Hepatitis A Through E

Front 1

What is the most common strain of hepatitis?

Back 1

Front 2

What are the three general presentations in viral hepatitis? What are the three complications of chronic hepatitis?

Back 2

Front 3

Which virus cause acute hepatitis? What percent and which virus type lead to fulminant liver failure?

Which viruses cause chronic hepatitis?

Back 3

Most B in US is acute but can progress to chronic.

Front 4

Which strains usually cause acute hepatitis in the US? Which strain associated with zoonosis? Which strain with IV drug users?

How will the AST/ALT, bilirubin, prothombin time be affected?

What does a very high INR indicate?

Back 4

Diagnosed by AST/ALT and high IgM

Front 5

The diagnosis of acute HAV infection is confirmed during the acute or early convalescent phase of infection by the presence of __ antibodies to HAV (__ anti-HAV). __ anti-HAV is generally present 5-10 days before the onset of symptoms and is no longer detectable in the vast majority of patients __ months later. __ anti-HAV, which also appears early in the course of infection, remains detectable for the lifetime of the individual and confers lifelong protection against infection. Commercial tests are available for the detection of __ and total (IgM and IgG) anti-HAV in serum.

Back 5

The diagnosis of acute HAV infection is confirmed during the acute or early convalescent phase of infection by the presence of IgM antibodies to HAV (IgM anti-HAV). IgM anti-HAV is generally present 5-10 days before the onset of symptoms and is no longer detectable in the vast majority of patients 6 months later. IgG anti-HAV, which also appears early in the course of infection, remains detectable for the lifetime of the individual and confers lifelong protection against infection. Commercial tests are available for the detection of IgM and total (IgM and IgG) anti-HAV in serum.

Front 6

In infected persons, HAV replicates in the liver, is excreted in __, and is shed in the __. Peak infectivity occurs during the 2-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus in stool is __. The concentration of virus in stool declines after __ appears. Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness. Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have __ illness. Viremia occurs soon after infection and persists through the period of liver enzyme (alanine aminotransferase [ALT]) elevation.

Back 6

In infected persons, HAV replicates in the liver, is excreted in bile, and is shed in the stool. Peak infectivity occurs during the 2-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus in stool is highest. The concentration of virus in stool declines after jaundice appears. Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness. Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness. Viremia occurs soon after infection and persists through the period of liver enzyme (alanine aminotransferase [ALT]) elevation.

Front 7

HAV RNA can be detected in the __ and stool of most persons during the __ phase of infection by using nucleic acid amplification methods, such as __, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates. These methods, however, are available in only a limited number of research laboratories and are not used generally for diagnostic purposes.

Back 7

HAV RNA can be detected in the blood and stool of most persons during the acute phase of infection by using nucleic acid amplification methods, such as PCR, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates. These methods, however, are available in only a limited number of research laboratories and are not used generally for diagnostic purposes.

Front 8

Back 8

Front 9

What is the most common outcome of acute hepatitis?

Which strain often professes to chronic infection?

Which stain can cause fulminant liver failure?

Back 9

Front 10

What is the KEY test for acute hepatitis A, E, and B diagnosis?

Which antibody indicates PREVIOUS infection?

What indicates active infection but DOES NOT differentiate between acute vs. chronic infection.

Back 10

Front 11

What is the most serious complication of acute viral hepatitis?

Which strains usually cause this? (one in pregnancy also)

What is the presentation (think brain effects specifically)?

What is the only cure?

Back 11

Acute hepatitis + confusion = fulminant hepatic failure

Front 12

What is the definition of chronic viral hepatitis?

How does it present?

Mild elevations of what two labs?

What serious conditions can occur in late stages?

Back 12

Front 13

Identify normal, fibrosis, cirrhosis, HCC

What are four things that can accelerate fibrosis?

Back 13

30 years to progress to cirrhosis.

Front 14

Which race is 2.7 times more likely to develop HCC and 2.4 times more likely to die from HCC?

Back 14

Highest rates of Hep B are in far east countries (China, india, etc.), in the US it is on the West Coast.

Front 15

Which group of patients with HBV experience an increased risk of medical consequences?

