Liver & Biliary Disease: Dr Anil Sabharwal Mbbs,md(medicine)

Liver & Biliary Disease Dr Anil Sabharwal MBBS,MD(Medicine)

Liver • Largest organ-1.2-1.5 kg, • Right & Left lobe- 8 segments • Blood supply1.Hepatic Art-rich in O2 (20 %) 2.Portal vein-rich in nutrients(80%) 3.Hepatic vein

Liver Functions: 1.Nutrient metabolism-Carbo., protein, fat 2.Protein synthesis-albumin, coagulation factor, complements 3.storage-Fe,Cu,Vit A,D&B12 4.Excretion:Bilesalts,Bilirubin,drugs&alcohol 5.Kupffer cells (cells of REsystem)(15%)-remove aged/damaged RBC, bacteria, viruses, Ag-Ab complexes & endotoxins

Liver Diseases • Alcohol Abuse • Nonalcoholic fatty liver disease • Infections-viral hepatitis, amoebiasis • Hepatobiliary cancers

Clinical Features • • • • • • •

Loss of appetite, nausea, vomiting, fatigue fever Dark colored urine Yellowish discoloration of sclera Whitish stools Pain right hypochondriac region Hemet emesis

Investigations • • • • • • •

LFT,GGT Coagulation tests: î Prothrobine time USG-color Doppler CT MRI-MRCP (cholangiopancreatography) ERCP Liver biopsy

Jaundice •Yellowish discoloration of sclera, bilirubin >3mg/dl •Bilirubin Metabolism: Metabolism Daily catabolism of Haem→250-300 mg/dl unconjugated bilirubin, which becomes conjugated in hepatocytes→ bile. Bile by colonic bacteria→ stercobilinogen (oxidized) → stercobilin •Small amount of stercobilin (4gm/day) is absorbed from liver & excreted in urine as urobilinogen & urobilin

Hemolytic Jaundice • Healthy adult liver can dispose of 6 times normal load of bilirubin. • Bilirubin usually<6mg/dl,unconjugated • New born-Hemolytic jaundice

Alcoholic Liver Disease • Chronic and excessive alcohol ingestion is one of the major causes of liver disease • Alcoholic liver injury comprises three major forms: (1) fatty liver, (2) alcoholic hepatitis, and (3) cirrhosis. • Fatty liver is present in over 90% of binge and heavy drinkers. • 10 to 20% of alcoholics develop alcoholic hepatitis which is precursor of cirrhosis.

Cirrhosis • Cirrhosis is irreversible chronic injury of the hepatic parenchyma and include extensive fibrosis with the formation of regenerative nodules. These features result from hepatocyte necrosis, collapse of the supporting reticulin network with subsequent connective tissue deposition, distortion of the vascular bed, and nodular regeneration of remaining liver parenchyma.. The pathologic process is a final common pathway of many types of chronic liver injury. Clinical features of cirrhosis : Hepatocyte loss→jaundice, edema, coagulopathy, Fibrosis and distorted vasculature → to portal hypertension and its sequelae, including gastroesophageal varices and splenomegaly. Ascites and hepatic encephalopathy result from both hepatocellular insufficiency and portal hypertension.

Hepatocellular Jaundice • Both conjugated &unconjugated bilirubin î

Cholestatic Jaundice • Cholestatic or obstructive jaundice • Pruritus, white stool • Increase Alkaline phosphatase

Ascites • Fluid in peritoneal cavity • Common causes: 1.Malignant disease-hepaic,peitoneal 2.CHF 3.Hepatic cirrhosis Others:Infection-tuberculosis,SBP Hypoprotenemia,hepatic vein occlusion,Pancreatitis

Ascites-Clinical Features • Abdominal Distention, Shifting dullness, fluid thrill,( volume>1 lt) • Pleural effusion-right side

Cirrhosis-Ascites-Pathogenesis • Splanchnic vasodilatation-mediated by nitric oxide which is released when portal HT causes shunting of blood into systemic circulation

Viral Hepatitis Acute viral hepatitis is a systemic infection affecting the liver predominantly: • Hepatitis A virus (HAV), • Hepatitis B virus (HBV), • Hepatitis C virus (HCV), • Hepatitis D virus (HDV), (HBV-associated delta agent). • Hepatitis E virus (HEV).

