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Pharmacology > Anti-fungals (year 2) > Flashcards

Anti-fungals (year 2) Flashcards

1
Q

Is Malassezia commensal or pathogenic?

A

commensal

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2
Q

what needs to happen for Malassezia to cause disease?

A

reduction in normal cutaneous barrier function/immune function

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3
Q

is dermatophytosis commensal or pathogenic?

A

pathogenic

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4
Q

what are some reason antifungals may fail? (4)

A

fungal cell wall and capsules
toxicity (fungi are eukaryotes)
poor penetration
not treating beyond cure

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5
Q

what are fungal cell walls made of? (3)

A

glycoprotein
glucan
chitin

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6
Q

why are fungal cell walls good targets for treatment?

A

mammalian cells lack a cell wall (limited toxicity)

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7
Q

what is the main sterol in fungal cell membranes?

A

ergosterol

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8
Q

what drugs groups target ergosterol? (3)

A

polyenes
azoles
allylamine

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9
Q

what type of protein is the enzyme that synthesises ergosterol from lanosterol?

A

cytochrome P450

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10
Q

where are cytochrome P450 enzymes found in the body?

A

most tissues (especially liver)

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11
Q

what is the major function of cytochrome P450 enzymes?

A

drug metabolism

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12
Q

what are the most common anti-fungal drug groups? (2)

A

azoles

allylamines

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13
Q

what do azoles target?

A

cytochrome P450 enzyme

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14
Q

what do azoles prevent the formation of? (what’s formed instead?)

A

ergosterols

toxic sterols

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15
Q

are azoles narrow or broad spectrum?

A

broad

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16
Q

what can decrease the absorption of azoles?

A

decrease acid environment (antacids)

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17
Q

what can increase the absorption of azoles?

A

giving with food (fatty)

18
Q

how are azoles circulated around the body?

A

highly protein bound (albumin)

19
Q

what are the two groups of azoles?

A

triazoles

imidazoles

20
Q

what are some examples of triazoles? (4)

A

itraconazole
fluconazole
voriconazole
posaconazole

21
Q

what are some examples of imidazoles? (4)

A

ketoconazole
miconazole
enilconazole
clotrimazole

22
Q

what has the addition of the triazole ring allowed? (4)

A

higher specificity for the fungal cytochrome P450
increased affinity for fungal cell membranes
lipophilic
keratophilic

23
Q

where are azoles metabolised?

A

liver

24
Q

where are azoles mainly excreted?

A

bile

25
Q

what is the most common side effect of azoles?

A

hepatotoxicity

26
Q

what are some other side effects of azoles? (other than hepatotoxicity)

A 
anorexia, vomiting, diarrhoea
thrombocytopenia
teratogenic 
hormone suppression
vasculitis
27
Q

what are some examples of medications that will decrease the absorption of azoles? (3)

A

H2 blockers
antacids
anticholinergics

28
Q

what do allylamines inhibit?

A

squalene epoxidase

29
Q

what do allylamines prevent the formation of?

A

lanesterol

30
Q

how are allylamines transported in blood?

A

highly protein bound

31
Q

where are allylamines metabolised?

A

liver

32
Q

where are allylamines excreted?

A

urine

33
Q

what are the side effects of allylamines?

A

(uncommon)
GI signs
hepatotoxicity

34
Q

what does polyene antibiotic target?

A

ergosterol

35
Q

how do polyene antibiotics work?

A

insert into the fungal cell membrane causing it to become leaky

36
Q

what is an example of a polyene antibiotic?

A

amphotericin B

37
Q

what does whether an anti-fungal in fungicidal or fungistatic depend on?

A

the dose

38
Q

what are the main side effect of amphotericin B?

A

nephrotoxicity

39
Q

what does griseofulvin effect?

A

interferes with microtubule formation

40
Q

what are the side effects of griseofulvin?

A

tertatogenic
hepatotoxic (idiosyncratic toxicity in cats)
GI issues
carcinogenic

Pharmacology (25 decks)

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