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. On 29 of them the answer is followed by the class most often mixed up with this one. Suffixes are why the classes are worth learning at all: 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.

What happens when you add it

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The button opens Memly and the whole deck lands in your account.
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Each card gets its own schedule, based on how well you actually recall it.
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What's inside

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

Front	Back
Pharmacokinetics — what is it?	What the body does to a drug, covering absorption, distribution, metabolism, and excretion. Pharmacodynamics, which is what the drug does to the body.
Pharmacodynamics — what is it?	What a drug does to the body, covering its molecular target and the response that follows. It is where mechanism, potency, and efficacy live, and it explains why a class shares an effect profile.
Drug metabolism — what is it?	The chemical alteration of a drug, mostly hepatic, that generally makes it more water-soluble and easier to excrete.
First-pass metabolism — what is it?	The metabolism of an orally absorbed drug by the gut wall and liver before it reaches the systemic circulation. Heavily extracted drugs have low oral bioavailability, which is why some agents exist only in parenteral or sublingual formulations.
Steady state — what is it?	The condition in which the amount of drug entering the body equals the amount leaving it, so concentration plateaus. 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 — what is it?	The macromolecule a drug binds to produce its effect, most often a membrane receptor, enzyme, ion channel, or transporter. Class membership is defined by this target, which is why agents sharing a target share an effect profile and an adverse effect profile.
Antagonist — what is it?	A drug that binds a receptor without activating it, blocking the action of an agonist. 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 — what is it?	A drug that binds a receptor with constitutive activity and reduces that baseline activity below its resting level. An antagonist, which holds baseline activity where it is rather than lowering it.
Potency — what is it?	The amount of drug needed to produce a given effect. 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 — what is it?	A ratio comparing the exposure that produces toxicity with the exposure that produces the desired effect. A narrow index means the two are close together, which is the pharmacological reason some classes are monitored and others are not.
Tolerance — what is it?	A reduced response to a drug after repeated exposure, so a larger exposure is needed for the same effect. Receptor downregulation, receptor desensitization, and induction of the enzymes that metabolize the drug.
Cytochrome P450 system — what is it?	The family of hepatic enzymes responsible for most phase I drug metabolism. 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 — what is it?	The two receptor families for acetylcholine, muscarinic and nicotinic. One transmitter acting at two unrelated receptor types is why cholinergic drugs can be selective for very different effects.
Nicotinic receptor — what is it?	A ligand-gated ion channel for acetylcholine, found at autonomic ganglia and at the neuromuscular junction. 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 — what is it?	A postsynaptic adrenergic receptor on vascular smooth muscle, the bladder neck, and the pupillary dilator.
Beta-1 adrenergic receptor — what is it?	An adrenergic receptor concentrated in cardiac tissue and the juxtaglomerular apparatus.
Direct cholinergic agonists — what is it?	Bind and activate muscarinic receptors directly, reproducing parasympathetic stimulation.
Ganglionic blockers — what is it?	Block nicotinic receptors at autonomic ganglia, interrupting both sympathetic and parasympathetic outflow. Blocking both limbs at once produces effects determined by whichever limb dominated at each organ, which is why the class is largely historical.
Catecholamines — what is it?	Endogenous and synthetic agents sharing the catechol structure and acting on adrenergic receptors. 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 — what is it?	Activate alpha-2 receptors in the brainstem, reducing sympathetic outflow to the heart and vessels.
Alpha-1 blockers — what is it?	Block alpha-1 receptors, relaxing vascular smooth muscle and the bladder neck.
Cardioselective beta blockers — what is it?	Preferentially block beta-1 receptors, sparing beta-2 at lower exposures. Nonselective agents. Selectivity is relative rather than absolute, and it falls away as exposure rises.
Anticholinergic effect profile — what is it?	The pattern produced by blocking muscarinic receptors, summarized as dry mouth, blurred vision, flushed dry skin, urinary retention, constipation, tachycardia, and confusion. Many classes outside autonomic pharmacology produce it as an off-target effect, so recognizing the pattern identifies the mechanism.
Sympathomimetic effect profile — what is it?	The pattern produced by adrenergic activation, including tachycardia, hypertension, tremor, sweating, and pupillary dilation. The anticholinergic profile, which also gives tachycardia and dilated pupils but leaves the skin dry rather than sweating.
