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Pathophysiology of Jaundice

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13 views23 pages

Pathophysiology of Jaundice

Uploaded by

harshdadhich29
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Pathophysiology of Jaundice

Learning objectives

• Define jaundice
• Describe the catabolism of hemoglobin
• List the different types of jaundice
• Describe the etiology of jaundice
• Describe the clinical and laboratory features of the different types of jaundice:
Hemolytic, Hepatic and Obstructive
• List the points of difference between the different types of jaundice
• Describe physiological jaundice of newborn
What is Jaundice?

• Jaundice is characterised by the yellowish discolouration of the skin and sclera


due to the deposition of the yellowish pigment, Bilirubin

• This occurs due to the increase in the concentration of bilirubin in blood

• Bilirubin is a normal product of erythrocyte breakdown


Destruction of erythrocytes

• Life span of erythrocytes is about 120 days

• Old erythrocytes are trapped by macrophages in the reticuloendothelial system

• Sites: Spleen, Liver, Lymph nodes and Bone marrow

• Erythrocytes are phagocytosed by the macrophages, which releases the


hemoglobin
Breakdown of hemoglobin

HEMOGLOBIN

HEME GLOBIN

HEME OXYGENASE

BILIVERDIN AMINO ACIDS

BILIVERDIN REDUCTASE

BILIRUBIN
Handling of Bilirubin by hepatocytes

• Bilirubin released by the macrophages enters the circulation

• Formation of Bilirubin-Albumin complex

• Reaches the Liver

• Bilirubin enters the hepatocytes; Albumin stays in circulation

• Liver handles the Bilirubin in 3 steps: Uptake, Conjugation and Excretion


HEPATOCYTE
ENDOPLASMIC RETICULUM
BLOOD BILE
Bile
Glucunoryl canaliculus
Bilirubin Transferase
Albumin Bilirubin Bilirubin Bilirubin Bilirubin
complex glucuronide glucuronide

UDP UDP
Ligandin Glucuronic
Albumin acid

UPTAKE CONJUGATION EXCRETION


Handling of Bilirubin by the hepatocytes
Bilirubin in bile enters small intestine

Enters large intestine

Bacterial flora splits glucuronic acid from Bilirubin and reduces it to Stercobilinogen

20%
80%

Absorbed into portal


Stercobilinogen
circulation
(colourless) is oxidised to
Stercobilin (brownish)
and excreted with faeces

Enters circulation and


Re-excreted by Liver into Bile and
excreted in urine as
enters small intestine
Urobilinogen
Etiology of jaundice

1. Increased production of Bilirubin 2. Decreased excretion of Bilirubin

Increased destruction of red


blood cells or hemolysis Liver cannot conjugate Obstruction in bile
bilirubin effectively duct
HEMOLYTIC JAUNDICE
HEPATIC JAUNDICE OBSTRUCTIVE
JAUNDICE
Jaundice
• It is the yellowish discolouration of skin and sclera due to increased concentration
of Bilirubin in blood

• Normal concentration is < 1mg/dl

• Jaundice can be detected clinically when Bilirubin > 2.5 mg/dl

• First site where jaundice is clinically detected is Sclera

• Because sclera is white in colour and contains Elastin, which has high affinity for
Bilirubin
Yellowish discolouration of sclera: Icterus
Clinical and laboratory features of
Jaundice
Hemolytic jaundice

• Excessive breakdown (hemolysis) of erythrocytes

• Increased release of Bilirubin into circulation

• Exceeds conjugation capacity of Liver

• Increase in Unconjugated Bilirubin

• Increase in conjugation by Liver causes increase in faecal Stercobilin and urinary


Urobilinogen
Hepatic jaundice

• Affects hepatic handling of hepatocytes

• Impaired conjugation of Bilirubin

• Excretion of conjugated Bilirubin is also affected

• Excess unconjugated and conjugated Bilirubin in blood

• Excretion of conjugated bilirubin in urine: Yellow urine


• Decreased excretion of conjugated bilirubin in Bile

• Reduced fecal Stercobilinogen and urinary urobilinogen

• Decreased secretion of bile salts impairs fat absorption: STEATORRHOEA

• Liver function tests are abnormal

• Altered Albumin:Globulin ratio

• Narrowing of biliary canaliculi by the inflammatory process adds an obstructive


element
Obstructive jaundice
• In complete obstruction, no bile reaches the intestine

• Neither Bilirubin nor bile salts reaches the intestine

• Absence of fecal Stercobilinogen: Clay coloured stools

• Increase in fecal fat content: Steatorrhoea

• Conjugated hyperbilirubinemia; Dark yellow urine

• Prolonged biliary stasis may damage the hepatocytes


Van den Bergh test

PRINCIPLE:
Excess of conjugated (water-soluble) bilirubin gives a reddish-violet colour with
diazo reagent (sulphanilic acid, sulphuric acid and sodium nitrite)

Direct positive test: Colour appears immediately

Indirect positive test: Colour appears on addition of alcohol


(Basis: Alcohol makes the Bilirubin albumin complex soluble)
HEMOLYTIC JAUNDICE HEPATIC JAUNDICE OBSTRUCTIVE JAUNDICE

Fecal Stercobilinogen

Urinary Urobilinogen

Urinary Bilirubin

Van den Bergh test

Liver function test


Physiological jaundice of newborn

• Seen in some newborn infants

• More common in premature infants

• Usually mild jaundice occurs

• Also known as neonatal jaundice

• Appears on 2nd/3rd day of life; disappears within a week


• Cause: Immaturity of liver function

• Decreased glucuronosyl transferase activity

• Management: Phototherapy (White light converts bilirubin to Lumirubin, which is


water soluble and excreted in urine)

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