Most medically useful antibiotics interfere with either peptidoglycan synthesis or ribosome function. Why would the cell membrane be a poor target for antimicrobial medication?

Why are gram-negative bacteria more resistant than gram-positive bacteria to the cytoplasmic target antibiotics?

In general, why might cell-wall inhibiting antimicrobial drugs be less effective on gram-negative bacteria compared to gram-positive bacteria? The gram-negative bacteria digest these drugs at a much higher rate than gram-positive bacteria. The mutation rate of gram-negative bacteria is much greater than that of gram-positive bacteria. The outer membrane of the gram-negative bacteria inhibits penetration of the drug. The peptidoglycan found in gram-positive bacteria is structurally different from that in gram-negative bacteria. The gram-negative bacteria do not synthesize peptidoglycan.

Broad-spectrum drugs target a wide variety of bacterial pathogens. Even when the broad-spectrum drug is capable of killing a target pathogen, it may not be the best treatment. Which statement best explains why a broad spectrum drug might be an undesirable treatment choice?   Broad-spectrum antimicrobials are usually toxic to the host cells. Broad-spectrum antimicrobials only work if they are used shortly after the infection begins. Broad-spectrum antimicrobials may kill much of the normal microbiota. Broad-spectrum antimicrobials are not able to kill bacteria that are in their log phase of growth. Broad-spectrum antimicrobials may stimulate excess growth of the normal microbiota.