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105 Cards in this Set
- Front
- Back
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What are the B-lactams, and what is their common mechanism?
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Penicillins, Cephalosporins, Carbapenems, and Monobactam. They inhibit the cell wall.
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Penicillin: action
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bind PBP (transpeptidase), inhibit PG cross-linking
cidal to actively growing bacteria |
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Penicillin: spectrum
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relatively narrow, some G+ and some G- Neisseria in particular
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Penicillin G vs Penicillin V
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Penicillin G is sensitive to stomach acid, IV only- Pen. V is acid stable, given orally
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Penicillin: intxns
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antag w/ static and synergy with cidals
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Penicillins: other derivatives
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Amino-penicillins- ampicillin, amoxicillin- extended spectrum, more G-
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Cephalosporin: action
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cidal- inhibits PG cross-linking -similar to penicillins
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Cephalosporin: spectrum
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4 generations, more widespread each one against G- and B-lactamase resistance
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Cephalosporin: pharm
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longer 1/2 life than penicillins
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Carbapenems: action
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cidal, resistant to most B-lactamases
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Carbapenems: spectrum
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broad, most G- and G+, good anti-pseudomonal and for mixed RT and UT
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Monobactam: action
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like other B-lactamases
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Monobactam: spectrum
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good for G- but not as effective for G+ or anaerobes.
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Monobactam (Aztreonam): What's so special about it?
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It's used as alternative to other B-lactams for allergic reasons- Monobactam has little cross-allergenicity with B-lactams.
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Glycopeptides: What and Action
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Vancomycin, binds D-Ala-D-Ala and inhibits PG transglycosylation, cidal to actively growing
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Vanc: Spectrum
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G+ only - can't get through G- cell wall pores- use against MRSA
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Vanc: Resistance
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Change D-Ala-D-Ala to D-Ala-D-Lactate, Vanc can no longer bind- problem in Staphylococcus and Enterococcus
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Bacitracin: action
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inhibits dephosph. of bactroprenol phosphate, blocks transfer of PG monomers across cell membrane; requires actively growing cells
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Bacitracin: spectrum
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G+ only- too large for pores of G-
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Bacitracin: adverse rxns
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toxic to eukaryotic cells, so use topically
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Cycloserine: structure
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D-Ala analog
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Cycloserine: action
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blocks L-Ala --> D-Ala conversion
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Cycloserine: use
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1st line for Mycobacterium tuberculosis
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Isoniazid: action
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cidal- inhibits mycolic acid synthesis, component unique to Mycobacteria cell walls
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Isoniazid: use
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1st line for Myco. tuberculosis- v. narrow spectrum
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Isoniazid: pharm
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intracellular and CNS penetration
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Ethambutol: action and use
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inhibits arabinogalactan synthesis, 1st line against m. tuberculosis
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Ethionamide: action and use
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inhibits mycolic acid synthesis, use for m. tuberculosis when 1st line fails
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Which two classes are considered "cell membrane disruptors?"
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Polymixins and Daptomycin
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Polymixin: action
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binds LPS- detergent action- cidal
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Polymixin: spectrum
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G- only since no LPS on G+ cells
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Polymixin: rxns
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nephrotoxicity, so only used topically (w/ bacitracin and neomycin)
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Daptomycin: action
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incorporates into membrane in Ca2+ dependent manner with lipid tail, depolarizes membrane
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Daptomycin: spectrum
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G+ bacteria, no activity against G-. Back up med for resistant pathogens, even those resistant to vanc
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Aminoglycosides: examples
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streptomycin, gentamicin, amikacin
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Aminoglycosides: action
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bind 30s rib. subunit irreversibly, cidal
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Aminoglycosides: spectrum
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broad for G- and G+ aerobes- needs Oxygen for transport, so not effective for anaerobes; use against facultative G- rods
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Aminoglycosides: resistance
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drug modifying enzymes on plasmids, modification of ribosomal target, changes in uptake
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Aminoglycosides: adverse rxns
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ototoxicity and nephrotoxicity
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Tetracyclines: examples
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tetracycline, doxycycline, tigecycline
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Tetracyclines: action
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static, bind 30s subunit, prevents binding of tRNA, blocks peptide elongation
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Tetracyclines: spectrum
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borad, G- and G+, and intracellular bacteria
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Tetracyclines: pharm
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good GI absorption, orally given, binds to bone and teeth
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Tetracyclines: adverse rxns
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impair bone growth, stain teeth in young children or fetus, liver tox in prego, photosensitivity
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Tetracyclines: resistance
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plasmid-encoded efflux pump (major source), changes in ribosomal binding site
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Tetracyclines: drug intxns
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antagonizs B-lactams, Ca supplements decrease absorption
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Chloramphenicol: action
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static, binds 50s subunit, inhibits peptide bond formation
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Chloramphenicol: spectrum
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broad, but toxic limits use. can cross blood-brain barrier (meningitis)
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Chloramphenicol: drug intxns
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antagonistic with macrolides, lincosamides- binds same site as these
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Chloramphenicol: adverse rxns
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bone marrow suppression
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Chloramphenicol: resistance
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acetyltransferase that modifies drug to disallow target binding mutations in G- porins- reduce ability of drug to enter cell
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Macrolides: examples
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erythromycin, azithromycin, telithromycin
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Macrolides: action
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binds 50s subunit, blocks peptide elongation by blocking translocation and/or transpeptidation, static
