diagnosis of liver disease based on clinical examination and laboratories

Diagnosis of liver disease may be based on the following as
1/clinical presentation:
       History: History taking should be focused on the following
*History of present illness
*Medicine usage and toxin exposure (including alcohol)
*Associated symptoms_development of swelling, screening for encephalopathy, GI bleeding
*Family history of liver disease
*Dietary habits
*Risk factors for infectio that is, intravenous/intranasal drug use, body piercings, tattooing, sexual history,travel to foreign countries, occupation
      Physical examination
physical stigmata of acute or chronic liver disease may be subtle or asent
*assess for icterus
*Ascites_shifting dullness; peripheral edema
*Hepatomegaly and splenomegaly
*Gynecomastia, testicular atrophy
*Muscle wasting,
*Telangiectasis , palmar erythema, pubic hair changes

2/Diagnostic testing
      Laboratories
*serum enzymes :hepatic disorders with elevation in aminotransferases referred to as hepatocellular;
      elevation in alkaline phosphatase (ALP) referred to as cholestatic.
      elevation of serum aspartate and alanine aminotransferases (AST and ALT) indicates              hepatocellular injury and necrosis
the ratio of serum AST to ALT is typically > 2 in alcoholic liver disease. in viral hepatitis, this ratio is characteristically >1
      -ALP is an enzyme that is present in a variety of tissues (bone, intestine, kidney, leukocytes, liver and placenta). serum ALP level elevated in biliary obstruction, space-occupying lesions or infiltrative disorders of the liver and condition caused by intrahepatic cholestasis
      -GGT is present in a variety of tissues. increases in GGT and ALP tend to ocur in similar hepatic diseases. Serum GGT level elevated in individuals who ingest barbiturates, phenloin, or alcohol when other liver enzyme and bilirubin levels are normal
     -5-Nucleotidase used to detect biliary obstruction, cholestasis and infiltrative hepaobiliary diseases.

* Synthetic products
    -Serum albumin
    -Several important proteins in hemostaisis and fibrinolysis (coagulation factors..), prothrombine time (PT) and the international normalized ratio (INR). PT/INR prolongation may result from impaired coagulation factor synthesis or vitamin K deficiency
    -cholesterol synthesized in the liver. A very low cholesterol level occurs in patients with advanced liver disease. in PBC, lvels of serum cholesterol may be markedly elevated

*excretory products
    -Bilirubin is a degradation product of hemoglobin and nonerythroid hemoproteins. total serum bilirubin is composed of conjugated (direct) and unconjugated (indirect)fractions. Increase in uncojugated bilirubin level occurs as a result of excessive bilirubin production (neonatal or physiologic jaundice,hemolysis and hemolytic anemias, ineffective erythroproiesis and resorption of hematomas), reduced hepatic bilirubin uptake (Gillbert's syndrome and drugs such as rifampin and probenecid) or impaired bilirubin conjugation
Elevation of both conjugated and unconjugated fractions occurs in Dubin-Johnson's and Rotor's syndromes and in conditions associated with intrahepatic and extrahepatic cholestasis
    -Bile acids
    -AFP is normally produced by fetal liver cells. AFP falls to normal adult levels of <10ng/ml. within 1 year of life. levels of >400ng/ml or a rapid doubling time are suggestive of HCC; mild to moderate elevation can also be seen in acute and chronic liver inflammation