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

Drugs - Treatment of Hepatitis (Kinder) Flashcards

(69 cards)

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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
what drugs interact with interferon alpha and may result in increased levels of these drugs
theophylline and methadone
26
co - administration of interferon alpha s and what other drugs are not recommended
not recommended with didanosine (increased risk of hepatic failure) zidovudine (exacerbates cytopenias)
27
MOA of nucleoside/nucleotide analogs (NA's) do you need to renal adjust?
interfere with viral replication dose adjust in renal impairment
28
what are the advantages of Nucleoside/nucleotide versus interferon alpha disadvantages
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
adefovir MOA
antiretroviral nucleoside/nucleotide (1) MOA: inhibits HBV DNA polymerase, chain termination after incorporation into viral DNA
30
ADR's of Adefovir
(2) ADRs: side effects include headache, diarrhea, abdominal pain; potential nephrotoxicity
31
why is adefovir not recommended for first-line therapy against HBV
(b) Not recommended as first-line agent for HBV due to slow response and low likelihood of HBeAg seroconversion
32
Entecavir MOA effect of food on this drug
inhibits DNA polymerase (base priming, reverse transcription, DNA synthesis) (2) PK: food decreases bioavailability (take on an empty stomach)
33
ADR's of entecavir
(3) ADRs: well-tolerated; side effects include headache, dizziness, nausea
34
therapeutic use of entecavir
(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
Lamivudine (3TC) MOA
(1) MOA: inhibits DNA polymerase, competes for incorporation into viral DNA, causes chain termination drug for HBV
36
ADR's of lamivudine (3TC)
(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
why is Lamivudine not first line therapy for hep B
due to high rate of resistance (15-30% at 1 year and 70% at 5 years) and progressive liver disease
38
MOA of Telbivudine
(1) MOA: inhibits DNA polymerase (competitive inhibition), causes chain termination used for HBV
39
ADR's of Telbivudine
(2) ADRs: well-tolerated; side effects are generally mild and may include fatigue, headache, abdominal pain, increased creatine kinase levels, nausea, and vomiting
40
CI's for telbivudine
(3) CIs: avoid concurrent use with interferon alfa due to increased risk of peripheral neuropathy
41
why is telbivudine not recommended as first line therapy
(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
tenofovir MOA ADR's
(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
what is the therapeutic use of Tenofovir
(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
Ribvarinin
drug for treatment of HCV i) MOA: inhibits initiation/elongation of RNA resulting in inhibition of viral protein synthesis
45
what are the ADR's for ribavirin
(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
what is Ribavirin used in combination with
chronic HCV treatment used with pepinterferon alfa and sofosbuvir
47
what are the CI's for ribavirin use
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
what is the MOA of Sofosbuvir (Sovaldi)
direct-acting antiviral (DAA), inhibits HCV NS5B RNA dependent RNA polymerase (essential for viral replication), acts as chain terminator
49
ADR's of sofosbuvir
fatigue, headache, insomnia, pruritus, nausea, diarrhea, flu-like symptoms, anemia, neutropenia, weakness, myalgia
50
therapeutic use of sofosbuvir
HCV
51
simeprevir MOA food impact on drug
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
adr's of semeprevir and therapeutic use
iii) ADRs: skin rash, pruritus, nausea, increased serum bilirubin, myalgia therapeutic use? HCV
53
what is the advantage of using pegylated interferon
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
what is seroconversion a predictor of ?
viral clearance
55
common side effect of peg interferon
flu like illness use with caution in depression pt's- causes mood disorders, somnolence, confusion, seizures
56
which drug class would be preferred if our pt had decompensated liver disease
nucleotide/side analogs don't use peginterferon
57
1st line therapy for HBV
Tenofovir, Entecavir
58
``` 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? ```
genotype 2 RNA of 350,000 --> >400,000 is high absence of cirrhosis
59
SVR
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
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
Peginterferon and ribavirin Sofosbuvir
61
which HEP C drug is CI in pregnancy
Ribavirin category X--- bad
62
MOA of sofosbuvir
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
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
adverse drug reaction secondary to ribavirin
64
Genotype 1 IFN eligible for HCV treatment
SOF, PEG/RBV
65
Genotype 1 | IFN ineligible for HCV treatment
SOF + SMV, RBV
66
what makes a person IFN ineligible
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
Genotype 2 HCV treatment
SOF + RBV x 12 weeks
68
Genotype 3 HCV treatment
SOF + RBV x 24 weeks
69
Polymorphism NS3/4A
something to consider in Simeprevir treatment decreased SVR - consider other treatment

GI II Exam I AP (8 decks)

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