Pharmacology Drug Classes: 300 Mechanism and Effect Cards

300 classes learned by mechanism, so the adverse effects follow.

300 cardsLast updated 2026-08-21

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Pharmacology becomes manageable the moment you stop learning drugs one at a time. Almost everything a drug does follows from what it binds: a beta blocker slows the heart and constricts airways for the same reason, an anticholinergic dries the mouth and blurs vision for the same reason, and the adverse effects of a class are usually its intended action turning up in the wrong tissue. Learn it in that order and the side-effect list stops being a second thing to memorize. It falls out of the mechanism you already know. These 300 cards are built that way. Every one opens with the mechanism or the definition, naming the receptor or enzyme where the class acts on one. Then 182 name representative agents, 126 set out the adverse effects the whole class shares, 54 give the naming suffix, and 29 name the class most often mixed up with this one. Those suffixes are worth the price on their own: once -olol, -pril, -statin and -azole mean something to you, you can place a drug you have never seen from its name alone. There are no doses anywhere, and that is deliberate. What is worth carrying in memory is the mechanism, and a number you would look up in a formulary before acting on it only crowds that out. Cards are tagged by body system and by class family, so you can drill just the autonomic classes, just the anti-infectives, or one family such as the beta-lactams on its own. Import it and the deck joins your spaced-repetition schedule, and the classes that keep slipping keep coming back until they stop slipping.

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What's inside

Showing 100 representative cards from the full 300-card deck.

