Jaundice  - labsstudies

Jaundice 

Jaundice 

Jaundice 

  • Jaundice is defined as a yellowish discoloration of body tissues and fluids visible in the sclera and mucous membrane caused by an excess of bilirubin in the serum (hyperbilirubinaemia).
  • It is also a disease condition in which a person turns yellow.
  • It is a disease condition whereby a person becomes yellow in color.
  • Skin pigmentation can be seen in light-colored people and neonates.
  • This pigment stains almost all of the body’s tissues and secretions.
  • Bilirubin is a byproduct of the metabolism of red blood cells.
  • Jaundice develops when serum bilirubin levels range between 17 and 34 umol/L (2 and 3 mg/dl).
  • A normal level is usually less than 10 umol/L.

Pathology of Jaundice

  • In order to understand how jaundice occurs, the pathological processes that cause jaundice must be understood.
  • Jaundice is not a disease in and of itself, but rather a symptom of one of many possible underlying pathological processes that occur at some point along the normal physiological pathway of bilirubin metabolism.
  • The majority of the bilirubin in the body is produced by the breakdown of old and abnormal red blood cells.
  • Other sources of bilirubin exist, such as myoglobin (from muscle cells), but this source is insignificant.
  • Red blood cells (RBCs) have an average lifespan of about 120 days. After this period, their efficiency is greatly reduced, and they are catabolized by the reticuloendothelial system (RES).
  • The breakdown of red blood cells (RBCs) begins with the removal of the globin component, which then enters the amino acids.
  • A number of enzymes work on the remaining heme, and iron (Fe 3+) contained in the four (4) pyrole rings is removed and taken by the liver for future use.  The remaining component is converted into biliverdin and then bilirubin.
  • Biliverdin is the end product of  haemoglobin catabolism.
  • Bilirubin is a yellowish pigment that exits the RES and enters the bloodstream, where it is strongly bound to plasma albumin.
  • This type of bilirubin is unconjugated because it is not soluble in water.
  • It (unconjugated bilirubin) must be eliminated via a process that increases its solubility in water.
  • Conjugation is a process that occurs in the liver.
  • Conjugation occurs in the liver using glucuronic acid and bilirubin diglucuronide to produce a highly water-soluble molecule.
  • Conjugated bilirubin is secreted from liver cells (hepatocytes) into the intrahepatic ducts and then transported to the gall bladder via the hepatic duct. It is then ejected into the gut along with bile.
  • Bilirubin is converted into urobilinogen by intestinal bacteria. The urobilinogen can proceed in one of two ways from here.
  • Bilirubin is hydrolyzed by the gut flora and converted into stercobilinogen, which is what colors our stool and has deodorant properties (reduces bad smell from the feaces).
  • However, stercobilinogen serves no important function in the stool or body; it is simply a means of elimination.
  • Alternatively, it can be reabsorbed by intestinal cells, transported by blood to the kidneys, and excreted in the urine as the oxidized product urobilin. The products responsible for the coloration of feces and urine, respectively, are stercobilin and urobilin.

 

Bilirubin in the Entero-Hepatic Circulation

  • Entero hepatic circulation refers to the continuous recycling of bilirubin between the gut and the liver.
  • The primary bile acids, cholic acid and chenodeoxycholic acid, are first deconjugated and then further metabolized by intestinal bacteria, which remove a hydroxyl group from the 7-position of the steroid molecule, forming deoxycholic acid from cholic acid and lithocholic acid from chenodeoxycholic acid.
  • The primary bile acids, cholic acid and chenodeoxycholic acid, are synthesized in the liver from cholesterol and are temporarily stored and concentrated in the gallbladder after conjugation with the amino acids glycine and taurine.
  • The bile acids then pass into the upper intestine in response to a fatty meal, where they play an important role in promoting fat digestion and absorption.
  • Bile acid reabsorption occurs primarily in the ileum via an active transport mechanism, and they return to the liver via the portal vein, completing the enterohepatic circulation.
  • Bile acid absorption in the intestine is extremely efficient, with approximately 95 to 98 percent of total circulating bile acids absorbed each day.
  • Only a small amount escapes reabsorption and is excreted in the feces, so the liver only needs to synthesize enough bile acids to match the fecal loss to maintain the status quo.

Also read: Body fluids, Electrolytes and Balance of Acid and Base

Types of Jaundice

The following are types of jaundice:

1. Obstructive Jaundice (Post-Hepatic Jaundice)

  • This occurs as a result of a blockage in the flow of already conjugated bilirubin from the hepatocytes to the intestines.
  • Occurs when the common bile duct is obstructed.
  • Also known as Post-hepatic Jaundice.
  • This can be extrahepatic or intrahepatic.

