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Module 11 - Gastrointestinal and Hepatobiliary Disorders > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

1
Q

What is viral hepatitis?

A

Any inflammatory process that occurs in the liver.
- can be viral or non-viral
- acute or chronic
- chronic can progress to cirrhosis and hepatocellular carcinoma

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2
Q

What are examples of non-viral hepatitis?

A

Hepatotoxic injury from:
- drug-induced liver injury
- alcohol-related liver disease
- mushroom poisoning

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3
Q

What are the outcomes of alcohol abuse?

A
  • Fatty liver, cirrhosis, alcoholic hepatitis
  • genetic predisposition to increased risk for some moderate to heavy drinkers
  • excess acetaldehyde is toxic and ethanol metabolism generates ROS which cause injury
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4
Q

What is metabolic dysfunction-associated steatotic liver disease (MASLD)?

A

Previously called non-alcoholic steatohepatits (NASH) or fatty liver disease (NAFLD).

It is the progression of metabolic dysfunction-associated fatty liver disease (MAFLD) resulting in a group of liver diseases.

It is the most common liver disease affecting Canadians.

MASLD causes:
- hapatocyte injury and inflammation and may progress to cause fibrosis, cirrhosis, and hepatocellular carcinoma.

  • autoimmune hepatitis (rare)
  • primary biliary cholangitis (chronic autoimmune intrahepatic biliary disorder)
  • genetic conditions (e.g. hemochromatosis, Wilsons’s disease, cystic fibrosis, alpha 1-antitrypsin deficiency
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5
Q

What are risk factors for MASLD?

A

Risk factors include genetics, obesity, type 2 diabetes, metabolic syndrome, diet (high fat, high fructose), and microbiome dysbiosis.

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6
Q

When is MAFLD and MASLD symptomatic?

A

MAFLD is most often symptomatic early on = may present with fatigue or RUQ discomfort.

MASLD = may be asymptomatic before fibrosis occurs and liver function is impaired. Liver enzymes elevated d/t hepatocyte injurt.

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7
Q

What are the types of viral hepatitis and how do they differ?

A

Viruses A,B,C,D,E specifically target hepatocytes.

Differ in terms of transmission, incubation period, degree of liver damage, chronicity and treatment.

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8
Q

How is viral hepatitis diagnosed?

A

Detection of viral antigens, antibodies, DNA or RNA.

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9
Q

Viral hepatitis may occur as part of the clinical course of which other viral infections?

A

CMV, Epstein-Barr virus, herpes simplex virus, varicella zoster virus etc. = not common but tends to occur in immunosuppressed individuals.

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10
Q

What are the there steps of viral hepatitis pathogenesis?

A
  1. viral entry and replication within hepatocytes.
  2. activation of immune response
  3. hepatocyte damage and inflammation
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11
Q

Describe the immune response that is activated with viral hepatitis.

A
  1. viruses taken up by Kupffer cells (macrophages) are presented to helper T cells.
  2. Helper T cells release cytokines that activate immune responses.
  3. Cytotoxic T cells directly attack and destroy infected hepatocytes.
  4. B cells are activated producing antibodies against the virus.
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12
Q

Describe the hepatocyte damage that occurs with the immune response to viral hepatitis.

A
  • some direct cytopathic effects of virus on hepatocytes, but most damage is from the immune response
  • causes inflammation (the infiltration of neutrophils) and necrosis)
  • inflammation blocks bile flow (Cholestasis)
  • damaged hepatocytes are removed by Kupffer cells (which proliferate)
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13
Q

What are the 4 phases of acute viral hepatitis?

A
  1. Incubation period
  2. Prodromal phase
  3. Icteric phase
  4. Recovery phase

S&S vary depending on extent of liver damage.

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14
Q

Describe the incubation period of hepatitis.

A

Virus is replicating in hepatocytes but individual is asymptomatic.

  • duration varies depending on the type of hepatitis, amount of virus and host factors

Ranges:
- HAV: 15-50 days
- HBV: 45-160 days
- HCV: 15-180 days

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15
Q

Describe the prodromal phase of viral hepatitis.

A

Immune responses are initiated, and hepatocyte damage starts causing the onset of symptoms.

  • non-specific manifestations of infection and inflammation (fatigue, anorexia, fever, nausea)
  • mild RUQ abdominal pain (liver distension)
  • arthralgia (joint pain) or uritcaria (hives) d/t immune complex deposition
  • elevated levels of serum ALT and AST (indicates hepatocyte damage)
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16
Q

Describe the icteric phase of acute viral hepatitis.

