Antimycotic agents Flashcards

1
Q

What is the different protein that makes up part of the cell wall in mycobacteria?

A

Mycolic acid

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2
Q

What is the classic culture result for mycobacterium?

A

Acid-fast

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3
Q

What does mycobacterium avium complex cause?

A

Pulmonary and disseminated infections

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4
Q

What does mycobacterium lepra cause?

A

leprosy

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5
Q

What is mycolic acid?

A

Lipid in the cell wall of TB

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6
Q

What is the gram stain of mycobacterium? Why?

A

gram stain poorly or not at all due to mycolic acid structure

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7
Q

Where does TB like to replicate?

A

macrophages

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8
Q

How fast does TB grow?

A

Slowly

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9
Q

What is the morphology of TB?

A

Rod

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10
Q

What infection is closely correlated with TB infection?

A

HIV

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11
Q

How is TB transmitted?

A

Respiratory droplets

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12
Q

True or false: most patient infected with TB show some type of symptoms

A

false-90% are asymptomatic

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13
Q

What are the classic symptoms for TB infection?

A

Night sweats
Weight loss
Hemoptysis
Fever/chills

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14
Q

In latent TB infection, what are the ssx? CXR results? Sputum smears/cultures? Are they infectious?

A

Nothing will show positive, except for blood tests (IFN-gamma release)

They are not infectious

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15
Q

What are the diagnostic criteria for active TB?

A

Positive blood tests
CXR abnormal
sputum

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16
Q

What is the IFN-gamma test for TB?

A

Expose WBCs of a pt to TB antigen, and see if they produce IFN-gamma. If they do, then positive for infection

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17
Q

What are the obstacles of treating TB?

A

Slow growing
Toxicity of TB drugs
Resistance

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18
Q

Why are patient not compliant with TB drugs?

A

Really toxic

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19
Q

Why do you always treat TB with 3-4 different drugs?

A

Resistance

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20
Q

What is the MOA of rifamycin? Is it bactericidal or bacteriostatic? Why is this drug particularly useful for treating TB?

A

Inhibits RNA synthesis by targeting bacterial RNA polymerase
Bactericidal
Goes into macrophages

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21
Q

What is the MOA of streptomycin?

A

Inhibits protein synthesis by targeting the 30s subunit

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22
Q

What is the MOA of isoniazid? Is this bactericidal or bacteriostatic? Why is this drug particularly useful for treating TB?

A

Inhibit mycolic acid synthesis by forming covalent bond with two proteins
Bactericidal
Can go into macrophages

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23
Q

What is the MOA of Ethambutol?

A

Inhibit arabinosyl which inhibits cell wall synthesis

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24
Q

What is the MOA of pyrazinamide? This is a synthetic analog to what compound?

A

Inhibits cell membrane synthesis (somehow?)

Synthetic analog to nicotinamide

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25
Q

What are the bacteria that are a part of the mycobacterium avium complex?

A

M. Avium

M. intracellulare

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26
Q

What are the ssx of MAC infection? In whom does each type of infection occur?

A

Pulmonary disease in immunocompetent individuals and disseminated disease in AIDS pts

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27
Q

How are the MAC bacteria acquired?

A

ingestion of contaminated food and water

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28
Q

What is the preferred regimen for active TB infection? (4 drugs, how long?)

A

Daily INH, Rifampin, pyrazinamide, and ethionamide x8 weeks

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29
Q

What is involved in the continuation phase of TB infection?

A

Daily INH and rifampin x18 weeks

30
Q

What is the treatment for latent TB? What is the alternative

A

Isoniazid x9 months

Rifampin is alternative

31
Q

Is isoniazid useful for MAC?

A

less effective than for TB

32
Q

What vitamin supplement should pts on isoniazid treatment be placed on? Why?

A

B6 since isoniazid resembles B6, and will inhibit heme synthesis pathway at AIP synthase

33
Q

Isoniazid is a prodrug. What converts it to the active form?

A

Mycobacterial catalase-peroxidase enzyme (Kat G)

34
Q

True or false: INH is one of the safest and most effective TB treatment we have

A

True

35
Q

What are the two ways in which TB develops resistance to INH?

A

Mutation in the Kat G gene

Overexpression of the inh A protein

36
Q

Why is a combination drug therapy used in the treatment of TB?

