2. HEPATITIS
• hepatitis is a broad term that means inflammation of liver.
• it is most commonly caused by viruses but also be caused by drugs
(alcohol), chemicals, autoimmune diseases and metabolic
abnormalities.
3. TYPES OF HEPATITIS
• Alcoholic Hepatitis
• Viral Hepatitis
• Drug Induced Hepatitis
• Autoimmune Hepatitis
4. ALCOHOLIC HEPATITIS
• alcohol is a major risk factor for fatty liver disease which manifests as
hepatitis.
• c/f : may be asymptomatic or present with fever
rapid onset of jaundice,
abdominal discomfort, muscle wasting
portal HTN,ascites , without cirrhosis
hepatomegaly and splenomegaly
5. INVESTIGATION :
• Biochemical findings :AST, ALT raised
raised bilirubin,decreased albumin
• Hematological findings: prolonged prothrombin time, leukocytosis
• Liver biopsy
TREATMENT:
• Stop consumption of alcohol
• Severe hepatitis – bed rest
• Nutrition –fine bore nasogastric tube
6. • Treatment for encephalopathy and ascites
• Corticosteroids – prednisolone
• Antimicrobial therapies for bacterial and fungal infection
• N-acetylcysteine – antioxidants – reduce inflammation
• Liver transplantation
7. VIRAL HEPATITIS
• Causative agents : Hepatitis A virus
Hepatitis B virus
Hepatitis C virus
Hepatitis D virus
Hepatitis E virus
8.
9. HEPATITIS B VIRUS
• Most common cause of chronic liver disease and hepatocellular
carcinoma
• Source of infection: human suffering from hepatitis or carriers
• Mode of transmission :
vertical transmission
Horizontal transmission
10. INVESTIGATION :
• viral markers : surface antigen , e- antigen, viral load (PCR)
• Liver markers : elevated levels of AST ,ALT and rarely ALP
• Specific antibody in blood against viral antigen , an IGM antibody
indicates acute infection while IG-G antibody indicates development
of secondary immune response
11. MANAGEMENT OF ACUTE HEPATITIS B
• Full spontaneous recovery occurs in more than 95./. Adults with
acute HBV infection
• If fulminant liver failure present –life threatening and requires liver
transplantation
• Treatment is supportive with monitoring of acute liver failure
• Antiviral therapy –severe liver injury with coagulopathy
• Recovery occurs within 6 months with appearance of antibody to
viral antigen
• Persistence of HBeAg andHBsAg indicates chronic infection
12. MANAGEMENT OF CHRONIC HEPATITIS B
• Goals of treatment :HBeAg seroconversion, reduction in HBV-DNA,
normalisation of LFTs
• DIRECT ACTING NUCLEOSIDE /NUCLEOTIDE ANTIVIRAL AGENTS:
lamivudine, entecavir, tenofovir
• PEGYLATED INTERFERON –ALFA – acts by augmenting host immune
response
• Liver transplantation
13. PREVENTION AND PROPHYLAXIS
• AVOIDING RISK FACTORS
• ACTIVE IMMUNIZATION: Recombinant vaccines (containing HBsAg)
dosage regimen – given into deltoid muscle at 0,1,6 months
for high risk groups and children
• Combined prophylaxis : vaccination and immunoglobulin
14. DRUG INDUCED HEPATITIS
• Drug and toxin induced hepatotoxicity- any degree of
liver injury by drugs and toxins
• Examples: acetaminophen, alcohol, carbon tetrachloride,
chloroform,
heavy metals, phosphorus
TREATMENT:
• Withdrawal of offending drug
• N-acetylcysteine – in paracetamol toxicity
• Supportive therapy for specific type of liver injury
15. AUTOIMMUNE HEPATITIS
• Chronic and progressive hepatitis
• Associated with circulating autoantibodies and
hypergammaglobulinemia
INVESTIGATIONS :
o biochemical findings : raised serum transferases, ALP, bilirubin
serum gamma globulin, low serum albumin
oProthrombin time, autoantibodies, liver biopsy
16. TREATMENT:
• Prednisolone 30 mg given orally (2 wks) maintenance
dose 10-15mg for 2yrs after LFT becomes normal
• Azathioprine – dose 1-2mg/kg daily
• Immunosuppressive agents: cyclosporin ,tacrolimus
• Duration of tx : lifelong
• Liver transplantation if treatment fails
17. CIRRHOSIS
• End stage of any chronic liver disease
• Diffuse process characterised by fibrosis and conversion of normal
architecture to structurally abnormal regenerating nodules of liver
cells
• 3 main characteristics: fibrosis
regenerating nodules
loss of architecture of entire liver
18. PATHOGENESIS
• Chronic liver injury results in inflammation & widespread necrosis of
liver cells and eventually fibrosis ( due toactivation of stellate cells
by many cytokines)
• Extensive fibrosis results in loss of liver architecture.
