PH2.6-8 | Autacoids and Pain Pharmacology — Glossary

IgE-mediated type I hypersensitivity reaction of the nasal mucosa to inhaled allergens, presenting with sneezing, rhinorrhoea, nasal itching, and congestion; classified as intermittent or persistent by ARIA guidelines.

Xanthine oxidase inhibitor; first-line urate-lowering therapy for gout; reduces uric acid synthesis; started only after an acute attack fully resolves; titrated to achieve UA <6 mg/dL.

Blockade of muscarinic acetylcholine receptors producing dry mouth, urinary retention, constipation, blurred vision, and tachycardia; a class effect of first-generation antihistamines limiting their use in BPH, glaucoma, and the elderly.

Allergic Rhinitis and its Impact on Asthma guidelines; classifies rhinitis by duration (intermittent vs persistent) and severity (mild vs moderate–severe) to guide stepwise therapy.

Aspirin acetylates a serine residue in the COX active site, permanently inactivating the enzyme; platelets (anucleate) cannot regenerate COX, so antiplatelet effect persists for the platelet lifespan (7–10 days).

Second-generation H1 antihistamine (active metabolite of hydroxyzine); 10 mg once daily; may cause mild sedation in some patients; dose reduction required in renal impairment.

A potent vasodilatory and pro-nociceptive neuropeptide released from trigeminal terminals around meningeal vessels during migraine; drives neurogenic inflammation and meningeal vasodilation; the target of newer anti-CGRP migraine therapies (erenumab, fremanezumab).

First-generation H1 antihistamine; the most common ingredient in OTC cold combinations in India; oral dose 4 mg 3–4 times daily; causes sedation and mild anticholinergic effects.

Plant alkaloid (from Colchicum autumnale) that inhibits tubulin polymerisation, impairing neutrophil chemotaxis and degranulation; used for acute gout (low-dose: 1 mg then 0.5 mg) and prophylaxis during ULT initiation (0.5 mg once or twice daily).

A slowly propagating wave of complete neuronal and glial depolarisation across the cortex, followed by sustained suppression; the electrophysiological event underlying migraine aura and thought to activate the trigeminovascular system initiating the headache phase.

Constitutively expressed isoform that produces prostaglandins for gastric mucosal cytoprotection, platelet TXA2 synthesis, and renal blood flow maintenance; its inhibition underlies NSAID-related GI and platelet adverse effects.

Predominantly inducible isoform expressed at sites of inflammation producing pro-inflammatory prostaglandins; also constitutive in kidney and endothelium; the selective target of coxibs.

The enzyme that converts arachidonic acid to prostaglandins and thromboxane A2; exists as constitutive COX-1 and inducible COX-2 isoforms that are the primary targets of NSAIDs.

A drug class that slows or prevents the structural joint damage of rheumatoid arthritis by targeting the underlying autoimmune process; conventional synthetic DMARDs include methotrexate, hydroxychloroquine, sulfasalazine; biologics target specific cytokines (TNF-α, IL-6).

Selective xanthine oxidase inhibitor; alternative to allopurinol; avoid co-administration with azathioprine (XO inhibition increases azathioprine toxicity); used when allopurinol is not tolerated or contraindicated.

Second-generation H1 antihistamine (active metabolite of terfenadine); 120–180 mg once daily; no CNS penetration; bioavailability reduced 36–73% by grapefruit, apple, or orange juice.

Lipophilic H1 antagonists that readily cross the blood-brain barrier, producing sedation and anticholinergic effects; examples include chlorpheniramine, diphenhydramine, and promethazine.

A G-protein-coupled histamine receptor found on smooth muscle, vascular endothelium, and sensory nerves; its activation mediates the cardinal symptoms of allergy including itching, sneezing, vasodilation, and increased permeability.

A G-protein-coupled histamine receptor predominantly on gastric parietal cells; its activation stimulates hydrochloric acid secretion and is targeted by H2 blockers for peptic ulcer disease, not allergy.

Non-selective NSAID (propionic acid class); reversible COX-1/COX-2 inhibitor; among the safest non-selective NSAIDs for GI adverse effects; short half-life requires 3-times daily dosing.

A drug that binds a receptor and reduces its constitutive (baseline) activity below the level seen in the absence of any ligand; modern H1 antihistamines act as inverse agonists, not merely competitive blockers.

Acetic acid NSAID available parenterally and orally; potent analgesic used for acute pain; maximum systemic duration 5 days to avoid GI and renal toxicity.

