Biochemical functions of
Liver
• Lipid metabolism
• Gathering of free fatty acids from diet and breaking down to acetyl coA it
can enter into several pathways to form TG, phospholipids, cholesterol.
• Approx 70% of cholesterol is produced from liver .
• Protien metabolism
• All protiens are synthesized from liver except immunoglobulins and adult
haemoglobin.
• Development of Hb in infants
• Synthesis of albumin,acute phase protiens, coagulation protiens also serve
as a pool of amino acids from protein degradation.
2) Synthetic function:
A number of proteins present in the plasma including albumin, globulin
, fibrinogen and other coagulation system proteins except calcium are
synthesized in liver, lipoproteins,cholesterol. Albumin also acts as a
ready source of amino acids whenever required. Coagulation factors,
except VIII C are synthesised in liver. Factor II, V, VII, IX, and X require
Vitamin K for their synthesis, the absorption of which is dependent on
the presence of bile in the small intestine.
3) Excretion and secretory function :Major haem waste product
bilirubin into bile. Excretion of bile pigments bile salts
4) Detoxification function and protective function: ammonia is
detoxified to urea and certain drugs Steroids are inactivated by
conjugation as glucuronides and sulphates before excretion in urine
• Kupffer cells: (phagocytosis), The Kupffer cells remove certain toxic
substances coming from portal circulation before they enter the
general circulation.
5) Storage function: glycogen, fat soluble vitamins D,A, trace elements
and iron.
• Derangement of liver functions, singly or in combination, may occur
when liver is assaulted by:
• • Viruses
• • Drugs
• • Industrial chemicals
• • Hypoxia due to shock, congestive cardiac failure ,liver cirrhosis
• • Prolonged biliary obstruction.
• In addition, the disease process also destroys the liver cells and this
causes leakage of intracellular enzymes into plasma where their level
rises.
Importance of LFTS
• To assess the severity of the disease
• To differentiate different types of jaundice
• To find out the presence of latent disease
LFTS
• These test simply provide exsistance, extent, damage
• Classification of LFTS
1. Test based on excretory function
2. Test based on detoxification function
3. Test based on synthetic function
4. Test based on enzymatic activity
5. Test on metabolic activity
Test based on excretory function
• Test related with bilirubin metabolism
• Test related with bile acid metabolism
• Deficiency of bile acids then patients will suffer from steahorrea
• Malabsorption of fats
• Test based on dye-excretion BSP bromosulphthalein test
• Estimation of urobilinogen in urine and feaces
• Colour of stool examination
2) Test based on serum enzymes derived from liver
• ALT
• AST
• ALP
• Gamma-glutamy transpeptidase GGT
• 5-nucletidase enzyme 5NT
3) Test based on metabolic activity
• Galactose tolerance test GTT
• Estimation of esterified cholesterol
4) Test based on synthetic function
• Serum albumin and A/G ratio
• Coagulation factors (Prothrombin time) PT
• Total protein estimation
5) Test based on detoxification
• Estimation of blood urea and ammonia
• Hippuric acid synthesis
Test based on Synthetic function
• Although these tests are not sensitive to minimal liver damage
• Useful in quantitating the severity of hepatic dysfunction
• A decreased serum Albumin correlates with severity of functional
impairement
• Found in chronic liver disease rather than in acute liver disease.
• Serum alpha globulin in CLD. Serum gamma globulins in acute
liver disease and CLD, cirrhosis.
• Ig G and Ig M in chronic active hepatitis
• Ig A in alcoholic cirrhosis
• Prothrombin time in jaundice and liver disease because the liver
is unable to synthesize adequate amount of clotting factor or because
of disruption of bile flow results in inadequate absorption of vitamin
K.
• Measurement of PT is useful in following the progression of disease
• May be prolonged by cholestasis
• Assesement of risk of bleeding
• A marked increase indicates diffuse liver disease and a poor
prognosis.
• Total protein estimation
• A/G ratio
• Globulin = albumin- total protein
Test based on Detoxification function
• Serum ammonia level
Liver failure ammonia other toxins increase in blood leads to hepatic coma
hepato-encephalopathy
• Hippuric acid test
Hippuric acid is produced in liver when benzoic acid combines with glycin
3gm should excreted in healthy person
Smaller amount when there is acute or chronic liver damage or infectious
hepatitis
Test based on Enzymatic function
• Enzymes play an important role in differentiating hepatocellular from
obstructive liver disease. If the obstruction not rapidly treated it may
leads to liver failure.
