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
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
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
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).
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