A

Reduce resistance

37
Q

Who has more toxic side effects with INH? What are the two chief toxicities associated with INH? Does this affect the efficacy of the drug?

A

Slow acetylators
Peripheral neuropathy and hepatitis
Does not affect efficacy

38
Q

True or false: INH, Rifampin, Ethambutol, and pyrazinamide are all readily absorbed from the GI tract

A

True

39
Q

What are the two factors that increase the probability that hepatitis will occur with INH treatment?

A

Age

EtOH dependence

40
Q

What is the MOA of INH causing peripheral neuropathy?

A

B6 inhibition

41
Q

In whom is peripheral neuropathy more likely?

A

Immunosuppressed

Slow Acetylators

42
Q

What is are the side effects of rifampin?

A

n/v
HA, dizziness
Hepatitis

43
Q

What is the benign side effect of rifampin that pts will worry about?

A

red-orange color of urine, feces, sweat, tears, and salive

44
Q

What is the major concern for rifampin, and why should AIDS patients not take it? What is the alternative for them (hint: not INH)?

A

induces p450 enzymes, which will interfere with HIV drugs

Rifabutin

45
Q

True or false: pyrazinamide is an alternative drug for INH or rifampin

A

False-always used in combination with one of these

46
Q

Pyrazinamide is administered as a prodrug. What activates it?

A

pyrazinamide enzyme of bacteria and low pH of macrophage lysosome

47
Q

Why is the fact that pyrazinamide needs a low pH useful for therapy?

A

Good at killing macrophage engulfed TB

48
Q

How does resistance to pyrazinamide develop?

A

Mutation in the pyrazinamide enzyme

49
Q

What are the two major adverse effects of pyrazinamide? Which is seen in a small percent of pts, and which is seen in nearly all patients?

A

Hepatotoxic (5% of pts)

Hyperuricemia (nearly all)

50
Q

Do you ever use pyrazinamide or ethambutol alone? Why or why not?

A

Nope

resistance

51
Q

Is ethambutol useful for MAC?

A

Yep

52
Q

How is resistance to ethambutol brought about?

A

Point mutations in the genes encoding arabinosyl transferase

53
Q

What are the two major adverse effects of ethambutol?

A
Retrobulbar neuritis (color blindness)
Hyperuricemia
54
Q

When is streptomycin used for TB treatment?

A

Strains that are resistant to other first-line drugs

55
Q

What is the major issue with streptomycin as compared to other TB treatments?

A

Does not penetrate into macrophages

56
Q

What are the two major side effects with streptomycin?

A

Ototoxic

Nephrotoxic

57
Q

What is the MOA of Rifabutin?

A

inhibits bacterial RNA polymerase (just like Rifampin)

58
Q

True or false: Rifabutin has lesser activity against MAC organisms than Rifampin

A

False–much greater activity

59
Q

When is Rifabutin used instead of Rifampin? Why?

A

In HIV pts to prevent the induction of p450 enzymes that may interfere with the antiretrovirals

60
Q

What are the three drugs that are used for a MAC infection

A
  1. macrolide
  2. Rifampin
  3. Ethambutol
61
Q

When do you start to prophylax HIV pts for MAC? What drug(s) do you use?

A

CD4

62
Q

What are the two forms of Mycobacterium leprae infection? What is the cellular response in each?

A
  1. Lepromatous form (Th2 response)

2. Tuberculoid form (Th1 response–they chose wisely)

63
Q

What are the ssx of the tuberculoid form of M. Leprae infection?

A

hypopigmented plaque or macules

64
Q

What are the ssx of the lepromatous form of M. Leprae infection?

A

Modules and disfiguring skin lesions that develop very slowly

65
Q

A biopsy of a lesion of the tuberculoid form of M. Leprae infection will show what? Lepromatous form?

A
Tuberculoid = few, if any bacteria
Lepromatous = tons o' bacteria
66
Q

What is the three drug regimen for leprosy?

A

Dapsone
Clofazimine
Rifampin

67
Q

What is the MOA of dapsone?

A

Structural analog of PABA, that competes for folic acid synthesis in bacteria

68
Q

What are the major side effects of dapsone?

A

non-hemolytic anemia if have G6PD

69
Q

What is the MOA of Clofazimine?

A

DNA intercalator (maybe)

70
Q

What are the major side effects of Clofazimine?

A

Red-brown to black skin discoloration