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JAUNDICE
= icterus Is a yellowish discoloration of tissue resulting from the deposition of bilirubin Sign of liver disease or hemolytic disorder DD/
Carotenoderma The use of quinacrine Excessive exposure to phenol
Bilirubin synthesis
Urobilinogen
Faeces (80-90%)
10-20% absorbed
ducts
HEMOLYTIC JAUNDICE
Excessive breakdown of Erythrocytes Breakdown of Hemoglobin into Heme and Globin. Heme is converted into Bilirubin. Breakdown of Erythrocytes is called Hemolysis. So this is Hemolytic Jaundice. Since this happens before the Liver, it is called Pre Hepatic Jaundice.
Due to damage, the liver cannot process Bilirubin and so its blood level increases.
HEPATIC JAUNDICE
Hepatocytes produce bile. The bile salts in it help in the emulsification and absorption of Fats. In Liver damage, bile is not produced and so fats are not emulsified or absorbed. So the feces in such patients will be:
Bulky: all the fats are unabsorbed Greasy: due to fat content Foul smelling: due to bacterial action
OBSTRUCTIVE JAUNDICE
Also called Post Hepatic Jaundice. The root cause is obstruction to the bile ducts. This causes a block in the flow of bile. Since there is an obstruction, it is called Obstructive Jaundice. Since the cause of the Jaundice is beyond the liver, it is called Post Hepatic Jaundice.
OBSTRUCTIVE JAUNDICE
Feces is greasy & foul smelling. If the obstruction is complete, the stools will be colorless. This is because the stools do not have stercobilin, which gives the characteristic color to normal stools.
INITIAL STEPS
Determine
Predominantly conjugated or unconjugated Other biochemical liver tests are abnormal or not
Aquired
Microangiopathic hemolytic anemias PNH Immune hemolysis
Ineffective erythropoeis
Cobalamin, folate and iron deficiencies
Inherited conditions
Crigler Najjar types I and II Gilberts syndrome
DIRECT HYPERBILIRUBINEMIA
Inherited conditions
Dubin-Johnson syndrome Rotors syndrome
Normal < 1 mg/dL The presence of scleral icterus indicates a serum bilirubin of at least 3.0 mg/dL
HISTORY
Recent travel history Exposure to people with jaundice Alcohol consumption Accompanying symptoms
Arthralgia, myalgia, rash, anorexia, weight loss, abdominal pain, fever, pruritus, changes in the urine and stool
PHYSICAL EXAMINATION
Assess patients nutritional status Muscle wasting Stigmata of CLD
Spider naevi, liver palm, gynecomastia, caput medusae, Dupuytrens contracture, parotid gland enlargement, testicular athropy
Jugular vein distention Right pleural effusion Size and consistency of the liver Spleen enlargement Ascites Murphys sign
LABORATORY TESTS
Enzyme for hepatic necrosis
ALT, AST
Environmental toxins
Vinyl chloride, Jamaica bush tea, wild mushrooms
Cholangiocarcinoma Pancreatic cancer Gall bladder cancer Ampullary cancer Malignant involvement of the porta hepatis lymph nodes
Choledocholithiasis Primary sclerosing cholangitis Chronic pancreatitis AIDS cholangiopathy
Benign
Summary points
An isolated raised serum bilirubin concentration is usually due to Gilbert's syndrome, which is confirmed by normal liver enzyme activities and full blood count Jaundice with dark urine, pale stools, and raised alkaline phosphatase and glutamyl transferase activity suggests an obstructive cause, which is confirmed by presence of dilated bile ducts on ultrasonography Jaundice in patients with low serum albumin concentration suggests chronic liver disease Patients with high concentrations of bilirubin ( > 100 mol/l) or signs of sepsis require emergency specialist referral Imaging of the bile ducts for obstructive jaundice is increasingly performed by magnetic resonance cholangiopancreatography, with endoscopy becoming reserved for therapeutic interventions
Dupuytrens contracture
A 67 year old woman, who has previously been healthy, undergoes emergency surgery for a ruptured abdominal aortic aneurysm. Intraoperatively she requires 8 units of PRC to maintain her BP and Ht. Following surgery she is hemodinamically stable. On the third post operative day she appears jaundiced, but abdominal exam is unremarkable and she is afebrile. Total serum bilirubin concentration at this time is 8.3 mg/dl (direct 6.3). Serum AP level is 110 units and serum AST level is 51 U/ml. The most likely explanation for the woman jaundice is A. a stone in the common bile duct B. halothane hepatitis C. post transfusion hepatitis D. acute hepatic infarct E. benign intrahepatic cholestasis
Case