❖ The liver is the largest organ in the body.
❖ It is located below the diaphragm in the right upper quadrant of the abdominal
cavity and extended approximately from the right 5 th rib to the lower border of
the rib cage.
❖ The liver's highly specialized tissue, consisting of mostly hepatocytes, regulates
a wide variety of vital biochemical reactions, including the synthesis and
breakdown of small and complex molecules, many of which are necessary for
normal vital functions.
1. Synthetic Function:
a. Synthesis of plasma proteins (albumin, coagulation factors, some globulins)
b. Synthesis of cholesterol.
d. Lipoprotein synthesis
E. Ketogenesis (synthesis of ketone body).
2.Metabolic Function:
a. Carbohydrates: Glycolysis; glycogen synthesis; glycogen breakdown;
gluconeogenesis
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b. Fatty acid synthesis and breakdown.
c. Protein catabolism.
d. Citric acid cycle, production of ATP.
3. Detoxification and Excretion:
a. Ammonia to urea.
b. Bilirubin (bile pigment).
c. Cholesterol.
d. Drug metabolites.
4. Homeostasis:
Blood glucose regulation.
5. Hormone metabolism.
Metabolism, conjugation &excretion of steroidal &poly peptide hormones.
6. Storage Function:
Vitamin A, D, K, B12, glycogen, iron.
7. Production of Bile Salts: help in digestion
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1- Serum Albumin
2- Blood Bilirubin
(Total, Direct & Indirect)
3- Blood Liver Enzymes:
• Alanine Amino Transferase (ALT)
• Aspartate Amino Transferase (AST)
• Gamma Glutamyl Transferase (GGT)
• Alkaline Phosphatase (ALP)
4- Blood Coagulation Factors
Prothrombin Time (PT)
1. Classification based on laboratory findings:
A- Tests of hepatic excretory function: Serum bilirubin and Urine bile pigments
(bile salts and urobilinogen).
B- Liver enzyme panel which are markers of liver injury and/or cholestasis:
Alanine amino transferase (ALT), Aspartate amino transferase (AST), Alkaline
phosphatase (ALP) and Gamma glutamyl transferase (GGT).
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C- Plasma proteins (Tests for synthetic function of liver): Total proteins, Serum
albumin, globulins, A/G ratio and Prothrombin time (PT).
D- Special tests: Ceruloplasmin, Ferritin, Alpha-1-antitrypsin (AAT), and Alpha
fetoprotein (AFP).
2. Classification based on clinical aspects:
A- Markers of Liver Dysfunction: Serum bilirubin, Urine Bile pigments (bile salts
and UBG), Total protein, serum albumin and A/G ratio, Prothrombin time and
Blood ammonia (when indicated).
B- Markers of hepatocellular injury: Alanine amino transferase (ALT) and
Aspartate amino transferase (AST).
C- Markers of cholestasis: Alkaline phosphatase and Gamma glutamyl transferase.
Bilirubin
RBC live approximately 120 days and are then destroyed by the mononuclear
phagocyte system (MPS), particularly in the liver and spleen.
Bilirubin is a waste product derived from hemoglobin destruction (from
porphyrin rings).
The route of excretion is through the biliary tract.
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Figure :The formation and metabolism of bilirubin and its excretion into the
intestine.
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Jaundice
Jaundice (or, icterus) refers to the yellow color of skin, nail beds, and sclerae
(whites of the eyes) caused by bilirubin deposition, secondary to increased
bilirubin levels in the blood (hyperbilirubinemia) as shown below
Jaundiced patient with the sclerae
of his eyes appearing yellow.
A. Hemolytic (prehepatic): The liver has the capacity to conjugate and excrete
>3,000 mg of bilirubin/day, whereas the normal production of bilirubin is only 300
mg/day. However, extensive hemolysis (e.g., in patients with sickle cell anemia or
deficiency of pyruvate kinase or glucose 6-phosphate dehydrogenase) may produce
bilirubin faster than it can be conjugated.
B. Hepatocellular (hepatic): Damage to liver cells (e.g., in patients with cirrhosis or
hepatitis) can cause unconjugated hyperbilirubinemia as a result of decreased
conjugation. The urine consequently darkens, whereas stools may be a pale, clay
color. Plasma levels of ALT and AST are elevated. If CB is made but is not
efficiently secreted from the liver into bile (intrahepatic cholestasis), it can leak
into the blood, causing a conjugated hyperbilirubinemia. In hepatic jaundice, both
UCB and CB levels are abnormally elevated in the blood.
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C. Obstructive (posthepatic): jaundice is not caused by overproduction of bilirubin
or decreased conjugation but, instead, results from obstruction of the common bile
duct (extrahepatic cholestasis). For example, the presence of a tumor or bile stones
may block the duct, preventing passage of CB into the intestine.
Patients with stools that are a pale, clay color. The CB regurgitates into the blood
(conjugated hyperbilirubinemia).
