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Pulmonology > Suttle Treatment of Tb > Flashcards

Suttle Treatment of Tb Flashcards

1
Q

bactericidal treatments require…

A

bacteria to be actively growing

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2
Q

Tb can survive within

A

macophages–> making them resistant to AB’s

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3
Q

general course of tx for TB infection

A

multi-agents (will become resisitant to single therapy) and for a protracted course of tx.

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4
Q

First line therapy against M. tuberculosis

A

INH + RIF+ pyrazinamide + (ethambutol or streptomycin)

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5
Q

First line tx for MAC

A

Clarithromycin + ethambutol or clofazamine or cipro or amikacin

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6
Q

why is rifabutin better than rifampin

A

less potent CYP inducer

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7
Q

why is rifampentene better than rifampin

A

longer half-life (once weekly dosing)

*intermediate CYp inducer

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8
Q

best LATENt therapy

A

IND-RPT under DOT

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9
Q

who does not get INH-RPT

A

, 2, pregnant, HIV, LTBI with INH or RIF resistance

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10
Q

Active cases of TB get what dosing regimine

A

initial phase –> 8 weeks
continuation phase-> 18 weeks
*2-4 drugs taken for 26 weeks on different dosing schedules

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11
Q

how to ensure compliance

A

DIRECT OBSERVED THERAPY

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12
Q

HIV NEGATIVE PT’S WITH NEGATIVE AFB SPUTUM AND CHEST X RAY CAN GET
*AFTER INHITIAL PHASE

A

CONTINUATION PHASE OF OCE WEEKLY INH/RPT

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13
Q

ISONIAZID TARGETS

A

cell wall synthesis

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14
Q

ethambutol targets

A

cell wall synthesis

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15
Q

pryazinamide targets

A

unknown–> disrupts plasma membrane and enables energy metabolism

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16
Q

MOA for isoniazid

A

interferes with mycolic acid synthesis

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17
Q
  • cidal for rapidly dividing bacilli

* static for latent/ slow growing

A

isoniazid

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18
Q

resistance to isonizaid

A

inability to take up the drug, alteraiton of taret enzyme, overproduction of target enzyme,
*rapid resistance, never as mono thereapy

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19
Q

metabolism of Isoniazid

A

acetylated by Nacetyl transferease
*chronic liver disease will decrease metabolism
normal half life 1-4 hours depending on acetylaiton status
(slow vs fast acetylators)

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20
Q

excretion of isoniazid

A

75% in the urine

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21
Q

can isoniazid reach therapeutic levels in the brain

A

yes, rapidly absorbed from GI (oral or IM) cna distributes to all tissues

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22
Q

Adverse effects of isoniazid

A

peripheral neuropathy
B6 depletions (competes with pyridoxal phosphate)
hepatotoxicity
allergic rxns )not dose rleated)

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23
Q

drug interactions

A

drugs with Al+ salts, give 1 hour prior to antacids
corticosteroids decrease efficacy
CYP inhibitors–> caution with phenytoin, diazepam, fluoxetine, nelfavir,

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24
Q

MOA for rifampin

A

inhibitio of RNA synthesis bind RNA pol beta subunit)

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25
Q

is rifampin cidal or static

A

cidal

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26
Q

resistance to RIFAMPIN

A

DNA dependent RNA polymerase does not bind drug, never given as mono therapy

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27
Q

spectrum of rifampin

A

intra or extracellular mycobacterium

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28
Q

name the rifamycins

A

rifampin, rifapentine, rifabutin *RIF is most common

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29
Q

Distribution of rifampin

A

well absorbed, distributes to tissues well, 75% bound to proteins+ CSF

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30
Q

absorption problems with rifampin

A

impaired by food of para-aminosalicylic acid

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31
Q

does rifampin get into the CSF

A

yes

32
Q

metabolism of Rifampin

A

deacetylated in the liver–> stil ctive just not re-absorbable (facilitates excertion)

33
Q

excetion of rifampin

A

bile (30% unchanged), small amount renal secretion

34
Q

adjustment for rifampin in renal insufficiency

A

NONE

35
Q

impairement of rifampin half life

A

increased by hepatic dysfunction

36
Q

adverse effects of rifampin

A

discolors body fluids, (orange red), hepatotoxicity, Nervous complaints,

37
Q

Drug interactions with rifampin

A

induces CYP’s–> reduces half life of pred, ketocon, NNRTI’s etc.
oral contraceptives less effective and anticoags less effective

