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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
ganciclovir toxicity
myelosuppression!
26
ganciclovir resistance
due to mutations in CMV kinase or CMV DNA polymerase
27
cross resistance with acyclovir
penciclovir due to viral kinase mutants
28
why can penciclovir have chain elongation
2 OH groups allow a couple more additions
29
ganciclovir cross resistance?
mutations in DNA polymerase have cross resistance with foscarnet or cidofovir NOT for mutations with kinase
30
valganciclovir is what
prodrug of ganciclovir used for CMV retinitis
31
foscarnet MOA
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
32
does foscarnet require phosphorylation?
NO!
33
foscarnet
34
foscarnet binding site
binds binding site usually belonging to gamma pyrophosphate which usually helps ass nucleotides on
35
clinical use of foscarnet
CMV retinitis use w ganciclovir
36
foscarnet toxicity
renal toxicity
37
foscarnet resistance
mutations in DNA polymerase or HIV reverse transcriptasec
38
cidofovir MOA
competitive inhibitor of viral DNA polymerase and chain terminator
39
cidofovir is an analog of what
cytosine
40
cidofovir
41
cidofovir, phosphorylations?
only needs 2 by cellular kinases
42
cidofovir highly selective for what
DNA polymerase
43
cidofovir used for what
CMV
44
letermovir MOA
inhibits CMV terminase complex by binding pUL56 and preventing packing and cleaving
45
letermovir non nucleoside
46
which of the anti-herpes drugs are chain terminators and incorporated into DNA
acyclovir valacyclovir famciclovir penciclovir cidofovir ganciclovir valganciclovir
47
which of the anti-herpes drugs are prodrugs
acyclovir valacyclovir famciclovir valganciclovir
48
influenza virus shape
negative stranded RNA virus
49
influenza vaccine protects against what
Flu A and B
50
2 genes that are subtypes of influenza A
hemagglutinin neuraminidase
51
how do neuramidase inhibitors work
mimic structure of sialic acid at transition state and stall the enzyme activity
52
what does neuramidase do
cleave the bond between hemaglutinin and sialic acid to release virus
53
neuramidase inhibitor drugs
oseltamivir zanamivir peramivir
54
baloxavir MOA
inhibits viral cap snatching of 5' catch from host mRNA to block transcription and inhibit viral RNA syntheiss and replication
55
baloxavir interactions
dairy, metals
56
spectrum of activity of baloxavir
flu A and B
57
oseltamivir MOA
neuramidase inhibitor
58
oseltamivir metabolism
prodrug converted to active form by liver esterases
59
resistance to oseltamivir
mutations in active site of neuramidase
60
which neuramidase inhibitor has the most resistance
oseltamivir
61
why does oseltamivir have the most resistance
floppy structure cant fit in the pocket of neuramidase with mutations but zanamivir can fit even with the mutations
62
zanamivir MOA
neuramidase inhibitor and transition state analog
63
zanamivr spectrum of acitvity
flu A and B
64
zanamivir dosage form
inhaler
65
is zanamivir a prodrug
NO
66
peramivir MOA
neuramidase inhibitor and transition state analog
67
peramivir spectrum
flu A and B
68
hepatitis C shape
small positive stranded RNA virus
69
HCV life cycle
hep c makes a single polyportein that is cleaved by cellular and viral proteases - replication complexes are formed - RNA replication occurs
70
how do interferons have defense against viruses
induce synthesis of cellular proteins and have antiviral effects
71
interferon use
used to be primary treatment for Hep B and C - not absorbed orally - used in combo with ribavairin
72
interferon toxicity
flu like symptoms, could cause life threatening side effects
73
ribavirin is what
guanisine analog
74
ribavirin MOA
inhibits inosine monophosphate dehydrogenase (IMPDH) - reduces GTP levels (host enzyme) direct inhibition of viral RNA polymerase incorporation into viral RNA
75
how do protease inhibitors work
mimic the substrate so protease binds and and locked in from being active - block cleavage of the HCV polyprotein
76
HCV NS3 protease inhibitors
grazoprevir voxilaprevir glecaprevir
77
-previr class
protease inhibitors NS3
78
grazoprevir voxilaprevir glecaprevir MOA
HCV protease inhibitors induced fit binding at active site
79
grazoprevir voxilaprevir glecaprevir resistance
