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272 Cards in this Set
- Front
- Back
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What are antibiotics?
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Antibiotics are agents produced naturally by microorganisms to suppress the growth of or to kill other organisms ^
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What are antimicrobials?
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Includes all antibiotics including synthetic preparations ^
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What are bacteriocidal drugs/what do they do and when are they used?
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Bacteriocidal drugs will kill bacteria – used for immunocompromised patients and areas that are hard to reach by the host immune system ^
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What are bacteriostatic drugs/what do they do and when are they used?
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Suppress growth of but not kill bacteria. Host defense mechanisms must help to completely eliminate infecting organisms ^
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What are the factors affecting selection of antimicrobials?
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Identification of offending organism, antimicrobial susceptibility, anatomic site of infection, and pharmacokinetics, allergies, age, pregnancy, host defense (AIDS, cancer, transplant pts) ^
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How is the anatomic site of infection an issue when selecting the proper antimicrobials?
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Isolation from host immune cells (e.g. vegetative heart valve), infection localized in the CNS – the drug administered must be able to cross the BBB. Antimicrobials must get to site of action. ^
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What are some of the pharmacokinetic issues affecting selection of antimicrobials?
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Hepatically metabolized/renally excreted, genetic variation in the hepatic CYP450 microsomal enzymes – possible increase or decrease in metabolism. Renal, hepatic dysfunction = dose adjustment. ^
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Why is pt age an issue in selection of antimicrobials?
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The very young and the very old have reduced metabolic pathways and therefore, potential for greater toxicity. ^
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What is the risk of using antimicrobials prophylactically?
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Risk of superinfection, selection of resistant flora, selection of resistant pathogenic organisms ^
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What are some reasons for prophylactic use of antimicrobials?
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Certain types of meningitis – prevention of spread when highly contagious, rapid spread, very deadly. Damaged heart valves – high risk of endocarditis – prophylaxis prior to dental or GI procedures. Immunocompromised pts. Neutropenic pts, post-splenectomy, GI sx, recurrent UTI, various sx ‘s ^
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What is the indifferent effect of combination of antibiotics?
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Activity together equals sum of separate independent activities (1-1=2) Ceftriaxone/Azithromiacin (covering different organisms) ^
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What is the synergism effect of combination of antibiotics?
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Activity together is greater than the sum of the independent activities (1+1=3) trimethoprim with sulfamethoxazole (increases the effect of both) or PCN /aminoglycosides ^
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What is the antagonism effect of combination of antibiotics
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Activity together isles than thesum of the independent activities. (1+1=1 or <1) Vancomycin with linezolid ^
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When do you consider combining antibiotics?
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Life threatening infections (eg septic shock), polymicrobial infections (eg trauma to the GI tract w/ a breach of bowel integrity, or the immunocompromised), permittance of administration of lower dose to therapeutics to avoid toxicity, desired synergism, prevention of resistant organisms ^
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Name some inhibitors of bacterial metabolism
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Sulfonamides, trimethoprim ^
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Name some inhibitors of bacterial cell wall synthesis
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Betalactams, vancomycin ^
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Name some inhibitors of bacterial protein synthesis
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Tetracycline, aminoglycosides, macrolides, clindemycin, chloramphenicol ^
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Name some inhibitors of nucleic acid function or synthesis
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Fluoroquinolones, rifampin ^
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Name some sulfonamides
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Sulfamethoxzaole, sulfadiazine ^
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What are some indications for the use of sulfonamides?
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Otitis media, meningitis, UTIs, toxoplasmosis, PCP, URIs, stenotrophomonas maltophilia ^
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MOA of sulfonamides?
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Mimics PABA and hihibits bacterial biosynthesis of folic acid ^
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Are sulfonamides bacteriocidal or bacteriostatic?
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Bacteriostatic ^
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AE of sulfonamides?
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Hypersensitivity, hemolytic anemia, megaloblastic anemia, neutropenia, agranulocytosis (rare), crystalluria/hematuria, photosensitivity ^
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DI of sulfonamides?
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PABA (paraaminobenzoic acid) containing compounds (ie: procaine), May potentiate effects of warfarin, sulfonylureas, phenytoin. Bactrim inhibits CYP2C9, ^
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Cross-sensitivity of sulfonamides?
