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21 Cards in this Set
- Front
- Back
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Sulfonamindes:
MOA Selective toxicity activity |
-similar to PABA so block first step of folate synth
-bacteria must synth folate, humans get from diet -static, less effective in presence of pus |
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Sulfonamides:
-admin -distribution -metabolism -excretion |
-oral, topical or IV
-well-distributed, CNS ++++ -liver -renal |
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sulfonamides:
spectrum resistance adverse effects |
-broad
-due to overproduction of PABA, efflux pump, DHPS enzyme mutation -GI distress, hemolytic anemia, SJS |
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Diaminopyrimidines:
-MOA -selective toxicity -activity |
-blocks folate step from DHF to THF
-100,000x more active against bacterial DHFR than mammalian -static, but cidal when combined with sulfonamides |
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diaminopyrimidines:
-administration -absorption/distribution -excretion |
-oral and IV
-good -urine |
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diaminopyrimidines:
spectrum resistance adverse effects |
-broad but no anaerobes
-overexpress DHFR, mutate DHFR -similar to other sulfa, SJS |
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Common uses of diaminopyrimidines
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-UTIs
-otitis media -pneumocystis pneumonia |
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Quinolone:
MOA x2 |
-bind to DNA/enzyme and induce damage
-interferes with DNA gyrase/topoisomerase |
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quinolone:
selective toxicity spectrum |
-low affinity for mammlian DNA gyrase
-cidal, but concentration dependent -Gm- enterics |
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quinolone:
adverse effects |
-GI disturbances, arthropathy (not for kiddos), tendon rupture, hepatotoxicity
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Quinolone:
-absorption -distribution -clearance |
-excellent GI absorption
-distributed to CNS -hepatic or renal clearance depending on drug |
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3 mechanisms of resistance to quinolones:
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-decreased permeability
-efflux pump -mutation of the enzymes |
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What 4 features make mycobacterium tb difficult to tx with drugs
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-slow growth rate, doubling time = 24 hrs
-facultative anaerobe (can go dormant) -high lipid content of cell wall (resistant to dessication) -intracellular pathogen (macrophage) |
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Why do we tx tb w/more than 1 drug
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to combat resistance
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What are the two main drugs used with tb
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-isoniazid and rifampin
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How does isoniazid work
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-inhibits mycolic acid synthesis = cidal to tb
-can be oral or IV/IM |
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How does rifampin work
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-inhibits RNA polymerase
-cidal to tb |
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What is the most effective individual agent against TB
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-rifampin
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What 3 other drugs can be used against TB
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-pyrazinamide (cidal)
-ethambutol (cell wall synthesis inhibitor - static), red/green colorblindeness -streptomycin (inhibits protein synthesis, cidal) toxicity |
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What 3 drugs are used to treat leprosy
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dapsone - like sulfonamide
rifampin - RNA pol inhibitor, given in combo clofazimine - cidal w/adverse effects |
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What is the first line combo used to treat leprosy
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dapsone + rifampin + clofazimine
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