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PHRM 865 > Stahlein > Flashcards

Stahlein Flashcards

1
Q

herpes virus shape

A

double stranded DNA

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2
Q

HSV-1 location and infects who

A

oral herpes
infected as child

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3
Q

HSV-1 ganglion location

A

trigeminal ganglion

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4
Q

HSV-2 location and infects who

A

genital herpes
infected as adult or teenager

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5
Q

HSV-2 ganglion location

A

sacral ganglion

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6
Q

VZV causes what

A

chickenpox as kids
shingles as reativation in adults

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7
Q

CMV is what

A

most adults have it but no symptoms, symptoms seen in immunocompromised
retinitis in AIDS pts

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8
Q

acyclovir MOA

A

competitive inhibitor of viral DNA polymerase
incorporates into DNA
chain terminator

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9
Q

does acyclovir require phosphorylations

A

yes, three
first by viral enzyme

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10
Q

acyclovir resistance

A

mutations in viral thymidine kinase and viral DNA polymerase

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11
Q

valacyclovir MOA

A

competitive inhibitor of viral DNA polymerase
incorporates into DNA to act as chain terminator

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12
Q

valacyclovir metabolism

A

converted to acyclovir by esterases in intestine and liver after intestinal transport

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13
Q

valacyclovir resistance

A

mutations in viral thymidine kinase and viral DNA polymerase

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14
Q

penciclovir is active form of what

A

famciclovir

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15
Q

penciclovir / famciclovir MOA

A

competitive inhibitor of viral DNA polymerase
chain termination but not immediate

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16
Q

which drug has chain termination but allows short elongation before

A

penciclovir
famciclovir

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17
Q
A

acyclovir

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18
Q
A

valacyclovir

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19
Q
A

penciclovir

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20
Q
A

famciclovir

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21
Q

how is famciclovir converted to penciclovir

A

first pass metabolism

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22
Q

ganciclovir MOA

A

competitive inhibitor of viral DNA polymerase
chain termination but not immediate
(same as penciclovir)

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23
Q

ganciclovir more active against what

A

CMV

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24
Q
A

ganciclovir

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25
Q

ganciclovir toxicity

A

myelosuppression!

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26
Q

ganciclovir resistance

A

due to mutations in CMV kinase or CMV DNA polymerase

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27
Q

cross resistance with acyclovir

A

penciclovir due to viral kinase mutants

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28
Q

why can penciclovir have chain elongation

A

2 OH groups allow a couple more additions

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29
Q

ganciclovir cross resistance?

A

mutations in DNA polymerase have cross resistance with foscarnet or cidofovir
NOT for mutations with kinase

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30
Q

valganciclovir is what

A

prodrug of ganciclovir
used for CMV retinitis

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31
Q

foscarnet MOA

A

inhibits viral DNA polymerase, RNA polymerase, and HIV reverse transcriptase
blocks pyrophosphate binding site of DNA polymerase
inhibits cleavage of pyrophosphate from dNTPs so new base can’t be added

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32
Q

does foscarnet require phosphorylation?

A

NO!

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33
Q
A

foscarnet

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34
Q

foscarnet binding site

A

binds binding site usually belonging to gamma pyrophosphate which usually helps ass nucleotides on

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35
Q

clinical use of foscarnet

A

CMV retinitis
use w ganciclovir

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36
Q

foscarnet toxicity

A

renal toxicity

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37
Q

foscarnet resistance

A

mutations in DNA polymerase or HIV reverse transcriptasec

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38
Q

cidofovir MOA

A

competitive inhibitor of viral DNA polymerase and chain terminator

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39
Q

cidofovir is an analog of what

A

cytosine

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40
Q
A

cidofovir

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41
Q

cidofovir, phosphorylations?

