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Therapeutics 5 Kappa Epsilon > Exam 4 - Tuberculosis > Flashcards

Exam 4 - Tuberculosis Flashcards

1
Q

what bug causes tuberculosis?

A

mycobacterium tuberculosis

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2
Q

gram stain of mycobacterium tuberculosis?

A

Aerobic
non-spore forming
bacillus

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3
Q

what are factors associated with MDR-TB?

A 
inadequate therapy (monotherapy or suboptimal dose)
Cavitary lesions
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4
Q

what drug combo is most commonly used for active TB treatment?

A

RIPPE

Rifampin, Isoniazid, Pyrazindamide, Pyridoxine (B6), Ethambutol

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5
Q

Mycobacterium tuberculosis:

_____ rich cell wall that contains _______ and is _______ to many durgs

A

Lipid rich
contains mycolic acid
impermeable to many drugs

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6
Q

Transmission of Tb:

Only _____ Tb infections can be transmitted

A

active

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7
Q

Transmission of Tb:

spread by __________

A

aerosol droplets (speaking, coughing, spitting)

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8
Q

what are the extrapulmonary tuberculosis things that can happen?

A

genitourethral tuberculosis
TB w/ arthritis or osteomyelitis
TB menigitis

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9
Q

Issues with HIV and diagnosis of TB?

A

HIV patients have weak immune systems —- they wont have a positive response to skin testing as easily (high false negative rate)

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10
Q

Clinical presentation for TB in healthy patients?

A 
Fever/chills
NIGHT SWEATS
anorexia
wt loss 
cough
hemoptysis/SOB
malaise
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11
Q

Clinical presentation of TB in HIV patients?

A

if early HIV — kinda similar… extrapulmonary at higher risk
if late HIV — v high extrapulmonary disease risk

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12
Q

2 main ways to screen for TB?

A

PPD (purified protein derivative)

IGRAs (interferon gamma release assays)

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13
Q

when to do IGRA over PPD for diagnosis?

A

when pts have rcvd BCG vaccinated

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14
Q

T or F: only need to do drug susceptibility for TB when i HIV pts?

A

false — do it for every isolate!!

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15
Q

Someone is deemed noninfectious when receiving effective therapy, improving clinically, and ??

A

pt has negative sputum smear results for 3 CONSECUTIVE days (each sputum collected on a different day)

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16
Q

what are the 2 phases for TB treatment?

A

intensive phase then continuation phase

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17
Q

If pts have HIV and you want to treat TB….

  • If pts have CD4 < 50 cells/uL start ART within ______ of TB therapy
  • If pts have CD4 >/= 50 cells/uL start ART within ______ of TB therapy
A

< 50: within 2 weeks

> 50: delay ART until 8 - 12 weeks

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18
Q

Rifampin is a hella _______ of CYP

A

inducer

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19
Q

_________ is the most active FQ against M. tuberculosis

A

Moxifloxacin

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20
Q

For MDR-TB:

Treat any patient with ______ resistant TB (or if _____ resistance is absent or unknown with a MDR-TB regimen

A

rifampin resistant; INH resistance unknown

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21
Q

For MDR-TB:

Must include what 3 drugs for sure for treatment?

A 
A FQ (Levo or moxi)
\+
Bedaquiline
\+
Linezolid
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22
Q

Treatment options for latent TB infection?

A

Rifampin QD x 4 mos
INH + Rifapentine once weekly x 12 weeks
INH daily x 6 - 9 mos

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23
Q

INH: how metabolized?

A

by liver — N-acetyltransferase

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24
Q

INH: into CSF?

A

yas – super well

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25
Q

INH: good or bad oral bioavail?

A

good

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26
Q

ADEs of INH?

A

Hepatitis

Neurotoxic = PERIPHERAL NEUROPATHY — give Vit. B6

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27
Q

Dose adjustments for INH?