• Regenerating nodules produced due to hyperplasia of remaining
surviving liver cells. Destruction and distortion of hepatic vasculature
by fibrosis leads to obstruction of blood flow
• Ascites and hepatic encephalopathy (hepatocellular insufficiency)
21. SYMPTOMS
• Some are asymptomatic (diagnosed at ultrasound)
• Weakness, fatigue, muscle cramps ,weight loss, anorexia, upper
abdominal discomfort
• Also present as shortness of breath due to large right pleural
effusion
22. CLINICAL FEATURES OF CIRRHOSIS
• Hepatomegaly (although may be small )
• Jaundice
• Ascites
• Circulatory changes :spider telangectasia, palmar erythema,
cynosis
• Endocrine changes :loss of libido, hair loss
men – gynaecomastia, testicular atrophy
women – breast atrophy, amenorrhoea
• Hemorrhagic tendency : bruises , purpura, epistaxis
• Portal hypertension: splenomegaly, collateral vessels ,variceal
bleeding
24. MANAGEMENT
INVESTIGATIONS:
• LIVER FUNCTION TESTS :
o hyperbilirubinemia
oSerum proteins: reversal of A:G ratio (hypoalbuminemia due to
reduced synthesis by liver)(hyperglobulinemia- stimulation of
reticuloendothelial system)
oSerum transaminases- AST,ALT raised, ALP slightly elevated
oProthrombin time prolonged
25. • Hematological tests- peripheral blood picture,serological markers
• Other biochemical markers- serum electrolytes blood ammonia
• Imaging – usg ,CT scan, MRI , endoscopy
• Liver biopsy- uses- to confirm diagnosis, assess severity and type
26. TREATMENT
• No treatment available to arrest or reverse the cirrhotic changes in
liver
• Liver transplantation is the specific treatment
• Progression can be halted by:
treatment of underlying cause, removal of causative agents –
drugs and alcohol, nutrition , treatment of complications
27. • . Diet : daily calorie intake – 35kcal/kg
daily protein intake -1.2-1.5g/kg
• Avoid hepatotoxic drugs
• Follow up- 6 monthly ultrasound and serum alpha
fetoprotein for detection of HCC
28. PROGNOSIS
• COMPENSATED CIRRHOSIS- good prognosis with median
survival >12 yrs
• DECOMPENSATED cirrhosis – median survival around 2 yrs
• Poor prognostic factors :
raised bilirubin, low albumin, prolonged PT, renal dysfunction,
hyponatremia
29. PORTAL HYPERTENSION
• Increased portal pressure or sinusoidal pressure
• Normal hepatic venous pressure gradient is 5-6mmhg
• Portal HTN is present when >10mmhg
• Risk of variceal bleeding increase beyond gradient of 12 mmhg
30.
31. PATHOLOGY
CAUSE : lobules of liver being replaced by nodules
separated by fibrous septations which compress sinusoids
(increased resistance)
portal pressure = flow X resistance
Increased resistance reduction in blood flow to liver
simultaneously development of
collateral
vessels
portal blood bypass liver and enter
32. CLINICAL FEATURES
• Splenomegaly is a cardinal finding . Spleen is rarely
enlarged more than 5 cm below the left costal margin in
adults but more marked splenomegaly can occur in
childhood and adolescence.
• Thrombocytopenia
• collateral vessels may be visible on the anterior
abdominal wall and occasionally several radiate from the
umbilicus to form a ‘caput medusae’ -
cruveilhier Baumgarten syndrome -venous hum from
33. • Ascites – partly due to portal HTN and mainly due to liver cell failure
(sodium retention)
• Variceal bleeding –from osephagial varices
35. INVESTIGATIONS
• diagnosis is often done clinically
• Portal venous pressure measurement –balloon catheter via
transjugular route
• Thrombocytopenia
• endoscopy is the most useful investigation to determine whether
gastro-oesophageal varices are present
36. • ultrasonography - splenomegaly and collateral vessels, and can
sometimes indicate the cause, such as liver disease or portal vein
thrombosis.
• ct and magnetic resonance angiography can identify the extent of
portal vein clot and are used to identify hepatic vein patency
37. MANAGEMENT
focused on the prevention and/or control of variceal haemorrhage.
• NON-BLEEDING VARICES : non selective β-adrenoceptor
antagonist (β-blocker) therapy : propranolol (80–160 mg/day) or
nadolol (40–240 mg/day)
reduce the heart rate by 25% has been shown to be effective in the
primary prevention of variceal bleeding.
38. • carvedilol: a non-cardioselective vasodilating β-blocker (6.25–12.5
mg/day).
39. FOR ACUTE VARICEAL BLEEDING
• Antibiotics – iv cephalosporin or piperacillin/ tazobactum
• Vasoactive medications- terlipressin-
• Endoscopic therapy( banding)
• Balloon tamponade
• Transjugular intrahepatic portosystemic stent shunt
40. • TERLIPRESSIN - synthetic vasopressin analogue
• given by intermittent injection rather than continuous infusion
• reduces portal blood flow &resistance ,hence decrease portal HTN
• is 2 mg iv 4 times daily until bleeding stops, and then 1 mg 4 times
daily for up to 72 hours
• caution - severe ischaemic heart disease or peripheral vascular
disease
41. VARICEAL LIGATION (‘BANDING’)
• stops variceal bleeding in 80% of patients and can be repeated if
bleeding recurs.
• band ligation involves the varices being sucked into a cap placed on the
end of the endoscope, allowing them to be occluded with a tight rubber
band.
• the occluded varix subsequently sloughs with variceal obliteration.
banding is repeated every 2–4 weeks until all varices are obliterated.
42. BALLOON TAMPONADE
• this technique employs a Minnesota tube which consists of 2
balloons – positioned in the fundus of the stomach and in the lower
oesophagus, respectively.
• additional lumens allow contents to be aspirated from the stomach
and from the oesophagus
• life-threatening haemorrhage
43. TIPSS :
• this technique uses a stent placed between the portal vein and the
hepatic vein within the liver to provide a portosystemic shunt and
therefore reduce portal pressure.
• it is carried out under radiological control via the internal jugular
vein
44. SECONDARY PREVENTION OF VARICEAL BLEEDING
•
• beta-blockers prevent recurrent variceal bleeding
• following successful endoscopic therapy
