy; what a rightward shift and a lowered ceiling each mean.
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Selective agents lose selectivity as dose rises, which is where the class side effect appears.
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Receptor downregulation over days vs mediator depletion within minutes.
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Enzyme inhibitors, transporter blockers, channel blockers, and chelators act without a receptor.
F. Adverse effects, allergy and interactions
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Dose-related predictable reactions vs idiosyncratic reactions that no dose reduction prevents.
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IgE-mediated anaphylaxis vs delayed T-cell reactions; intolerance is not allergy.
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What earns a boxed warning and how it constrains use rather than forbidding it.
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Interactions at absorption, binding, metabolism, and transport, including P-glycoprotein.
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Additive sedation, serotonergic stacking, QT stacking, and dual pathway blockade.
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Grapefruit, tyramine, vitamin K, and herbal inducers change exposure predictably.
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Which classes own hepatotoxicity, nephrotoxicity, ototoxicity, and myelosuppression.
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Insulin, opioids, anticoagulants, and concentrated electrolytes are defined by error severity.
G. Cholinergic pharmacology
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Nicotinic receptors at ganglia and neuromuscular junction; muscarinic receptors at target organs.
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Bethanechol and pilocarpine; the secretory-and-motility effect cluster is the class signature.
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Reversible agents for myasthenia and dementia vs irreversible organophosphate poisoning.
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Atropine-class blockade produces the dry, flushed, tachycardic, confused pattern.
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Cumulative blockade from many drugs drives falls, delirium, and retention in older adults.
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Depolarizing vs nondepolarizing blockade and why reversal strategies differ.
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Too much drug and too little drug look alike until you test the tone.
H. Adrenergic pharmacology
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Alpha-1, alpha-2, beta-1, beta-2, and beta-3 locations and the effect each mediates.
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Epinephrine, norepinephrine, and dopamine differ by which receptors they reach.
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Peripheral alpha-1 agonists raise pressure while central alpha-2 agonists lower it.
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Beta-2 bronchodilation with tremor and potassium shift vs beta-1 cardiac stimulation.
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First-dose orthostatic hypotension, urinary flow benefit, and intraoperative iris effects.
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Cardioselectivity, masking of hypoglycemia, and rebound ischemia on abrupt withdrawal.
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Releasers, reuptake blockers, and MAO inhibitors raise synaptic catecholamines without binding the receptor.
I. Antihypertensives and heart-failure drugs
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Where renin inhibitors, ACE inhibitors, ARBs, and aldosterone antagonists interrupt the cascade.
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Bradykinin accumulation explains cough and angioedema; potassium and creatinine rise are expected.
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Receptor-level blockade without bradykinin buildup, and what that changes.
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Dihydropyridines act on vessels with reflex tachycardia and edema; non-dihydropyridines slow the heart.
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Nephron site of action predicts both the diuresis and the electrolyte loss.
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Aldosterone antagonists and epithelial sodium channel blockers; hyperkalemia risk compounds with RAAS blockade.
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Neurohormonal blockade changes outcome; diuresis changes how the patient feels.
J. Antianginals, antiarrhythmics and lipid drugs
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Venodilation drops preload; tolerance requires a nitrate-free interval; PDE5 combination is prohibited.
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Vaughan Williams classes I to IV grouped by the ion current each blocks.
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Multichannel action with thyroid, pulmonary, hepatic, and corneal toxicity over time.
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Sodium-potassium ATPase inhibition; narrow index; hypokalemia magnifies toxicity.
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Adenosine and rate-control agents work by transiently blocking conduction, not by fixing the atria.
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HMG-CoA reductase inhibition; myopathy risk climbs with CYP3A4 inhibitors.
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Which classes stack repolarization delay and how torsades follows.
K. Anticoagulants, antiplatelets and thrombolytics
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Antithrombin potentiation, aPTT monitoring, and protamine as the specific reversal.
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Predictable kinetics and anti-Xa monitoring; renal clearance limits use.
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Vitamin K epoxide reductase inhibition, INR monitoring, and diet plus CYP2C9 variability.
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Direct factor Xa and thrombin inhibitors, their reversal agents, and renal dosing.
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An immune reaction that causes clotting, not bleeding, and forbids further heparin.
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Aspirin, P2Y12 inhibitors, and glycoprotein IIb/IIIa blockers hit different steps of the same plug.
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Plasminogen activation dissolves formed clot; contraindications are all bleeding-risk logic.
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Vitamin K, prothrombin complex, antifibrinolytics, and desmopressin by mechanism.
L. Antibacterials — cell-wall agents
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Natural, aminopenicillin, antistaphylococcal, and antipseudomonal spectra differ by side chain.
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Clavulanate and tazobactam protect the partner drug; they are not antibiotics alone.
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Gram-negative reach and CNS penetration change with generation.
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Broadest beta-lactam coverage and the monobactam option in severe penicillin allergy.
