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23 y/o male admitted to the hospital with 1 week hx of fever, RUQ pain,…
23 y/o male admitted to the hospital with 1 week hx of fever, RUQ pain, nausea and lethargy. he is also jaundice 3 days prior to admission
Lab Test
Full blood count
Liver function test
Renal profile
Coagulation profile
Hepatitis and HIV serology
Abdomen ultrasound
Serological profile of Hep B
Hepatitis B surface antigen
(HBsAg)Appears during incubation period (1-6 months)
Peaks when the patient is most ill.
Becomes undetectable in 3-6 months.
Indicates infection – recent or chronic.
Hepatitis B surface antibody (anti-HBs)
Arises once the acute disease has resolved.
Hepatitis B core antibody (anti-HBc)
- Anti-HBc IgM and elevated serum transaminases also appear shortly before the symptom onset.
Hepatitis B e-antigen (HBeAg)
Shortly after HBsAg appears, HBeAg and HBV DNA can be detected in the serum and are markers of the acute viral replication.
Predictor of infectivity.
Hepatitis B e-antibody (anti-HBe)
Anti-HBe appears shortly after HBeAg vanishes
Predictor of low infectivity.
MANAGEMENT:
a) Interferon (combined antiviral & immunomodulatory effect)
IFN-a
b) Nucleoside/nucleotide analogues (direct antiviral effect)
Lamivudine
Adefovir
Entecavir
Telbivudine
Tenofovir
c) Liver transplant
PREVENTION:
a) Vaccination
b) Hepatitis B Ig
c) Others
Screening of blood donors
Antenatal screening
Blood & body fluid precaution
Practice safe sex
Don't become IVDU
causative agent of viral hepatitis
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Metabolism of bilirubin
Function of liver - Metabolism of carbohydrates, lipid and protein,
Catabolism of steroid hormone,
bile production,
Storage and metabolism of vitamins and mineral,
Storage of iron and copper
bilirubin metabolism
Diagnosis: HBV infection
Immune Response to Hep B
Innate and the adaptive immune system are important.
The innate immune system is responsible for early containment of the viruses and initial activation of adaptive immune responses.
It is generally thought that HBV is poorly sensed by the innate immune system and can escape innate immune recognition at the early stages of infection.
Natural killer (NK) cells, are activated early during infection, before HBV-specific T cells arise.
As time goes, functionally active HBV-specific T cells (especially cytotoxic CD8+ T cell) can be detected, which are thought to play an important role in viral clearance, there are also B cell being activated to mature into plasma cell for HBV antibody production (dendritic > T helper > B cell activation).
During chronic infection, HBV-specific T cells are exhausted and their function is impaired.
acute hepatitis
ballooning degeneration
cholestasis
apoptosis
macrophage aggregates
eosinophilic
infiltration of inflammatory cells
bridging necrosis
chronic hepatitis
lymphoid aggregates
apoptosis
fibrosis
Possible outcome of HBV infection
Acute hepatitis
Fulminant Hepatitis
Nonprogressive Chronic Hepatitis
Progressive Chronic Hepatitis to Cirrhosis
Asymptomatic Hep B carrier
Pathogenesis & clinical manifestation
immune mediated cytotoxic killing of hepatocytes is that cause of inflammation of the liver
hepatocytes are further damaged -the cell lyses releasing the cell contents = aspartate aminotransferase & alanine amino transferase
Summary
fatigue, nausea, vomiting, fever, hepatomegaly, jaundice, dark urine, anorexia, and rash
symptoms
:
jaundice
fever
fatigue
loss of appetide
nausea
vomiting
abdominal pain
Jaundice:
3 types:
pre-hepatic jaundice
hepatocellular jaundice
post-hepatic jaundice
Causes:
haemolytic anaemia
genetic disoders
autoimmune hepatitis
viruses
alcohol
gallstones
tumours
Risk factors for viral hepatitis
Environmental
Lack of sanitation
Contact with used needles, syringes
Unsafe water
Behavioral
Sharing needles
Engaging in unsafe sexual contact
Large quantities of alcohol
Working around toxic chemicals
Health
Not being vaccinated
Immunocompromised
Mother who has hepatitis
