Types of Jaundice and their causes

1 Like 1 Comment
Types of jaundice

Jaundice is an unnatural yellow coloration of the skin or sclera which is due to the presence of bilirubin in plasma in concentrations greater than 40 mmol / L. The normal concentration of bilirubin in the plasma is under 22 mmol / L.

There are three main causes of elevated bilirubin content in the blood which are

  • Increase rate of  bilirubin synthesis; it exceeds the excretory capacity of the liver (syt hemolytic jaundice).
  • Inhibition of conjugation and / or excretory mechanisms in the liver: the liver’s ability to metabolize bilirubin synthesized in normal amounts is reduced (hepatic, or hepatocellular jaundice).
  • Obstruction of the biliary system, this  prevents the outflow of bile (cholestatic, obstructive, mechanical, obstructive jaundice).

Types of jaundice

Hemolytic jaundice

This is most often caused by an increased destruction of red blood cells that is both mature cells and their precursors. Destruction of mature red  cells may be the result of hemolysis or an effect of blood utilization after internal bleeding, like in soft tissue injuries.

Ineffective hematopoiesis occurs in pernicious anemia  that is disturbed maturation of red blood cells or thalassemia (anomalous structures of hemoglobin).

In hemolytic jaundice,Hyperbilirubinemia is caused by accumulation of unconjugated bilirubin that is not excreted by the kidneys. This increases the flow of bilirubin from the liver to the intestine. Urobilinogen is produced in large amounts, and its urine content is elevated.

Hepatocellular jaundice

The congenital disturbances of bilirubin transport lead to jaundice due to imperfect absorption, decreased conjugation or impaired excretion of bilirubin. Generalized hepatocellular dysfunction may occur in hepatitis and decompensated liver cirrhosis.

Pathogenesis of jaundice in these cases is complicated; the contributing factors are disturbance of the uptake, intracellular transport, and reduced conjugation of bilirubin.

Drugs can cause hepatocellular lesion in connection with its dose-related hepatotoxicity (e.g., acetaminophen) or idiosyncratic sensitivity (e.g., isoniazid).

If hyperbilirubinemia is caused by disturbance of conjugation, bilirubin is not conjugated, and the flow of bilirubin in the liver is not increased. As a consequence, bilirubinuria is absent, and urobilinogen content in the urine is not elevated. If there is generalized dysfunction of the liver, the uptake of bilirubin is reduced, and, therefore, the kidneys excrete it in greater quantities. Serum bilirubin can be both conjugated and unconjugated, due to defective UDP-glucuronyl transferase and intracellular transport of bilirubin.

If the rate of conjugation exceeds the excretory capacity, blood levels of conjugated bilirubin go up, and it can be excreted in the urine. This sometimes happens during convalescence after viral hepatitis.  

Also read  WBC Count : Principle, Procedure and Calculation

Cholestatic jaundice

Cholestatic jaundice

Cholestatic jaundice

Cholestatic jaundice may be the effect of obstruction of an outflow of bile from the hepatocytes in the duodenum. It can be caused by lesions in the liver (intrahepatic cholestasis) or in the bile ducts and pancreas head (extrahepatic cholestasis).

Intra- and extrahepatic cholestasis can be differentiated by ultrasound or biopsy of the liver; evaluative tests of liver function do not help.

Intrahepatic cholestasis is often the result of generalized hepatocellular dysfunction developing, for instance, in hepatitis or decompensated cirrhosis. This condition is also a sign of primary biliary cirrhosis. The branches of biliary tree can be blocked by malignancies. Some medications such as anabolic steroids, phenothiazines, and sulfonylurea may lead to intrahepatic cholestasis.  

Extrahepatic obstruction is often the result of large biliary tract tumors, tumors of the head of the pancreas and lymph nodes at the porta hepatis. Obstruction of bile ducts can be also caused by gallstones or sclerosing cholangitis.

Jaundice is caused by a disturbance of excretion of conjugated bilirubin and its accumulation, which is filtered by the glomerulus and appears in the urine. However, bilirubin may not be detected in the urine, possibly because changes in the processes of conjugation lead to formation of less soluble bilirubin bound to albumin. In complete obstruction, bilirubin cannot reach the intestine, urobilinogen is not formed or detected in the urine, and feces may have whitish coloration.

Hyperbilirubinemia and bilirubinuria. Bilirubin and its fractions in the blood, liver, intestines and kidneys. Free (indirect) and conjugated (direct) bilirubin, urobilinogen and stercobilinogen, bile pigments. Bilirubin toxicity.

Bilirubin is formed from the breakdown of hemoglobin in the cells of the reticuloendothelial system (RES), it is particularly active in the spleen and hepatic Kupffer cells. In an adult, 250-350 mg of bilirubin is formed daily. Bilirubin is poorly soluble in water; in the plasma bilirubin appears primarily in the unconjugated form bound to albumin (indirect, unconjugated bilirubin). Unconjugated bilirubin cannot pass through the kidney barrier.

In the liver bilirubin is transferred from albumin to the sinusoidal surface of hepatocytes. In liver cells, indirect bilirubin undergoes enzymatic conjugation with glucuronic acid and is converted to bilirubin mono- and bilirubin diglucuronide (conjugated, or direct bilirubin). Conjugated bilirubin is water soluble; it comes from the bile in the gallbladder, or directly into the intestine. It loses bilirubin glucuronic acid and is reduced to urobilinogen.