A

only needs 2 by cellular kinases

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42
Q

cidofovir highly selective for what

A

DNA polymerase

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43
Q

cidofovir used for what

A

CMV

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44
Q

letermovir MOA

A

inhibits CMV terminase complex by binding pUL56 and preventing packing and cleaving

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45
Q
A

letermovir
non nucleoside

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46
Q

which of the anti-herpes drugs are chain terminators and incorporated into DNA

A

acyclovir
valacyclovir
famciclovir
penciclovir
cidofovir
ganciclovir
valganciclovir

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47
Q

which of the anti-herpes drugs are prodrugs

A

acyclovir
valacyclovir
famciclovir
valganciclovir

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48
Q

influenza virus shape

A

negative stranded RNA virus

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49
Q

influenza vaccine protects against what

A

Flu A and B

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50
Q

2 genes that are subtypes of influenza A

A

hemagglutinin
neuraminidase

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51
Q

how do neuramidase inhibitors work

A

mimic structure of sialic acid at transition state and stall the enzyme activity

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52
Q

what does neuramidase do

A

cleave the bond between hemaglutinin and sialic acid to release virus

53
Q

neuramidase inhibitor drugs

A

oseltamivir
zanamivir
peramivir

54
Q

baloxavir MOA

A

inhibits viral cap snatching of 5’ catch from host mRNA to block transcription and inhibit viral RNA syntheiss and replication

55
Q

baloxavir interactions

A

dairy, metals

56
Q

spectrum of activity of baloxavir

A

flu A and B

57
Q

oseltamivir MOA

A

neuramidase inhibitor

58
Q

oseltamivir metabolism

A

prodrug converted to active form by liver esterases

59
Q

resistance to oseltamivir

A

mutations in active site of neuramidase

60
Q

which neuramidase inhibitor has the most resistance

A

oseltamivir

61
Q

why does oseltamivir have the most resistance

A

floppy structure cant fit in the pocket of neuramidase with mutations but zanamivir can fit even with the mutations

62
Q

zanamivir MOA

A

neuramidase inhibitor and transition state analog

63
Q

zanamivr spectrum of acitvity

A

flu A and B

64
Q

zanamivir dosage form

65
Q

is zanamivir a prodrug

66
Q

peramivir MOA

A

neuramidase inhibitor and transition state analog

67
Q

peramivir spectrum

A

flu A and B

68
Q

hepatitis C shape

A

small positive stranded RNA virus

69
Q

HCV life cycle

A

hep c makes a single polyportein that is cleaved by cellular and viral proteases
- replication complexes are formed
- RNA replication occurs

70
Q

how do interferons have defense against viruses

A

induce synthesis of cellular proteins and have antiviral effects

71
Q

interferon use

A

used to be primary treatment for Hep B and C
- not absorbed orally
- used in combo with ribavairin

72
Q

interferon toxicity

A

flu like symptoms, could cause life threatening side effects

73
Q

ribavirin is what

A

guanisine analog

74
Q

ribavirin MOA

A

inhibits inosine monophosphate dehydrogenase (IMPDH)
- reduces GTP levels (host enzyme)
direct inhibition of viral RNA polymerase
incorporation into viral RNA

75
Q

how do protease inhibitors work

A

mimic the substrate so protease binds and and locked in from being active
- block cleavage of the HCV polyprotein

76
Q

HCV NS3 protease inhibitors

A

grazoprevir
voxilaprevir
glecaprevir

77
Q

-previr class

A

protease inhibitors NS3

78
Q

grazoprevir
voxilaprevir
glecaprevir MOA

A

HCV protease inhibitors
induced fit binding at active site

79
Q

grazoprevir
voxilaprevir
glecaprevir resistance

A

mutations at NS3 active site

80
Q

sofosubir metabolism

A

prodrug, nucleotide analog
converted to monophosphate by liver enzymes

81
Q

sofosubir MOA

A

HCV RNA polymerase inhibitor
incorporated into RNA chain and causes termination

82
Q

sofosubir resistance

A

single mutation in active site of HCV RNA polymerase

83
Q

dasabuvir MOA

A

non nucleoside RNA polymerase inhibitor NS5B

84
Q

dasabuvir binding site

A

palm I site of HCV RNA polymerase (allosteric)
blocks nucleotide incorporation into viral RNA

85
Q

NS5B inhibitors

A

sofosbuvir
dasabuvir

86
Q

NS5A inhibitors

A

ledipasivir
elbasvir
daclatasvir
velpatasvir
pibrentasvir

87
Q

ledipasivir
elbasvir
daclatasvir
velpatasvir
pibrentasvir MOA

A

bind NS5A protein
inhibits viral RNA replication and assem ble or release of infectious viral particles

