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GI II Exam I AP > Drugs - Treatment of Hepatitis (Kinder) > Flashcards

Drugs - Treatment of Hepatitis (Kinder) Flashcards

1
Q

how do you confirm the specific hepatitis diagnosis

A

serologic tests

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2
Q

what are the symptoms of hepatitis

A

nausea, anorexia, fever, malaise, or abdominal pain

b) – PLUS – jaundice or elevation in serum aminotransferase levels

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3
Q

what type of viruses are Hep A and C

A

RNA virus

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4
Q

Hep B is what type of virus

A

DNA virus

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5
Q

Hep A
transmission
incubation period

popultations at risk

A

fecal- oral

28 days

  • Travelers to countries with high/intermediate prevalence of HAV
  • Children, household, or personal contacts
  • Low socioeconomic status (poor sanitation and overcrowding)
  • Persons working with nonhuman primates
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6
Q

Hep B

transmission
incubation period
populations at risk

A

sexual, parenteral, perinatal

6-24 weeks

sero - test is IgM Ab to HAV

  • Sex partners of infected persons
  • Infants born to infected mothers
  • Men who have sex with men
  • Injection drug users
  • Household contacts of persons with chronic HBV
  • Healthcare workers at risk for occupational exposure
  • Hemodialysis patients
  • Travelers to countries with high/intermediate prevalence of HBV
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7
Q

Hep C

transmission
Incubation period

populations at risk

A

***most common blood borne pathogen

sexual
parenteral***, perinatal

4-12 weeks

  • Current or former injection drug users
  • Recipients of clotting factor concentrates before 1987
  • Recipients of blood transfusions or solid organ transplants before July 1992
  • Chronic hemodialysis patients
  • Persons with known exposure to HCV
  • Persons with HIV
  • Children born to HCV-positive mothers
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8
Q

how do you treat Hep A

A

supportive care

prevention and prophylaxis–> good hand hygiene

Ig for pre-exposure and post-exposure

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9
Q

what are the symptoms of HepB

A

fever, anorexia, nausea, vomiting, jaundice, dark urine, pale stools, abdominal pain

i) Many neonates, children, and adults have no clinical symptoms
ii) Children (perinatal exposure) pose a special problem:
(1) Viral replication may last decades while patient is asymptomatic, undiagnosed, and highly infectious

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10
Q

what does it mean if HBsAg is found

A

pt is infectious

high levels occur during acute or chronic infection

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11
Q

what does it mean if you find hepatitis B surface antibodies

A

identification of surface antibodies may be interpreted as recovery or immunity from HBV. These antibodies will also arise after successful vaccination

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12
Q

what does total hep B core antibody mean

A

appears at onset of infection (will persist for life) and indicates previous or ongoing infection.

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13
Q

IgM anti-HBc means what

A

delineates recent infection with HBV within previous 6 months

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14
Q

hep B e antigen

A

indicates high levels of HBV. Found during acute and chronic infection and indicates viral replication.

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15
Q

hep B e antibody

A

indicates lower levels of HBV. Immune system may produce these antibodies after acute infection or after a burst in viral replication. Spontaneous antigen to antibody conversion (aka “seroconversion”) is a good predictor of viral clearance in those receiving treatment.

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16
Q

what are the symptoms of Hep C

A

c) Mild/non-specific symptoms (33% of patients): fatigue, anorexia, weakness, jaundice, abdominal pain, dark urine
e) Chronic symptoms: few if any; persistent fatigue, right upper quadrant pain, nausea, poor appetite

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17
Q

what is the progression of Hep C

A

d) Acute infections rarely progress to fulminant hepatitis, but 85% will go on to develop chronic HCV
i) Increases risk of cirrhosis, end-stage liver disease, HCC

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18
Q

what are the indications for treatment of HCV

A

i) ALL patients with virologic evidence of chronic HCV infection (detectable HCV viral level over a 6 month period)
ii) Untreated patients with chronic HCV infection, circulating HCV-RNA, increased ALT levels, advanced fibrosis, or compensated liver disease

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19
Q

what are the contraindications for treatment of HCV

A

(1) Treatment not recommended for patients with decompensated liver disease or history of severe, uncontrolled psychiatric disorder

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20
Q

what are the factors associated with a favorable treatment response in HCV

A

i) HCV genotype 2 or 3
ii) Absence of cirrhosis
iii) Low pretreatment HCV RNA level

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21
Q

what is the MOA of interferon alfa

A

agent used for HBV

inhibits viral penetration, translation, transcription, protein processing, maturation, and release. Enhanced phagocytic activity of macrophages and augmentation of proliferation/survival of cytotoxic T-cells.

