Icterus

Nikita Garg

Icterus / Jaundice
Jaundice, or icterus, is a yellowish discoloration of tissue resulting from the
deposition of bilirubin.
-Serum hyperbilirubinemia and is a sign of either liver disease or, less often, a hemolytic
disorder.

The presence of scleral icterus indicates a

serum bilirubin of at least 3 mg/dL.
The second place to check for icterus is to examine underneath the Tongue.

Physiology
Bilirubin metabolism and elimination.
(1) Normal bilirubin production from heme (0.20.3
gm/day) is derived primarily from the breakdown of
senescent circulating erythrocytes.
(2) Extrahepatic bilirubin is bound to serum albumin and
delivered to the liver.
(3) Hepatocellular uptake
(4) Glucuronidation in the endoplasmic reticulum generate
bilirubin monoglucuronides and diglucuronides, which are
water soluble and readily excreted into bile.
-The conjugation of glucuronic acid to bilirubin is
catalyzed by bilirubin uridine diphosphateglucuronosyl transferase (UDPGT).

(5) Gut bacteria deconjugate the bilirubin and degrade it to

colorless urobilinogens.
The urobilinogens and the residue of intact pigments are
excreted in the feces, with some reabsorption and
excretion into urine.

Pathophysiology
Hyperbilirubinemia may result
from
1. Excessive extrahepatic production
of bilirubin
2. Reduced hepatocyte uptake

An increase in unconjugated bilirubin

in serum results from either
Overproduction
Impairment of uptake
Impaired Conjugation of bilirubin

3. Impaired conjugation
4. Decreased hepatocellular excretion
5. Impaired bile flow.

An increase in conjugated bilirubin is

due to
Decreased excretion into the bile ductules
Backward leakage of the pigment.

Types
1. Prehepatic Jaundice
2. Hepatocellular Jaundice
3. Obstructive Jaundice

Prehepatic Jaundice - Unconjugated

Bilirubin overproduction may result from excessive breakdown of heme
derived from hemoglobin
Hemolysis
Inherited disorders include spherocytosis, sickle cell anemia, thalassemia, and deficiency
of red cell enzymes such as pyruvate kinase and glucose-6-phosphate dehydrogenase.
Acquired hemolytic disorders include microangiopathic hemolytic anemia (e.g.,
hemolytic-uremic syndrome), paroxysmal nocturnal hemoglobinuria, immune hemolysis
and parasitic infections including malaria.
In these conditions, the serum bilirubin rarely exceeds 86 mol/L (5 mg/dL).
Higher levels may occur when there is coexistent renal or hepatocellular dysfunction or in
acute hemolysis such as a sickle cell crisis.

Hepatocellular Jaundice
Unconjugated and Conjugated Jaundice
Most liver diseases affect canalicular excretion, resulting in the accumulation of both
conjugated and unconjugated bilirubin in hepatocytes
Inability of liver to transport bilirubin across the hepatocytes due to liver disease
Usually associated with increased levels of transaminases AST> 1000 U/L
Increase in AST and ALT more than increase in ALP
This type of jaundice is usually caused by liver failure, cirrhosis, hepatitis or taking certain
drugs.
Ethanol, Paracetamol, Halothane, Methyldopa, Barbiturates
It may also be caused by a tumour in the liver.
Imaging
Liver biopsy

Obstructive Jaundice Conjugated

Obstruction of bile flow in the
Extrahepatic Bile ducts between Porta
Hepatis and the Papilla of Vater

The most common cause of

obstructive jaundice is the presence
of gallstones in the ducts of the biliary
system
Other Causes:

Biliary stricture (narrowing of the bile duct)

Cancer of the gallbladder or pancreas
Cholangitis (infection or inflammation of
the common bile duct)
Congenital structural defects
Cysts of the bile duct
Lymph node enlargement
Pancreatitis
Parasitic infection
Trauma, including surgical complications

Characterstically associated with dark urine

and pale stools
Prurutis and skin excoriations
CHARCOTs TRIAD
Jaundice
Right upper quadrant pain
Fever

Increase in ALP more than increase in ALT

and AST

Thank You