Back 15

Front 16

What are six possible blood tests for HBV? Can the core antigen be measured?

Back 16

Front 17

What will indicate active infection (acute or chronic)?

What will indicate resolved infection or prior exposure/vaccination?

What will indicate definite exposure? (which one for acute and which for resolved or chronic)

What will indicate active replication and high risk of transmission?

1. Anti HBs antibody

2. Anti HB core antibody

3. Hepatitis B e antigen and high DNA

4. Positive HBs Ag surface antigen

Back 17

Front 18

Complete

Back 18

Front 19

The phases of chronic HBV infection consists of four successive phases:
The immune tolerant phase, in which there is __ hepatic inflammation despite a __ serum level of HBV DNA and positive HBeAg.
The immune clearance phase, in which there is hepatic __ and __ in serum HBV DNA level and ultimately loss of HBeAg. This phase is also known as HBeAg+ CHB.
The inactive carrier state, during which patients have __ level of HBV DNA, __ (positive or negative) HBeAg, and __ aminotransferases.
The reactivation phase, during which __ levels of HBV DNA can be detected in serum along with hepatic inflammation. Many patients remain HBeAg negative, but some patients may revert to HBeAg positive. This phase is also known as HBeAg- CHB.

Back 19

The phases of chronic HBV infection consists of four successive phases:
The immune tolerant phase, in which there is little hepatic inflammation despite a high serum level of HBV DNA and positive HBeAg.
The immune clearance phase, in which there is hepatic inflammation and decrease in serum HBV DNA level and ultimately loss of HBeAg. This phase is also known as HBeAg+ CHB.
The inactive carrier state, during which patients have low level of HBV DNA, negative HBeAg, and normal aminotransferases.
The reactivation phase, during which high levels of HBV DNA can be detected in serum along with hepatic inflammation. Many patients remain HBeAg negative, but some patients may revert to HBeAg positive. This phase is also known as HBeAg- CHB.

Front 20

Back 20

Front 21

Not all patients go through all the four phases. The immune clearance phase is most common in young __ patients with perinatally acquired HBV infection. Some patients remain in the inactive carrier phase with no evidence of reactivation, these patients have better prognosis than those who develop reactivation. The immune clearance phase and reactivation phase may be prolonged with recurrent exacerbations of hepatitis and fluctuations in serum HBV DNA levels.

Back 21

Not all patients go through all the four phases. The immune clearance phase is most common in young Asian patients with perinatally acquired HBV infection. Some patients remain in the inactive carrier phase with no evidence of reactivation, these patients have better prognosis than those who develop reactivation. The immune clearance phase and reactivation phase may be prolonged with recurrent exacerbations of hepatitis and fluctuations in serum HBV DNA levels.

Front 22

When do you treat chronic HBV (two things)?

Back 22

1. When evidence of liver injury.

2. When there is evidence of advanced fibrosis.

Front 23

Can chronic HBV be cured in most patients? What is the goal of treatment? What is the secondary goal?

Back 23

Front 24

What are three drugs to treat HBV?

Which two are oral, require a long duration, and are well tolerated?

Which one is SQ, has finite duration, several side effects, contraindicated in cirrhosis, and best for GENOTYPE A?

Back 24

Front 25

Is hepatitis D a complete virus? What does it need to infect? Seen only in patients who have what other hepatitis?

What are the two infections types?

Back 25

Front 26

What is the effect of hepatitis delta on the severity of HBV and the risk of cirrhosis?

How can you diagnose it? What should all patients have?

Back 26

Front 27

What is the most common chronic viral hepatitis in the US?

Back 27

Hepatitis C

"C for chronic"

Front 28

How many people in the US have chronic hep c infection?

Back 28

Front 29

Back 29

Front 30

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Front 31

Back 31

Front 32

Draw out the natural history of hepatitis C infection from acute infection to development of disease complications.

Back 32

Front 33

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Front 34

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Front 35

How many HCV genotypes are there? 75% in the US are which type?

Back 35

Front 36

Draw the HCV life cycle.

Back 36

Hepatitis C always stays outside the nucleus.

Front 37

Is HCV curable with treatment? What can you use?

