Pod: Viral Hepatitis

Front 1

T/F: Liver destruction associated with hepatitis A,B,C is caused by viral invasion and replication.

Back 1

F. Destruction is immune mediated by influx of acute or chronic inflammatory cells(cytotoxic lymphocytes).

Front 2

What three systemic viral infection cause hepatitis?

Back 2

1. Epsterin Barr virus
2. Cytomegalovirus
3. Yellow fever virus

Front 3

What liver enzymes are elevated in viral hepatitis?

Back 3

ALT elevated to a greater degree.
AST
*Jaundice follows the elevated enzyme levels.

Front 4

Define mild, moderately active, and severe viral hepatitis.

Back 4

1. Mild: quiescent lymphocytescollect in portal tracts.
2. Moderately active: activated lymphocytes spill over to periportal parenchyma.
3. Severe: activated lymphocytes suffuse the entire paranchyma.

Front 5

Histologically, what would you find in viral hepatits?

Back 5

1. Ballooning degeneration of hepatocyte in response to lymphocytic injury.
2. Regenerating hepatocyte(except in fulminant infections).
3. Fibrosis, cirrhosis overtime(irreversible).

Front 6

Describe HAV:
1. genome
2. enveloped or not?

Back 6

1. ssRNA (picornavirus)
2. non-enveloped

*Stable at low pH
*Resistant to detergent, drying, cold/warm temperatures.
*Single serotype.
*Human only.

Front 7

Describe the pathogenesis of HAV.

Back 7

1. bind to receptors on hepatocytes and Kupffer cells and internalized.
2. viral replication: RNA translated to proteins.
3. excreted in bile
4. shed in stool(large quantity): 10 days before symptom or antibodies are detectable.Viremia:persist during enzyme elevation.

Front 8

How does HAV transmit? What is the key reservoir?

Back 8

1. fecal orally (contaminated food, shell fish).
2. Asmptomatic children(underdeveloped CMI) and adults.

Front 9

Where are the endemic areas of HAV?

Back 9

Africa, Mongolia, India, Southeast Asia.

Front 10

What is the typical incubation period for HAV?

Back 10

28days(15-50).

Front 11

A young man presents with jaundice, abdominal pain, and fatigue. He mentioned some flu-like symptoms such as nasea, vomiting, low grade, and headache less than a week ago.
1. What was going on a week ago?
2. What is happending now?
3. What is the cause?
4. How to diagnose?
5. How to treat it?

Back 11

1. Prodromal period of viral hepatitis A.
2. Icteric phase of hepatitis A.
3. HAV
4. measure HAV-IgM for acute or recent infection.
5. Symptomatic relief.

Front 12

What test can be used to test past infection and vaccination of HAV?

Back 12

Measure HAV-total(IgM amd IgG).

Front 13

Interpret the following result for HAV:
IgM-
total-

Back 13

HAV -

Front 14

Interpret the following result for HAV:
IgM+
total+

Back 14

HAV +

Front 15

Interpret the following result for HAV:
IgM-
total+

Back 15

Past infection or vaccination

Front 16

How to prevent HAV?

Back 16

1. Hygiene, sanitation
2. HepA immunoglobulins for travelers or during incunation period.
3. Vaccine: inactivated whole rirus. Pediatric and adult formulations. Lon lasting, no boosting needed.

Front 17

What is the major difference between HAV and HEV?

Back 17

HEV has more severe infection in pregnant women(esp 3rd trimester): more of a Th2 response and hormonal stimulation of abnormal viral protein production.

Front 18

What are the endemic areas of HEV?

Back 18

Asia, North Africa.

Front 19

Describe HBV:
1. genome
2. enveloped or not?

Back 19

1. overlapping dsDNA, hepadnavirus.
2. enveloped(HBsAG)
3. capsid( HBcAg, HBeAg).

*DNA encode for reverse transcriptase.
*Human and chimpanzees
*Relatively resistant to low pH, ether, freezing, moderate heat.

Front 20

What is Dane particles?

Back 20

complete virion of HBV.

Front 21

A blood smear showed several small spheres or filamentous structures).
1. What are they?
2. What are their functions?

Back 21

1. HB surface antigen containing particles.
2. Act as decoys to bind to antibodies and prevent clearing of the viruses. (May cause immune-complex problems such as vasculitis, arthralgia, rash, kidney damage similar to type III hypersensitivity.

