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Antifungals Flashcards

(50 cards)

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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

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A

Eye and CNS infections as small

22
Q

What are the pharmacokinetic of flucytosine

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A

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

23
Q

Strenghts of flucytosine

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A

Good absorption and distibtuion

24
Q

Weaknesses of flucytosine

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A

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

SHOUDL NOT USE AS A SINGLE AGESNT!!!

25
HOw can you get resistance to flucytosine
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
How do azole wosk
Inhibits CP450 demethylase (Encoded for by ERGII gene) --> hence disupts the funcal cell membrane structure and fucntions
27
Pharmacokinetics of fluconazole
Oral bioaviabilility: 100% Protein Binding: 12% Elimination: Renal Half Life: 20-30 hours
28
Advantages of fluconazole
``` IV or Oral Few interactions SE uncommon Good tissue penetration Potential of combo therapy ```
29
Disaddvantages of fluconazole
Limited spectum of action --> goesnt cover moulds (hence no aspregillosis) Drug resistance
30
Pharmackinetics o f itraconazole
Oral bioavilability: 55% Protein binding: 99% ElimitaionL Metabolic --> cauting in hepatic insufficiency Half life: 20-30hours
31
Strenghts of itraconazole
``` IV or Oral Broad spectrum Low drug resistance Good for invasive aspergillosis and candidiasis --> HAS MOULD ACIVITY Potential of combination therapy ```
32
Weaknesses of itraconazole
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
What azoles are generally used for more invasive disaese in immunocomprosimed patietns
Voriconzaole and Posiconzazole
34
Strenghts of voriconzaole
``` IV or Oral Broad specturm Fungicidal Low toxicity GOod brain penetiration Potential for combinations ```
35
What is first line for invasive aspergillosis
Voriconzaole
36
Weaknesses of voriconazole
Needs monitoring --> due to varial metablism SEL Visual disturbances and cardiac and cerebreal No mucoromycosis activity Drug interactions
37
Strenghts of posiconazole
Oral or Iv Broad specturm with action against Mucromyctina --> only other one than AmpB Fungicidal activity Low toxicity
38
Weaknesses of Posiconzaole
Likely drug interactions | Variable absoprtions --> needs monitorin
39
How can you get azole resistance
Overexpression of ERGII ERGII Pointmutaitons Efflux pumps
40
Strenghts of caspofungin
``` Unique mode of action Fungicidal activity agisnt candida Reasonbly broad spectrum Few drug interacitons Activity and P. Jiroveci Portential for combination ```
41
What are the diasdvantages of caspofungin
IV onlr no activity aginst cryptococcus, fusoirum , siedosporim and the zygomycetes Saery not established in children or pregnancy limitations in hepatic insufficiency
42
How might resitance arise to echingocandanins
Mutations in FSK1 which is amembrane bound portein that functions as a catalytic subunit of 1,3,B-D glucan synthase
43
What is an established combination of clnical synergry
AmpB and Flucytosine for cryptococcal meningitis
44
What is a suffested benefit
AmpB and flucytosine for certain candida infections
45
What is a theoretic combo
AmpB and Azoles
46
What is a potential ocmbinations
Echinocandins and anything else as they have a unique mode of action!
47
Name some other antifungal that can be used in combo
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
Which agents do we want to monitor
Flucytosine Itraconzole Voriconaloe and Posiconazole
49
Give an example of how fungi react differently i.e. cidal or static to different antifuncals
ASpergillus fumigatus AmpB = cidal Caspofungin = statis Itraconazole = resistant
50
How can we monitor treatment of antifuncals
HPLC | Bioassays - generally only o if HPLC isnt available

Microbiology (14 decks)

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