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  1. Name the 6 general Cell Wall Synthesis Inhibitors (two general classes)
    • Beta-Lactams: penicillins, cephalosporins, carbapenems, monobactams (all inhibit transpeptidases)
    • Others: vancomycin (transglycosylase), fosfomycin (enolpyruvate transferase)
  2. Name the 9 general Protein Synthesis Inhibitors
    • Aminoglycosides: 30S; block initiation complex, misread mRNA template, block A=>P translocation
    • Spectinomycin: 30S; similar to aminoglycosides without mRNA misreads
    • Tetracyclines/Glycylcyclines: 30S; block aminoacyl-tRNA binding to A site
    • Macrolides/Ketolides/Lincosamides: 50S; block A=>P translocation
    • Linezolid: 50S; block ribosome initiation complex formation
    • Chloramphenicol: 50S; block P=>A transpeptidation
    • Streptogramins: 50S; quinupristin/dalfopristin (A=>P translocation/conformational change respectively)
  3. Name the 4 general Inhibitors of Nucleic Acid Synthesis or Function
    • Sulfonamides: cytoplasmic; inhibit dihydropteroate synthetase (purine synth)
    • Trimethoprim: cytoplasmic; inhibit dihydrofolate reductase (purine synth)
    • Fluoroquinolones: cytoplasmic; inhibit topoisomerases II (G-) and IV (G+)
    • Metronidazole: DNA; direct damage via free nitrogen radical
  4. Name the main bactericidal drugs/classes (7 single agents and 2 combos)
    • Beta-Lactams (cell wall synth)
    • Vancomycin/Fosfomycin (cell wall synth)
    • Aminoglycosides (protein synth 30s)
    • Quinupristin-Dalfopristin (protein synth 50s)
    • Sulfonamide-Trimethoprim (purine synth)
    • Fluoroquinolones (topoisomerase)
    • Metronidazole (DNA)
    • Isoniazid (anti-mycobacterial)
    • Rifampin (anti-mycobacterial)
    • Pyrasinamide (anti-mycobacterial)
  5. Name the 6 main bacteriostatic drugs/classes
    • Tetracyclines (protein synth 30s)
    • Macrolides (protein synth 50s)
    • Clindamycin (protein synth 50s)
    • Chloramphenicol (protein synth 50s)
    • Linezolid (ribosome formation)
    • Sulfonamides (purine synth)
  6. Define concentration-dependent killing.
    Significant increase in bacterial killing as [drug] increases; give high doses once per day for rapid killing.
  7. Define time-dependent killing.
    Do not increase rate of killing as [drug] increases; rate of killing is proportional to time the [drug] remains above Minimum Bactericidal Concentration.
  8. Define post-antibiotic effect.
    When drugs (e.g. aminoglycosides, fluoroquinolones) maintain persistent suppression of growth after [drug] has fallen below Minimum Inhibitory Concentration; often only require one dose per day.
  9. Define/compare MIC vs MBC.
    • MIC: minimum inhibitory concentration; lowest concentration that inhibits growth; related to postantibiotic effect
    • MBC: minimum bactericidal concentration; lowest concentration that kills; related to concentration dependent killing and time-dependent killing
  10. Compare concentration-dependent killing and time-dependent killing.
    • Concentration: given in high and fewer (daily) doses to get better kill; includes aminoglycosides, fluoroquinolones, carbapenems
    • Time: higher doses not more effective, given in smaller doses over time to maintain regular concentration; includes B-lactams, macrolides, clindamycin, linezolid
  11. List the 5 classes of β-lactam related drugs, general MOA, efficacy, susceptibility, and resistance.
    • Penicillins
    • Cephalosporins
    • Carbapenems
    • Monobactams
    • β-lactamase inhibitors
    • All inhibit penicillin-binding proteins, most importantly transpeptidases for final peptidoglycan x-linking, and many can activate autolytic enzymes to further precipitate lysis.
    • They exhibit time-dependent killing and are bacteriocidal.
    • Susceptibility depends on outer cell membrane and peptidoglycan thickness.
    • Natural or acquired (via plasmid); through β-lactamase, mutations in PBPs, decreased permeability, or active efflux.
  12. List 4 classes of penicillins and their drugs.
    • Standards: penicillin G, benzathine penicillin
    • Penicillinase resistant: nafcillin, dicloxacillin, methicillin
    • Amino: ampicillin, amoxicillin
    • Antipseudomonal: piperacillin
  13. List the 1 β-lactamase inhibitor and some general properties.
    Clavulanate: inhibits a wide variety of β-lactamases; given with amino penicillins to extend their spectrum (+amoxicillin = augmentin).
  14. List 4 classes of cephalosporins and their drugs.
    • 1st Gen: cefazolin (IM/IV), cephalexin (oral), 1=L
    • 2nd Gen: cefuroxime, cefoxitin, cefotetan (IM/IV)
    • 3rd Gen: cefotaxime, ceftriaxone, ceftazidime (IM/IV), 3=T
    • 4th Gen: cefepime (IM/IV), 4=P
  15. List 2 carbapenems.
    • Imipenem: hydrolyzed by dehydropeptidase-1 (DHP-1), must be given with cilastatin (DHP1 inhibitor)
    • Meropenem: not degraded by DHP1
    • Both have broad spectrum against G+, G-, and anaerobes; resistant to most β-lactamases.