Front 22

Each of the following is a marker for:
1. HBsAg
2. HBeAg
3. Anti-Hbe
4. Anti-Hbc
5. Anti-Hbs

Back 22

1. infectivity(active infection)
2. high viral replication
3. decreasing viral replication
4. recent/past infection
5. recovery from infection

Front 23

Describe the pathogenesis of HBV.

Back 23

1. virus attach to receptor on liver cell.
2. transcription and translation of RT, HBsAg, core proteins
3. RT makes -strand
4. + strand production
5. viral packaging or repeat
6. release by exocytosis

Front 24

What is the incubation of HBV?

Back 24

>45 days.

Front 25

What do hepatocytes look like in HBV infection?

Back 25

Ground-glass appearance

Front 26

What happens to people with insufficient T-cell response in HBV infection?
What about people with massive T cell response?

Back 26

1. Mostly infants: mild symptoms, unresolved infection, development of chronic hepatitis.
2. fulminant hepatitis may result.(co-infection of HDV increases the risk)

Front 27

T/F: Hepatocelluar carcinoma may result when viral DNA incorporated into host genome.

Back 27

T.

Front 28

How does HBV transmit?

Back 28

1. via blood, semen, saliva, cerival secretions.
2. mother to fetus/infant: perianal, blood.

Front 29

What are the endemic areas of HBV?

Back 29

Asia and south Africa.

Front 30

How to prevent HBV?

Back 30

1. HepB immunoglobulin: post-exposure prophylaxis, and to infants borne to infected mother.
2. vaccine(not for immunocompromised).

Front 31

How to treat HBV?

Back 31

3 drugs that also treat HIV: FTC, 3TC, TDF.
Interferons

Front 32

What marker is the overall indicator of infectivity of HBV?

Back 32

HBsAg

Front 33

Which marker is the indicator of a high level of viral replicaiton and is a bad prognostic sign in someone with chronic HBV?

Back 33

HBeAg

Front 34

Which marker indicates recovery from HBV?

Back 34

Anti-Hbs

Front 35

Which marker can be measured to detect someone in the window phase of HBV(undetectable HBsAg or anti-Hbs)?

Back 35

IgM anti-Hbc

Front 36

Interpret the following result:
HBsAg-
HBeAg-
anti-Hbc total-
anti-Hbc IgM-
anti-Hbe-
anti-Hbs-

Back 36

susceptible to HBV

Front 37

Interpret the following result:
HBsAg-
HBeAg-
anti-Hbc total+
anti-Hbc IgM+
anti-Hbe+
anti-Hbs+

Back 37

Recently had it and recovered.

Front 38

Interpret the following result:
HBsAg-
HBeAg-
anti-Hbc total+
anti-Hbc IgM-
anti-Hbe- or +
anti-Hbs+

Back 38

Had it awhile ago and recovered.

Front 39

Interpret the following result:
HBsAg-
HBeAg-
anti-Hbc total-
anti-Hbc IgM-
anti-Hbe-
anti-Hbs+

Back 39

Vaccinated.

Front 40

Interpret the following result:
HBsAg+
HBeAg+
anti-Hbc total+
anti-Hbc IgM+
anti-Hbe-
anti-Hbs-

Back 40

Acute phase hepatitis
highly infective

Front 41

Interpret the following result:
HBsAg+
HBeAg-
anti-Hbc total+
anti-Hbc IgM+
anti-Hbe+
anti-Hbs-

Back 41

getting better but still infective

Front 42

Interpret the following result:
HBsAg+
HBeAg+
anti-Hbc total+
anti-Hbc IgM-
anti-Hbe-
anti-Hbs-

Back 42

chronic hepatitis and high infectiive

Front 43

Interpret the following result:
HBsAg-
HBeAg-
anti-Hbc total+
anti-Hbc IgM+
anti-Hbe+
anti-Hbs-

Back 43

window phase

Front 44

Why is HDV considered a "viral parasite"?

Back 44

Becaues it requires HBV to complete its life cycle (coinfection increases the risk of develop fulminant hepatitis.

Front 45

Describe HDV:
1. genome
2. enveloped or not?

Back 45

1. ss circular RNA
2. enveloped(HBsAg)
3. Delta antigen on core.

Front 46

Differentiate coinfection and superinfection of HBV and HDV.