88
Q

ledipasivir
elbasvir
daclatasvir
velpatasvir
pibrentasvir resistance to NS5A inhibitors

A

mutations in first 100 amino acids
1st gen high resistance for single mutations

89
Q

black box warning for HCV antivirals

A

Hep B reactivation in pts infected with Hep C if taking a direct acting antiviral without interferons

90
Q

hep B infection shape

A

partially double stranded DNA virus

91
Q

anti retrovirals for Hep B

A

lamivudine
tenofovir
entecavir

92
Q

lamivudine MOA

A

incorporated into viral DNA and causes chain termination due to lack of OH group

93
Q

tenofovir metabolism

A

prodrug
only requires two phosphorylatiuions and is stable due to already having a phosphate

94
Q

tenofovir is an analog of what

95
Q

protease inhibitors - previr drug interasctions

A

CYP3A4 substrates
weak inhibitors

96
Q

SARS CoV-2 drugs

A

remdesivir
nirmatrelvir
molnupiravir

97
Q

remdisivir MOA

A

inhibits RNA polymerase
(adenosine analog)

98
Q

nirmatrelvir MOA

A

protease inhibitor
peptidomimetic inhibits active site cysteine residue

99
Q

molnupiravir MOA

A

polymearse inhibitor and chain terminator

100
Q
A

tenofovir
does not have ribose ring
NRTI

101
Q
A

lamivudine
sulfur instead of OH
NRTI

102
Q
A

emtracitibine
sulfur instead of OH
NRTI

103
Q
A

abacavir
double bond instead of OH
NRTI

104
Q

NRTI MOA

A

competitive inhibitors of reverse transcriptase
DNA chain terminator

105
Q

NRTIs

A

abacavir
lamivudine
emtricitabine
tenofovir

106
Q

how are NRTIs activated

A

cellular enzymes phosphorylate

107
Q

tenofovir alefenamide metabolism

A

activated once inside the lymphocytes so drug gets right to infected cells
decreased plasma concentration so decreased toxicities like kidney damage

108
Q

tenofovir alefenamide becomes what

109
Q

TAF dose compared to TDF

A

can use 10 x lower dose

110
Q

tenofovir AF consideration

A

only 2 phosphoryaltions
higher lipid levels

111
Q

NRTIs have a high affinity for what

A

reverse transcriptase than for DNA polymerases

112
Q

how do we get resistasnce to NRTIs

A

NRTIs can’t suppress viral replication 100% so we still have some
we must maintain drug levels above MIC as mutations related to drug conc

113
Q

which drug should we test for HLAB5701 for before starting

A

abacavir
could be lethal

114
Q

non nucleoside RT inhibitors MOA

A

block RNA and DNA dependent polymerase activities
- bind hydrophobic pocket and confer confirmational change

115
Q

NNRTIs drug interactions

116
Q

NNRTI drugs

A

efavirenz
nevirapine
etravirine
rilpivirine

117
Q

do NNRTIs require activation?

118
Q

do mutations that cause resistance to NRTIs confer resistance to NNRTIs?

A

no they are different

119
Q

integrase inhibitors MOA

A

inhibits insertion of HIV DNA into human genome by blocking the strand transfer at the chelating metal level

120
Q

key structural component of integrase inhibitors that enables them to inhibit

A

oxygen atoms chelate with the metals

121
Q

elvitegravir
dolutegravir
bictegravir class

A

integrase inhibitors

122
Q

elvitegravir considerations

A

metabolized by CYP3A4 so taken with cobicistat

123
Q

HIV protease inhibitors mechanism

A

peptidomimetics bind protease and prevent it from cleaving further
causes confirmational change in protease

124
Q

why do we use CYP3A4 inhibitors with proteast inhibitors

A

PIs are metabolized by CYP3A4 so giving ritonavir with it will boost the levels

125
Q

what drug can we use for PI boosting

A

ritonavir to inhibit CYP3A4

126
Q

HIV protease inhibitor drugs

A

darunavir
tipranavir
atazanivir

127
Q

unique features of darunavir

A

makes extensive hydrogen bonds with protease backbone
inhibits HIV protease dimerization

128
Q

HIV protease inhiitors bette4r for resistance

A

darunavir
atazanivir

PHRM 865 (31 decks)

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