Front	Back
Pharmacokinetics	Definition: What the body does to a drug, covering absorption, distribution, metabolism, and excretion. Why it matters: It determines how much drug reaches its target and for how long, which is why two agents with the same mechanism can behave very differently. Often confused with: Pharmacodynamics, which is what the drug does to the body.
Pharmacodynamics	Definition: What a drug does to the body, covering its molecular target and the response that follows. Why it matters: It is where mechanism, potency, and efficacy live, and it explains why a class shares an effect profile.
Drug metabolism	Definition: The chemical alteration of a drug, mostly hepatic, that generally makes it more water-soluble and easier to excrete. Phases: Phase I reactions modify the molecule by oxidation, reduction, or hydrolysis. Phase II reactions attach a polar group by conjugation.
First-pass metabolism	Definition: The metabolism of an orally absorbed drug by the gut wall and liver before it reaches the systemic circulation. Why it matters: Heavily extracted drugs have low oral bioavailability, which is why some agents exist only in parenteral or sublingual formulations.
Steady state	Definition: The condition in which the amount of drug entering the body equals the amount leaving it, so concentration plateaus. Why it matters: It is reached after several half-lives regardless of how often the drug is taken, so frequency changes the fluctuation rather than the time to plateau.
Drug receptor	Definition: The macromolecule a drug binds to produce its effect, most often a membrane receptor, enzyme, ion channel, or transporter. Why it matters: Class membership is defined by this target, which is why agents sharing a target share an effect profile and an adverse effect profile.
Antagonist	Definition: A drug that binds a receptor without activating it, blocking the action of an agonist. Why it matters: It has no effect of its own where there is no ongoing agonist activity, which is why a blocker's visible effect depends on baseline tone.
Inverse agonist	Definition: A drug that binds a receptor with constitutive activity and reduces that baseline activity below its resting level. Often confused with: An antagonist, which holds baseline activity where it is rather than lowering it.
Potency	Definition: The amount of drug needed to produce a given effect. Often confused with: Efficacy. Potency is a position on the horizontal axis and efficacy is the height of the plateau, so a more potent drug is not a stronger one.
Therapeutic index	Definition: A ratio comparing the exposure that produces toxicity with the exposure that produces the desired effect. Why it matters: A narrow index means the two are close together, which is the pharmacological reason some classes are monitored and others are not.
Tolerance	Definition: A reduced response to a drug after repeated exposure, so a larger exposure is needed for the same effect. Mechanisms: Receptor downregulation, receptor desensitization, and induction of the enzymes that metabolize the drug.
Cytochrome P450 system	Definition: The family of hepatic enzymes responsible for most phase I drug metabolism. Why it matters: Many drugs are substrates, inducers, or inhibitors of the same isoenzyme, which is the mechanism behind a large share of drug interactions.
Cholinergic receptor types	Definition: The two receptor families for acetylcholine, muscarinic and nicotinic. Why it matters: One transmitter acting at two unrelated receptor types is why cholinergic drugs can be selective for very different effects.
Nicotinic receptor	Definition: A ligand-gated ion channel for acetylcholine, found at autonomic ganglia and at the neuromuscular junction. Why it matters: The ganglionic and muscle subtypes differ, which is what allows a neuromuscular blocker to act at muscle without blocking autonomic ganglia.
Alpha-1 adrenergic receptor	Definition: A postsynaptic adrenergic receptor on vascular smooth muscle, the bladder neck, and the pupillary dilator. Effect when activated: Vasoconstriction with a rise in blood pressure, bladder outlet contraction, and pupillary dilation.
Beta-1 adrenergic receptor	Definition: An adrenergic receptor concentrated in cardiac tissue and the juxtaglomerular apparatus. Effect when activated: Increased heart rate, conduction velocity, and contractility, and increased renin release.
Direct cholinergic agonists	Mechanism: Bind and activate muscarinic receptors directly, reproducing parasympathetic stimulation. Examples: Bethanechol, pilocarpine, carbachol. Class adverse effects: Salivation, lacrimation, sweating, bradycardia, bronchospasm, and abdominal cramping, all of which are the intended action appearing where it is not wanted.
Ganglionic blockers	Mechanism: Block nicotinic receptors at autonomic ganglia, interrupting both sympathetic and parasympathetic outflow. Why it matters: Blocking both limbs at once produces effects determined by whichever limb dominated at each organ, which is why the class is largely historical.
Catecholamines	Definition: Endogenous and synthetic agents sharing the catechol structure and acting on adrenergic receptors. Examples: Adrenaline, noradrenaline, dopamine, dobutamine, isoprenaline. Why it matters: They are rapidly broken down by monoamine oxidase and catechol-O-methyltransferase and are poorly absorbed from the gut, which is why the class is not given orally.
Central alpha-2 agonists	Mechanism: Activate alpha-2 receptors in the brainstem, reducing sympathetic outflow to the heart and vessels. Examples: Clonidine, methyldopa, dexmedetomidine. Class adverse effects: Sedation, dry mouth, and a rebound rise in blood pressure if the drug is stopped abruptly, which follows from the loss of suppressed sympathetic tone.