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Thiazides, furosemide, sulfonylureas, sulfones ^
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What drug inhibits dihydrofolate reductase decreasing folic acid synthesis?
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Trimethoprim, bactrim, methotrexate ^
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What drug is often used in combination with trimethoprim?
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Sulfamethoxazole ^
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If a pt is on both bactrim and warfarin what changes would you expect to see in the INR?
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Increase! Bactrim inhibits CYP2C9 which metabolizes warfarin ^
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What is the effect of trimethoprim with sulfamethoxazole? Indifferent, synergistic, antagonistic?
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Synergistic ^
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T/F sulfamethoxazole when used with trimethoprim increases effectiveness and decreases resistance
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TRUE ^
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When would you use trimethoprim alone?
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With sulfonamide allergy or reaction to bactrim. ^
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What drugs prevent the formation of dihydropteroic acid?
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Sulfonamides ^
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What is the drug of choice for leprosy?
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Dapsone ^
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Is Dapsone more or less toxic than the sulfonamides?
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More toxic! ^
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AE of Dapsone?
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Hemolytic anemia, leucopenia, methemoglobinemia, anorexia, N/V, HA, dizziness, nervousness, lethargy, psychosis, mononucleosis-like syndrome (potentially lethal!) ^
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What levels should be checked in a pt taking Dapsone?
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G6PD levels ^
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If a pt is G6PD deficient they are at greater risk for developing _______ and thus, the level MUST be checked prior to starting a pt on Dapsone
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Hemolytic anemia ^
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Can dapsone be used if a pt has an allergy to sulfamethoxazole?
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Yes, if G6PD level is checked. But usually another treatment can be found ^
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What are some of the uses for Dapsone?
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Tx or prophylaxis of PCP or prophylaxis of toxoplasmosis when pt has allergy to sulfamethoxazole ^
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Uses of Phenazopyridine (Pyridium)?
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UTI ^
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Can Phenazopyridine (Pyridium) be used in combination?
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Yes,often used in combination with sulfonamides. ^
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What is the site of antibacterial action for phenazopyridine (pyridium)?
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NONE! It is an anesthetic for the urinary tract ^
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What should pts be told about phenazopyridine (pyridium)?
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Discoloration of urine ^
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What is nitrofurantoin used for?
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UTI (particularly effective against e-coli) ^
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MOA of nitrofurantoin?
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Inhibits a number of bacterial enzymes necessary for protein, DNA, RNA, and cell wall synthesis. ^
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Why is nitrofurantoin used specifically for UTI?
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Because it has a very high concentration in the urine ^
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Is nitrofurantoin bacteriocidal or bacteriostatic?
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Bacteriocidal in urine at therapeutic concentrations ^
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AE of nitrofurantoin?
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GI distress, HSR, HA, vertigo, dizziness, polyneuropathy (high doses), alteration of urince color to dark orange-brown ^
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Why should nitrofurantoin not be prescribed for pyelonephritis or severe UTI?
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Poor tissue penetration ^
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Pts with significant kidney dysfunction should be prescribed nitrofurantoin. T/F?
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FALSE! Should ONLY be used for simple UTI with no other kidney dysfunction ^
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Nitrofurantoin comes in two forms, name them and tell how they are different.
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Macrodantin 4 times/day dosing, Macrobid 2 times/day dosing (longer ½ life) ^
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Can nitrofurantoin be given to pregnant pts?
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Yes, exception: not close to delivery date as it can interfere with newborn enzymes and result in anemia ^
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What is betalactamase?
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An enzyme produced by bacteria to destroy penicillins ^
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Name the Betalactam antibiotics
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Penicillins, penicillins with betalactamase inhibitors, cephalosporins, carbapenems, monobactams. ^
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MOA of betalactams
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Irreversible inhibition of transpeptidase which inhibits cell wall synthesis. Production of bacterial cell lysis ^
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Are betalactams bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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How are betalactams eliminated (except nafcillin)?
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Active renal excretion, urinary excretion. ^
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How does probenacid effect elimination of betalactams?
