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4 Pharma > Antiviral and Antifungal > Flashcards

Antiviral and Antifungal Flashcards

1
Q

HIV receptor?

A

CD4+

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2
Q

HIV co-receptor?

A

CCR5

CXCR4

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3
Q

What part of HIV binds to CD4+ receptor?

A

Env gp 120

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4
Q

What part of HIV fuses with host membrane?

A

gp 41

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5
Q

This anti-HIV drug TARGET that splices polyproteins

A

protease

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6
Q

This anti-HIV drug TARGET which acts on host DNA to form proviral DNA

A

reverse transcriptase

RNA-dependent DNA polymerase

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7
Q

This entry/fusion inhibitor (anti-HIV) binds to CCR5

A

maraviroc

gp120 cannot bind to CCR5 –> blocks entry

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8
Q

This entry/fusion inhibitor (anti-HIV) binds to gp41

A

enfuviritide

blocks fusion of membranes. uses gp41 not gp120 because of gp120’s mutation frequency

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9
Q

This entry/fusion inhibitor requires tropism test (HIV tropism = what cell the HIV infects) and Tx-experienced adults.

(Not for CXCR4 tropic or dual/mixed R5X4)

A

maraviroc

Binds to CCR5 not CXCR4

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10
Q

This entry/fusion inhibitor acts on T-cell

A

Maraviroc (CCR5)

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11
Q

This entry/fusion inhibitor acts on HIV

A

enfuviritide (gp41)

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12
Q

Anti-HIV drug TARGET that inserts viral cDNA into host genome.

A

integrase

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13
Q

RTI subgroup that:

1) are prodrugs: chain terminators
2) are myelosuppressive

A

NRTIs

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14
Q

RTI subgroup that are NOT prodrugs and do not cause myelosuppression

A

NNRTIs

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15
Q

Which nucleoside reverse transcriptase inhibitor acts on nucleoTide not nucleoSide

A

tenofovir

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16
Q

Non-competitive inhibition of RT by NNRTI is achieved by:

A

binding to HIV-1 RT away from catalytic site

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17
Q

These anti-HIV drugs cause lactic acidosis and hepatic steatosis

A

NRTIs

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18
Q

NRTI that causes most BM depression

A

zidovudine, ZDV

aka azidothymidine or AZT

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19
Q

NRTI that causes peripheral neuropathy and pacreatitis

A

stavudine
didanosine
zalcitabine

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20
Q

NRTI that causes headache/nausea/fatigue

A

lamivudine

LEAST TOXIC NRTI

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21
Q

NRTI that causes hyperpigmentation

A

emtricitabine

Newer, more active form of lamivudine

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22
Q

NRTI that causes rash/HSR (5% patients develop allergy)

A

abacavir

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23
Q

NRTI that causes nephropathy

A

tenofovir

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24
Q

Which group of anti-HIV drugs require phosphorylation? (thymidine kinsase)

A

NRTIs

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25
Q

NNRTIs are metabolized by

A

CYP450 (CYP3A4 inducer)

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26
Q

HIV drug that causes insomnia and nightmares:

A

efavirenz

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27
Q

HIV drug that causes insomnia and depression

A

rilpivirine

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28
Q

NNRTI’s that causes rash

A

nevirapine
delavirine
etravirine

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29
Q

Integrase inhibitor:

A

raltegravir

inhibiting HIV integrase prevents the insertion of HIV DNA into human genome

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30
Q

HIV drug that causes toxic epidermal necrolysis

A

raltegravir

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31
Q

-navir drugs =

A

protease inhibitors

think NAVIR/never TEASE

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32
Q

These HIV drugs block cleavage of polyproteins

A

protease inhibitors

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33
Q

Inhibition of HIV-1 protease results in the production of these particles:

A

non-infectious virions

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34
Q

Least potent protease inhibitor, also least toxic and lowest bioavail

A

saquinavir

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35
Q

Most potent protease inhibitor.

