Antibiotics used for Tuberculosis Flashcards

1
Q

Why is TB hard to treat?

A
it is slow growing.
It is intracellular
It develops resistance quickly
Patient compliance
Drug Toxicity
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2
Q

What are the first-line therapies for M. tuberculosis?

A

Combo of Isoniazid, Rifampin, pyrazinamide, and ethambutol (or streptomycin).

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3
Q

What are the first-line therapies for M. Avium complex?

A

clarithromycin and ethambutol (or clofazimine or ciprofloxacin or amikacin)

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4
Q

What is most effective treatment for Latent TB?

A

INH-RPT with direct observed therapy.

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5
Q

Who is INH-RPT not recommended for?

A

children < 2 years of age and HIV patients on HAART

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6
Q

What is the MOA of isoniazid?

A

interferes with mycolic acid synthesis. Bacteriostatic. Penetrates host cells so good for intracellular.

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7
Q

What is the primary elimination route of isoniazid?

A

Metabolized in liver. 75% excreted in urine. No dosage adjustment necessary for renal failure.

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8
Q

What are the main adverse effects of isoniazid?

A

Hand-foot neuropathy. Hepatotoxicity. Give Vitamin B6 supplements to prevent Hand-foot neuropathy.

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9
Q

What are contraindications of isoniazid?

A

Can’t give with antacids containing Al.

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10
Q

What is the MOA of rifampin? Resistance?

A

inhibition of RNA synthesis, binds B subunit of RNA polymerase. Bactericidal.
Resistance if DNA-dependent RAN polymerase does not bind drug. Effective against slow growing and rapidly dividing cells. First line drug for TB

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11
Q

What are the main adverse effects of rifampin drugs?

A

discolors body fluid to orange-red. Hepatotoxicity, P450 interactions. No adjustment needed for renal failure.

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12
Q

What is the MOA of ethambutol? Resistance?

A

inhibition of RNA synthesis. Disruption of cell wall synthesis by inhibiting arabinosyl transferase.
Bacteriostatic. Bacilli MUST be rapidly dividing. Not good for latent phase.

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13
Q

What is the most active antileprosy drug?

A

Rifampin - inhibition of RNA synthesis by binding B subunit of RNA polymerase.

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14
Q

What are the main adverse effects of ethambutol? Any contraindications?

A
optic neuritis (vision problems) and hyperuricemia.
Cant give with antacids.
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15
Q

What is MOA of pyrazinamide?

A

Bacilli convert pyrazinamide to pyrazinoic acid and this decreases pH below growth threshold. Cidal and static. Active against tubercle bacilli intracellularly.

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16
Q

What are main adverse effects of pyrazinamide?

A

hepatotoxicity, non-gouty arthralgia, hyperuricemia. Must stop is gout occurs.

17
Q

What is MDR TB?

A

resistant to the two best antibiotics, isoniazid and rifampin.

18
Q

What is the MOA of cycloserine?

A

broad spectrum, second line agent. Blocks cell wall synthesis. It is a structural analog of D-alanine. cidal or static. Not protein bound.

19
Q

What are main adverse effects of cycloserine?

A

CNS problems and suicidal tendencies. Contraindicated in history of epilepsy.

20
Q

What is XDR TB?

A

resistant to two best antibiotics, INH and RIF, as well as most of the alternative drugs.