Renin-angiotensin-aldosterone system — what is it?	The hormonal cascade in which renin generates angiotensin I, converting enzyme generates angiotensin II, and angiotensin II raises vascular tone and drives aldosterone release. 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 — what is it?	Block the angiotensin II type 1 receptor, so angiotensin II is formed normally but cannot act at that receptor. ACE inhibitors. Because bradykinin is not affected, cough is far less prominent, but the potassium and renal effects are shared.
Aldosterone antagonists — what is it?	Block the mineralocorticoid receptor in the distal nephron, reducing sodium reabsorption and potassium excretion.
Thiazide diuretics — what is it?	Block the sodium-chloride cotransporter in the distal convoluted tubule.
Potassium-sparing diuretics — what is it?	Block the epithelial sodium channel in the collecting duct, so sodium is lost without the potassium exchange that normally accompanies it.
Osmotic diuretics — what is it?	Filtered but not reabsorbed, so they hold water within the tubule by osmosis.
Dihydropyridine calcium channel blockers — what is it?	Block L-type calcium channels preferentially in vascular smooth muscle, producing arterial vasodilation.
Direct arterial vasodilators — what is it?	Relax arterial smooth muscle directly, without acting on adrenergic or calcium channel targets.
Endothelin receptor antagonists — what is it?	Block endothelin receptors, removing one of the strongest endogenous vasoconstrictor signals in the pulmonary circulation.
Cardiac glycosides — what is it?	Inhibit the sodium-potassium ATPase, raising intracellular sodium and therefore intracellular calcium through the sodium-calcium exchanger, while also increasing vagal tone.
Class IB antiarrhythmics — what is it?	Block sodium channels with fast on-off kinetics, acting preferentially on depolarized or ischaemic tissue and shortening repolarization. The kinetics explain the selectivity for damaged ventricular tissue, since healthy tissue recovers between beats before the block can build.
Class II antiarrhythmics — what is it?	Beta-adrenergic blockade, which slows sinoatrial firing and atrioventricular conduction by removing sympathetic drive. The antiarrhythmic action and the antihypertensive action of beta blockers are the same mechanism seen at different tissues.
Class IV antiarrhythmics — what is it?	Calcium channel blockade at nodal tissue, slowing sinoatrial and atrioventricular conduction. Dihydropyridines, which share the channel but act on vascular smooth muscle rather than nodal tissue and so are not antiarrhythmic.
Statins — what is it?	Competitively inhibit HMG-CoA reductase, the rate-limiting enzyme of hepatic cholesterol synthesis, which upregulates LDL receptors and clears LDL from plasma.
Fibrates — what is it?	Activate the nuclear receptor PPAR-alpha, increasing lipoprotein lipase activity and clearing triglyceride-rich particles.
Vitamin K antagonists — what is it?	Inhibit vitamin K epoxide reductase, so clotting factors II, VII, IX, and X cannot be carboxylated into active form. 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.
Direct factor Xa inhibitors — what is it?	Bind factor Xa directly, without needing antithrombin as an intermediary. Heparins, which inhibit the same factor indirectly through antithrombin.
Cyclo-oxygenase inhibition as antiplatelet action — what is it?	Irreversible acetylation of cyclo-oxygenase-1 in platelets blocks thromboxane A2 production. Platelets have no nucleus and cannot replace the enzyme. 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 — what is it?	A ligand-gated chloride channel whose opening hyperpolarizes the neuron, making it the main inhibitory target in the central nervous system. Several unrelated sedative classes converge on this one channel, which is why their effects are additive and their profiles overlap.
Barbiturates — what is it?	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. 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 — what is it?	Block the presynaptic serotonin transporter, raising synaptic serotonin.
Monoamine oxidase inhibitors — what is it?	Inhibit monoamine oxidase, so serotonin, noradrenaline, and dopamine are not broken down within the neuron.
First-generation antipsychotics — what is it?	Block dopamine D2 receptors, with the antipsychotic effect attributed to the mesolimbic pathway.
Neuroleptic malignant syndrome — what is it?	A syndrome of rigidity, hyperthermia, autonomic instability, and altered consciousness associated with dopamine blockade.
Sodium channel blocking antiepileptics — what is it?	Bind voltage-gated sodium channels in their inactivated state, limiting high-frequency repetitive firing while leaving normal firing largely intact.
