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ID > Antivirals and Antifungals > Flashcards

Antivirals and Antifungals Flashcards

1
Q

what are the oral nucleoside analogs

A

acyclovir, valacyclovir, famciclovir

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2
Q

acyclovir requires what steps

A

3 phosphorylation steps: becomes acyclovir monophosphate via viral thymidine kinase. then converts to diphosphate and triphosphate by host cell kinases like guanylate kinase. the drug requires viral kinase for initial phosphorylation, so acyclovir is selectively activated only in infected cells

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3
Q

acyclovir mechanism

A

inhibits viral DNA synthesis by competition with deoxyGTP for viral DNA polymerase, resulting in binding to DNA template as an irreversible complex. chain termination following incorporation into the viral DNA

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4
Q

valacyclovir structure

A

L-valyl ester of acyclovir

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5
Q

famciclovir structure

A

diacetyl ester prodrug of 6-deoxy penciclovir, an acyclic guanosine analog

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6
Q

what is different about penciclovir from acyclovir

A

does not cause chain termination

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7
Q

docosanol structure

A

saturated 22 carbon aliphatic alcohol

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8
Q

docosanol mechanism

A

inhibits fusion between the host cell membrane and the HSV envelope, thereby preventing entry into cells and subsequent viral replication

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9
Q

baloxavir marboxil mechanism

A

prodrug converted by hydrolysis to baloxavir, a cap-dependent endonuclease inhibitor that interferes with viral RNA transcription and blocks virus replication

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10
Q

neuraminidase inhibitors

A

oseltamivir, zanamivir

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11
Q

neuraminidase inhibitors mechanism

A

interfere with the release of progeny influenza A and B virus from infected host cells, thus halting spread. competitively and reversibly interact with the enzyme active site to inhibit viral neuraminidase activity

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12
Q

adamantanes

A

amantadine, rimantadine

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13
Q

adamantanes mechanism

A

block the M2 protein ion channel of the virus particle and inhibit uncoating of the viral RNA within infected host cells, thus preventing its replication

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14
Q

griseofulvin mechanism

A

fungistatic: interferes with fungal mitosis and nuclear acid synthesis.

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15
Q

nystatin structure

A

polyene macrolide

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16
Q

nystatin mechanism

A

binds to sterols in fungal cell membrane, changing the cell wall permeability allowing for leakage of cellular contents

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17
Q

terbinafine structure

A

synthetic allylamine

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18
Q

terbinafine mechanism

A

inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi. results in a deficiency in ergosterol within the fungal cell membrane and results in fungal cell death. leads to the accumulation of sterol squalene, which is toxic to the organism

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19
Q

what are the imidazoles

A

clotrimazole, miconazole, ketoconazole

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20
Q

structure of imidazoles

A

2-nitrogen azole ring

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21
Q

imidazoles mechanism

A

inhibits the CYP51 enzyme lanosterol 14-alpha-demethylase which converts lanosterol to ergosterol in fungi cellular membranes. inability to produce ergosterol increases membrane permeability, which results in cell lysis and death

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22
Q

what is ergosterol

A

the most abundant sterol in fungal cell membranes, aids in the regulation of permeability and fluidity

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23
Q

what are the triazoles

A

voriconazole, itraconazole, fluconazole, posaconazole

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24
Q

triazoles structure

A

3-nitrogen ring

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25
Q

acyclovir activity against?

A

HSV1, HSV2, VSV. FAR MORE POTENT AGAINST HSV COMPARED TO VSV

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26
Q

bioavailability of acyclovir

A

very low, 15-20% and unaffected by food

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27
Q

elimination considerations for acyclovir

A

eliminated via the kidney, so reduction in dose may be necessary in reduced kidney function

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28
Q

counseling for acyclovir

A

take the dose with plenty of water to reduce the likelihood of acute kidney injury secondary to crystal-induced nephropathy

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29
Q

what happens to valacyclovir upon PO administration

A

it is rapidly converted to acyclovir via first pass enzymatic hydrolysis in the liver and intestine. results in serum levels that are 3-5x greater

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30
Q

valacyclovir bioavailability

A

54-70%

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31
Q

what happens to famciclovir after PO administration

A

it is rapidly deacetylated and oxidized by first pass metabolism to penciclovir

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32
Q

famciclovir bioavailability

A

70%

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33
Q

what are the instructions for docosanol

A

specific time: apply within 12 hours of the onset of prodromal symptoms, 5x daily

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34
Q

what does baloxavir have activity against

A

influenza A and B

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35
Q

half life of baloxavir

A

LONG, 80 hours. given as a single dose treatment initiated within 48 hours of the onset of symptoms

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36
Q

how is baloxavir metabolized

A

UGT1A3, minor contributions from CYP3A4

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37
Q

what is an advantage with baloxavir

A

it binds to a different active site than the neuraminidase inhibitors, so you can enhance activity by combining these agents. it is well tolerated.