A

Juandice (intrahepatic) appears.

  • dark (tea-coloured) urin, pale stools, pruritis
  • occurrence depends on age (more common in adults) and virus type (rare with HCV)
  • follow the prodromal phase by 1-2 weeks
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17
Q

If someone with viral hepatitis is asymptomatic, what might that indicate?

A
  • the incubation phase of infection
  • low-grade infection, minimal liver injury
  • insufficient immune response (less injury to hepatocytes)
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18
Q

Describe the recovery phase of acute viral hepatitis.

A
  • Most patients recover completely (= acute hepatitis)
  • virus is eliminated by the immune response and the liver regenerates
  • decline in symptoms and ALT levels
  • liver function returns to normal
  • long-term immunity d/t antibody production
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19
Q

What is fluminant hepatitis?

A

AKA = acute liver failure

Necrosis of hepatocytes leading to acute liver failure (in 6-8 weeks)

  • rare
  • can occur with any type of viral hepatitis (most common with HBV)
  • potentially fatal; usually requires liver transplantation
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20
Q

What is the most common cause of acute liver injury and failure?

A

45% of cases relate to acetaminophen overdose.

  • chronic use of high therapeutic doses (greater than or equal to 4g/day) or intentional (greater than or equal to 7.5g single dose)
  • may be unintentional (fasting, malnutrition, alcohol, existing liver disease, taking multiple drugs that contain acetaminophen, etc.)
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21
Q

Describe the metabolism of acetaminophen.

A

NOTE: most PO drugs are lipophilic and need to be converted to a water-soluble form for excretion (bile or urine).

Acetaminophen is metabolised by enzyme cytochrome P450 into NABQI (toxic) = N-acetyl-p-benzoquinoneimine

NABQI is normally conjugated to glutathione and secreted.

At high doses NABQI overwhelms this pathway, accumulates, and causes injury.

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22
Q

How does acute liver failure present?

A
  • elevated liver enzymes (often greater than 10x the upper limit of normal)
  • rapid onset of symptoms (abdominal pain, nausea, jaundice)
  • coagulopathy (INR > 1.5 or PT > 3 secs prolonged)
  • hepatic encephalopathy (confusion, disorientation, asterixis “flapping tremour”, bradykinesia, etc.)
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23
Q

What is chronic hepatitis?

A

The virus cannot be removed completely typically d/t insufficient immune response.
- continued infection beyond 6 months (symptoms and/or serologic evidence of infection)
- hepatitis A is never chronic
- occurs in hepatitis B (5% of adult cases) and hepatitis C (75% of cases)

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24
Q

What are some extrahepatic manifestations that may be present with chronic infection and what is thought to be the cause?

A

Thought to be caused by circulating immune complexes.

  • Polyarteritis nodosa: A systemic vasculitis affecting medium-sized arteries
  • Membranous nephropathy: causes increased glomerular permeability and proteinuira
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25
Q

What are the hepatic manifestations of chronic hepatitis?

A

Chronic hepatitis causes inflammation and fibrosis (scarring)

Extensive fibrosis over decades progresses to cirrhosis (scarring that impairs liver functioning)

Increases risk of hepatocellular carcinoma

26
Q

What labwork is used to support diagnosis of acute viral hepatitis?

A

Very high ALT and AST and relatively normal ALP = suggests hepatocellular injury and hepatitis

ALT to AST ratio = ALT>AST suggests viral hepatitis (AST>ALT suggests alcoholic hepatitis).

27
Q

How is the type of acute viral hepatitis identified?

A

A risk factor assessment.

28
Q

What is Hepatitis A?

A
  • RNA virus
  • most common hepatitis infection world-wide
  • endemic in countries without modern sanitation and hygiene standards.
29
Q

How is HAV transmitted?

A
  • virus replicates in liver - excreted in the bile - shed in the stool (=fecal shedding)
  • mode of transmission is fecal-oral
  • virus enters the GI tract - travels via the hepatic portal vein to the liver

NOTE: HAV transmission via the blood is possible, but not common.

30
Q

In BC in 2018, there were 25 reported cases of HAV. Most cases occur in?

A

Unimmunized persons who:
- consumed contaminated food products
- travelled to or immigrated from endemic countries

31
Q

How does HAV present across the lifespan?

A
  • asymptomatic in young children (<30% of children < 6 yrs have symptoms)
  • > 70% of older children and adults have symptoms, including jaundice (symptoms typically resolve within 8 weeks)
  • acute, self-limiting, not chronic
  • full recovery (no lasting liver damage)
  • fulminant hepatitis is rare (more common in people with underlying liver disease)
  • immune to re-infection
32
Q

How is HAV diagnosed?

