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Pharm Exam 4 > Antimicrobials - Mycobacterial Infections > Flashcards

Antimicrobials - Mycobacterial Infections Flashcards

1
Q

mycobacteria -

  • stain?
  • replication where?
  • growth rate?
A
  • acid fast - not gram bc they down have peptidoglycan cell wall - instead they have lipid rich cell wall (mycolic acids)
  • inside macrophages - need to get drugs here!
  • slow growing - dormancy = challenge bc we like to target fast growing things and mess with growth!
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2
Q

Latent TB infection vs TB disease

A
  • inactive/active multiplying
  • Chest X-ray normal/abnormal
  • Sputum neg/sputum pos
  • No Symptoms/Yes Symptoms
  • Not infectious/Infectious b4 tx
  • Not a case of TB/Yes a case
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3
Q

Obstacles and solutions when treating TB?

A

Bad=slow growth, viable but dormant-slow metabolism, rapid resistance, toxicity

Solutions=multiple drug therapy, regularly taken for sufficient time

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4
Q

What to give for drug resistant TB?

A

streptomycin

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5
Q
  • How to get M Avium complex (MAC)?

- What organisms make up MAC?

A

-M avium and M intracellulare

  • ingestion of contaminated food/water
  • -> respiratory droplets
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6
Q

Preferred Initial phase of treatment for active TB?

A 
RIPE:
Rifampin
isoniazid
pyrazinamide
ethambutol

DAILY 8 weeks of treatment

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7
Q

Preferred continuation phase for active TB?

A
  • Rifampin
  • Isoniazid

DAILY OR TWICE WEEKLY-18 weeks of treatment

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8
Q

Alternative regimentS - initial tx for active TB?

A
  • RIPE drugs but dosing different - DAILY FOR 2 WEEKS AND THEN TWICE WEEKLY FOR 6 WEEKS
  • RIPE drugs for THRICE WEEKLY FOR 8 WEEKS
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9
Q

Alternative regimentS - continuation phase for active TB:

A
  • RI drugs TWICE WEEKLY FOR 18 WEEKS

- RI drugs THRICE WEEKLY FOR 18 WEEKS

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10
Q

Daily preferred treatment for LATENT TB?

A

Isoiazid - 9 months Daily or Thrice weekly

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11
Q

best drug for active and latent TB?

A

isoniazid

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12
Q

Isoniazid

-not MOA but how does it kill stuff?

A
  • bactericidal for actively growing bacilli

- penetrates macrophages - extracellular and intracellular

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13
Q

Isoniazid is less effective against what organisms?

A

-atypical mycobacterial infections (M avium complex MAC)

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14
Q

Isoniazid MOA:

A
  • inhibits synthesis of mycolic acid –> needed for cell wall
  • -> forms covalent bond with at least 2 proteins involved in mycolic acid - impedes function
  • prodrug activated by mycobacterial catalase peroxidase enzyme (Kat G)
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15
Q

Isoniazid

  • safety?
  • absorption?
A

-safest and most effective anti-mycobacterial drug we have

  • readily absorbed from GI tract
  • penetrates the CNS and goes everywhere
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16
Q

Primary drug for nearly all therapeutic or prophylactic TB regimens?

A

-isoniazid

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17
Q

MOA mycobac uses to be resistant to isoniazid?

How to avoid active TB resistance?

A
  • mutation of Kat G pro-drug activation enzyme
  • over expression of Inh A protein which is involved in mycolic acid synthesis

-MUST use at least two active antiTB agents!

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18
Q

Slow acetylator patients - issues with isoniazid?

A

-isoniazid has an acetyl group so if slow acetylator the = peripheral neuropathy

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19
Q

Isoniazid adverse rxns?

A

-hepatitis: risk inc with age and alcoholics

-peripheral neuropathy - risk inc with slow acetylators, malnourished, alcoholics, diabetics, or AIDS patients
(fixable by giving pyridoxine)

20
Q

What are the rifamycin drugs used to treat active TB?

A
  • *-rifampin
  • *-rifabutin
  • rifapentine
21
Q

Rifampin

  • MOA?
  • cidal or static?
  • penetration?
A
  • inhibits RNA synthesis (transcription) - binds to BACTERIAL DNA dependent RNA polymerase
  • CIDAL
  • absorbed well from GI -
  • penetrates most tissues and phagocytic cells = kills intracellularly too!
22
Q

Primary and alternative tx for latent TB?

A
  • primary = isoniazid

- alternative = rifampin

23
Q

Development of resistance to rifampin MOA?