Opioid receptor subtypes — what is it?	The mu, kappa, and delta G protein-coupled receptors on which opioids act. 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 — what is it?	The constellation of effects shared across mu agonists, comprising analgesia, respiratory depression, miosis, constipation, sedation, and euphoria. 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 — what is it?	Block voltage-gated sodium channels from the inside of the axon, preventing action potential propagation.
Levodopa with a peripheral decarboxylase inhibitor — what is it?	Levodopa crosses the blood-brain barrier and is converted to dopamine, which cannot cross. The added inhibitor blocks that conversion outside the brain only.
COMT inhibitors — what is it?	Inhibit catechol-O-methyltransferase, the enzyme that methylates levodopa peripherally, so more of it survives to reach the brain. The class has no antiparkinsonian effect of its own and acts only by extending the availability of levodopa.
Triptans — what is it?	Agonists at serotonin 5-HT1B and 5-HT1D receptors, constricting cranial vessels and inhibiting release of vasoactive neuropeptides.
Selective norepinephrine reuptake inhibitors — what is it?	Block the noradrenaline transporter without appreciable dopamine release. 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 — what is it?	Bactericidal agents kill the organism, while bacteriostatic agents halt replication and leave clearance to host defences. 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 — what is it?	The beta-lactam ring binds penicillin-binding proteins, the transpeptidases that cross-link peptidoglycan, so the wall cannot be completed and the cell lyses. Every penicillin, cephalosporin, carbapenem, and monobactam shares this target, which is why they share both their action and the hypersensitivity concern.
Antistaphylococcal penicillins — what is it?	A bulky side chain sterically shields the beta-lactam ring from staphylococcal beta-lactamase.
First-generation cephalosporins — what is it?	Beta-lactam action with a spectrum weighted toward gram-positive cocci. 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 — what is it?	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.
Glycopeptides — what is it?	Bind the D-alanyl-D-alanine terminus of the peptidoglycan precursor, blocking cross-linking at a different point from the beta-lactams.
Aminoglycosides — what is it?	Bind the 30S ribosomal subunit, causing misreading of messenger RNA. Uptake into the bacterium is oxygen-dependent.
Macrolides — what is it?	Bind the 50S ribosomal subunit and block translocation along the messenger RNA.
Fluoroquinolones — what is it?	Inhibit DNA gyrase and topoisomerase IV, so bacterial DNA cannot be supercoiled or separated after replication.
Rifamycins — what is it?	Inhibit bacterial DNA-dependent RNA polymerase.
Beta-lactamase resistance — what is it?	Bacterial enzymes hydrolyse the beta-lactam ring before it can reach its target. It is the reason for beta-lactamase inhibitor combinations and for the structural modifications that define several penicillin subclasses.
Azole antifungals — what is it?	Inhibit fungal lanosterol 14-alpha-demethylase, blocking ergosterol synthesis and destabilizing the fungal membrane.
Nucleoside reverse transcriptase inhibitors — what is it?	Nucleoside analogues that, once phosphorylated in the cell, are incorporated by reverse transcriptase and terminate the growing DNA chain.
Integrase strand transfer inhibitors — what is it?	Block the viral integrase enzyme, preventing insertion of viral DNA into the host genome.
Insulin as a therapeutic class — what is it?	Activates the insulin receptor tyrosine kinase, promoting glucose uptake into muscle and fat, glycogen synthesis, and suppression of hepatic glucose output. It is a protein and is digested if swallowed, which is why the class exists only in parenteral and inhaled formulations.
Thiazolidinediones — what is it?	Activate the nuclear receptor PPAR-gamma, altering transcription of genes governing fatty acid handling and insulin sensitivity. Because the mechanism is transcriptional, the effect builds over weeks rather than hours.
SGLT2 inhibitors — what is it?	Block the sodium-glucose cotransporter-2 in the proximal tubule, so filtered glucose is excreted rather than reabsorbed. The action is renal and independent of insulin, which is why it works regardless of beta cell reserve.
Thyroid hormone replacement — what is it?	Synthetic thyroxine acts as a prohormone, converted peripherally to the more active triiodothyronine, which binds nuclear receptors and alters transcription.
Glucocorticoids — what is it?	Bind the cytosolic glucocorticoid receptor, which moves to the nucleus and alters transcription, suppressing inflammatory mediators and immune cell function. The mechanism is transcriptional, so the anti-inflammatory effect takes hours to appear regardless of how the drug is given.
