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Chronic Liver Disease
Dr. Salman Ahmad Ansari
Kanachur Institute of Medical Sciences
Contents
● Liver Function Tests(LFT)
● Jaundice
● Hepatitis
● Alcoholic liver disease
● Portal hypertension
Liver Function Tests(LFT)
I. Tests to assess liver function
Serum bilirubin:
- It is a degradation product of hemoglobin and heme-containing
proteins
- Conjugated and unconjugated bilirubin
- Total bilirubin=conjugated + unconjugated bilirubin
- Increased in gallstones, chronic hepatitis, hemolytic anemias,
Gilberts syndrome
Bilirubin metabolism pic
Serum enzymes:
- These enzymes are present in hepatocytes and leak
into the blood with liver cell damage.
- These include 2 enzymes:
- Aspartate aminotransferase(AST/SGOT)
- Alanine aminotransferase(ALT/SGPT)
- Normal value: 10-40 U/L
- AST is found in liver as well as heart, muscle, kidney and
brain
- AST is increased in: hepatic necrosis, MI, CCF
- ALT is more specific for liver
- ALT is increased in: autoimmune hepatitis, chronic viral
hepatitis(B, C and D)
- AST:ALT ratio: ratio of >2:1 is suggestive of alcoholic liver
disease
- <1 indicates chronic viral hepatitis and non-alcoholic fatty
liver disease
Other enzymes:
- Alkaline phosphatase
- Normal value: 80-240 IU/L
- Increased in cholestasis
- 5’-nucleotidase
- Ɣ-glutamyl transferase(GGT)
- Screening test for alcoholism: raised serum
GGT
II. Tests to measure synthetic function of liver
- Serum albumin
- Made only by liver - excellent marker of hepatic synthetic
function
- Normal value: 4-5.5 g/dl
- Serum globulins
- Group of proteins made up of ϒ-
globulins(immunoglobulins)
- Increased in chronic liver disease
- Coagulation factors: liver produces all coagulation factors
except factor 8
JAUNDICE
Jaundice
Definition: yellowish pigmentation of skin, mucous
membranes and sclera, due to increased levels of bilirubin in
the blood
Normal values
● Normal S. bilirubin: 0.3 to 1.2 mg/dl
● Jaundice: S.bilirubin above 2.0-2.5 mg/dl
● Latent jaundice: S.bilirubin between 1.2-2.5 mg/dl
Classification of jaundice
1. On the basis of cause: conjugated and unconjugated
hyperbilirubinemia
2. On the basis of pathology:
Pre-hepatic Hepatic Post-hepatic
A) Pre-hepatic jaundice:
● Called ‘hemolytic jaundice’
● Occurs due to increased destruction of RBCs
● Unconjugated type of hyperbilirubinemia
● Mild jaundice
● Causes:
● Sickle cell disease
● Thalassemia
● Vitamin B12 and folate deficiency
● malaria
B) Hepatic jaundice:
● Called ‘hepatocellular jaundice’
● Due to inability of damaged liver cells to transport and
conjugate bilirubin, leading to leakage of bilirubin
● Both unconjugated and conjugated bilirubin are increased
● Causes:
● Viral hepatitis
● Alcoholic hepatitis
● Chronic hepatitis
● Drug-induced hepatitis: chlorpromazine, erythromycin
C) Post-hepatic jaundice:
● Called ‘obstructive jaundice’
● Due to narrowing or blockage of pancreatic duct
● Causes:
● Primary biliary cholangitis
● Gallstones in bile duct
● Carcinoma of head of pancreas
● Bile duct carcinoma(cholangiocarcinoma)
● Sclerosing cholangitis
Clinical features of jaundice
● Pallor
● Jaundice
● Hepatosplenomegaly
● Dark stools
● Urine turns dark yellow on standing
Investigations
● Serum bilirubin: conjugated and unconjugated
● LFT
● USG abdomen
● Liver biopsy
Treatment
● Depends upon cause of jaundice
● For mild pruritus: warm baths or oatmeal baths,
antihistamines
● bile acid sequestrants such as cholestyramine or
colestipol
● In some cases, liver transplantation
Gilbert syndrome
Gilbert syndrome
- Mild deficiency of UGT1 enzyme -> results in
unconjugated hyperbilirubinemia
- Autosomal dominant
Clinical features:
- Usually asymptomatic
- Mild jaundice
- Fatigue
Investigations:
- Unconjugated hyperbilirubinemia: <6 mg/dl
- Urobilinogen
Treatment:
- self-limiting
Charcot’s triad
● Suggests inflammation of the bile duct - cholangitis
● Consists of:
● Pain in the right hypochondrium
● Jaundice
● Fever with chills and rigor
Viral hepatitis
5 common types:
● Hepatitis A
● Hepatitis B
● Hepatitis D(Delta Hepatitis)
● Hepatitis C
● Hepatitis E
Hepatitis B
- Caused by hepatitis B virus
- It has several different antigens
- Hepatitis B surface antigen - HBsAg
- Hepatitis B core antigen - HBcAg
- Antigen in nucleocapsid - HBeAg
- Antibodies produced in response:
- Anti-HBs
- Anti-HBc
- Anti-HBe.