• Hepatocyte damage
• AST and ALT
• A rise in plasma aminotransferase activity sensitive indicator of
damage to cytoplasmic or mitochondrial membrane
• Liver cells contain more AST than ALT.ALT is confined to cytoplasm in
which its concentration is high than AST.
• In viral hepatitis the cytoplasmic membrane sustains the more
damage thus ALT greater increase than AST.
• In infiltrative disorders in which there is damage to both
mitochondrial and cytoplasmic membrane there is greater increase in
AST than ALT.
• The relative plasma activities of ALT and AST may help to indicate
type of cell damage.
• A plasma AST:ALT ratio of > 2 suggestive but not diagnostic of
alcoholic disease
• <1 ratio suggests chronic viral hepatitis.
• ALT is found mainly in liver(lesser amount in kidney,skeletal muscle)
• ALT is more liver specific
• AST is widely distributed in equal amounts in heart ,skeletal muscle
and liver.
• AST and ALT raised in acute conditions acute viral hepatitis drug and
toxin induced liver necrosis and ischemia.
• ALT is more elevated than AST.
• Test of obstruction
• ALP (Alkaline phosphatase)
• Localized in microvilli of bile canaliculi
• Widely distributed in all tissues high in liver bone kidney and placenta
• Marker of extra hepatic biliary obstruction
• Intra hepatic cholestasis
• Thus both conjugated bilirubin and ALP will be elevated in cholestasis
liver disease.
• Bone related disorders
GGT
• Gamma-glutamyl transferase
• It is an enzyme derived from endoplasic reticulum of cells of
hepatobiliary tract.
• Also found in liver kidney pancreas intestine prostate but not in bone.
• As this reticulum proliferates for example in response to prolonged
alcohol intake and drugs synthesis of enzyme is induced. There fore
raised plasma activity does not indicate hepatocellular damage but
may reflect enzyme induction or cholestasis.
• Highest level in biliary obstruction

Biochemical functions of Liver.pptx

  • 1.
  • 2.
    • Lipid metabolism •Gathering of free fatty acids from diet and breaking down to acetyl coA it can enter into several pathways to form TG, phospholipids, cholesterol. • Approx 70% of cholesterol is produced from liver . • Protien metabolism • All protiens are synthesized from liver except immunoglobulins and adult haemoglobin. • Development of Hb in infants • Synthesis of albumin,acute phase protiens, coagulation protiens also serve as a pool of amino acids from protein degradation.
  • 3.
    2) Synthetic function: Anumber of proteins present in the plasma including albumin, globulin , fibrinogen and other coagulation system proteins except calcium are synthesized in liver, lipoproteins,cholesterol. Albumin also acts as a ready source of amino acids whenever required. Coagulation factors, except VIII C are synthesised in liver. Factor II, V, VII, IX, and X require Vitamin K for their synthesis, the absorption of which is dependent on the presence of bile in the small intestine.
  • 4.
    3) Excretion andsecretory function :Major haem waste product bilirubin into bile. Excretion of bile pigments bile salts 4) Detoxification function and protective function: ammonia is detoxified to urea and certain drugs Steroids are inactivated by conjugation as glucuronides and sulphates before excretion in urine • Kupffer cells: (phagocytosis), The Kupffer cells remove certain toxic substances coming from portal circulation before they enter the general circulation. 5) Storage function: glycogen, fat soluble vitamins D,A, trace elements and iron.
  • 5.
    • Derangement ofliver functions, singly or in combination, may occur when liver is assaulted by: • • Viruses • • Drugs • • Industrial chemicals • • Hypoxia due to shock, congestive cardiac failure ,liver cirrhosis • • Prolonged biliary obstruction. • In addition, the disease process also destroys the liver cells and this causes leakage of intracellular enzymes into plasma where their level rises.
  • 6.
    Importance of LFTS •To assess the severity of the disease • To differentiate different types of jaundice • To find out the presence of latent disease
  • 7.
    LFTS • These testsimply provide exsistance, extent, damage • Classification of LFTS 1. Test based on excretory function 2. Test based on detoxification function 3. Test based on synthetic function 4. Test based on enzymatic activity 5. Test on metabolic activity
  • 8.
