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G.I & Nutrition > Hepatobiliary Pharmacology > Flashcards

Hepatobiliary Pharmacology Flashcards

1
Q

T/F HepC viral RNA dependent RNAp lacks proofreading activity

A

T –> leads to a high mutation rate

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2
Q

Most common HCV genotype in US

A

genotype 1

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3
Q

% of people with acute phase who will get chronic HCV

A

85%

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4
Q

% of people with chronic HCV who get cirrhosis

A

20% over 20 years

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5
Q

Factors that increase progression of liver injury due to HCV

A

age >40, male, caucasian/hispanic, smoking, additional liver injury, immunocompromise

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6
Q

How do genotypes of HCV compare in tx response?

A

genotype 1 responds less than 2 and 3

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7
Q

Responsiveness to HCV tx? high viral load

A

less responsive

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8
Q

Responsiveness to HCV tx? age> 40

A

less responsive

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9
Q

Responsiveness to HCV tx? males

A

less responsive

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10
Q

Responsiveness to HCV tx? African Americans

A

less responsive

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11
Q

What genetic polymorphism is associated with less responsiveness to HCV tx?

A

IL28B

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12
Q

Gold standard response to HCV tx?

A

absence of detectable HCV at 6 months after therapy = sustained viral response (SVR) –> <1% chance of relapse at this point, 5x reduction in risk of HCC, elimination of decompensation risk

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13
Q

Traditional tx for HCV

A

peg interferon alpha + ribavirin

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14
Q

MOA of interferon in HCV

A

immune activation (MHC1 expression, tc/NK cell/macrophage activity) and potential direct antiviral activity (inhibition of attachment/uncoating/activation of RNAses)

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15
Q

Traditional tx for HCV

A

peg interferon alpha + ribavirin

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16
Q

MOA of interferon in HCV

A

immune activation (MHC1 expression, tc/NK cell/macrophage activity) and potential direct antiviral activity (inhibition of attachment/uncoating/activation of RNAses)

17
Q

Adverse effects of interferon

A

flu-like symptoms, depression/suicidal ideation, pancytopenia, activation of autoimmune disease, weight loss, infection/cirrhosis, worsening of liver function

18
Q

Ribavirin MOA

A

guanosine analogue –> inhibtion of viral RNAp, induction of lethal mutations in HCV, GTP depletion, modulation of tcell response, favoring Th1–> only works as combination tx by preventing relapse

19
Q

Conceptual complication of monotherapy with specific antivirals

A

development of resistance –> use specific antivirals in combination therapy

e.g. Peg IFN + RBV + Boceprevir/Telaprevir

20
Q

Adverse effects of viral protease inhibitors boceprevir/telaprevir

A

anemia, rash, dysgeusia, anorectal discomfort

21
Q

Adverse effects of viral protease inhibitors boceprevir/telaprevir

A

anemia, rash, dysgeusia, anorectal discomfort

22
Q

What does e antigen indicate in HBV?

A

that the virus is currently replicating (wild type only)

23
Q

Why can’t we resolve HBV infection?

A

we can treat cytoplasmic processes but can’t get the viral DNA out once it’s been incorporated

24
Q

How does HBV cause damage to hepatocytes?

A

mostly due to immune response –> degree of immune tolerance determines whether a chronic infection will develop

25
Q

What does eAg neg/eAb pos in chronic HBV indicate?

A

eAg seroconversion –> to a inactive carrier state/no current replication

OR

core/precore mutation eAg neg chronic Hep B

26
Q

How do we differentiate seroconverted inactive carriers and eAg neg Chronic Hep B?

A

in the mutated state, will have high DNA and high ALT because the virus is still replication and doing its thing

27
Q

What are the benefits of eAg seroconversion?

A

decreased risk of hepatic decompensation and decreased risk of hcc

28
Q

What are the benefits of eAg seroconversion?

A

decreased risk of hepatic decompensation and decreased risk of hcc

29
Q

Is HBsAg loss a good endpoint of therapy

A

No–> rare

30
Q

Is HBsAg loss a good endpoint of therapy

A

No–> rare

31
Q

Tx of chronic HBV

A

peg interferon, viral polymerase inhibitor

*eAg negative patients better off w/o PegIFN

32
Q

Disadvantages of IFN in HBV tx

A

relapse rate in eAg negative pts, side effects, can’t use in decompensated liver disease, limited efficacy in high HBV DNA and low ALT

33
Q

Disadvantages of oral tx in HBV

A

development of drug resistance (e.g. Lamivudine YMDD mutation), long term tx, occasional post-withdrawal flares

34
Q

Disadvantages of oral tx in HBV

A

development of drug resistance (e.g. Lamivudine YMDD mutation), long term tx, occasional post-withdrawal flares

G.I & Nutrition (43 decks)

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