Alpha-1 blockers	Mechanism: Block alpha-1 receptors, relaxing vascular smooth muscle and the bladder neck. Suffix: Many end in -osin. Examples: Prazosin, doxazosin, tamsulosin. Class adverse effects: Postural hypotension, most marked at the start of treatment, and nasal congestion.
Cardioselective beta blockers	Mechanism: Preferentially block beta-1 receptors, sparing beta-2 at lower exposures. Examples: Metoprolol, atenolol, bisoprolol. Often confused with: Nonselective agents. Selectivity is relative rather than absolute, and it falls away as exposure rises.
Anticholinergic effect profile	Definition: The pattern produced by blocking muscarinic receptors, summarized as dry mouth, blurred vision, flushed dry skin, urinary retention, constipation, tachycardia, and confusion. Why it matters: Many classes outside autonomic pharmacology produce it as an off-target effect, so recognizing the pattern identifies the mechanism.
Sympathomimetic effect profile	Definition: The pattern produced by adrenergic activation, including tachycardia, hypertension, tremor, sweating, and pupillary dilation. Often confused with: The anticholinergic profile, which also gives tachycardia and dilated pupils but leaves the skin dry rather than sweating.
Renin-angiotensin-aldosterone system	Definition: The hormonal cascade in which renin generates angiotensin I, converting enzyme generates angiotensin II, and angiotensin II raises vascular tone and drives aldosterone release. Why it matters: Four separate drug classes act at four points of this one cascade, which is why their effects and adverse effects overlap so heavily.
Angiotensin II receptor blockers	Mechanism: Block the angiotensin II type 1 receptor, so angiotensin II is formed normally but cannot act at that receptor. Suffix: End in -sartan. Examples: Losartan, valsartan, candesartan. Often confused with: ACE inhibitors. Because bradykinin is not affected, cough is far less prominent, but the potassium and renal effects are shared.
Aldosterone antagonists	Mechanism: Block the mineralocorticoid receptor in the distal nephron, reducing sodium reabsorption and potassium excretion. Examples: Spironolactone, eplerenone. Class adverse effects: Raised serum potassium, and with spironolactone gynaecomastia and menstrual irregularity from its additional activity at androgen and progesterone receptors.
Thiazide diuretics	Mechanism: Block the sodium-chloride cotransporter in the distal convoluted tubule. Suffix: Most contain -thiazide. Examples: Hydrochlorothiazide, chlortalidone, indapamide. Class adverse effects: Low sodium, low potassium, low magnesium, raised calcium, raised urate, and raised glucose.
Potassium-sparing diuretics	Mechanism: Block the epithelial sodium channel in the collecting duct, so sodium is lost without the potassium exchange that normally accompanies it. Examples: Amiloride, triamterene. Class adverse effects: Raised serum potassium, which is the mirror image of the loss caused by loop and thiazide agents.
Osmotic diuretics	Mechanism: Filtered but not reabsorbed, so they hold water within the tubule by osmosis. Example: Mannitol. Mechanistic note: They also draw water out of tissues into plasma before reaching the kidney, which transiently expands intravascular volume.
Dihydropyridine calcium channel blockers	Mechanism: Block L-type calcium channels preferentially in vascular smooth muscle, producing arterial vasodilation. Suffix: End in -dipine. Examples: Amlodipine, nifedipine, felodipine. Class adverse effects: Ankle oedema, flushing, headache, and reflex tachycardia, all consequences of selective arterial dilation.
Direct arterial vasodilators	Mechanism: Relax arterial smooth muscle directly, without acting on adrenergic or calcium channel targets. Examples: Hydralazine, minoxidil. Class adverse effects: Reflex tachycardia and fluid retention, because the fall in resistance triggers baroreceptor and renal compensation.
Endothelin receptor antagonists	Mechanism: Block endothelin receptors, removing one of the strongest endogenous vasoconstrictor signals in the pulmonary circulation. Suffix: End in -sentan. Class adverse effects: Hepatic enzyme elevation, fluid retention, and teratogenic potential.
Cardiac glycosides	Mechanism: Inhibit the sodium-potassium ATPase, raising intracellular sodium and therefore intracellular calcium through the sodium-calcium exchanger, while also increasing vagal tone. Example: Digoxin. Class adverse effects: Nausea, visual disturbance with altered colour perception, and a wide range of arrhythmias. Mechanistic note: Low serum potassium increases binding at the pump, so potassium-losing diuretics amplify this class pharmacologically.
Class IB antiarrhythmics	Mechanism: Block sodium channels with fast on-off kinetics, acting preferentially on depolarized or ischaemic tissue and shortening repolarization. Examples: Lidocaine, mexiletine. Why it matters: The kinetics explain the selectivity for damaged ventricular tissue, since healthy tissue recovers between beats before the block can build.
Class II antiarrhythmics	Mechanism: Beta-adrenergic blockade, which slows sinoatrial firing and atrioventricular conduction by removing sympathetic drive. Why it matters: The antiarrhythmic action and the antihypertensive action of beta blockers are the same mechanism seen at different tissues.
Class IV antiarrhythmics	Mechanism: Calcium channel blockade at nodal tissue, slowing sinoatrial and atrioventricular conduction. Examples: Verapamil, diltiazem. Often confused with: Dihydropyridines, which share the channel but act on vascular smooth muscle rather than nodal tissue and so are not antiarrhythmic.