A part of urobilinogen absorbed in the small intestine and the portal vein enters the liver again, where it is oxidized to bipyrrole. In the colon, bile bilirubin becomes stercobilinogen under the impact of normal intestinal flora. In the lower portion of the major part of the colon, colorless stercobilinogen is oxidized into brown stercobilin, and is excreted in the feces. A small part of stercobilinogen absorbed into the blood and through the hemorrhoidal veins and inferior vena cava enters the kidneys and then into the urine. Normal urine contains a minimal amount of conjugated bilirubin (7 – 20 mg /L) that are not detectable by qualitative methods.  

Also read  ABO and Rhesus Blood Grouping principles and Result interpretation

Bile pigments are breakdown products of hemoglobin and other derivatives of porphyrin excreted in the bile, urine and feces.

Their greater portion is formed during the catabolism of hemoglobin in red blood cells in the cells of mononuclear phagocytes system. Bile pigments are compounds containing four pyrrole groups linked by one-carbon bridges in the open, non-closed circuit (in contrast to the closed structure of the heme). As a result of a-methine bridge of heme breakdown in hemoglobin, verdoglobin (holeglobin) is formed, which is an iron-porphyrin pyrrole compound with an open structure, of green color. After release of globin protein and iron by the molecule of verdoglobin, green bile pigment biliverdin is produced.

An alternative way of biliverdin formation is cleavage of the protein part of hemoglobin, formation of iron porphyrin hematin pigment and oxidation of hematin with a breakdown of methine bridge and loss of iron. In the cells of the mononuclear phagocyte system, biliverdin is reduced to bilirubin, which is delivered into the liver with the blood. A small amount of bilirubin is formed in the cells of the mononuclear phagocyte system of the heme that was not used for the synthesis of hemoglobin; as well as from the heme formed in the liver for catabolism of other heme-containing proteins (myoglobin, cytochromes, etc.), or from hemoglobin renovated in the process of maturation of erythrocytes.

Bilirubin is the main and most diagnostically valuable bile pigment that occurs in human bile. Biliverdin is present in the bile in trace amounts (15-20% of its dry weight). In the liver, bilirubin forms pairs of compounds, or conjugates, mainly with glucuronic acid, and to a lesser extent – with sulfuric acid. About 300 mg of bilirubin is produced in the body daily. About 75% of bilirubin is formed from bilirubin glucuronide, and 15% – from bilirubin sulfate.

Neonatal jaundice

Hemolytic disease of newborn


Incompatibility of the mother’s and fetal blood in the group or Rh factor. Accumulation of hydrophobic forms of bilirubin in the subcutaneous fat causes yellowness of the skin. However, the real danger is posed by accumulation of bilirubin in the gray matter of nervous tissue and stem nuclei with development of “kernicterus” (bilirubin encephalopathy).

Also read  Hemolytic Disease of the Newborn (Causes and investigation)

Clinical diagnosis.

Its manifestations are drowsiness, poor sucking, mental retardation, stiff neck, tonic convulsions, tremor of limbs, changed reflexes; development of deafness and paralysis is possible.

Laboratory diagnosis.

Severe anemia, reticulocytosis, erythropoietin and normoblastosis are detected in the blood. Hyperbilirubinemia due to indirect fraction from 100 to 342 mmol / L, in the future, and direct attached fraction. Bilirubin content in the blood increases rapidly reaching its peak by the 3-5 day of life.

Physiological (transient) neonatal jaundice


  • relative reduction of UDP-glucuronyl transferase activity in the first days of life associated with intensified degradation of fetal hemoglobin,  
  • an absolute decrease in the activity of UDP-glucuronyl in the first days of life,
  • ligandin deficit,
  • poor activity of the biliary tract.

Clinical diagnosis

  • skin coloration for 3-4 days after birth,  
  • no hemolysis or anemia can be detected.

Symptoms resolve within 1-2 weeks after birth.

Laboratory diagnosis.

Increased concentrations of free serum bilirubin to 140-240 mmol/L.  

Jaundice of prematurity


  • relative reduction of UDP-glucuronyl transferase activity in the first days of life associated with increased degradation of fetal hemoglobin,  
  • an absolute decrease in the activity of UDP-glucuronyl in the first days of life, – ligandin deficit,
  • poor activity of the biliary tract.

Clinical diagnosis

  • skin coloration for 3-4 days after birth,  
  • no hemolysis or anemia can be detected.
  • Symptoms resolve within 3-4 weeks after birth

Laboratory diagnosis.

Increased concentrations of free serum bilirubin reaching the peak on day 5-6 after birth, more pronounced in comparison with physiological jaundice. .  

Nonhemolytic neonatal hyperbilirubinemia caused by breast milk.

This condition develops in 1% of breast-fed infants.  


Inhibition of UDP-glucuronyl presumably by milk estrogen.

Clinical diagnosis.

Manifested as jaundice, sometimes with CNS symptoms.

Laboratory diagnosis.

Increased concentrations of free bilirubin in the serum.

How useful was this post?

Click on a star to rate it!

Average rating / 5. Vote count:

No votes so far! Be the first to rate this post.

As you found this post useful...

Follow us on social media!

We are sorry that this post was not useful for you!

Let us improve this post!

Tell us how we can improve this post?

You might like

About the Author: Arthur Westmann

DEFFE ARTHUR (AMOEBAMANN) is the founder and author of MLTGEEKS and MLTEXPO.He’s from Cameroon and is currently a Final year State Medical Laboratory Technician (MLT MA). Beyond lab works, he’s a passionate internet user with a keen interest in web design and blogging. Furthermore He likes traveling, hanging around with friends and social networking to do in his spare time.

1 Comment

Leave a Reply

Your email address will not be published. Required fields are marked *