Estrogens — what is it?	Bind nuclear estrogen receptors and alter transcription in reproductive tissue, bone, liver, and vasculature.
Androgens — what is it?	Bind the androgen receptor, driving transcription in muscle, bone, skin, and reproductive tissue.
Bisphosphonates — what is it?	Bind hydroxyapatite in bone and are taken up by osteoclasts, where they disrupt the mevalonate pathway and impair osteoclast function and survival. 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 — what is it?	Activate the growth hormone receptor, with most peripheral growth effects mediated by insulin-like growth factor 1 produced in the liver.
Beta-2 agonist duration classes — what is it?	Inhaled beta-2 agonists grouped as short-acting and long-acting. Long-acting members carry a lipophilic side chain that anchors them in the membrane near the receptor, so they leave the site slowly.
Leukotriene receptor antagonists — what is it?	Block the cysteinyl leukotriene receptor, preventing leukotriene-driven bronchoconstriction, mucus secretion, and eosinophil recruitment.
Anti-IgE monoclonal antibodies — what is it?	Bind free IgE and prevent it attaching to receptors on mast cells and basophils. It removes the trigger for degranulation rather than blocking any mediator, which places it upstream of the other anti-inflammatory classes.
First-generation antihistamines — what is it?	Block histamine H1 receptors, and cross the blood-brain barrier readily while also blocking muscarinic and alpha-1 receptors.
Antitussives — what is it?	Suppress the cough reflex, centrally by acting on medullary pathways or peripherally by reducing sensory input from the airway.
Proton pump inhibitors — what is it?	Prodrugs activated in the acidic canaliculus of the parietal cell, where they irreversibly inhibit the hydrogen-potassium ATPase, the final step of acid secretion. Because inhibition is irreversible, the effect outlasts the drug in plasma until new pumps are made.
5-HT3 receptor antagonists — what is it?	Block serotonin 5-HT3 receptors on vagal afferents in the gut and in the chemoreceptor trigger zone.
Prokinetic agents — what is it?	Increase gastrointestinal motility, through dopamine D2 blockade, 5-HT4 agonism, or motilin receptor agonism. An antibiotic appearing in this list is a reminder that class membership follows the receptor, not the therapeutic label.
Stimulant laxatives — what is it?	Act on the enteric nervous system to increase motility and reduce absorption of water and electrolytes.
Conventional disease-modifying antirheumatic drugs — what is it?	Slow the disease process rather than only relieving symptoms, by varied routes including dihydrofolate reductase inhibition and effects on lymphocyte function.
JAK inhibitors — what is it?	Inhibit Janus kinases, the intracellular enzymes that transmit signals from many cytokine receptors to the nucleus. Blocking a shared intracellular step affects many cytokines at once, which is why the class is broader in effect than a single antibody.
Alkylating agents — what is it?	Attach alkyl groups to DNA, forming cross-links that prevent strand separation and replication.
Microtubule stabilizers — what is it?	Bind tubulin and prevent microtubule disassembly, so the mitotic spindle cannot be taken apart.
Monoclonal antibody naming convention — what is it?	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. The more non-human sequence an antibody contains, the more likely an immune response against it, so the name carries a pharmacological hint.
Toxidrome — what is it?	A recognizable cluster of signs produced by a class of agents acting on a shared receptor system. Recognizing the pattern identifies the receptor mechanism, which is why toxidromes are organized by pharmacology rather than by substance.
Benzodiazepine receptor antagonists — what is it?	Competitively block the benzodiazepine site on the GABA-A receptor. Removing benzodiazepine potentiation abruptly can unmask withdrawal in an adapted nervous system, which is a pharmacological consequence of the mechanism.
Cholinesterase reactivators — what is it?	Displace an organophosphate from the enzyme's active site, restoring acetylcholinesterase activity. 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 — what is it?	Blockade of the rapid delayed rectifier potassium current lengthens ventricular repolarization.
Ototoxicity mechanisms — what is it?	Damage to cochlear or vestibular hair cells, or to the auditory nerve, caused by drug exposure. Hair cells do not regenerate in mammals, which is why cochlear damage from these classes is generally permanent.
Drug-induced hyperkalaemia mechanisms — what is it?	A rise in serum potassium caused by drug action on its handling.
Boxed warning — what is it?	The most prominent warning a medicines regulator can require on a product's labelling, marking a serious or life-threatening risk. 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: -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 does not use your AI allowance, 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.