Pharmacology
Autacoids and Anti-inflammatory Drugs
NSAIDs, antihistamines and gout drugs for MBBS and NEET-PG: aspirin, paracetamol, COX-2 inhibitors, allopurinol and colchicine, mapped to NMC codes.
MedNext Academy | 3 min read
Autacoids and Anti-inflammatory Drugs
NSAIDs, antihistamines and gout drugs for MBBS and NEET-PG: aspirin, paracetamol, COX-2 inhibitors, allopurinol and colchicine, mapped to NMC codes.
This chapter covers the local hormones known as autacoids, including histamine, serotonin, prostaglandins and their antagonists, together with the non-steroidal anti-inflammatory drugs and the drugs used in gout. These agents underpin the management of pain, fever, inflammation, allergy, migraine and hyperuricaemia.
High-yield: Autacoids and Anti-inflammatory Drugs
- Non-steroidal anti-inflammatory drugs inhibit cyclo-oxygenase, reducing prostaglandin synthesis and giving analgesic, antipyretic and anti-inflammatory effects.
- COX-1 is constitutive and protects the gastric mucosa, while COX-2 is induced at sites of inflammation.
- Aspirin irreversibly acetylates cyclo-oxygenase, so low-dose aspirin gives lasting antiplatelet action for the life of the platelet.
- Aspirin is avoided in children with viral illness because of the risk of Reye syndrome.
- Paracetamol is antipyretic and analgesic but has little anti-inflammatory action; overdose causes hepatotoxicity treated with N-acetylcysteine.
- Selective COX-2 inhibitors such as celecoxib spare the stomach but carry an increased cardiovascular thrombotic risk.
- The classic NSAID adverse effects are peptic ulceration, renal impairment, fluid retention and inhibition of platelet aggregation.
- Histamine acts on H1 receptors to cause bronchoconstriction and vascular leak and on H2 receptors to stimulate gastric acid secretion.
- First-generation antihistamines such as chlorpheniramine cross the blood-brain barrier and cause sedation and antimuscarinic effects.
- Second-generation antihistamines such as cetirizine and loratadine are non-sedating as they poorly cross into the brain.
- 5-HT3 antagonists such as ondansetron are potent antiemetics, especially for chemotherapy-induced nausea.
- Sumatriptan, a 5-HT1B/1D agonist, aborts acute migraine but is contraindicated in ischaemic heart disease.
- Allopurinol lowers uric acid by inhibiting xanthine oxidase and is used for chronic gout prophylaxis, not acute attacks.
- Colchicine relieves acute gout by inhibiting microtubule assembly and neutrophil migration; diarrhoea is the dose-limiting effect.
NSAIDs and gout drugs
- **Aspirin:** Irreversible COX inhibitor; low dose is antiplatelet; avoid in children with viral illness.
- **Paracetamol:** Antipyretic analgesic; overdose causes liver failure treated with N-acetylcysteine.
- **Acute gout:** NSAIDs, colchicine or corticosteroids; do not start or stop allopurinol during an attack.
- **Chronic gout:** Allopurinol or febuxostat lower urate by inhibiting xanthine oxidase.
NMC competencies in this chapter
- **PH1.16:** Autacoids, NSAIDs, antihistamines and drugs for gout
Frequently Asked Questions
Why does low-dose aspirin work as an antiplatelet agent?
Aspirin irreversibly blocks cyclo-oxygenase in platelets, which cannot make new enzyme, so the antiplatelet effect lasts for the platelet lifespan of about a week.
What is the antidote for paracetamol overdose?
N-acetylcysteine replenishes glutathione and neutralises the toxic metabolite, and it is most effective when started early after ingestion.
Why are second-generation antihistamines preferred?
Drugs like cetirizine and loratadine poorly cross the blood-brain barrier, so they relieve allergy without the sedation of older agents such as chlorpheniramine.
Why is allopurinol not used in an acute gout attack?
Sudden changes in urate can worsen or prolong the acute attack, so allopurinol is started only after the flare settles, under cover of an anti-inflammatory.
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