Ebright: Viral Hepatitis Flashcards by Andrew Kumar

Viral Hepatitis Definition:

Inflammation and damage to the liver (can be caused by infectious and non-infectious agents)

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Viral Hepatitis

Most Common Agents: (3)

HAV
HBV
HCV

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Viral Hepatitis

Less Common Agents: (6)

HDV
HEV
Epstein-Barr
CMV
HSV
Yellow Fever

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Is Bacteria Hepatitis common?

Less common

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Bacteria Hepatitis

Less Common Agents: (5)

Leptospirosis
Syphilis
Q fever (Ricketssia)
Tuberculosis
Brucellosis

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Fungal Hepatitis

Less Common Agents: (2)

Histoplasmosis*
Candidiasis*
(*especially in immunocompromised)

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Parasitic Hepatitis

Less Common Agents: (2)

Schistosomiasis

Liver flukes

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Hepatitis
Non-Infectious Causes
Most Common: (4)

Drugs/mediations

Alcohol

Cholecystitis (primary problem outside liver, but can be confused with hepatitis)

Obstructed bile duct (primary problem outside liver, but can be confused with hepatitis)

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Hepatitis
Non-Infectious Causes
Less Common: (4)

Toxins

Anoxia (Lack of O2)

Autoimmune

Wilson’s disease

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Acute Hepatitis

Liver Changes:

Inflammation, ballooning degeneration, apoptosis, macrophage aggregates, fatty change
- pg: 620

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Chronic Hepatitis
Liver Changes:
What distinguishes this from acute hepatitis?

Bridging necrosis and bridging fibrosis (signs of cirrhosis or scarring of the liver) are the major distinguishers from acute disease; also fatty change, apoptosis, macrophage aggregates and other symptoms similar to acute
- pg: 620

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CLINICAL PRESENTATION OF VIRAL HEPATITIS:

Range: asymptomatic to fulminant (life-threatening)

Four Clinical Stages:

Range: asymptomatic to fulminant (life-threatening)

Four Clinical Stages:
Incubation
Preicteric
Icteric
Convalescence

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Viral Hepatitis Presentation

Incubation:

Clinically silent

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Viral Hepatitis Presentation
Preicteric

When?
Most common initial symptoms:

Preicteric: early, prior to appearance of jaundice

Most common initial symptoms: malaise, weakness, anorexia, N/V, vague-dull RUQ pain, low grade fever (not always), hepatomegaly, splenomegaly (~25% of the time)

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Viral Hepatitis Presentation
Preicteric

Other variations can occur:
Serum-Sickness Like Syndrome may occur especially with:
Symptoms of Serum-Sickness Like Syndrome: (3)

Other variations can occur: headache, myalgia, sore throat, cough

Serum-Sickness Like Syndrome: may also occur before jaundice, especially with HBV

Symptoms: arthralgias/arthritis, urticaria (hives) and fever

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Viral Hepatitis Presentation
Icetric

Definition:
Symptoms: (3)
What may develop due to severe jaundice?

Icetric: presence of jaundice (50-80% do not become jaundiced)

Symptoms: jaundice, dark urine and light stools

Severe Jaundice: pruritis may develop (generalized itching)

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Viral Hepatitis Presentation

Convalescence

Convalescence: recovery

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Fulminant Viral Hepatitis

How common?
Characteristics: (5)
Mortality rate:

Fulminant Viral Hepatitis: uncommon

Characteristics: lethargy, somnolence, stupor, asterixis (flapping tremor) or coma; widespread necrosis of liver

High mortality rate

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Acute Viral Hepatitis Presentation
Lab findings

What is dramatically elevated?
How are Alkaline phosphatase, 5’ nucleotidase, gamma-glutamytransferase levels affected? In a patient with cholestasis?
How is bilirubin affected?

Dramatically elevated AST and ALT: 8-100 times normal

Other Findings:

Alkaline phosphatase, 5’ nucleotidase, gamma-glutamytransferase all modestly elevated (except when patients present with cholestasis)

Bilirubin is elevated (icteric disease; usually equally direct and indirect forms)

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In acute hepatic disease, what happens to:

Prothrombin time?
Albumin?
Globulin?
Hb?
WBC counts?

