Definitions

jaundice

jaundice

[jawn-dis, jahn-]
jaundice, abnormal condition in which the body fluids and tissues, particularly the skin and eyes, take on a yellowish color as a result of an excess of bilirubin. During the normal breakdown of old erythrocytes (red blood cells), their hemoglobin is converted into bilirubin. Normally the bilirubin is removed from the bloodstream by the liver and eliminated from the body in the bile, which passes from the liver into the intestines. There are several conditions that may interrupt the elimination of bilirubin from the blood and cause jaundice. Hemolytic jaundice is caused by excessive disintegration of erythrocytes; it occurs in hemolytic and other types of anemia and in some infectious diseases like malaria. Another type of jaundice results from obstruction in or about the liver; usually a stone or stricture of the bile duct blocks the passage of bile from the liver into the intestines. A third type of jaundice occurs when the liver cells are damaged by diseases such as hepatitis or cirrhosis of the liver; the damaged liver is unable to remove bilirubin from the blood. Treatment of jaundice is directed to the underlying cause. Many instances of obstructive jaundice may require surgery.

Excess bile pigments (bilirubin) in the bloodstream and tissues, causing a yellow to orange—even greenish—colour in the skin, the whites of the eyes, and the mucous membranes. Bilirubin may be overproduced or inadequately removed by the liver or leak into the bloodstream after removal; jaundice may also be due to impaired bile flow. Causes include anemia, pneumonia, and liver disorders (e.g., infection or cirrhosis). While bilirubin excess usually does no harm, retention jaundice signals severe liver malfunction.

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Jaundice, also known as icterus (attributive adjective: "icteric"), is yellowish discoloration of the skin, sclerae (whites of the eyes) and mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL, three times the usual value of approximately 0.5mg/dL, for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow.

Normal Physiology

In order to understand how jaundice results, it is important to understand where the pathological processes that cause jaundice take their effect. It is also important to further recognize that jaundice itself is not a disease, but rather a symptom of an underlying pathological process that occurs at some point along the normal physiological pathway of the metabolism of bilirubin.

Pre-hepatic events

When red blood cells have completed their life span of approximately 120 days, their membranes become fragile and prone to rupture. As the cell traverses through the reticuloendothelial system, their cell membranes rupture and the contents of the red blood cell is released into the blood. The component of the red blood cell that is involved in jaundice is hemoglobin. The hemoglobin released into the blood is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, being protein, is degraded into amino acids and plays no further role in jaundice. Two reactions then take place to the heme molecule. The first reaction is the oxidation of heme to form biliverdin.This reaction is catalyzed by microsomal enzyme heme oxygenase and it results in biliverdin (green color pigment), iron and carbon monoxide. Next step is reduction of biliverdin to yellow color tetrapyrol pigment bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is known as "unconjugated", "free" or "indirect" bilirubin. Approximately 4 mg per kg of bilirubin is produced each day. The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 per cent comes from other heme sources, including ineffective erythropoiesis, breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.

Hepatic events

The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.

Post-hepatic events

This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here the urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the faeces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.

Causes

When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

  • Pre-hepatic: The pathology is occurring prior the liver
  • Hepatic: The pathology is located within the liver
  • Post-Hepatic: The pathology is located after the conjugation of bilirubin in the liver

Pre-hepatic

Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers.

Laboratory findings include:

  • Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).
  • Serum: increased unconjugated bilirubin.

Hepatic

Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver's ability to metabolise and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome, metastatic carcinoma and Niemann Pick Type C disease. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.

Laboratory Findings include:

  • Urine: Conjugated bilirubin present, Urobilirubin > 2 units but variable (Except in children)

Post-hepatic

Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".

Laboratory Tests

No one test can differentiate between various classifications of jaundice. A combinations of liver function tests is essential to arrive at a diagnosis.

Pre-hepatic Jaundice Hepatic Jaundice Post-hepatic Jaundice
Total bilirubin Normal / Increased Increased Increased
Conjugated bilirubin Normal Normal / Decreased Increased
Unconjugated bilirubin Increased Normal / Increased Normal
Urobilinogen Increased Normal / Increased Decreased / Negative
Urine Colour Normal Dark Dark
Stool colour Normal Normal Pale
Alkaline phosphate levels normal normal increased
Alanine transferase n Aspartate transferase levels normal increased normal

Neonatal jaundice

Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. Neonatal jaundice is a risk factor for hearing loss.

Jaundiced eye

It was once believed persons suffering from the medical condition jaundice saw everything as yellow. By extension, the jaundiced eye came to mean a prejudiced view, usually rather negative or critical. Alexander Pope, in 'An Essay on Criticism' (1711), wrote: "All seems infected that the infected spy, As all looks yellow to the jaundiced eye." Similarly in the mid 19th century the English poet Lord Alfred Tennyson wrote in the poem 'Locksley Hall': "So I triumphe'd ere my passion sweeping thro' me left me dry, left me with the palsied heart, and left me with a jaundiced eye."

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