Pharmacology

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• Antibiotics — Antibiotics are antibacterial medicines that target essential structures or processes within bacteria. Grouping them by their main mechanism of action makes their spectrum, clinical uses, adverse effects and resistance patterns far easier to learn.
• Cardiovascular drugs — Cardiovascular medicines are grouped here by the mechanism they act through, because spectrum of use, adverse effects and monitoring follow the mechanism far more closely than they follow the indication. A medicine used for hypertension, heart failure and angina behaves according to its family, not its label.
• Central nervous system and psychiatry — Neurological and psychiatric medicines are grouped here by the transmitter system they act on, because that is what predicts their adverse effects, their interactions and their withdrawal behaviour. Two drugs used for the same diagnosis often behave nothing alike, while a single drug frequently spans epilepsy, mood and pain because one mechanism serves all three.
• Endocrine and metabolic drugs — Endocrine medicines are grouped here by the hormonal axis or metabolic pathway they act on, because that is what predicts their monitoring, their interactions and the consequences of stopping them abruptly. Many replace or oppose a hormone the body already makes, which is why both excess and deficiency states appear as adverse effects. (in preparation)
• Respiratory and allergy drugs — Respiratory medicines separate cleanly into those that relieve airway narrowing within minutes and those that suppress the inflammation causing it over weeks. Confusing the two is the commonest clinical error in this area, so the grouping here follows that division.
• Analgesia and anaesthesia — Pain and anaesthesia medicines are grouped by where they interrupt the pain pathway: at the peripheral inflammatory source, along the conducting nerve, or centrally at the opioid receptor. That location predicts both the usefulness of a drug and the harm it can do. (in preparation)
• Gastrointestinal drugs — Gastrointestinal medicines are grouped by the process they change: acid secretion, transit through the gut, the vomiting reflex, or mucosal inflammation. Symptoms overlap heavily across these mechanisms, which is why the mechanism rather than the complaint organises the section.
• Antivirals, antifungals and antiparasitics — These medicines complete the anti-infective story the antibiotics section begins. They are separated from antibacterials because the targets differ fundamentally: viruses replicate inside host cells, fungi and parasites are eukaryotes, and the selective margin is narrower in every case. (in preparation)
• Immunomodulators — These medicines change how the immune system behaves rather than treating an organism or a receptor. They share a common trade-off that organises the whole section: the benefit is suppression of a damaging immune response, and the cost is reduced defence against infection and, for some, against malignancy. (in preparation)

How the antibacterial classes are grouped

Grouping antibacterial drugs by their main mechanism of action is what makes their spectrum, resistance patterns and adverse effects learnable rather than memorisable.

• Cell wall synthesis inhibitors — These antibiotics interfere with bacterial cell-wall formation, weakening susceptible bacteria and ultimately causing cell death or inhibition of growth.
• Protein synthesis inhibitors — These antibiotics bind bacterial ribosomal subunits and prevent production of the proteins required for bacterial growth and survival.
• Nucleic acid synthesis inhibitors — These drugs interfere with bacterial DNA replication or RNA synthesis.
• Folate synthesis inhibitors — These drugs interrupt bacterial folate metabolism, a pathway required for the synthesis of nucleic acids.
• Cell membrane–active antibiotics — These agents disrupt the bacterial cell membrane and interfere with membrane integrity.
• Other important antibacterial agents — These clinically important antibacterial drugs have mechanisms that are best studied separately.
• Renin–angiotensin–aldosterone system agents — These medicines act at different points of the renin–angiotensin–aldosterone system to lower blood pressure, reduce cardiac workload and limit adverse cardiac and renal remodelling.
• Adrenergic receptor agents — These medicines block or stimulate adrenergic receptors, changing heart rate, contractility and vascular tone.
• Calcium channel blockers — These medicines reduce calcium entry through voltage-gated channels in vascular smooth muscle and cardiac tissue, causing vasodilation or reduced cardiac conduction depending on subclass.
• Diuretics — These medicines increase renal sodium and water excretion at defined nephron sites, reducing fluid overload and blood pressure.
• Antithrombotic agents — These medicines reduce clot formation or dissolve existing clot by acting on platelets, the coagulation cascade or fibrin, and they carry the bleeding risk that dominates their monitoring.
• Lipid-modifying agents — These medicines lower atherogenic lipoproteins by inhibiting synthesis, reducing absorption or increasing clearance, and are central to cardiovascular risk reduction.