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38
Q

counseling point for baloxavir

A

do not take with cation-containing products (antacids) or dairy products

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39
Q

what do the neuraminidase inhibitors have activity against

A

influenza A and B

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40
Q

neuraminidase inhibitors bioavailability

A

80%

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41
Q

elimination considerations for neuraminidase inhibitors

A

eliminated via the kidney, dose adjustment is necessary in patients with impaired kidney function

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42
Q

when to give neuraminidase inhibitors

A

early administration is crucial: influenza illness peaks at 24-72 hours after the onset of illness

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43
Q

how long is neuraminidase inhibitor course of therapy

A

5-days within 48h after onset of symptoms

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44
Q

how is zanamivir given

A

it is given via inhalation and administered directly to the respiratory tract: 10-20% reaches the lungs. Not recommended in patients with underlying airway disease

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45
Q

what do the adamantanes have activity against

A

influenza A only

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46
Q

dose reductions for amantadine

A

elderly and reduced kidney function

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47
Q

dose reductions for rimantadine

A

elderly, reduced kidney function, severe reduced hepatic function

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48
Q

griseofulvin absorption

A

Ultra-microsize almost complete absorption. Microsize 27-72%

49
Q

counseling point for griseofulvin

A

take with a fatty meal: absorption is enhanced by fatty meal

50
Q

griseofulvin adverse effects

A

rash: can be phototoxic/photoallergic or not. transient headaches that occur early in therapy and cease spontaneously. dizziness, mental confusion, GI upset

51
Q

microsize dose

A

500 mg/day

52
Q

ultra-microsize dose

A

375 mg/day

53
Q

griseofulvin duration for ringworm

A

2-4wks

54
Q

griseofulvin duration for jock itch

A

6 wks

55
Q

griseofulvin duration for scalp ringworm

A

4-6wks

56
Q

griseofulvin duration for athlete’s foot

A

4-8wks

57
Q

griseofulvin duration for onychomycosis

A

4-6 months

58
Q

nystatin major PK consideration

A

absorption is minimal, used topically only

59
Q

nystatin adverse effects

A

diarrhea, nausea, stomach pain, vomiting

60
Q

terbinafine adverse effects

A

rash, d/v, dyspepsia, abdom pain, vision color confusion, decreased visual acuity, depression, taste disturbance, reversible severe neutropenia, hepatic failure, hypersensitivity, changes in ocular lens and retina, smell disturbance

61
Q

terbinafine drug interactions

A

CYP2D6

62
Q

difference in safety profile between imidazoles and triazoles?

A

imidazoles exhibit less selectivity for target enzyme, so greater frequency of ADRs. triazoles exhibit greater selectivity for target enzyme, thus have a better safety profile.

63
Q

uncomplicated vaginal candidiasis

A

mild/moderate symptoms, sporadic, candida albicans, normal host

64
Q

complicated vaginal candidiasis

A

ANY of the following: severe symptoms, recurrent, nonalbicans, abnormal host (DM, pregnant, immunosuppressed, recurrent)

65
Q

duration for topical, vaginal candidiasis

A

uncomplicated: 1-3 days, complicated: 7-14 days

66
Q

duration for systemic, vaginal candidiasis

A

uncomplicated: fluconazole 150 mg x 1. complicated: q72h x 2

67
Q

vaginal candidiasis in pregnancy

A

use topicals

68
Q

what defines recurrent vaginal candidiasis

A

4+ infections/year

69
Q

treatment for recurrent vaginal candidiasis

A

fluconazole q72h x 3, then weekly x 6 months

70
Q

options for oral candidiasis, mild

A

nystatin suspension 400,000-600,000 u 4x/day swish, retain, swallow. or clotrimazole troches 10 mg dissolved BID. x 7-14 days

71
Q

options for oral candidiasis, severe

A

systemic: fluconazole 100 mg Day 1. 100-200 mg/day x 7-14 days (choice for immunocompromised)

72
Q

who typically gets oral candidiasis

A

denture-wearers, dry mouth, antibiotics, inhaled steroids

73
Q

topical options for onychomycosis

A

ciclopirox 8% or efinaconazole 10% daily x 48 weeks

74
Q

1st line systemic option for onychomycosis

A

terbinafine daily x 6 weeks if fingernail or 12 weeks if toenail

75
Q

other systemic options for onychomycosis

A

itraconazole, fluconazole, griseofulvin (4-6 months)

76
Q

BCS class of griseofulvin

A

class II: very insoluble, high permeability

77
Q

griseofulvin is fungi____

A

static

78
Q

in addition to inhibiting fungal cell mitosis, griseofulvin binds to _____

A

alpha and beta tubulin to interfere with the function of spindle and cytoplasmic microtubules

