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Systemic Pharm I > Antifungal Drugs > Flashcards

Antifungal Drugs Flashcards

1
Q

What are the azoles?

A

clotrimazole, fluconazole, itraconazole, ketoconazole, miconazole, posaconazole, voriconazole

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2
Q

What are the echinocandins?

A

anidulafungin, caspofungin, micafungin

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3
Q

What are the polyene macrolides?

A

amphotericin B, natamycin, nystatin

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4
Q

What are the allylamines?

A

naftifine, terbinafine, tolnaftate

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5
Q

What is the “other” antifungal drug?

A

flucytosine

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6
Q

What is mycoses?

A

an infectious disease caused by fungi

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7
Q

What are the most common locations of fungi infection?

A

skin, mucous membranes, hair, nails

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8
Q

Can there be deep fungal infections?

A

yes, can spread to blood and organs and be life threatening and difficult to treat

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9
Q

T/F Antifungals are only topical

A

false, they are systemic or topical

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10
Q

What are the characteristics of fungi?

A

eukaryote with rigid cell wall composed of chitin NOT peptidoglycan, cell membrane contains ergosterol, can exist in yeast or mold form

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11
Q

T/F fungi are usually resistant to antibiotics and bacteria are usually resistant to antifungals

A

true

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12
Q

Why is the incidence of fungal infections on the rise?

A

more organ transplants (with chronic immune suppression), chemotherapy, HIV, antibiotic treatment

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13
Q

What are azoles good for?

A

wide clinical use but good for superficial infections like candida and dermatophytes

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14
Q

What is the MOA of azoles?

A

inhibits enzyme responsible for converting lanosterol to ergosterol (disrupts fungal cell membrane structure and function)

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15
Q

What is the secondary MOA of azoles?

A

inhibit human gonadal and adrenal steroid synthesis leading to decreased testosterone and cortisol production

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16
Q

What are the adverse effects of azoles?

A

allergies and minor GI disturbances

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17
Q

What are the drug interactions of azoles?

A

inhibits CYP450 (potentiates toxicities of other drugs), decreased absorption when co-administered with agent decreasing gastric activity

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18
Q

What should azoles not be combined with?

A

amphotericin B because it needs ergosterol in the membrane

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19
Q

What shortens the duration of action of ketoconazole?

A

rifampin because it is an inducer of CYP450

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20
Q

What is ketoconzaole?

A

the first azole used, limited to topical, less selective for fungal enzyme=more side effects

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21
Q

What is true of fluconazole?

A

high oral availability and penetration to CNS

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22
Q

What is itraconazole?

A

drug of choice for histoplasmosis (not exactly fungus), administered orally or parenterally

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23
Q

What is the bioavailability of voriconazole?

A

96% bioavailability, oral or parenteral administration

24
Q

T/F coriconazole is an extensive CYP450 inhibitor?

A

true, dose reduction may be needed for other meds

25
Q

What are the adverse effects of voriconazole?

A

30% of patients report visual disturbances (blur, changes in color/brightness, occur immediately then resolve) photosensitivity dermatitis also common

26
Q

What is posaconazole?

A

new oral/parenteral, broadest spectrum, developed to prevent infections in immunocompromised patients

27
Q

Does posaconazole inhibit or induce CYP450?

A

inhibits some enzymes

28
Q

Which three azoles are most common topically?

A

clotrimoazole, miconazole, and ketoconazole (shampoo too)

29
Q

What is the MOA of echinocandins?

A

interferes with synthesis of B-glucan which disrupts fungal cell wall and causes lysis and cell death

30
Q

What is the absorption of echinocandins?

A

IV only, poor oral absorption

31
Q

What is caspofungin?

A

the second line if failure of amphotericin B or azole, requires dose adjustment if given with CYP450 inducer

32
Q

What are the adverse effects of echinocandins?

A

well tolerated with few side effects, infrequent GI problems, flushing which may be histamine mediated

33
Q

What is amphotericin B?

A

the only antifungal for years, high toxic potential but still drug of choice for life-threatening systemic mycoses

34
Q

What is the MOA of amphotericin B?

A

binds to ergosterol in plasma membrane and forms a pore allowing electrolytes and small molecules to escape causing cell death

35
Q

What is resistance of amphotericin B related to?

A

decreased ergosterol content of fungal membranes

36
Q

What are the pharmacokinetic considerations of amphotericin B?

A

mainly given by slow IV infusion, extensively bound to plasma proteins, kidney and liver elimination

37
Q

What are the adverse effects of amphotericin B?

A

low therapeutic index, infusion related toxicity, cumulative toxicity

38
Q

What are the infusion related toxicity aspects of amphotericin B?

A

fever/chills, muscle spasm, vomiting, headache, hypotension

39
Q

What is the cumulative toxicity aspect of amphotericin B?

A

renal impairment from decreased glomerular filtration rate (reversible) and anemia

40
Q

What are nystatin and natamycin?

A

antifungals restricted to topical treatment of candida or corneal infections that resemble amphotericin B

41
Q

What is the MOA of nystatin and natamycin?

A

binds ergosterol in plasma membrane and forms a pore

42
Q

What is the only commercially available ophthalmic anti-fungal medication?

A

natamycin

43
Q

What is available for the treatment of thrush?

A

oral mouthwash of nystatin or natamycin

44
Q

What is flucytosine?

A

developed as anti-cancer with no real effectivity, now a antifungal

45
Q

What is the MOA of flucytosine?

A

enters fungal cell and disrupts DNA/protein synthesis, converted intracellularly into 5FU an antimetabolite

46
Q

What is resistance to flucytosine caused by?

A

decreased levels of enzymes used to convert 5FC to 5FU, rate is lower if given with additional antifungal

47
Q

What is flucytosine often combined with?

A

amphotericin B, enters pores easily

48
Q

What are the pharmacokinetics of flucytosine?

A

only available as oral drug, excretion via glomerular filtration, can penetrate CNS

49
Q

What are the adverse effects of flucytosine?

A

neutropenia, thrombocytopenia, bone marrow depression, GI disturbances

50
Q

What is the MOA of allylamines?

A

inhibits enzyme (squalene epoxidase) that converts squalene to lanosterol (aka blocks biosynthesis of ergosterol) –squalene builds up and becomes toxic

51
Q

Which allylamine is topical and oral?

A

terbinafine

52
Q

Which allylamine is topical only?

A

naftifine

53
Q

What is the drug of choice for treating fungal infections of nails?

A

terbinafine (effective for skin infection as well)

54
Q

What are the pharmacokinetics of allylamines?

A

40% bioavailability orally, deposited in skin, nails and fat, urinary excretion

55
Q

What are the adverse effects of allylamines?

A

orally– GI disturbance, headache, rash, some visual disturbances

topically– irritation and redness when in contact with mucous membranes

Systemic Pharm I (13 decks)

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