Statins	Mechanism: Competitively inhibit HMG-CoA reductase, the rate-limiting enzyme of hepatic cholesterol synthesis, which upregulates LDL receptors and clears LDL from plasma. Suffix: End in -statin. Examples: Atorvastatin, simvastatin, rosuvastatin. Class adverse effects: Muscle aching, raised creatine kinase, rarely rhabdomyolysis, and raised hepatic transaminases.
Fibrates	Mechanism: Activate the nuclear receptor PPAR-alpha, increasing lipoprotein lipase activity and clearing triglyceride-rich particles. Suffix: Contain -fibr-. Examples: Fenofibrate, gemfibrozil. Mechanistic note: They act on the same muscle toxicity pathway as statins, so the myopathy risk of the two mechanisms is additive.
Vitamin K antagonists	Mechanism: Inhibit vitamin K epoxide reductase, so clotting factors II, VII, IX, and X cannot be carboxylated into active form. Example: Warfarin. Why it matters: Existing factors must be cleared before the effect appears, which is why onset lags by days and why the effect is measured rather than assumed. Mechanistic note: It is metabolized by cytochrome P450, so inducers and inhibitors of those enzymes shift its exposure substantially.
Direct factor Xa inhibitors	Mechanism: Bind factor Xa directly, without needing antithrombin as an intermediary. Suffix: Contain -xaban. Examples: Apixaban, rivaroxaban, edoxaban. Often confused with: Heparins, which inhibit the same factor indirectly through antithrombin.
Cyclo-oxygenase inhibition as antiplatelet action	Mechanism: Irreversible acetylation of cyclo-oxygenase-1 in platelets blocks thromboxane A2 production. Platelets have no nucleus and cannot replace the enzyme. Example: Aspirin. Why it matters: The antiplatelet effect lasts the lifespan of the platelet rather than the lifespan of the drug in plasma.
GABA-A receptor as a drug target	Definition: A ligand-gated chloride channel whose opening hyperpolarizes the neuron, making it the main inhibitory target in the central nervous system. Why it matters: Several unrelated sedative classes converge on this one channel, which is why their effects are additive and their profiles overlap.
Barbiturates	Mechanism: Bind a separate site on the GABA-A receptor and increase the duration of channel opening, and at higher exposure open the channel without GABA at all. Suffix: End in -barbital. Often confused with: Benzodiazepines. Acting without GABA means there is no ceiling to the effect, which is why the therapeutic index of this class is far narrower.
Selective serotonin reuptake inhibitors	Mechanism: Block the presynaptic serotonin transporter, raising synaptic serotonin. Examples: Fluoxetine, sertraline, escitalopram. Class adverse effects: Nausea, sexual dysfunction, low serum sodium, and a discontinuation syndrome after abrupt cessation. Mechanistic note: The transporter is blocked within hours while the clinical effect takes weeks, so the therapeutic action is attributed to downstream receptor adaptation rather than to the block itself.
Monoamine oxidase inhibitors	Mechanism: Inhibit monoamine oxidase, so serotonin, noradrenaline, and dopamine are not broken down within the neuron. Examples: Phenelzine, tranylcypromine. Mechanistic note: Monoamine oxidase in the gut wall normally destroys dietary tyramine. With the enzyme inhibited, tyramine reaches the circulation and displaces stored noradrenaline, which is the mechanism behind the tyramine reaction.
First-generation antipsychotics	Mechanism: Block dopamine D2 receptors, with the antipsychotic effect attributed to the mesolimbic pathway. Examples: Haloperidol, chlorpromazine, fluphenazine. Class adverse effects: Movement disorders from D2 blockade in the nigrostriatal pathway, and raised prolactin from blockade in the tuberoinfundibular pathway.
Neuroleptic malignant syndrome	Definition: A syndrome of rigidity, hyperthermia, autonomic instability, and altered consciousness associated with dopamine blockade. Mechanistic note: It is attributed to abrupt loss of dopaminergic transmission, which is why it can also follow sudden withdrawal of a dopamine agonist.
Sodium channel blocking antiepileptics	Mechanism: Bind voltage-gated sodium channels in their inactivated state, limiting high-frequency repetitive firing while leaving normal firing largely intact. Examples: Carbamazepine, phenytoin, lamotrigine. Class adverse effects: Dizziness, double vision, ataxia, and serious cutaneous reactions.
Opioid receptor subtypes	Definition: The mu, kappa, and delta G protein-coupled receptors on which opioids act. Why it matters: Analgesia, respiratory depression, euphoria, and constipation are all attributed principally to the mu receptor, which is why they travel together as a class profile.
Opioid class effect profile	Definition: The constellation of effects shared across mu agonists, comprising analgesia, respiratory depression, miosis, constipation, sedation, and euphoria. Why it matters: Tolerance develops to most of these but not to constipation or miosis, because the gut and pupillary effects do not adapt in the same way.
Local anesthetics	Mechanism: Block voltage-gated sodium channels from the inside of the axon, preventing action potential propagation. Suffix: End in -caine. Examples: Lidocaine, bupivacaine, ropivacaine. Mechanistic note: They are weak bases, so an acidic inflamed environment keeps more of the molecule ionized and less able to cross the membrane to reach its site.
Levodopa with a peripheral decarboxylase inhibitor	Mechanism: Levodopa crosses the blood-brain barrier and is converted to dopamine, which cannot cross. The added inhibitor blocks that conversion outside the brain only. Examples: Levodopa with carbidopa or with benserazide. Class adverse effects: Nausea, postural hypotension, and with prolonged use motor fluctuations and dyskinesia.