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Inhibits active renal excretion ^
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Should you prescribe betalactams to a pt with renal impairment?
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Yes, but dose must be adjusted ^
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AE of betalactams?
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Hypersensitivity, IgE mediated anaphylaxis within 20 min., cross sensitivity among agents, GI distress ^
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Difference in betalactams between PCNs, carbapenems, cephalosporins, and monobactams?
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PCNs, carbapenems, and cephalosporins have double ring structure, and monobactam only has single ring structure ^
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What are the naturally occurring penicillins?
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Penicillin G+, Penicillin G benzathine+, Penicillin G procaine+, and penicillin V* ^
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What are the PCNase resistant antibiotics?
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Nafcillin+, Oxacillin+, Dicloxacilln* ^
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What are the amino penicillins?
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Ampicillin*,+, Ampicillin/sulbactam+, amoxicillin*, amoxicillin/clavulanate* ^
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What are the extended spectrum penicillins?
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Piperacillin+, piperacillin/tazobactam+, Ticarcillin+, Ticarcillin/clavulanate ^
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If a pt has a penicillin allergy, what do you need to know about cross-sensitivity in order to prescribe another antibiotic?
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10% or greater cross-sensitivity reaction to cephalosporins. 50% cross-sensitivity reactions to carbapenems. 0% cross-reactivity reactions with monobactams (aztreonam) ^
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What are the 4 sub-classes of PCNs?
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Naturally occurring, PCNase resistant, Amino PCNs, extended spectrum ^
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What is the half-life of Pencillin G?
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0.5hrs ^
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Why is Penicillin G administered parenterally?
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Short half life and destroyed by stomach acid ^
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What is Penicillin G used for?
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Neurosyphilis ^
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AE of penicillin G
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Jarish-Herxheimer (especially after first or second dose of the drug)^
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IM forms of Penicillin G?
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Bicillin L-A (benzatine only), and Bicillin C-R (50/50 benzathine/procaine) ^
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What is Bicillin L-A prescribed for?
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Syphilis (except neuro), prevention of rheumatic fever ^
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Naturally occurring PCNs are used primarily against gram (+/-) organisms and some gram (+/-) cocci such as meningococcus?
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Gram(+)/Gram (-) ^
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How often is bicillin L-A given?
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IM once/week ^
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What should be monitored in pts receiving high amounts of PenG?
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Significant build-up of K+ or Na+, monitor levels ^
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What are the PCNase resistant PCNs?
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Methicillin, Oxacillin, Dicloxacillin ^
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Common uses for PCNase resistant PCNs?
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Methicillin Sensitive StaphAureus (MSSA), Coag negative staph (STACN), and S. pneumonia ^
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AE of methicillin?
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Nephrotoxicity, interstitial nephritis ^
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AE of Oxacillin?
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Hepatotoxic ^
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If a pt has MRSA would you use methicillin?
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NO
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What is ampicillin prescribed for?
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Listeria
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Are ampicillin and amoxicillin used to treat gram + or – organisms?
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Better gram negative coverage, such as non-beta-lactamase-producing H. influenza, E. coli, and P. mirabilis; Salmonella, and shigella ^
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How do you determine whether you want to use ampicillin or sulbactam, or some other antibiotic?
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Sensitivity testing ^
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What betalactamase inhibitors would you use in combination with aminopenicillins for a broader spectrum?
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Sulbactam, clavulanate ^
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What is an aminopenicillin/betalactamase inhibitor used to treat?
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MSSA, H. influenza, N. gonorrhoeae, moraxella catarrhalis, bacteriodes, E. coli, and K. pneumonia ^
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What are exended –spectrum penicillins used for?
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Antipseudomonal activity ^
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What bacteria are extended-spectrum penicillins used against?
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Similar to ampicillin PLUS enterobacter, serratia, P. aeruginosa ^
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If used in combination with a betalactamase inhibitor, what organisms can extended-spectrum penicillins treat?
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Beta-lactamase producing MSSA, E. coli, K. pneumonia, H. influenza, and gram neg anaerobic bacilli ^
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What levels should be checked when prescribing Ticarcillin?
