NSAIDs Quiz: Pharmacology and Paracetamol Chapter 3

What is the effect of sodium and water retention on renal chloride reabsorption?

Which NSAID is contraindicated in patients with gout due to its effect on serum urate levels?

What is the pharmacokinetic characteristic of aspirin when taken at a low dose of less than 600mg per day?

Which adverse effect is considered an early sign of salicylate toxicity?

What treatment is recommended for severe anaphylactic reactions caused by salicylates?

In which condition should children avoid the use of aspirin to prevent Reye's Syndrome?

Which enzyme is potently inhibited by Paracetamol?

What is the main role of prostaglandins in the body?

How do NSAIDs affect pain perception?

What is the main cause of gastrointestinal ulceration induced by NSAIDs?

Which type of fever is triggered by the release of prostaglandins?

Which type of enzyme is COX-3 in relation to COX-1 and COX-2?

Which NSAID is known to be one of the most potent inhibitors of COX isozymes?

What is a characteristic feature of Piroxicam among NSAIDs?

Which NSAID is contraindicated in patients with gout?

Which drug should be used for short-term management of moderate pain states, but for less than 5 days due to hematologic toxicity?

What is unique about Nabumetone among NSAIDs?

What is a notable characteristic of Phenylbutazone and Oxyphenbutazone among the mentioned drugs?

Inflammation and NSAIDs

Inflammation is the body's way to defend itself from invading bacteria, fungi, viruses, and non-living substances that appear foreign and harmful.
Fever is an abnormally high temperature associated with infection and is triggered by the release of prostaglandins.

Cyclooxygenase (COX) Enzymes

COX-1 is a constitutive enzyme, constantly expressed, and important for maintenance functions such as platelet aggregation, cytoprotection, and vasodilation.
COX-2 is an inducible enzyme, low at normal states but increases during inflammatory processes.
COX-3 is an alternative splice variant of COX-1 and is potently inhibited by paracetamol.

Mechanism of Action of NSAIDs

NSAIDs inhibit COX enzymes, leading to decreased prostaglandin synthesis, which reduces pain, inflammation, and fever.

Side/Adverse Effects of NSAIDs

Gastrointestinal ulceration due to inhibition of prostaglandins that protect the gastric mucosa.
Sodium and water retention due to reduction in PG-induced inhibition of renal chloride reabsorption and inhibition of ADH.
Reversible inhibition in GFR.
Effect on serum urate level (ASA and Tolmetin are contraindicated in patients with gout).
Hypersensitivity reactions.

Non-Selective COX Inhibitors

Salicylates: aspirin, bismuth subsalicylate, and methyl salicylate.
Indole derivatives: indomethacin.
Oxicam derivatives: piroxicam.
Phenylacetic acid derivatives: diclofenac, sulindac, and ketorolac.
Propionic acid derivatives: ibuprofen and naproxen.
Pyrrolealkanoic acid derivatives: tolmetin.
Pyrazolone derivatives: phenylbutazone and oxyphenbutazone.

Selective COX-2 Inhibitors

Oxicam derivatives: meloxicam.
Phenylacetic acid derivatives: etodolac.

Adverse Effects of Aspirin

Salicylism: tinnitus, hyperventilation, metabolic acidosis, fever, and dehydration.
Severe anaphylactic reactions.
Reye's syndrome in children with viral infections.

This quiz covers the pharmacology of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and Paracetamol as discussed in Chapter 3 of Cristopherson P. Mata's book. Topics include the immune response, inflammation, and the body's defense mechanisms against harmful substances.