38
Q

which drug icreases serum concentration of rifampin

A

probenacid

39
Q

rifampin can cuase death from

A

liver failure–> in pt.’s with hepatitis, and chornic liver diseae, on other hepatotosic drugs and alcohol

40
Q

only cyp not induced by Rifampin

A

2d6

41
Q

Other uses of rifampin

A

first line for MB TB rapid and slow
–> MRSA, Leprosy, eradiates nasal staph, prophylactics for household members exposed to H flu or meningococcal meningitis

42
Q

ethambutol MOA

A

INhibits RNA synthesis ??*

disrupts cell wall (arabinosyl transferase)

43
Q

spectrum of Ethambutol

A

static–> cidal at higher concentrations

*bacillia must be actively dividing

44
Q

resistance to Ethambutol

A

slow, no cross resistance

45
Q

Distribution of Ethambutol

A

wide–> concentrates in (kidneys, lungs, saliva), CSF access +, placenta crossing, breast milk as well

46
Q

eliminiation of ethambutol

A

pertially metab. n liver, excerted in urine,

47
Q

half life of ethambutol

A

3.5 hours–> up to 15 hours in kidney disease

48
Q

absorptoin of ethambutol

A

75%with oral dosing

49
Q

adverse rxns with ethambutol

A

optic neuritis (loss of visual accuity, color blind, reversible)
allergic rhinitis
hyperuricemia

50
Q

interactions with ethambutol

A

Al++_ antacids reduce absorption

51
Q

before ehtmabutol therapy begins pt. must have

A

vision test, and must be monitored throughout treatment

52
Q

MOA for pyrazinamide

A

?????

decreases pH below threshold growth

53
Q

bacilli conver pyrazinamide to

A

pyrazinoic acid

54
Q

resistant strains

A

lack pyrazinamidase

55
Q

cidal or static for pyrzainamide

A

depends on cencentration

56
Q

Is pyrazinamide therapeutic in CSF

A

yes

57
Q

metabolism pf pyrazinamide

A

liver and excreted in urine via Glomerular filtration not secrteion

58
Q

adverse effects of pyrazinamide

A

dose related hepatoxocity

  • -> non-gouty arthritis
  • ->hyperuricemia
59
Q

MDR TB-> definition

A

cannot be killed by INH or rifampin

60
Q

TX for DMR -TB and MAC when other dont work and for UTI’s

A

cycloserin (broad spectrum)

61
Q

MOA for cycloserine

A

cell wall inhibition of synthesis
(strcutural analog od D-alanine–> can block L alanine racemase and D alanine synthase–> required for encorporation into peptidoglycan strands)

62
Q

Cycloserine cidal or static

A

depends on concentraiton

63
Q

Canc cylsoerine penentrate meninges

A

yes 86% noninflammed, 100% inflammed

64
Q

can cycloserine cross placenta

A

yess—immensely

65
Q

excretion of cycloserine

A

unchanged by renals (change dose for Renal impairment)

66
Q

distribution of cycloserine

A

widely, 70-90% absorbed from GI, NOT PROTEIN BOUND< lungs, pleura, synovial folds)

67
Q

adverse effects of cycloserine

A

Central Nervous system (suizide, seizure)

68
Q

Cycloserine containdicated in pt’s with

A

epilepsy

69
Q

ethonamide MOA

A

inhibits peptide synthesis

70
Q

structural analog of isoniazid

A

ethonamide

71
Q

why is ethonamide reserved as last line agent

A

GI
Neuro
Hepato-toxicites

72
Q

given along side Ethonamide

A

pyridoxine (reverses CNS disturbances)

73
Q

ethonamide is active or inactive as adinsiteres

A

inactive, activated by bacerial redux system

74
Q

resistance to ethonamide

A

rapid, never a solo drug, can icnrease resistance to isoniazid

75
Q

XDR-TB

A

inh and RPt resistance + alternatives (floroquinolones and any one of 1. amikacin, kinamycin, capreomycin)
*aminoglycosides

76
Q

static drug reserved for last ditch effor to treat XDR TB

A

cepreomycin

bad side effects–>IM route

77
Q

side effects of Capreomycin

A

nephrotoxicity and ototoxicity

Pulmonology (10 decks)

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