Antimycobacterials Flashcards

1
Q

Do you treat Tb with a single or combo of drugs

A

Combo. Long duration of multiple drugs to prevent resistance.

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2
Q

What is the most common mycobacterial infection?

A

Tuberculosis

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3
Q

Results of tuberculosis infection?

A

Causes granulomatous lesions= pulmonary destruction. (most common site)

Grows slow, asymptomatic early on.

High resistance to antibiotics, and impermeable to many drugs.

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4
Q

Latent vs active Tb infection

A

Latent: Cannot be spread, but you have a positive Tb skin test. This does need to be treated, but not as aggressively. Can use 1 drug 1x per day for months.

Active: Can be spread. Must treat more aggressively. Ex: 4 drugs a day for months.

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5
Q

Strategies to address resistance of tuberculosis

A

Resistant strains emerge during treatment with a single drug. Must use multi drug therapy- however this may cause a decrease in patient compliance.

Directly observed therapy helps increase compliance.

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6
Q

Isoniazid

  1. MOA
  2. Spectrum
  3. Resistance
  4. Pharmacokinetics
  5. Adverse effects
A
  1. Prevents mycolic acid synthesis.
  2. Bactericidal for Tb
  3. Cross resistance does not occur. If resistant to isoniazid, shouldn’t be resistant to others.
  4. Absorbed orally, impaired if taken with food. Metabolized by P450.
  5. Severe liver probs- pt will be monitored. Caused by toxic metabolite. Paresthesia (numbing) of hands and feet.
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7
Q

Brief overview of the Rifamycins

A

All block transcription by interacting with RNA pol.
Never given as single agent.
All excreted by liver

Rifampin- broader spec that isoniazid.
Rifabutin- Less C450 induction than rifampin.
Rifapentin- Longer 1/2 life than rifampin.

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8
Q

Rifampin

  1. MOA
  2. Spectrum
  3. Resistance
  4. Pharmacokinetics
  5. Adverse effects
A
  1. Blocks transcription
  2. Broader than isoniazid. Tb, gram positive and negative, leprosy, and prophylactically in pts exposed to meningitis.
  3. Mutation in affinity of RNA pol
  4. Widely distributed in body. Liver metabolism- potent P450 inducer. Can interact with lots of drugs and shorten their half lives. Excreted by liver
  5. LOTS of drug/drug interactions. Secretions will have an orange-red color, including tears.
    Nausea, vomiting, rash
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9
Q

How is rifampin excreted

A

Liver

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10
Q

Rifampin liver metabolism

A

potent inducer of P450. Can interact with lots of drugs and shorten their half lives. Ex: birth control.

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11
Q

Which drug causes red secretions?

A

Rifamycins

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12
Q

Rifabuten

  1. MOA
  2. Spectrum
  3. Resistance
  4. Pharmacokinetics
  5. Adverse effects
A
  1. Block transcription.
  2. same as rifampin. Broad. Preferred in pts with HIV because it won’t decrease effectivity of HIV meds.
  3. Mutation in affinity of RNA pol
  4. Widely distributed in body. Less P450 interactions than Rifampin!
  5. Secretions will have an orange-red color, including tears. Nausea, vomiting, rash
    * may cause uveitis.
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13
Q

Rifapentine main diff from rifampin

A

Longer 1/2 life than rifampin.

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14
Q

Pyrazinamide

  1. MOA
  2. Spectrum
  3. Adverse effects
A
  1. Lowers intracellular pH and inhibits growth.
  2. Bactericidal to actively dividing organisms.
  3. Liver disfunction when used with isoniazid and rifampin. Be careful. Hyperuricemia= precipitate gout.
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15
Q

Ethambutol

  1. MOA
  2. Resistance
  3. Adverse effects
A
  1. Interferes with cell wall synthesis
  2. Never give alone. No resistance problems when given with others.
  3. *****OPTIC NEURITIS. Inflammation of ON, typically unilateral. Sometimes inflam is behind eye (retrobulbar). Reversed upon discontinuation of drug. Decreased vision and red/green color VA loss.
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