Comprehensive Nsaids Quiz MCQs: Get The Answers You Need

These five are the five groups that inflammatory mediators can be classified into.

The correct answer is "All of the above" because NSAIDs can indeed be divided into non-selective COX inhibitors, COX-2 selective inhibitors, and CINODs (cyclooxygenase-inhibiting nitric oxide-donating drugs) such as Nitroaspirins. This categorization helps to differentiate the different types of NSAIDs based on their mechanism of action and selectivity for specific COX enzymes.

They readily cross the placental barrier.

Propionic acid derivatives such as ibuprofen, naproxen, ketoprofen, fenoprofen, oxaprozin, and flurbiprofen are indeed better tolerated by patients compared to phenylbutazone, or indomethacin. This means that patients experience fewer side effects or adverse reactions when taking propionic acid derivatives.

Glucocorticoids do not cause pain. They reduce it by decreasing inflammation.

NSAIDs (Nonsteroidal anti-inflammatory drugs) cause an anticoagulation effect by inhibiting platelet thromboxane A2 production. Thromboxane A2 is a substance that promotes platelet aggregation and vasoconstriction. By inhibiting its production, NSAIDs prevent platelet aggregation and reduce the risk of blood clot formation. This anticoagulation effect can be beneficial in conditions such as cardiovascular diseases or after surgical procedures to prevent excessive blood clotting.

Indomethacin, a medication commonly used for pain and inflammation, has been known to cause central nervous system (CNS) disturbances. These disturbances can manifest as depression, psychosis, and hallucinations. Due to this potential side effect, indomethacin is contraindicated in individuals with psychiatric disorders. Therefore, the given statement is true.

Aspirin is the correct answer because it binds irreversibly to COX (cyclooxygenase), an enzyme involved in the production of prostaglandins, which are responsible for inflammation, pain, and fever. Unlike other NSAIDs (nonsteroidal anti-inflammatory drugs) such as ibuprofen and celebrex, aspirin irreversibly acetylates COX, inhibiting its activity permanently. This irreversible binding makes aspirin unique among NSAIDs and gives it its long-lasting effects.

The antipyretic effect of NSAIDs is not due to their inhibitory effect on the biosynthesis of thromboxane A2. Instead, NSAIDs reduce fever by inhibiting the synthesis of prostaglandins, which are involved in the regulation of body temperature. While NSAIDs do inhibit the production of thromboxane A2, this is not the mechanism responsible for their antipyretic effect.

Although used in rheumatoid arthritis and osteoarthritis, they are not recommended as initial therapy.

The statement is true because coxibs, which are a class of nonsteroidal anti-inflammatory drugs (NSAIDs), have been found to have a cardiotoxic effect. This effect is partly attributed to their ability to inhibit the biosynthesis of vascular PGI2, also known as prostacyclin. Prostacyclin is a substance that helps regulate blood clotting and blood vessel constriction, and its inhibition can lead to an increased risk of cardiovascular events such as heart attacks and strokes. Therefore, the statement is accurate in stating that the cardiotoxic effect of coxibs is partly due to their ability to inhibit the biosynthesis of vascular PGI2.

NSAIDs and aspirin are examples of first line drugs for low grade pain (headaches, for example). Codeine is an example of a drug given for moderate pain. Morphine, oxycodone, and fentanyl are examples of drugs given for severe pain.

Acetaminophen is a  preferred drug for children because it is generally considered safe and effective for relieving pain and reducing fever in children. Unlike aspirin, acetaminophen does not have the risk of causing a rare but serious condition called Reye's syndrome in children. Ketoprofen, on the other hand, is not commonly used in children and may have more side effects compared to acetaminophen. Therefore, acetaminophen is the preferred choice for children due to its safety profile and effectiveness.

The analgesic actions of NSAIDs include decreased PG generation, which reduces the sensitization of nociceptive nerve endings to inflammatory mediators. Additionally, NSAIDs also decrease PG-mediated vasodilation, which can provide relief from headaches. Therefore, the correct answer is that all of the above actions contribute to the analgesic effects of NSAIDs.

IRREVERSIBLE!

Stimulus (infection, inflammation, malignancy) causes release of cytokines and pyrogens - PGE2 - increase of cyclic AMP - increase of hypothalamic set point = fever. Treat fever by getting rid of PGE2 - NSAIDs.

