Hepatic Disorders: Liver Cirrhosis

• Slides about hepatic disorders

Liver Cirrhosis

• A chronic liver condition arises from hepatocytes necrosis, leading to fibrous tissue deposits.
• Regenerating nodules form and hepatic architecture is lost.
• Portal hypertension & liver cell failure can result from the described derangement.

Causes of Cirrhosis

• Chronic viral hepatitis caused by Hepatitis B ± D and Hepatitis C
• Autoimmune hepatitis
• Alcohol
• Nonalcoholic fatty liver disease (NAFLD)
• Primary biliary cholangitis
• Hereditary hemochromatosis
• Budd-Chiari syndrome
• Wilson's disease
• α1-Antitrypsin deficiency
• Idiopathic or cryptogenic causes

Clinical Features

• Symptoms include general malaise, fatigue, anorexia, and weight loss
• Swollen abdomen/legs with feeling of enlarged abdomen
• Nose bleed/bleeding from lower limbs, jaundice/itch and hand tremors
• Physical findings include skin pigmentation, xanthoma, and spider angioma
• Palmar erythema and finger clubbing
• Ascites, lower thigh edema, hepatic encephalopathy, bleeding plaques/purpura are also clinical features
• Other clinical signs include caput medusae, gynecomastia, and fever

Investigations for Hepatic Disorders

• Serum albumin and prothrombin time are tests for severity
• Liver biochemistry will be tested, especially alanine transaminase (ALT) is specific
• Serum electrolyte and creatinine levels
• Serum alpha-fetoprotein levels >200 ng/mL suggest hepatocellular carcinoma (HCC)
• Viral markers, serum autoantibodies, and immunoglobulins indicate cause or type of cirrhosis
• Genetic markers are tested
• To exclude hereditary hemochromatosis, TIBC and ferritin are examined
• Imaging: Ultrasound, CT scan, MRI
• Endoscopy
• Liver biopsy remains the 'gold standard' for confirming liver disease type and severity.

Complications of Liver Cirrhosis

• Can include portal hypertension, variceal bleeding, ascites
• Edema, hepatic encephalopathy, hepatorenal syndrome and hepatopulmonary syndromes are other possible complications
• Hepatocellular carcinoma (HCC) may develop

Prognostic Parameters

• Child-Pugh Score is used for classification
• Total bilirubin, serum albumin, PT INR are assessed
• Severity of ascites and hepatic encephalopathy are taken into account to determine class
• Class A has a 1-year survival of 100%
• Class C has a survival rate of only 45%

Portal Hypertension

• Esophageal varices are dilated submucosal veins in patients with portal hypertension
• They may result in serious upper gastrointestinal bleeding
• Esophageal varices are the most common cause of significant gastrointestinal bleeding
• Gastric and, rarely, intestinal varices may also bleed
• Band ligation can treat bleeding

Clinical Signs

• History includes color, amount, abdominal pain, hemodynamic instability, weight loss and anorexia
• Clinical signs include drugs, alcohol, liver history, fresh, coffee ground, black tarry stool
• Physical examination involves vital signs, clubbing, stigmata of chronic liver disease
• Findings from the abdominal exam include masses and tenderness
• CBC: Hb, platelet.
• Other tests: Urea, Creatinine,Liver function tests, Coagulation profile, Abdominal US, Upper Endoscopy

Ascites

• Straw colored ascites can be caused by Cirrhosis, malignancy
• Tuberculosis, Spontaneous infective cirrhosis, Budd-Chiari syndrome
• Chronic pancreatitis, Congestive cardiac failure, Constrictive pericarditis, and Hypoproteinemia (e.g., nephrotic syndrome)
• Chylous ascites can be caused by lymphatic duct obstruction, e.g. by carcinoma
• Hemorrhagic can be caused by malignancy, ruptured ectopic pregnancy, abdominal trauma or acute pancreatitis
• Serum-ascites albumin gradient (SAAG) is measured, high if >1.1 g/dL and low if <1.1 g/dL
• High portal hypertension indicates Hepatic outflow obstruction; Budd-Chiari syndrome, Hepatic veno-occlusive disease and Tricuspid regurgitation
• Low serum-ascites results from Peritoneal carcinomatosis or tuberculosis
• Pancreatitis and Nephrotic syndrome

Hepatic Encephalopathy

• It's an altered neuropsychiatric state in patients with liver cell failure
• Primarily occurs in liver cirrhosis, though can occur in acute hepatic failure
• Stages 0-4 exist based on severity, increasing from minimal abnormalities to coma
• Portal blood bypasses the liver, and 'toxic' metabolites directly affect the brain
• Leading pathophysiological mechanism is ammonia-induced alteration of brain neurotransmitter balance

Acute Hepatitis

• Acute hepatitis:
• • Viral hepatitis
• • Autoimmune hepatitis
• • Nonalcoholic steatohepatitis

Hepatitis A Virus (HAV)

• Hepatitis A virus (HAV) travels the fecal-oral route
• Incubation lasts 1-2 weeks
• Resolution is the rule, but fulmination may occur in 0.5% of cases
• Chronic hepatitis does not occur
• Hepatitis A anitbodies such as IgM indicates recent infection while IgG shows old infections
• Is prevented prophylactically with inactivated (HAV) vaccine.
• Supportive care is the treatment

Hepatitis E (HEV)

• HEV is a single stranded RNA virus that is self-limiting and enteric transmitted
• Transmission: fecal-oral
• Chronicity may occur in immunocompromised patients
• Diagnosis is typically based on the detection of IgM antibodies to HEV
• Fulmination with pregnancy may occur

Hepatitis B Virus (HBV)

• DNA virus
• Route of infection: Blood and all blood products, sexual intercourse, saliva, Transplacental.
• Incubation period: 2-6 months.
• Immunity response and fate of hepatitis B infection:
• -Resloution
• -Carrier
• Chronic hepatitis (5-10%).

Hepatitis C Virus (HCV)

• Viral incubation period of approximately 8 weeks
• Most cases of acute HCV infection are asymptomatic
• Mild course
• 55-85% of newly infected patients remain virement and may develop chronic liver disease
• 15-30% of patients with chronic hepatitis C experience progression to cirrhosis.
• Patients with HCV-induced cirrhosis at a risk for the development of HCC especially in the setting of HBV coinfection
• HCV antibody is used for screening of infection, and PCR to assess viral load and follow up response to treatment

Hepatitis D

• Needs HepB(Bivirius Antigent)
• Simultaneous infection of HBV and HDV results in the same clinical picture of acute infection with HBV alone with mild to severe results
• Risk of developing chronic HBV and HDV infection is the same as the rate of developing chronic HBV infection
• Chronic HBV and HDV disease tend to progress more rapidly to cirrhosis than chronic HBV infection alone
• Introduction of HDV into an individual already infected with HBV may have dramatic consequences
• Superinfection may give HBsAg-positive patients the appearance of a sudden worsening or flare of hepatitis B

Key Points

• Cirrhosis secondary to HBV and HCV is the most common risk factor for HCC development.
• All cirrhotic patients should be routinely monitored with abdominal ultrasonography every 6 months.