TB meds-Table 1 Flashcards

1
Q

What is mycobacterium?

A

Slow-growing, slender rod shaped aerobic with a lipid rich cell wall
Can remain dormant in the host for long periods of time

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2
Q

What does mycolic acid do?

A

Makes up60% of the cell wall of mycobacterium and makes it relatively impermeable to many abx

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3
Q

Where can mycobateria reside?

A

Inside non activated macrophages

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4
Q

What is the importance of living in the macrophages?

A

Creates another permeability barrier

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5
Q

What is the defining pathologic feature of TB?

A

Granuloma mass enclosed by mono, lympho, and neutrophils recruited by an inflammatory response around the foamy macrophages within a fibrous cuff

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6
Q

What is the MOA of isoniazid (INH)?

A

Inhibition of cell wall synthesis by inhibiting mycolic acid synthesis through the formation of reactive oxygen radicals and isonicotinic acid

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7
Q

Is INH cidal or static?

A

Static in the stationary phase and cidal in the rapid dividing phase

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8
Q

What metabolizes INH?

A

N-acetylation and hydrolysis

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9
Q

Is there cross-resistance in INH?

A

No cross resistance to other TB drugs

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10
Q

What are the ADRs of INH?

A

Peripheral neuritis ( B6 def, make sure you supplement)
Hepatitis/hepatotoxic
Inhibits phenytoin met and may produce convulsions in pts prone to seizures

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11
Q

What is the most severe side effect of INH? What increase this effect?

A

Hepatitis/ hepatotoxicity- rifampin and EtOH

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12
Q

What is the Black Box warning associated with INH?

A

Severe and sometimes fatal hepatitis associated with isoniazid therapy may occur and may develop even after many months of tx

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13
Q

What are the rifamycins?

A

Rifampin, rifabutin, rifapentin

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14
Q

What is the mechanism of rifampin?

A

Blocks transcription by interacting with the Bsub unit of bacterial DNA-dependent RNA polymerase

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15
Q

Is INH or rifampin have a greater antimicrobial spectrum?

A

Rifampin

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16
Q

Is rifampin static or cidal?

A

Cidal against gram + and –

17
Q

When is rifampin used prophylactically?

A

Individuals exposed to meningitis

18
Q

What is rifabutin?

A

Analog of rifampin active against mycobacterium avium complex but less active against TB

19
Q

What is rifapentin?

A

Newer, induces 3A4

20
Q

How are the rifamycins administered?

A

Orally to get to all body fluids and organs

21
Q

What doe the rifamycins induce?

A

Hepatic mixed function that oxidases increasing its own metabolism as well as other drugs like OCPs

22
Q

How are the rifamycins eliminated?

A

Feces and urine- may give orange red color

23
Q

What should you warn contact lens wearers about?

A

Tears may permanently stain soft lenses orange red

24
Q

What are the ADRs of rifamycins?

A

Minor- N/V

25
Q

What is the MOA of pyrazinamide?

A

Bactericidal.

1) Enters Mtub by passive diffusion, converted to POA by nicotinamidase/pyrazinamidas (PZase)
2) Inhibits fatty acid synthase I- stops mycolic acid biosynthesis
3) Accumulates w/in acidic environment of macrophages and monocytes and kills tubercle bacilli – help prolong therapy

26
Q

What are the ADRs of Pyrazinamide?

A

Liver injury with jaundice- rarely fatal

27
Q

What should you do if tx with pyra?

A

Get liver fxn tests! Shouldn’t tx if they have preexisting liver dysfxn

28
Q

What is the MOA of ethambutol?

A

Static

Inhibits cell wall synthesis by inhibiting synthesis of polysaccharides and transfer of mycolic acids to the cell wall

29
Q

What is the role of ethambutol?

A

Helps to prevent the emergence of RIF resistant organisms when primary resistance to INH may be present

30
Q

What are the ADRs of Ethambutol?

A

Optic neuritis – most imp
Diminished visual acuity and loss of green red discrimination – do visual exams
Decreases urate excretion – careful if gout