79
Q

name for body surface ringworm

A

tinea corporis

80
Q

name for jock itch

A

tinea cruris

81
Q

name for scalp ringworm

A

tinea capitis

82
Q

name for athlete’s foot

A

tinea pedis

83
Q

name for onychomycosis

A

tinea unguium

84
Q

besides taking griseofulvin with a high fat meal, what else should you counsel the patient

A

use suncreen

85
Q

nystatin works similarly to _____

A

amphotericin b

86
Q

terbinafine is largely associated with treatment of _____

A

onychomycosis

87
Q

terbinafine is fungi____ and ____philic

A

fungicidal and keratophilic

88
Q

what is the difference in mechanism between terbinafine and the imidazoles if they both cause ergosterol deficiency?

A

imidazoles interfere with the CYP51 enzyme

89
Q

what labs to check with terbinafine

A

LFTs baseline and at 6 weeks

90
Q

pros and cons of pulsed dosing with terbinafine

A

less effective, but reduces ADE, cost, and improves patient compliance

91
Q

drug options when the fungal infection reaches follicles, dermis, or nails

A

terbinafine, itraconazole, fluconazole, griseofulvin

92
Q

what to avoid with diaper dermatitis

A

topical corticosteroids with antifungal creams

93
Q

ketoconazole drug interactions

A

CYP3A4 inhibitor

94
Q

characteristics of viruses

A

obligate intracellular parasites, cannot replicate independent of host, must be infectious to endure, most use host cellular machinery to produce necessary components, must self-assemble, cannot make energy/proteins outside of host cell

95
Q

components of viruses

A

contain RNA or DNA (not both), have a naked capsid or envelope morphology. viral components are ASSEMBLED (not replicated by cell division)

96
Q

surface structures of the capsid or envelope are critical for interaction with the target host cell through _____

A

viral attachment proteins (VAPs)

97
Q

viruses contain ______ that are crucial for entry into host cell and replication

A

enzymes that catalyze reactions

98
Q

nucleocapsid characteristics

A

viral nucleic acid genome, protein coat serves as rigid structure, serves to package/protect/deliver during viral transmission, surrounded by lipid layer with insertions, may be contained in an envelope made of lipids/proteins/glycoproteins in aqueous conditions

99
Q

envelope characteristics

A

environmentally labile, must stay in aqueous medium and cannot survive GI tract, spreads via large droplets/secretions/transfusions, does not need to kill host cell in order to spread, antibody and cell-mediated immune response often secondary to envelope, elicits hypersensitivity and inflammatory responses

100
Q

naked capsid characteristics

A

environmentally stable (temp, acidic, detergents, drying), spread via fomites/hand to hand/dust/small droplets, may dry out but still infectious, ability to survive harsh acidic pH of the stomach, resistant to detergents, antibodies must be generated for immune protection

101
Q

viruses penetrate a host cell membrane via a ______

A

receptor-mediated interaction

102
Q

once the virus attaches to the host cell membrane, the viral genetic material enters the host cell and what happens

A

the cellular machinery of the host transcribes the viral genome, followed by translation of viral proteins

103
Q

if RNA virus

A

host cell ribosomes translate RNA into protein

104
Q

if retrovirus

A

RNA transcribed into DNA (reverse transcriptase) before entering viral genome

105
Q

if DNA virus

A

transcription into mRNA, then translation into viral proteins

106
Q

viral enzymes assemble material into ____ which are then released

A

VIRIONS

107
Q

_____ is the complete infective form of a virus outside of a host cell

A

virion

108
Q

steps of viral pathogenesis

A

acquisition, primary site of infection, activation of innate, incubation period, replication in target tissue, adaptive immune response, contagion, resolution or persistent/chronic infection

109
Q

common cold/flu follows what patten of infection

A

acute

110
Q

HSV follows what pattern of infection

A

latent

111
Q

varicella-zoster follows that pattern of infection

A

chronic

112
Q

susceptibility to viral infection and severity: the virus

A

viral load, genetics of virus, stability of virion in environment, replication and secretion into aerosols

113
Q

susceptibility to viral infection and severity: the host

A

genetics of the host, immune status, age, overall general health, asymptomatic transmission, risk factors (travel, environment like daycare, sexual activity)

114
Q

how is valacyclovir prodrug converted to acyclovir

A

first pass enzymatic hydrolysis in liver and intestine

115
Q

in pregnant women with recurrent HSV, when is suppressive therapy recommended

A

36 weeks gestation

116
Q

how is famciclovir prodrug converted to penciclovir

A

deacetylated and oxidized by first pass metabolism

117
Q

influenza b viruses infect

A

only people

118
Q

influenza a viruses infect

A

people and animals

119
Q

neuraminidase inhibitors are analogs of ___

A

sialic acid

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