COMT inhibitors	Mechanism: Inhibit catechol-O-methyltransferase, the enzyme that methylates levodopa peripherally, so more of it survives to reach the brain. Suffix: End in -capone. Why it matters: The class has no antiparkinsonian effect of its own and acts only by extending the availability of levodopa.
Triptans	Mechanism: Agonists at serotonin 5-HT1B and 5-HT1D receptors, constricting cranial vessels and inhibiting release of vasoactive neuropeptides. Suffix: End in -triptan. Class adverse effects: Chest and throat tightness, flushing, and paraesthesia. Mechanistic note: The vasoconstrictor action is not confined to cranial vessels, which is the basis of caution in vascular disease.
Selective norepinephrine reuptake inhibitors	Mechanism: Block the noradrenaline transporter without appreciable dopamine release. Example: Atomoxetine. Often confused with: Stimulants. The absence of a dopamine-releasing action is why this class is not a controlled stimulant, and why its onset is gradual.
Bactericidal versus bacteriostatic	Definition: Bactericidal agents kill the organism, while bacteriostatic agents halt replication and leave clearance to host defences. Why it matters: The distinction is a laboratory property measured under defined conditions and it varies with organism and concentration, so it is not a fixed label for a class.
Beta-lactam mechanism	Mechanism: The beta-lactam ring binds penicillin-binding proteins, the transpeptidases that cross-link peptidoglycan, so the wall cannot be completed and the cell lyses. Why it matters: Every penicillin, cephalosporin, carbapenem, and monobactam shares this target, which is why they share both their action and the hypersensitivity concern.
Antistaphylococcal penicillins	Mechanism: A bulky side chain sterically shields the beta-lactam ring from staphylococcal beta-lactamase. Examples: Flucloxacillin, nafcillin, oxacillin. Mechanistic note: Resistance in this group arises not from beta-lactamase but from an altered penicillin-binding protein with low beta-lactam affinity.
First-generation cephalosporins	Mechanism: Beta-lactam action with a spectrum weighted toward gram-positive cocci. Examples: Cefazolin, cefalexin. Why it matters: Successive cephalosporin generations trade gram-positive activity for gram-negative activity, and this is the gram-positive end of that gradient.
Fourth and fifth generation cephalosporins	Mechanism: The fourth generation combines broad gram-negative coverage with retained gram-positive activity and greater stability to some beta-lactamases. The fifth binds the altered penicillin-binding protein that confers methicillin resistance. Examples: Cefepime, ceftaroline.
Glycopeptides	Mechanism: Bind the D-alanyl-D-alanine terminus of the peptidoglycan precursor, blocking cross-linking at a different point from the beta-lactams. Examples: Vancomycin, teicoplanin. Class adverse effects: Nephrotoxicity, and an infusion-related histamine release reaction that is not immune-mediated. Mechanistic note: Resistance arises when the organism substitutes D-lactate for the terminal D-alanine, so the binding site is no longer recognized.
Aminoglycosides	Mechanism: Bind the 30S ribosomal subunit, causing misreading of messenger RNA. Uptake into the bacterium is oxygen-dependent. Suffix: Contain -micin or -mycin. Examples: Gentamicin, tobramycin, amikacin. Class adverse effects: Nephrotoxicity and ototoxicity affecting both hearing and balance. Mechanistic note: Oxygen-dependent uptake is why the class has no activity against anaerobes.
Macrolides	Mechanism: Bind the 50S ribosomal subunit and block translocation along the messenger RNA. Suffix: End in -thromycin. Examples: Azithromycin, clarithromycin, erythromycin. Class adverse effects: QT interval prolongation, and gastrointestinal upset from motilin receptor agonism. Mechanistic note: Erythromycin and clarithromycin inhibit cytochrome P450 3A4, raising exposure to substrates of that enzyme.
Fluoroquinolones	Mechanism: Inhibit DNA gyrase and topoisomerase IV, so bacterial DNA cannot be supercoiled or separated after replication. Suffix: End in -floxacin. Examples: Ciprofloxacin, levofloxacin, moxifloxacin. Class adverse effects: Tendinopathy and tendon rupture, peripheral neuropathy, QT prolongation, central nervous system effects, and aortic wall weakening. Mechanistic note: Like tetracyclines, the molecule chelates divalent cations, which reduces absorption when they share the gut lumen.
Rifamycins	Mechanism: Inhibit bacterial DNA-dependent RNA polymerase. Suffix: Begin with rif-. Examples: Rifampicin, rifabutin. Class adverse effects: Orange discolouration of urine, sweat, and tears, and hepatitis. Mechanistic note: Rifampicin is a powerful inducer of cytochrome P450 enzymes, so exposure to many co-administered substrates falls substantially.
Beta-lactamase resistance	Mechanism: Bacterial enzymes hydrolyse the beta-lactam ring before it can reach its target. Why it matters: It is the reason for beta-lactamase inhibitor combinations and for the structural modifications that define several penicillin subclasses.
Azole antifungals	Mechanism: Inhibit fungal lanosterol 14-alpha-demethylase, blocking ergosterol synthesis and destabilizing the fungal membrane. Suffix: End in -azole. Examples: Fluconazole, itraconazole, voriconazole. Class adverse effects: Hepatotoxicity and QT prolongation. Mechanistic note: The target is a cytochrome P450 enzyme, and the class also inhibits human P450 isoenzymes, which is the basis of its many metabolic interactions.
