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37 Cards in this Set
- Front
- Back
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Name 5 important nosocomial infections
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Staph aureus
Acinetobacter baumannii Klebsiella pneumoniae Psuedomonas aeruginosa Enterococcus faecium |
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What are the 2 broad classes of abx?
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Bactericidal (results in cell death) and Bacteriostatic (prevents cell growth; growth resumes when abx are removed)
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What is the Minimum Inhibitory Concentration (MIC)?
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Lowest [] of abx that prevents growth of a specific organism (determined in the lab)
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What is concentration-dependent killing?
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An increase in rate & extent of killing as concentration increases.
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What treatment strategy is used for bacteriocidal drugs that exhibit concentration-dept killing?
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maximize the concentration and decrease the time the drug is administered
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What is time-dependent killing?
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Drugs that kill bacteria at a constant rate as long as the concentration is > MIC.
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Give two classes of abx that exhibit concentration-dependent killing.
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aminoglycosides and fluoroquinolones
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What treatment strategy is used for bacteriocidal drugs that exhibit time-dept killing?
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maximize the time the abx is above the MIC
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Give two classes of abx that exhibit time-dependent killing.
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beta-lactams and vancomycin
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What is Post Antibiotic Effect?
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The time reqd for abx-treated cultures to return to log growth after removal of the drug.
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What are two positive corollaries of post antibiotic effect?
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1. Allows for once daily dosing of drugs that exhibit this effect
2. Decreases toxicity and lowers cost |
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What are superinfections?
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outgrowths of indigenous pathogenic organisms that are normally held "in check" by the competition w/ normal flora
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True or False: Superinfections occur more frequently with broad-spectrum antibiotics?
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TRUE
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How are superinfections generally started?
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Normal flora is eliminated by an antibiotic which allows for the superinfection to grow unabated (it's not affected by the drug).
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True or False: Combining antibiotics is always synergistic?
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FALSE!!! Can by synergistic, antagonistic, or indifferent
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What are three methods by which drug resistance is increasing?
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1. Mutation and selection
2. Uptake of extracellular DNA and homologous recombination (H. flu, Neisseria, Strep) 3. Plasmid-mediated transfer of R-factors |
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What is the mechanism of action of Sulfonamides?
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Analog of PABA --> inhibits Folic Acid synthesis --> inhibits pteroate synthetase
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What is the mechanism of action of Trimethoprim?
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Analog of dihydrofolate --> Inhibits DHFR.
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Why doe sulfonamides and trimethoprim display synergism?
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because they inhibit two distinct steps in the same pathway
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What is the therapeutic use of sulfonamides (alone)?
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Sulfadiazine is used with pyrimethamine for treating toxoplasmosis
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What is the therapeutic use of trimethoprim (alone)?
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None!!!
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What are 4 therapeutic use of TMP/SMZ?
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Broad spectrum coverage:
1. UTIs caused by lots of stuff 2. Resp. tract infxn caused by H. influenza and S. pneumoniae 3. Shigella enteritis 4. PCP pneumonia (AIDS pts) |
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What are the major toxicities of sulfonamides?
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1. hematopoietic disorders
2. hypersensitivity rxns (skin rashes) 3. kernicterus -- protein-bound bilirubin is displaced and deposits in basal ganglia of newborns |
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What is the major drug-drug interaction of sulfonamides?
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potentiates the effects of warfarin by interfering w/ it's metabolism by the CYP450 enzymes.
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What are the major toxicities of TMP/SMZ combination therapy?
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same as for sulfonamides alone plus:
1. meglobalstosis, leukopenia, and thrombocytopenia in pts w/ folic acid deficiency (alcoholics, homeless, malnourished, etc.) 2. rash, fever, hepatitis in AIDS pts being treated for PCP. |
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What are the three major mechanisms of resistance to sulfonamides?
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1. synthesis of an altered Dihydropteroate synthase with lower affinity for the drug.
2. increased production of PABA (up to 70x) 3. reduced uptake of the drug NOTE: These are listed from most to least common |
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What are the 2 major mechanisms of resistance to TMP/SMZ therapy?
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1. Overproduction of DHFR
2. Expression of an altered DHFR w/ reduced affinity for trimethoprim |
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What is the mechanism of action of quinolones and fluoroquinolones?
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Inhibit two enzymes involved in DNA replication:
1. DNA gyrase 2. Topoisomerase IV |
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What are three examples of fluroquinolones?
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ciprofloxacin, oxafloxacin, and norfloxacin
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Why don't fluroquinolones mess up human DNA gyrase?
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They inhibit bacterial DNA gyrase at much lower concentration than mamallian enzyme (topo II) --> This is an example of selective toxicity.
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How are fluoroquinolones administered?
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orally
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What are the 2 major therapeutic uses of fluroquinolones?
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1. UTIs caused by lots of stuff incl. Pseudomonas aeruginosa
2. Enteritis caused by Salmonella, Shigella, E. coli, and Campylobacter |
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True or False: Fluoroquinolones are used for treated Neisseria gonorrhea?
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FALSE
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What are the 3 major toxicities of fluoroquinolones?
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1. Nausea and GI distress
2. CNS effects (confusion, HA, dizziness) 3. Damages growing cartilage --> contraindicated in pts <= 18 yo and pregnant women |
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What are the major drug-drug interactions assoc. w/ fluoroquinolones?
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Inhibits degradation of Theophylline (asthma) and caffeine (heavy coffee drinkers) --> possibly leading to seizures.
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What are the 2 major mechanisms of resistance to fluoroquinolones?
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1. Alterations in the DNA Gyrase and Topo IV that lower affinity for the drug
2. Decreased permeability to the drug. |
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What two agents which are both effective against uncomplicated UTIs are antagonistic and should never be used together?
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Nalidixic acid and Nitrofurantoin
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