Cephalosporins Antibiotics Mechanisms Quiz

Cephalosporins are bactericidal because they disrupt bacterial cell wall synthesis, leading to cell lysis rather than growth inhibition.

Resistance mainly occurs through beta-lactamase enzymes that inactivate the drug, altered PBPs that reduce binding, and efflux pumps removing the drug.

Most cephalosporins can be given orally, intramuscularly, or intravenously. Fourth-generation agents are IV only due to pharmacokinetics.

Early-generation cephalosporins poorly cross the blood–brain barrier, limiting CSF concentrations needed to treat meningitis.

Cephalosporins are minimally metabolized and eliminated primarily by the kidneys, making dose adjustment necessary in renal impairment.

They are commonly used for uncomplicated infections caused by streptococci and methicillin-sensitive staphylococci.

Second-generation agents expand Gram-negative coverage while retaining some Gram-positive activity.

They treat mixed infections involving Gram-positive and select Gram-negative organisms such as E. coli and Klebsiella.

They are used for meningitis, severe Gram-negative infections, and Neisseria species.

Cefepime is especially useful for Pseudomonas infections and neutropenic fever due to its broad activity.

Across generations, Gram-negative activity and beta-lactamase resistance increase, while Gram-positive activity may decrease.

Sensitivity depends on outer membrane penetration, resistance to beta-lactamases, and binding affinity to PBPs.

Adverse effects include hypersensitivity reactions, nephrotoxicity, and bleeding risk with specific agents.

Patients with penicillin anaphylaxis have a 5–10% risk of cross-reactivity, making cephalosporins unsafe in this context.

Cephalosporins share the beta-lactam ring with penicillins but differ structurally by having a six-membered dihydrothiazine ring instead of a five-membered thiazolidine ring. They also possess two variable R-groups, increasing spectrum and resistance.

Cephalosporins inhibit penicillin-binding proteins (PBPs), blocking peptidoglycan cross-linking. This weakens the cell wall and triggers autolysis.

First-generation cephalosporins are highly effective against Gram-positive organisms but limited against Gram-negative bacteria.

Third-generation cephalosporins offer strong Gram-negative coverage, improved beta-lactamase resistance, and effective CSF penetration.

Fourth-generation cephalosporins combine broad spectrum activity with enhanced beta-lactamase resistance and bacterial penetration.

Drug half-life in plasma does not equal CSF half-life. Cefotaxime distributes and persists differently in CSF despite shorter plasma duration.