Nucleoside reverse transcriptase inhibitors	Mechanism: Nucleoside analogues that, once phosphorylated in the cell, are incorporated by reverse transcriptase and terminate the growing DNA chain. Examples: Tenofovir, emtricitabine, abacavir, zidovudine. Class adverse effects: Mitochondrial toxicity, since the same analogues can inhibit human mitochondrial DNA polymerase.
Integrase strand transfer inhibitors	Mechanism: Block the viral integrase enzyme, preventing insertion of viral DNA into the host genome. Suffix: End in -tegravir. Examples: Dolutegravir, bictegravir, raltegravir. Mechanistic note: The molecules chelate divalent cations, so antacids and mineral supplements sharing the gut lumen reduce absorption.
Insulin as a therapeutic class	Mechanism: Activates the insulin receptor tyrosine kinase, promoting glucose uptake into muscle and fat, glycogen synthesis, and suppression of hepatic glucose output. Class adverse effects: Low blood glucose, weight gain, and low serum potassium as insulin drives potassium into cells. Why it matters: It is a protein and is digested if swallowed, which is why the class exists only in parenteral and inhaled formulations.
Thiazolidinediones	Mechanism: Activate the nuclear receptor PPAR-gamma, altering transcription of genes governing fatty acid handling and insulin sensitivity. Suffix: End in -glitazone. Class adverse effects: Fluid retention with oedema and heart failure risk, weight gain, and reduced bone density. Why it matters: Because the mechanism is transcriptional, the effect builds over weeks rather than hours.
SGLT2 inhibitors	Mechanism: Block the sodium-glucose cotransporter-2 in the proximal tubule, so filtered glucose is excreted rather than reabsorbed. Suffix: End in -gliflozin. Class adverse effects: Genital fungal infection and volume depletion from the osmotic diuresis, and ketoacidosis that can occur without markedly raised glucose. Why it matters: The action is renal and independent of insulin, which is why it works regardless of beta cell reserve.
Thyroid hormone replacement	Mechanism: Synthetic thyroxine acts as a prohormone, converted peripherally to the more active triiodothyronine, which binds nuclear receptors and alters transcription. Example: Levothyroxine. Mechanistic note: Absorption is reduced by calcium and iron salts sharing the gut lumen, which bind the molecule. Class adverse effects: Features of excess thyroid activity, including palpitations, tremor, and bone loss.
Glucocorticoids	Mechanism: Bind the cytosolic glucocorticoid receptor, which moves to the nucleus and alters transcription, suppressing inflammatory mediators and immune cell function. Examples: Prednisolone, dexamethasone, hydrocortisone. Why it matters: The mechanism is transcriptional, so the anti-inflammatory effect takes hours to appear regardless of how the drug is given.
Estrogens	Mechanism: Bind nuclear estrogen receptors and alter transcription in reproductive tissue, bone, liver, and vasculature. Class adverse effects: Increased venous thromboembolism risk through raised hepatic synthesis of clotting factors, breast tenderness, and nausea.
Androgens	Mechanism: Bind the androgen receptor, driving transcription in muscle, bone, skin, and reproductive tissue. Class adverse effects: Acne, suppression of endogenous gonadotropins and spermatogenesis, polycythaemia, and adverse changes in lipid profile.
Bisphosphonates	Mechanism: Bind hydroxyapatite in bone and are taken up by osteoclasts, where they disrupt the mevalonate pathway and impair osteoclast function and survival. Suffix: End in -dronate or -dronic acid. Class adverse effects: Oesophageal irritation, osteonecrosis of the jaw, and atypical femoral fracture. Why it matters: Oral absorption is very poor and is abolished by food and by divalent cations, which is a property of the molecule.
Growth hormone and analogues	Mechanism: Activate the growth hormone receptor, with most peripheral growth effects mediated by insulin-like growth factor 1 produced in the liver. Class adverse effects: Fluid retention, joint pain, and reduced insulin sensitivity.
Beta-2 agonist duration classes	Definition: Inhaled beta-2 agonists grouped as short-acting and long-acting. Mechanism of the difference: Long-acting members carry a lipophilic side chain that anchors them in the membrane near the receptor, so they leave the site slowly. Why it matters: Both categories act at the same receptor with the same effect and the same adverse effect profile, and only the duration differs.
Leukotriene receptor antagonists	Mechanism: Block the cysteinyl leukotriene receptor, preventing leukotriene-driven bronchoconstriction, mucus secretion, and eosinophil recruitment. Suffix: End in -lukast. Class adverse effects: Neuropsychiatric effects including mood change and sleep disturbance.
Anti-IgE monoclonal antibodies	Mechanism: Bind free IgE and prevent it attaching to receptors on mast cells and basophils. Example: Omalizumab. Why it matters: It removes the trigger for degranulation rather than blocking any mediator, which places it upstream of the other anti-inflammatory classes.
First-generation antihistamines	Mechanism: Block histamine H1 receptors, and cross the blood-brain barrier readily while also blocking muscarinic and alpha-1 receptors. Examples: Diphenhydramine, chlorphenamine, promethazine. Class adverse effects: Sedation, anticholinergic effects, and postural hypotension, none of which come from the intended H1 target.
Antitussives	Mechanism: Suppress the cough reflex, centrally by acting on medullary pathways or peripherally by reducing sensory input from the airway. Examples: Dextromethorphan, codeine, benzonatate. Mechanistic note: Dextromethorphan is an NMDA receptor antagonist and serotonin reuptake inhibitor at higher exposure, which is why it interacts with serotonergic mechanisms.
