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20 Cards in this Set
- Front
- Back
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What is the mechanism of action of fluoroquinolones?
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FQ's inhibit DNA gyrase in Gm(-) and topoisomerase IV in Gm(+).
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How do bacteria become resistant to fluoroquinolones?
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FQ's inhibit DNA gyrase, which is encoded by gyrA and gyrB genes. FQ's bind to the A subunit of DNA gyrase.
gyrA mutations result in significant FQ resistance due to decreased binding affinity of the FQs. gyrB mutations cause a low level resistance and are less common. Resistance to FQ's can also be achieved by efflux of the drug from the bacterial cell. |
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Name the 4 fluoroquinolones discussed in class.
Do these agents show cross-resistance? Three of these agents have higher activity against S.pneumo, including MDRSP. Identify them. |
1) Ciprofloxacin
2) Levofloxacin*** 3) Gatifloxacin*** 4) Moxifloxacin*** ***These agents are more active vs. S.pneumo, including MDRSP. Cross-resistance between FQ's is almost complete. |
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What are the adverse effects of fluoroquinolones?
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--GI disturbance
--rash --CNS disturbaces (headache, vertigo, excitement) --tendon rupture --cartilage damage in kids |
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Why aren't fluoroquinolones recommended for use in children?
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FQ's may damage cartilage which is why they are not used in kids.
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What is the mechanism of action of rifampin?
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Rifampin inhibits DNA-dependent RNA polymerase.
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What are the clinical uses of rifampin?
What are the clinical uses of rifabutin? |
Rifampin is often used in combination to treat tuberculosis, MRSA, legionella and leprosy. Used alone, it can be used to prophylactically treat a person who has been exposed to N.meningitidis or can treat a known N.meningitidis carrier.
Rifabutin is used to treat M.avium. |
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What is the mechanism of action of the sulfonamides?
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Dihydropteroate synthase is a bacterial enzyme that catalyzes the bond between PABA and dihydropteridine. This bond formation is the first step in folic acid synthesis in bacteria.
Sulfonamides are PABA analogs and competitively inhibit dihydropteroate synthetase. This causes depletion of folic acid in the bacteria. Without folic acid, purines and thymidine cannot be synthesized, and, as a result, DNA and RNA synthesis is inhibited. |
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Describe the pharmacokinetics of the sulfonamides..
1) absorption 2) distribution 3) metabolism 4) excretion |
1) Sulfonamides are rapidly absorbed following oral administration.
2) Sulfonamides distribute in extracellular water into CSF 3) Sulfonamides are metabolized by acetylation. 4) They are excreted via the urine |
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How do bacteria become resistant to sulfonamides?
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Bacteria become resistant to sulfonamides in three ways:
1) bacteria increase their PABA synthesis 2) bacteria synthesize altered dihydropteroate synthetase that doesn't bind sulfonamides 3) bacteria use exogenous folic acid |
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List the sulfonamide agents discussed in class.
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1) sulfisoxazole, sulfamethoxazole
2) sulfacetamide 3) silver sulfadiazine 4) sulfasalazine |
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What are the adverse effects associated with sulfonamides?
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--75% of adverse effects involve skin
--drug fever --blood dyscrasias --hepatitis --kernicterus in newborns |
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Identify the sulfonamide agent described by the following..
1) prevents colonization of burns by bacteria 2) treats ulcerative colitis 3) treats UTIs 4) treats conjunctivitis by topical application |
1) prevents colonization of burns by bacteria = SILVER SULFADIAZINE
2) treats ulcerative colitis = SULFASALAZINE 3) treats UTIs = SULFISOXAZOLE, SULFAMETHOXAZOLE 4) treats conjunctivitis by topical application = SULFACETAMIDE |
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How do sulfonamide drugs cause kernicterus in newborns?
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The sulfonamide drugs displace bilirubin from plasma albumin in newborns, causing kernicterus.
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When combined with this drug, sulfonamides are used to treat toxoplasmosis.
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When combined with PYRIMETHAMINE, sulfonamides are used to treat toxoplasmosis.
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What is the mechanism of action of trimethoprim?
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Trimethoprim interferes with folate utilization by inhibiting dihydrofolate reductase.
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Trimethoprim + sulfamethoxazole results in a(n):
a) additive + bactericidal effect b) synergistic + bactericidal effect c) additive + bacteriostatic effect d) synergistic + bacteriostatic effect |
Trimethoprim + sulfamethoxazole results in a:
b) synergistic + bactericidal effect |
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Why doesn't trimethoprim interefere with folate utilization in humans?
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The affinity of TMP is 50,000x greater for bacterial dihydrofolate reductase than mammalian reductase.
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The adverse effects of TMP-SMX are mostly due to:
a) trimethoprim b) sulfamethoxazole What are these adverse effects? |
The adverse effects of TMP-SMX are mostly due to:
b) sulfamethoxazole The major TMP-SMX adverse effect is interference of folate metabolism in malnourished people, which may lead to megaloblastic anemia, leukopenia and granulocytopenia. |
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What are the clinical uses of TMP-SMX?
For which of these uses is TMP-SMX the drug of choice? |
TMP-SMX uses:
--bronchitis --otitis media --Pneumocystis jiroveci*** --conditions in which sulfonamides are ineffective **TMP-SMX is the drug of choice for treatment of pneumonia due to Pneumocystis jiroveci. |
