Jaundice (Icterus

Jaundice ( icterus )

Most of liver diseases are characterized by icterus , which is the apparent symptom . Icterus occurs due to an excessive amount of bilirubin in the plasma over normal range which is 0.2 - 0.8 mg/dl .When the level reaches about 3 mg/dl , jaundice become clinically obvious especially noticeable in the sclera of the eyes , skin and palatal mucosa .

Types of jaundice

Jaundice can be classified into 3 types according to the course or its relation to the liver as follow :
1- Hemolytic or prehepatic jaundice .
2 - Toxic or hepatic jaundice
3 - Obstructive or post hepatic jaundice

1 - Hemolytic jaundice

It occurs due to excessive breakdown of the erythrocytes causing an increase in the level oftotal bilirubin and jaundice occurred .
This condition is usually associated with hemolytic anemia .

Causes 

- Erythroblastosis  fetalis
- The post- blood transfusion period
- Hematoma
- Hemolytic anemia
- Pernicious anemia
- Physiologic jaundice of the newborn
- Red blood cell enzyme abnormalities (i.e G-6-PD, Pyruvate kinase, spherocytosis) .

Biochemical features

1 - Increased level of total bilirubin ( moderat).
2 - Increased amount of indirect bilirubin .
3 - Normal level of direct reacting bilirubin
4 - Icterus index is high
5 - Marked increase of urobilinogen in the urine .
6 - Increase stercobilinogen  in the stool giving dark orange color .

2 - Toxic or hepatic jaundice

This type of jaundice occures due to destruction of hepatocytes by inflammation due to virus or some chemicals or toxic substances as follow:

- Bilirubin conjugation failure
- Disturbance in bilirubin transport
- Liver damage or necrosis
- Alcoholism
- Cholangitis
- Cholestatic drug reactions
- Cholecystitis
- Cirrhosis
- Hepatitis
- Hepatocellular damage
- Infectious mononucleosis

. Jaundice occurs either due to the failure in the conjugation mechanism witin the hepatocytes or to an obstruction the escape of the conjugated bilirubin ( either from cells to the canaliculi or from the canaliculi itself, which constitute the intra-hepatic cholestasis) .
Obstruction occurs due to presure  from the swollen degenerating hepatocytes . So that direct bilirubin may be escaped to the blood raising its level

Biochemical Features

1 - Marked increase in the total bilirubin
2 - Increase in conjugated bilirubin about 50%
3 -Increase in the unconjugated bilirubin about 50% due to inability of hepatocytes to take up unconjugated bilirubin perfectly .

4 -Variable increase in the ictrus index
5 - Slightly increase in urine urobilinogen
6 -Urine bilirubin is positive
7 - Fecal strecobilinogen is normal
8-Increased activity of GPT and alkaline phospatase due to destruction of hepatocytes with cholestasis .

3 - Post Hepatic Jaundice

- This type of jaundice occurs due to hindrance of normal out flow of the bile .This may be due to obstruction in the liver( intrahepatic cholestasis ) or in the bile duct outside the liver .

- Intrahepatic cholestasis occurs due to closure of the bile caniculi or collecting ducts inside the liver either due to pressure from outside the canaliculi as by tumor , cirrhosis or due to inflammation . Also may occurs due to some drugs which are called cholestatic druge jaundice such as chloropromazine or steroids .

- Extrahepatic  cholestasis occurs due to obstruction in the bile duct by pancreatic neoplasia or cholelithiasis

Biochemical Manifestation

1- Marked increase of total protein
2 - High increased direct bilirubin
3- Normal level of unconjugated bilirubine
4- Increase icterus index
5- Absence of urine urobilinogen
6- Presence of bilirubin and bile salts
7- Decrease amount of stercobilongen in the stool so that appeared pale in color  (bulky and frothy)
8- Increased level of serum alkaline phosphatase
9- Increased level of gamma glutamyle transferase
10- Hyper cholesterolemia due to the increased production by the liver .