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Macrolides: spectrum
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G+ plus some others: chlamydia, legionella, mycoplasma, bordetella, EC and IC pathogens
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Macrolides: pharm
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long 1/2 life, concentrates in phagocytes, can be used as alternative in penicillin-allergic patients
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Macrolides: intxns
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binds same site as chloramphenicol, lincosamides, so antag with those drugs
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Macrolides: resistance
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efflux pump, alteration in binding site, enzymatic modification (methylases)
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Lincosamides: example
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Clindamycin
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Lincosamides: action
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binds 50s subunit, blocks peptide bond formation, static
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Lincosamides: spectrum
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mostly G+ anaerobes, bacterial vaginosis and topical for acne, no G- activity
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Lincosamides: drug intxns
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binds same site as macrolides and chloramphenicol, so antagonistic with those
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Lincosamides: resistance
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efflux pumps, alteration in binding site, enzymatic modification (same as macrolides)
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Oxazolidinones: example
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linezolid
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Oxazolidinones: action
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binds 50s subunit, inhibits initiation step in protein synth, static
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Oxazolidinones: spectrum
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VRE and MRSA
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Oxazolidinones: adverse rxns
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thrombocytopenia, neuropathy, serotonin syndrome w/ SSRIs
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Streptogramins: examples
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dalfopristin + quinupristin = synercid
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Streptogramins: action
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binds 50s subunit, blocks protein synth at two steps in elongation
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Streptogramins: spectrum
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VRE and MRSA
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Streptogramins: adverse rxns
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myalgias, phlebitis
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Streptogramins: drug intxns
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dalfoprostin (strepto A) and quinupristin (strepto B) are synergistic- together are cidal, individually static
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Mupirosin: action
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binds isoleucyl-tRNA synthase enzyme, blocks formation of Ile-tRNA; leads to protein synthesis arrest at codons for Ile; cidal at topical concentrations
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Mupirosin: spectrum
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good for S. aureus, MRSA, use topically for impetigo and folliculitis from S. aureus
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Mupirosin: adverse rxns
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toxic, topical use only
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What are the three classes of nucleic acid inhibitors?
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Quinolones/Fluoroquinolones, Nitroimidazoles, and Rifamycins
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Quinolones/Fluoroquinolones: examples
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ciprofloxacin, moxifloxacin, gatifloxacin
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Quinolones/Fluoroquinolones: action
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bind to DNA gyrase in G- and topoisomerase IV in G+ in complex with DNA. , promote DNA cleavage and interfere w/ supercoiling of DNA, cidal
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Quinolones/Fluoroquinolones: spectrum
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broad range, but not effective against streptococci or staphylococci. used for UTI and prostatitis, RT, GI, soft tissue and skin, osteomyelitis, STDs
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Quinolones/Fluoroquinolones: drug intxns
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metals in things like antacids and iron supplements chelate and block absorption
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Quinolones/Fluoroquinolones: pharm
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wide tissue distribution, including CNS and prostate
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Quin/Fluoro: adverse rxns
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don't use in children or pregos
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Quin/Fluoro: resistance
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alteration in DNA gyrase or topoisomerase (main), changes in uptake via porins, efflux pumps
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Nitroimidazoles: examples
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Metronidazole, Tinidazole
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Nitroimidazoles: action
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bacterial nitroreductase reduces drug's nitro group, this newly converted compound damages DNA
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Nitroimidazole: spectrum
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anaerobes, microaerophiles, some parasites
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Rifamycins: examples
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Rifampin, Rifabutin, Rifamaxin
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Rifamycins: action
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binds B-subunit of bacterial DNA dependent RNA pol, inhibits transcription initiation, cidal
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Rifamycins: pharm
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well aborbed orally, penetrates host cell
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Rifamycins: spectrum
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combo therapy for TB and prophylaxis for bacterial meningitis
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Rifamycin: adverse rxns
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orange urine and sweat, serious issues due to cytochrome P450 induction that alters other drug levels
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Rifamycin: resistance
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alteration in bacterial RNA pol
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What are the two classes of antimetabolites and what is their general action?
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Sulfonamides and Trimethoprim, folic acid metabolism inhibitors
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Sulfonamides: examples
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Sulfamethoxazole (SMX) and Dapsone
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Sulfonamides: action
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inhibit para-aminobenzoic acid conversion to dihydropteroic acid- stops purine and pyrimidine synthesis. static alone, TMP-SMX is cidal
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Sulfonamides: resistance
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quickly developed if used alone
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Trimethoprim (TMP): action
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inhibits dihydrofolate reductase, blocks folic acid synth, static alone TMP-SMX cidal
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Methenamine: action
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at pH<6, drug is converted to ammonia and formaldehyde- formaldehyde is cidal, ineffective if pathogen raises pH
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Methenamine: pharm
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delivered to bladder after oral ingestion
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Methenamine: use
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prophylaxis of recurrent bladder infections
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Nitrofurantoin: action
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weak acid, requires reduction inside bacterial cell for activity. reduced form inhibits several cellular processes. active against most bacteria that cause UTI
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Nitrofurantoin: spectrum
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most UTIs, usually recurrent UTI
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Pyrazinamide (PZA): action
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cleaved by bacterial enzyme (pyrazinamidase) to pyrazinoic acid (active form)- mechanism unclear
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Pyrazinamide: spectrum
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v. narrow, only effective against M. tuberculosis
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Pyrazinamide: use
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1st line for M. tuberculosis, combo w/ INH, EMB, and rifampin
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Pyrazinamide: resistance
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rapid if used alone, mutations in pyrazinamidase enzyme
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