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b-lactam, common penicillin 2. acid labile, b-lactamase snesitive: cant be given orally 3 use: .G+ and G- cocci 4. oral iv and im 5. side effects: toxic when renally insuficcient. |
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antistaph, no g negative. 2, acid stable, b= lactamse resistant. 3. Use against g plus cocci, particularly staph 4. oral, iv and im 5. microbes. Some allaergic reactiosn- |
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extended spectrum2. b-lactamase sensitive (can beused with inhibitor) 3. g+ and G- , acide stable 4. oral, iv and im |
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1.1st gen cephalosporin all cephaosporinis have some b-actamase resistnace 2. braod spectrum: Gplus and G-, better for Gplsu 3. oral and iv 4. hypersensitivity. Superinfection. Crossreaction not issue with 2nd gen and above, TOXIC when renally insuficcient |
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2nd gen 2. G- increased action 3. oral and iv |
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3rd gen 2. further extension of g-, at expense of gplus. Resistant to inducible, but no consistiucve b lactamases. CNS penetration 3. oral and iv |
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4 gen 2. penetrates CNS. True broad spectrum- good coverage of both Gs. Good lactamase ersistance 3 . oral and iv |
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1. monobactams 2. no activity towards Gplus 3. G- rods, restaitant to blactams 4. iv 5. no penicillin crossreactivity, low toxicity, occasional skin rash |
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carbapenems 2. braod spectrum, useful against serine blactamases but not metalloblactamases. Penetrates CNS 4. iv- cleared by renal dehydropeptidase. Na 5. nausea, vomiting diarrgea , rashes. Seizures in patients w renal insuff. Cross reactivity with penicillin allergies. |
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non b-lactam cell wall synth inhibitor, tar\ets wall , not enzyme 2. Gplus, bactericidal for actively growing cells. Used for methicilin resistance, good brain distrib, can be used with aminoglycosides, gentamicin. 4. oral, iv 5. minor adverse effects. |
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pore former- potassium releasing, no cell reputure 2. Gplus MRSA 3. significant nepgro and neurotoxicity reduces its use to last resort parentally |
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outerlayer perforator 2. does not work against G plus. 3. specific to LPS on outer membrane G- |
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precursor inhibitor: targets MurA= enzyme involved in first step conversion of NAG to NAM 2. G plus and G- |
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precurosor inhibitor: targets lipid phosphotase 2. significant nepgrotoxicity 3. Gplus 4. topical only 5. serious nephrotoxicity. |
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precursor inhibitor : inhibitor of alanine racemization and ligation. 2. CNS toxicity 3. TB usage 4. second line drug 5. serious CNS toxicity |
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aminoglycoside: 2. blocks 30s subunit: inhibits translocation, initaition, and incorporates incorrrect a.a. Rapidly bactercidial, postantibiotic effect,can be used synergetstically 4. 2nd line tuberculosis 5. reversible nephrotoxicity, avoide concurrent use w other nephrotoxic drugs.otoxic e ffects- both auditory and vestibular- irreversible. |
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aminoglycoside 2. blocks 30s subunit: inhibits translocation, initaition, and incorporates incorrrect a.a. Rapidly bactercidial, postantibiotic effect,can be used synergetstically 3. g- |
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aminoglycoside . Same mechanism as streptomycin. Can be used to gneative bacteria htat are resitsant |
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aminoglycoside 2. same mechanism streptomycin, uses for mechanical cleansing to prepare for colorectal surgery 3. oral for c olorectal, otherwise topical |
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no longer used systemically, due to toxicity and widespread ressistance binds 50s subunit, blocking protein acceptor site , and blocks peptidyl transferase enzyme. Broad spectrum and bacteriostatic. topically for certain eye infections, useful against some penicillin resistant mening, useful for ricketsia . gi disturbances, bone marrow d isturbances (i.e. anemia.), gray baby syndrome (glucoronide deficiency) inhibits hepatic enzyems resposnible for drug detox., don’t use w bactericidial |
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tetracycline (i.e. doxyccyline) |
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1. binds 30s subunit, prevents access to Asite . Broad spectrum and bacteriostatic, but can be usedwith aminoglycosides. Drug of choice mycoplasma pneumoniae. Used in combo for H pylori 2. orally/IV 3. gi disturbances, binds to teeth amd bone in young children (<8) SO DON’T GIVE TO PREGNANT WOMEN. Hepatic funciton, kidney function (RTA and N retention). Photosensitziation and vestibular reactions 4. Gi disturbances. Liver toxicity Cytp450 enzyme user. |
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macrolide 2. binds 50s subunit, inhibits translocation step, Gplus cocci
Gi disturbances. Liver toxicity Cytp450 enzyme user. |
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macrolide 2.binds 50s subunit, inhibits translocation step, Gplus 3. Gi disturbances. Liver toxicity Cytp450 enzyme user. |
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macrolide 2. macrolides, longest half life (3 days). 3. toxicity same as macrolides, except no cyp450 usage. |
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lincosamide. Binds 50s subunit, inhibits translocation. Gplus cocci,anaeorbes of both types, useful for MRSA. 4. Gi disturbances. Liver toxicity , C dif. Infection possiblity |
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quinipristin-dalfopristin (synercid |
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streptogramin. quinipristin= 50s subunit,m prevents elongation, dalfopristin- increases quinipristin affinity , each alone = bacteriostatic, together= bacteriocidal. Gplus, MDR cocci. Given via IV, all toxicities are infusion related |
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oxazilidzones. 1. Gplus bacteria: rods and cocci. Bacteriostatic. Targets 23srRNA of 50s subuinit. Inhibits formation of protein synth complex. 3. reserved for mdr usage 4. toxicity not that important- some bone marrow related, |
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sulfonamides 2. inhibits PABA to DHF step, works against UTIS and stomach bugs.3. Good FoR Gplus and G negative bacteria 4. all are partially crossa allergenic. Cause fever, can crystallize in urine. Hemolytic anemia. |
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inhibits DHFR , leading to decreasedTHF. Works synergystically with sulfonamides. When used synergystically are braod spectrum and good agaisnt MDR. |
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cipproflaxacin, all xacins |
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1.flouroquinolones 2. blocks DNA gyrase/topo II (G-) which inhibits unfolding of supercoild DNA. Blocks topo IV (G plus) , which inhibits replication of daughter cells , by inhibiting strand seperation. 4. first choice agent against anthrax. Also used for MDR UTIs and gastric infecitons. 5. Generally well tolerated. Gi disturbances, some bone issues with chio;ldren |
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