A

-point mutations in bac RNA poly

–> MUST COMBINE WITH OTHER ANTI TB DRUGS

24
Q

Rifampin Adverse effects:

A
  • GI issues - nausea, vomit
  • Nervous system=headache, dizziness, fatigue
  • hepatitis=usually in those with some hidden liver disease and slow acetylators
  • RED-ORANGE COLOR in pee, poop, sweat, tears, and saliva
25
Q

Rifampin Drug interactions:

A

-Increases the elimination of MANY anti-viral drugs!!! ViA P450s
esp protease inhibitors and non-nucleoside reverse transcriptase inhibitor drugs

26
Q

Which rifamycin drug should NOT be given to HIV+ patients?

A
  • rifampin SHOULD NOT be given
  • –> causes INCREASED elimination of antivirals

-GIVE RIFABUTIN! Not as strong of a P450 inducer

27
Q

Pyrazinamide

-MOA

A
  • inh mycolic acid synthesis

- its a prodrug - active form = pyrazinoic acid – converted via pyrazinamidase enzyme

28
Q

Environment needed for good pyrazinamide activity?

A

-ACIDIC! = very effective killer of intracellular mycobacteria inside acidic environment of macrophage phagolysosome

29
Q

Resistance to pyrazinamide how?

A

mutation in pyrazinamidase enzyme

30
Q

Pyrazinamide - Adverse rxns:

A
  • liver tox
  • hyperuricemia - ALMOST ALL PATIENTs
  • some get gouty arthritis
31
Q

Which TB drug is good to treat MAC mycobacteria?

A

ETHAMBUTOL

32
Q

Ethambutol

-MOA>

A

-inhibits arabinosyl transferases - mycobacterial cell wall synthesis

33
Q

Resistance development to ethambutol how?

A

-Point mutations in genes for arabinosyl transferases

–> MUST GIVE IN COMBO WITH OTHER DRUGS!

34
Q

Ethambutol - Adverse effects?

A
  • retrobulbar neuritis (reversible after stopping drug) = impaired visual acuity - red-green color blind
  • hyperuricemia =NOT AS BAD AS PYRAZINAMIDE - some acute gouty arthritis
35
Q

red-green color blindness drug?

A

-ethambutol

36
Q

Streptomycin

  • MOA?
  • activity against what bugs?
  • issue with drug?
  • resistance development?
A
  • interfere with bac protein synthesis (aminoglycoside)
  • M Tuberculosis
  • M Avium
  • Doesnt penetrate cells well - only good against extracellular
  • point mutation in ribosomal proteins
37
Q

Streptomycin -

adverse reactions?

A
  • ototoxic = vertigo or permanent hearing loss

- nephrotic

38
Q

Give which drug to HIV+ patients?

A

Rifabutin instead of rifampin in RIPE drugs

39
Q

Rifabutin

  • MOA
  • compared to rifampin this drug is better at?
A
  • inhibits RNA synthesis (transcription) - binds to BACTERIAL DNA dependent RNA polymerase
  • better for HIV+ and killing MAC organisms
40
Q

What is the combo therapy for M avium complex (MAC)?

A
  • macrolide (clarithromycin or azithromycin) = protein synth inh
  • rifampin (or other rifamycin)
  • ethambutol
  • w/ or w/out streptomycin
41
Q

What is the combo therapy for M avium complex (MAC) Disseminated disease?

A
  • macrolide (clarithromycin or azithromycin) = protein synth inh
  • rifampin (or other rifamycin - like rifabutin)
  • ethambutol
42
Q

What prophylaxis to give HIV Patient with serious AIDS (CD4<50)..

A

clarithromycin or azithromycin

43
Q

M Leprae -

  • lepromatous form
  • tuberculoid form
A

1) lepro=
- disfiguring skin lesions (nodules and plaques)
- absence/poor cell mediated immune response–>neg skin test
- MANY organisms in tissues
2) tubercu=
- milder form
- hypopigmented plaques or macules
- strong cell mediated immune response –> + skin test
- few organism present

44
Q

Leprosy

  • Tx drugs?
  • duration?
A

-MULTIDRUG REGIMEN= dapsone, clofazimine, rifampin

  • 1-2 years for tuberculoid
  • 5 years for lepromatous
45
Q

Dapsone

  • what kind of drug/MOA?
  • high concentrations where in body?
  • Adverse effects?
A
  • analog of PABA = competitive inh of folate synthesis
  • good distribution everywhere but highest in kidney, muscle and skin
  • induce non-hemolytic anemias & acute hemolytic anemias with G6PD deficiency
46
Q

Clofazimine

  • what kind of drug/mOA?
  • solubitily?
  • AE?
A
  • bactericidal dye - DNA binding?
  • highly lipophilic = poor solubility
  • skin color change -red-brown to black after years of use

Pharm Exam 4 (10 decks)

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