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IC10 Flashcards

1
Q

types of subcutaneous & systemic antifungals (x3)

A

amphotericin B, echinocandins, triazoles

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2
Q

amphotericin B general

A
  • polyene antifungal
  • broad spectru,
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3
Q

MOA of amphotericin

A

bind to ergosterol in plasma membrane -> disrupt function -> allow content to leak out -> death

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4
Q

types of amphotericin B

A

1) amphotericin B deoxycholate
2) amphotericin B liposomal

  • reduced renal toxicity
  • VERY expensive
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5
Q

amphotericin B PK

A
  • Parenteral
  • appear in urine over long period of time
  • renal tox
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6
Q

amphotericin B adverse effect

A

1) fever, chills
2) renal tox (renal vasoconstriction, reduced eGFR)
3) electrolyte imbalance

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7
Q

amphotericin - pregnant

A

most suitable

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8
Q

echinocandin MOA

A

1) inhibit cell wall synthesis
2) inhibit activity of glucan synthase complex (impt for assembly of fungi cell wall)

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9
Q

echinocandin types

A

1) micafungin
2) anidulafungin

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10
Q

echinocandin PK

A

parenteral
X penetrate CSF

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11
Q

echinocandin indications

A

1) asperigullus
2) 1st line for invasive candidiasis (candida species)

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12
Q

AE for echinocandin

A

fever, chill

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13
Q

triazole MOA

A

inhibit C-14 alpha-demethylase that is required for demethylation of lanosterol to ergosterol so inhibit ergosterol synthesis

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14
Q

types of triazoles

A

1) fluconazole
2) posaconazole

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15
Q

fluconazole PK

A

smaller size = better CSF
good O
- high fat meal, acidic improve absorption
- avoid w PPi

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16
Q

fluconazole indication

A

1) Cryptococcal meningitis
2) single dose treatment for vulvovaginal candidiasis

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17
Q

fluconazole special population

A

1) not safe pregnancy
2) dose adjust if renal impair

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18
Q

adverse effect for fluconazole

A

GI
hepatotox
QT prolongation
hair loss if long term use

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19
Q

posaconazole PK

A

larger = poorer CSF
good O
- high fat meal & acidic improve absorption
- avoid PPi

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20
Q

posaconazole pregnant

A

NO

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21
Q

posaconazole AE

A

GI
hepatotox
QT prolongation

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22
Q

triazoles vs imidazoles

A

triazoles for systemic, imidazoles for cutaneous

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23
Q

types of imidazole

A

1) itraconazole
2) voriconazole

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24
Q

itraconazole PK

A

larger in size = poorer CSF
good O
- high fat meal, acidic help absorption
- avoid PPi

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25
Q

indication of itraconazole

A

broad spectrum
onychomycosis

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26
Q

AE for itraconazole

A

1) GI
2) hepatotox
3) QT prolongation
4) hair loss if long term use
5) cardiotoxicity

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27
Q

voriconazole PK

A

smaller size = better CSF penetration
good O
- high fat meal or acidic to improve absorption
- avoid PPi

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28
Q

indication for voriconazole

A

broad spectrum
first line invasive aspergillus

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29
Q

adverse effect for voriconazole

A

GI
hepatotox
QT prolongation
hair loss if prolonged use
neurotox

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30
Q

all azoles drug interaction

A

CYP450 inhbitors

31
Q

types of cutaneous antifungals

A

imidazoles, nystatin, terbinafine

32
Q

imidazoles - moa

A

bind to C-14 alpha-demethylases required for demethylation of lanosterol to ergosterol -> inhibit ergosterol synthesis

33
Q

cutaneous imidazoles AE

A

contact dermatitis, vulvar irritation, oedema

34
Q

types of cutaneous imidazoles (@x)

A

clotrimazole
miconazole

35
Q

clotrimazole indication

A

1) cutaneous candidiasis
2) vulvovaginal candidiasis
3) pharyngeal candidiasis

36
Q

miconazole indication

A

1) cutaneous candidiasis
2) vulvovaginal candidiasis
3) pharnygeal candidiasis

37
Q

nystatin MOA

A

bind to ergosterol -> form pores

38
Q

indication for nystatin

A

broad sepctrum
- oral/GI fungal infection
- vulvovaginal candidiasis

39
Q

terbinafine MOA

A

upstream of lanosterol
- inhibit squalene epoxidase -> no conversion of squalene to lanosterol
- accumulation of squalene toxic -> increase membrane permeability -> death

