Presentation (1).pptx medicine cirrhosis

Medicine

1. Management of Hepatitis, Cirrhosis and Portal Hypertension -Raichel babu

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. 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

9. 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

10. 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

11. 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

12. 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

13. 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

14. Autoimmune hepatitis Chronic and progressive hepatitis Associated with circulating autoantibodies and hypergammaglobulinemia INVESTIGATIONS : biochemical findings : raised serum transferases, ALP, bilirubin serum gamma globulin, low serum albumin Prothrombin time, autoantibodies, liver biopsy

15. 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

16. 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

17. 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)

18. CAUSES OF CIRRHOSIS Alcohol Chronic viral hepatitis (B or C) Non alcoholic fatty liver disease Immune : primary sclerosing cholangitis autoimmune liver disease Biliary : primary biliary cholangitis secondary biliary cholangitis cystic fibrosis Genetic :haemochromatosis wilson’s disease alpha 1 antitrypsin deficiency Cryptogenic Chronic venous outflow obstruction Any chronic liver disease

19. 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

20. 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 Hepatic encephalopathy

21. COMPLICATIONS Portal hypertension Hepatic encephalopathy Ascites Renal failure

22. MANAGEMENT INVESTIGATIONS: LIVER FUNCTION TESTS : hyperbilirubinemia Serum proteins: reversal of A:G ratio (hypoalbuminemia due to reduced synthesis by liver)(hyperglobulinemia- stimulation of reticuloendothelial system) Serum transaminases- AST,ALT raised, ALP slightly elevated Prothrombin time prolonged

23. 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

24. 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

25. . 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

26. 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

27. 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

28. 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 systemic circulation

29. 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 large umbilical collateral vessel

30. Ascites – partly due to portal HTN and mainly due to liver cell failure (sodium retention) Variceal bleeding –from osephagial varices

31. Complications of portal HTN Variceal bleeding: oesophageal, gastric,other Congestive gastropathy Hypersplenism Ascites Iron deficiency anaemia Renal failure Hepatic encephalopathy

32. 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

33. 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

34. 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.

35. carvedilol: a non- cardioselective vasodilating β-blocker (6.25–12.5 mg/day).

36. For acute variceal bleeding Antibiotics – iv cephalosporin or piperacillin/ tazobactum Vasoactive medications- terlipressin - Endoscopic therapy( banding) Balloon tamponade Transjugular intrahepatic portosystemic stent shunt

37. 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

38. 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 .

39. 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

40. 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

41. Secondary prevention of variceal bleeding beta-blockers prevent recurrent variceal bleeding following successful endoscopic therapy

42. Thank you