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Has a high Na+ content, monitor Na+ levels ^
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Name the first generation cephalosporins
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Cefadroxil*, cefazolin+, cephalexin*, cephrdadrine* ^
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Name the second generation cephalosporins
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Cefaclor*. Cefotetan+, cefoxitin+, cefprozil*, cefuroxime*+ ^
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Name the third generation cephalosporins
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Cefixime*, Cedinir*, Cefpodoxime*, ceftibutin*, cefditoren*, cefaperazone+, cefotaxime+, ceftazidime+, ceftriaxone+ ^
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Name the fourth generation cephalosporins
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Cefepime+ ^
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Cephalosporin generation designation is based on ____ and ______ to betalactamases
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Spectrum and stability to beta-lactamases ^
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First generation cephalosporins have good gram (+/-) coverage and not as good gram (+/-) coverage
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+ / - ^
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Third generation cephalosporins have good gram (+/-) coverage and not as good gram (+/-) coverage
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- / + ^
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What are the differences between cephalosporins from PCNs?
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Broader spectrum, more resistant to betalactamases, many are ineffective orally due to gastric acid ^
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Which generation of cephalosporins has the broadest spectrum coverage of both gram – and + organisms?
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4th generation ^
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Which cephalosporin has the longest half-life with once/day dosing?
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Ceftriaxone ^
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Which cephalosporin is not renally eliminated but instead uses biliary excretion alone?
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Cefoperazone ^
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Which cephalosporin is best against P. aeruginosa?
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Ceftazidime ^
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Which cephalosporin is better against gram (+) than third generation but is also good against P. aeruginosa?
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Cefepime ^
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Which cephalosporin is excreted both renally and biliary
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Ceftriaxone ^
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Are carbapenems typically administered PO, IM, or IV?
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Parenteral only! ^
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What are the carbapenems?
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Ertapenem, imipenem, meropenem, doripenem ^
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What would be a good DOC for an organism with an extended spectrum betalactamase? (ESBL)
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CARBAPENEMS (resistant to beta-lactamases) ^
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Do carbapenems have a high Vd or low Vd?
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High Vd, distributed to most tissues ^
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AE of carbapenems?
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Seizures (esp. imipenem in those predisposed) ^
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Which carbapenem has a narrower spectrum of activity and may not be effective against p. aeruginosa?
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Ertapenem ^
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_______ is inactivated by renal dipeptidases so it is always used in combination with cilastin, a dipeptidase inhibitor
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Imipenem ^
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What is the name of a monobactam?
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Aztreonam ^
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What is a benefit of aztreonam regarding cross-reactivity with other beta-lactams?
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Very different structure means no cross-reactivity with other betalactams ^
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Aztreonam is effective against gram (+/-) and is anaerobic/aerobic
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Gram -/ aerobic. NO gram+ and NO anaerobic activity. ^
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Is aztreonam effective against P. aeruginosa?
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Yes ^
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Staph aureus produces an enzyme effective against many antibiotics. What is this enzyme?
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Betalactamase ^
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MRSA is a gram (+/-) bacteria
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+ ^
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MRSA is resistant to ______ antibiotics
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Betalactam ^
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Hospital/community acquired MRSA is the most common form
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Community acquired ^
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What is VRE?
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Vancomycin resistant enterococcus faecium/faecalis ^
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2 forms of VRE – name them
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Vancomycin resistant enterococcus faecium and/or faecalis ^
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E. faecalis/faecium is more prevalent
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Faecalis ^
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E. faecalis/faecium is more likely vancomycin resistant
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Faecium ^
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E. Faecalis and E. faecium are gram (+/-)?
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+ ^
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Vancomycin is the mainstay treatment for MRSA or VRE?
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Both as long as the pt does not have VRE ^
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MOA of Vancomycin
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Inhibition of cell wall synthesis ^
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Is vancomycin bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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Is vancomycin given PO or IV?
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IV for systemic infections, PO for C.diff for local antibacterial effect in GI tract. ^
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AE of vancomycin?
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Ototoxicity, nephrotoxicity (rare), hypersensitivity, red man’s syndrome ^
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How is vancomycin excreted?
