Jaundice by dr anita teli

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Introduction Definition Classification Causes Clinical features

Introduction :

Introduction Bilirubin is the end product of the catabolism of heme . It is formed in the reticuloendothelial system. One gram of hemoglobin yields 35mg of bilirubin . 75% of daily bilirubin production is from circulating senescent erythrocytes. 25% is from the trunover of nonhemoglobin heme proteins & destruction of immature & ineffective erythrocytes. Normal levels are 0.2 – 0.8 mg% (average 0.5mg%)


Definition Jaundice (derived from French word ‘ jaune ’ for yellow) or icterus (Latin word for jaundice) is a yellowish staining of the skin, sclera and mucous membranes by deposition of bilirubin (a yellow orange bile pigment) in these tissues. Jaundice was once called the " morbus regius " (the regal disease) in the belief that only the touch of a king could cure it.

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Clinically jaundice occurs when serum bilirubin exceeds 2mg%. Latent jaundice is said to occur when serum bilirubin is between 1 – 2mg%.

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It is most apparent in natural sunlight. In fact, it may be undetectable in artificial or poor light. Pseudo jaundice may be found in black patients with pigmented sclera, from carotinemia , uremia (a sallow yellowish pallor), and quinacrine (a yellow-green color).


Classification Physiological jaundice Pathological jaundice

Classification :

Classification Physiological jaundice 1. Physiological jaundice of new born 2. Breastfeeding jaundice 3. Breastmilk jaundice

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Pathological jaundice 1. Pre -Hepatic (Hemolytic) jaundice 2. Hepatic ( Hepatocellular ) jaundice 3. Post- Hepatic (Obstructive ) jaundice


Causes Physiological jaundice : elevation of unconjugated bilirubin in first week of birth , where the bilirubin level is raised by 5 mg/dl. Increase bilirubin load on liver cells a. Increased erythrocyte volume : seen in - Infants with polycythemia - Infants of diabetic mothers - Delayed cord clamping

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Defective hepatic uptake of bilirubin from plasma a. Decreased Y protein ( ligandin ) due to caloric deprivation. b. Decreased binding of Y protein by other anions 3. Defective bilirubin conjugation a. Decreased UDPG activity : Hypothyroidism, inhibitors of breast milk . 4. Defective bilirubin excretion

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Physiological jaundice has be functionally classified into 2 phases: Phase one : lasts for 5 days in term infants & about 7 days in preterm infants. There is rapid rise of serum bilirubin levels to 12 & 15 mg/dl respectively. Phase two : decline in levels to about 2mg/dl & lasts for 2 weeks, after which adult values are attained. This phase may lasts for more than a month in preterm infants.

Breastfeeding jaundice:

Breastfeeding jaundice Studies have found that jaundice is seen to occur in first few weeks of birth in breast fed babies compared to those who are formula fed. This has been called as breastfeeding jaundice

Breast milk jaundice:

Breast milk jaundice This is seen in babies who are exclusively breast fed. Develops in second week of life & continue well into the third month. A bilirubin level of over 20mg/dl may be attained. It is due to inhibitory substances in the breastmilk that interfere with bilirubin conjugation e.g pregananediol & free fatty acids. Temporary interruption of feeding will reduce the serum levels of bilirubin .

Pre – Hepatic Jaundice:

Pre – Hepatic Jaundice The pathology is occurring prior to the liver . It is also called as hemolytic jaundice. Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells ). Excessive breakdown of red cells produce unconjugated bilirubin in amounts more than the healthy liver can conjugate & excrete.

Causes of Pre-hepatic Jaundice:

Causes of Pre-hepatic Jaundice A . Inherited disorders 1. Spherocytosis , Elliptocytosis 2. Glucose 6-PD deficiency 3. Pyruvate kinase deficiency 4. Sickle cell anemia 5. Gilbert's syndrome : A genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population. 6. Crigler - Najjar syndrome : rare disease with complete absence of hepatic glucoronyl transferase activity.