• Antiarrhythmic agents — These medicines alter cardiac ion currents or conduction to restore or maintain rhythm, and several are themselves proarrhythmic.
• Vasodilators and other cardiac agents — These medicines reduce preload or afterload, or act through mechanisms best studied separately from the main cardiovascular families.
• Anticonvulsant and membrane-stabilising agents — These medicines reduce pathological neuronal firing by acting on voltage-gated sodium or calcium channels, by enhancing GABAergic inhibition, or by binding synaptic vesicle protein 2A. The same mechanisms underlie their use in epilepsy, in mood stabilisation and in neuropathic pain.
• Monoamine-modulating antidepressants — These medicines raise synaptic serotonin, noradrenaline or both, most often by blocking reuptake. Their classes are separated far more by receptor selectivity and adverse-effect burden than by antidepressant efficacy.
• GABAergic and sedative agents — These medicines enhance inhibitory transmission at the GABA-A receptor, producing anxiolysis, sedation, hypnosis and anticonvulsant activity. Tolerance, dependence and withdrawal are class properties rather than agent-specific surprises.
• Dopamine receptor agents — These medicines block or stimulate dopamine receptors, chiefly D2. Blockade underlies antipsychotic effect and extrapyramidal adverse effects; stimulation underlies antiparkinsonian effect and its own impulse-control and psychiatric risks.
• Headache and neurovascular agents — These medicines act on cranial vascular tone and trigeminal nociception, principally through serotonin 5-HT1B/1D receptors or the calcitonin gene-related peptide pathway, and are separated into acute and preventive roles.
• CNS stimulant and cognitive agents — These medicines increase catecholaminergic or cholinergic transmission to improve attention, wakefulness or cognitive symptoms. They span controlled stimulants and the symptomatic agents used in dementia.
• Sex hormones and reproductive agents — These agents supply, oppose or modulate oestrogen, progestogen and androgen signalling. Thrombotic risk, hepatic enzyme interactions and hormone-sensitive cancer dominate their safety profile.
• Glucose-lowering agents — These medicines lower blood glucose by increasing insulin supply, improving insulin sensitivity, slowing carbohydrate absorption or promoting urinary glucose loss. Hypoglycaemia risk follows the mechanism, not the potency.
• Bone and mineral agents — These medicines act on bone turnover and on calcium and phosphate handling, and are used where fracture risk or mineral homeostasis is the clinical problem.
• Corticosteroids and adrenal agents — These agents act at the glucocorticoid or mineralocorticoid receptor, or on adrenal steroid synthesis. Duration of exposure, rather than dose alone, governs most of their harm.
• Thyroid and antithyroid agents — These medicines replace thyroid hormone or suppress its synthesis, and are monitored biochemically rather than symptomatically.
• Antihistamines and allergy agents — These medicines block the histamine H1 receptor or otherwise interrupt allergic mediator release. Generation determines sedation far more than potency does.
• Bronchodilators — These medicines relax airway smooth muscle through beta-2 adrenoceptor stimulation, muscarinic blockade or phosphodiesterase inhibition, and are separated into reliever and maintenance roles.
• Inhaled and anti-inflammatory airway agents — These medicines suppress airway inflammation rather than relieving bronchoconstriction, and act over days to weeks rather than minutes.
• Opioid analgesics — These medicines act at mu, kappa and delta opioid receptors to reduce pain perception. Respiratory depression, tolerance and dependence are properties of the mechanism itself.
• Non-opioid analgesics — These medicines relieve pain without acting at opioid receptors, mostly by inhibiting cyclo-oxygenase or by mechanisms that remain incompletely characterised.
• Anaesthetic and neuromuscular agents — These agents produce loss of sensation, loss of consciousness or skeletal muscle paralysis, and are used almost exclusively in monitored settings.
• Neuropathic pain agents — These medicines act on neuronal excitability rather than on inflammation, which is why conventional analgesics work poorly in nerve-related pain.
• Acid-suppressing agents — These medicines reduce gastric acid secretion or neutralise acid already secreted, and differ principally in the speed and completeness of that effect.
• Gut motility and antiemetic agents — These medicines alter gastrointestinal transit or interrupt the receptors that drive nausea and vomiting, and are chosen by the mechanism of the symptom rather than by its severity.
• Intestinal anti-inflammatory agents — These medicines suppress mucosal inflammation in inflammatory bowel disease, acting topically within the bowel or systemically on the immune response.
• Antiviral agents — These medicines inhibit viral entry, replication or maturation. Because they target a replicating organism, resistance and treatment adherence are inseparable.
• Antifungal agents — These medicines exploit differences between fungal and human cell membranes and cell walls, chiefly through ergosterol synthesis, membrane binding or glucan synthesis.
• Antimycobacterial agents — These medicines treat tuberculosis and related mycobacterial infection, where combination therapy and long duration are dictated by the organism's biology.
• Antiparasitic and anthelmintic agents — These medicines act against protozoa and helminths, organisms whose eukaryotic biology leaves a narrower selective margin than bacteria do.
• Disease-modifying antirheumatic agents — These medicines alter the course of inflammatory rheumatic disease rather than only relieving its symptoms, and share a requirement for infection screening and ongoing monitoring.
• Immunosuppressant agents — These medicines suppress lymphocyte activation or proliferation, principally in transplantation and severe autoimmune disease, at the cost of infection and malignancy risk.

All drug classes

• Opioid analgesics — Mu receptor agonists; respiratory depression, tolerance and dependence follow directly from the mechanism. (in preparation)
• NSAIDs, including COX-2 selective agents — Cyclo-oxygenase inhibitors; gastrointestinal, renal and cardiovascular risk define their limits. (in preparation)
• Paracetamol and other non-opioid analgesics — Safe at licensed doses and hepatotoxic above them; the mechanism remains incompletely established. (in preparation)
• General anaesthetics — Intravenous and inhalational agents producing reversible loss of consciousness. (in preparation)
• Local anaesthetics — Sodium channel blockers acting on conduction; systemic toxicity is the critical hazard. (in preparation)
• Neuromuscular blockers — Depolarising and non-depolarising paralytic agents used only with airway control. (in preparation)
• Gabapentinoids and neuropathic pain agents — Alpha-2-delta ligands and related agents; misuse potential and opioid interaction matter. (in preparation)
• Penicillins — β-lactams that bind penicillin-binding proteins; spectrum differs sharply by subclass.
• Cephalosporins — β-lactams conventionally grouped into generations with broadly shifting spectrum.
• Carbapenems — Very broad-spectrum β-lactams reserved for serious or resistant infections.
• Monobactams — A monocyclic β-lactam class represented in practice by aztreonam.
• Glycopeptides — Non-β-lactam cell-wall inhibitors active against Gram-positive organisms including MRSA.
• Aminoglycosides — 30S-binding bactericidal agents with important toxicity monitoring.
• Tetracyclines — 30S-binding bacteriostatic agents with broad atypical coverage.
• Macrolides — 50S-binding agents widely used in respiratory and atypical infections.
• Lincosamides — 50S-binding agents with anaerobic and Gram-positive activity.
• Oxazolidinones — 50S-binding agents active against resistant Gram-positive organisms.
• Fluoroquinolones — DNA gyrase and topoisomerase IV inhibitors with significant safety warnings.
• Rifamycins — RNA polymerase inhibitors central to antimycobacterial therapy.
• Sulfonamides — Dihydropteroate synthase inhibitors, usually combined with trimethoprim.
• Trimethoprim — Dihydrofolate reductase inhibitor used alone or with sulfamethoxazole.
• Polymyxins — Last-resort agents against multidrug-resistant Gram-negative organisms.
• Daptomycin — Lipopeptide active against Gram-positive organisms, inactivated by surfactant.
• Metronidazole — Nitroimidazole active against anaerobes and several protozoa.
• Fosfomycin — Single-dose oral option for selected uncomplicated urinary infections.
• Mupirocin — Topical agent used for selected skin and nasal staphylococcal indications.
• Antiretrovirals — Combination therapy for HIV, grouped by the replication step each drug blocks. (in preparation)
• Hepatitis antivirals — Direct-acting agents for hepatitis C and suppressive therapy for hepatitis B. (in preparation)
• Antiherpes and other DNA-virus antivirals — Nucleoside analogues activated by viral kinases; renal handling matters. (in preparation)
• Influenza antivirals — Neuraminidase and endonuclease inhibitors, effective only when started early. (in preparation)
• Azole antifungals — Ergosterol synthesis inhibitors; hepatic and cytochrome interactions are the defining problem. (in preparation)
• Other antifungals: polyenes, echinocandins and allylamines — Membrane-binding, glucan synthesis and squalene epoxidase inhibitors. (in preparation)
• Antimycobacterials — Combination regimens for tuberculosis and leprosy; hepatotoxicity and adherence dominate. (in preparation)
• Antiparasitics and anthelmintics — Antimalarials, antiprotozoals and anthelmintics grouped by target organism. (in preparation)
• ACE inhibitors — Block conversion of angiotensin I to II; cough and angio-oedema are the classic class effects.