Remain normal

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Pathologic findings in acute viral hepatitis

What happens to the hepatic sinusoidal cords?
What does eosinophilic generation result in?
What type of necrosis?

Lobular Disarray: disorderly pattern of hepatic sinusoidal cords

Ballooning and eosinophilic degeneration of hepatocytes: eosinophilic generation resulting in free hyaline bodies or Councilman bodies

Spotty necrosis

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Pathologic findings in acute viral hepatitis

Where is lymphocyte infiltration?
What are pathologic changes in viral hepatitis probably more likely due to?
Cholestasis:

Lymphocyte infiltration: primarily in portal tracts
o Pathologic changes in viral hepatitis probably more likely due to cell mediated immunity that viral cytopathic effects (esp. HBV)

Cholestasis: variable degree; any condition in which bile flow is blocked from the liver

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Chronic Hepatitis develops in what percent of adult patients with the hepatitis B virus?
Newborns?

Develops in ~10% of adult patients and ~90% of newborns infected with the virus

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Inactive Carrier carries what for greater than 6 months?

LFTs:

Inactive Carrier: chronic carrier of HBsAg (but HBsAb negative) for greater than 6 months with normal LFTs

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Chronic Hepatitis: Carries what for greater than 6 months? LFTs: Indicates either:

Chronic carrier of HBsAg (but HBsAb negative) for greater than 6 months with abnormal LFTs and abnormal liver biopsy Indicates either: - Immune tolerate hepatitis: mild - Immune active hepatitis: moderate to severe

In Chronic HBV, what is the patient positive for? (3) What about acute HBV? What can this result in?

Patient also often positive for “e” Ab (elaborated b virus when it is actively replicating), HBV DNA and DNA polymerase Note: the patient would also be positive for these during active acute HBV, however, these are not tested for in this type of scenario Can result in cirrhosis (25-30% of the time) and hepatocellular carcinoma (less common)

What happens to 85% of people infected with chronic HCV? | What happens to the other 15%?

85% of people infected go on to develop chronic disease (15% spontaneously cured)

Chronic HCV | Characteristics: (3)

Fluctuating AST/ALTs Varying degrees of chronic hepatitis Patients often do not feel sick until very late in its course (advanced disease)

Chronic HCV | Can result in:

Can result in cirrhosis and hepatocellular carcinoma as well.

If a patient has HBV or HCV, it is important to check for Abs to what?

If a patient has HBV or HCV, it is important to check for Abs to HAV.

Co-infection with HAV increases risk for developing what? What if there are no Abs to HAV?

Co-infection with HAV increases risk for developing fulminant hepatitis If no Abs to HAV, give vaccine

HAV Virus Particle: Genome: Family:

Virus Particle: Non-enveloped Genome: RNA Family: Picornaviridae

HBV Virus Particle: Genome: Family:

Virus Particle: Enveloped Genome: DNA (replicates by reverse transcriptase) Family: Hepadnaviridae

HCV Virus Particle: Genome: Family:

Virus Particle: Enveloped Genome: RNA Family: Flaviviridae

HDV Virus Particle: Genome:

Virus Particle: Defective virus that uses HBsAg for its envelope Genome: RNA

HEV Virus Particle: Genome:

Virus Particle: Non-enveloped | Genome: RNA

HAV Incubation Period: Transmission: Age Preference: Pattern of Onset:

Incubation Period: ~30 days Transmission: Fecal-oral Age Preference: Children and adolescents Pattern of Onset: Acute

HBV Incubation Period: Transmission: (4) Age Preference: Percutaneous vs endemic areas Pattern of Onset:

Incubation Period: ~60-90 days ``` Transmission: Percutaneous Sexual Vertical Unspecified (saliva) ``` Age Preference: All ages (percutaneous) Neonates (endemic areas) Pattern of Onset: Acute or insidious

HCV Incubation Period: Transmission: (4) Age Preference: Pattern of Onset:

Incubation Period: ~50 days ``` Transmission: Percutaneous Sexual Vertical (predominantly with HIV coinfection) Unspecified ``` Age Preference: All ages Pattern of Onset: Insidious

HDV Incubation Period: Transmission: (2) Age Preference: Percutaneous vs endemic areas Pattern of Onset:

Incubation Period: ~60 days Transmission: Percutaneous Close personal contact Age Preference: All ages (percutaneous) Children and young adults (endemic areas) Pattern of Onset: Acute

HEV Incubation Period: Transmission: Age Preference: Pattern of Onset:

Incubation Period: ~40 days Transmission: Fecal-oral Age Preference: Adolescents and young adults Pattern of Onset: Acute

HAV Fulminant Hepatitis? Chronic Hepatitis? Cirrhosis? Predisposition to Hepatoma?

