Pharmacology Drug Classes: 300 Mechanism and Effect Cards
300 classes learned by mechanism, so the adverse effects follow.
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| Front | Back |
|---|---|
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
About this deck
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.
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.
Educational material about how drug classes work, not prescribing guidance and not clinical advice. Drug availability, approved names, and labelling differ by country and change over time. Compiled 2026-08-21.