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MD3001resp > anti fungals > Flashcards

anti fungals Flashcards

1
Q

what are some key characteristics of fungi?

A
  • cells contain nuclei like chromosomes (unlike bacteria)
  • they cannot photosynthesis (they are heterotrophic, like animals)
  • hyphae are key to growth (exude enzymes and absorb food)
  • spores are important for reproduction (sexual and asexual)
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2
Q

what type of cell are fungi?

how do they reproduce ?

A
  • they are single cells/ complex filamentous networks
  • ‘dimorphic’ switching between Yeats and filaments
  • sexual or asexual reproduction
  • highly adaptable to their new environment
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3
Q

what are the key differences between fungi and bacteria?

A
  • fungal walls contain polysaccharide not found in other micro-organisms
  • CHITIN = this adds rigidity and support, this confers resistance to cell wall antibiotics (eg- penicillin)
  • B- glucan = site of action of some anti fungals
  • cell membranes consist of ergosterol rather than cholesterol (this is a good target for some anti funagls)
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4
Q

why will antibiotics not work against fungus?

A

because of the chitin protein in the cell wall - adding support and rigidity.

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5
Q

what type of pathogen are fungals

A

they are opportunistic pathogens - this means that they will target immunocompromised people

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6
Q

what fungus is going to cause superficial mycoses?

A

malassezia furfur

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7
Q

what fungus Is going to cause cutaneous mycoses?

A
  • tinea capitus
  • tinea cruris
  • tinea pedis
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8
Q

what fungal pathogens are able to induce disease of an immunocompetent host?

A
  • histoplasmosis
  • coccoidomycosis
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9
Q

due to what, will most ‘opportunistic pathogens’ cause systemic disease in patients with compromised cell mediated immunity due to:

A
  • HIV
  • immunosuppressive medication
  • concurrent illnesses/long term lines.
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10
Q

what type of yeast will cause meningitis

A

crytococcus neoformans

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11
Q

yeast?

A

single oval cells replicate by BUDDING or FISSION
(some are dimorphic, can be filamentous too)

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12
Q

disease entity:
candida spp.

A

thrush, fungaemia

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13
Q

disease entity:
cryptococcus neoformans

A

meningitis
pneumonia
fungaemia

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14
Q

disease entity:
systemic Yeasts

A

pulmonary or disseminated infections

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15
Q

disease entity:
aspergillus spp., mucor, rhizopius, absidia.

A
  • allergic bronchopulmonary aspergillosis
  • aspergilloma
  • invasive aspergillois
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16
Q

disease entity:
dermatophytes; epidermophyton, microsporum, trichophyton

A

chronic infection of skin and nails, kerion

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17
Q

what are the 6 anti fungal drugs

A
  • azoles
  • terbinafine
  • polyenes
  • flucytosine
  • griseofulvin
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18
Q

describe the ergosterol biosynthetic pathway?

A
  • selective toxicity= key principle underpinning anti-infective therapy
  • ergosterol biosynthetic pathway is essential to fungal but not to eukaryotic cell membranes
  • anti fungal drugs can exhibit inhibitory mechanisms on ergosterol synthesis
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19
Q

what 2 drugs will act as ergosterol inhibitors?

A

azoles
terbinafine

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20
Q

describe the mechanism of action of Fluconazole

A
  • it will inhibit fungal cytochrome P450 enzyme 14a-demethylase
  • prevents conversion of lanosterol to ergosterol
  • primarily fungistatic (prevents growth)
  • will need a high dose to be fungicidal
21
Q

what are 4 specific try-azole drugs ?

A
  • fluconazole
  • itraconazole
  • voriconazole
  • posaconazole
22
Q

fluconazole

A
  • well absorbed after oral administration
  • good penetration into the cerebrospinal fluid to treat neurological infection
  • excreted largely unchanged in the urine so can be used to treat candiduria.
23
Q

itraconazole?

