Antimycobacterials Flashcards Preview

Pharmacology Block 3 > Antimycobacterials > Flashcards

Flashcards in Antimycobacterials Deck (10):
1

Tb treatment drugs:

-Rifampin
-Isoniazid
-Pyrazinamide
-Ethambutol
-Streptomycin

2

Rifampin MOA:

Inhibits RNAP, thereby stopping RNA synthesis.

3

Isoniazid MOA:

-Inhibits synthesis of mycolic acids.
-Is a prodrug that is activated by KatG protein of the tubercle bacillus.
-Activated drug target is the enoyl-acyl carrier-protein reductase (InhA).

4

Isoniazid misc:

-All patients with Tb should receive this drug in combination with others.
-May produce peripheral neuritis.
-Watch for polymorphisms in N-acetyltransferase-2.

5

Ethambutol MOA and misc:

-Blocks mycobacterial cell wall synthesis by interfering with arabinosyltransferase.
-May produce optic neuritis, but not heptotoxicity.

6

Pyrazinamide:

-Blocks mycolic acid synthesis by inhibiting fatty acid synthase I.
-Important component of short-term combination therapy due to hepatotoxicity (can lead to severe hepatic damage).

7

Streptomycin class and use:

Aminoglycoside, reserved for only the most serious cases of Tb.

8

Which two drugs are for M. avium-intracellulare (MAC) treatment and prophylaxis?

1. Rifabutin
2. Clarithromycin

9

Dapsone MOA, SEs, use:

MOA: Inhibits synthesis of folic acid

SE: Hemolytic anemia

Use: -Used in combination therapy (rifampin) for leprosy.
-Prophylaxis and treatment of Pneumocystis.
-Genetic polymorphisms in N-acetyltransferase.

10

Clofazimine:

MOA: Binds to mycobacterial DNA, interfering with reproduction and growth.

SE: Red-brown pigmentation in skin.

Use: Combination therapy for leprosy.