• Angiotensin receptor blockers — Block the AT1 receptor directly, avoiding the bradykinin-mediated cough.
• Mineralocorticoid receptor antagonists — Aldosterone antagonists with prognostic benefit in heart failure and a hyperkalaemia risk.
• Angiotensin receptor–neprilysin inhibitors — Combined AT1 blockade and neprilysin inhibition; the ACE-inhibitor washout is the key safety point.
• Beta blockers — Reduce heart rate and contractility; selectivity and intrinsic activity differ sharply across the class.
• Alpha blockers — Reduce vascular tone through alpha-1 blockade; first-dose hypotension is characteristic.
• Centrally acting antihypertensives — Reduce central sympathetic outflow; rebound hypertension on abrupt withdrawal is the classic trap.
• Dihydropyridine calcium channel blockers — Vascular-selective agents; peripheral oedema is the dose-limiting effect.
• Non-dihydropyridine calcium channel blockers — Rate-limiting agents acting on cardiac conduction; combination with beta blockers needs care.
• Thiazide and thiazide-like diuretics — Distal tubule agents; hyponatraemia and hypokalaemia dominate monitoring.
• Loop diuretics — Powerful ascending-limb agents used for fluid overload; ototoxicity at high doses.
• Potassium-sparing diuretics — Distal agents that conserve potassium; hyperkalaemia is the principal risk.
• Antiplatelet agents — Reduce platelet aggregation by distinct pathways; bleeding risk governs combination use.
• Vitamin K antagonists — Warfarin and relatives; INR monitoring and interactions define their use.
• Direct oral anticoagulants — Direct factor Xa or thrombin inhibitors with fixed dosing and renal dose adjustment.
• Heparins and related parenteral anticoagulants — Antithrombin-dependent agents; heparin-induced thrombocytopenia is the key adverse effect.
• Thrombolytics — Fibrinolytic agents for time-critical occlusion; contraindications are largely bleeding-related.
• Statins — HMG-CoA reductase inhibitors; myopathy and interaction profile are the examinable points.
• Cholesterol absorption inhibitors — Reduce intestinal cholesterol absorption; commonly added to a statin.
• PCSK9 inhibitors — Monoclonal or RNA-based agents that increase LDL receptor recycling.
• Fibrates — PPAR-alpha agonists used mainly for hypertriglyceridaemia; myopathy risk with statins.
• Class I antiarrhythmics (sodium channel blockers) — Sodium channel blockers subdivided by kinetics; proarrhythmia limits use.
• Class III antiarrhythmics (potassium channel blockers) — Prolong repolarisation; amiodarone toxicity is a major examinable topic.
• Nitrates — Nitric oxide donors reducing preload; tolerance and PDE5-inhibitor interaction are critical.
• Cardiac glycosides — Digoxin and relatives; narrow therapeutic index and toxicity recognition dominate.
• Sinus node and metabolic cardiac agents — Ivabradine, ranolazine and related agents acting outside the main families.
• Antiepileptics — Reduce pathological neuronal firing by several distinct mechanisms; enzyme induction and teratogenicity dominate the safety picture.
• Mood stabilisers — Lithium and the anticonvulsant mood stabilisers; narrow therapeutic index and monitoring are the examinable points.
• SSRI antidepressants — Selective serotonin reuptake inhibitors; hyponatraemia, bleeding risk and discontinuation symptoms are the class concerns.
• SNRIs and other antidepressants — Serotonin–noradrenaline reuptake inhibitors and the atypical agents that fit no other class.
• Tricyclic antidepressants — Older non-selective agents; antimuscarinic burden and cardiotoxicity in overdose are why they are second-line.
• Benzodiazepines — GABA-A positive allosteric modulators; duration of action, dependence and flumazenil are the high-yield points.
• Z-drugs and other hypnotics — Non-benzodiazepine hypnotics and newer agents used for insomnia, with a similar dependence caution.
• Atypical antipsychotics — Second-generation agents with lower extrapyramidal risk but substantial metabolic effects; clozapine is monitored separately.
• Typical antipsychotics — First-generation D2 antagonists; extrapyramidal effects and tardive dyskinesia define their profile.
