W5-Local Hormones 2:Anti-inflammatory Agents Lecture

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Questions and Answers

What are the main pharmacological actions of NSAIDs?

Anticoagulant action, antihypertensive action, antidiabetic action
Antibiotic action, antiviral action, antifungal action
Antihistamine action, antiemetic action, anticonvulsant action
Antipyretic action, analgesic action, anti-inflammatory action (correct)

Which is an example of an archetypal NSAID mentioned in the text?

Paracetamol
Ibuprofen
Naproxen
Aspirin (ASA) (correct)

What are the uses of NSAIDs?

Treatment of viral infections
Treatment of high blood pressure
Treatment of bacterial infections
Treatment of chronic pain and inflammation (correct)

Which system is not affected by the pharmacological actions of NSAIDs mentioned in the text?

Endocrine system (C) Signup and view all the answers

What are the primary uses of NSAIDs mentioned in the text?

Treatment of pain and inflammation (C) Signup and view all the answers

What is the main function of NSAIDs in relation to immune response?

Suppressing immune response (C) Signup and view all the answers

Which condition is NOT mentioned as a potential treatment target for NSAIDs in the text?

Bacterial infections (D) Signup and view all the answers

What are the typical side effects of NSAIDs?

Stomach ulcers, kidney problems, increased risk of bleeding (D) Signup and view all the answers

What is the mechanism of action of sulfasalazine in the treatment of ulcerative colitis?

Inhibits cyclooxygenase and lipoxygenase activities (A) Signup and view all the answers

Which NSAID is selective for COX-2 but inhibits COX-1 in the gastrointestinal tract, leading to ulcers?

Diclofenac (C) Signup and view all the answers

What is the mode of action of allopurinol in the treatment of gout?

Prevents the production of uric acid crystals in the joints (C) Signup and view all the answers

What is a common side effect of naproxen use?

Dizziness and nausea (C) Signup and view all the answers

Which NSAID exhibits analgesic, anti-inflammatory, and antipyretic activity by inhibiting COX1/COX2 levels?

Naproxen (D) Signup and view all the answers

What is the risk associated with using NSAIDs with warfarin?

Increased gastrointestinal bleeding (D) Signup and view all the answers

What is the major aim of drug treatment for ulcerative colitis?

Reduce symptoms and induce remission (C) Signup and view all the answers

What is a potential side effect of sulfasalazine use in the treatment of ulcerative colitis?

Itchy rash and sore mouth (D) Signup and view all the answers

What is a possible indication for the use of NSAIDs besides treating inflammation and pain?

Preventing Alzheimer's disease (B) Signup and view all the answers

What is the impact of NSAIDs on renal blood flow?

Reduction in renal blood flow (D) Signup and view all the answers

Which enzyme do non-steroidal anti-inflammatory drugs (NSAIDs) inhibit?

Both COX-1 and COX-2 (D) Signup and view all the answers

Which type of NSAIDs are considered 'super aspirins'?

COX-2 selective agents (C) Signup and view all the answers

Which NSAID acts irreversibly on COX?

Aspirin (D) Signup and view all the answers

What effect do bacterial endotoxins have on the release of interleukin-1 (IL-1β)?

Stimulate the release of IL-1β (D) Signup and view all the answers

How do NSAIDs provide symptomatic relief?

By blocking prostaglandin production (B) Signup and view all the answers

What is the benefit of aspirin in cardiovascular disorders?

All of the above (D) Signup and view all the answers

How do NSAIDs affect the gastrointestinal tract?

Decrease mucus secretion and acid production (D) Signup and view all the answers

Which COX-2 selective inhibitor was withdrawn due to cardiovascular effects?

Rofecoxib (B) Signup and view all the answers

What is the reason for aspirin's ability to inhibit the production of new COX proteins in endothelial cells?

It inhibits PGE2 synthesis at its site of action (A) Signup and view all the answers

What distinguishes aspirin from ibuprofen in terms of gastroprotective effects?

Aspirin inhibits PGE2 synthesis at its site of action (B) Signup and view all the answers

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Study Notes

Arthritis, bone pain, fever, and inflammation are cardinal signs of inflammation.
Non-steroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the enzyme COX, which converts arachidonic acid (AA) into prostaglandins (PGs) and thromboxanes (TXs).
Aspirin acts irreversibly on COX, while others act reversibly, which is significant in its use as a prophylactic in cardiovascular disease.
Older generation NSAIDs inhibit both COX-1 and COX-2, while newer COX-2 selective agents are considered "super aspirins".
Paracetamol is a non-NSAID analgesic that weakly inhibits COX-3 in the CNS and has little effect on COX-1 or COX-2 in peripheral tissue.
Bacterial endotoxins stimulate the release of interleukin-1 (IL-1β), which acts on the hypothalamus to cause the release of prostaglandin E2 (PGE2). PGE2 elevates the set point temperature and causes fever. NSAIDs block PGE2 production, lowering the set point temperature and dissipating the fever.
Prostaglandins sensitize and stimulate nociceptors and directly activate nociceptive nerve fibres, contributing to pain and hyperalgesia. NSAIDs provide symptomatic relief by blocking PG production and breaking this cycle.
NSAIDs have effects on various systems in the body, such as the cardiovascular system, skeletal system, gastrointestinal tract, CNS, genital tract, kidney, and body fluids, lung & respiratory system, and skin.
Aspirin is beneficial in cardiovascular disorders because it inhibits both COX-1 and COX-2 and has anti-aggregatory and vasodilatory effects. The benefits are due to the inhibition of TXA2, a pro-aggregatory vasoconstrictor, and the preservation of PGI2, an anti-aggregatory vasodilator.
Aspirin is beneficial in cardiovascular disorders due to its ability to inhibit the production of new COX proteins in endothelial cells, while platelets cannot synthesize new COX, which leads to less irritant effects and the preservation of the benefits of PGI2 and PGE2.
Skeletal PGs contribute to swelling and pain in arthritis through various mechanisms, including arteriolar dilatation, increased microvascular permeability, and hyperalgesia. NSAIDs diminish these effects, but do not treat the underlying cause of inflammation.
NSAIDs have negative effects on the gastrointestinal tract, including decreased mucus secretion, increased acid secretion, and increased production of leukotrienes, which can lead to bleeding and ulceration. COX-2 selective inhibitors may be less irritant to the gastrointestinal tract as they have less effect on gastric cytoprotective mechanisms.
NSAIDs are acidic and can increase blood loss. They interfere with tissue healing by inhibiting COX-2 and can cause nausea, dyspepsia, and gastrointestinal contraction due to COX-1 inhibition.
Examples of COX-2 selective inhibitors include celecoxib, etoricoxib, rofecoxib, and valdecoxib. Etoricoxib is the most selective COX-2 inhibitor and has no effect on TXA2 in platelets but decreases PGI2 in blood vessels. However, it was withdrawn due to cardiovascular effects and is not recommended for use in rheumatoid arthritis or osteoarthritis. Instead, meloxicam or etodolac are recommended.
Aspirin inhibits the synthesis of PGE2 at its site of action, while ibuprofen does not. This is important in understanding the gastroprotective effects attributed to PGE2 and TXA2.

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