Class Explorer
Medications as families
Learn the family first: shared mechanism, shared effects, shared warnings, then the differences that actually change decisions. Trivia without practical relevance did not make the page.
Cardiovascular
Beta blockers
Competitive antagonists at beta adrenergic receptors; the clinical personality of each agent is its selectivity and its pharmacokinetics.
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ACE inhibitors
Inhibit angiotensin-converting enzyme: less angiotensin II and aldosterone, more bradykinin.
3 full pages · 4 more members noted
Angiotensin receptor blockers
Block angiotensin II at the AT1 receptor; RAAS interruption without bradykinin accumulation.
3 full pages · 4 more members noted
Calcium channel blockers
Block L-type calcium channels; the split that matters is vascular (dihydropyridines) versus cardiac (non-dihydropyridines).
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Loop diuretics
Block the Na-K-2Cl cotransporter in the thick ascending limb: the most powerful diuresis the nephron can give.
1 full page · 2 more members noted
Thiazide diuretics
Block the distal Na-Cl cotransporter; modest diuresis, durable vascular antihypertensive effect.
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Statins
HMG-CoA reductase inhibitors: upregulate hepatic LDL receptors by throttling cholesterol synthesis.
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Mineralocorticoid receptor antagonists
Competitive antagonists at the aldosterone receptor in the distal nephron: sodium out, potassium retained, and, in the heart, less fibrosis. The diuretic effect is modest; the outcome benefit is not.
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Antiplatelet agents
Drugs that stop platelets aggregating, each at a different point: thromboxane synthesis, ADP signalling, or the final common receptor. They prevent arterial (white, platelet-rich) clot, which is why they are not interchangeable with anticoagulants.
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Nitrates
Nitric oxide donors that relax vascular smooth muscle. Venodilation at low doses drops preload, which is where most of the anginal relief comes from; arterial dilation follows at higher doses.
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Antiarrhythmics
Drugs that alter cardiac conduction or refractoriness. Every one of them can also cause the arrhythmia it treats, which is the single most important fact about the class.
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Hematology
Anticoagulants
Interrupt the coagulation cascade: warfarin starves factor synthesis upstream; DOACs inhibit factor Xa or thrombin directly.
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Hematinics
Replacement of the substrates of erythropoiesis. Each one corrects a different deficiency, and giving the wrong one is a way to delay the diagnosis.
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Endocrine
Diabetes agents
A mechanistically diverse family: less hepatic glucose (metformin), urinary glucose disposal (SGLT2i), incretin amplification (GLP-1 RA, DPP-4i), insulin release (sulfonylureas), insulin itself.
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Sulfonylureas
Close the ATP-sensitive potassium channel on the beta cell, depolarising it and forcing insulin release whether or not glucose is high. That last clause is the whole safety story.
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Incretin-based agents
Amplify the incretin signal that makes oral glucose release more insulin than intravenous glucose does. Because the effect is glucose-dependent, insulin only rises when glucose is high, which is why hypoglycemia is not a feature.
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Insulins
Replacement of the hormone itself. The molecule is the same job in every product; what is bought and sold is the time-action profile.
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Thyroid agents
Replace thyroid hormone, or block its synthesis. Both directions are titrated against TSH, and both are slow.
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Systemic corticosteroids
Bind the glucocorticoid receptor and rewrite transcription across every tissue. Powerfully anti-inflammatory, and there is no such thing as an organ they miss.
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Bisphosphonates
Bind hydroxyapatite, are swallowed by osteoclasts as they resorb, and kill them from the inside. Bone formation then outpaces resorption.
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Psychiatry
SSRIs
Selective serotonin reuptake inhibition at SERT; weeks-long receptor adaptation delivers the clinical effect.
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SNRIs
Serotonin plus noradrenaline reuptake inhibition; the noradrenaline arrives with dose and brings blood pressure along.
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Atypical antidepressants
Antidepressants that do not fit the SSRI or SNRI template. Their differences are the reason they exist: each one is chosen for a side effect somebody wants.
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Antipsychotics
Dopamine D2 receptor blockade is the common thread; the atypicals add serotonin antagonism, which buys fewer movement disorders at the price of metabolic ones.
