Which bone is affected more by glucocorticoid-induced osteoporosis?

Correct Answer: D

Rationale: In glucocorticoid-induced osteoporosis, the lumbar vertebra (option D) is affected more compared to other bones. Glucocorticoids exert their effects by decreasing bone formation and increasing bone resorption, leading to decreased bone mineral density. The vertebrae, especially the lumbar vertebrae, are predominantly affected due to their high trabecular bone content and increased bone turnover rate. Option A, the femur, is less affected because it consists of more cortical bone which is less susceptible to the effects of glucocorticoids. Option B, the humerus, and option C, the radius, are also less affected compared to the lumbar vertebra due to similar reasons. In an educational context, understanding the differential effects of glucocorticoids on various bone types is crucial for healthcare professionals managing patients on long-term glucocorticoid therapy. This knowledge helps in implementing preventive strategies and appropriate monitoring to mitigate the risk of osteoporosis and fractures in these patients.

Correct Answer: C

Rationale: In this question, the correct answer is C) Phospholipase - A. Corticosteroids exert their anti-inflammatory effects by inhibiting the enzyme phospholipase A2. Phospholipase A2 is responsible for the release of arachidonic acid from cell membrane phospholipids. This arachidonic acid is then metabolized into inflammatory mediators like prostaglandins and leukotrienes by cyclooxygenase and lipoxygenase enzymes. Option A) Cyclooxygenase is incorrect because it is the enzyme responsible for converting arachidonic acid into prostaglandins, not the enzyme inhibited by corticosteroids. Option B) Lipoxygenase is incorrect for the same reason as option A. Lipoxygenase converts arachidonic acid into leukotrienes, not the enzyme inhibited by corticosteroids. Option D) Phosphodiesterase is incorrect because it is not directly involved in the arachidonic acid pathway or the mechanism of corticosteroids. Understanding the mechanism of action of corticosteroids is crucial in pharmacology as it helps in comprehending their therapeutic uses and potential side effects. By inhibiting phospholipase A2, corticosteroids reduce the production of inflammatory mediators, leading to their anti-inflammatory effects. This knowledge is essential for healthcare professionals in selecting appropriate treatments for inflammatory conditions involving the central nervous system.

Correct Answer: C

Rationale: In a comatose patient suspected of poisoning, the finding of hyperreflexia would be against the drug being morphine. Morphine, a potent opioid, typically presents with pinpoint pupils and severe respiratory depression due to its central nervous system depressant effects. Loss of consciousness is also expected with opioid toxicity. Hyperreflexia, on the other hand, is not a typical feature of opioid poisoning. It is more commonly associated with stimulant toxicity or conditions affecting the upper motor neuron pathways. In an educational context, understanding these differential effects can help healthcare professionals make accurate clinical assessments and provide appropriate treatment in cases of drug poisoning. It is crucial for pharmacology students to grasp these nuances to differentiate between drug toxicities accurately. This knowledge is vital in clinical settings to ensure timely and effective management of patients presenting with overdose or poisoning scenarios involving CNS drugs.

Correct Answer: B

Rationale: The correct answer is B) It is inducible. Cyclooxygenase-2 (COX-2) is an isoenzyme that is not constitutively expressed in most tissues, unlike cyclooxygenase-1 (COX-1). COX-2 is inducible in response to stimuli such as inflammation, cytokines, and growth factors. This induction allows for the production of prostaglandins involved in the inflammatory response. Understanding this distinction is crucial in pharmacology because drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) selectively inhibit COX-2 to reduce inflammation without affecting the cytoprotective functions of COX-1. Option A) It is not inhibited by indomethacin is incorrect because both COX-1 and COX-2 can be inhibited by indomethacin. Option C) It generates cytoprotective prostaglandins in gastric mucosa is incorrect because this function is attributed to COX-1, not COX-2. Option D) It is found only in fetal tissues is incorrect as COX-2 can be induced in various tissues in response to different stimuli beyond fetal development. In a clinical context, understanding the distinct features of COX-2 helps in the development of drugs with fewer gastrointestinal side effects compared to non-selective NSAIDs, making them a preferred choice in certain patient populations. This knowledge is essential for healthcare professionals in optimizing drug therapy and patient care.

Correct Answer: B

Rationale: In the context of a patient with a peptic ulcer, the safest nonopioid analgesic option among the ones provided is Paracetamol (option B). Paracetamol is preferred due to its minimal effects on the gastrointestinal (GI) system compared to other nonsteroidal anti-inflammatory drugs (NSAIDs) like Ketorolac, Diclofenac sodium, and Ibuprofen. Paracetamol is not associated with causing or exacerbating peptic ulcers as it does not have significant effects on prostaglandin synthesis within the GI tract, unlike NSAIDs. NSAIDs, such as Ketorolac, Diclofenac sodium, and Ibuprofen, can increase the risk of GI bleeding, ulcer formation, and perforation, especially in patients with a history of peptic ulcers. Educationally, this question highlights the importance of considering a patient's comorbid conditions when selecting pharmacological treatments. Understanding the mechanisms of action and side effect profiles of different analgesics is crucial for making safe and effective clinical decisions. In the case of peptic ulcers, selecting a nonopioid analgesic with minimal GI side effects, like Paracetamol, is essential to prevent further harm to the patient.