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Pharmacyology 3 > Anti-TB > Flashcards

Anti-TB Flashcards

1
Q

innate resistance TB

A
  • highly complex
  • impermeable mycobacterium wall
  • efflux transporters
  • intracellular location of infection
  • slow proliferation, dormancy
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2
Q

Acquired resistance TB

A
  • spontaneous mutations (therapy long term)

- each mutation confers resistance to one drug

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3
Q

mutation frequency in TB

A

1 in 10^6

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4
Q

The chance of one bacterium developing resistance to 2 drugs is

A

1 in 10^12

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5
Q

What reduces incidence of relapse in TB?

A

multi drug therapy

- some drugs are effective against active bacilli other against dormant

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6
Q

Why dose multi drug anti-TB therapy not lead to superinfection?

A
  • standard drugs highly selective for TB
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7
Q

MDR to TB due to what? and what drugs?

A

Isoniazid + rifampin

  • inadequate drug therapy
  • lack of compliance
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8
Q

Extensive drug resistance (XDR)

A

MDR + fluoroquinolone and aminoglycosides

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9
Q

INH MOA

A
  • inhibit synthesis of mycolic acid

- prodrug activated by KatG

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10
Q

INH bactericidal or bacteriostatic?

A

bactericidal –> active

bacteriostatic –> quiescent

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11
Q

INH active against extracellular or intracellular?

A

both!

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12
Q

INH resistance

A

mutation or deletion of katG gene

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13
Q

INH in host liver

A

NAT2 –> inactive

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14
Q

INH in bacillus

A

KatG –> INH radical –> active form

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15
Q

INH metabolism

A
  • inactivated by liver by acetylation

- N-acetyl-INH excreted by kidneys

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16
Q

Which drug has slow or rapid acetylators?

A

INH

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17
Q

T/F acetylator status effects dosing and therapeutic outcomes?

A

false!

dose not

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18
Q

INH use

A

Latent: alone
Active: combo

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19
Q

Adverse reaction INH

A
  • peripheral neuropathy
  • hepatotoxicity
  • hepatitis
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20
Q

peripheral neuropathy in INH

A
  • caused by drug induced deficiency in pyridoxine
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21
Q

peripheral neuropathy in INH can be reduced by

A

taking B6

22
Q

BBW INH

A

hepatitis: fatal hepatic necrosis

23
Q

Rifampin MOA

A

inhibit DNA dependent RNA polymerase

24
Q

Rifampin bacteriostatic or bactericidal?

A

bactericidal

25
Q

Rifampin for intracellular or extracellular organisms?

A

intracellular

26
Q

Rifampin resistance

A
  • mutation in rpoB gene for B subunit

- not used for mono therapy!

27
Q

Rifampin use

A

active: combo with INH
MAC: combo with macrolide
serious deep seated staph infection: combo with other antibiotics

28
Q

Rifampin adverse reactions

A
  • hepatotoxicity: cholestatic jaundice
  • discoloration of body fluids (red/orange)
  • strong induction of CYP
29
Q

Which drug can increase elimination of contraceptives, warfarin and hIV drugs?

A

rifampin

30
Q

Ethambutol MOA

A

inhibit mycobacterial arabinosyl transferase

31
Q

Ethambutol bacteriostatic or bactericidal

A

bacteriostatic

32
Q

Ethambutol intracellular or extracellular organisms

A

both!!!

33
Q

ethambutol resistance

A

mutation of embAB

34
Q

Ethambutol use

A

active: combo

MAC

35
Q

ethambutol adverse effect

A

optic neuritis (loss of visual acuity, red/green blindness)

36
Q

Pyrazinamide MOA

A
  • prodrug converted to POA (active in acidic conditions)

- molecular target unknown

37
Q

Pyrazinamide bacteriostatic or bactericidal

A

bactericidal

38
Q

pyrazinamide intracellular or extracellular oganisms

A

intracellular organisms

39
Q

Pyrazinamide use

A

combo

40
Q

Pyrazinamide adverse effects

A
  • hepatotoxicity

- hyperuricemia

41
Q

2nd line antimycobacterial agents

A

streptomycin

42
Q

Streptomycin use

A

severe life threatening TB

43
Q

streptomycin intracellular or extracellular organisms

A

extracellular

44
Q

TB prophylaxis use

A
  • high risk patients with latent infections to prevent emergence of active
45
Q

TB prophylaxis therapy

A
  • daily mono therapy 9 months: INH

- daily mono therapy 4months: rifampin alternative

46
Q

TB combination therapy use

A

confirmed active infection

47
Q

2 phases of TB combo therapy

A 
induction phase (first 2 months)
continuation phase (next 4 months)
48
Q

Induction phase TB

A

Rifampin, INH, pyrazinamide, ethambutol

49
Q

Goal of induction phase TB

A
  • eliminate actively dividing extracellular organisms
  • render non-infectious
  • prevent development of resistance
50
Q

Most common cause of treatment failure in induction phase TB

A

non-adherence

- Directly observed therapy (DOT) is standard of care

51
Q

Continuation phase TB

A 
intermittent therapy (2 weekly): INH + rifampin
- may prolong to 7 months if more severe
52
Q

In continuation phase TP what should you monitor for?

A

hepatotoxicity

Pharmacyology 3 (12 decks)

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