AIM STEP 10
Student Memory Support
Anti-Inflammatory Pharmacology: NSAIDs, COX-2 Inhibitors and Paracetamol
3rd Year MBBS • Infection and Inflammation • High-yield memory reinforcement and last-minute revision
1. High-Yield Flashcards
Tap each question to reveal the answer.
Which drug is the prototype non-selective cyclooxygenase inhibitor?
Aspirin.
How does aspirin differ from most other conventional NSAIDs at the COX enzyme?
It inhibits cyclooxygenase irreversibly by acetylation.
What explains the prolonged antiplatelet effect of low-dose aspirin?
Irreversible platelet COX-1 inhibition reduces thromboxane A₂ until new platelets are formed.
What is the approximate aspirin dose used for antiplatelet therapy?
Approximately 75–150 mg daily.
Why can conventional NSAIDs cause peptic ulceration and gastrointestinal bleeding?
COX-1 inhibition reduces protective gastric prostaglandins.
Which commonly tested NSAID has a very long elimination half-life?
Piroxicam, with a half-life of about 45–50 hours.
What is the major gastrointestinal advantage of selective COX-2 inhibitors?
They relatively spare COX-1-mediated gastric mucosal protection.
What important cardiovascular concern is associated with selective COX-2 inhibitors?
Increased thrombotic risk due to reduced prostacyclin with relatively preserved platelet thromboxane.
What is the main pharmacological profile of paracetamol?
Analgesic and antipyretic action with weak peripheral anti-inflammatory activity.
Which toxic metabolite accumulates in paracetamol overdose?
NAPQI.
Which antidote is used for significant paracetamol poisoning?
N-acetylcysteine.
How does sodium bicarbonate help in salicylate poisoning?
Urinary alkalinization increases ionized salicylate and enhances renal elimination.
2. Mnemonics
Mnemonic Title: Major NSAID Adverse Effects
Mnemonic Word: G-R-B-C
Mnemonic Word: G-R-B-C
Meaning: Gastric injury, Renal impairment, Bleeding tendency, Cardiovascular concern.
Mnemonic Title: Aspirin Main Actions
Mnemonic Word: A-A-A-A
Mnemonic Word: A-A-A-A
Meaning: Antiplatelet, Analgesic, Antipyretic, Anti-inflammatory.
Mnemonic Title: Paracetamol Overdose Sequence
Mnemonic Word: N-G-H-N
Mnemonic Word: N-G-H-N
Meaning: NAPQI rises → Glutathione falls → Hepatic necrosis → N-acetylcysteine treatment.
3. Memory Tables
Non-Selective NSAIDs vs Selective COX-2 Inhibitors
| Feature | Non-Selective NSAIDs | Selective COX-2 Inhibitors |
|---|---|---|
| Target | COX-1 + COX-2 | Preferential COX-2 |
| GI injury | Greater | Generally less |
| Platelet effect | Important with aspirin | No aspirin-like effect |
| Renal effects | Present | Still present |
| Thrombotic concern | Varies with drug | Important class concern |
NSAIDs vs Paracetamol
| Feature | Conventional NSAIDs | Paracetamol |
|---|---|---|
| Analgesia | Effective | Effective |
| Antipyresis | Effective | Effective |
| Peripheral anti-inflammatory action | Strong | Weak |
| Platelet inhibition | Especially aspirin | Minimal at therapeutic doses |
| Major overdose toxicity | Salicylate acid-base toxicity | Hepatic necrosis |
4. Rapid Revision Points — Last-Minute Revision
Must Remember:
- Aspirin is the prototype non-selective COX inhibitor.
- Aspirin irreversibly inhibits platelet COX-1 and reduces thromboxane A₂.
- Antiplatelet aspirin doses are much lower than anti-inflammatory doses.
- NSAID analgesia results from reduced prostaglandin-mediated nociceptor sensitization.
- COX-1 inhibition explains much of the gastric toxicity of conventional NSAIDs.
- Renal prostaglandin inhibition can cause sodium retention and reduced renal function.
- Piroxicam is long acting; ibuprofen is relatively short acting.
- Selective COX-2 inhibitors reduce GI injury but may increase thrombotic risk.
- Paracetamol is mainly analgesic and antipyretic, with weak peripheral anti-inflammatory action.
- Paracetamol overdose causes NAPQI accumulation and is treated with N-acetylcysteine.
KMU Trap: COX-2 selectivity lowers gastrointestinal toxicity but does not remove renal risk and does not provide aspirin-like antiplatelet protection.
5. Clinical Memory Hooks
Epigastric pain after prolonged NSAID use → reduced gastric protective prostaglandins → mucosal injury and bleeding.
Edema and rising creatinine after starting an NSAID → reduced renal prostaglandin-mediated perfusion → sodium retention and renal dysfunction.
Hyperventilation after aspirin overdose → salicylate-induced acid-base disturbance → consider bicarbonate-based alkalinization.
Large paracetamol ingestion → glutathione depletion and NAPQI accumulation → hepatic necrosis → N-acetylcysteine.
6. Starred High-Yield Exam Points
- ⭐ Aspirin irreversibly inhibits platelet COX-1, producing prolonged suppression of thromboxane A₂.
- ⭐ Low-dose aspirin is used for antiplatelet therapy, while much larger doses are needed for anti-inflammatory action.
- ⭐ Selective COX-2 inhibitors generally cause less gastric mucosal injury but may increase thrombotic cardiovascular risk.
- ⭐ Salicylate poisoning may produce respiratory alkalosis together with metabolic acidosis; urinary alkalinization enhances elimination.
- ⭐ Paracetamol overdose causes glutathione depletion, NAPQI accumulation and hepatic necrosis.
- ⭐ N-acetylcysteine is the specific antidotal treatment for significant paracetamol poisoning.