Hepatitis Flashcards

(40 cards)

1
Q

Hepatitis A overview

A

Fecal-oral

Perinatal transmission? No

Most common risk factor: direct contact with someone with HAV

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2
Q

Hepatitis B overview

A

Transmission: Blood, sexual

Perinatal transmission? Yes

Most common risk factor: born to infected mother

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3
Q

Hepatitis C overview

A

Transmission: blood

Perinatal transmission? Yes

Most common risk factor: injection drug use

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4
Q

HAV risk of chronic infection?

A

No

Acute, then resolved

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5
Q

HBV risk of chronic infection?

A

Yes

Course of infection: acute then sometimes chronic
- 90% of infants
- 20-25% of children ages 1-5
- 5% of adults

Treatment of chronic infection: Yes but no curable

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6
Q

HCV risk of chronic infection

A

Yes

Acute then sometimes chronic
- > 50% develop chronic infection

Treatment: Yes, curative

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7
Q

Hepatitis A Symptoms

A

Can be asymptomatic or symptomatic

Abrupt onset, usually last less than 2 months:
Abdominal pain, nausea, or vomiting
Dark urine or clay colored stools
Fatigue
Fever
Jaundice
Joint pain
Loss of appetite

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8
Q

Hepatitis A diagnosis

A

IgM anti-HAV serum (usually detectable within 5-10 days of symptom onset) OR HAV RNA in serum or stool

IgG anti-HAV appears early in the infection, remains detectable providing lifelong immunity

Total anti-HAV (measuring both IgG and IgM) used to assess immunity

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9
Q

Hepatitis A management

A

Supportive Care

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10
Q

Hepatitis A prevention (who should be vaccinated)

A

All children age 12-23 months
MSM
People who anticipate close contact
Pregnant women at risk for HAV
Homeless
People who use drugs
Unvaccinated ages 2-18
Anyone who requests vaccination
International traveler
People at risk for exposure
People with chronic liver disease or HIV

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11
Q

HAV vaccine

A

Inactivated–safe in pregnancy

Two doses at 0 and 6-12 months

Pre and post vaccination serologic screening is typically not recommended

Post exposure prophylaxis to be given ASAP after exposure
- > 12 months of age
- IM immune globulin if < 12 months
- give both if > 40 years with increased risk of severe disease

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12
Q

Hepatitis B transmission

A

Sexual contact
Injecting drugs
Mother to child
Contact with blood or open sores
Needle stick
Sharing razors or toothbrushes

CANNOT BE SPREAD by:
Food
water
sharing utensils
kissing
coughing
sneezing
holding hands

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13
Q

Hepatitis B symptoms

A

Similar to HAV expect don’t see much diarrhea

Chronic infection is typically asymptomatic until onset of cirrhosis, end-stage liver disease or hepatocellular carcinoma

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14
Q

Hepatitis B screening

A

All adults aged 18 years and older at least once in their lifetime using a triple panel test

Screen for HBsAg during each pregnancy regardless of vaccination status

People who are at ongoing risk for exposure should be tested periodically

Or anyone who requests it

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15
Q

Hepatitis B serologic markers

A

Hepatitis B surface antigen
- marker of presence of ongoing infection
- Is the patient infectious?

Antibody to hepatitis B surface antigen
- marker of immunity
- Is the patient immune?

Antibody to hepatitis B core antigen
- marker of exposure to infection
- How has the patient been exposed?

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16
Q

Interpreting HBV test results

A

HBsAg, anti-Hbs, anti-HBc: all negative, never infected, if not vaccination then offer vaccine

HbsAg: negative, anti-HBs: positive, anti-HBc: positive, resolved infection, counsel about HBV infection reactivation risk

HBsAg: negative, anti-HBs: positive, anti-HBc: negative, immune from receipt of prior vaccination, complete vaccine series

HBsAg: positive, anti-HBs: negative, anti-HBc: positive, IgM anti-HBc: positive, acute infection, link to hepatitis B care

HBsAg: positive, anti-HBs: negative, anti-HBc: positive, IgM anti-HBc: negative, chronic infection, link to hepatitis B care

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17
Q

Hepatitis B acute management

A

Acute infection: no treatment, supportive care

18
Q

Hepatitis B chronic infection goals of therapy

A

Achieve sustained suppression of HBV replication

Remission of liver disease

Prevent cirrhosis, hepatic failure, and HCC

Functional cure: HBsAg loss with or without anti-HBe gain is attainable

Virological cure: eradication of cccDNA from hepatocyte nuclei– not yet attainable

19
Q

Hepatitis B chronic infection management

A

History (risk factors) and physical exam

CBC, liver panel, INR, HBeAg, anti-HBe, HBV DNA PCR

Test for coinfection, HCV, HDV, HIV, anti-HAV

Baseline alfa fetoprotein assay, abdominal US, and fibrosis staging to assess for evidence of HCC