Back 37

Front 38

What are the three-four drug types used for HCV treatment?

Which drug has no major side effects, no food interaction, limited drug interactions, and is $1,000 per pill?

Back 38

Front 39

Which drug is this?

It is the first and only once-daily, single-tablet regimen containing ledipasvir (90 mg), a hepatitis C virus (HCV) NS5A inhibitor, and sofosbuvir (400 mg), an HCV nucleotide analog NS5B polymerase inhibitor
is an interferon (IFN)-free and ribavirin (RBV)-free regimen

Back 39

Havaroni

Indicated for chronic hep c (type 1) infection in adults

Front 40

What two drugs are used to treat type 1 with a cure rate of 95%

Which two drugs for types 2 and 3?

Back 40

Front 41

Complete

Back 41

Front 42

Does achieving sustained virologic response result in reductions in HCC incidence?

Back 42

Yep

Front 43

Just be aware.

Back 43

Transition
Patient adherence to a medication regimen is critical to good patient outcomes.1

Main Message
Poor adherence is the result of factors spanning several dimensions. Issues related to the patient, socioeconomic conditions, therapy administration, and the healthcare system may all adversely affect adherence.1,2

Front 44

Is there a hepatitis A vaccine?

Hepatitis B vaccine?

What envelope proteins does the HCV vaccine contain? What type of response will it induce against non structural protein of HCV?

Back 44

Front 45

All HIV patients should be tested for which two hepatitis viruses? Why?

What is the leading cause of death tin HIV patients?

Do many anti-HIV drugs have anti-HBV activity?

Back 45

Front 46

What is the most common cancer worldwide? Which hepatitis causes HCC only with cirrhosis? Which can cause HCC without cirrhosis?

Back 46

Front 47

These are all indications for what?

Back 47

Liver transplantation in viral hepatitis

Front 48

What are all of these associated with?

Back 48

Extra hepatic manifestations in viral hepatitis

Front 49

Do extra hepatic manifestations correlate with viral RNA/DNA levels?

When is treatment indicated and can be successful?

Back 49

Front 50

Look over

Back 50

Front 51

What are three other viral infections that can cause acute hepatitis?

What range will the ALT and AST be in?

Are most self-limiting?

Serious infections can result in which patients?

Back 51

CMV

EBV

Herpes

Front 52

What are the clinical symptoms of CMV hepatitis?

How will the ALT and AST change?

How can diagnose? What is the treatment (and prophylaxis)

Back 52

Front 53

What is the arrow pointing to? What is the condition?

Back 53

Inclusion bodies

CMV hepatitis

Front 54

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Front 55

Back 55

Front 56

58 year old white male

No symptoms

No risk factors

Everything looks normal

What test should he get?

Back 56

HCV antibody (based on the screening guidelines).

Front 57

32 yo w/ jaundice

Drink 6 pack beer during weekends

Icterus and mild upper Rt quadrant pain

BMI 31

Normal liver ultrasound but stones seen in gall bladder

ALT 1500, AST 1400, Bilirubin 12

What is diagnosis?

Back 57

Acute hepatitis E

Front 58

22 yo medical student seen for checkup

Born in US, parents from Taiwan

Liver function tests normal

Hepatitis B surface antigen positive

HBcore IGG antibody positive

HBV DNA very high

HBe antigen positive => previously vaccinated for hep A and B

Back 58

He's in the immune tolerant stage! No treatment

Chronic HBV immune tolerant stage

Front 59

24 yo jaundice

Active IV drug user

High AST/ALT/bilirubin => acute hepatitis

Acute hepatitis C

What is the best management for this patient?

Back 59

Just wait, most people will resolve

Repeat HCV RNA in 3 months

Front 60

50 year ol referred for HCV

NO medical history

HepC positive, HCV RNA negative

HB surface antibody positive

What do you do?

Exposed to hepatitis C but does not have active infection.

Back 60

No further tests.

Front 61

32 yo w/ history of HBV presents with jaundice

Entecavir regularly

Recent traveled to mediterranean countries and uses heroin

Chronic hepatitis B with acute hepatitis.

What is most likely cause of present illness?

Back 61

Super infection with Hepatitis Delta