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22
Q

what are the advantages of inteferon alpha versus nucleoside/nucleotide analog (NA’s)

A

finite duration of treatment, resistance is not a problem, responses are more durable

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23
Q

what are the ADR’s of interferon alpha

transient
chronic

A

> 30% of patients will experience flu-like illness within the first week of therapy (headache, fever, chills, myalgias, malaise) which occur ~6 hours following dose (generally resolves with continued therapy)

(1) Transient increase in hepatic enzymes (first 8-12 weeks) → common in treatment responders
(2) Chronic therapy: neurotoxicity (mood disorders, depression, somnolence, confusion, seizures), myelosuppression, profound fatigue, weight loss, rash, cough, myalgia, alopecia, tinnitus, reversible hearing loss, retinopathy, pneumonitis, possibly cardiotoxicity

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24
Q

what are the contraidications of interferon alpha s

A

hepatic decompensation

autoimmune disease (induction of antibodies)

history of cardiac arrhythmia

pregnancy

use with caution in :
(1) Cautions: psychiatric disease, epilepsy, thyroid disease, ischemic cardiac disease, severe renal insufficiency, cytopenia

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25
Q

what drugs interact with interferon alpha and may result in increased levels of these drugs

A

theophylline and methadone

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26
Q

co - administration of interferon alpha s and what other drugs are not recommended

A

not recommended with didanosine (increased risk of hepatic failure)

zidovudine (exacerbates cytopenias)

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27
Q

MOA of nucleoside/nucleotide analogs (NA’s)

do you need to renal adjust?

A

interfere with viral replication

dose adjust in renal impairment

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28
Q

what are the advantages of Nucleoside/nucleotide versus interferon alpha

disadvantages

A

iii) Advantages versus interferon: PO administration (tablets or solution), better tolerated, higher response rate, can be used for chronic therapy or in patients with significant liver disease
iv) Disadvantages: sustained response limited after discontinuation of therapy, resistance can be a problem, some agents cause peripheral neuropathy, general warning for lactic acidosis and hepatic steatosis

29
Q

adefovir MOA

A

antiretroviral nucleoside/nucleotide

(1) MOA: inhibits HBV DNA polymerase, chain termination after incorporation into viral DNA

30
Q

ADR’s of Adefovir

A

(2) ADRs: side effects include headache, diarrhea, abdominal pain; potential nephrotoxicity

31
Q

why is adefovir not recommended for first-line therapy against HBV

A

(b) Not recommended as first-line agent for HBV due to slow response and low likelihood of HBeAg seroconversion

32
Q

Entecavir MOA

effect of food on this drug

A

inhibits DNA polymerase (base priming, reverse transcription, DNA synthesis)
(2) PK: food decreases bioavailability (take on an empty stomach)

33
Q

ADR’s of entecavir

A

(3) ADRs: well-tolerated; side effects include headache, dizziness, nausea

34
Q

therapeutic use of entecavir

A

(4) Therapeutic use: recommended first-line therapy for HBV; exhibits good viral suppression and normalization of liver enzymes with slowing of liver damage

resistance is rare

35
Q

Lamivudine (3TC)

MOA

A

(1) MOA: inhibits DNA polymerase, competes for incorporation into viral DNA, causes chain termination

drug for HBV

36
Q

ADR’s of lamivudine (3TC)

A

(2) ADRs: excellent safety profile, including use during pregnancy; side effects are rare, but include headache, nausea, and dizziness; co-infection with HIV may increase risk of pancreatitis

37
Q

why is Lamivudine not first line therapy for hep B

A

due to high rate of resistance (15-30% at 1 year and 70% at 5 years) and progressive liver disease

38
Q

MOA of Telbivudine

A

(1) MOA: inhibits DNA polymerase (competitive inhibition), causes chain termination

used for HBV

39
Q

ADR’s of Telbivudine

A

(2) ADRs: well-tolerated; side effects are generally mild and may include fatigue, headache, abdominal pain, increased creatine kinase levels, nausea, and vomiting

40
Q

CI’s for telbivudine

A

(3) CIs: avoid concurrent use with interferon alfa due to increased risk of peripheral neuropathy

41
Q

why is telbivudine not recommended as first line therapy

A

(a) Rapidly suppresses HBV and causes HBeAg seroconversion with reduced liver damage, but not recommended as first-line therapy due to high rate of resistance (22%), which increases after one year of therapy.