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Renally ^
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Is red man’s syndrome an allergic reaction?
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No – slow rate of infusion and administer antihistamines with vanco if necessary. ^
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When do you need to check a vancomycin trough?
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Vanco therapy >4 days, unstable renal function, altered Vd such as significant edema, burns, CF, obesity, concomitant nephrotoxic drugs, intermittent or continuous hemodialysis (random level), poor response to vanco, 2nd level in addition to a trough may be necessary for pt specific pharmacokinetics ^
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Vanco displays _____ dependent pharmacokinetics (time/concentration)
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Time ^
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Why do you check the trough instead of the peak for vancomycin?
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Need to make sure the trough is high enough to be therapeutic. Peak not as important ^
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When do you check the first trough for vancomcin?
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Immediately prior to administration of 3rd dose. (within 30 minutes) ^
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MIC?
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Minimum inhibitory concentration ^
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MOA of streptogramins
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Inhibition of protein synthesis via action at 50s subunit ^
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What type of antibiotic is quinupristin/dalfopristin (syndercid)?
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Streptogramins ^
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Are streptogramins bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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Is a quinupristin/dalfopristin (Synercid) administered PO or IV?
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IV only ^
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What is quinepristin/dalfopristin (Synercid) used to treat?
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VRE (E. faecium only) and MRSA ^
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AE of quinepristin/dalfopristin (Synercid)
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Infusion site effects, athralgias, myalgias, increased transaminases ^
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DI of quinepristin/dalfopristin (Synercid)
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Inhibition of CYP3A4 ^
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MOA of Linezolid?
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Inhibition of protein synthesis via inhibition of 70S ribosomal initiation complex ^
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Is linezolid administered PO or IV?
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PO and IV ^
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What is Linezolid prescribed to treat?
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VRE (E. faecium and faecalis), and MRSA ^
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AE of Linezolid?
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N/V/D, thrombocytopenia, elevated transaminases, leucopenia ^
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Drug and food interactions with Linezolid?
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Inhibition of MAO – SEVERE HTN if taken with tyramine-rich foods, serotonin syndrome in combination with SSRIs ^
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Daptomycin MOA?
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Binds to cell membranes and causes cell death via rapid depolarization ^
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Daptomycin is a broad/narrow spectrum gram (+/-) drug.
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Broad, + ^
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Daptomycin is prescribed for the treatment of ?
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MRSA, VRE (E. faecalis, E. faecium) ^
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AE of Daptomycin?
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N/V/C/D, dizziness, HA, insomnia, pruritis, rash ^
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DI of Daptomycin?
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Possible HMG CoA reductase inhibitors (statins) – increased myopathy, elevated CPKs ^
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What is the synthetic derivative of vancomycin (lipoglycopeptide)?
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Telavancin ^
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Is Telavancin administered PO or IV?
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IV ^
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What is Telavancin prescribed to treat?
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MRSA complicated skin/subQ tissue infections ^
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Black Box warning for Telavancin?
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Pregnancy test prior to administration to women of child-bearing potential! ^
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What is the benefit of Telavancin over Vancomycin?
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Less monitoring ^
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Is Telavancin bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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Telavancin displays Time/concentration dependent pharmacokinetics?
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Concentration ^
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What is the new generation cephalosporin (“5th generation”)?
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Ceftaroline ^
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Why is ceftaroline better than ceftriaxone?
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Like ceftriazone except better gram + coverage, covers MRSA skin/skin structure infections, and has a better drug interaction profile ^
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Is ceftaroline administered PO or IV?
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IV ^
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Is ceftaroline bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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Does ceftaroline kill gram neg or pos bacteria?
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Both! Good at gram – and also covers gram + ^
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Ceftaroline is ineffective against what 2 bacteria?
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Enterococcus and pseudomonas ^
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Can ceftaroline be used against MRSA an VRE?
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Only MRSA – ineffective against enterococcus ^
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MOA of tigecycline?
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Inhibits protein synthesis by binding to 30S subunit ^
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Is Tigecycline bacteriocidal or bacteriostatic?
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Bacteriostatic ^
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Is Tigecycline administered PO or IV?