Incubation period is about 90 days (50--150 days)
Route of infection:
● Parenteral - transfusion of infected blood products,
contaminated needles(needlestick injury,), IV drug
use with needle sharing, tattooing
● Sexual intercourse, male homosexuals
● Mother-to-child transmission
ALCOHOLIC LIVER DISEASE
Alcoholic liver disease
Alcoholic liver disease (ALD) is defined as liver damage,
caused by over consumption of alcohol, leading to fat
accumulation, liver inflammation, and liver scarring.
Spectrum of disease and comprises of three pathological
forms of liver damage. These are:
(1) Alcoholic fatty liver,
(2) alcoholic hepatitis, and
(3) alcoholic cirrhosis.
Alcoholic fatty liver or steatosis: At this stage, fat
accumulates in the liver parenchyma.
Alcoholic hepatitis: Here, there is inflammation of liver
parenchyma. Appropriate treatment along with alcohol
abstinence can reverse this stage. Recurrent episodes can
occur and are often associated with binge alcohol intake.
More severe cases may end up in liver failure.
Alcoholic cirrhosis: Liver damage at this stage is
irreversible and leads to complications of cirrhosis and portal
hypertension.
Etiology
● Alcohol is a major hepatotoxin
● Fatty liver/steatosis -> alcoholic hepatitis -> cirrhosis
● Quantity and duration of alcohol intake are the
highest risk factors for the development of the liver
disease
● Concurrent infection with hepatitis B or hepatitis C
increases the chances of liver damage.
Clinical features
Patients develop problems during their 30s or 40s.
● Alcoholic fatty liver is often asymptomatic. Liver may be
enlarged and smooth, but is not usually tender.
● Alcoholic hepatitis presents with fatigue, fever, jaundice,
right upper quadrant pain, tender hepatomegaly, and
sometimes a hepatic bruit.
● Severe alcoholic hepatitis may present with features of
liver failure such as ascites, encephalopathy, variceal
bleeding, and hypoglycemia.
● Cirrhosis, if compensated, may be asymptomatic. If it is
decompensated features of liver cell failure and portal
hypertension are present which include hepatic
encephalopathy, coagulopathy, ascites, variceal
bleeding, and splenomegaly.
Investigations
● Liver function tests: ratio of aspartate
aminotransferase (AST) to alanine aminotransferase
(ALT) is ≥2
● CBC
● USG abdomen
Treatment
● Abstinence from alcohol.
● Supportive care
● Corticosteroids or pentoxifylline for severe alcoholic
hepatitis.
● Rarely liver transplantation
PORTAL HYPERTENSION
Portal hypertension
Definition: Portal hypertension is chronic elevation of the
portal venous pressure more than 10 mm Hg or 15 cm of
saline (normal, 5–10 mmHg or 10–15 cm of saline).
Etiology
- Prehepatic: Portal vein obstruction
- Intrahepatic: Cirrhosis, Drug toxicity (e.g. vinyl
chloride, arsenic), Malignant or metastatic hepatic
diseases, Wilson’s disease
- Posthepatic: Hepatic vein thrombosis (Budd-
Chiari syndrome)
• Cardiac disease (e.g. constrictive
pericarditis)
• Inferior vena cava obstruction
Clinical features
● The clinical features of portal hypertension result
mainly from portal venous congestion and collateral
vessel formation.
● Splenomegaly
● Dilated veins may be seen on the anterior abdominal
wall. Dilated veins radiating from the umbilicus are
called caput medusae
● Dilated veins in the esophagus and
stomach(gastroesophageal varices) can bleed and
cause hematemesis and melena.