    Test based onexcretory function • Test related with bilirubin metabolism • Test related with bile acid metabolism • Deficiency of bile acids then patients will suffer from steahorrea • Malabsorption of fats • Test based on dye-excretion BSP bromosulphthalein test • Estimation of urobilinogen in urine and feaces • Colour of stool examination
  • 9.
    2) Test basedon serum enzymes derived from liver • ALT • AST • ALP • Gamma-glutamy transpeptidase GGT • 5-nucletidase enzyme 5NT
  • 10.
    3) Test basedon metabolic activity • Galactose tolerance test GTT • Estimation of esterified cholesterol 4) Test based on synthetic function • Serum albumin and A/G ratio • Coagulation factors (Prothrombin time) PT • Total protein estimation 5) Test based on detoxification • Estimation of blood urea and ammonia • Hippuric acid synthesis
  • 11.
    Test based onSynthetic function • Although these tests are not sensitive to minimal liver damage • Useful in quantitating the severity of hepatic dysfunction • A decreased serum Albumin correlates with severity of functional impairement • Found in chronic liver disease rather than in acute liver disease. • Serum alpha globulin in CLD. Serum gamma globulins in acute liver disease and CLD, cirrhosis. • Ig G and Ig M in chronic active hepatitis • Ig A in alcoholic cirrhosis
  • 12.
    • Prothrombin timein jaundice and liver disease because the liver is unable to synthesize adequate amount of clotting factor or because of disruption of bile flow results in inadequate absorption of vitamin K. • Measurement of PT is useful in following the progression of disease • May be prolonged by cholestasis • Assesement of risk of bleeding • A marked increase indicates diffuse liver disease and a poor prognosis.
  • 13.
    • Total proteinestimation • A/G ratio • Globulin = albumin- total protein
  • 14.
    Test based onDetoxification function • Serum ammonia level Liver failure ammonia other toxins increase in blood leads to hepatic coma hepato-encephalopathy • Hippuric acid test Hippuric acid is produced in liver when benzoic acid combines with glycin 3gm should excreted in healthy person Smaller amount when there is acute or chronic liver damage or infectious hepatitis
  • 15.
    Test based onEnzymatic function • Enzymes play an important role in differentiating hepatocellular from obstructive liver disease. If the obstruction not rapidly treated it may leads to liver failure. • Hepatocyte damage • AST and ALT • A rise in plasma aminotransferase activity sensitive indicator of damage to cytoplasmic or mitochondrial membrane • Liver cells contain more AST than ALT.ALT is confined to cytoplasm in which its concentration is high than AST.
  • 16.
    • In viralhepatitis the cytoplasmic membrane sustains the more damage thus ALT greater increase than AST. • In infiltrative disorders in which there is damage to both mitochondrial and cytoplasmic membrane there is greater increase in AST than ALT. • The relative plasma activities of ALT and AST may help to indicate type of cell damage. • A plasma AST:ALT ratio of > 2 suggestive but not diagnostic of alcoholic disease • <1 ratio suggests chronic viral hepatitis.
  • 17.
    • ALT isfound mainly in liver(lesser amount in kidney,skeletal muscle) • ALT is more liver specific • AST is widely distributed in equal amounts in heart ,skeletal muscle and liver. • AST and ALT raised in acute conditions acute viral hepatitis drug and toxin induced liver necrosis and ischemia. • ALT is more elevated than AST.
  • 18.
    • Test ofobstruction • ALP (Alkaline phosphatase) • Localized in microvilli of bile canaliculi • Widely distributed in all tissues high in liver bone kidney and placenta • Marker of extra hepatic biliary obstruction • Intra hepatic cholestasis • Thus both conjugated bilirubin and ALP will be elevated in cholestasis liver disease. • Bone related disorders
  • 19.
    GGT • Gamma-glutamyl transferase •It is an enzyme derived from endoplasic reticulum of cells of hepatobiliary tract. • Also found in liver kidney pancreas intestine prostate but not in bone. • As this reticulum proliferates for example in response to prolonged alcohol intake and drugs synthesis of enzyme is induced. There fore raised plasma activity does not indicate hepatocellular damage but may reflect enzyme induction or cholestasis. • Highest level in biliary obstruction