Choose the characteristics of vancomicin:

Correct Answer: D

Rationale: Step-by-step rationale for why answer D is correct: 1. Vancomycin is a glycopeptide antibiotic known to inhibit cell wall synthesis. 2. It is effective against Gram-positive bacteria such as Staphylococcus and Streptococcus. 3. Vancomycin is not active against Gram-negative bacteria due to differences in cell wall structure. 4. Options A, B, and C are incorrect as they provide inaccurate information about vancomycin's characteristics.

Correct Answer: B

Rationale: The correct answer is B: Zalcitabine. Zalcitabine is a nucleoside reverse transcriptase inhibitor commonly associated with peripheral neuropathy and oral ulceration as side effects. These adverse effects are well-documented in clinical studies and are known to be dose-dependent. Zalcitabine can cause damage to peripheral nerves leading to neuropathy and can also irritate the mucous membranes in the mouth causing oral ulceration. Incorrect Choices: A: Acyclovir - Acyclovir is an antiviral medication used to treat herpes infections and does not typically cause peripheral neuropathy or oral ulceration. C: Zidovudine - Zidovudine is also a nucleoside reverse transcriptase inhibitor used in the treatment of HIV, but it is not associated with peripheral neuropathy or oral ulceration. D: Saquinavir - Saquinavir is a protease inhibitor used to treat HIV and does not commonly induce peripheral neurop

Correct Answer: D

Rationale: Correct Answer: D Rationale: 1. Hypermagnesemia can exacerbate heart failure. 2. Vomiting may further worsen magnesium levels. 3. Digoxin toxicity is a concern in hypermagnesemia. 4. Discontinuing digoxin is crucial to avoid adverse effects. 5. Starting losartan can help manage heart failure without worsening hypermagnesemia. Summary: A: Adding potassium may worsen hypermagnesemia. B: Atropine is not indicated for hypermagnesemia or heart failure. C: Increasing furosemide may lead to electrolyte imbalances. D: Discontinuing digoxin and starting losartan is the appropriate therapeutic adjustment.

Correct Answer: A

Rationale: The correct answer is A: By binding to fibrin. Plasminogen is converted into active plasmin by binding to fibrin through the tissue plasminogen activator (tPA). This binding triggers the activation of plasminogen into plasmin, which then degrades fibrin clots. The other choices (B: collagen, C: heparin, D: platelets) are incorrect because plasminogen activation specifically involves binding to fibrin to initiate the fibrinolytic cascade. Collagen, heparin, and platelets do not play a direct role in the conversion of plasminogen to plasmin.

Correct Answer: B

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.