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Pharm > Block V- Pulm TB & Mycobacterium Treatment > Flashcards

Block V- Pulm TB & Mycobacterium Treatment Flashcards

1
Q

Why use multi-drug therapy with active TB?

A
  • enhances rates of response/cure

- reduces emergence of resistance

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2
Q

What are methods of increasing adherence/Rx completion?

A
  • shortest possible course of therapy

- DOT

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3
Q

Why do you need an adequate duration of TB therapy?

A
  • increase cure rate

- reduce relapse

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4
Q

How is Isoniazid HCL used clinically?

A
  • first line drug for active pulmonary TB

- used in combo with at least 2 other active drugs, except for when treating LTBI

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5
Q

What is the MOA of INH?

A
  • pro drug that is activated by catalase peroxidase

- targets inhA gene products (cell wall my colic acid)

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6
Q

what is the gene which encodes catalase peroxidase?

A

TB katG gene

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7
Q

How dose INH resistance develop?

A
  • mutations in the katG gene

- mtuations in the inha gene

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8
Q

does INH reach the CNS?

A

you bet

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9
Q

What is INH toxicity?

A
  • Hepatotoxic: inc w/ pregnancy
  • Neurotoxic
  • Hypersensitivity Rxn
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10
Q

How can you reduce neurotoxicity in INH therapy?

A

-give them Vitamin B6 (pyridoxine)

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11
Q

What are some notable INH drug interactions?

A
  • rifampin (hepatitis)
  • Dilantin (reduced clearance)
  • intraconazole and levadopa (dec. levels)
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12
Q

What are the clinical uses of Rifampin?

A
  • first line for TB (in combo , xc for LTBI)
  • Gram + like S. aureus in combo
  • N. meningitidis (alone)
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13
Q

Why can’t you use Rifampin alone?

A

-rapid development of resistance

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14
Q

what is the MOA of Rifampin?

A
  • inhibits DNA dependent RNA polymerase

- endocded by rpoB gene

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15
Q

How does resistance to Rifampin develop?

A

-mutations in the rpoB gene

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16
Q

is Rifampin bactericidal or static?

A

cidal all the way

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17
Q

Does Rifampin get to the CNS?

A

it does

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18
Q

what are some adverse effects of Rifampin?

A
  • Hepatotoxicity
  • Red discoloration of body fluids
  • ARF, interstitial nephritis
  • influenza syndrome
  • thrombocytopenia
  • cholestatic jaundice
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19
Q

What are drug interactions in Rifampin?

A
  • too many to count (over 100!)

- coumadin, estrogen, anticonvulsants, antiretrovral drugs, etc.

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20
Q

What is the clinical use of Ethambutol?

A
  • first line TB therapy

- helper drug to inhibit resistance to other drugs

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21
Q

What is the MOA of Ethambutol?

A
  • inhibits TB arabinosyl transferase encoded by the embB gene
  • effects wall synthesis
22
Q

is Ethambutol tidal or static?

A

static

23
Q

Does Ethambutol reach the CNS

A

no

24
Q

What are adverse effects of Ethambutol?

A
  • Optic neuritis CAN MAKE YOU BLIND

- Peripheral neuropathy - less common

25
Q

What is the clinical use of Pyrazinamide?

A
  • first line TB drug for the FIRST TWO MONTHS OF THERAPY

- always used in combo

26
Q

what is the MOA of Pyrazinamide?

A

-prodrug activated by TB pyrazinamidase encoded by pncA gene

27
Q

How dose PZA resistance occur?

A

-mutations of the pncA gene

28
Q

is PZA cidal or static?

A

cidal

29
Q

Does PZA reach the CNS?

A

yes!

30
Q

What are adverse effects of PZA?

A

Hepatitis
rash
GI issues
inc. serum uric acid (but no gout)

31
Q

What are clinical uses of Streptomycin?

A

-second line TB drug

32
Q

What is the MOA of Streptomycin?

A

-inhibits protein synthesis by binding to ribosome

33
Q

how dose resistance to Streptomycin occur?

A
  • mutation of ribosomal binding site

- not cross resistant to amikacin, kanamycin, capreomycin

34
Q

Does Streptomycin enter the CNS?

A

only in the presence of inflamed meninges

35
Q

What are adverse effects of Streptomycin?

A
  • Ototoxicity

- Nephrotoxicity

36
Q

What is Primary Resistance?

A

infection by a source case with drug resistant TB

37
Q

What is secondary resistance?

A

From ineffective therapy (poor treatment design or adherence)

  • too few drugs to prevent emergence of resistance
  • suboptinal drug dosing or absorption
38
Q

How do you calculate the risk of evolution of resistance to two drugs?

A

the product of the risk of the development of resistance to each drug – INH®~10-8 + Rifampin®~10-9 INH/Rifampin = 10-8 x 10-9 = 10-17

39
Q

Define MDR-TB

A

resistance to both INH and Rifampin

-more common with HIV infected patients

40
Q

What will it mean for therapy if Rifampin resistance develops?

A

you will not be able to use short course (6month) TB therapy and will need therapy for 18-24 months

41
Q

How effective is 6 month TB treatment?

A

95% cure rate

42
Q

What is the 4 drug regimen for 6 month TB therapy?

A

RIPE (initial)
-rifampin, INH, PZA, and Ethambutol
RI (continual)

43
Q

When can you use intermittent therapy plans?

A

only with DOT

44
Q

When can 6 month therapy be used?

A
  • Adherence is high
  • Sputum cultures convert by 2 months
  • no major cavitary lung disease
  • no rifampin resistance
45
Q

How do you treat a latent TB infection?

A
  • INH mono therapy for 9 mo
  • Rifampin for 4 mo
  • INH + Rifampin for 3 mo (DOT)
46
Q

Which drugs are only active against TB?

A

INH

PZA

47
Q

which drugs are active against TB and NTM?

A

Rifampin
Ethambutol
fluroquinolones
aminoglycosides

48
Q

Which drugs are only active against NTM?

A

Clarithromyocin

Azithromyocin

49
Q

How does the treatment of leprosy compare to the treatment of TB?

A

it’s very different

50
Q

How do you treat Paucibacillary leprosy?

A

Rifampin and dapson daily for 12 mo

51
Q

How do you treat multibacillary leprosy?

A

rifampin and dapson and clofazimine daily for 24 months

Pharm (9 decks)

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