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JAUNDICE
JAUNDICE
TOPIC : JAUNDICE
JAUNDICE
INTRODUCTION
BILURUBIN
Bilirubin (formerly referred to as haematoidin) is the yellow breakdown product of normal heme
catabolism, caused by the body's clearance of aged red blood cells which contain hemoglobin.[1]
Bilirubin is excreted in bile and urine, and elevated levels may indicate certain diseases. It is
responsible for the yellow color of bruises and the yellow discoloration in jaundice. It is also
responsible for the brown color of feces, via its conversion to stercobilin, and the background straw-
yellow color of urine via its breakdown product, urobilin.
JAUNDICE :
When the bilirubin concentration in the blood is abnormally elevated, all the body tissues, including
the sclerae
condition called jaundice. Jaundice becomes clinically evident when the serum bilirubin level exceeds
2.5 mg/dL (43
There are several types of jaundice: hemolytic, hepatocellular, and obstructive jaundice, and jaundice
due to hereditary
hyperbilirubinemia. Hepatocellular and obstructive jaundice are the two types commonly associated
with liver disease
DEFINITION
This is the yellowish discoloration of the skin of sclerae and other mucus membrane as a result of
increase core of bilirubin bilurubin concentration in the blood greater than 1.5g /dl
CLASSIFICATION
DEF: is a the type of jaundice occur due to increase hemolysis of the red blood cell, which result in
production of excess bilurubin.
It occur outside of the liver i.e before the bilurubin concentration reaching the liver
S/S
Spleenomegaly
Hepatomegaly
2. HEPATIC JAUNDICE
It's a type of jaundice in which the liver fail to clear the amount of bilirubin from the blood
It is cause by :
Hepatitis virus
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of
bile containing conjugated bilirubin 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" can live in the common bile duct, causing obstructive
jaundice.
S/S
- pruritis
PATHOPHYSIOLOGY
Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological
processes that occur at some point along the normal physiological pathway of the metabolism of
bilirubin in blood.
When red blood cells have completed their life span of approximately 120 days, or when they are
damaged, their membranes become fragile and prone to rupture.
Cellular contents, including hemoglobin, are subsequently released into the blood.
The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The
globin portion, a protein, is degraded into amino acids and plays no role in jaundice.
Two reactions then take place with the heme molecule. The first oxidation reaction is catalyzed by the
microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron and carbon
monoxide.
The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by
cytosolic enzyme biliverdin reductase.
The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the
process just described
However approximately 20 percent comes from other heme sources, including ineffective
erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and
cytochromes