• Antiparkinsonian agents — Levodopa and the dopaminergic agents around it; wearing-off and impulse-control effects are examinable.
• Triptans and migraine agents — 5-HT1B/1D agonists for acute attacks alongside the preventive agents; cardiovascular contraindications matter.
• CNS stimulants and ADHD agents — Controlled stimulants and the non-stimulant alternatives; cardiovascular and growth monitoring are required.
• Dementia agents — Cholinesterase inhibitors and memantine; symptomatic benefit only, with a modest effect size.
• Sex hormones and hormonal contraceptives — Oestrogens, progestogens and androgens; thrombotic risk and enzyme-inducer interactions are the key safety points. (in preparation)
• Biguanides — Metformin and relatives; lactic acidosis and renal thresholds define their cautions. (in preparation)
• Sulfonylureas — Insulin secretagogues; hypoglycaemia and weight gain are the class effects. (in preparation)
• SGLT2 inhibitors — Promote urinary glucose loss; euglycaemic ketoacidosis and genital infection are characteristic. (in preparation)
• GLP-1 receptor agonists — Incretin mimetics with weight loss and gastrointestinal effects; thyroid C-cell warnings apply. (in preparation)
• DPP-4 inhibitors — Prolong endogenous incretin action; generally weight-neutral with a low hypoglycaemia risk. (in preparation)
• Insulins — Replacement therapy classified by onset and duration; hypoglycaemia is the dose-limiting effect. (in preparation)
• Bisphosphonates and bone agents — Reduce osteoclastic resorption; osteonecrosis of the jaw and atypical femoral fracture are the notable risks. (in preparation)
• Systemic corticosteroids — Broad anti-inflammatory action; adrenal suppression and the hazard of abrupt withdrawal dominate. (in preparation)
• Thyroid and antithyroid agents — Levothyroxine and the thionamides; agranulocytosis is the antithyroid class warning. (in preparation)
• Proton pump inhibitors — Irreversible inhibitors of the gastric proton pump; long-term use carries its own risks.
• H2-receptor antagonists — Reversible histamine H2 blockers; a class reshaped by the withdrawal of ranitidine.
• Antacids and alginates — Neutralise or raft over gastric acid; interactions arise chiefly through altered absorption. (in preparation)
• Laxatives and antidiarrhoeals — Agents that speed or slow transit, grouped by osmotic, stimulant, bulking or antimotility action. (in preparation)
• Antiemetics — Chosen by the receptor driving the nausea: dopaminergic, serotonergic, histaminergic or NK1. (in preparation)
• Antispasmodics — Reduce intestinal smooth muscle spasm, principally in irritable bowel syndrome. (in preparation)
• Aminosalicylates and IBD agents — Topical mucosal anti-inflammatories central to ulcerative colitis maintenance. (in preparation)
• Conventional DMARDs — Methotrexate and relatives; monitoring for marrow, hepatic and pulmonary toxicity is mandatory. (in preparation)
• Biologic DMARDs — Monoclonal antibodies and fusion proteins; tuberculosis screening precedes treatment. (in preparation)
• JAK inhibitors — Small-molecule intracellular signalling inhibitors carrying cardiovascular and malignancy warnings. (in preparation)
• Calcineurin inhibitors — Ciclosporin and tacrolimus; nephrotoxicity and narrow therapeutic index govern their use. (in preparation)
• Antimetabolite immunosuppressants — Azathioprine and mycophenolate; TPMT status and teratogenicity are the key points. (in preparation)
• Antihistamines — H1 receptor antagonists; the first- and second-generation split is entirely about central nervous system penetration.
• Beta-2 agonist bronchodilators — Short- and long-acting relievers and maintenance agents; tremor and hypokalaemia are class effects.
• Antimuscarinic bronchodilators — Block airway muscarinic receptors; central in COPD maintenance therapy.
• Methylxanthines — Theophylline and relatives; a narrow therapeutic index with major interaction potential.
• Inhaled and intranasal corticosteroids — The maintenance backbone of asthma therapy; local and systemic effects follow dose and device technique.
• Leukotriene receptor antagonists — Oral anti-inflammatory agents carrying a neuropsychiatric safety warning.

How this differs from the Drug Library

The Study Corner explains the pharmacology of a whole class — why the drugs in it behave the way they do. The Drug Library remains the reference for an individual medicine, including its uses, side effects and interactions. Class pages link out to the individual medicines wherever a page exists.