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Acquired disord ers 1. Microangiopathic hemolytic anemia 2. Paroxysmal noctural hemoglobinuria 3. Spur cell anemia 4. Immune hemolysis - Warm & cold antibodies - Hemolytic diseases of newborn - Incompatible blood transfusion 5. Drug induced ( rifampicin , probenacid ) 6. Burn

Hepatic Jaundice:

Hepatic Jaundice The pathology is located within the liver. It is also called as hepatocellular jaundice. Damage to the liver cells is caused by infective or toxic products. Here the all three steps of bilirubin metabolism(uptake, conjugation & excretion) are affected. Inability of the liver to efficiently conjugate as well as transport bilirubin into the bile due to liver cell damage Produces both unconjugated as well as conjugated bilirubin is increased in serum.

Causes of Hepatic Jaundice:

Causes of Hepatic Jaundice 1. Acute hepatitis 2. Chronic hepatitis 3. Hepatotoxicity 4. Drug induced hepatitis 5. Cirrhosis 6. Alcoholic liver disease 7. Primary biliary cirrhosis 8. Leptospirosis .

Post – Hepatic Jaundice:

Post – Hepatic Jaundice The pathology is located after the conjugation of bilirubin in the liver. Post-hepatic jaundice, also called obstructive jaundice. Is caused by an interruption to the drainage of bile in the biliary system. Conjugated hyperbilirubinemia results due to impaired flow to the bile.

Causes of Post Hepatic Jaundice:

Causes of Post Hepatic Jaundice Most common cause is Gall stones in common bile duct Carcinoma head of the pancrease Parasitic infection by liver flukes in common bile duct Biliary atresia Cholangiocarcinoma Pancreatitis Pancreatic pseudocysts .

Clinical features:

Clinical features Physiological jaundice 1. Jaundice is detected by blanching of skin in newborn. 2. Icterus is noticed first in face with 5mg/dl. 3. With increase in bilirubin levels, icterus proceeds caudal to trunk & extremities. 4. Palms & soles become yellow when the level exceeds 15mg/dl.

Haemolytic Jaundice:

Haemolytic Jaundice Icterus : yellowish discolouration of skin & conjunctiva. In fair-skinned patients, jaundice is most noticeable on the face, trunk, and sclerae In dark-skinned patients, it’s noticeable on the hard palate, sclerae , and conjunctivae.

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Abdominal pain, rigors, itching Palpable liver more than 2cm below the costal margin There is no stigmata of chronic liver disease Pallor due odema Normal or dark coloured stools due to increased stercobilinogen Urine darkens on standing due to excessive urobilinogen . Spleenomegaly due to excess RE activity Pigment stones Leg ulcers may be noticed.

Hepatic jaundice:

Hepatic jaundice Clinical features of hepatic jaundice include History of alcohol abuse, Lemon yellow jaundice Yellow colour urine & pale stools Clubbing , low grade fever & pigmentation Acute hepatitis, and

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Stigmata of chronic liver disease like - palmar erythema , -caput medusae , - ascites and - dupuytren’s contracture, - hair loss, - gynaecomastia , - bleeding tendency Manifestation of hepatic encephalopathy Manifestation of portal hypertension

Obstructive jaundice:

Obstructive jaundice A good history, physical examination and diagnostic tests are the requisites for the evaluation of the jaundiced patient. Jaundice, dark yellow urine due to conjugated bilirubin , pale stools or clay coloured stools due to absent stercobilinogen and generalized pruritus are the hallmark of obstructive jaundice. History of fever, biliary colic and intermittent jaundice may be suggestive of cholangitis / choledocholithiasis . Weight loss, osteomalacia & bleeding tendency.

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Weight loss, abdominal mass, pain radiating to the back. Progressively deepening jaundice may be suggestive of pancreatic cancer. Deep jaundice (with a greenish hue) that appears to fluctuate in intensity may be due to a periampullary cancer. A palpably enlarged gall bladder in a jaundiced patient is also suggestive of an extrahepatic malignancy .

References :

References Text book of physiology – Guyton Text book of physiology – Indu khurana Text book of medicine – Harrison Text book of pediatrics – O.P.Ghai Internet sources

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