Possible but rare No No No

HBV Fulminant Hepatitis? Chronic Hepatitis? Cirrhosis? Predisposition to Hepatoma?

Possible but rare 5-10% of infected adults 90% of infected neonates ~25% of patients with chronic disease Yes

HCV Fulminant Hepatitis? Chronic Hepatitis? Cirrhosis? Predisposition to Hepatoma?

Possible but rare Increased risk with HAV superinfection 85% of infected patients ~20% of patients with chronic disease Yes

HDV Fulminant Hepatitis? Chronic Hepatitis? Cirrhosis? Predisposition to Hepatoma?

Common <5% in patients co-infected with HBV 80-95% in patients with pre-existing chronic HBV 15-30% of patients with chronic disease Possible

HEV Fulminant Hepatitis? Chronic Hepatitis? Cirrhosis? Predisposition to Hepatoma?

Common, especially in pregnant women No No No

HAV Diagnosis Acute Infection Chronic Infection

Acute Infection: IgM anti-HAV | Chronic Infection: --

HBV Diagnosis Acute Infection: Chronic Infection:

Acute Infection: IgM anti-HBc (core Ag) Chronic Infection: HbsAg IgG anti-HBc

HCV Diagnosis Acute Infection: Chronic Infection:

Acute Infection: Serum HCV RNA Chronic Infection: Anti-HCV Serum HCV RNA

HDV Diagnosis Acute Infection: Chronic Infection:

Acute Infection: Acute and convalescent anti-HDV Chronic Infection: Anti-HDV (high titer)

HEV Diagnosis Acute Infection: Chronic Infection:

Acute Infection: | Chronic Infection: Anti-HEV

HAV ``` PREVENTION AND TREATMENT Passive Immunization: Protective: Effective Therapies: (need to consider liver transplant for fulminant hepatitis and endstage chronic disease) ```

Immune globulin Vaccine No

HBV ``` PREVENTION AND TREATMENT Passive Immunization: Protective: Effective Therapies: (need to consider liver transplant for fulminant hepatitis and endstage chronic disease) ```

HBV immune globulin Vaccine IFN-alpha Lamivudine Other anti-virals

HCV ``` PREVENTION AND TREATMENT Passive Immunization: Protective: Effective Therapies: (need to consider liver transplant for fulminant hepatitis and endstage chronic disease) ```

No No vaccine IFN-alpha + ribavirin Other anti-virals

HDV ``` PREVENTION AND TREATMENT Passive Immunization: Protective: Effective Therapies: (need to consider liver transplant for fulminant hepatitis and endstage chronic disease) ```

No HBV vaccine (indirect protection) IFN-alpha (possibly)

HEV ``` PREVENTION AND TREATMENT Passive Immunization: Protective: Effective Therapies: (need to consider liver transplant for fulminant hepatitis and endstage chronic disease) ```

No Vaccine in production No

Acute HAV diagnosis: | Check for what? Why?

IgM Anti-HAV: check for IgM because that is indicative of a new infection; IgG is present for life

Acute HBV diagnosis: Why check for the Ab to the core Ag? What causes a false negative?

IgM Anti-HBc: check for Ab to the core Ag because of the possible window period Time during acute illness where HbsAg starts to go away (Abs being formed) but that HbsAb is not yet detectable; results in a false negative

Acute HBV What indicates recovery from infection? When does HBsAg disappear?

Development of Anti-HBs antibodies: indicates recovery from infection (protective Ab); after this Ab develops, HBsAg disappears

Chronic HBV Anti-HBs: What happens to HBsAg?

Anti-HBs does not develop: therefore, HBsAg stays elevated for years after exposure to HBV (HBeAg also present along with DNA polymerase)

Chronic Hepatitis C Anti-HCV ab: What happens due to the development of ab?

Anti-HCV antibody is NOT protective: even though this Ab develops, chronic disease occurs anyways