An opioid analgesic is preferred over aspirin-like analgesics in

Correct Answer: D

Rationale: In the context of CNS Drugs Pharmacology, the correct answer, option D) Neuralgia, is preferred for opioid analgesics over aspirin-like analgesics due to the severity and nature of the pain associated with neuralgia. Neuralgia is a chronic condition characterized by intense, stabbing, or burning pain along the course of a nerve. Opioid analgesics are more effective in managing severe, neuropathic pain like neuralgia compared to aspirin-like analgesics. Option A) Acute gout is better managed with aspirin-like analgesics or NSAIDs due to the inflammatory nature of gout attacks. Aspirin-like analgesics help reduce inflammation and pain associated with acute gout. Option B) Burn pain is also more effectively managed with aspirin-like analgesics due to their anti-inflammatory properties, which can help reduce swelling and pain associated with burns. Option C) Toothache, typically caused by inflammation or infection, is better managed with aspirin-like analgesics or NSAIDs to address the inflammatory component of the pain. In an educational context, understanding the appropriate use of different classes of analgesics for specific types of pain conditions is crucial for healthcare providers to provide optimal pain management for their patients. This rationale highlights the importance of selecting the most appropriate analgesic based on the underlying cause and nature of the pain to achieve effective pain relief and improve patient outcomes.

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.

Correct Answer: A

Rationale: In understanding why nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the diuretic action of furosemide, it is crucial to have a grasp on the pharmacological mechanisms involved. The correct answer is A) Preventing prostaglandin-mediated intrarenal hemodynamic actions. Furosemide is a loop diuretic that acts on the ascending limb of the loop of Henle to inhibit the Na+/K+/2Cl- co-transporter, thus promoting diuresis. Prostaglandins play a role in maintaining renal blood flow and glomerular filtration rate by dilating afferent arterioles. NSAIDs inhibit cyclooxygenase enzymes, leading to decreased prostaglandin synthesis. By inhibiting prostaglandins, NSAIDs disrupt the normal intrarenal hemodynamic balance, including the vasodilatory effects on the afferent arteriole. This disruption ultimately reduces the efficacy of loop diuretics like furosemide, as the renal blood flow is reduced, impacting the delivery of the diuretic to its site of action in the loop of Henle. Now, let's address why the other options are incorrect: B) Blocking the action in ascending limb of loop of Henle: Furosemide itself acts on the ascending limb, so blocking its action here would not explain the reduced diuretic effect. C) Enhancing salt and water reabsorption in the distal tubule: This would actually oppose the diuretic effect of furosemide, making it an unlikely explanation for the reduced diuretic action. D) Increasing aldosterone secretion: Aldosterone acts on the distal tubule to enhance sodium reabsorption, which would not directly impact the action of loop diuretics like furosemide. Understanding the interaction between different classes of drugs is essential in pharmacology to predict and manage potential drug interactions and their implications for treatment outcomes. This scenario highlights the importance of considering the physiological and pharmacological mechanisms at play when multiple drugs are used concurrently.