Jaundice is a symptom complex which is characterized by yellow coloration of tissues and body fluids due to an increase in bile pigments i.e. Bilrubin and related products
It may arise due to:
- Increased bile pigment load to the liver.
- Affection of bilirubin diffusion into the liver cells.
- Defective conjugation.
- Defective excretion.
Other causes of yellow coloration of tissues
Yellow coloration of tissues can occur due to carotenemia and mepacrine therapy.
Bilirubin Metabolism
- Breakdown phase: Hemoglobin released by breakdown of aged cells is broken down into globin and heme. The heme is further broken into iron and bilirubin. Bilirubin attaches to serum albumin and is transported to the liver where it is taken up.
- Conjugation phase: In the liver, bilirubin is separated from albumin and conjugated to glucuronide by glucuronyl transferase. The conjugated bilirubin is water soluble and can be excreted by kidneys.
- Alimentary phase: The conjugated bilirubin is excreted through the bile canaliculi and reaches the intestines where it is converted to stercobilinogen and urobilinogen by the intestinal bacteria. About 70% of this is absorbed in the colon and brought back to the liver and re-excreted (enterohepatic circulation). Unabsorbed stercobilinogen gives brown color to the faces.
- Excretion phase: Circulating urobilinogen is carried to the kidneys for excretion in the urine as urobilinogen.
Normal values
Serum bilirubin: Total: 1 mg%; Direct: 0.25 mg%. Urinary bilirubin is present if direct bilirubin is greater than 0.4 mg% in serum.
Urine Urobilinogen: 100-200 mg/day.
Fecal stercobilinogen: 300 mg/day
Distribution of Jaundice
High concentration of bilirubin (hyperbilirubinemia), the bile product and its congeners are responsible for yellow discoloratrion of skin in jaundice. They bind with circulating proteins.
Bilirubin has more affinity for nervous tissue like basal ganglia and elastic tissues such as skin, sclera and blood vessels.
Infections:
- Viral hepatitis
- Weil’s disease (Leptospirosis)
- Septicemia
- Malaria
- Typhoid
Toxicity
- Anesthetic agents: Halothane, chloroform
- Anticoagulants: Phenindione
- Anti-tuberculous drugs: Rifampicin, P.A.S., I.N.H., Thiacetazone
- Metals: Arsenic, mercury, gold, bismuth
- Chemicals: DDT
- X-ray irradiations
Cirrhosis
- Portal Hypertension
- Biliary cirrhosis
- Hemochromatosis
Extra Hepatic Obstruction
- Stone
- Stricture
- Parasites
- Acute cholecystitis
- Carcinoma of the head of the pancreas
- Neoplasm of bile ducts, gall bladder and ampulla of Vater
- Congenital: Biliary atresia
Intra Hepatic Obstruction
1. Cholestatic phase of infective hepatitis
2. Drugs – Steroids, chlorpromazine, PAS, sulfonamides, chlorpropamide tolbutamide, methyl testosterone
Hemolytic Causes of Jaundice
There is an increased destruction of red blood cells which causes increase in production of bilirubin. This may occur due to
- Infections like Malaria, Clostridium welchi
- Drugs like L. Methyldopa, quinine, phenacetin, sulfonamides
- Burns
- Irradiation
- Poisons as in: Snake Venom, Favism
- Mismatched blood-tranfusion
- Paroxysmal Cold Hemoglobinuria
- Lymphoma
- Leukemia
- Systemic lupus erythematosis
- Uremia
Congenital Hyperbilirubinemia
- Gilbert’s syndrome
- Crigler-Najjar syndrome
- Dubin Johnson syndrome
- Rotor’s syndrome.