Acute Hepatitis • All these human hepatitis viruses are RNA , except for hepatitis B, which is DNA virus. • All types of viral hepatitis produce clinically similar illnesses. These range from asymptomatic to fulminant acute infections on the one hand, and from subclinical persistent infections to rapidly progressive chronic liver disease with cirrhosis and even hepatocellular carcinoma, common to the bloodborne types (HBV, HCV, and HDV), on the other.

Clinical Features • Anorexia,nausea,vomiting,URTI,aversion to smoking • Fever, enlarged & tender liver,Jaundice • TLC –normal or low • LFT-grossly derranged

Hepatitis A • Virus transmits by fecal-oral routecontaminated water or food • Incubation period -30 days. • Mortality rate is low. • Chronic hepatitis does not occur. • In adults it is more severe

Hepatitis B • Parenteral route of transmission-infected blood & it’s product, sexual contact, mother to child during delivery. • Incubation period 6 weeks to 6 months • Arthritis, AGN may be associated. • Complications: Chronic hepatitis, cirrhosis & hepatocellular carcinoma.

Hepatitis B-Markers • HBsAg- detection establishes infection & implies infectivity • Anti-HBs-appears after clearance of HBsAg & after successful vaccination • Anti-HBc-IgM-(HBcAg does not appear in serum) • HbeAg-indicate viral replication & infectivity suggests chronic infection • HBV-DNA-parallels the presence of HBeAg

Hepatitis-D (Delta agent) • Hepatitis D virus is a defective RNA virus which causes hepatitis only in the presence of HBsAg. When HBsAg is cleared Hepatitis D also clears. • Hepatitis D is either co-infection or super infection of hepatitis B

Hepatitis-C • Transmission by Blood transfusion, I/V drug abuser, multiple sexual partners. • Incubation period-6-7 weeks • Illness is usually mild • Testing of donated blood for HCV has helped reduce it’s incidence

Hepatitis-E,G • Hepatitis E-Waterborne, self limited ,no carrier state. But has high mortality 10-20% in pregnant women. • Hepatitis G- percutaneous transmission , chronic viremia

Prevention • • • • •

Strict isolation-not required Hand washing after bowel movement Hand washing by medical attendants. Proper disposal of needles-NOT to be Recapped. Screening of donated blood for HBsAg, anti-HBc & anti HCV • Vaccination for HAV & HBV is recommended.

Wilson’s disease • Wilson’s Disease-Hepato lenticular degeneration-excessive deposition of fat in liver & brain. • There is excessive absorption of copper from the small intestine& decreased excretion from liver. • Low serum ceruloplasmin level • Treatment-d-Penicillamine

Amoebic Liver Abscess • Entamoeba Histolytica

Hepatic Malignancy • Primary:Cirrhosis, hemochromatosis, aflatoxin exposure →Carcinoma • Secondary-from GIT

Diseases of Biliary tract • Cholelithiasis (gall stones); more in females, • Risk factors: Obesity, Rapid wt loss or wt gain, diabetes, cirrhosis. Diseases of terminal iluem (eg Crohn’s disease) affects absorption of bile & hence it’s solubility→ Gall stones • Pregnancy ↑ risk • Low carbohydrate diet & Physical activity ↓ risk

Cholelithiasis • Stones are formed by cholesterol,Calcium bilirubinate. • Clinical Features: asymptomatic & discovered by USG, Biliary colic • Laproscopic Cholecystectomy is treatment of choice

Acute cholecystitis • Steady severe pain & tenderness in right hypochondrium or epigastrium • Nausea & vomiting - after fatty meal • Fever & leucocytosis • 90 % cases associated with gall stones • Acalculous cholecystitis(10%)