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TB and Mycobacterium Treatment
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Why use multi-drug therapy with active TB?
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-enhances rates of response/cure
-reduces emergence of resistance
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Terms in this set (57)
Why use multi-drug therapy with active TB?
-enhances rates of response/cure
-reduces emergence of resistance
What are methods of increasing adherence/Rx completion?
-shortest possible course of therapy
-DOT
Why do you need an adequate duration of TB therapy?
-increase cure rate
-reduce relapse
How is Isoniazid HCL used clinically?
-first line drug for active pulmonary TB
-used in combo with at least 2 other active drugs, except for when treating LTBI
What is the MOA of INH?
-pro drug that is activated by catalase peroxidase
-targets inhA gene products (cell wall my colic acid)
Is INH cidal or static?
-cidal for replicating organisms
-static for resting organisms
what is the gene which encodes catalase peroxidase?
TB katG gene
How dose INH resistance develop?
-mutations in the katG gene
-mtuations in the inha gene
how is INH acetylation rate controlled?
genetics (slow, rapid, nl)
does INH reach the CNS?
you bet
What is INH toxicity?
-Hepatotoxic
-Neurotoxic
-Hypersensitivity Rxn
How can you reduce neurotoxicity in INH therapy?
-give them Vitamin B6 (pyridoxine)
What are some notable INH drug interactions?
-rifampin (hepatitis)
-Dilantin (reduced clearance)
-intraconazole and levadopa (dec. levels)
What are the clinical uses of Rifampin?
-first line for TB (in combo , xc for LTBI)
-Gram + like S. aureus in combo
-N. meningitidis (alone)
Why can't you use Rifampin alone?
-rapid development of resistance