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Multisystem Pharm > Anti-mycobacterial Therapies > Flashcards

Anti-mycobacterial Therapies Flashcards

1
Q

What is MDR TB?

A

Multi-drug resistant TB. These strains are resistant to two different first line drugs (like isoniazid and rifampin).

This form has increased mortality, more drug side effects and much more expensive to treat.

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2
Q

What is XDR TB?

A

Extremely drug resistant TB.

Recently emerged, and is resistant to at least 3 different first line drugs. This strain is typically 50% fatal, more expensive, and take longer to treat.

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3
Q

TB And HIV: twin epidemics?

A

TB can remain in the latent form, but when you have HIV its more likely to become active again faster.

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4
Q

Brief characteristics of mycobacteria

A
  1. Stain acid fast with aryl methane dyes (like carbon fuchsin)
  2. Aerobic
  3. Mycolic acid in cell wall
  4. Genome has 59-65% GC content
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5
Q

Cell wall of mycobacterium (4 layers from the inside out)

A
  1. Cytoplasmic membrane
  2. Peptidogylcan layer
  3. Arabinogalactan layer
  4. Mycolic acid layer
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6
Q

What complicates treatment of TB? 4 things.

A
  1. Infection is chronic (long term tx)
  2. Bacteria often intracellular
  3. Bacteria develop resistance to single drugs
  4. Often dormant w/ slow growth rate
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7
Q

First line drugs:

A

RIPE

  1. Rifampin
  2. Isoniazid
  3. Pyrazinamide
  4. Ethambutol
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8
Q

Isoniazid. How does it work?

A
  1. It inhibits mycotic acid synthesis.
  2. Active against extra and intracellular mycobacteria.
  3. Bactericial
  4. High specificity
  5. Pro-drug that must be converted to active form by KatG enzyme
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9
Q

Describe the pharmacokinetics of isoniazid.

A

Absorbed from the GIT and diffuses into all body fluids and tissue (Even CNS).

Similar intra and extracellular concentrations

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10
Q

How is isoniazid inactivated?

A

Acetylation

There is genetic variation in how fast or slow a person acetylates this drug, affecting its therapeutic and toxic effects

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11
Q

What are the side effect of isoniazid?

A
  1. Neurotoxicity
  2. Hepatotoxicity: caused by acylated metabolites
  3. Allergic rxns
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12
Q

What drug can be given to counteract the neurotoxic side effects of isoniazid?

A

Pyridoxine (vitamin B6)

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13
Q

What drug-drug interaction should you look out for with isoniazid?

A

Isoniazid and phenytoin (epileptic drug)

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14
Q

Rifapmpin mechanism?

A
  1. Inhibits DNA dependent RNA polymerase (no effect on host enzyme). This makes it more broad spectrum than other TB drugs
  2. Bactericidal
  3. Can kill intra and extracellular mycobacteria
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15
Q

Describe the pharmacokinetics

A
  1. Absorbed via GIT
  2. Excreted into bile and undergoes enterohepatic recirculation.
  3. Excreted into bodily builds, causing orange-red colorant of urine, feces, saliva

rifamPIN makes your pee PUMPKIN colored

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16
Q

Side effects of rifampin

A

Well tolerated but:

  1. Jaundice, rash, thrombocytopenia, nephritis
  2. If you give it less often (
17
Q

Drug interactions with rifampin

A

Potent inducer of CYP450 enzymes (can reduce half life of anticoagulants, OCPs, chloramphenicol, methadone, PIs etc)

18
Q

Rifapentine. Same as rifampin?

A

Pretty much. The “long-acting rifampin” (2x week dosage=patient compliance). Same side effects and drug interactions as rifampin

19
Q

Ethambutol mechanism of action?

A
  1. Inhibits arabinogalactan synthesis (remember, 2nd from the outside layer, right under mycotic acid)
  2. Bacteriostatic for mycobacteria
  3. Specific for mycobacteria
20
Q

Pharmacokinetics of ethambutol?

A

Absorbed in GIT, excreted in urein

21
Q

Side effects of ethambutol (2).

A
  1. Optic neuritis: loss of ability to differentiate red from green.
  2. Decrease urate secretion–>gout
22
Q

Mechanism of action of pyrazinamide?

A
  1. Inhibits fatty acid synthetase1 (FAS1) or mycobacterium TB.
  2. Can enter cells
  3. Prodrug
23
Q

Pharmacokinetics of pyrazinamide?

A

Absorbed in GIT, excreted in urine mainly

24
Q

Side effects of pyrazinamide?

A
  1. Hepatotoxicity
  2. Nongouty polyarthralgia
  3. GI sx
  4. Gout arthritis
25
Q

What a common (and stupid) reason for drug resistance in TB? What do we do about it?

A

People start taking their meds and then stop, leading to an increase in resistance.

This is where DOT (direct observed therapy) comes in (having pt come in or someone go out to pt to make sure they take their drugs)

26
Q

Describe the typical TB treatment regiment?

A

RIPE therapy for 2 months while susceptibility to drugs is tested

If susceptible: continue RI for either 4 or 7 months

27
Q

Latent TB: when should you treat?

A
  1. They have HIV

2. kids

28
Q

Treatment for Latent TB?

A
  1. Isoniazid and Rifapentine (3 month, 1x/wk) (most recent regiment)
  2. Isoniazid for 9 months (daily, or 2x/wk DOT)
29
Q

What are some second line drugs for TB?

A
  1. Steptomycin
  2. Ethionamide
  3. PAS
  4. Cycloserine
  5. Careomycin
  6. Fluoroquinolones

*Use when you get drug resistance to first line drugs
(Tx for 9-18 months, with way worse side effects :( )

30
Q

Mycobacterium avim complex is a common infection in AIDS patients. What is the treatment?

A
  1. Clarithromycin or Azithromycin + ethambutol (ACE)

2. Use AC for prophylaxis in HIV pts

31
Q

Leprosy is caused by Mycobacterium leprae. What sx does it cause?

A

Causes peripheral nerve damage, skin and mucous membranes affected too. Difficult to transmit to others.

32
Q

What animal can transmit leprosy to us?

A

Armadillos

33
Q

Treatment for leprosy

A 
Paucibacillary leprosy (skin smear negative): dapsone and rifampin
Multibacillary leprosy (skin smear pos): dapsone, rifampin, clofazimine
34
Q

How does dapsone work?

A

Inhibits folate synthesis and competes with PABA for active site of dihydropteroate synthetase

35
Q

Side effects of dapsone?

A
  1. Hemolysis

2. Hemolytic anemia

36
Q

Clofazimine mechanism of action?

A

Unknown

37
Q

Side effects of clofazimine?

A
  1. GI sx

2. Red discoloration of skin

Multisystem Pharm (9 decks)

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