42
Q

tenofovir
MOA

ADR’s

A

(1) MOA: competitively inhibits DNA polymerase, causes chain termination
(2) ADRs: nausea, diarrhea, vomiting, decreased bone mineral density (consider calcium and vitamin D supplementation and monitor bone density in long-term use) **

43
Q

what is the therapeutic use of Tenofovir

A

(3) Therapeutic use:
(a) Recommended first-line therapy for HBV; treats lamivudine- and entecavir-resistant isolates, but exhibits reduced activity against adefovir-resistant strains

44
Q

Ribvarinin

A

drug for treatment of HCV

i) MOA: inhibits initiation/elongation of RNA resulting in inhibition of viral protein synthesis

45
Q

what are the ADR’s for ribavirin

A

(1) Dose dependent hemolytic anemia (10-20%), depression, fatigue, nausea, rash, insomnia
(2) Preclinical studies indicate ribavirin is teratogenic, embryotoxic, oncogenic, and possibly gonadotoxic

46
Q

what is Ribavirin used in combination with

A

chronic HCV treatment used with pepinterferon alfa and sofosbuvir

47
Q

what are the CI’s for ribavirin use

A

anemia,

end-stage renal failure,

ischemic vascular disease,

pregnancy (pregnant women and their partners);

pregnant women should not directly care for patients receiving aerosolized ribavirin

48
Q

what is the MOA of Sofosbuvir (Sovaldi)

A

direct-acting antiviral (DAA), inhibits HCV NS5B RNA dependent RNA polymerase (essential for viral replication), acts as chain terminator

49
Q

ADR’s of sofosbuvir

A

fatigue, headache, insomnia, pruritus, nausea, diarrhea, flu-like symptoms, anemia, neutropenia, weakness, myalgia

50
Q

therapeutic use of sofosbuvir

A

HCV

51
Q

simeprevir MOA

food impact on drug

A

direct-acting antiviral (DAA), inhibits HCV NS3/4A protease (essential for viral replication)

ii) PK: absorption enhanced by food, CYP3A4 oxidative metabolism, excreted in feces

52
Q

adr’s of semeprevir and therapeutic use

A

iii) ADRs: skin rash, pruritus, nausea, increased serum bilirubin, myalgia

therapeutic use? HCV

53
Q

what is the advantage of using pegylated interferon

A

polyethylene glycol complexed (non-toxic polymer excreted in the urine); always given subcutaneously; slower clearance (30% renal – dose adjust in impairment),

longer t1/2 of 40 hours, steadier concentration allows for less frequent dosing (once-weekly compared to daily or thrice-weekly dosing)

listen again

54
Q

what is seroconversion a predictor of ?

A

viral clearance

55
Q

common side effect of peg interferon

A

flu like illness

use with caution in depression pt’s- causes mood disorders, somnolence, confusion, seizures

56
Q

which drug class would be preferred if our pt had decompensated liver disease

A

nucleotide/side analogs

don’t use peginterferon

57
Q

1st line therapy for HBV

A

Tenofovir, Entecavir

58
Q 
pt with HEP c virus in the past
no complaints at his visit today
HCV genotype 2 
Baseline HCV RNA 350,000
does he have any characteristics that might predict a more favorable response to treatment?
A

genotype 2
RNA of 350,000 –> >400,000 is high

absence of cirrhosis

59
Q

SVR

A

absence of HCV RNA by polymerase chain reaction for 6 months after completion of therapy

(2) SVR is associated with improved liver histology, decreased HCC, and occasionally regression of cirrhosis

60
Q

44 year old female presents for follow up after receiving a recent diagnosis of HCV genotype 1

IV drug use in the past
what drugs should be included in her treatment

A

Peginterferon and ribavirin

Sofosbuvir

61
Q

which HEP C drug is CI in pregnancy

A

Ribavirin

category X— bad

62
Q

MOA of sofosbuvir

A

direct-acting antiviral (DAA), inhibits HCV NS5B RNA dependent RNA polymerase (essential for viral replication), acts as chain terminator

incorporated into the HCV RNA

63
Q

Peginterferon and ribavirin

Sofosbuvir

pt is started on these and develops fatigue, scleral icterus, pallor
no evidence of bleeding

AST and ALT- not worsening or increased

what is most likely causing the pt’s symptoms
hematocrit has decreased
total bili is elevated

A

adverse drug reaction secondary to ribavirin

64
Q

Genotype 1

IFN eligible for HCV treatment

A

SOF, PEG/RBV

65
Q

Genotype 1

IFN ineligible for HCV treatment

A

SOF + SMV, RBV

66
Q

what makes a person IFN ineligible

A

pregnancy - b/c you have to have treatment with ribovirin as well (used in combo with IFN)

decompensated liver disease

autoimmune disease

cardiac arrythmia

caution:
psychiatric disease, epilepsy, thyroid disease, renal insufficiency

67
Q

Genotype 2 HCV treatment

A

SOF + RBV x 12 weeks

68
Q

Genotype 3 HCV treatment

A

SOF + RBV x 24 weeks

69
Q

Polymorphism NS3/4A

A

something to consider in Simeprevir treatment

decreased SVR - consider other treatment

GI II Exam I AP (8 decks)

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