A

anti-HAV IgM = appears first, may be detectable 5-10 days before symptom onset, remains elevated for up to 12 months

anti-HAV IgG = appears later and remains elevated providing life-long immunity

If symptomatic and HAV suspected, anti-HAV IgM and anti-HAV total are ordered.
If anti-HAV IgM reactive:
- recent HAV infection
- recent HAV immunization
- false positive
If anti-HAV total reactive but anti-HAV IgM not reactive:
- resolved infection
- prior immunization

33
Q

What are preventative measures against HAV?

A
  • vaccination = production of anti-HAV IgG. Not part of normal routine but recommended and free for high risk of exposure
  • personal hygiene
  • travel precautions
34
Q

Infection with HAV is self-limiting. What might be recommended during recovery?

A
  • rest, proper nutrition, and fluids
  • alcohol abstinence (6 months)
  • avoid drugs metabolized by liver
  • prevention education
35
Q

What does post-exposure prophylaxis (PEP) for Hep A include?

A
  • Hep A vaccine (preferred) and/or immune globulin (HAIg) should be given to individuals within 14 days of a known exposure to a confirmed case while in the infectious period

HAIg is derived from plasma donors with high concentrations of anti-HAV IgG, and provides immediate, short-term protection against HAV

36
Q

What is HBV?

A
  • DNA virus
  • outer lipid envelope contains HBsAg (surface antigen)
  • inner nucleocapsid composed of HBcAg (core antigen)
  • HBeAg is synthesized during viral replication and is secreted (function not known)
37
Q

Describe HBV transmission.

A
  • virus replicates in the liver - released into the blood
  • low levels in semen and vaginal secretions
  • transmitted via percutaneous, perinatal and permucosal routes
  • when transmitted, the virus travels in the blood via the hepatic artery to the liver
38
Q

What are risk factors for HBV?

A
  • unprotected sexual contact
  • injection drug use
  • perinatal (usually during childbirth)
  • body piercings and tattoos (poor infection control practices)
  • unscreened blood products or transfusion recipient prior to 1970
  • sharing razors or toothbrushes contaminated with blood
  • iatrogenic exposure (e.g., hemodialysis d/t to poor sterilization)
  • occupational exposure to infected blood or body fluids (e.g. needle stick)
39
Q

What kind of protection does the HBV vaccine provide?

A

Individuals vaccinated for HBV or who have cleared a natural infection are protected from subsequent HBV infections.

40
Q

What is the prevalence of HBV in BC?

A
  • perinatal transmission is the predominant mode of transmission world-wide (one of the most common infections worldwide)
  • acute HBV infection rates declined in Canada d/t universal vaccination programs (started in BC in 1992)
  • IV drug use and unprotected sex are the most common causes in BC
  • 70% of chronic cases in Canada are seen in individuals immigrating from HBV endemic areas
41
Q

Describe the progression of acute HBV infection.

A
  1. Virus infects hepatocytes and viremia occurs before symptom onset
  2. HBV DNA indicates viral load
  3. HBsAg indicates infection and infectivity
  4. HBeAg indicates active viral replication and infectivity
  5. Infectivity period starts from 1 week to 1 month
  6. Acute phase: <10% of children and 30-50% of adults with acute HBV infection have symptoms in the acute phase. Symptoms last up to 4 weeks.
  7. Symptoms resolve and HBsAg levels decline as an immune response is mounted.
42
Q

What are the outcomes of acute HBV infection?

A

An acute HBV infection can have several outcomes:

  1. recovery = life-long immunity
  2. Chronic HBV infection rates based on age and no prophylaxis:
    - neonates: 90%
    - child (<6): 50%
    - adults: 5% (more likely if immunocomprimised or coinfected with HIV, HCV or HDV.
    - chronic can either progress to cirrhosis or chronic liver vailure (15-40%), hepatocellular carcinoma (5%) or spontaneous clearance of HBV infection (loss of HbsAg)
  3. 1-2% of adults (rare, but > risk than HAV) fulminant hepatitis - 63-93% fatality rate.
43
Q

How is acute HBV infection diagnosed?

A

HBsAg:
- used to screen for HBV infection
- marker of HBV infection (acute or chronic) and infectivity

Anti-HBc IgM:
- indicates acute infection
- undetectable within 6-9 months

Anti-HBc Total (IgM + IgG)
- indicates prior infection with HBV

Anti-HBs:
- recovery and immunity from past HBV infection
- immunity d/t vaccination

44
Q

What is in the HBV vaccination?

