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4 Pharm Self > Antimicrobials: antifungals > Flashcards

Antimicrobials: antifungals Flashcards

1
Q

What fungus is most frequently associated with oral lesions?

A
  1. Candida albicans

[mucocutaneous mycoses, thrush, denture stomatitis]

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2
Q

Is candida albicans the 1st most common organism isolated from US blood cultures?

A

NO, 4TH

HARD TO TELL IF IT IS COMMENSAL COLONIZATION OR PATHOGEN/INFECTION

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3
Q

What are the 2 categories of anti fungal drugs?

A 
a. oral and parenteral drugs for
systemic therapy of systemic
infections
b. topical drugs for local therapy, and
oral drugs (for local or systemic
therapy) of mucocutaneous infections
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4
Q

What type of anifungals bind to ergosterol ?

A

polyene antibiotics

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5
Q

What type of anifungals associates with polymerized microtubules?

A

griseofulvin

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6
Q

What type of antifungals block ergosterol synthesis? 2

A
  1. Azoles- bind fungal cytochrome P450 enzyme lanosterol 14-alpha-demethylase
  2. allylamine
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7
Q

What structure is found in amphotericin B and nystatin?

A

lactone ring–(macrolide) polyene antibiotics

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8
Q

What anti-fungal has the broadest spectrum of anti fungal activity? when is it drug of choice? fungicidal?

A
  1. Amphotericin
  2. most life threatening systemic fungal infections
  3. yes but may be static depending on environment etc.
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9
Q

What causes amphotericin adverse effects?

A

binding cholesterols [much less than ergosterol, but it does happen]

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10
Q

When is resistance to amphotericin B found? Is it rare?

A
  1. when ergosterol concentration is low (azole treatment etc.)
  2. if ergosterol affinity for amphotericin B is reduced

YES BUT MAY BE OBSERVED WITH CANDIDA SPECIES OTHER THAN C. CLBICANS

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11
Q

Is amphotericin absorbed well?

A

No- oral administration is only topical for GI

Must be parenteral for systemic infections. Not soluble

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12
Q

How are amphotericin metabolites excreted

A

renal

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13
Q

T-F–broad distribution of deoxycholate formulation of amphotericin B is a significant factor in toxicity?

A

True

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14
Q

What adverse effect is almost always seen to some degree with IV?

A

nephrotoxicity- slower with IV infusion as opposed to allergic/immediate

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15
Q

What 3 types of drugs have bad interactions with amphotericin B?

A
  1. digitalis
  2. azoles
  3. nephrotoxic agents [aminoglycosides and cyclosporine]
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16
Q

What is critical for patients with renal dysfunction or requiring long-term amphotericin B therapy?

A

Liposomal preparations

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17
Q

Can nystatin be used parenterally?

A

No- too toxic

No absorbed through membranes so can be used topically everywhere

18
Q

What does nystatin taste like?

A

bitter and very unpleasant taste

19
Q

Is griseofulvin static or cidal?

A

statis

20
Q

T-F–griseofulvin induces various CYP isoforms?

A

True–> alters effectiveness of various drugs including warfarin and oral contraceptives

21
Q

is flucytosine static or tidal? oral or parenteral?

A
  1. static

2. oral

22
Q

What converts flu cytosine to 5-FU? What does 5-FU inhibit?

A
  1. cytosine deaminase

2. Nothing–> 5-FdUMP which competitively inhibits thymidylate synthetase

23
Q

What do we use flu cytosine in combination with to yield a synergistic effect? what disease?

A
  1. amphotericin B -

2. Cryptococcus meningitis and severe candida

24
Q

How do we get resistance to flucytosine?

A

mutations in cytosine permease or

cytosine deaminase

25
Q

With flucytosine is oral bioavailability good? CNS penetration? hepatic excretions?

A
  1. 90%
  2. good CNS penetration
  3. Renal excretion
26
Q

Are azoles static or tidal? Oral or parenteral?

A
  1. Static

2. both

27
Q

T-F–triazoles are much less specific for fungal CYPs than imidazoles? T-f— numerous drug interactions overall for this class?

A
  1. False- other way around

2. True

28
Q

What class of azoles is ketoconazole, miconazole, clotrimazole? Which azole has the greatest propensity to inhibit mammalian CYPS?

A
  1. Imidazoles

2. Ketoconazole- may cause symptomatic hepatitis that can be fatal and dose independent

29
Q

Is micronazole often used systemically?

A

no- thrombophlebitis after IV

30
Q

What drug class is itraconazole, fluconazole, voriconazole, posaconazole, efinazonazole?

A

Triazoles

31
Q

Is itraconazole absorbed well in the GI?

A

Yes

32
Q

What are 3 key resistance facts of fluconazole

A
  1. intrinsic resistance to C. krusei
  2. Common in C. glabrata
  3. Not active against mols like aspergillus
33
Q

T-F– voriconazole is less potent in vitro against yeast and molds than itraconazole? Is vori oral biovailability high? Which CYP is largely effected?

A
  1. False- more potent in vitro
  2. yes
  3. CYP3A4
34
Q

Does posaconazole have good oral bioavailability? what is it largely effective against?

A
  1. Yes

2. zygomycoses

35
Q

Is efinaconazole safe?

A

YES!! mono therapy for fungal toenail infections

36
Q

What anti fungal class has a terbinafine structure? are they cidal or static?

A
  1. allyamines

2. cidal

37
Q

T-F– allylamines and griseofulvins have the same dermatophyte target?

A

True

38
Q

Where does terbinafine accumulate?

A

in the skin, nails, and fatty tissues

39
Q

Co administration of terbinafine with what doubles its clearance? decreases its clearance?

A
  1. Rifampicin

2. cimetidine

40
Q

T-F–besides skin and nail infections, terbinafine is used for unusual refractory yeast infections?

A

False- mold infections

41
Q

WHAT IS the newest class of antifungals? what does it cause to the cell wall? oral or parenteral?

A
  1. glucan synthesis inhibitors
  2. osmotic shock and lysis
  3. parenteral IV

4 Pharm Self (17 decks)

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