Antibiotics Flashcards
Penicillins
-MOA: Inhibit bacterial cell wall synthesis (bind penicillin binding proteins, prevent peptidoglycan cross-linking)
-Static/Cidal: Cidal
-Time/Conc: Time
-Spectrum:
Naturals - G+ & anaerobes
Aminopencillins - G+ & anaerobes, some G-
Anti-pseud - excellent pseud, variable otherwise (ticaracillin broad spec)
Anti-staph - increase B-lactamase resistance, not effective MRSA; good G+, anaerobes, poor G-
-Elimination: Active tubular secretion in renal tubules
-Synergism/Antagonism: Drugs that inhibit protein synthesis may enhance efficacy against beta-lactamase. Synergism with aminoglycosides. Antagonistic with inhibitors of ribosomal activity. May inactive aminoglycosides/FQ at high conc.
-Addtl facts: B-lactamase inhibitors (Amoxi-clav, ticarciliin-clav); impaired activity in hypertonic environment. Penicillins inactivated in acidic environment.
-Examples:
Natural - penicillin
Amino - amoxicillin, ampicillin
Anti-pseud - ticaracillin, piperacillin
Anti-staph - oxacillin, methicillin, nafcillin, dicloxacillin
Carbapenems
-MOA: Inhibit cell wall synthesis
-Static/Cidal: Cidal
-Time/Conc: Time
-Spectrum: Broadest spectrum
(G+) - 4/4
(G-) - 4/4
(An) - 3-4/4
Staph - 4/4
Pseud - Y
-Elimination: Tubular secretion, concentrate in urine
-Synergism/Antagonism:
-Addtl facts: Imipenem associated with least endotoxin release. Can cross BBB unlike other b-lactams.
-Adverse effects: GI effects, CNS toxicity, hypersensitivity, renal failure
-Examples: Meropenem, imipenem
1st gen Cephalosporins
-MOA: Inhibit cell wall synthesis
-Static/Cidal: Cidal
-Time/Conc: Time
-Spectrum: Gram + and some G- (e.coli, klebsiella, proteus);(cefazolin better G- but worse staph)
(G+) - 3/4
(G-) - 1-2+/4
(An) - 1-2/4
Staph - 3-4/4
Pseud - N
-Elimination: Active renal tubular secretion
-Synergism/Antagonism: See penicillins
-Addtl facts: More resistant to B-lactamases
-Examples: Cephalexin, cefazolin
2nd gen Cephalosporins
-MOA: Inhibit cell wall synthesis
-Static/Cidal: Cidal
-Time/Conc: Time
-Spectrum: Better G- (enterobacter, proteus, e coli, klebsiella), good anaerobe (cefoxitin excellent anaerobe)
Pseud - N
-Elimination: Active renal tubular secretion
-Synergism/Antagonism: See penicillins
-Addtl facts:
-Examples: Cefoxitin, cefotiam, cefuroxime
3rd gen Cephalosporins
-MOA: Inhibit cell wall synthesis
-Static/Cidal: Cidal
-Time/Conc: Time
-Spectrum: Improved G- spectrum at expense of G+
Moderate G+ (less effective cocci), Good-excellent G-, good anaerobic
Pseud - Variable
-Elimination: Active renal tubular secretion
-Synergism/Antagonism:
-Addtl facts: Usually used for severe G- infection (pseud, enterobacter, serratia)
-Examples: Ceftazidime, ceftiofur, cefpodoxime, cefovecin
Aminoglycosides
-MOA: Protein synthesis inhibition via irreversible binding to 30S ribosome
-Static/Cidal: Cidal
-Time/Conc: Conc
-Spectrum:
(G+) - 1/4
(G-) - 4/4
(An) - NO (O2 required for transport into cell)
Staph - 3-4/4
Pseud - 3-4/4
-Elimination: Renal
-Synergism/Antagonism: Synergistic with B-lactam (improved movement into cell with increased cell wall permeability); chemically inactivated by penicillins at high concentrations
-Addtl facts: Inherent anaerobic resistance, O2 required for cell entry. Poor GI absorption. Nephrotoxic (tubular > glomerular) - avoid concurrent NSAID, diuretic, ACEi, shock, endotoxemia; once daily dosing, monitor with glutamyltransferase:creatinine ratio; inactivated in acidic environment (e.g. acidic urine, abscess), bound to sediment in pus, chelated to Ca/Mg; higher risk of nephrotoxicity in alkaline urine; may cause ototoxicity, neuromuscular blockade. No CNS, distribute to ECF
-Examples: Amikacin, Gentamycin
Fluoroquinolones
-MOA: Nucleic acid synthesis inhibitor - inhibits topoisomerase 2 (DNA Gyrase) and 4
-Static/Cidal: Cidal
-Time/Conc: Concentration
-Spectrum: Broad Gram - with some Gram +
(G+) - Variable
(G-) - 3-4/4
(An) - Poor
Staph - 3-4/4
Pseud - Y
-Elimination: Enro 100% renal, others some hepatic metabolism w/renal excretion
-Synergism/Antagonism: Chemically inactived by penicillins at high concentrations
-Addtl facts: Cartilage deformities/joint disorders in immature animals, blindness in cats (enro). Reaches prostate well, decent CNS. More effective in alkaline pH. Accumulate in WBC. Good against rickettsial.
-Examples: Enrofloxacin, pradofloxacin, ciprofloxacin
Sulfonamides
-MOA: Inhibit folic acid synthesis
-Static/Cidal: Static (cidal in combo with trimethoprim)
-Time/Conc:
-Spectrum: Broad but limited by resistance. Gets Nocardia.