40
Q

terbinafine indication

A

tinea infection
onychomycoses

41
Q

terbinafine PK

A

extensively metabolised, avoid if renal/hepatic tox

42
Q

caution for terbinafine

A

vaginal cat A
oral cat B

43
Q

general Tb

A
  • caused by mucobacterium tuberculosis
    ** obligate aerobic, slow-growing, fast-acting bacilli
  • mode of transmission: airborne droplet
44
Q

phases of tb infection

A

1) dormant
- start of infection, X symptoms

2) latent: X infectious

45
Q

what populations are more susceptible to tb infection

A

elderly, immunocompromised, HIV +ve

46
Q

why combination therapy for tb

A

different subpopulation of mycobacterium tb w different rates of metabolic activity

monotherapy = higher chance of resistance

47
Q

what abx to avoid for tb infection

A

respi quinolones

48
Q

clinical diagnosis for tb

A

1) the standard stuff
2) sputum obtained for Ziehl-Neelsan stain for acid fast bacilli

  • start treatment if +ve
49
Q

standard regiment for tb treatment

A

1) 2 month intensive daily RIPE
2) 4 month continuation daily/3x per wk rifampicin & isoniazid

50
Q

adverse effect of RIPE

A

rash (self limiting)

RIP: GI symp (weight loss, abdominal discomfort), careful hepatotox if persist

51
Q

what is RIPE

A

rifampicin, isoniazid, pyrazinamide, ethambutol

52
Q

rifampicin MOA

A

block DNA dependent RNA polymerase -> prevent mRNA & protein synthesis -> cell death

53
Q

resistance mechanism to rifampicin

A

mutation in gene which encode RNA polymerase

54
Q

rifampicin PK

A

oral, well absorbed, hepatic metabolism, CNS infection

55
Q

special population rifampicin

A

used in pregnancy, give Vit K
dose adjust if liver failure

56
Q

DDI rifampicin

A

CYP450 inducer

57
Q

adverse effect rifampicin

A

rash, GI, hepatitis, orange discolouration of fluids

58
Q

isoniazid MOA

A

activated by catalase-peroxidase enzyme of M. tb -> produce free radical -> inhibit formation of mycolic acid of bacterial cell wall -> death

59
Q

resistance mechanism for isoniazid

A

mutation to catalase-peroxidase enzyme & mutation of regulatory genes involved in mycolic

60
Q

isoniazid PK

A
  • oral
  • metabolised in liver by N-acetyltransferase
  • good CSFspec
61
Q

special population

A

1) used w pyridoxine in pregnancy
2) monitor if liver failure
3) X dose adjustment for kidney failure

62
Q

food drug interactions for isoniazid

A

tyramine & histamine cuz MAOi

63
Q

DDI isoniazid

A

CYP450 inhibitor

64
Q

isoniazid adverse effect

A

peripheral neuropathy (give w pyridoxine), hepatitis (stop & recontinue after liver test value normalise)

65
Q

pyrazinamide MOA

A

converted to pyrazinoic acid by pryazinamidase
pyrazinoic acid accumulate = drop in intracellular pH

66
Q

resistance mechanism for pyrazinamide

A

mutation to gene encoding for pyrazinamidase enzyme

67
Q

special population for pyrazinamide

A

1) can use pregnant
2) very hepatotoxic
3) dose adjust if kidney failure

68
Q

pyrazinamide AE

A

1) hepatotox
2) hyperurecemia & arthalgia

69
Q

ethambutol MOA

A

inhibit arabinos/transferase enzyme -> interfere w polymerisation of arabinose into arabinogalactan

70
Q

resistance mechanism for ethambutol

A

mutation to gene encoding for arabinoyltransferase enzyme

71
Q

ethambutol PK

A
  • oral
  • liver metabolise
  • excreted in urine unchanged
72
Q

ethambutol AE

A

1) visual tox
- need assess baseline
- higher in pt w kidney failure
- dose dependent
- recovery dependent on early withdrawal
- caution in children

2) hyperuricemia, gout

73
Q

ethambutol special population

A

can pregnant
X dose adjust if liver faiure
dose adjust if renal impair

abx ca2 (6 decks)

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