Fluconazole:

Questions 52

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Ch 30 principles of pharmacology Questions

Question 1 of 5

Fluconazole:

Correct Answer: C

Rationale: Fluconazole penetrates the central nervous system well (C), making it ideal for cryptococcal meningitis and other CNS fungal infections, due to its small size and hydrophilicity ensuring high CSF levels. Oral absorption is excellent regardless of food (A is incorrect), with nearly complete bioavailability. Presystemic metabolism is minimal (B is incorrect), unlike voriconazole, enhancing its systemic availability. It's excreted 80% by the kidney (D), requiring dose adjustment in renal failure. It doesn't cause gynecomastia (original E). Fluconazole's efficacy in Candida infections (e.g., thrush, esophagitis) and its favorable pharmacokinetics, including a long half-life, make it a mainstay antifungal, though resistance in non-albicans species is a growing concern.

Question 2 of 5

The following anticancer drugs are considered highly emetogenic:

Correct Answer: D

Rationale: Cisplatin (D) is considered highly emetogenic, causing severe nausea and vomiting in most patients due to its action on the chemoreceptor trigger zone and GI tract, requiring aggressive antiemetic prophylaxis (e.g., 5HT3 antagonists, dexamethasone). Cyclophosphamide (A) is moderately to highly emetogenic, depending on dose, but less than cisplatin. Methotrexate (B) is mildly emetogenic at standard doses. 5-Fluorouracil (C) causes moderate nausea. Interleukin-2 (original E) is variably emetogenic, not a cytotoxic drug. Cisplatin's alkylating action on DNA is potent against testicular and ovarian cancers, but its emetic potential, linked to serotonin release, makes premedication critical for patient tolerability.

Question 3 of 5

Paclitaxel (a taxane):

Correct Answer: C

Rationale: Paclitaxel causes sensory neuropathies (C), a dose-limiting toxicity from microtubule stabilization, affecting peripheral nerves, common in breast and ovarian cancer treatment. It's used alone or in combination for epithelial tumors and lymphomas (A), enhancing efficacy. It doesn't inhibit purine synthesis (B); it prevents microtubule disassembly. Glucocorticoid premedication (D) prevents hypersensitivity from its Cremophor vehicle. It causes myelosuppression (original E is incorrect). Paclitaxel's broad antitumor activity and synergy in regimens like AC make it vital, though neuropathy and alopecia require supportive care.

Question 4 of 5

Distribution of drugs to specific tissues

Correct Answer: C

Rationale: The correct answer is that distribution depends on the unbound drug concentration gradient between blood and tissue (C). Only free (unbound) drug can cross membranes into tissues, driven by the concentration gradient, as per Fick's law of diffusion. Option A is false; blood flow (e.g., high to brain, low to fat) significantly affects distribution, as seen with anesthetics. Option B is incorrect; tissue solubility (lipid vs. aqueous) determines partitioning, like thiopental in fat. Option D is wrong; strong plasma protein binding (e.g., warfarin) reduces free drug, limiting distribution. Option E (original) about half-life is unrelated. This gradient-driven process explains rapid onset in highly perfused organs and prolonged effects in poorly perfused ones, critical for therapeutic targeting and avoiding toxicity.

Question 5 of 5

Which of the following provides information about the variation in sensitivity of the drug within the population studied?

Correct Answer: D

Rationale: Quantal dose-response curves (D) provide information about variation in drug sensitivity within a population, plotting the percentage of subjects responding (e.g., pain relief) against dose, revealing ED50 and variability (e.g., standard deviation). Maximal efficacy (A) measures the maximum effect (graded curves). Therapeutic index (B) is TD50/ED50, assessing safety, not sensitivity spread. Drug potency (C) compares doses for equal effects (e.g., ED50), not population variation. Graded curves (original E) measure continuous responses, not all-or-none. Quantal curves, used in clinical and preclinical studies, highlight interindividual differences (e.g., genetic polymorphisms), guiding dosing adjustments for diverse populations.

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