20
Q

Phases of chronic HBV

A

e+ Immune-tolerant
- normal ALT
- elevated HBV DNA (++++)
- monitor ALT q2-6 months, eAg q6-12 months

e+ Immune-active
- elevated ALT
- elevated HBV DNA (+++)
- TREAT if ALT > 2x ULN, HBV DNA > 20,000 IU/mL, otherwise monitor

e+ cirrhosis
- elevated ALT
- elevated HBV DNA (++)
- low albumin, low platelets
- TREAT INDEFINITELY if HBV > 2,000 IU/mL, otherwise monitor

e- Inactive (carrier)
- normal ALT
- low/undetectable HBV DNA (+/-)
- monitor ALT q6-12 months

e- Immune reactivation
- elevated ALT
- elevated HBV DNA (+++)
- TREAT INDEFINITELY if ALT > 2x ULN, HBV DNA > 2,000 IU/mL, otherwise monitor

e- Cirrhosis
- elevated ALT
- elevated HBV DNA (++)
- low albumin, low platelets
- TREAT INDEFINITELY if HBV > 2,000 IU/mL, otherwise monitor

21
Q

HBV principles of treamtment

A

HBV DNA > 2,000 IU/mL (> 10,000 copies/mL) associated with increased risk of cirrhosis and HCC

ALT upper limit of normal (ULN) is 35 U/L for males and 25 U/L for females

Treatment does not eradicated HBV

Combination therapy has not shown higher response rates than monotherapy

For most, duration of NA therapy is indefinite

22
Q

HBV treatment eligibility

A

HBV DNA > 2,000 IU/mL; plus
- ALT > 2x ULN; or if they have cirrhosis: if they meet the major one and 1 of the other two then offer treatment

23
Q

Tenofovir 1st line treatment

A

MOA: inhibit HBV replication through incorporation into viral DNA by the HBV reverse transcriptase

300 mg PO daily

76% of e+ and 93% of e- maintain suppressed HBV DNA levels after 3 years of therapy

Maintenance of HBsAg loss after 3 years: e+ 8%, e- 0%

SE: nephropathy, faconi syndrome, osteomalacia, lactic acidosis

24
Q

Tenofovir alafenamide 1st line

A

25 mg PO daily

Improved safety (less renal impairment)

73% of e+ and 90% of e- maintain suppressed HBV DNA levels after 2 years of therapy

maintenance of HBsAg loss after 2 years: e+1%, e- < 1%

SE: lactic acidosis

25
Entevacir 1st line
0.5 mg PO daily in nucleoside naive patients 1 mg PO daily in nucleoside-experienced patients take on empty stomach 61% of e+ and 90% of e- maintain suppressed HBV DNA levels after 3 years of therapy Maintenance of HBsAg loss after 3 years: e+ 4-5%, e- 0-1% SE: lactic acidosis
26
Treatment monitoring
For patients on therapy, HBV DNA levels should be monitored q3 months on NA therapy until undetectable; then q3-6 months thereafter If therapy is stopped, monitor q3 months for at least one year for recurrent viremia, ALT flares, seroreversion, and decompensation All HBsAg+ patients with cirrhosis and high risk non-cirrhotics, should receive HCC surveillance (ultrasound of abdomen) q6 months
27
HBV reactivation/flares
28
Special populations
Renal insufficiency: adjust dose of NA Pregnancy: to minimize risk of perinatal transmission, beginning at weeks 28-32 of gestation, treat pregnant women with HBV DNA > 200,000 IU/mL with tenofovir DF HIV coinfection: some NA used for HBV also have antiretroviral activity against HIV, fully suppressive three-drug therapy should be initiated against HIV when treatment of HBV is warranted, combination of emtricitabine/tenofovir is frequently used
29
Who should be vaccinated?
All infants, beginning at birth Unvaccinated children aged < 19 years Adults 19-59 Adults aged 60 years or older with at least one of the risk factors (chronic liver dx, HIV, sexual exposure, drug use, percutaneous or mucosal risk for exposure to blood, people in jail, travelling)
30
HBV vaccine
All inactivated 3 injections at 0, 1, and 6 months Post vaccination testing for immunity is recommended for: infants born with HBV, people at risk for exposure, immunocompromised, sex partners who have HBV chronic infection
31
HCV symptoms
> 50% with acute HCV will develop chronic infection Persistently detectable HCV RNA for > 6 months fatigue and depression right upper quadrant pain nausea poor appetite hepatomegaly on PE
32
HCV serologic testing
anti-HCV is detectable 8-11 weeks after infection HCV RNA is diagnostic of current HCV infection: detectable 1-2 weeks after infection A diagnosis of HCV is many times incidental after having persistent elevated LFTs
33
HCV goals of therapy
Obtain virological cure by achieving a sustained virological response (SVR): check 12 weeks after completion of treatment Prevent complications
34
HCV agents
NS3/4A protease inhibitors NS5B polymerase inhibitors: nucleoside/nucleotide, non-nucleoside NS5A replication complex inhibitors
35
NS3/4A protease inhibitors
Blocks this: Serine protease cleaves the HCV RNA-encoded polyprotein into its functional units (NS4A, NS5B, NS5A, and NS5B) CYP3A4 inhibitors
36
Grazoprevir
AE: fatigue, headache, nausea, anemia, ALT elevations Patients should have ALT checked at 8 weeks; discontinue if > 5xULN Contraindicated in Child-pugh class B and C
37
Sofosbuvir
NS5B Polymerase inhibitors Avoid amiodarone coadministration due to risk of symptomatic bradycardia No dose adjustment needed in hepatic impairment
38
Elbasvir
Prior to use in patients with genotype 1a, and NS5a genotype must be performed to screen for presence of resistance-associated substitutions (RASs) at baseline
39
Velpatasvir
Check for genotype 3 must be performed to screen for presence of the Y93H substitution; presence requires ribavirin or voxilaprevir No dose adjustment in hepatic impairment
40
Ribavirin