25-hydroxyvitamin D3 (calcifediol) is less effective than 1,25-dihydroxyvitamin D3 (calcitriol) in stimulating intestinal calcium transport, so that hypercalcemia is less of a problem with calcifediol. This consideration is:

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Question 1 of 5

25-hydroxyvitamin D3 (calcifediol) is less effective than 1,25-dihydroxyvitamin D3 (calcitriol) in stimulating intestinal calcium transport, so that hypercalcemia is less of a problem with calcifediol. This consideration is:

Correct Answer: A

Rationale: Step 1: 25-hydroxyvitamin D3 (calcifediol) is a precursor to 1,25-dihydroxyvitamin D3 (calcitriol). Step 2: Calcitriol is the active form of vitamin D that stimulates intestinal calcium transport. Step 3: Calcifediol is converted into calcitriol in the kidneys. Step 4: Since calcifediol is less potent than calcitriol, it is less effective in stimulating intestinal calcium transport. Step 5: Therefore, hypercalcemia, a condition of high calcium levels in the blood, is less likely to occur with calcifediol compared to calcitriol. Summary: Choice A is correct because calcifediol is indeed less effective than calcitriol in stimulating intestinal calcium transport, leading to a lower risk of hypercalcemia. Choices B, C, and D are incorrect as they do not accurately reflect the relationship between

Question 2 of 5

All of the following drugs are antibiotics, EXCEPT:

Correct Answer: C

Rationale: The correct answer is C: Co-trimoxazole. Co-trimoxazole is a combination of sulfamethoxazole and trimethoprim, which are not antibiotics but rather antimicrobial agents. Streptomycin, Penicillin, and Chloramphenicol are all antibiotics that target and kill bacteria. Antibiotics specifically target bacterial infections, while antimicrobial agents can target a broader range of microbes. Therefore, Co-trimoxazole does not fall under the category of antibiotics, making it the correct answer.

Question 3 of 5

Combination of sulfonamides with trimethoprim:

Correct Answer: B

Rationale: Step-by-step rationale for Choice B being correct: 1. Trimethoprim inhibits bacterial dihydrofolate reductase. 2. Sulfonamides inhibit dihydropteroate synthetase. 3. Combination blocks sequential steps in folate synthesis. 4. Synergistic effect enhances antimicrobial activity. Summary: A: Incorrect. Combination does not decrease unwanted effects of sulfonamides. C: Incorrect. Combination does not decrease antimicrobial activity. D: Incorrect. Combination does not increase elimination of sulfonamides.

Question 4 of 5

Tick the drug for the treatment of a hepatic form of amebiasis:

Correct Answer: C

Rationale: Rationale for Correct Answer (C - Metronidazole or emetine): 1. Metronidazole is the drug of choice for hepatic amebiasis due to its high efficacy against Entamoeba histolytica in the liver. 2. Emetine is an alternative option for hepatic amebiasis treatment, especially in cases of resistance to metronidazole. 3. Both drugs have good tissue penetration and are effective against the protozoa causing hepatic amebiasis. Summary of Incorrect Choices: A: Diloxanide or iodoquinol - These drugs are primarily used for treating non-invasive intestinal amebiasis, not the hepatic form. B: Tetracycline or doxycycline - These antibiotics are not the first-line treatment for hepatic amebiasis. D: Erythromycin or azithromycin - These antibiotics are not effective against Entamoeba histolytica in the liver

Question 5 of 5

Tick the action mechanism of anticancer drugs belonging to plant alkaloids:

Correct Answer: C

Rationale: The correct answer is C: Mitotic arrest at metaphase. Plant alkaloids like vinca alkaloids and taxanes disrupt microtubule function, leading to mitotic arrest at metaphase. This prevents cell division and ultimately inhibits cancer cell growth. Option A is incorrect because plant alkaloids do not directly inhibit DNA-dependent RNA synthesis. Option B is incorrect as cross-linking of DNA is not a mechanism of action for plant alkaloids. Option D is incorrect as plant alkaloids do not target aromatases. In summary, the correct mechanism for plant alkaloids is disrupting microtubule function, leading to mitotic arrest at metaphase.

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