  16. List 1 monobactam and its properties.
    Aztreonam: no activity against G+ and anaerobes; resistant to G- β-lactamases; tolerated by penicillin/cephalosporin allergics; used for nosocomial Pseudomonas infections
  17. List 2 other cell wall inhibitors.
    • Vancomycin: no activity against G-; parenteral admin; flushing and hypotension after rapid IV; DOC for MRSA, used for C. difficile enterocolitis, combo with aminoglycosides for Enterococcal endocarditis and ceftriaxone for pneumococcal meningitis
    • Fosfomycin: inhibits enolpyruvate transferase (NAG to NAM synth, early step); active against G+ and G-
  18. List the 6+1 drugs that bind the 30S ribosomal subunit and block initiation complex formation and A=>P translocation.
    • Aminoglycosides - bactericidal, concentration-dependent killers with long post-antibiotic effect used primarily against G- aerobes
    • Streptomycin: generally less active, but highly effective for Yersinia, Mycobacterium, and Francisella
    • Gentamycin: commonly used against G-, combo with β-lactams for synergy
    • Tobramycin: esp. active against P. aeruginosa, combos with piperacillin
    • Amikacin: highest resistance to aminoglycoside inactivators
    • Neomycin: primarily topical, otherwise nephrotoxic
    • Paromomycin: good for protozoa (esp. Entamoeba, Cryptosporidium, Taenia)
    • Spectinomycin: does not cause mRNA misreading! Used as alternative N. gonorrhea treatment.
  19. Name the 3+1 drugs that bind to the 30S subunit and block aminoacyl tRNA binding to the A site.
    • Tetracyclines - broad spectrum, especially useful for atypicals, anaerobes, G+ bugs, G- rods, and protozoa; bacteriostatic; resistance can arise easily
    • Tetracycline
    • Doxycycline
    • Demeclocycline
    • Glycylcyclines - same as tetracyclines, but bugs exhibit less resistance to tigecycline
    • Tigecycline
  20. Name the 1 drug that binds to the 50S subunit and inhibits transpeptidation.
    Chloramphenicol: broad spectrum, but many side effects, toxicities, and drug interactions coupled with widespread resistance; can cause bone marrow suppression and gray-baby syndrome
  21. Name 3+1 drugs that bind the 50S subunit and inhibit tRNA translocation.
    • Macrolides - bacteriostatic, good against G+s, anaerobes, and atypicals; clar- and azithromycin broader and more effective
    • Erythromycin: low bioavailability, inhibits CYP450
    • Clarithromycin: improved acid stability over erythro
    • Azithromycin: also acid stable, doesn't inhibit CYP450
    • Clindamycin: lincosamide, not macrolide; Bacteroides fragilis treatment
  22. Name the drug that binds to the 50S subunit and blocks formation of initiation complex.
    Linezolid: bacteriostatic drug with poor activity on G-; reserved for vancomycin and multi-drug resistant bugs (Enterococcus faecium, S. aureus) and nosocomial S. aureus pneumonia
  23. Name the 2 streptogramins.
    • Quinupristin/Dalfopristin - bactericidal combo with long post-antibiotic effect; active against G+ cocci, inactive against G-; used for VRSA and VREF
    • Quinupristin: binds 50S to prevent A=>P translocation
    • Dalfopristin: binds 50S and induces conformational change
  24. Name 4 drugs that block topoisomerase II and IV.
    • Fluoroquinolones - concentration-dependent bactericidals with post-antibiotic effect; resistance is uncommon
    • Ciprofloxacin: potent against Pseudomonas, DOC for anthrax
    • Ofloxacin: chlamydial urethritis/cervicitis
    • Levofloxacin: community acquired pneumonias
    • Moxifloxacin: good for anaerobes; poor activity against Pseudomonas
  25. Name 3 drugs that block dihydropteroate synthetase.
    • Sulfonamides - bacteriostatic; prevents PABA -> dihydropteroate, inhibiting purine synth
    • Sulfamethoxazole: often combined with trimethoprim (aka bactrim or cotrimoxazole, TMP-SMZ)
    • Sulfadiazine: topical, active against bacteria and fungi
    • Sulfasalazine: ulcerative colitis and rheumatoid arthritis
  26. Name the drug that blocks dihydrofolate reductase.
    Trimethoprim: prevents purine synth; bacteriostatic, much more potent than sulfonamides; cidal when combo'd 1T:5S with sulfamethoxazole
  27. Name the drug that causes DNA damage through nitrogenous free radical formation.
    Metronidazole: cidal prodrug converted by anaerobics that donate electrons from ferredoxins; teratogenic
  28. Name 2 urinary antiseptics.
    • Methenamine: converted to formaldehyde at urine pH ( < 5.5); cannot use with sulfonamides
    • Nitrofurantoin: intermediates formed by susceptible bacs that damage DNA, rapidly excreted in urine
Card Set
General classifications and mechanisms, specific drug classes, drug names
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