A

when severe hepatic insufficiency or renal failure

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28
Q

why supplement B6 with INH therapy?

A

INH increases pyridoxine excretion — need it to prevent peripheral neuropathy

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29
Q

INH: inducer or inhibitor of P450?

A

inhibitor

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30
Q

ADEs of rifampin?

A 
Hepatoxicity
discolored urine (sweat and tears)/(orange color) -- can permanently stain contact lenses
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31
Q

ADEs of Pyrazinamide?

A

Hepatoxicity
Hyperuricemia
Joint pain - arthralgias (MCMP notes)

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32
Q

ADEs of Ethambutol?

A 
Peripheral neuropathy
Optic neuritis (can be irreversible if not discontinued)
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33
Q

ADEs of streptomycin?

A

otoxicity
nephrotoxicty
(it is a aminoglycoside!!)

34
Q

Do you renal dose adjust for Pyrazinamide or Ethambutol?

A

Ethambutol

35
Q

ADE with PAS (P-aminosalicylic acid)

A

GI!! -take with meals

36
Q

ADEs of Cycloserine?

A

“PSYCHO-serine”

depression/personality changes/psychosis/seizures

37
Q

INH has to be activated by the ______ protein

A

KatG (comes M.tb)

38
Q

INH forms adducts with _______ and ______

A

NAD+ and NADP+

39
Q

what enzymes are inhibited by the INH/NAD+/NADP+?

A

InhA and KasA (inhibits mycolic acid synthesis)

DHFR (dihydrofolate reductase)

40
Q

Activated INH inhibits _______ which is a component of ________ synthase

A 
inhibits: InhA
FAS II (fatty acid synthase)

(overall affects arabino-galactan – part of mycobacterium

41
Q

Overall INH leads to a ________ (why it is good at killing Tb)

A

leads to defective cell wall

42
Q

INH resistance happens via what?

A

by over expression of InhA

and somehow activation of INH by KatG is stopped (Tb probs stops making Katg)

43
Q

INH is metabolized how?

A

acetylated by N-acetyltransferase

44
Q

INH Toxicity Mechanism:

Acetylisoniazed can become _________ (which I think is a toxic metabolite…)

A

acetylhydrazine

45
Q

INH Toxicity Mechanism:

_______ converts to hepatotoxic metabolites

A

CYP2E1

46
Q

INH Toxicity Mechanism:

_____ can acetylate acetylhydrazine to nontoxic diacetyhdrazine

A

NAT2

47
Q

what does AFB stand for

A

acid fast bacteria

48
Q

what does it mean to be AFB?

A

the bug stains SUPER well and cannot be decolorized

49
Q

Pathology of Tb:

  1. bacteria phagocytosed by alveolar macrophages in the lung/ cause proinflammatory response
  2. Recruited cells (such as _______ cells) will form a _______
A

recruited cells = mononuclear cells

form a granuloma (tubercle)

50
Q

Pathology of Tb:

  1. Granuloma forms a _________ with fewer ________ in later stages
  2. When immune status change containment fails
  3. The granuloma ________ and spills viable/infectious bacilli into airways
A

forms a fibrous sheath; fewer penetrating blood vessels in later stages
granuloma caseates/decays/ruptures

51
Q

Always a 10% lifetime risk of developing active infection when pt has latent Tb

but what things increase risk of activation of Tb?

A

Diabetes
HIV
Old age
malnutrition

52
Q

INH Toxicity Mechanism:
(fast or slow) acetylators will lead to toxic metabolites
(fast or slow) acetylators will remove acetylhydrazine

A 
slow = toxic
fast = removes the toxic metab
53
Q

INH Toxicity Mechanism:

Induction of CYP________ leads to toxic metabolites

A

CYP2E1

54
Q

INH Toxicity Mechanism:

_______ induces CYP2E1 and potentiates INH hepatotoxicity

A

rifampin

55
Q

MCMP reason why we need to supplement B6 with INH therapy?