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IV ^
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Tigecycline is effective against gram (+/-) organisms
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BOTH + & - including resistant organisms (MRSA) ^
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AE of Tigecycline?
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GI side effects, teeth/bone effects in children ^
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What drug is structurally similar to tetracycline but is effective against MRSA?
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Tigecycline ^
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What other agents can be used against MRSA/VRE besides vancomycin, linezolid, ceftaroline, telavancin,or Synercid?
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Clindamycin, Clindamycin (bactrim) (at a very different dose than for UTI), minocycline, doxycycline, mupirocin ^
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How is tetracycline administered?
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PO, IV, IM ^
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How is tetracycline eliminated?
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Renal elimination (hydrophilic) ^
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How are doxycycline and minocycline eliminated?
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Hepatically metabolized (lipophilic) ^
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MOA of Tetracyclines?
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Reversible binding to 30S ribosomal subunit, prevents rTNA from binding to rRNA which inhibits protein synthesis ^
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AE of tetracyclines?
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GI distress (minimized w/food), phototoxicity (doxycycline), dose-related vestibular toxicity (minocycline), hepatotoxicity (less w/ tetracycline), permanent tooth discoloration, tooth enamel defects, bone growth retardation in children ^
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Should tetracyclines be prescribed for children?
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No – permanent tooth discoloration, tooth enamel defects, bone growth retardation in children ^
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DI of tetracyclines?
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Dairy products, iron, antacids/laxatives containing cations can decrease absorption (except doxycycline) ^
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Are tetracyclines bacteriocidal or bacteriostatic?
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Bacteriostatic ^
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Spectrum of Tetracyclines?
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Chlamydia, rickettsia, mycoplasma pneumonia, borrelia, minocycline – acne vulgaris ^
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MOA of chloramphenicol?
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Similar to tetracyclines, prevents rRNA from binding to rRNA which inhibits protein synthesis (binds to 50S ribosomal subunit) ^
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Is chloramphenicol administered PO or IV?
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Effective PO, penetrates membranes well, reaches CNS. Can also be given IV ^
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Is chloramphenicol bacteriocidal or bacteriostatic?
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Bacteriostatic ^
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How is chloramphenicol eliminated?
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Hepatically metabolized via conjugation ^
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AE of chloramphenicol?
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Toxic bone marrow suppression, aplastic anemia, Gray Baby Syndrome (infants), ^
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DI of chloramphenicol?
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CYP450 inhibition
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MOA of Clindamycin?
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MOA same as chloramphemicol; prevents tRNA from binding to rRNA which inhibits protein synthesis ^
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Is Clindamycin bacteriocidal or bacteriostatic?
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Bacteriostatic ^
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What type of bacteria is clindamycin effective against?
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Anaerobes ^
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AE of Clindamycin?
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Blood dyscrasias (eosinophilia, leucopenia, thrombocytopenia), pseudomembranous colitis, rash, N/V/D. ^
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How is bactitracin administered? Why?
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Topically, irrigation. Nephrotoxicity limits systemic use ^
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What is mupirocin used to treat?
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Impetigo caused by Staph and Strep ^
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How is mupurocin administered?
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Topically ^
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AE of polymyxin B and Colisitin?
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VERY nephrotoxic ^
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What are polymyxin B and Colisitin prescribed to treat?
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Multi Drug Resistant P. aeruginosa ^
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What drug can be used to treat multidrug resistant P. aeruginasa?
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Polymyxin B and Colisitin ^
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Name the macrolide antibiotics
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Erythromucin, azithromycin, clarithromycin, and telithromycin (ketolide) ^
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MOA of macrolide antibiotics?
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Inhibition of protein synthesis (50S). Overlaps with binding site of clindamycin and chloramphemicol (do not use together). ^
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Are macrolides bacteriocidal or bacteriostatic?
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Bacteriostatic ^
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Macrolides treat gram (+/-) and intra/extracellular bacteria
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+/intracellular ^
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What are macrolides prescribed to treat?
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Chlamydia, mycoplasma, legionella as well as gram + and intracellular bacteria, CAP, acute exacerbation of chronic bronchitis, MAC (azithromycin, clarithromycin) H. pylori (clarithromycin) ^
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Azithromycin has a short/long intracellular half-life?