The IgE-triggered exocytosis of preformed mediators (histamine, tryptase, heparin) from mast cells, occurring within seconds of allergen re-exposure and initiating the immediate allergic response.

Paradoxical chronic daily headache resulting from regular overuse of acute migraine treatments (analgesics, triptans, or ergotamine on >10–15 days per month); prevented by limiting acute treatment days and initiating prophylaxis when attacks are frequent.

Anchor DMARD for rheumatoid arthritis; inhibits dihydrofolate reductase; 7.5–25 mg/week; must be co-prescribed with folic acid; teratogenic (Category X); monitor CBC, LFTs, and renal function regularly.

Preventive pharmacotherapy (propranolol, topiramate, amitriptyline, valproate) used when migraine attacks occur ≥4 days per month or are severely debilitating; reduces attack frequency by ≥50% in responders.

Needle-shaped crystals formed when serum uric acid exceeds its solubility limit (~6.8 mg/dL); deposited in joints and periarticular tissues, they trigger NLRP3 inflammasome activation and intense neutrophil-mediated inflammation — the substrate for acute gout attacks.

The antidote for paracetamol overdose; replenishes hepatic glutathione stores by serving as a cysteine precursor, most effective when given within 8 hours of ingestion.

The toxic reactive metabolite of paracetamol generated by CYP2E1 and CYP3A4; conjugated harmlessly with glutathione at therapeutic doses but causes centrilobular hepatic necrosis when glutathione is depleted in overdose.

Bronchoconstriction precipitated by aspirin or NSAIDs in ~10–20% of adult asthmatics; mechanism is LOX-shunting of arachidonic acid to excess leukotriene synthesis when COX is inhibited.

Invasive hyperplastic synovial tissue in rheumatoid arthritis, driven by activated synovial fibroblasts and macrophages; erodes cartilage and bone at the joint margin; responsible for structural joint damage and deformity.

Uricosuric agent that blocks URAT1 transporters in the renal proximal tubule, reducing urate reabsorption and increasing urinary uric acid excretion; contraindicated in CKD (eGFR <30), uric acid nephrolithiasis, and salicylate co-use.

First-generation phenothiazine-derivative H1 antihistamine with strong D2 and muscarinic blockade; used as antiemetic, antipruritic, and preoperative sedative; causes significant sedation and extrapyramidal effects at high doses.

COX-2-derived prostaglandin from vascular endothelium that inhibits platelet aggregation and promotes vasodilation; selective COX-2 inhibition (coxibs) suppresses PGI2 without suppressing TXA2, increasing thrombosis risk.

The principal prostaglandin mediating peripheral nociceptor sensitisation (hyperalgesia), fever (via hypothalamic thermostat), and gastric mucosal protection; its synthesis is inhibited by all NSAIDs.

Rare but potentially fatal syndrome of acute encephalopathy and hepatic failure in children following aspirin use during viral illness (varicella, influenza); mechanism unclear but aspirin-related mitochondrial dysfunction implicated.

Rebound nasal congestion caused by prolonged use (>3–5 days) of topical nasal decongestants such as oxymetazoline, due to downregulation of α-adrenergic receptors in nasal mucosa.

H1 antagonists engineered for minimal CNS penetration via P-glycoprotein efflux and high molecular weight, producing negligible sedation and no anticholinergic effects; examples include cetirizine, loratadine, and fexofenadine.

An NSAID with >50-fold greater affinity for COX-2 over COX-1; reduces GI ulceration risk vs non-selective NSAIDs but increases cardiovascular risk (MACE) via PGI2 suppression; examples: celecoxib, etoricoxib.

COX-1-derived prostaglandin in platelets that promotes platelet aggregation and vasoconstriction; irreversibly inhibited by aspirin, explaining its unique antiplatelet effect.

The combination of an NSAID + ACE inhibitor + diuretic that simultaneously reduces renal prostaglandin vasodilation, afferent arteriole perfusion, and intravascular volume, precipitating acute kidney injury.

Class of selective 5-HT1B/1D receptor agonists (sumatriptan, rizatriptan, zolmitriptan) used for acute moderate-to-severe migraine; act by constricting dilated meningeal vessels and inhibiting trigeminal nociceptive transmission; contraindicated in established CVD.

Drug treatment (allopurinol, febuxostat, uricosurics) aimed at reducing serum uric acid to below the saturation threshold (<6 mg/dL) to prevent gout attacks, dissolve tophi, and protect joints and kidneys from hyperuricaemic damage.