A

INH inhibits metabolism of pyridoxine to pyridoxal phosphate….

56
Q

How is Pyrazinamid activated?

A

by pncA which is a nicotinamidase from M.Tb

gets converted to pyrazinoic acid

57
Q

Pyrazinamide (PZA) is structurally similar to ________

A

nictinamide

58
Q

Pyrazinamide (PZA):

facts about it being active in relation to pH?

A

NOT active at neutral pH/

WILL BE active if pH < 5.5

59
Q

3 ideas of how Pyrazindamide works?

A
  • inhibition of trans-translation
  • inhibition of aspartate decarboxylase PanD
  • Acidification of cytoplasm followed by disruption of energy metabolism
60
Q

Pyrazinamide MOA Guess: Trans-Translation:

It gets converted to pyrazinoic acid and will bind and inhibit ______________

A

ribosomal protein S1 (RpsA) = proteins won’t fold correctly

61
Q 
PZA = ?
POA  = ?
A 
PZA = pyrazinamide
POA = Pyrazinoic Acid
62
Q

Pyrazinamide MOA Guess: inhibit PanD

panD normally converts ________ to ______

A

L-aspartate to alanine

63
Q

Pyrazinamide MOA Guess: inhibit PanD

(PZA or POA) binds to PanD

A

POA (the activated form) does bind

wont bind to mutant panD tho = resistance

64
Q

Pyrazinamide MOA Guess: inhibit PanD
overall will reduce the accumulation of ________ after the panD step

which will increase levels of _______

A

coA precursors;

free fatty acids

65
Q 
MOA of Ethambutol:
Inhibits \_\_\_\_\_\_\_\_\_\_ (which is involved in \_\_\_\_\_\_\_\_\_)

this causes a build up of ________

A

mycobacterial arabinosyl transferases;
polymerization of arabinogalactan;

build up of arabinan

66
Q

Ethambutol:

is synergistic with _______

A

rifampin (increases penetration into cell)

67
Q

Resistance to Ethambutol happens how?

A

over expression of or mutations of arabinosyl transferase

68
Q

INH:

active against latent, growing or both forms of Tb?

A

JUST growing forms

69
Q

Rifampin:

active against latent, growing or both forms of Tb?

A

both!!

70
Q

Rifampin is most effective when the cell is _______

A

dividing

71
Q

MOA of Rifampin:

Binds to ________ deep within the ________

A

to RNA pol

within DNA/RNA channel

72
Q

Bacteriocidal or Bacteriostatic?
Rifampin?
Ethambutol?

A

Rifampin:cidal
Ethambutol: static

73
Q

Rifapentine:
is a derivative of rifampin
it is more _______ and has a ______ half life

A

lipophilic

longer 1/2 life

74
Q

Which aminoglycoside can be used for Tb?

A

Streptomycin (idk if others cant but they talk about streptomycin…)

75
Q

Streptomycin and Tb:

most active against ______ forms

A

extracellular

76
Q

Streptomycin and Tb:

used mainly when severe tuberculosis (ex: _______ or _______0

A

meningitis or disseminated

77
Q

Bedaquiline:
Given PO or IV?
cidal or static?
active against latent, growing or both forms of Tb?

A

PO
cidal
both!

78
Q

Bedaquiline MOA?

A

inhibits ATP synthase

79
Q

what are some 2nd line agents fro Tb?

A 
FQs
Ethionamide
para-aminosalicylic acid
Cycloserine
Carpreomycin
80
Q

when to consider 2nd line agents for Tb?

A

if resistant to 1st line…
failure of clinical response to first line agents
intolerance of first line
have expert guidance available to deal with toxic side effects

81
Q

why are the 2nd line agents for Tb used as 2nd line?

A

less well tolerated/greater incidence of side effects…..(SHOCKING)

Therapeutics 5 Kappa Epsilon (27 decks)

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