A

ritonavir

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36
Q

Protease inhibitor always formulated in combination with ritonavir

A

lopinavir

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37
Q

Ritonavir inhibits CYP34A metabolism of this protease inhibitor

A

lopinavir

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38
Q

Protease inhibitors that cause sulfa allergy

A

darunavir
tipranavir
fosamprenavir

DTF

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39
Q

Protease inhibitor that has replaced amprenavir

A

fosamprenavir

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40
Q

Protease that causes most drug interactions by acting on CYP450 groups

A

ritonavir

induce 1A2
inhibit 2D6, 3A4

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41
Q

Fixed combo of elvitegravir, cobicistat, tenofovir, emtricitabine:

A

Stribild

Elvitegravir is ONLY used in this combination.

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42
Q

Fixed combination of tenofovir + emtricabone

A

Truvada

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43
Q

Drug group that causes DM Type 2 like syndrome: hyperglycemia, lipodystrophy

A

Protease inhibitors

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44
Q

Fusion inhibitor for HSV-1?

A

docosanol

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45
Q

When to use docosanol?

A

during PRODROME, before visible lesions

46
Q

DNA Polymerase inhibitor used in HSV and VZV

A

acyclovir

newer drugs: famciclovir, valaciclovir

47
Q

Prodrug of acyclovir (+valine)

A

valaciclovir

better bioavailabilty than acyclovir

48
Q

Prodrug of penciclovir

A

famciclovir

[valaciclovir –> acyclovir
famciclovir –> penciclovir]

49
Q

Ophthalmic herpetic drugs

A

vidarabine
trifluridine
idoxuridine

50
Q

Drug therapy for herpes labialis

A

oral acyclobir, famciclovir, valaciclovir

then
decosanol (oral), acyclovir (topical)

51
Q

Drug therapy for disseminated herpes simplex

A

IV acyclovir

52
Q

Drug therapy for herpes simplex genitalis

A

Oral therapy not topical

53
Q

Drug therapy for chicken pox

A

acyclovir, valaciclovir

54
Q

DNA polymerase inhibitors used for CMV infection (CMV retinitis)

A

ganciclovir
valganciclovir
cidofovir

55
Q

What drug is a prodrug of ganciclovir?

A

valganciclovir

better BA

56
Q

DNA polymerase inhibitors REQUIRE vrial kinase phosphorylation except for:

A

cidofovir - nucleoside DNA PI
foscarnet - non-nucleoside DNA PI

cidofovir requires cellular kinases.
foscarnet does not require phosphorylation.

57
Q

Foscarnet is an analog of

A

pyrophosphate

NON-NUCLEOSIDE analog DNA polymerase inhibitor –> THEREFORE not an antimetabolite –> does NOT cause BMS!!

58
Q

MoA: inhibit pyrophosphate exchange during DNA replication

A

foscarnet

59
Q

DNA polymeriase inhibitor used as 2nd line of defense against infections which are resistant to ganciclovir or acyclovir

A

foscarnet

60
Q

Mechanism of resistance against acyclovir

A

lack of thymidine kinase

61
Q

Mechanism of resistance against ganciclovir

A

lack of viral kinase

mutated CMV DNA polymerase

62
Q

Drug therapy for Influenza A only

A

amantidine

rimantidine

63
Q

MoA of anti-influenza A only drugs:

A

Blocks M2 protein (proton channel) –> blocks influx of protons –> THEREBY blocking uncoating (uncoating occurs AFTER viral ENTRY)

64
Q

Derivative of amantadine with fewer CNS effects and extensive hepatic metabolism

A

rimantidine

65
Q

Anti-viral used as weak therapy in Parkinson’s

A

amantidine

66
Q

Drug therapy for Influenza A or B

A

zanamivir

oseltamivir

67
Q

MoA of anti-influenza A/B:

A

Inhibits neuraminidase (NA) –> inhibits RELEASE and spread

68
Q

Release inhibitor (influenza A/B) delivered directly via diskhaler

A

zanamivir

69
Q

Release inhibitor (Influenza A/B) delivered orally

A

oseltamivir

70
Q

Oseltamivir is activated by what enzymes?

A

hepatic esterases

71
Q

DNA polymerase inhibitors for Hep B

A 
lamivudine (least toxic NRTI for HIV)
entecavir
telbivudin
adefovir
tenofovir (NtRTI for HIV)
72
Q

HIV NRTI/NtRTI also used in Hep B?