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D-Ala-D-Ala binding; infusion reaction is not allergy; level monitoring guards the kidney.
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Cross-reactivity is driven by side-chain similarity, not by class membership alone.
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Beta-lactamases, altered penicillin-binding proteins, porin loss, and efflux pumps.
M. Antibacterials — protein, DNA and folate agents
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30S binding, concentration-dependent killing, and paired nephrotoxicity plus ototoxicity.
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30S binding; cation chelation, photosensitivity, and tissue-deposition cautions.
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50S binding with QT prolongation and heavy CYP3A4 inhibition.
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Anaerobic coverage bought at the price of Clostridioides difficile risk.
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Linezolid blocks initiation, carries serotonergic risk, and suppresses marrow with duration.
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Gyrase and topoisomerase IV inhibition; tendon, aortic, and neuropathy warnings.
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Sulfonamide plus trimethoprim blocks sequential steps; rash, hyperkalemia, and displacement effects.
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Narrowing spectrum, shortening duration, and deciding when not to treat at all.
N. Antifungals, antivirals, antiparasitics and antitubercular drugs
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Ergosterol synthesis blockade with strong CYP inhibition and hepatic monitoring.
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Membrane binding with infusion and renal toxicity vs fungal cell-wall inhibition.
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Acyclovir requires viral thymidine kinase, which is why it spares host cells.
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Reverse transcriptase, protease, integrase, and entry targets and why combinations are used.
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Neuraminidase inhibitors have a treatment window; direct-acting antivirals cure hepatitis C.
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Rifampin induction, isoniazid neuropathy and pyridoxine, ethambutol optic effects, pyrazinamide urate.
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Antimalarial, antihelminthic, and antiprotozoal targets and prophylaxis timing.
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Active immunization vs immunoglobulin, and why live vaccines are restricted in immunosuppression.
O. Sedative-hypnotics, anxiolytics and anesthetics
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GABA-A channel-opening frequency; flumazenil reversal; synergy with opioids is the lethal combination.
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Z-drugs, melatonin receptor agonists, and orexin antagonists by target.
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Duration-based GABA modulation with no ceiling, which is why they were displaced.
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Propofol, etomidate, and ketamine differ in blood pressure, adrenal, and airway effects.
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Minimum alveolar concentration as a potency measure; malignant hyperthermia as a trigger reaction.
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Sodium-channel blockade; acidic infected tissue resists; systemic toxicity has a lipid rescue.
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Cross-tolerance explains why a long-acting agent covers a short-acting withdrawal.
P. Antidepressants, antipsychotics and mood stabilizers
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Reuptake blockade with delayed clinical effect and a discontinuation syndrome on abrupt stop.
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Anticholinergic and antihistaminic burden plus cardiac sodium-channel toxicity in overdose.
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Tyramine hypertensive crisis and mandatory washout before serotonergic agents.
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Bupropion, mirtazapine, and trazodone chosen for their distinct side-effect profiles.
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Mental status change, autonomic instability, and neuromuscular excitation from serotonergic stacking.
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D2 blockade with dystonia, akathisia, parkinsonism, and late tardive dyskinesia.
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Serotonin-dopamine profile trades movement effects for metabolic effects; clozapine needs marrow monitoring.
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Narrow index with sodium and hydration dependence, plus thyroid and renal effects.
Q. Antiepileptics and neurodegenerative-disease drugs
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Use-dependent block; enzyme induction and serious rash define the class risks.
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Valproate, levetiracetam, and topiramate mechanisms and their signature toxicities.
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Why regimens are reviewed before pregnancy rather than after a positive test.
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A benzodiazepine aborts; a loading antiepileptic prevents recurrence; the order is the point.
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Levodopa with a decarboxylase inhibitor, dopamine agonists, and MAO-B or COMT inhibitors.
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Cholinesterase inhibitors and NMDA modulation are symptomatic, not disease-reversing.
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Disease-modifying immunomodulation vs steroids for an acute relapse.
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Centrally acting spasmolytics vs peripheral action at the muscle itself.
R. Opioids, NSAIDs and non-opioid analgesia
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Mu receptor analgesia comes bundled with constipation, sedation, and respiratory depression.
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Kinetics and active metabolites separate morphine, hydromorphone, fentanyl, and methadone.
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A ceiling effect and the ability to precipitate withdrawal in a tolerant patient.
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Competitive reversal wears off faster than the agonist, so re-sedation is expected.
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Tolerance, hyperalgesia, and the pharmacology behind maintenance treatment.
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COX-1 vs COX-2 inhibition explains the gastric, renal, and cardiovascular trade-offs.
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NAPQI accumulation after glutathione depletion, and why N-acetylcysteine works.
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Abortive serotonin-receptor agonists and CGRP-directed agents vs preventive therapy.
S. Diabetes and thyroid pharmacology
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Onset, peak, and duration profiles are what make a basal-bolus regimen work.
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Hypoglycemia recognition, intracellular potassium shift, and concentrated-product errors.
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Reduced hepatic glucose output without hypoglycemia; lactate and renal-function considerations.
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Sulfonylureas and meglitinides close ATP-sensitive potassium channels and can cause hypoglycemia.
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GLP-1 receptor agonists and DPP-4 inhibitors; delayed gastric emptying is the shared effect.
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Renal glucose loss with euglycemic ketoacidosis and genital infection risk.
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Absorption rules, feedback monitoring, and the signs of over-replacement.
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Thionamides block hormone synthesis; agranulocytosis is the warning symptom to teach.
T. Corticosteroids, sex hormones and bone drugs
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Anti-inflammatory benefit paid for in glucose, bone, immunity, skin, and mood.
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Exogenous steroid silences the axis, which is why tapering and stress dosing exist.
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Relative potency at each receptor decides which agent fits which deficiency.
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Ovulation suppression mechanism, thrombotic risk, and failure with enzyme inducers.
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Testosterone therapy risks, 5-alpha-reductase inhibition, and receptor blockade.
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Osteoclast inhibition with esophageal and jaw precautions and long skeletal residence.
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RANKL inhibition, parathyroid-hormone analogues, and selective estrogen receptor modulators.
U. Respiratory and allergy pharmacology
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Rescue and maintenance roles are not interchangeable, and monotherapy risk differs.
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Controller therapy; local deposition explains both the benefit and the mouth-care teaching.
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Muscarinic blockade in the airway with ocular and urinary cautions.
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Blocking the leukotriene pathway; the neuropsychiatric warning is class-defining.
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Narrow therapeutic index and a heavy interaction load explain their decline.
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First-generation sedation and anticholinergic load vs second-generation peripheral selectivity.
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Alpha-agonist rebound congestion; central cough suppression and its abuse potential.
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Anti-IgE and anti-interleukin agents target a phenotype rather than the whole disease.
V. Gastrointestinal pharmacology
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Irreversible pump inhibition, pre-meal timing, and the long-term-use concerns.
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Faster but weaker acid control, plus absorption interactions from raised gastric pH.
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Barrier formation vs prostaglandin replacement, and the pregnancy contraindication.
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Serotonin, dopamine, neurokinin, histamine, and muscarinic pathways map to different nausea causes.
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Bulk, osmotic, stimulant, softener, and peripheral opioid antagonists by mechanism.
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Peripheral opioid receptor action, and when slowing the bowel is harmful.
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Aminosalicylates, corticosteroids, immunomodulators, and biologics as an escalation ladder.
W. Antineoplastics and immunomodulators
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Phase-specific vs nonspecific agents and why the marrow nadir is predictable.
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DNA cross-linking with bladder, renal, and auditory toxicity signatures.
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Folate and pyrimidine pathway blockade, and the logic of a rescue agent.
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Spindle and DNA-unwinding targets; neuropathy and vesicant extravasation risk.
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Kinase inhibitors and monoclonal antibodies act only where the biomarker is present.
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Releasing the immune brake produces autoimmune-style adverse events.
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Calcineurin, mTOR, and antiproliferative agents; level monitoring and infection risk.
X. Toxicology, antidotes and overdose mechanisms
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Anticholinergic, cholinergic, opioid, sympathomimetic, and sedative patterns as diagnostic clusters.
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Each antidote works by competition, bypass, chelation, or metabolic blockade.
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Charcoal timing, urinary alkalinization, and what makes a drug dialyzable.
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Time-based risk assessment and why the antidote replenishes glutathione.
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Simultaneous respiratory alkalosis and metabolic acidosis with tinnitus as an early clue.
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The metabolite, not the parent alcohol, causes injury, which is what the antidote exploits.
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Lead, iron, and mercury each pair with a specific chelator.
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Carbon monoxide blocks oxygen carriage; cyanide blocks its use in the mitochondrion.
Y. Special populations and lifespan pharmacology
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Weight and surface-area scaling plus organ immaturity change both dose and choice.
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Falling clearance, altered body composition, and potentially inappropriate medication lists.
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Risk-benefit framing, known teratogen classes, and transfer into milk.
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Which classes require adjustment and what accumulation looks like clinically.
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Lost first-pass extraction, low albumin, and heightened sedative sensitivity.
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Total, ideal, and adjusted body weight follow the drug lipophilicity.
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Reviewing indication, benefit horizon, and prescribing cascades.
Z. Drug development, labeling and safety systems
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Preclinical through post-marketing, and which harms each phase can actually detect.
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Bioequivalence for small molecules vs biosimilarity and interchangeability for biologics.
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Indications, warnings, interactions, and clinical pharmacology sections answer different questions.
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Shared suffixes encode the class, which turns an unfamiliar name into a prediction.
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Spontaneous reporting, signal detection, and risk-mitigation programs.
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Schedules rank abuse potential against accepted use and constrain prescribing.
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Off-label prescribing, compendial support, and the evidence hierarchy behind a claim.
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