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Long (even after drug is stopped, the intracellular level is present for several more days – Z-pack) ^
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AE of macrolides?
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GI distress, hepatotoxicity (telithromycin) (benefit may not outweigh the risk if just sinusitis for example), dose dependent ototoxicity ^
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DI of macrolides?
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Erythromycin/clarithromycin/telithromycin –inhibition of CYP3A4, telithromycin substrate of 3A4, erythromycin/azithromycin –biliary excretion, clarithromycin – hepatic, urinary, and biliary excretion ^
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What is the one macrolide that does not interfere with CYP450 enzymes?
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Azithromycin produces least amount of drug interactions, does not interfere with CYP450 ^
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Name the quinolones
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Norloxacin, ciprofloxacin, ofloxcin, levofloxacin, sparfloxacin, lomefloxacin, moxifloxacin, trovafloxacin ^
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MOA of quinolones?
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Inhibit DNA gyrase ^
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Are quinolones bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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How does resistance to quinolones occur?
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Resistance secondary to mutation change in gyrase ^
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Spectrum of Quinolones?
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Gram+, gram -, atypical, Micobacterium tuberculosis. Poor anaerobic coverage ^
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Are quinolones administered PO or IV?
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Both – bioequivalence ^
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How are quinolones eliminated?
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Most really cleared, moxifloxacin –hepatically metabolized, some renally excreted unchanged ^
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AE of quinolones?
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Erosion of cartilage can lead to tendonitis and tendon rupture, QTc interval prolongation, photosensitivity, hepatic damage (trovafloxacin) ^
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DI of quinolones?
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Antacids, and other products containing cations significantly decrease absorption. ^
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Contraindications of quinolones?
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Children, pregnancy, and lactation. ^
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What is ciprofloxacin used to treat?
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Pseudomonas, UTI, intra-abdominal infections ^
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What is Levofloxacin used to treat?
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L-isomer of ofloxacin; UTI, URI; broad spectrum ^
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Moxifloxacin differences from other quinolones?
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Lower kidney concentrations, poor pseudomonos coverage (not good for UTI!) ^
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What is Norfloxacin used to treat?
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BMT prophylaxis ^
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You always want to use the narrowest/broadest spectrum agent to prevent resistance
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Narrowest ^
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Name the aminoglycosides
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Amikacin, gentamicin, Tobramycin (IV, IM), Neomycin (oral, topical), Streptomycin (IM) ^
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How is streptomycin different from other aminoglycosides?
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Structurally, mechanistically, therapeutically different. Only 1st line agent for TB. MOA inhibits initiation of bacterial protein synthesis ^
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MOA of aminoglycosides (other than streptomycin)?
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Irreversible binding to 30S ribosomal subunit, produces misreading of bacterial mRNA resulting in faulty bacterial protein synthesis ^
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What class of antibiotic causes irreversible binding to the 30S ribosomal subunit producing misreading of bacterial mRNA resulting in faulty bacterial protein synthesis?
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Aminoglycosides ^
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Are aminoglycosides bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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Are aminoglycosides time/concentration dependent?
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Concentration dependent ^
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Aminoglycosides have a synergistic effect with what class of antibiotics?
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Betalactams ^
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Aminoglycosides are effective against gram (+/-) including pseudomonas?
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Gram - ^
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Aminoglycosides are hydrophilic/lipophilic?
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Hydrophilic ^
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Do aminoglycosides produce good CNS penetration?
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No! hydrophilic, not significantly metabolized – lack of CNS penetration ^
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AE of aminoglycosides?
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Ototoxicity (streptomycin > amikacin = gentamicin = tobramycin), Nephrotoxicity (neomycin > amikacin = gentamycin = tobramycin > streptomycin) Neuromuscular blockade w/ high doses ^
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What should be monitored when a pt is taking aminoglycosides?
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Serum creatinine, peak & trough levels if unstable renal function or volume status, poor clinical response, or change in aminoglycoside dose. Peak level not necessary when using gentamycin for gram+ synergy. Rough levels obtained for synergy but NOT if dose is adjusted for renal function. ^
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When drug levels in plasma have subsided (are at 0) and yet the drug continues to have an effect, this is called?
