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Skin/MS--Week 2 > Antifungals - Sheet1 > Flashcards

Antifungals - Sheet1 Flashcards

1
Q

Individuals with lowered immunity commonly see what in regards to fungal infections?

A

an increase in almost every type of fungal infection

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2
Q

What are the common cutaneous fungal infections?

A

Malassezia (tinea versicolor); Dermatophytes (Microsporum, Epidermophyton, Trichophyton)

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3
Q

Autotrophic, what does it mean?

A

It means making it’s own energy… fungi are NOT autotrophic, they are heterotrophic

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4
Q

Do fungi produce spores?

A

Yes,

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5
Q

Are fungi multicellular? Do they have a cell wall?

A

Yes, and Yes. Yes; single cell = yeast, multicelluar = mold. Yes; ergosterol and lanosterol in cell wall.

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6
Q

Do fungi have mito?

A

Yes! Eukaryotic

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7
Q

Yeast

A

single cell, spherical or elliptical. Asexual budding (aka blastoconidia);

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8
Q

blastoconidia

A

asexual budding of yeast. if bud stays attached it is called pseudohyphae.

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9
Q

Molds

A

multicellular, form hyphae

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10
Q

mycelium

A

a mass of hyphae

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11
Q

Dimorphic fungi

A

mold at cold temp, and yeast at warm temp (body temp)

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12
Q

fungal spore

A

produced via sexual reproduction.

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13
Q

fungal conidia

A

produced via asexual reproduction

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14
Q

Why do we see a higher amount of toxicity with fungi than bacteria?

A

Fungi = eukaryotes, bacteria = prokaryotes

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15
Q

What is the mechanism of Amphotericin B and Nystatin?

A

Binds ergosterol in cell wall and creates holes in membrane allowing electrolytes to leak. Fungicidal!!

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16
Q

If a patient is immunocompromized, what antifungal drug(s) would you use?

A

Amphotericin B/Nystatin (fungicidal)

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17
Q

What are the toxicities of Nystatin?

A

Binds cholesterol, decreases renal blood flow, 80% of patients have nephrotoxicity

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18
Q

What is the mechanism of Azoles?

A

Binds fungal CYP-450 enzyme (ERG11) blocking the production of ergosterol from lanosterol, and causing the toxic accumulation of lanosterol. Fungistatic!

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19
Q

What resistance do we see with Azoles?

A

altered CYP-450 and upregulation of efflux transporters.

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20
Q

Name the three Azoles…

A

Fluconazole, Itraconazole, Ketoconazole

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21
Q

What are the toxicities of Azoles?

A

Testosterone synthesis inhibition (gynecomastia, esp. with ketoconazole), Teratogenic, hepatotoxicity, nephrotoxicity

22
Q

Terbinafine (Lamisil)–mechanism?

A

Fungicidal. Inhibits squalene epoxidase, which leads to toxic accumulation of squalene.

23
Q

Terbinafine (Lamisil)–spectrum?

A

Dermatophytes (esp. onychomycosi–fungal infection of finger or toe nails)

24
Q

What is the toxicity of Terbinafine?

A

Abnormal liver function tests. visual disterbances. drug interactions with CYP2D6 substrates.

25
Q

Resistance mechs for terbinafine?

A

Rare. decreased uptake, mutant binding site, substrate for efflux transporters

26
Q

Mechanism of Flucytosine…

A

inhibits DNA and RNA biosynthesis through conversion to 5-fluorouracil in fungi. Fungistatic

27
Q

Spectrum of flucytosine?

A

Narrow! Yeast. Candida albicans and Cryptococcus.

28
Q

How do you administer flucytosine and what is unique about its’ distribution?

A

Oral, penetrates CNS

29
Q

What other antifungal is Flucytosine commonly combined with?

A

amphotericin B; increases uptake and minimizes dev. of resistance.

30
Q

Do you know the mechanism of Griseofulvin?

A

Interferes with microtubule function, disrupts mitosis. Deposits in keratin-containing tissues (i.e. nails)

31
Q

What is Griseofulvin commonly used to treat?

A

Dermatophytes (tinea, ringworm)

32
Q

What is unique about Griseofulvin absorbion and what is its’ toxicity?

A

Lipids increase absorption and it conc. in dead keratin. Teratogenic

33
Q

What’s the mech. for caspofungin?

A

Inhibits cell wall synthesis by inhibiting synthesis of beta-glucan.

34
Q

Caspofungin’s spectrum?

A

Candida Albicans, invasive aspergillosis.

35
Q

Tox of Caspofungin?

A

little known (new drug), fever, rash at site of INJECTION!

36
Q

Two main diagnostic tools for cutaneous fungal infections…

A

1) KOH prep 2) Wood’s lamp (only some fluoresce)

37
Q

Tinea versicolor, what?

A

Malassezia furfur-yeast, part of normal flora. But converts to MOLD in disease. Reqs. lipids so increased in sebacious glands and indiv 15-24 yrs.

38
Q

seborrheic dermatitis, scaly cradle cap–huh? Dx? Tx?

A

Dx: KOH prep, yellow-green by Wood’s lamp (UVa). Microscopy “spaghetti and meatballs” Tx: Selenium sulfide or ketoconazole shampoo. Recurrence common.

39
Q

Top three for Dermatophytoses?

A

Trichophyton, Microsporum, Epidermophyton

40
Q

Dermatophytosis Dx?

A

KOH prep, grow on Sabouraud’s agar.

41
Q

Dermatophytosis Tx?

A

Topical griseofulvin; terbinafine or itraconazole (1 month oral)

42
Q

tinea capitis

A

scalp (Microsporum canis [zoophilic], Microsporum fulvum [geophilic])

43
Q

tinea barbae

A

Beard

44
Q

tinea axillaris

A

armpit

45
Q

tinea cruris

A

groin

46
Q

tinea pedis

A

feet (Trichophyton rubum)

47
Q

tinea unguium (onychomycosis)

A

nail

48
Q

What organisms appear blue under a Wood’s Lamp?

A

Microsporum canis and fulvum.

49
Q

Epidermophyton floccosum lacks what? How is it spread?

A

microconidia; anthropophilic

50
Q

Sporothix schenckii causes what? Dx, Tx?

A

“rose gardener’s disease” Tx with oral itraconazole (3-6 months). Dx with biopsy of lymph node.

51
Q

Candida albicans Dx?

A

base on clinic appearance… in skin folds and anus, corners of mouth (cheilitis). Opportunistic!

52
Q

What may the presense of Candida albicans potentially suggest?

A

Diabetes, or T-cell dysfunction

Skin/MS--Week 2 (6 decks)

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