A

lamivudine

tenofovir

73
Q

Hep C drug

A

ribavirin

74
Q

Quadrivalent HPV vaccine (6, 11, 16, 18)

A

gardasil

75
Q

Bivalent HPV vaccine (16 and 18)

A

cervarix

76
Q

This drug is a guanosine analog (antimetabolite) that inhibits IMP dehydrogenase which inhibits GUANINE nucleotide synthesis.

A

ribavirin

77
Q

Drug therapy for HPV – antimitotic

A

podofilox

78
Q

Drug therapy for HPV – immunomodulation

A

imiquimod

induces cytokines/chemokines for antiviral effects.

79
Q

Anti-fungals which bind to ERGOSTEROL as their MoA

A

polyene macrolides (amphotericin B, nystatin)

80
Q

Polyene macrolide for systemic, serious infections

A

amphotericin B

81
Q

Polyene macrolide used for topical

A

nystatin

82
Q

Immediate toxic effects of amphotericin B can be countered by using:

A

paracetamol (fever/chills/headache)

83
Q

Most significant toxicity caused by ampho B

A

nephrotoxicity

also hematotoxic (anemia) and causes phlebitis

84
Q

Newer preparation of amphotericin B that reduces toxicity

A

lipid formulation –> promotes slower release of drug

85
Q

Drug therapy for mucocutaneous candidiasis

A

nystatin

86
Q

Anti-fungal MoA: inhibit ergosterol SYNTHESIS by inhibiting CYP450 enzyme that converts lanosterol to ergosterol (also substrate of human CYP)

A

Azoles

87
Q

Only imidazole with oral and topical preparation

A

ketoconazole

88
Q

Azole subgroup with HIGHER selectivity for fungal CYP450

A

triazole

89
Q

Ketoconazole decreases absorption of these drugs

A

antacids
H2 blockers
PPIs
anticholinergics

90
Q

Most popular purely topical imidazole

A

clotrimazole

91
Q

Triazole used for tinea unguium and as an alternative to amphotericin B for aspergillosis

A

itraconazole

92
Q

Triazole used in cryptococcus meningitis, candidiasis BUT NO activity against aspergillus

A

fluconazole

93
Q

DOC for invasive aspergillosis

A

voriconazole

94
Q

Azole with BROADEST spectrum; only azole active against mucormycosis and zygomycosis

A

posaconazole

95
Q

Azole that can cause changes in vision like blurring or color changes

A

voriconazole

96
Q

Drug therapy for dermatophytosis AND fungicidal?

A

allylamine (terbinafine)

fungistatic drug for dermatophytosis = griseofulvin

97
Q

MoA: binds to fungal TUBULIN (antimitotic)

A

griseofulvin

fungistatic –> does not treat infected structures but protects new structures

98
Q

Antifungal drug that is converted to 5-FU and inhibits fungal thymidylate synthetase

A

flucytosine

99
Q

MoA of allylamines

A

inhibits squalene epoxidase –> which inhibits ergosterol synthesis

squalene is toxic to fungus as well

100
Q

Combination therapy in cryptococcal meningitis

A

Amphotericin B + flucytosine

also treated with fluconazole

101
Q

Combination therapy in chromoblastomycosis

A

itraconazole + flucytosine

102
Q

Inhibits SQUALENE epoxidase causing accumulation of squalene

A

terbinafine

103
Q

Drug used in invasive aspergillosis and approved as empiric therapy during FEBRILE NEUTROPENIA (presumed fungal infections)

A

caspofungin

104
Q

Echinocandins MoA

A

inhibit glucan synthase complex resulting in a disruption of fungal cell wall –> cell death

105
Q

Treatment of tinea capitis (mode of delivery)

A

oral

106
Q

Treatment of tinea barbae

A

topical - mild

oral - severe

107
Q

Treatment of tinea corporis

A

topical - small

oral - extensive

108
Q

Treatment of tinea manuum

A

oral or topical

109
Q

Treatment of tinea cruris

A

oral and topical combination

110
Q

Treatment of tinea pedis

A

topical

oral - thickening of soles

111
Q

Treatment of unguium

A

oral (itraconazole, terbinafine, griseofulvin)

4 Pharma (7 decks)

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