Back 46

coinfection: at the same time.
superinfection: chronic HBV infection acquire HDV.

Superinfection results in more rapid, severe progression.

Front 47

Which viral hepatitis cause direct cell death and immune mediated damage?

Back 47

HDV

Front 48

How does HDV transmit?

Back 48

via blood and body fluid

require HBV to complete its life cycle.

Front 49

How to diagnose HDV?
How to prevent it?
How to treat it?

Back 49

1. IgM or total antibody against delta antigen.
2. HBV vaccine.
3. interferon alpha may be of help.

Front 50

Describe HCV:
1. genome
2. enveloped or not?
3. family

Back 50

1. +,- RNA
2. enveloped
3. flavivirus family, hepacivirus genus.

*2 hypervariable glycoproteins: E1,E2.
*6 genotypes: 1a, 1b most common in US and Western Europe.

Front 51

Describe the pathogenesis of HCV.

Back 51

1. bind to LDL, VLDL receptors, CD81 on lymphocytes and internalized.
2. replication: RNA dependent RNA polymerase with no proofreading capability. HCV proteins inhibit IFN-α and apoptosis.
3. persistent viremia: hepatic inflammation and fibrosis.

Front 52

List histological stages of HCV infection.

Back 52

1. Dense portal lymphocytic infiltrate.
2. Infiltrate extend to lobules.
3. scant fibrous tissue.
4. expansion of fibrosis.
5. cirrhosis.
6. carcinoma.

Front 53

Who are more at risk of HCV infection?

Back 53

female, alcoholics, older age.

Front 54

Which 2 viral hepatitis may have vasculitis, glomerulonephritis complications?

Back 54

Immune complex development.
1. HBsAg
2. HCV antigenic variation E1,E2 due to lack of proofreading from RNA dependent RNA polymerase.

Front 55

T/F: Superinfection of HAV with HCV can result in a severe hepatitis.

Back 55

T.

Front 56

T/F: Coinfection of HCV with HIV accelerates the course of HCV.

Back 56

T.

Front 57

How to diagnose HCV infection?

Back 57

1. EIA for anti-HCV
2. RIBA(westernblot) ot RT PCR to conform.
3. genotyping can indicate the duration of treatment.
4. liver enzyme(ALT) can access degree of liver damage.

Front 58

How to treat HCV infection?

Back 58

IFN-α and ribavirin combination. for 24-48 weeks.
Last resort: liver transplant, may get reinfected.

Front 59

Name the Chinese(Oriental) liver fluke. What does it c

Back 59

Clonorchis sinensis

Front 60

Name tow organims that associated with fish.

Clue: one cause GI problem, the other cause liver problem.

Back 60

1. Diphyllobothrium latum:fish tape worm.
2. Clonorchis sinensis (Chinese liver fluke): heavy infections caues liver necrosis and jaundice.

Front 61

How to diagnise Clonorchis sinensis infection?
How to treat it?

Back 61

Ova in feces.
Praziquantel.

Front 62

Name the sheep liver fluke.

Back 62

Fasciola hepatica.

Front 63

How does fascoila hepatica transmit?

Back 63

ingestion of plants with attached metacercaria, adults located in hepatic parencyma.(more pathogenic than clonorchis sinensis)

Front 64

How to diagnose fasciola hepatica infection?

Back 64

1. chronic case: eggs in feces.
2. acute disease: complement-fixation serology.

Front 65

Name three spirochetes.

Back 65

leptospira
borrelia
treponemal pallidum

Front 66

Describe the pathogenesis of leptospirosis.

Back 66

1. penetration through skin or mucus membrane.
2. 1-2 wks: spread in blood to all tissues including CSF.
3. multiplication, endothelial cell damage.
4. flu-like symptoms: fever, myalgia.
5. go in CSF, blood, urine.
6. If not recovered: Weil's disease: headache, myalgia, chills, abdominal pain, conjunctival reddening, vascular collapse, thrombocytopenia, hemorrhage, hepatic and renal dysfunction.

Front 67

Describe leptocpira:
1. gram stain morphology

Back 67

1. GN, thin coiled.

Front 68

2 wks ago, a guy went diving in a cave and had a minor cut. He has flu-like symptoms, but later developed headache, hepatitis, jaudice, and hemorrhage.
1. What is likely the cause?
2. How to diagose?
3. How to treat?

Back 68

1. Leptopira
2. serology
3. ?