The description of acute inflammation includes local vasodilation of small vessels and increased capillary permeability, which is characterized by redness, swelling, and tenderness. This matches with option C. The description of delayed subacute inflammation includes tissue degradation and fibrosis, which matches with option A. The description of chronic proliferative inflammation is not given, but based on the remaining option, it can be inferred that chronic inflammation matches with option B. Therefore, the correct answer is Acute = C, Delayed = A, Chronic = B.

Exception: CINODs - NO antagonizes intrarenal effects of vasoconstrictors in absence of PGs, therefore CINODs are protective to the intra-renal system.

Indomethacin is not routinely used as an analgesic-antipyretic agent because of its side-effects. However, it is useful in special conditions: acute gouty arthritis, ankylosing spondylitis, Bartters's syndrome, osteoarthritis, and used to accelerate the closure of patent ductus arteriosus.

Reduces the synthesis of uric acid by inhibiting xanthine oxidase - confers a long duration of action so qd dosing is appropriate..

Fibrosis is a late phase/chronic development of inflammation.

The correct answer matches the descriptors with the drugs as follows: 1 = colchicine, 2 = colchicine and NSAIDs and corticosteroids, 3 = allopurinol, 4 = Febuxostat, 5 = Uricosuric agents, and aspirin. This means that colchicine is an anti-gout drug that inhibits mitosis, allopurinol is an anti-gout drug that is not protein bound, Febuxostat is a non-purine xanthine oxidase inhibitor, and uricosuric agents and aspirin cause an increase in uric acid excretion.

Mr. X is likely to experience increased retention of fluids. Congestive heart failure is a condition where the heart is unable to pump blood effectively, leading to fluid buildup in the body. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are known to cause fluid retention as a side effect. Therefore, when Mr. X took the NSAID tablets, it is probable that his fluid retention increased, exacerbating his congestive heart failure symptoms.

NSAIDs have anti-inflammatory actions by decreasing the levels of vasodilator prostaglandins, which results in less vasodilation and edema. They also inhibit the migration of certain immune cells, such as polymorphonuclear leukocytes and macrophages, to the site of inflammation. Additionally, NSAIDs stabilize lysosomal membranes, preventing the release of inflammatory mediators. Therefore, all of the given options describe the anti-inflammatory actions of NSAIDs.

During inflammation, these residents and recruited cells also become a source of a number of mediators that alter smooth muscle function, including IL1-β, nitric oxide (NO), IL-6, and TNF-α

The salicylates have uricosuric effects - low doses (1-2 g per day) decrease urate excretion (uric acid is retained - large doses (>5g per day) uricosuria and low plasma urate levels - excreted from kidneys.

CINODs - NO provides cytoprotection to gastric mucosa.

The correct answer is "have less GI side effects." This means that the oxicams (piroxicam, tenoxicam, and meloxicam) are similar to the salicylates in terms of anti-inflammatory actions, analgesic actions, and antipyretic actions. However, they differ in that they have less gastrointestinal (GI) side effects. This suggests that the oxicams may be a preferred choice over salicylates for individuals who are prone to GI issues or have a higher risk of developing GI side effects.

base binds the acid for excretion

The acetic acid derivatives, including indomethacin, sulindac, and etodolac, are more potent than aspirin. These drugs belong to the class of nonsteroidal anti-inflammatory drugs (NSAIDs) and are known for their strong anti-inflammatory and analgesic effects. Compared to aspirin, they have a higher potency in inhibiting the production of prostaglandins, which are responsible for pain and inflammation. Therefore, these acetic acid derivatives are considered to be more effective in relieving pain and reducing inflammation than aspirin.

Coxibs do not exhibit a potent antiplatelet effect.

The correct answer includes mediators such as IL-1, IL-6, PGE2, IL-1beta, and TNFalpha. These mediators are known for their role in promoting inflammation and fever. IL-1 and TNFalpha are pro-inflammatory cytokines that play a crucial role in initiating the inflammatory response and inducing fever. IL-6 is another pro-inflammatory cytokine that is involved in the immune response. PGE2 is a prostaglandin that is released during inflammation and can contribute to fever. IL-1beta is a pro-inflammatory cytokine that is produced in response to infection or injury and can also induce fever. Overall, these mediators play a significant role in the immunological response to pyrogens.