Proton pump inhibitors	Mechanism: Prodrugs activated in the acidic canaliculus of the parietal cell, where they irreversibly inhibit the hydrogen-potassium ATPase, the final step of acid secretion. Suffix: End in -prazole. Examples: Omeprazole, pantoprazole, esomeprazole. Class adverse effects: Reduced magnesium and vitamin B12 absorption, enteric infection risk from reduced gastric acidity, and rebound acid hypersecretion on stopping. Why it matters: Because inhibition is irreversible, the effect outlasts the drug in plasma until new pumps are made.
5-HT3 receptor antagonists	Mechanism: Block serotonin 5-HT3 receptors on vagal afferents in the gut and in the chemoreceptor trigger zone. Suffix: End in -setron. Examples: Ondansetron, granisetron. Class adverse effects: Constipation, headache, and QT interval prolongation.
Prokinetic agents	Mechanism: Increase gastrointestinal motility, through dopamine D2 blockade, 5-HT4 agonism, or motilin receptor agonism. Examples: Metoclopramide, prucalopride, erythromycin acting at motilin receptors. Why it matters: An antibiotic appearing in this list is a reminder that class membership follows the receptor, not the therapeutic label.
Stimulant laxatives	Mechanism: Act on the enteric nervous system to increase motility and reduce absorption of water and electrolytes. Examples: Senna, bisacodyl. Class adverse effects: Cramping and electrolyte loss with prolonged use.
Conventional disease-modifying antirheumatic drugs	Mechanism: Slow the disease process rather than only relieving symptoms, by varied routes including dihydrofolate reductase inhibition and effects on lymphocyte function. Examples: Methotrexate, leflunomide, hydroxychloroquine, sulfasalazine. Class adverse effects: Bone marrow suppression, hepatotoxicity, and increased infection susceptibility, varying by agent.
JAK inhibitors	Mechanism: Inhibit Janus kinases, the intracellular enzymes that transmit signals from many cytokine receptors to the nucleus. Suffix: End in -citinib. Why it matters: Blocking a shared intracellular step affects many cytokines at once, which is why the class is broader in effect than a single antibody. Class adverse effects: Infection including herpes zoster reactivation, raised lipids, and thromboembolic signals.
Alkylating agents	Mechanism: Attach alkyl groups to DNA, forming cross-links that prevent strand separation and replication. Examples: Cyclophosphamide, ifosfamide, temozolomide. Class adverse effects: Bone marrow suppression, infertility, and secondary malignancy. Cyclophosphamide produces a bladder-irritant metabolite.
Microtubule stabilizers	Mechanism: Bind tubulin and prevent microtubule disassembly, so the mitotic spindle cannot be taken apart. Suffix: Contain -taxel. Examples: Paclitaxel, docetaxel. Class adverse effects: Peripheral neuropathy from disrupted axonal transport, and hypersensitivity related to the solubilizing vehicle.
Monoclonal antibody naming convention	Definition: The stem -mab identifies a monoclonal antibody, and preceding syllables indicate the source, such as -ximab for chimeric, -zumab for humanized, and -umab for fully human. Why it matters: The more non-human sequence an antibody contains, the more likely an immune response against it, so the name carries a pharmacological hint.
Toxidrome	Definition: A recognizable cluster of signs produced by a class of agents acting on a shared receptor system. Why it matters: Recognizing the pattern identifies the receptor mechanism, which is why toxidromes are organized by pharmacology rather than by substance.
Benzodiazepine receptor antagonists	Mechanism: Competitively block the benzodiazepine site on the GABA-A receptor. Example: Flumazenil. Why it matters: Removing benzodiazepine potentiation abruptly can unmask withdrawal in an adapted nervous system, which is a pharmacological consequence of the mechanism.
Cholinesterase reactivators	Mechanism: Displace an organophosphate from the enzyme's active site, restoring acetylcholinesterase activity. Example: Pralidoxime. Why it matters: The bond ages into an irreversible form over time, after which reactivation is no longer possible, which is a chemical property of the complex.
QT interval prolongation as a class effect	Mechanism: Blockade of the rapid delayed rectifier potassium current lengthens ventricular repolarization. Classes involved: Class IA and class III antiarrhythmics, macrolides, fluoroquinolones, azole antifungals, several antipsychotics, and 5-HT3 antagonists. Mechanistic note: Agents acting on the same current add to one another, and low potassium or magnesium deepens the effect.
Ototoxicity mechanisms	Definition: Damage to cochlear or vestibular hair cells, or to the auditory nerve, caused by drug exposure. Classes involved: Aminoglycosides, loop diuretics, platinum agents, and high sustained salicylate exposure. Why it matters: Hair cells do not regenerate in mammals, which is why cochlear damage from these classes is generally permanent.
Drug-induced hyperkalaemia mechanisms	Definition: A rise in serum potassium caused by drug action on its handling. Mechanisms involved: Reduced aldosterone effect with renin-angiotensin blockers and aldosterone antagonists, blocked distal sodium channels with potassium-sparing agents, reduced cellular uptake with beta blockade, and shift out of cells with digoxin at the sodium-potassium pump.
Boxed warning	Definition: The most prominent warning a medicines regulator can require on a product's labelling, marking a serious or life-threatening risk. Why it matters: It signals a risk that regulators judged severe enough to need highlighting, and it is a regulatory instrument rather than a pharmacological property.