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Benzodiazepines and Z-drugs
Positive allosteric modulators at GABA-A: they do not open the channel themselves, they make the body's own GABA more effective. That distinction is why they are safer alone than barbiturates and still lethal with opioids.
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Anti-infectives
Penicillins
Beta-lactams binding penicillin-binding proteins: wall synthesis stops, bactericidal, time-dependent killing.
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Fluoroquinolones
DNA gyrase/topoisomerase IV inhibitors: concentration-dependent killing, excellent oral bioavailability.
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Glycopeptides
Bind D-Ala-D-Ala peptidoglycan termini in gram-positives; too bulky for gram-negative outer membranes.
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Cephalosporins
Beta-lactams that bind penicillin-binding proteins and stop cell-wall cross-linking. Generations describe a march from Gram-positive coverage toward Gram-negative and resistance stability.
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Macrolides
Bind the 50S ribosomal subunit and block translocation. Bacteriostatic, excellent intracellular and atypical coverage, and the interaction profile of a CYP3A4 inhibitor.
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Tetracyclines
Bind the 30S ribosomal subunit and block tRNA docking. Broad, intracellular, and reliably active against the organisms nothing else reaches.
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Sulfonamide antibacterials
Sequential blockade of folate synthesis: sulfamethoxazole blocks dihydropteroate synthase, trimethoprim blocks dihydrofolate reductase. Bacteria make folate, we eat it, which is the selectivity.
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Nitroimidazoles
Reduced inside anaerobic organisms to radicals that fragment DNA. The reduction only happens in a low-oxygen environment, which is the entire basis of the spectrum.
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Urinary antiseptics
Agents that concentrate in urine and act there. They treat the bladder and nothing else, which is both their strength and their hard limit.
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Respiratory
Inhaled bronchodilators
Beta-2 agonists (cAMP-mediated relaxation) and muscarinic antagonists (blocking vagal tone), in short- and long-acting forms.
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Inhaled corticosteroids
Topical anti-inflammatory therapy delivered to the airway, with high first-pass metabolism of whatever is swallowed so that systemic exposure stays low.
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Leukotriene receptor antagonists
Block the cysteinyl leukotriene receptor, cutting the bronchoconstriction, mucus and eosinophil recruitment that arachidonic acid's other branch produces.
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Gastrointestinal
Proton pump inhibitors
Irreversible H+/K+-ATPase inhibition in active parietal cells: the deepest acid suppression available.
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Antiemetics
Vomiting has several afferent routes, and each antiemetic class blocks one of them. Choosing by mechanism rather than by habit is what separates effective antiemesis from a sequence of failures.
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Laxatives
Soften stool, draw water in, or stimulate propulsion. The mechanism decides the pairing: a stimulant for opioid constipation, an osmotic for hard stool.
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Pain & inflammation
NSAIDs
COX inhibition: prostaglandin-dependent pain and inflammation fall, and so do the prostaglandin-dependent defenses (gastric mucosa, renal perfusion, platelets).
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Simple analgesics
Acetaminophen's central COX action: analgesia and antipyresis without anti-inflammatory or antiplatelet effects.
1 full page
Opioids
Mu receptor agonists in the dorsal horn, brainstem and limbic system: less pain signal ascending, less distress about the pain that arrives, and less respiratory drive.
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Gout agents
Two entirely separate jobs that are constantly confused: putting out the fire of an acute attack, and lowering urate over months so the fires stop.
2 full pages · 3 more members noted
Conventional DMARDs
Disease-modifying agents that slow the immune process itself rather than treating its symptoms. Slow to work, and monitored for as long as they are taken.
2 full pages · 3 more members noted
Neurology
Gabapentinoids
Bind the alpha-2-delta subunit of voltage-gated calcium channels and reduce excitatory transmitter release. Named after GABA and acting nowhere near it.
1 full page · 1 more members noted
Antiseizure medications
Reduce neuronal excitability by blocking sodium channels, enhancing GABA, or modulating synaptic vesicle release. Choice is driven as much by interactions, pregnancy and monitoring burden as by efficacy.
4 full pages · 3 more members noted