A
  • capsules require an acid environment in the stomach for optimal absorption
  • hepatotoxic
  • issues with drug to drug interaction
24
Q

voriconazole

A

complex issues with drug to drug interaction

25
Q

posaconazole

A

lisensed for the treatment of invasive fungal infections unresponsive to conventional treatment

26
Q

what enzyme will terbinafine

A

squalene epoxidase

27
Q

terbinafine:
indications?

A

dermatophyte infections of the nails, ringworm infections, where oral therapy is appropriate.

28
Q

terbinfine:
cautions?

A

psoriasis, autoimmune disease

29
Q

terbinafine:
hepatic/renal impairment?

A

manufacturer advises avoid in liver disease - elimination reduced.
- use half the normal dose if eGFR is less than 50mL/minute/1.73m2 and no suitable alternative is available.

30
Q

terbinafine:
pregnancy and breast feeding?

A
  • only use in pregnancy if potential benefit outweighs the risk
  • avoid in breast feeding as present in milk
31
Q

Polyenes:
mechanism of action?

A

amphotercin B binds with ergosterol in fungal cell membranes, pores form which cause rapid leakage of monovalent ions and fungal cell death.

32
Q

describe the use/action of polyenes?

A
  • not absorbed well when given by mouth
  • nystatin is applied locally for oral, oropharyngeal and peri oral infections.
  • amphotercin B by intravenous fusion is used to treat systemic fungal infections and is active against most fungi
  • it is highly protein bound and penetrates poorly into tissues
  • amphotercin B is toxic and side effects are common
  • less toxic than Ampotericin B liposomal formulations are increasingly used
33
Q

Flucytosine indications

A

systemic yeast and fungal infections, often as an adjunct to amphotericin B

34
Q

how does flucytosine work?

A

it disrupts the replication of dna by interfering with the nucleic acid chain as a false nuceltide.
but it is non selective so it will also do this to the host cells.

35
Q

renal impairment for flucytosine

A

reduce the dose in case of renal impairment and measure the drug concentration.

36
Q

pregnancy and breast feeding indications for flucytosine?

A

avoid in breast feeding
teratogenic in animal studies, only use if potential benefits outweigh the risks.

37
Q

what are the side effects for flucytosine?

A

hepatoxicity
blood disorders

38
Q

mechanism of echinocandins?
examples?

A

examples = andifulafungin, caspofungin, micafungin

  • they act by inhibiting beta -(1,3)-D-glucan synthase.
  • fungicidal against candida spp.
  • fungistatic against aspergillum spp. but are not used for the treatment of aspergillosis
  • not effective against fungal infections of the CNS
  • CAN ONLY BE GIVEN INTRAVENOUSLY
39
Q

griseofulvin indications

A

dermatophyte infections of the skin, scalp, hair and nails where topical therapy has failed

40
Q

griseofulvin cautions

A

may pair perofmrnace of skilled tasks, the effects of alcohol will be enhanced.

41
Q

griseofulvin contra indications

A

avoid in severe liver disease

42
Q

griseofulvin pregnancy and breast feeding

A

avoid!!!!!

43
Q

side effects of griseofulvin

A

nausea, vomitting, diarrhoea, headache, glossitis

44
Q

summary: mode of action
tri-azoles

A

blocks P450 and sterol 14 alpha demthylase in the cell wall

45
Q

summary: mode of action
terbinafine

A

inhibits squalene epoxidase that accumulates toxic steroid in the cell wall

46
Q

summary: mode of action
polyenes

A

inhibits form pores in funga membrane

47
Q

summary: mode of action
flucytosine

A

inhibits protein synthesis

48
Q

summary: mode of action
echinocandins

A

inhibits 1,3 beta glucan in cell wall polysaccharide

49
Q

summary: mode of action
griseofulvin

A

inhibits fungal mitosis (induces hepatic CYP450)

MD3001resp (41 decks)

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