Liver & Biliary Disease

Dr Anil Sabharwal
MBBS,MD(Medicine)
 Liver
• Largest organ-1.2-1.5 kg,
• Right & Left lobe- 8 segments
• Blood supply-
1.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 route-
contaminated 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%)