● Fetor hepaticus
● Ascites
Investigations
● CBC: anemia
● Endoscopy: GI varices
● USG abdomen
Complications of portal HTN
● Variceal bleeding
● Congestive gastropathy
● Hypersplenism
● Ascites
● Renal failure
● Hepatic encephalopathy
Treatment
● Reduction of portal pressure: beta blockers, nitrates
● Portosystemic shunt surgeries
● TIPS(transjugular intrahepatic portosystemic shunt): it
decompresses portal circulation
● Treat the underlying cause of portal HTN
● Liver transplantation
References:
● Manipal Prep Manual of Medicine
● Archith Boloor - Prep Manual
Questions:
salman.s.ansari92@gmail.com
For PPT, scan:

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Chronic liver disease, Jaundice, Alcoholic Liver Disease - Medicine - ATOT

  • 1. Chronic Liver Disease Dr. Salman Ahmad Ansari Kanachur Institute of Medical Sciences
  • 2. Contents ● Liver Function Tests(LFT) ● Jaundice ● Hepatitis ● Alcoholic liver disease ● Portal hypertension
  • 3. Liver Function Tests(LFT) I. Tests to assess liver function Serum bilirubin: - It is a degradation product of hemoglobin and heme-containing proteins - Conjugated and unconjugated bilirubin - Total bilirubin=conjugated + unconjugated bilirubin - Increased in gallstones, chronic hepatitis, hemolytic anemias, Gilberts syndrome
  • 5. Serum enzymes: - These enzymes are present in hepatocytes and leak into the blood with liver cell damage. - These include 2 enzymes: - Aspartate aminotransferase(AST/SGOT) - Alanine aminotransferase(ALT/SGPT) - Normal value: 10-40 U/L
  • 6. - AST is found in liver as well as heart, muscle, kidney and brain - AST is increased in: hepatic necrosis, MI, CCF - ALT is more specific for liver - ALT is increased in: autoimmune hepatitis, chronic viral hepatitis(B, C and D) - AST:ALT ratio: ratio of >2:1 is suggestive of alcoholic liver disease - <1 indicates chronic viral hepatitis and non-alcoholic fatty liver disease
  • 7. Other enzymes: - Alkaline phosphatase - Normal value: 80-240 IU/L - Increased in cholestasis - 5’-nucleotidase - Ɣ-glutamyl transferase(GGT) - Screening test for alcoholism: raised serum GGT
  • 8. II. Tests to measure synthetic function of liver - Serum albumin - Made only by liver - excellent marker of hepatic synthetic function - Normal value: 4-5.5 g/dl - Serum globulins - Group of proteins made up of ϒ- globulins(immunoglobulins) - Increased in chronic liver disease - Coagulation factors: liver produces all coagulation factors except factor 8
  • 10. Jaundice Definition: yellowish pigmentation of skin, mucous membranes and sclera, due to increased levels of bilirubin in the blood
  • 11. Normal values ● Normal S. bilirubin: 0.3 to 1.2 mg/dl ● Jaundice: S.bilirubin above 2.0-2.5 mg/dl ● Latent jaundice: S.bilirubin between 1.2-2.5 mg/dl
  • 12. Classification of jaundice 1. On the basis of cause: conjugated and unconjugated hyperbilirubinemia 2. On the basis of pathology: Pre-hepatic Hepatic Post-hepatic
  • 13. A) Pre-hepatic jaundice: ● Called ‘hemolytic jaundice’ ● Occurs due to increased destruction of RBCs ● Unconjugated type of hyperbilirubinemia ● Mild jaundice ● Causes: ● Sickle cell disease ● Thalassemia ● Vitamin B12 and folate deficiency ● malaria
  • 14. B) Hepatic jaundice: ● Called ‘hepatocellular jaundice’ ● Due to inability of damaged liver cells to transport and conjugate bilirubin, leading to leakage of bilirubin ● Both unconjugated and conjugated bilirubin are increased ● Causes: ● Viral hepatitis ● Alcoholic hepatitis ● Chronic hepatitis ● Drug-induced hepatitis: chlorpromazine, erythromycin
  • 15. C) Post-hepatic jaundice: ● Called ‘obstructive jaundice’ ● Due to narrowing or blockage of pancreatic duct ● Causes: ● Primary biliary cholangitis ● Gallstones in bile duct ● Carcinoma of head of pancreas ● Bile duct carcinoma(cholangiocarcinoma) ● Sclerosing cholangitis
  • 16.
  • 17. Clinical features of jaundice ● Pallor ● Jaundice ● Hepatosplenomegaly ● Dark stools ● Urine turns dark yellow on standing
  • 18.
  • 19. Investigations ● Serum bilirubin: conjugated and unconjugated ● LFT ● USG abdomen ● Liver biopsy
  • 20. Treatment ● Depends upon cause of jaundice ● For mild pruritus: warm baths or oatmeal baths, antihistamines ● bile acid sequestrants such as cholestyramine or colestipol ● In some cases, liver transplantation
  • 22. Gilbert syndrome - Mild deficiency of UGT1 enzyme -> results in unconjugated hyperbilirubinemia - Autosomal dominant Clinical features: - Usually asymptomatic - Mild jaundice - Fatigue
  • 23. Investigations: - Unconjugated hyperbilirubinemia: <6 mg/dl - Urobilinogen Treatment: - self-limiting
  • 24. Charcot’s triad ● Suggests inflammation of the bile duct - cholangitis ● Consists of: ● Pain in the right hypochondrium ● Jaundice ● Fever with chills and rigor
  • 25.
