VIRAL HEPATITIS

1. Hepatitis:
- liver inflammation
- causes:
• Infectious, cytomegalovirus, EBV
• Drugs: paracetamol overdose, co-amoxicalv
• Autoimmune
• Ischaemic

2. Functions of liver:
- Clotting factor
- Conjugation of bilirubin
- Complement factors
- Metabolism of drugs and hormones and toxins
- Carbohydrate metabolism
- Production of bile salts
- Synthesis of albumin

3. Symptoms of hepatitis:
- Asymptomatic
- Fever
- Jaundice
- Malaise
- Diarrhoea/vomiting
- Acute liber failure – bruising, ascites, encephalopathy

4. Liver cirrhosis:
- Normal liver tissue is replaced by fibrotic/ scar tissue

5. Liver cancer:
- Risk factors: hep B (WORLDWIDE) /C (IN EUROPE)
- Alcohol
- Obesity
- Smoking
- measure alpha fetoprotein (tumour marker)

Name epidemiology Presentation investigations Vaccine Management

Hepatitis +ssRNA -hepatomegaly hepA IgM – YES – NO CURE
-Faeco-roal -jaundice positive in acute lifelong -self resolving
A
-Water borne infection protection -supprotive
-Shellfish hepA IgG – (but treatment
-poor hygiene indicates recommended -once infected →
and sanitation immunity (and only when lifelong immunity
previous going away)
infection)
Hepatitis dsDNA -asymptomatic (66%) 1. SURFACE YES – since NO CURE
-blood-borne -jaundice MARKERS: 2017 all Only treatment that
B
-Africa, Asia -tender hepatomegaly -Ag: have newborn at suppresses viral
and Western -severity: based on infection 8,12 and 16 replication
Pacific Rim immune response (the -Anti sAb: NO weeks 1. Nucleotide
-vertical better, the more INFECTION Analogues:
transmission damage to but immunity -Inhibit DNA
hepatocytes) (from infection polymerase
- HIGH RISK OF or vaccination) -tablet
HEPATOCELLULAR -tenofovir
CARCINOMA IS 200 2. CORE -well-tolarated
HIGHER MARKERS: -lifelong
Anti IgM: acute
infection 2. Pegylated
Anti IgG: alpha
chronic inf or interferon:
recovery (NOT -activation of genes
VACCINE) involved in
immunity
3. SOLUBLE E- -subcytaneous
PROTEIN: injection
-Ag: high viral -pegylated
replication and interferon alpha
transmissibility -flu-like symptoms
-Anti eAb: -48 weeks
reduction
(immunological
control)

4. PCR virus
detection:
HBV-DNA:
viral load
Hepatitis ssRNA -asymptomatic -85% 1. Hepatitis C NO (due to Cure in 95% →
-most (during acute phase) RNA: active rapid antivirals (only 8
C
common - risk of hepatocellular infections emergence of weeks)
cause of carcinoma 2. antiHepCAb: genetic 1. Protease
chronic viral -Extrahepatic recovery or variatns) inhibitors,
hepatitis manfestations: chronic 2. NS5A
(chronic Thyroid disease; infection inhibitors
defined as lymphoma; fibrosis; 3. RNA
infection glomerulonephritis; Polymerase
persisting lichen planus; inhibitors
beyond 6 porphyria cunea tardia
months of
diagnosis)
-blood-borne
(needles most
common
route)
Hepatitis RNA virus Not distinguishable Hep D IgM – Antivirals don’t
-infection only between hep B and D acute infection work; Peg
D
if you already -Rapid progression Hep D IgG – Interferons the only
have hepatitis and development of immunity treatment option
B hepatocellular
-blood borne carnicoma
-transmission
associated
with IV drug
use
Hepatitis RNA virus -95% asymptomatic YES – but -self limiting
-Zoonotic -males over 50 are only in China -supportive care
E
disease most severely affected
-middle aged -10% of symptoms are
men neurological
-pig -increasing prevalence
farming/pork -most common acute
-faeco-oral hepatitis in the UK
route -25% of pregnant
women die

6. Hep B markers:
- Chronic: persists beyond 6 months of diagnosis; positive HBsAg (antigen)
without development fo HBsAb (antibody)

7. Summary
- Hep C: blood borne, few acute features, high risk of progression to chronic
disease, there is a cure
- Hep D: RNA, co-infection with hep B, no treatment (only interferons)
- Hep A and E – usually present with acute hepatitis; self- limiting but
fulminant disease can occur
- HepE dangerous for pregnant women
- Hep B and C – chronic hepatitis
- Hep A and B – vaccine, no cure
- Hep C – no vaccine but cure
 LIVERS FUNCTION TESTS (LFTs)
1. Chronic liver disease causes:
- Alcoholic fatty liver
- Chronic active hepatitis
- Primary biliary cirrhosis
- Alfa-1 AT deficiency
- Haemochromatosis
- Wilson’s disease

2. Liver failure signs:

- Failure to synthesize albumin: Oedema and ascites
- Inadequate synthesis of clotting factors: bruising
- Inability to elinate bilirubin: jaundice
- Inability to eliminate ammonia: hepatic encephalopathy

3. Albumin:
- Main plasma protein
- Produced by the liver
- Used as an assessment of liver synthetic function
- BUT ALSO FOUND:
o Post-surgical
o Significant malnutraition
o Nephrotic syndrome (not sieving the molecules)

4. ALT and AST:

- Damage to hepatocytes
- Nonspecific: also found in cardiac muscle and erythrocytes as well as the liver
(and raised in skeletal muscle disorders, MI)
- Increased in all forms of liver injury

5. Alkaline Phosphatase (ALP):

- For biliary epithelial damage and obstruction (cholestasis)
- ALSO:
▪ In preganancy
▪ Broken bone
▪ Drugs

6. Gamma gT
- Biliary epithelial damage and obstruction (cholestatis)
- Super sensitive
- ALSO: affected by alcohol and drugs such as phenytoin

7. Bilirubin:
- Raised results in jaundice
- Indicator of cholestasis
- Unconjugated raised in haemolysis and Gilbert’s syndrome (AUTOSOMAL
DOMINANT)

8. Gilbert’s syndrome:
- Fluctuating Hyperbilirubinemia
 - Common autosomal dominant disorder found in up to 7% of population
- Intermittent mild jaundice
- Due to conjugating defect in liver
- Benign and no treatment required

9. Other steps:
- Hepatitis serology for viral causes or autoantibodies
- Imaging: obstruction, hepatomegaly
- Proteins: alfa-1 antitrypsin deficienct
- Iron studies: haemochromatosis (rel common)
- Caeruloplasmin/Cu studies – Wilson’s disease (rare)
- Alfa-fetoperotein – hepatocellular carcinoma
- Liver biopsy

10. Intelligent LFTs (iFLT):

- Combination of published diagnostic guidelines and expert opinion (panel)
- Patients with abnormal LFTs in whom the cause in unclear
- Patient specific data
- LFTs and FBC
- ALT, Alk phos and gammaGT all normal: no further tests
- When abnormal:
▪ Aetiology screen - hepatitis serology, liver immunology, ferritin, alpha
1 antitrypsin, caerulopasmin
▪ Fibrosis staging (FIB4 + NAFLD score)
▪ Addition of ELF (enhanced live fibrosis test) when NAFLD or FIB4 are
raised