Frequently asked

Why are there no doses in the deck?

Because at this level the mechanism is what repays memorizing and a number is not. Doses vary by country, formulation and situation, and anyone acting on one checks a current source first. Leaving them out keeps every card about how the class works, which is what an exam asks you to reason from. It also means the deck is a study aid on mechanism rather than a clinical reference.

How do the naming suffixes help?

Drug classes are often named to a pattern, so the ending of a generic name places the drug. 54 cards give the suffix for classes that have one: -olol for beta blockers, -pril for ACE inhibitors, -statin for HMG-CoA reductase inhibitors, -azole for the azole antifungals, -prazole for proton pump inhibitors, -tinib for tyrosine kinase inhibitors. Learn those and an unfamiliar name stops being unfamiliar.

Why does it teach classes instead of individual drugs?

Because the class is where the explanation lives. Agents sharing a target share their effects and their adverse effects, so learning the class explains many agents at once. Named drugs are generic names used as representative examples. A handful of cards are headed by a single agent, such as lithium or isoniazid, where that agent effectively is its own class.

How is it organized for studying one area at a time?

Every card carries a system tag and a class-family tag below it, across principles, autonomic, cardiovascular, CNS, anti-infective, endocrine, respiratory, gastrointestinal, immune and oncology, and toxicology. Filter by a tag to drill one system, or by the finer tag to drill a single family such as beta-lactams or diuretics.

Does the content apply in every country?

Mechanisms are the same everywhere. Which agents are available, what they are called and how they are labelled all vary and change over time, so treat the mechanism as portable and the names around it as something to check locally.

Can I import the whole deck on the free plan?

Yes. Importing a saved deck runs no new AI generation and spends no AI credits, so the free plan imports every card. You can study, edit and delete them afterwards.

Will importing it twice create duplicates?

No. Cards you already have are skipped and only cards added in a revision come through. Including re-imports after deleting it, one official deck can be imported three times per account.

Can I edit the cards after importing?

Yes. Once imported they are your cards: edit either side, delete the ones your course does not cover, retag them, or move them into another deck.