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Post-antibiotic effect ^
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What class of antibiotics has a post-antibiotic effect?
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Aminoglycosides ^
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When should peak level of aminoglycosides be drawn?
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Draw AFTER 3rd dose (30minutes after the end of the infusion). ^
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When should trough level of aminoglycosides be drawn?
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Draw PRIOR to 3rd dose; within 30 min before administration of 3rd dose. ^
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When should a random level for aminoglycosides be drawn for a pt on dialysis?
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Draw 2 hrs after end of dialysis ^
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How to prevent antibiotic resistance?
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Choose narrowest spectrum possible, check sensitivity, only administer antibiotics when necessary ^
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What is the most common cause of TB?
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M. tuberculosis ^
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What 2 types of Mycobacterium are typically only found in immune suppressed pts?
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M. avium and M. kansasii ^
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Mycobacterium has a slow/fast growth rate and intra/extracellular location?
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Slow/intracellular ^
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T/F treatment for TB is short and only one drug is necessary to treat.
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FALSE treatment is anywhere from 6 mos-2yrs and combination therapy is necessary to prevent resistance prior to irradication ^
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First line TB agents?
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Isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin ^
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Usually, after 2 mos of treatment a pt with TB can reduce medications to just 2, which 2 medications are these?
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Isoniazid and rifampin ^
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Second-line TB agents?
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Aminoglycosides (amikacin, kanamycin), moxifloxacin, levofloxacin, capreomycin, cyclosterine, p-aminoslicylic acid, and ethionamide ^
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MOA of isoniazid?
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Inhibits synthesis of mycolic acid, an important component of the cell wall of mycobacteria ^
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AE of isoniazid?
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Hepatotoxicity, esp in slow acetylators, neurotoxicity (prevent with B6) ^
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What are the 2 main uses for isoniazid?
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Active TB and latent TB (LTBI) (positive PPD but no active disease at this time). ^
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MOA of rifampin?
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Inhibits DNA-dependent RNA polymerase (not specific to mycobacteria) ^
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What drug is used alone or in combination for treatment of LTBI?
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Isoniazid ^
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AE of rifampin?
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Hepatotoxicity ^
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Important to inform pts about rifampin?
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Orange-red color to all body secretions! Tears, sweat, urine etc… ^
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DI of rifampin?
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Broadly and significantly induces CYP450 and glucoronidation enzymes decreases efficacy of other drugs. (ie: protease inhibitors – drug levels will plummet and will not be recoverable. If no other option available, try rifabutin) ^
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What is rifabutin?
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Part of the rifamycin drug class, alternative to rifampin, less drug interactions compared to rifampin. ^
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How is rifabutin metabolized?
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CYP3A4 ^
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AE of rifabutin?
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Neutropenia, uveitis ^
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MOA of ethambutol?
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Inhibits incorporation of mycolic acids into mycobacterial cell wall ^
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AE of ethambutol?
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Optic neuritis ^
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How is ethambutol excreted?
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Renally eliminated ^
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MOA of Pyrazinamide?
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Unclear ^
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Is pyrazinamide bacteriocidal or bacteriostatic?
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Bacteriocidal ^
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Which of the four first-line TB agents is the only one to be renally eliminated and therefore must be dose adjusted with renal impairment?
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Ethambutol ^
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What is the problem with using pyrazinamide alone to treat TB?
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Resistance develops rapidly if used alone ^
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AE of pyrazinamide?
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Dose-related hepatotoxicity ^
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The metabolite of pyrazinamide causes ______
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Hyperuricemia ^
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What 3 of the four first-line TB agents can cuase hepatotoxicity?
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Isoniazid, rifampin, & pyrazinamide ^
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MDR-TB involves resistance to what drugs? (multi drug resistant)
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INH and rifampin ^
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XDR-TB involves resistance to what drugs?
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INH and rifampin plus any fluoroquinolone and one second-line injectable drug ^
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How does resistance to TB medication occur?
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Transmitted resistant TB, non-adherance to medication regimen, inappropriate or incomplete treatment by provider. ^
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