Anti-Mycobacterials Flashcards

1
Q

Which drugs are considered “Antimycobacterials”? These drugs are also considered “first lines”?

A
Isoniazid    (INH)
Rifampin
Ethambutol
Pyrazinamide 
Streptomycin
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2
Q

What stain is specific to Mycobacterium?

A

Acid Fast

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3
Q

What are the 2 divisions of treatment for Mycobacterium?

A
  1. Chemoprophylaxis

2. Active Disease

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4
Q

What is Chemoprophylaxis?

A

Giving a drug to prevent the development of clinically active disease in people already infected with the organism

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5
Q

In treating mycobacterium tuberculosis, how many drugs and what type (cidal or static) should the person be taking?

A

2 drugs concurrently

CIDAL

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6
Q

Which drug is almost always the initial drug?

A

INH (Isoniazid)

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7
Q

Which combination of drugs has good efficacy to treat TB?

A

INH + Rifampin

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8
Q

How long should the person be on the treatment?

A

for at least 3-6 mo after sputum becomes negative to sterilize the lesions and prevent relapse

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9
Q

What triple therapy should be given if the treatment is to last 2 mo?

A

INH + rifampin + pyrazinamide for two months

plus either ethambutol or streptomycin

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10
Q

After the 2 mo treatment for TB, what therapy follows?

A

INH + rifampin for four months

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11
Q

What other 9 mo alternative to treat TB is there?

A

INH + rifampin is also effective

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12
Q

What treatment should be administered if the patient is resistant to INH and Rifampin?

A

treat with 3 or more drugs to which the organism is susceptible & continue for 12-24 months after the culture becomes negative

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13
Q

What is DOT and who would benefit from it?

A

Intermittent therapy & Directed observed therapy

For patients who can not be relied upon to take daily medication, but who can be followed as OP in a clinic

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14
Q

What does the DOT therapy consist of?

A

Consists of daily therapy for 2 weeks (INH, rifampin, pyrazinamide, & streptomycin) followed by therapy 2 times a week for 6 weeks, followed by INH + rifampin twice weekly for 18 weeks

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15
Q

Is Isoniazid CIDAL or STATIC?

A

CIDAL

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16
Q

What is Isoniazid active against?

A

against actively growing bacilli, both extracellular & intracellular

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17
Q

What is the MOA of Isoniazid ?

A

Interferes with biosynthesis of cell wall mycolic acids

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18
Q

How does TB gain resistance of Isoniazid and Rifampin?

A

due to drug accumulation or alteration of target enzyme

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19
Q

How is Isoniazid administered?

A

Readily absorbed orally or parenterally

20
Q

Does Isoniazid get into the CSF?

A

Yes and caseous lesions

21
Q

What is the primary metabolic route of Isoniazid?

A

Acetylation

22
Q

How is INH excreted ?

A

75-95% of the dose is excreted in the urine in 24 hrs

also excreted in the saliva, sputum, and breast milk

23
Q

What are the adv eff of INH?

A
  1. Peripheral neuritis
  2. Hepatotoxicity
  3. Potential for seizures
  4. Inhibits metabolism of phenytoin
  5. Hypersensitivity – rash; fever
24
Q

A patient is experiencing peripheral neuritis? What caused the agent and what should be done to alleviate the patient?

A
  1. INH

2. Pyridoxine

25
Q

What is Rifampin?

A

Complex macrocyclic antibiotic

26
Q

Is Rifampin CIDAL or STATIC?

A

CIDAL

27
Q

What bacteria is Rifampin active against?

A

against extracellular cavitary bacilli & organisms in closed lesions (macrophages & caseous lesions)

  • M. tuberculosis, M. leprae, atypical mycobacteria
  • Prophylaxis for exposure to meningococcal or H. influenzae meningitis
28
Q

What is the MOA of Rifampin?

A

Inhibits bacterial DNA-dependent RNA polymerase

29
Q

How is Rifampin administered?

A

Well absorbed from orally

30
Q

Does Rifampin get into the brain?

A

Yes

31
Q

This drug has a progressively shortened half-life owing it to it’s own ability to induce hepatic enzymes that accelerate its own metabolism. What is the drug?

A

Rifampin

32
Q

This drug is rapidly eliminated via bile, followed by enterohepatic recirculation that goes to the feces and urine. What drug is this?

A

Rifampin

33
Q

What are some adverse rxs of Rifampin?

A

Hypersensitivity
GI: epigastric distress, N/V, cramps, diarrhea
Fever
Hepatotoxicity leading to: jaundice

34
Q

A patient is complaining of orange-red colored saliva, tears, and urine–even their sweat is orange. And have noticed a discoloration of their contact lens. What is the causative agent?

A

Rifampin

35
Q

What drugs should a patient avoid if they are taking Rifampin? and why?

A
Rifampin is a potent inducer of P 450 : increases metabolism of other drugs 
Oral contraceptives	Warfarin
Prednisone 			Digoxin
Quinidine			Ketoconazole
Propranolol			Clofibrate
Sulfonylureas
36
Q

What is the MOA of Pyrazinamide?

A

Unknown

37
Q

How is Pyrazinamide used clinically?

A

INH and Rifampin

38
Q

Is Pyrazinamide CIDAL or STATIC?

A

CIDAL to actively dividing bugs

39
Q

How is Pyrazinamide administered?

A

absorbed well orally

40
Q

Does Pyrazinamide get into the CSF?

A

Yes

41
Q

What are some adverse effects of Pyrazinamide?

A

Hepatotoxic
Hyperuricemic = Gout
Occasional GI effects

42
Q

What is the MOA of Ethambutol?

A

Unknown

43
Q

Is Ethambutol CIDAL or STATIC?

A

STATIC

44
Q

How is Ethambutol administered?

A

Orally

45
Q

What are some adverse effects of Ethambutol?

A

OPTIC NEURITIS: bi- or unilateral – loss red/green discrimination examine visual acuity periodically
Urate retention & gouty attacks