Pharmacology Drug Classes: 300 Mechanism and Effect Cards
300 classes learned by mechanism, so the adverse effects follow.
300枚のカード
収録カードを見る（30枚）
全300枚から30枚を抜粋して表示しています。
| 表 | 裏 |
|---|---|
| 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. |
| Direct cholinergic agonists — what is it? | Bind and activate muscarinic receptors directly, reproducing parasympathetic stimulation. |
| 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. |
| 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. |
| Selective serotonin reuptake inhibitors — what is it? | Block the presynaptic serotonin transporter, raising synaptic serotonin. |
| First-generation antipsychotics — what is it? | Block dopamine D2 receptors, with the antipsychotic effect attributed to the mesolimbic pathway. |
| 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. |
| Local anesthetics — what is it? | Block voltage-gated sodium channels from the inside of the axon, preventing action potential propagation. |
| Triptans — what is it? | Agonists at serotonin 5-HT1B and 5-HT1D receptors, constricting cranial vessels and inhibiting release of vasoactive neuropeptides. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
このデッキについて
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.
よくある質問
- 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.
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.