Extrahepatic jaundice

  • Extrahepatic jaundice is well-known because it includes surgical jaundice. The type of jaundice that can be surgically corrected.

Causes of Extrahepatic jaundice are:

  • Gall stone in the large bile duct
  • Tumour compressing the billiary flow
  • Pancreatic cancer in the head of pancreas
  • Cancer of the bile duct
  • Cancer gut near the bile duct opening
  • Wandering worm – Ascaris lumbricoides (rare cause)

Intrahepatic jaundice

  •  Intrahepatic jaundice is not caused by a direct mechanical bile duct obstruction, but it may be linked to billiary tree diseases and other conditions.

Causes of Intrahepatic jaundice are:

  • Steroids, chlorpromazine, halothane, para-amino-salicylic acids, and Thiouracil are some of the drugs that can cause intrahepatic obstructive jaundice.
  • Cholangitis sclerosing (secondary form can be seen in AIDS).
  • Complications of pregnancy (mainly as a result of oestrogen effect).

Biochemical manifestations of Obstructive jaundice include:

  •  The presence of bilirubin in the urine.
  • Urobilinogen in urine is reduced or absent.
  •  Low/no stercobilinogen levels in the stool.
  •  Serum direct reacting bilirubin elevation.
  •  Increased serum alkaline phosphotase levels.
  •  Bile salt deposition in the skin can cause severe itching (pruritis) in patients with obstructive jaundice.

 

2. Haemolytic Jaundice (Pre-hepatic Jaundice)

  • This is due to an increased rate of RBC destruction.
  • Also known as Pre-hepatic Jaundice.

The following are some of the causes of haemolytic jaundice:

Infections

  • Infections with some microorganisms do cause haemolysis because they directly affect the RBCs.
  • Infection with protozoa Plasmodium malariae is the most common parasite in the Tropics, causing haemolytic anaemia and jaundice.
  • Jaundice can also be caused by bacteremia or septicaemia.

Haemoglobinopathies

  • Haemoglobinopathies are genetically inherited haemoglobin abnormalities in which the shape of red cells becomes abnormal under certain conditions and their lifespan is greatly reduced, resulting in jaundice.
  • Sickle cell anaemia is one such condition common in the Tropics.
  • Thalassaemia is another haemoglobinopathy that is common in Mediterranean countries.

Incompatibility of blood or rhesus factor

  • Transfusion of mismatched blood can result in adverse reactions, one of which is increased hemolysis.
  • Neonatal hemolytic disease (HDN).

G-6-PD (glucose 6-phosphate dehydrogenase) deficiency.

  • G-6-PD is an X-linked condition in which haemolytic crisis is precipitated by infection, administration of some drugs such as quinine, phenacetin, and aspirin, and ingestion of some legumes.

Drugs

  • Some chemicals, including methyl chloride, arsine, lead, and nitrobenzene, can cause haemolysis and, in severe cases, jaundice.

Biochemical manifestations of haemolytic jaundice include:

  •  an increase in unconjugated bilirubin in the serum
  • an increase in stercobilinogen in the stool, and an increase in urine urobilinogen.
  •  The absence of bilirubin in the urine (acholuric). Unlike in obstruction, because all conjugated bilirubin from the liver reaches the intestines, none refluxes back into the plasma to be excreted by the kidneys.
  • Although unconjugated bilirubin is almost insoluble in water, it has a high affinity for fat.
  •  In young infants (with a poorly developed blood brain barrier), toxins can be deposited in fat-rich areas of the brain, causing irreversible damage, a condition known as kernicterus.

3. Hepatocellular Jaundice

  • This occurs as a result of liver cell damage, a lack of enzymes required for conjugation, or a failure to secrete already conjugated bilirubin-from the hepatocytes.
  • Also known as Hepatic Jaundice.

Causes include:

  •  Viral hepatitis (most common)
  •  Drugs- halothane
  • Cirrhosis
  •  Crigler-Najar syndrome-congenital disorder characterized by a lack of conjugating enzymes

Biochemical manifestations of hepatocellular jaundice include:

  •  Serum analysis reveals both haemolytic and obstructive features.
  •  This indicates that there are elements of conjugation failure, secretion (of conjugated bilirubin) failure, and possibly increased haemolysis.
  •  The characteristics of cholestasis and haemolysis are mixed in many cases of hepatocellular jaundice.

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