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Questions and Answers
What was the major mechanism of action of all NSAIDs demonstrated by Vane and co-workers?
What was the major mechanism of action of all NSAIDs demonstrated by Vane and co-workers?
- Inhibition of leukotriene synthesis
- Inhibition of prostaglandin synthesis (correct)
- Enhancement of lipoxygenase activity
- Promotion of prostaglandin production
Which compound obtained from willow bark led to the discovery of aspirin in 1899?
Which compound obtained from willow bark led to the discovery of aspirin in 1899?
- Acetyl salicylate
- Bitter glycoside
- Salicylic acid (correct)
- Sodium salicylate
What strategy was proposed by WHO to provide adequate pain relief for cancer patients?
What strategy was proposed by WHO to provide adequate pain relief for cancer patients?
- Intermittent pain relief
- Around-the-clock pain relief (correct)
- On-demand pain relief
- Opioid-based pain relief only
What is the main difference between NSAIDs and opioids in terms of analgesic strength?
What is the main difference between NSAIDs and opioids in terms of analgesic strength?
Which enzyme is responsible for the synthesis of leukotrienes in the prostaglandin synthesis pathway?
Which enzyme is responsible for the synthesis of leukotrienes in the prostaglandin synthesis pathway?
What is the IASP definition of pain based on the provided text?
What is the IASP definition of pain based on the provided text?
Which enzymes are inhibited by NSAIDs to reduce prostaglandin synthesis?
Which enzymes are inhibited by NSAIDs to reduce prostaglandin synthesis?
According to the WHO Analgesic Ladder Strategy, what is the recommended step for moderate to severe pain?
According to the WHO Analgesic Ladder Strategy, what is the recommended step for moderate to severe pain?
How do weaker analgesics differ from opioids in terms of pain management effectiveness?
How do weaker analgesics differ from opioids in terms of pain management effectiveness?
Which class of analgesics primarily target COX-2 to reduce inflammation and pain?
Which class of analgesics primarily target COX-2 to reduce inflammation and pain?
What is a key difference between the mechanism of action of NSAIDs and opioids in pain management?
What is a key difference between the mechanism of action of NSAIDs and opioids in pain management?
What is the mechanism by which NSAIDs exert their anti-inflammatory effect?
What is the mechanism by which NSAIDs exert their anti-inflammatory effect?
Which prostaglandin is primarily responsible for vascular endothelium vasodilation and inhibition of platelet aggregation?
Which prostaglandin is primarily responsible for vascular endothelium vasodilation and inhibition of platelet aggregation?
Which class of NSAIDs includes aspirin, ibuprofen, and naproxen?
Which class of NSAIDs includes aspirin, ibuprofen, and naproxen?
What is the primary effect of NSAIDs on platelet function?
What is the primary effect of NSAIDs on platelet function?
Which event is a common consequence of NSAID-induced deficiency of prostaglandins (PGs)?
Which event is a common consequence of NSAID-induced deficiency of prostaglandins (PGs)?
Which prostaglandin is primarily responsible for smooth muscle contraction throughout the body and inhibition of gastric acid secretion?
Which prostaglandin is primarily responsible for smooth muscle contraction throughout the body and inhibition of gastric acid secretion?
What is the main difference between non-selective and selective COX-2 inhibitors in terms of COX enzyme inhibition?
What is the main difference between non-selective and selective COX-2 inhibitors in terms of COX enzyme inhibition?
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Study Notes
Pain and NSAIDs
- Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, influenced by biological, psychological, and social factors.
History of NSAIDs
- Willow bark was used for centuries as an analgesic.
- Salicylic acid was obtained by hydrolysis of the bitter glycoside extracted from willow bark in 1838.
- Sodium salicylate was developed in 1875, and acetyl salicylate (Aspirin) was introduced in 1899.
- Vane and co-workers demonstrated that aspirin inhibits prostaglandin production in guinea-pig isolated lungs in 1971, earning a Nobel Prize in Medicine in 1982.
Mechanism of Action of NSAIDs
- NSAIDs inhibit prostaglandin synthesis by blocking the action of cyclooxygenase (COX) enzymes.
- There are two isoforms of COX enzyme: COX-1 and COX-2.
- NSAIDs can block both COX enzymes or selectively block COX-2 enzyme.
Classification of NSAIDs
- Classification based on chemical structure:
- Salicylates (Aspirin)
- Arylalkanoic acids (Indomethacin, Sulindac)
- Heteroarylalkanoic acids (Tolmetin, Diclofenac)
- Oxicams (Piroxicam, Tenoxicam)
- Classification based on COX affinity:
- Non-selective COX inhibitors (Aspirin, Ibuprofen, Diclofenac)
- Selective COX-2 inhibitors (Celecoxib, Etoricoxib)
Effects of NSAIDs
- Beneficial actions:
- Analgesia: prevention of nerve ending sensitization
- Antipyresis: reduction of body temperature
- Anti-inflammatory: reduction in signs of inflammation
- Antithrombotic: inhibition of platelet aggregation
- Adverse effects:
- Gastric mucosal damage
- Prolonged bleeding time
- Limitation of renal blood flow
- Delay/prolongation of labor
- Asthma, hypersensitivity, and anaphylactic reactions
Specific NSAIDs
- Aspirin:
- Non-selective and irreversibly inhibits both COX enzymes
- Classic actions: analgesic, antipyretic, and anti-inflammatory
- Inhibits platelet aggregation
- ADR: salicylism (mild intoxication) and acute salicylate poisoning (severe intoxication)
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