TB drugs- Allman Flashcards

1
Q

define multidrug-resistant (MDR) TB

A
  • resistant to at lead INH AND RIF
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2
Q

what are MDR patients at high risk for

A

-treatment failure and further acquired drug resistance

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3
Q

what happens to patients with just strain resistant to RIFAMPIN alone

A
  • better prognosis

- increase risk for treatment failure

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4
Q

What is extensive drug Resistant (XDR) TB

A
  • MDR TB plus resistance to FQN
  • AND resistant to at least one other of the 3 injectable drugs
  • amikacin
  • kanamycin
  • capreomycin
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5
Q

what defines therapeutic failure

A

positive sputum coherent scattering after 4 months of compliant therapy

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6
Q

what is the dosing guideline for TB drugs

A
  • daily dosing
  • twice or thrice weekly dosing
  • Directly observed therapy
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7
Q

MOA for Rifampin

A

inhibits DNA-dependent RNA polymerase
- suppression of initiation of chain formation in RNA synthesis

Bactericidal: kills slow-growing mycobacteria present within macrophages and in caseating granulomas

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8
Q

where is Rifampin distributed

A

CNS
tuberculosis abscesses
intracellular sites

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9
Q

How is Rifampin metabolized

A

deacetylation

  • autoinductin of metabolism occurs
  • Rifampin Revs up Liver
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10
Q

3 major adverse effects of Rifampin

A
  • transient elevation in serum transaminases
  • hepatotoxicity
  • orange discoloration ( sweat, tears, urine)
  • Rifampin revs up and red
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11
Q

Drug interaction of Rifampin

A
  • increase in cytochrome P-459
  • increases metabolism of
  • warfarin
  • narcotics
  • steroids ( oral contraceptives)
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12
Q

place in therapy: Rifampin

A
  • treats active TB

- 2nd line agent for preventative therapy

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13
Q

MOA for Isoniazid ( INH)

A

inhibits synthesis of mycolic acid

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14
Q

metabolism of Isoniazid

A

acetylation

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15
Q

Rate of acetylation of Isoniazid depend son what

A

genes: can be slow or rapid acetylator

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16
Q

Adverse effects of Isoniazid

A
  • transient elevation in serum transaminases
  • hepatotoxicity
  • Neurotoxicity
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17
Q

who is neurotoxicity seen in with Isoniazid, treatment?

A
  • alcoholics, homeless

- Pyridoxine ( B6)

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18
Q

MOA for Pyrazinamide

A
  • not well known

- toward dormant organism

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19
Q

Adverse effects of Pyrazinamide

A

Hepatotoxicity

hyperuricemia : decreased renal excretion of uric acid, bad for gout patients

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20
Q

MOA for Ethambutol

A

not well known

bacteriostatic

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21
Q

how is Ethambutol excreted

A

urine

22
Q

Adverse effects of Ethambutol

A
optic neuritis ( retrobulbar neuritis)
-decrease visual acuity and red-green color blindess
23
Q

Ethambutol should be used with caution in what patient group

A

children

24
Q

MOA for Streptomycin

A

Aminoglycoside antibiotic

- inhibit protein synthesis

25
Q

how is streptomycin absorbed and administered

A

poorly absorbed in GI tract

- given IM or IV

26
Q

Adverse effects of Streptomcin

A

nephrotoxicity

impairment of 8th cranial nerve function

27
Q

which is better ethambutol or streptomycin

A

ethambutol

28
Q

when can you not give rifabutin

A
  • unacceptable interactions with Rifampin

- or intolerance to Rifampin

29
Q

Adverse reactions for Rifabutin

A

rash
GI
NEUTROPENIA

30
Q

who can receive Rifapentine

A

HIV negative

- non-cavitary, drug susceptible pulmonary tuberculosis

31
Q

what is the most widely used antilieprosy agent

A

Clofazaime

32
Q

MOA of Clofazaomine

A

binds preferentially to mycobacterial DNA causing inhibition of transcription

33
Q

Adverse effects of Clofazamine

A
  • GI
  • severe and life threatening abdominal pain and organ damage caused by crystal deposition
  • discoloration of skin and eyes
34
Q

how long is general treatment for TB

A

6 months

35
Q

how long is treatment for osteo/miliary/meningitis

A

12-24 months

36
Q

if a TB patient has renal failure what should you avoid

A

Streptomycin
Kanamycin
Capreomycin

37
Q

TB children should avoid what medicine

A

Ethambutol

38
Q

when is suspected treatment failure seen

A
  • lack of clinical progression 6-8 wks into therapy

- add 2 or more new TB agents

39
Q

treatment for Mycobacterium leprae should include

A

Dapsone
Rifampin
Clofazimine
DR. C

40
Q

MOA for Dapsone

A

competitive inhibitor of folic acid synthesis

41
Q

what are 2 major categories for Leprosy

A
  1. lepromatous - disseminated

2. Tuberculoid - localized

42
Q

How is leprosy transmitted

A

prolonged contact

43
Q

how long is drug course of leprosy

A

2-5 years

44
Q

what are symptoms for MAC

A

fever
night sweats
weight loss
anemia

45
Q

Who does MAC usually occur in

A

HIV less than 100 CD4

46
Q

when is primary prophylaxis recommended for HIV MAC

A

CD4 less than 50

47
Q

How do non-HIV patients present with MAC

A

in lungs

chronic productive cough

48
Q

prophylaxis regimen for MAC

A

Clarithromycin
Azithromycin
Alternative Rifabutin if above2 not tolerated

49
Q

Treatment regimen for MAC

A

at least 2 agents

  • Clarithromycin or Azithromycin plus Ethambutol
  • consider adding one of the following: Clofazamine, Rifampin, Rifabutin or Cipro
50
Q

how long is RIPE regiment

A

6 months total

  • 2 months RIPE
  • 4 months RI
51
Q

how long is RIP regiment

A

6 months total

  • 2 months RIPS
  • 4 months RI
52
Q

which drug is more active against MAC

A

Clarithromycin