Questions
1–2 questions per semester paper
Difficulty
Medium
Importance
Core topic for B.Pharm pharmacology exams
Overview
Autacoids are local hormones that act near their site of synthesis, playing a critical role in inflammation and allergic responses. Understanding their mechanism of action alongside NSAIDs is essential for managing pain, fever, and hypersensitivity reactions in clinical practice.
Histamine and Receptors
Histamine is a biogenic amine stored in mast cells and basophils, released during allergic reactions or tissue injury. It exerts its effects via H1, H2, H3, and H4 receptors, mediating diverse physiological responses from vasodilation to gastric acid secretion.
- H1 receptors mediate smooth muscle contraction and increased capillary permeability.
- H2 receptors are primarily responsible for gastric acid secretion in the stomach.
- Released via IgE-mediated degranulation or physical trauma.
- Involved in the triple response of Lewis: flush, flare, and wheal.
Antihistamines
Antihistamines are competitive antagonists that block the effects of histamine at receptor sites. They are broadly categorized into first-generation (sedating) and second-generation (non-sedating) agents based on their ability to cross the blood-brain barrier.
- First-generation: Diphenhydramine, Chlorpheniramine (high sedation).
- Second-generation: Cetirizine, Loratadine, Fexofenadine (minimal CNS penetration).
- Used in allergic rhinitis, urticaria, and motion sickness.
- First-generation drugs exhibit significant anticholinergic side effects.
NSAIDs Mechanism of Action
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) primarily exert their therapeutic effects by inhibiting the enzyme cyclooxygenase (COX). This inhibition prevents the conversion of arachidonic acid into prostaglandins, which are key mediators of pain, inflammation, and fever.
- COX-1: Constitutive form, involved in gastric mucosal protection and platelet function.
- COX-2: Inducible form, up-regulated during inflammation.
- Aspirin irreversibly inhibits COX-1 and COX-2 via acetylation.
- Prostaglandins sensitize nociceptors, increasing pain perception.
NSAIDs Classification and Clinical Use
NSAIDs are classified based on their chemical structure and selectivity for COX isoforms. Their primary clinical indications include analgesia, antipyresis, and anti-inflammatory therapy, though they carry risks of gastrointestinal and renal toxicity.
- Salicylates: Aspirin.
- Propionic acid derivatives: Ibuprofen, Naproxen.
- Selective COX-2 inhibitors: Celecoxib, Etoricoxib.
- Acetic acid derivatives: Diclofenac, Indomethacin.
- Paracetamol is an analgesic-antipyretic with weak anti-inflammatory activity.
Exam Tip
Always link the side effect profile of NSAIDs back to the inhibition of constitutive COX-1 (gastric ulcers) versus inducible COX-2 (inflammation).
Common Mistakes
- Confusing the receptor selectivity (H1 vs H2) leading to incorrect drug choice for conditions like peptic ulcers versus allergies.
- Assuming all NSAIDs have the same cardiovascular and gastrointestinal safety profile, ignoring the risk of selective COX-2 inhibitors.
- Failing to distinguish between reversible and irreversible enzyme inhibition, particularly regarding Aspirin's unique role.
More Revision Notes
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