PT
● MODULE 07 / 20
Autacoids, Pain, Inflammation & Gout
Link inflammatory mediators to antihistamines, analgesics, anti-inflammatory drugs and urate therapy.
Quick revision ↓ Medical Dictionary
FULL CHAPTER EXPLANATION
Deep Learning — Module 07
Read this section in sequence. It moves from drug targets to therapeutic effects, adverse reactions and safe use.
01
Histamine and other mediators
Histamine H1 signaling contributes to itch, vascular permeability and allergic symptoms, whereas H2 signaling promotes gastric acid secretion. Older H1 antihistamines enter the brain and often cause sedation and antimuscarinic effects; many newer agents are less sedating. Eicosanoids include prostaglandins and leukotrienes. Bradykinin contributes to pain and vascular permeability; substance P participates in nociception. These pathways overlap, so blocking one mediator does not neutralize every allergic or inflammatory process.
02
NSAIDs and paracetamol
NSAIDs inhibit cyclooxygenase and reduce prostaglandin synthesis, providing analgesic, antipyretic and anti-inflammatory effects. Reduced protective prostaglandins help explain gastrointestinal injury, renal perfusion effects and fluid retention. Aspirin irreversibly inhibits platelet cyclooxygenase; most other NSAIDs inhibit reversibly. COX-2 selectivity does not remove cardiovascular or renal concerns. Paracetamol is useful for pain and fever but has little peripheral anti-inflammatory action; overdose can generate a hepatotoxic metabolite when protective glutathione is depleted.
03
Opioid analgesia
Mu-opioid receptor activation can relieve severe pain but also depress breathing, impair alertness and reduce bowel motility. Tolerance develops to several effects but constipation often persists. Combining opioids with alcohol or sedative drugs increases harm. Naloxone competitively reverses opioid effects but may act for less time than the opioid, requiring continued monitoring in overdose care. Physical dependence and withdrawal can occur without establishing addiction; assessment should distinguish these concepts.
04
Gout and rheumatoid arthritis
Acute gout inflammation can be treated with anti-inflammatory approaches selected for the patient; colchicine disrupts microtubule-dependent inflammatory functions and can cause severe toxicity with renal impairment or interacting drugs. Allopurinol and febuxostat reduce urate production by inhibiting xanthine oxidase and are long-term urate-lowering agents rather than immediate analgesics. Rheumatoid arthritis requires disease-modifying therapy, such as methotrexate, to limit structural progression; symptomatic NSAID relief alone does not accomplish this.
05
Migraine and monitoring
Triptans activate serotonin 5-HT1B/1D receptors and act on trigeminovascular pathways; vasoconstrictive effects limit their suitability in some vascular disease. Preventive and acute migraine treatments serve different purposes. Analgesic overuse can perpetuate headache. Match monitoring to mechanism: bleeding and renal function with NSAIDs, respiratory status with opioids, and organ-specific toxicity with disease-modifying drugs. Glucocorticoid benefits and risks are developed further in the endocrine unit.
High-Yield Revision
- Analgesia, anti-inflammatory action and disease modification are different goals.
- Naloxone response does not remove the need for ongoing observation.
- Urate-lowering therapy is not an immediate painkiller.
Common Exam & Concept Pitfalls
- COX-2 selectivity does not mean freedom from renal or cardiovascular harm.
- Antihistamines do not replace adrenaline in anaphylaxis.
Sources & Further Reading
Curriculum scope checked 23 September 2026. These original study notes summarize established principles; current institutional guidance and product information govern clinical use. Faculty review is pending.
RAHBAR study structure: target → drug action → therapeutic use → adverse effects → monitoring. Use institutional curriculum and faculty guidance for local sequencing, practical requirements and assessment specifications.