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Microbiology > Antifungals > Flashcards

Antifungals Flashcards

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Biology 101 flashcards
1
Q

How do allyamines work

A

Prevent conversion of squalene into lanestrerol

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2
Q

How do azoles work

A

Prevent converiosn of lanesterol into ergosterol

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3
Q

What targets elongation factor

A

Sodarins –> affects protein synthesis and ribosomes

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4
Q

What affects nucleic acid synethsis

A

5-flucytosine

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5
Q

What affects chitin synthesis

A

Nikkamycin –> chitin is a key cell wall component

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6
Q

What affects mannoprotein inhibition

A

Pradimicin -

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7
Q

What affects B-1,3 glucan synthesis

A

echinocandins

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8
Q

What inhibits mitosis

A

Griseofulvin

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9
Q

Which antifungals can we not use in humans

A

Pradimicin, Sodarins, Nikkomycin

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10
Q

Where doesnt amphotericin B work

A

CNS and eyes as too large

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11
Q

How deos AmpB work

A

binds to ergosterol in the cell wall –> 8 come together to form a pore causing electrolysis loss and death

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12
Q

Descrbie pharmockinetics of AmpB

A

Protein Binding: 80%
Metabolism: Not extensively metabolised mainly urinary excreted
Half life: 24hours in blood 360 hours in tissue

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13
Q

What is pulse therapy

A

Used with ampB idea of giving for like one week and then stopping –> as long half life in tissues so will continue to have antifungal effects but will reduce side effects

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14
Q

what are the SE of AmpB

A

Infusion related: Fever, chills, rigors, thrombophlebitis

General: Anaemia, potassim loss, nephrotixicty due to renal tubular damage

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15
Q

What makes ampB less nephrotoxic

A

Liposomal Form

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16
Q

What are the advantages of AmpB

A 
Broad spectrum
Fungicidal
Low cost
Low drug resistance
Long Half Life
Exprience
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17
Q

What are the disadvantages of AmpB

A

Difficult administration –> mainly IV
Infusion Toxitiy
Kidney Toxicity
Can cause anaemia

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18
Q

Is there resistance to AmpB

A

Not common
But can occur due to changes in ergosterol content, oreintation, or subsitution

Can occur due to mutations in ERG2 or ERG3 gene

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19
Q

What is flucytosin

A

A pyrimidine analogue that inhibits nucelic acid synthesis

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20
Q

Describe the metabolic pathway of flucytosin

A

FLY–> 5-flurouracil then converted into either

FUTP –> inhibits RNA mediated protein syntehsis
FdUMP –> inhibits DNA synthesis

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21
Q

What is flucytosine good for

A

Eye and CNS infections as small

22
Q

What are the pharmacokinetic of flucytosine

A

Oral biolavailabilit: 80%
Protein binding: <5%
Elimitaion: Renal
Half life: 3-6 hours

23
Q

Strenghts of flucytosine

A

Good absorption and distibtuion

24
Q

Weaknesses of flucytosine

A

Limited specturm of action
Reistance arrises easily
Toxic side effects
Needs monitoring

SHOUDL NOT USE AS A SINGLE AGESNT!!!

25
Q

HOw can you get resistance to flucytosine

A

10% C. albicans resistant due to defects in intracellular resistance

30% can acquire resistance on exposure due to alteraiton in teh 5-fluorourail metablism or incrase in pyramidines that can compete with FUTP and FdUMP

26
Q

How do azole wosk

A

Inhibits CP450 demethylase (Encoded for by ERGII gene) –> hence disupts the funcal cell membrane structure and fucntions

27
Q

Pharmacokinetics of fluconazole

A

Oral bioaviabilility: 100%
Protein Binding: 12%
Elimination: Renal
Half Life: 20-30 hours

28
Q

Advantages of fluconazole

A 
IV or Oral
Few interactions
SE uncommon
Good tissue penetration
Potential of combo therapy
29
Q

Disaddvantages of fluconazole

A

Limited spectum of action –> goesnt cover moulds (hence no aspregillosis)
Drug resistance

30
Q

Pharmackinetics o f itraconazole

A

Oral bioavilability: 55%
Protein binding: 99%
ElimitaionL Metabolic –> cauting in hepatic insufficiency
Half life: 20-30hours

31
Q

Strenghts of itraconazole

A 
IV or Oral
Broad spectrum
Low drug resistance
Good for invasive aspergillosis and candidiasis --> HAS MOULD ACIVITY
Potential of combination therapy
32
Q

Weaknesses of itraconazole

A

Variable oral absorption –> need to moitor levels and LFTs
SE not uncommon
Can get line blocckage with IV prep in paediatrics
Drug interactions i.e. vinristine –> GI Toxicity and peripheral neuropathy
Warning in patietns with heart disease

33
Q

What azoles are generally used for more invasive disaese in immunocomprosimed patietns

A

Voriconzaole and Posiconzazole

34
Q

Strenghts of voriconzaole

A 
IV or Oral
Broad specturm
Fungicidal
Low toxicity
GOod brain penetiration
Potential for combinations
35
Q

What is first line for invasive aspergillosis

A

Voriconzaole

36
Q

Weaknesses of voriconazole

A

Needs monitoring –> due to varial metablism
SEL Visual disturbances and cardiac and cerebreal
No mucoromycosis activity
Drug interactions

37
Q

Strenghts of posiconazole

A

Oral or Iv
Broad specturm with action against Mucromyctina –> only other one than AmpB
Fungicidal activity
Low toxicity

38
Q

Weaknesses of Posiconzaole

A

Likely drug interactions

Variable absoprtions –> needs monitorin

39
Q

How can you get azole resistance

A

Overexpression of ERGII
ERGII Pointmutaitons
Efflux pumps

40
Q

Strenghts of caspofungin

A 
Unique mode of action
Fungicidal activity agisnt candida
Reasonbly broad spectrum
Few drug interacitons
Activity and P. Jiroveci
Portential for combination
41
Q

What are the diasdvantages of caspofungin

A

IV onlr
no activity aginst cryptococcus, fusoirum , siedosporim and the zygomycetes
Saery not established in children or pregnancy
limitations in hepatic insufficiency

42
Q

How might resitance arise to echingocandanins

A

Mutations in FSK1 which is amembrane bound portein that functions as a catalytic subunit of 1,3,B-D glucan synthase

43
Q

What is an established combination of clnical synergry

A

AmpB and Flucytosine for cryptococcal meningitis

44
Q

What is a suffested benefit

A

AmpB and flucytosine for certain candida infections

45
Q

What is a theoretic combo

A

AmpB and Azoles

46
Q

What is a potential ocmbinations

A

Echinocandins and anything else as they have a unique mode of action!

47
Q

Name some other antifungal that can be used in combo

A

1) Cytokines e.g. GM-CSF
2) Granulocyte transfusion
3) aspericillus - specific T Cel therapy
4) Radioimmunotherapy –> i.e. mAB for cyptococcus
5) Ab to HSP90 e.g. mycograb –> however not come to fruitition!

48
Q

Which agents do we want to monitor

A

Flucytosine
Itraconzole
Voriconaloe and Posiconazole

49
Q

Give an example of how fungi react differently i.e. cidal or static to different antifuncals

A

ASpergillus fumigatus
AmpB = cidal
Caspofungin = statis
Itraconazole = resistant

50
Q

How can we monitor treatment of antifuncals

A

HPLC

Bioassays - generally only o if HPLC isnt available

Microbiology (14 decks)

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