1. A. The aminoglycosides appear to act by binding to various sites on bacterial 30S ribosomal subunits and disrupting the initiation of protein synthesis. The other agents appear to have the capacity to directly inhibit bacterial cell-wall synthesis.

2. C. The selection of agents to treat brain infections is quite limited because most agents do not penetrate into cerebrospinal fluid or the brain itself.

3. B. A synergistic effect when the combination of an aminoglycoside and p-lactam antibiotic are administered concurrently is well documented. The reasons for the synergistic response are not well documented but may be related to the actions of the p-lactam antibiotic to raise pH and oxygen tension in areas of abscess and thereby increase the penetrability of the aminoglycoside.

4. C. Aminoglycosides can cause neuromuscular junction blockade by the mechanism of displacing Ca++ from the neuromuscular junction and thus leading to the Ca++-dependent prejunctional release of acetylcholine. This is of clinical significance only in patients with myasthenia gravis, hypocalcemia, and hypermagnesemia.

5. D. Aminoglycosides do not penetrate most cells, and most drug-metabolizing enzymes are found on the inside of the cells. Therefore, aminoglycosides are poorly metabolized, and nearly all of an intravenous dose can be recovered in the urine.

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