CINODs are indevelopment - NO releasing NSAID - gets rid of some of the adverse effects of getting rid of prostaglandins.

No antidote for aspirin overdose - alkalyze the urine and perform gastric lavage. Activated charcoal can also be given - universal antidote - binds almost anything.

direct - stimulation of the respiratory center in the medulla in medium to large doses = hyperventilation
indirect - salicylate-induced uncoupling of oxidative phosphorylation - O2 coming in, but instead of ATP, have heat coming out - profus sweating and hyperventilation

Fenamates, such as mefenamic acid and meclofenamate, are known to inhibit the enzyme COX. In addition to this, they can also block prostaglandin receptors. Prostaglandins are lipid compounds that play a role in inflammation and pain. By blocking their receptors, fenamates can further reduce inflammation and alleviate pain. This additional mechanism of action makes fenamates effective in managing conditions associated with inflammation and pain.

*unique*

All of the given options are actually ways to treat gout. Inhibiting uric acid synthesis can help reduce the production of uric acid, while increasing uric acid secretion can help eliminate excess uric acid from the body. Inhibiting leukocyte migration into the joint can reduce inflammation and pain associated with gout. General anti-inflammatory and analgesic effects can also help alleviate symptoms of gout. Therefore, all of the above options are valid treatment approaches for gout.

Probenacid is the correct answer because it acts by inhibiting the proximal tubular reabsorption of uric acid, which leads to increased excretion of urate. This helps in reducing the levels of uric acid in the body, which is beneficial in the treatment of gout. Allopurinol and sulfinpyrazone are also used in the treatment of gout, but they work through different mechanisms and do not directly inhibit the proximal tubular reabsorption of uric acid.

Naproxen is a nonsteroidal anti-inflammatory drug (NSAIDs) that inhibits the activity of both COX-1 and COX-2 enzymes. This means that they are equally selective for both COX-1 and COX-2. COX-1 is involved in protecting the stomach lining and promoting platelet aggregation, while COX-2 is associated with inflammation and pain. By inhibiting both enzymes, naproxen and diclofenac effectively reduce inflammation and pain, but they may also cause side effects such as gastrointestinal irritation and increased bleeding risk.

Due to inhibition of contractile PGs in the uterus wall, thereby delaying the onset of labor and prolonging the gestation period. (Morning after pill)

Acetaminophen does not inhibit neutrophil activation. Neutrophil activation plays a crucial role in the inflammatory response, and many nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit this activation. However, acetaminophen primarily works by inhibiting the production of prostaglandins in the central nervous system, which helps to reduce pain and fever. Unlike other NSAIDs, it has minimal anti-inflammatory effects and does not significantly affect neutrophil activation. Therefore, acetaminophen is the correct answer as it does not inhibit neutrophil activation.

Stimuli such as injury and inflammation triggers the release of cytokines and pain mediators. Cytokines stimulate the synthesis of PGs which not only cause pain but also sensitize the nerves to pain mediators such as bradykinin, histamine, and serotonin.

In therapeutic doses, the body is able to get rid of the toxic intermediate and it is harmless - becomes a problem in overdose. Max = 4 grams/day. Toxicity is due to reaction of the intermediate with -SH groups in hepatic proteins (cell death.

The absorption of propionic acid derivatives is slowed down by the presence of food in the stomach. When food is present, it delays the emptying of the stomach and slows down the passage of the propionic acid derivatives into the small intestine, where absorption takes place. This can affect the effectiveness and onset of action of the propionic acid derivatives.

Acetylation (irreversible) of the active site of COX in platelets leads to a reduction in the biosynthesis of thromboxane A2 - I  takes days to replace the platelets.

While these drugs are still considered non-selective, they seem to be relatively selective for COX-1.

While these drugs are still considered non-selective, they seem to be relatively selective for COX-2.

It is thought to provide cysteine for glutathione synthesis and possibly to form an adduct directly with the toxic metabolite of acetaminophen, N-acetyl-p-benzoquinoneimine. 

Aspiring is a big no - contraindicated in hemophilia and gout. A CINOD might work but it's not as strong an anti-platelet. A coxib would be the best choice as their are NO effects on platelets with these drugs.