(G+) - 2-3/4
(G-) - 2/4
(An) - 2-3/4
Staph - 2-3/4
Pseud - N
-Elimination: Renal & hepatic, prolonged by intrahepatic circulation
-Synergism/Antagonism: Sulfonamides cidal when combined with trimethoprim
-Addtl facts: Penetrates tissues well including CNS & prostate. Can cause KCS. Acute idiosyncratic hepatopathies, aplastic anemia, arthropathies. Dobermans & other black/tan predisposed to hypersensitivity rxn.
-Examples: TMS
Tetracyclines
-MOA: Inhibit protein synthesis - 30S ribosome
-Static/Cidal: Static
-Time/Conc: Time
-Spectrum: Moderately broad spectrum, good for atypical organisms (rickettsial, borrelia, chlamydophila, mycoplasma)
(G+) - 2-3/4
(G-) - 2-3/4
(An) - 2-3/4
Staph - 2-3/4
Pseud - N
-Elimination: Enterohepatic circulation. Most renal & biliary; minocycline only renal, doxy ? (fecal?)
-Synergism/Antagonism:
-Addtl facts: Incorporated into forming bone/enamel. Lipophilic (doxy) cross BBB, others no. Esophageal stricture in cats. Don’t give with antacids. Resistance via efflux.
-Examples: Doxycycline, minocycline
Phenicols
-MOA: Inhibit protein synthesis - bind 50s ribosome
-Static/Cidal: Static
-Time/Conc: Time
-Spectrum: Broad spectrum but no enterococci or pseud. All anaerobes (variable based on source)
(G+) - 2-3/4
(G-) - 2-3/4
(An) - 2-3/4
Staph - 2-3/4
Pseud - N
-Elimination: Hepatic conjugation w/glucuronic acid, some urine excretion
-Synergism/Antagonism: Will bind 50s with clindamycin & antagonize (tetracyclines bind 30s)
-Addtl facts: Aplastic anemia in ppl. Dose/duration dependent bone marrow suppression. Peripheral neuropathy. Good CNS penetration. Resistance via enzymatic destruction.
-Examples: Chloramphenicol
Macrolides
-MOA: Inhibit protein synthesis - bind 50s ribosome
-Static/Cidal: Static
-Time/Conc: Time
-Spectrum: Good g+ & anaerobic, variable G-
(G+) - 2-3/4
(G-) - 1-2/4
(An) - 2-3/4
Staph - 2-4/4
Pseud - N
-Elimination: Excreted unchanged in bile
-Synergism/Antagonism: Antagonism with other 50s ribosome binders (e.g. chloramphenicol)
-Addtl facts: Erythromycin binds motilin receptor (pyloric & duodenal contractions); accumulate in WBC
-Examples: Azithromycin, erythromycin
Lincosamides
-MOA: Inhibit protein synthesis - binds 50s ribosome
-Static/Cidal: Static (clindamycin cidal at high conc, high pH?)
-Time/Conc: Time
-Spectrum: Excellent g+ & anaerobe, poor G-. Good for toxo.
(G+) - 4/4
(G-) - 1/4
(An) - 3-4/4
Staph - 3-4/4
Pseud - N
-Elimination: Unchanged in bile (clinda hepatic metabolism)
-Synergism/Antagonism: Antagonize other 50s binders
-Addtl facts: Accumulate in WBC, bile. Can achieve cidal concentrations at some sites. Penetrates biofilm, good for dental dz.
-Examples: Clindamycin, lincosamycin
Nitroimidazoles
-MOA: Inhibits bacterial RNA & DNA synthesis of nucleic acid
-Static/Cidal: Cidal
-Time/Conc: Conc
-Spectrum: Excellent anaerobe, no aerobic, good for protozoal
(G+) - N
(G-) - N
(An) - 4/4
Staph - N
Pseud - N
-Elimination: Microsomal oxidation, glucorinde conjugation with renal excretion.
-Synergism/Antagonism:
-Addtl facts: Good CNS penetration. Rare side effects (Vomiting, nausea, hepatoxicity, CNS). Used for IBD, SIBO, HE, etc.
-Examples: Metronidazole
Oxazolidinones
-MOA: Inhibit protein synthesis, 50s-70s ribosome (unique mechanism @ 50s?)
-Static/Cidal: Static (cidal against strep)
-Time/Conc: Time
-Spectrum: Excellent G+ (including MRSA), no G-
(G+) - 4/4
(G-) - N
(An) - 3/4
Staph - 4/4
Pseud - N
-Elimination: Hepatic metabolization, renal & fecal excretion
-Synergism/Antagonism: May not antagonize other 50s ribosome inhibitors d/t different binding region?
-Addtl facts: 100% oral bioavailability, minimal resistance documented. Mostly used for people.
-Examples: Linezolid
Rifamycin (Rifampin)
-MOA: RNA synthesis - inhibits B subunit of DNA dependent RNA polymerase
-Static/Cidal: Cidal
-Time/Conc: Conc (? - variable)
-Spectrum: Good G+, anaerobic, mycoplasma, no G-
(G+) - 3/4
(G-) - N
(An) - Y
Staph - 3/4
Pseud - N
-Elimination: Hepatic metabolism, bile excretion.
-Synergism/Antagonism: Always use with addtl drug.
-Addtl facts: Generally not used as sole therapeutic - rapid resistance development. Concentrates in WBC, crosses BBB. Enterohepatic circulation, can cause hepatopathy (don’t use in hepatic dz), caution with MDR1.
-Examples: Rifampin
