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Skin/MS > Fungi > Flashcards

Fungi Flashcards

1
Q

What is a fungi?

A

Eukaryotic, heterotroph, often saphrophytic

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2
Q

Yeast

A

Single cell, spherical or elliptical, reproduce asexually by budding

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3
Q

Budding produces what?

A

Conidia

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4
Q

Molds

A

Multicellular, form thread-like filaments call hypae

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5
Q

Mycellium

A

Mass of hyphae

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6
Q

Dimporphic fungi

A

Mold-cold environment, yeast-warm environment

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7
Q

What do fungi produce through sexual reproduction?

A

Spores

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8
Q

Hyphae filaments

A

Grow toward nutrients, can facilitate invasion

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9
Q

Haustoria

A

Hyphae on parasitic fungi

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10
Q

What is important issue when treating eukaryotic fungi?

A

Selective toxicity

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11
Q

What are good targets for antifungal medications?

A

Cell walls–cotain chitin and glucans. Ergosterol in plasma membrane (may have some toxicity…similar to cholesterol)

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12
Q

Polyenes

A

Amphotericin B and Nystatin

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13
Q

Mechanism of polyenes

A

Binds ergosterol, creates holes in membrane, allow for leaking of electrolytes, bactericidal

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14
Q

Spectrum of polyenes

A

Broad. Used for invasive systemic fungal infections in immunocompromised patients. Active against yeast and molds

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15
Q

Polyene distribution

A

Small fraction of drug excreted, long tissue half life. Liposomal form can cross blood brain barrier!!!

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16
Q

Polyene adverse effects

A

Nystatin treats Candida topically. Toxic because it is able to bind cholesterol! Decreases renal blood flow, can cause permanent destruction of basement membrane, up to 80% of patients have nephrotoxicity!

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17
Q

Polyene resistance

A

Rare, decrease ergosterol in membrane

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18
Q

Azoles

A

Fluconazole, Itraconazole, Ketoconazole

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19
Q

Azoles mechanism

A

binds fungal P-450 enzyme (Erg11), blocking production of ergosterol and causing accumulation of lanosterol, fungistatic

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20
Q

Azoles spectrum

A

Most widely used antifungal, spectrum varies by agents

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21
Q

Azoles distribution

A

Orally available through cola/acid (helps facilitate absorption of itraconazole and ketoconazole)

22
Q

Azoles toxicity

A

Drug-drug interactions, hepatotoxicity, neurotoxicity, alters hormone synthesis. Avoid during pregnancy!!!

23
Q

Azoles resistance

A

Altered cytochrome P-450, upregulation of efflux transporters

24
Q

Allylamines

A

Terbinafine (Lamisil)

25
Q

Allylamines mechanism

A

Fungicidal, inhibits squalene epoxidase, leads to toxic accumulation of squalene

26
Q

Allylamines spectrum

A

Dermatophytes

27
Q

Allylamines toxicity

A

Topical, drug interactions with CYP2D6 substrates

28
Q

Allylamines resistance

A

Rare in human pathogens but could include decreased uptake, mutant binding site, and substrate for efflux transporters

29
Q

Flucytosine (5-FC) mechanism

A

Nucleic acid synthesis inhibitor. Antimetabolite secectively taken up and converted to 5-flurouracil in fungi, interfering with DNA and RNA synthesis. Fungistatic

30
Q

Flucytosine spectrum

A

Narrow-yeast. Candida albicans and cryptococcus

31
Q

Flucytosine distribution

A

Oral, penetrates the CNS

32
Q

Flucytosine toxicity

A

Only partially selective for yeast, can lead to bone marrow suppression, follow patient’s cell count carefully

33
Q

Flucytosine resistance

A

Loss of converting enzyme or transporters, rarely used as monotherapy. Often cotreat with amphotericin B to increase uptake and minimize the likelihood of developing resistance

34
Q

Griseofulvin mechanism

A

Binds microtubules, inhibits spindle leading to multinucleate cells, fungistatic

35
Q

Griseofulvin spectrum

A

Dermatophytes

36
Q

Griseofulvin distribution

A

Lipids increase oral absorption and then concentrates in dead keratinized layer of the skin

37
Q

Griseofulvin toxicity

A

Teratogenic. Do NOT use if pregnant!!!

38
Q

Griseofulvin resistance

A

Change to beta-tubulin, need to take orally for months and if patient not compliant, resistance mutations more likely to occur

39
Q

Echinocandins (caspofungin) mechanism

A

Cell wall inhibitor blocks synthesis of beta (1,3)-d-glucan polysaccharide. Fungicidal for candida, fungistatic for aspergillus

40
Q

Echinocandins (caspofungin) spectrum

A

Candida albicans, system

41
Q

Echinocandins (caspofungin) distribution

A

IV, large molecular weight prohibits CNS penetration

42
Q

Echinocandins (caspofungin) toxicity

A

Limited, fever, rash at site of infection

43
Q

Echinocandins (caspofungin) resistance

A

Change in (1,3) beta D-glucan synthase gene

44
Q

What percentage of spores are capable of initiating fungal infection?

A

0.1%. Begins in lungs or on skin

45
Q

Mtcotoxicoses

A

Poisoning from toxins made by a fungus

46
Q

Mycosis

A

Fungus grows on or in the individual

47
Q

How rapidly do fungal infections develop?

A

Very slowly unless individual has suppressed immune system

48
Q

Cutaneous fungal infections

A

Malassezia (tinea versicolor)

Dermatophytes-microsporum, epidermophyton, trichophyton

49
Q

Subcutaneous fungal infections

A

Infection through skin, followed by subcutaneous or lymphatic spread (ex. Sporothrix)

50
Q

Opportunistic mycoses

A

Candida albicans part of normal flora. Infections in patients with immune deficiencies

51
Q

Diagnosis of fungal skin infection

A

Collect skin, hair, or nail with scraping. 10% KOH, can add stain, view under microscope. Some fungi fluoresce under Wood’ lamp (UV-A), can also do PCR or culture

Skin/MS (4 decks)

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