mutations at NS3 active site
80
sofosubir metabolism
prodrug, nucleotide analog converted to monophosphate by liver enzymes
81
sofosubir MOA
HCV RNA polymerase inhibitor incorporated into RNA chain and causes termination
82
sofosubir resistance
single mutation in active site of HCV RNA polymerase
83
dasabuvir MOA
non nucleoside RNA polymerase inhibitor NS5B
84
dasabuvir binding site
palm I site of HCV RNA polymerase (allosteric) blocks nucleotide incorporation into viral RNA
85
NS5B inhibitors
sofosbuvir dasabuvir
86
NS5A inhibitors
ledipasivir elbasvir daclatasvir velpatasvir pibrentasvir
87
ledipasivir elbasvir daclatasvir velpatasvir pibrentasvir MOA
bind NS5A protein inhibits viral RNA replication and assem ble or release of infectious viral particles
88
ledipasivir elbasvir daclatasvir velpatasvir pibrentasvir resistance to NS5A inhibitors
mutations in first 100 amino acids 1st gen high resistance for single mutations
89
black box warning for HCV antivirals
Hep B reactivation in pts infected with Hep C if taking a direct acting antiviral without interferons
90
hep B infection shape
partially double stranded DNA virus
91
anti retrovirals for Hep B
lamivudine tenofovir entecavir
92
lamivudine MOA
incorporated into viral DNA and causes chain termination due to lack of OH group
93
tenofovir metabolism
prodrug only requires two phosphorylatiuions and is stable due to already having a phosphate
94
tenofovir is an analog of what
adenosine
95
protease inhibitors - previr drug interasctions
CYP3A4 substrates weak inhibitors
96
SARS CoV-2 drugs
remdesivir nirmatrelvir molnupiravir
97
remdisivir MOA
inhibits RNA polymerase (adenosine analog)
98
nirmatrelvir MOA
protease inhibitor peptidomimetic inhibits active site cysteine residue
99
molnupiravir MOA
polymearse inhibitor and chain terminator
100
tenofovir does not have ribose ring NRTI
101
lamivudine sulfur instead of OH NRTI
102
emtracitibine sulfur instead of OH NRTI
103
abacavir double bond instead of OH NRTI
104
NRTI MOA
competitive inhibitors of reverse transcriptase DNA chain terminator
105
NRTIs
abacavir lamivudine emtricitabine tenofovir
106
how are NRTIs activated
cellular enzymes phosphorylate
107
tenofovir alefenamide metabolism
activated once inside the lymphocytes so drug gets right to infected cells decreased plasma concentration so decreased toxicities like kidney damage
108
tenofovir alefenamide becomes what
TDF
109
TAF dose compared to TDF
can use 10 x lower dose
110
tenofovir AF consideration
only 2 phosphoryaltions higher lipid levels
111
NRTIs have a high affinity for what
reverse transcriptase than for DNA polymerases
112
how do we get resistasnce to NRTIs
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
which drug should we test for HLAB5701 for before starting
abacavir could be lethal
114
non nucleoside RT inhibitors MOA
block RNA and DNA dependent polymerase activities - bind hydrophobic pocket and confer confirmational change
115
NNRTIs drug interactions
CYP3A4
116
NNRTI drugs
efavirenz nevirapine etravirine rilpivirine
117
do NNRTIs require activation?
no
118
do mutations that cause resistance to NRTIs confer resistance to NNRTIs?
no they are different
119
integrase inhibitors MOA
inhibits insertion of HIV DNA into human genome by blocking the strand transfer at the chelating metal level
120
key structural component of integrase inhibitors that enables them to inhibit
oxygen atoms chelate with the metals
121
elvitegravir dolutegravir bictegravir class
integrase inhibitors
122
elvitegravir considerations
metabolized by CYP3A4 so taken with cobicistat
123
HIV protease inhibitors mechanism
peptidomimetics bind protease and prevent it from cleaving further causes confirmational change in protease
124
why do we use CYP3A4 inhibitors with proteast inhibitors
PIs are metabolized by CYP3A4 so giving ritonavir with it will boost the levels
125
what drug can we use for PI boosting
ritonavir to inhibit CYP3A4
126
HIV protease inhibitor drugs
darunavir tipranavir atazanivir
127
unique features of darunavir
makes extensive hydrogen bonds with protease backbone inhibits HIV protease dimerization
128
HIV protease inhiitors bette4r for resistance
darunavir atazanivir

PHRM 865 (33 decks)

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