A
  • HBsAg is the antigen used to make the HepB vaccine
  • vaccination indicated by a positive anti-HBs and negative anti-HBc
  • anti-HBs levels may wane over time, but most are still immune
45
Q

What are host factors that increase risk for cirrhosis in patients with chronic HBV?

A
  • > 40 years
  • male
  • positive family history
  • immune status
46
Q

What are virus factors that increase risk for cirrhosis in patients with chronic HBV?

A
  • high serum HBV DNA level (key marker of risk)
  • prolonged time frame for HBeAg seroconversion
  • development of HBeAg(-) chronic hepatitis
  • precore and core promoter: HBV variant
  • genotype C
47
Q

What are environmental factors that increase risk for cirrhosis in patients with chronic HBV?

A
  • concurrent infection (HCV, HDV, HIV)
  • alcohol consumption
  • diabetes mellitus
  • obesity
48
Q

How is chronic HBV infection diagnosed?

A
  • HBsAg & HBeAg remain elevated 6 months or more
  • anti-HBe not produced until years later
  • anti-HBc (IgM and IgG) is present, but not protective
  • anti-HBs is not present
49
Q

Is breastfeeding when positive for HBV safe?

A

Yes, as long as nipples are not cracked or bleeding.

50
Q

How are infants of HBsAg+ mothers treated?

A

Given HBIg and the vaccine within 12 hours after birth. 90% of infected babies will develop chronic HBV but vaccine reduces that to 2-4%

51
Q

What are HBV preventative measures?

A
  • vaccination (included in primary childhood vaccination series)
  • decrease risky behaviours
  • blood donor screening
  • screening during pregnancy
52
Q

Describe treatment for HBV?

A
  • usually self-limiting (precautions to prevent transmission)
  • post-exposure prophylaxis - HBIg (within 48 hours) and/or hep B vaccine (needle stick, sexual assault etc.)
  • treatment of chronic active infection with antivirals (interferon and nucleos(t)ide analogues) to prevent progression to higher levels of fibrosis, cirrhosis and HCC - no complete cure.
53
Q

What is Hepatitis C?

A
  • a blood-borne RNA virus
  • 8 genotypes and numerous subtypes (genotype 1 is most common in BC)
  • mutating virus - resistant to immune defences
  • no vaccine, but there is a cure
54
Q

How is HCV transmitted?

A
  • primarily through percutaneous exposure to infectious blood
  • similar to HBV, but transmission through sexual contact and from mother-to-child are less common
  • prior to 1992 when screening was available, transmission through blood products was most common cause
55
Q

Describe the course of HCV infection.

A

Acute HCV:
- 75% are asymptomatic
- symptoms, if present, typically start 6-7 weeks after infection and resolve in a few weeks
- jaundice occurs in <10% of cases
- fulminant hepatitis is rare
- 25% of people spontaneously clear the virus within six months

56
Q

What happens to ALT levels and antibodies in acute HCV?

A

ALT levels are markedly increased during acute infection, but fluctuate widely in cases of chronic infection.

Antibodies remain elevated after clearing the infection

57
Q

Describe chronic HCV infection.

A
  • 75% develop chronic HCV
  • most people are asymptomatic for years. Some will experience fatigue, mental fog, digestive problems, and/or extrahepatic manifestations.
  • over decades, 10-20% will develop cirrhosis (reversible in the early stages if treated) and 1-5% will develop liver cancer.
58
Q

What percentage of Canadians with chronic HCV remain undiagnosed?

A

Estimated range = 44-70%

59
Q

How is HCV diagnosed?

A

HCV RNA
- detectable 1-3 weeks after infection
- indicates active infection

Anti-HCV
- detectable 5-10 weeks after infection
- levels decline after infection, but are present for life
- NOT protective (risk of HCV reinfection)

Screening;
- Anti-HCV first. If negative = no current or past infection. If positive then test for HCV RNA = confirms active (versus resolved) infection and does NOT distinguish between acute and chronic infection

60
Q

What is the management for HCV?

A
  • No vaccine or postexposure prophylaxis
  • precautions to prevent transmission
  • Test for hepatitis A and B (offer vaccination if appropriate)
  • Education to prevent chronic (avoid alcohol, healthy lifestyle, avoid hepatotoxic drugs, etc.)
  • direct-acting antivirals to treat (early) and cure

Module 11 - Gastrointestinal and Hepatobiliary Disorders (5 decks)

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