Jaundice / Icetrus : Abnormalities, Types, Causes, Sign, Symptoms, Diagnosis and Home Remedies of Jaundice / Icterus
Although newborns are the most frequent victims, adults also get jaundice, a yellow discoloration of the skin and the whites of the eyes. Jaundice is not a disease in itself. Usually it signals some type of liver damage---such as hepatitis (an inflammation of the liver) or cirrhosis (a slow deterioration of the liver)---or an obstruction in the ducts that drain bile from the liver.
What is Jaundice/ Icterus?
Jaundice , also known as icterus. Jaundice is yellow discolouration of skin, sclera, mucous membranes, and other tissues due to excess of bilirubin in the blood. Jaundice is a medical condition that occurs when there is too much bilirubin circulating in the blood. Bilirubin is a compound produced when hemoglobin is broken down in the blood. The excess bilirubin causes the skin, eyes and mucus membranes in the mouth to appear yellowish in color. Jaundice is common in newborns and usually clears up on its own without treatment, but when an adult is diagnosed with jaundice, it usually points to liver damage. Examination in bright daylight is absolutely essential to detect mild jaundice.
Biochemical Abnormalities in Jaundice
Approximately 30 mg of bilirubin is formed in the body every day of which 80 percent is derived from senescent erythrocytes and 20 percent from other sources. Bilirubin combines with albumin and this product being insoluble in water does not appear in urine. In hemolytic jaundice in which most of the bilirubin is unconjugated, urine does not contain bilirubin.
Three main phases are recognized in the metabolism of bilirubin. These are:
Entry into the liver cell
Excretion into the bile.
After uptake, bilirubin is conjugated with glucuronic acid in the endoplasmic reticulum of hepatocytes with the help of glucuronyl transferase. Reduced levels of this enzyme are responsible for certain forms of congenital hyperbilirubinemias like Criggler-Najjar syndrome. Conjugated bilirubin is water-soluble and it freely passes into urine. Bilirubin diglucuronide in the gut is acted upon by bacteria present in the distal small intestine and the colon and is converted into urobilinogen. Urobilinogen is reabsorbed mainly from the small intestine and to a small extent from the largeintestine into the portal blood. It is subjected to enterohepatic circulation. The portion that is present in stool without being absorbed is called stercobilinogen.
Both unconjugated and conjugated bilirubin stain tissues. Collagenous and elastic tissues have the maximum affinity for bilirubin and, therefore, tissues rich in these are stained deepest.
Types of JaundicePre-hepatic / hemolyptic - This is where too many red blood cells are broken down. Gilbert's syndrome is a congenital disorder of bilirubin metabolism and may affect up to 5% of the population.
Hepatic-jaundice - This is the appearance of jaundice due to the disturbances in liver function. Drugs such as the contraceptive pill, anti-diabetic drugs and some antibiotics may also cause inflammation of the liver cells.
Obstructive jaundice - The commonest cause of obstructive jaundice is a gallstone lodged in the common bile duct. The bile duct may become blocked if there is a tumour pressing on it.
Causes of Jaundice
Jaundice is caused by too much bilirubin in the blood. Newborns frequently develop jaundice when they are unable to eliminate excess bilirubin following birth. Jaundice usually appears within 1 or 2 days after birth and lasts a week or two with no need for treatment.
Signs/Symptoms of Jaundice
Telltale signs include yellowing of the skin and the whites of the eyes, a dark, tea-colored tinge to the urine, and pale or whitish stools. Depending on the underlying cause, you may experience other symptoms. For example, if hepatitis is at fault, you may also suffer from a loss of appetite, nausea, vomiting, diarrhea, and fever.
Diagnosis of Jaundice
Majority of cases can be diagnosed by the history, physical examination. and simple biochemical tests. Preliminary tests include urinalysis, examination of feces and biochemical and immunological tests of the serum. More definitive diagnostic tests to delineate the anatomy of the biliary tree are ultrasonography, radiological studies, liver biopsy, isotopic investigations, endoscopic investigations, CT scan, and laparotomy. If the diagnosis is not clear by all these tests, laparot<?my may have to be perfonned for initiating the treatment without further delay. Moreover, even in incurable malignant obstruction, drainage of bile through a cholecystojejunostomy helps to relieve symptoms and allay misery for considerable periods.
Biochemical test of Jaundice
Preliminary investigations: Laboratory investigations are necessary to detennine the type of jaundice and its etiology.
Examination of feces: The stools are dark colored in hemolytic jaundice que to excessive bile pigment, whereas it is pale and chalky white (clay coloured) in obstructive jaundice due to absence of bile. Ulcerating malignant lesions give rise to occult blood in stools. Silvery color of feces occurring in obstructive jaundice indicates the presen~e of altered blood.
Serum bilirubin: The total, conjugated and unconjugated fractions can be estimated. This helps in assessing the severity of jaundice and also in identifying the type. Vandenberg reaction is a qualitative test used in detecting the type of bile pigment in the serum. Direct positive test is given by conjugated bilirubin, unconjugated bilirubin gives rise to the indirect reaction. When both pigments are present the reaction is biphasic.
Complication due to Jaundice
Jaundice may give rise to further complications, apart from those caused by the primary disease.
(a) Obstructive Jaundice
Skin: Skin changes include melanotic pigment~tion, chronic pruritus, thickening, and excoriation. Xanthomas develop due to hypercholesterolemia. Bleeding tendency manifests as purpura and bruises.
Malabsorption: Since bile does not reach the intestine, absorption of fat and fat soluble vitamins is defective. This leads to steatorrhea and deficiencies of vitamins A, D and K and calcium.
Accumulation of copper: Copper is nonnally excretedin bile. In chronic obstructive jaundice copper accumulates in the liver and may reach high values. Unlike as in Wilson's disease in which copper is deposited in the lysosomes, in biliary cirrhosis the copper is present in the cytosol.
Hepatocellular failure: Back pressure of bile and prolonged obstruction. leads to hepatocellular necrosis, secondary biliary cirrhosis, and hepatic failure. Elderly subjects are more prone to develop these complications.
Renal failure: This may develop during the icteric stage or after surgical relief of the obstruction..
(b) Hemolytic Jaundice
Damage to nervous system: In the newborn the blood brain barrier for unconjugated bile pigment is not developed. The bilirubin is bound to albumin, but when the level exceeds 20 mg/dl, it passes into nervous tissue and causes extensive damage to the basal ganglia. This used to be a complication of severe Rh hemolytic disease.
Pigment gall stones: Presence of excess of bilirubin in bile results in its precipitation and formation of pigment gall stones. Though asymptomatic in many cases, rarely they may become symptomatic and lead to obstructive jaundice.
Home Remedies Of Jaundice
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