  • 26. Viral hepatitis 5 common types: ● Hepatitis A ● Hepatitis B ● Hepatitis D(Delta Hepatitis) ● Hepatitis C ● Hepatitis E
  • 27. Hepatitis B - Caused by hepatitis B virus - It has several different antigens - Hepatitis B surface antigen - HBsAg - Hepatitis B core antigen - HBcAg - Antigen in nucleocapsid - HBeAg - Antibodies produced in response: - Anti-HBs - Anti-HBc - Anti-HBe.
  • 28. Incubation period is about 90 days (50--150 days) Route of infection: ● Parenteral - transfusion of infected blood products, contaminated needles(needlestick injury,), IV drug use with needle sharing, tattooing ● Sexual intercourse, male homosexuals ● Mother-to-child transmission
  • 30. Alcoholic liver disease Alcoholic liver disease (ALD) is defined as liver damage, caused by over consumption of alcohol, leading to fat accumulation, liver inflammation, and liver scarring.
  • 31. Spectrum of disease and comprises of three pathological forms of liver damage. These are: (1) Alcoholic fatty liver, (2) alcoholic hepatitis, and (3) alcoholic cirrhosis.
  • 32. Alcoholic fatty liver or steatosis: At this stage, fat accumulates in the liver parenchyma. Alcoholic hepatitis: Here, there is inflammation of liver parenchyma. Appropriate treatment along with alcohol abstinence can reverse this stage. Recurrent episodes can occur and are often associated with binge alcohol intake. More severe cases may end up in liver failure. Alcoholic cirrhosis: Liver damage at this stage is irreversible and leads to complications of cirrhosis and portal hypertension.
  • 33. Etiology ● Alcohol is a major hepatotoxin ● Fatty liver/steatosis -> alcoholic hepatitis -> cirrhosis ● Quantity and duration of alcohol intake are the highest risk factors for the development of the liver disease ● Concurrent infection with hepatitis B or hepatitis C increases the chances of liver damage.
  • 34. Clinical features Patients develop problems during their 30s or 40s. ● Alcoholic fatty liver is often asymptomatic. Liver may be enlarged and smooth, but is not usually tender. ● Alcoholic hepatitis presents with fatigue, fever, jaundice, right upper quadrant pain, tender hepatomegaly, and sometimes a hepatic bruit. ● Severe alcoholic hepatitis may present with features of liver failure such as ascites, encephalopathy, variceal bleeding, and hypoglycemia.
  • 35. ● Cirrhosis, if compensated, may be asymptomatic. If it is decompensated features of liver cell failure and portal hypertension are present which include hepatic encephalopathy, coagulopathy, ascites, variceal bleeding, and splenomegaly.
  • 36. Investigations ● Liver function tests: ratio of aspartate aminotransferase (AST) to alanine aminotransferase (ALT) is ≥2 ● CBC ● USG abdomen
  • 37. Treatment ● Abstinence from alcohol. ● Supportive care ● Corticosteroids or pentoxifylline for severe alcoholic hepatitis. ● Rarely liver transplantation
  • 39. Portal hypertension Definition: Portal hypertension is chronic elevation of the portal venous pressure more than 10 mm Hg or 15 cm of saline (normal, 5–10 mmHg or 10–15 cm of saline).
  • 40.
  • 41. Etiology - Prehepatic: Portal vein obstruction - Intrahepatic: Cirrhosis, Drug toxicity (e.g. vinyl chloride, arsenic), Malignant or metastatic hepatic diseases, Wilson’s disease - Posthepatic: Hepatic vein thrombosis (Budd- Chiari syndrome) • Cardiac disease (e.g. constrictive pericarditis) • Inferior vena cava obstruction
  • 42. Clinical features ● The clinical features of portal hypertension result mainly from portal venous congestion and collateral vessel formation. ● Splenomegaly ● Dilated veins may be seen on the anterior abdominal wall. Dilated veins radiating from the umbilicus are called caput medusae
  • 43. ● Dilated veins in the esophagus and stomach(gastroesophageal varices) can bleed and cause hematemesis and melena. ● Fetor hepaticus ● Ascites
  • 44.
  • 45. Investigations ● CBC: anemia ● Endoscopy: GI varices ● USG abdomen
  • 46. Complications of portal HTN ● Variceal bleeding ● Congestive gastropathy ● Hypersplenism ● Ascites ● Renal failure ● Hepatic encephalopathy
  • 47. Treatment ● Reduction of portal pressure: beta blockers, nitrates ● Portosystemic shunt surgeries ● TIPS(transjugular intrahepatic portosystemic shunt): it decompresses portal circulation ● Treat the underlying cause of portal HTN ● Liver transplantation
  • 48.
  • 49. References: ● Manipal Prep Manual of Medicine ● Archith Boloor - Prep Manual Questions: salman.s.ansari92@gmail.com For PPT, scan: