Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PHRM 840 > Pharmacology of Antifungals > Flashcards

Pharmacology of Antifungals Flashcards

1
Q

Properties of cells in humans

A
  1. ribosomes 60S/40S
  2. no cell wall
  3. dietary folate
  4. differences in DNA gyrase/topoisomerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Humans and fungi are what cells?

A

eukaryotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antifungal agents two basic targets?

A
  1. action on cell wall

2. block nucleic acid aynthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which group of drops target action on cell wall? 4

A
  1. Azoles
  2. Allylamine
  3. polyenes
  4. echinocandin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which group of drugs block nucleic acid synthesis?

A

pyrimidine analog

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Azoles can be broken down into?

A

Imidazoles and triazoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Imidazoles (3)

A
  1. Ketoconazole
  2. Clotrimazole
  3. Miconazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Triazole (2)

A
  1. Fluconazole
  2. Posaconazole
  3. Voriconazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Itraconazole

A

Sporanox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fluconazole

A

Diflucan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Voriconazole

A

Vfend

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Posaconazol

A

Noxafil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Isavuconazonium - Isavuconazole

A

Cresemba

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Allylamines

A

Terbinafine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Polyenes

A

amphotericin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Amphotericin B desoxycholate

A

Fungisone IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Liposomal AmpB

A

AmBisome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lipid complex AmpB

A

Abelcet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Echinocandin (3)

A
  1. Anidulafungin
  2. Caspofungin
  3. Micafungin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Caspofungin

A

Cancidas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Anidulafungin

A

Eraxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Micafungin

A

Mycamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Localized manifestations of fungal infections are not life

threatening and usually do not disseminate in

A

immunocompetent hosts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Fungi can become opportunistic, systemic pathogens in

A

normal hosts with parenteral administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Opportunistic, systemic fungal infections also occur in patients
with

A

underlying medical problems or immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What inhibits the enzyme that synthesizes beta-glucans called the penicillin of antifungasl?

A

enchinocandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What binds ergosterol, weaken the membrane, cause pore formation, leakage of k+ and Na+, fungal cell death

A

polyenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What inhibits the enzyme that synthesizes ergosterol?

A

azoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is converted to 5-FU to inhibit DNA synthesis as a pyrimidine analog

A

5-flucytosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pregnancy category for polyenes

A

category B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pregnancy category for echinocandins

A

category c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Pregnancy category for azoles

A

category D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What antifungals are recommended to be avoided during the. first trimester of pregnancy?

A

azoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Formulations of enchinocandins?

A

IV only slow infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Metabolism of enchinocandins

A

slow metabolism by hydrolysis/N-acetylation

36
Q

Excretion of echinocandins

A

primarily in urine

37
Q

Enchinocandins in order of increasing half life

A

Caspofungin, Micafungin, Anidulafungi

38
Q

SE of enchinocandins

A 
Histamine-mediated symptoms 
Hepatic toxicity (Monitoring: LFTs)
39
Q

Dose adjustment is required for enchinocandins in renal impairment pts

A

False, no dose adjustment needed

40
Q

Does echinocandins have CSF penetration?

A

no, do not use for meningitis

41
Q

Mutations in FKS1 or FKS2 (Candida glabrata) gene
which encode glucan synthase
(increased or decreased) sensitivity to echinocandins

42
Q

Mechanisms of resistance to echinocandins (3)

A
  1. Upregulation of multidrug transporters
  2. Biofilms
  3. Increased chitin synthase gene expression (chitin also a fungal cell wall component)
43
Q

Amphotericin B is selective for

A

fungal erosterol

44
Q

main sterol of mammalian cell membranes

A

cholesterol

45
Q

What Induces ROS in fungal cell - accumulation of free radicals

A

Amphotericin B

46
Q

Is there a dose adjustment needed for amphotericin B for renal impairment?

A

no dose adjustment needed

47
Q

Does amphotericin B have CSF penetration?

A

No, poor CSF penetration

48
Q

What bind ergosterol in the fungal membrane and cause leakage of intracellular contents?

49
Q

What formulations of amphotericin B reduce toxicity?

A

lipid formulations

50
Q

Dosage forms for amphotericin B

A

IV and oral

51
Q

When to use IV formulatinn of amphotericin B

A

life threatening systemic

infections

52
Q

When to use oral formulation of amphotericin B

A

for GI infections

53
Q

Adverse effects of amp-B

A

rapid toxicity and delayed toxicity

54
Q

Rapid toxicity w/ non-lipid formulations

A

nfusion-related fever, chills, malaise,
rigors (pre-medication -NSAIDs,
diphenhydramine, acetaminophen,
meperidine, hydrocortisone)

55
Q

Delayed toxicity:

A

Nephrotoxicity (may
add to nephrotoxicity of other drugs)
(dose adjustment for conventional form
only)

56
Q

The risk of severe kidney damage during amphotericin B therapy depends on

A

dose and duration of treatment, underlying health and fluid status of the patient, previous or underlying kidney disease, and the receipt of other potentially nephrotoxic drugs

57
Q

What to monitor for kidney damage during ampB therapy

A

Serum creatinine
BUN
Renal Function - Electrolytes LFTs PTT CBC

58
Q

Mechanisms of resistance to Amphotericin B (2)

A
  1. Decreased ergosterol content (defective ERG2 or ERG3 genes)
  2. Alterations in sterol content to those with reduced affinity
    (fecosterol, episterol)
59
Q

Which antifungals decrease ergosterol synthesis and cell membrane formation by inhibiting cytochrome P450 activity (lanosterol 14-α-demethylase)?

60
Q

Azoles are classified as Imidazoles or Triazoles based on

A

number of nitrogen atoms in the five-membered azole ring (Imidazoles = 2; triazoles = 3)

61
Q

What dosage forms are available for azoles?

62
Q

Azoles toxicity is largely due to

A

potential inhibition of mammalian CYP 450s

63
Q

Azoles are substrates/ inhibitors of which CYP 450

A

CYP 3A4, 2C9 and 2C19

64
Q

ADE of azoles

A

risk of GI upset and possible
hepatic toxicities!
drug interactions

65
Q

Mechanisms of resistance to Azoles (4)

A
  1. overexpression or alteration of the drug target
  2. production of low affinity sterols (14α-methylfecosterol)
  3. up-regulation of drug transporters
  4. cellular changes that reduce drug toxicity or enable tolerance of
    drug-induced stress
66
Q

What formulation of azoles can help limit toxicity

A

topical azoles

67
Q

Topical azoles may cause what ADE

A

hypersensitivity reactions

68
Q

Systemic azoles differ in their

A

water solubility, absorption, half-life, etc.

69
Q

Itraconazole (Sporanox®) should not be used in patients with

A

history of CHF

70
Q

Itraconazole (Sporanox®)

A
  • GI upset
  • poor CSF penetration
  • absorption increased by food
71
Q

widest therapeutic index of all the azoles

A

fluconazole

72
Q

Fluconazole (Diflucan)

A
  • oral/IV
  • GI upset
  • 60-80% CSF penetration
73
Q

Only antifungal that achieves therapeutic concentrations in urinary tract

A

fluconazole

74
Q

Voriconazole (Vfend®) toxicities may include

A

rash, elevated hepatic enzymes and visual disturbances

75
Q

Voriconazole (Vfend®)

A
  • oral/IV

- good tissue penetration

76
Q

What co-administration with statins that prolong the QT interval should be avoided

A

Posaconazole (Noxafil®)

77
Q

Posaconazole (Noxafil®)

A
  • oral suspension, tablets, IV

- rash, GI upset, elevated ALT,

78
Q

Posaconazole Oral suspension: Must be taken with

A

high fat meal

79
Q

Isavuconazonium (Cresemba®)

A
  • Oral/IV
  • GI upset
  • shorten QT interval
80
Q

Non-Azole inhibitors of ergosterol synthesis

A

Terbinafine (Lamisil AT®) and Butenafine (Lotrimin Ultra®)

81
Q

Terbinafine (Lamisil AT®) and Butenafine (Lotrimin Ultra®) inhibit

A

ergosterol biosynthesis by
inhibiting the squalene epoxidase -
an earlier step in ergosterol biosynthesis

82
Q

taken up by fungal cytosine permease and converted to active metabolites intracellularly

A

5-flucytosine (Ancobon®)

83
Q

5-flucytosine (Ancobon®)

A
  • active only against yeast
  • oral
  • penetrates CSF
84
Q

5-flucytosine (Ancobon®) moa

A
  • Flucytosine enters cells by cytosine permease
  • Converted to 5-fluorouracil by cytosine deamination, and further
    metabolized to FdUMP and FUTP
  • FdUMP inhibits Thymidylate synthase = inhibits DNA synthesis.
  • FUTP incorporates into RNA and inhibits protein synthesis
85
Q

5-flucytosine (Ancobon®) toxicity is due to

A

metabolism to fluorouracil (possibly by intestinal flora)

86
Q

Fluorouracil metabolite can cause

A
  • reversible bone marrow toxicity

- hepatotoxicity

PHRM 840 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions