chlorAmphenicol — inhibits peptidyl transferase on 50S; aplastic anemia risk
C
Clindamycin — blocks translocation on 50S; excellent anaerobic and Gram+ coverage
💊 Antimicrobials · Fluoroquinolones
Fluoroquinolones: "-floxacin" ending. Inhibit DNA gyrase (Gram−) and topoisomerase IV (Gram+).
Fluoroquinolone Antibiotics — DNA gyrase inhibitors with broad-spectrum coverage
Broad-spectrum DNA-targeting antibiotic class — recognize by "-floxacin"
Ciprofloxacin: excellent Gram− (Pseudomonas, E. coli, Salmonella). Levofloxacin/moxifloxacin: respiratory fluoroquinolones — add Gram+ (S. pneumoniae). Adverse effects: tendon rupture (Achilles), QT prolongation, avoid in children and pregnancy.
💊 Antimicrobials · MRSA
Vancomycin: binds D-Ala-D-Ala. MRSA drug of choice. "Red man syndrome" from fast infusion.
Vancomycin — glycopeptide that blocks cell wall synthesis by binding D-Ala-D-Ala peptidoglycan precursor
The go-to antibiotic for MRSA — and what Red Man Syndrome actually is
Mechanism: binds D-Ala-D-Ala → blocks cell wall synthesis — no beta-lactam ring, so unaffected by beta-lactamase. VRE resistance: altered target (D-Ala-D-Lac) → use linezolid or daptomycin. Red man syndrome: histamine release from rapid infusion — NOT a true allergy. Monitor renal function (nephrotoxic).
Bacteriostatic = stops growth. Bactericidal = kills directly. Immunocompromised → must use bactericidal.
Bacteriostatic vs Bactericidal — critical distinction for immunocompromised patients who lack immune backup
Why this distinction matters most when the immune system is down
Bacteriostatic (tetracyclines, macrolides, clindamycin, TMP-SMX, chloramphenicol): halt replication — rely on immune system to finish the job. Bactericidal (beta-lactams, aminoglycosides, fluoroquinolones, vancomycin, metronidazole): kill directly. In HIV, transplant, neutropenia: no immune backup → must use bactericidal drugs.
💊 Antimicrobials · Anaerobes
Metronidazole: "Metro kills what has no O₂" — anaerobes and protozoa. DNA strand breakage mechanism.
Metronidazole (Flagyl) — reduced by anaerobes to a toxic metabolite that causes DNA strand breaks
The antibiotic of choice for anaerobic bacteria and certain parasites
Coverage: anaerobes (Bacteroides fragilis, C. difficile), protozoa (Giardia, Trichomonas, Entamoeba). Uses: C. diff colitis, bacterial vaginosis, intraabdominal infections. Adverse: disulfiram-like reaction with alcohol — warn patients. Metallic taste. Bactericidal against anaerobes.
💊 Antimicrobials · Folate
TMP-SMX: "Double block" — blocks folate synthesis at 2 sequential steps. First-line for PCP and UTIs.
Acyclovir — prodrug activated by viral thymidine kinase → inhibits viral DNA polymerase
Why acyclovir only works on herpes viruses and is non-toxic to human cells
Acyclovir enters all cells, but only herpes-infected cells have viral thymidine kinase (TK) to phosphorylate it. Activated form inhibits viral DNA polymerase. Uses: HSV-1/2 (cold sores, genital herpes), VZV (chickenpox, shingles), HSV encephalitis (IV). Valacyclovir: oral prodrug of acyclovir — better bioavailability. Resistance: TK mutation in immunocompromised.
The four-drug TB regimen — and why four drugs are required
RIPE for 2 months (intensive phase), then Rifampin + Isoniazid for 4 more months. Four drugs because M. tuberculosis mutates frequently — any two-drug combo will select for resistant mutants. Isoniazid (INH): give B6 (pyridoxine) to prevent peripheral neuropathy. Rifampin: red-orange urine/tears (warn patients), induces cytochrome P450.
Q: What does BET stand for and how does each mechanism confer antibiotic resistance?
A: BET: Beta-lactamase (enzyme that destroys the beta-lactam ring; ESBL = extended-spectrum version affecting cephalosporins too) · Efflux pumps (membrane proteins that actively export drug from the bacterial cell before it can act; major in fluoroquinolone and tetracycline resistance) · Target modification (altered binding site so drug cannot attach — MRSA: altered PBP2a; VRE: D-Ala-D-Lac instead of D-Ala-D-Ala). Also: decreased outer membrane permeability (loss of porins in Gram− bacteria) and enzymatic inactivation (aminoglycoside-modifying enzymes).
Q: Which antibiotics inhibit the 30S ribosome and which inhibit the 50S? Which are bactericidal vs bacteriostatic?
Q: What does RIPE stand for and what are the key side effects of each TB drug?
A: RIPE: Rifampin (inhibits RNA polymerase — red-orange body fluids, CYP450 inducer — many drug interactions) · Isoniazid/INH (inhibits mycolic acid synthesis — add pyridoxine/B6 to prevent peripheral neuropathy; hepatotoxicity) · Pyrazinamide (active in acidic macrophage environment — hyperuricemia, hepatotoxicity) · Ethambutol (inhibits arabinoglycan synthesis — optic neuritis, monitor color vision). Four drugs for 2 months then Rifampin + INH for 4 more months (total 6 months for drug-sensitive TB).
Q: What is vancomycin's mechanism, what is it used for, and what are Red Man Syndrome and VRE resistance?
A: Mechanism: binds D-Ala-D-Ala terminus of peptidoglycan precursors → blocks transglycosylation and transpeptidation → no cell wall cross-linking. No beta-lactam ring → unaffected by beta-lactamases. Uses: MRSA (IV), C. difficile colitis (oral — not absorbed), Gram+ endocarditis. Red Man Syndrome: histamine release from mast cell degranulation due to RAPID infusion — NOT a true IgE allergy; slow the infusion rate. VRE resistance: D-Ala-D-Lac replaces D-Ala-D-Ala → vancomycin cannot bind → use linezolid or daptomycin.
Q: What are the four HIV drug classes (NRTI, NNRTI, PI, INSTI) and why is triple therapy (ART) required?
A: NRTI (tenofovir, emtricitabine, abacavir): chain terminators lacking 3'-OH → block reverse transcription. NNRTI (efavirenz, nevirapine): bind RT allosterically — non-competitive. PI (ritonavir, atazanavir): block protease from cleaving polyproteins → immature, non-infectious virions. INSTI (dolutegravir, raltegravir): prevent viral DNA from integrating into host chromosome — currently preferred first-line. Triple therapy required because HIV reverse transcriptase is error-prone (no proofreading) → mutations arise rapidly → monotherapy or dual therapy selects for resistance within weeks.