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Pharm exam 4 > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

what composes mycobacterias cell wall

A

lipid-rich

mycolic acids

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2
Q

how do you treat active TB

A

4 drugs for 2 months

continuation phase for 18 weeks - reduce to 2 drugs

INH, Rif, PZA, EMB

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3
Q

how do you treat latent TB

A

Isoniazid - 9 months

Rifampin - 4 motnhs

INH and Rifapentne for 3 months

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4
Q

what is the most active drug used in the treatment of acute and latent TB

A

Isoniazid

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5
Q

Isoniazid:

1 (bacterostatic/cidal) for actively growing bacilli
Penetrates into 2. Active against both extracellular and intracellular organisms
Less effective against treating 3
Structural similarity to 4

A
  1. bacteriocidal
  2. macrophages
  3. atypical mycobacterial infections (M. avium complex)
  4. pyridoxine (vit. B6)
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6
Q

MOA of isoniazid

A

inhibits synthesis of mycolic acid

delivered as prodrug, activated by a mycobacterial catalase-peroxidase enzyme (Kat G)

activated INH forms a covalent bond with at least 2 proteins involved in mycolic acid synthesis and impedes function

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7
Q

how is resistance developed against INH

A

mutation in Kat G gene - lack of prodrug activation

overexpression of Inh A protein - enzyme involved in mycolic acid synthesis

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8
Q

what is necessary when treating TB to prevent emergence of drug resistance during therapy

A

at least 2 antituberculosis agents are used

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9
Q

INH is readily absorbed from the 1

Achieves peak plasma concentration in 2 hours - diffuses into all body fluids and tissues (including CNS)

INH is acetylated to acetyl-INH in the 2. Slow acetylators are prone to develop 3. (peripheral neuropathy)

A
  1. GI tract
  2. liver, bowel, kidney
  3. toxicity
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10
Q

Adverse rxns to INH

A

Hepatitis - risk increases with age and greater in individuals with alcohol dependence

peripheral neuropathy - results from structural similairty to pyridoxine; slow metabolism of drug; malnourished, alcoholic, diabetic, or suffers AIDs
- reverse with low doses of pyridoxine

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11
Q

first line tx for active TB

alternative to INH tx of latent TB

A

rifampin

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12
Q

MOA of rifampin

A

inhibits RNA synthesis

binds to bacteria DNA dependent RNA polymerase

bactericidal

penetrates most tissues as well as phagocytic cells - kill intracellular

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13
Q

resistance to rifampin

A

point mutation in bacterial RNA polymerase gene (target)

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14
Q

Rifampin is well absorbed from ___ and is widely distributed to all tissues/fluids

A

GI tract

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15
Q

Adverse rxns to rifampin

A

GI

Nervous system: HA, dizziness, fatigue

hepatitis - most common in those with underlying liver condition, INH slow acetylators (combo therapy)

harmless red-orange color in urine, feces, sweat, tears, and saliva

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16
Q

Rifampin drug interactions

A

strong inducer of cytochrome p450

increase elimination of many drugs

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17
Q

In HIV patients what drug is used instead of rifampinfor treated TB

A

rifabutin

18
Q

essential component of multidrug regimens used in treating active TB

synthetic analogue of nicotinamide

A

Pyrazinamide

19
Q

MOA of pyrazinamide

A

inhibit mycolic acid synthesis

activity is dependent on an acidic environemtn

prodrug - pyrazinamidase enzyme –> active form

20
Q

resistance to pyrazinamide

A

mutation in pyrazinamidase enzyme

21
Q

Pyrazinamide

Well absorbed from the 1

Widely distributed throughout the body, can enter 2 and 3

A
  1. GI tract
  2. macrophages
  3. TB cavities
22
Q

Adverse reactions to pyrazinamide

A

Hepatoxicity

hyperuricemia - nearly all patients

23
Q

___ is essential component in tx of combo therapy used to treat active TB and infections caused by M. avium

A

Ethambutol

24
Q

MOA of ethambutol

A

inhibits arabinosyl transferases (involved in mycobacterial cellw all synthesis)

25
Q

resistance to ethambutol

A

point mutations in genes encoding arabinosyl transferases

should always be given in combo with other drugs

26
Q

Adverse reactions to ethambutol

A

retrobulbar neuritis - reversible following discontinuation

hyperuicemia - less than pyradinazole

27
Q

aminoglycoside antibiotic used in tx of TB caused by strains resistant to first line drugs - used in combo with other drugs to prevent resistance

A

Streptomycin

28
Q

MOA of streptomycin

A

interferes with bacterial protein synthesis

29
Q

streptomycin effective against intracellular, extracellular or both?

A

extracellular - penetrates cells poorly

30
Q

what does streptomycin have antimicrobial activity against

A

M. tuberculosis

M. avium

31
Q

resistance to streptomycin

A

point mutations in ribosomal proteins

32
Q

Streptomycin:

delivered as a 1

distributed in most 2

penetrates 3 poorly

A
  1. injectable
  2. body fluids
  3. cells and tissues
33
Q

adverse reactions to streptomycin

A
  1. ototoxic - vertigo, hearing loss

2. nephrotic

34
Q

what is rifabutin active against?

A

M. tuberculosis and M. avium complex

MAC organisms more that rifampin

35
Q

Rifabutin is a less potent induced of _____

A

cytochrome p450

36
Q

how do you treat M. avium complex (MAC)

A

combination therapy

  1. macrolide (clarithromycin or azithromycin) - protein synthesis inhibitor
  2. rifampin
  3. ethambutol
  4. (+/-) streptomycin
37
Q

drugs used for prophylaxis of MAC in HIV pts (CD4<50)

A

Clarithromycin or azithromycin

38
Q

tx of leprosy

A

multidrug regimen:

  • dapsone
  • clofazimine
  • rifampin

therapy last for years:
1-2 years for tuberculoid
5 years for lepromatous

39
Q

Dapsone is a competitive inhibitor of what

A

folic acid synthesis

40
Q

Adverse effects of Dapsone

A

non-hemolytic anemia

acute hemolytic anemia in pts with G6P deficiency

41
Q

what drug for leprosy can cuase skin to turn red-brown to black

A

Clofazimine

Pharm exam 4 (15 decks)

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