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Jaundice
This document provides an overview of jaundice and its causes. It defines jaundice as a yellowish discoloration of the skin and eyes. Jaundice can be classified as pre-hepatic (haemolytic), hepatocellular, or obstructive based on its underlying mechanism. Common causes discussed include viral hepatitis, alcoholic liver disease, gallstones, and tumors. The document outlines approaches to evaluating a jaundiced patient through history, examination, and laboratory and imaging tests. It also describes treatment principles and specific therapies for acute viral hepatitis and liver failure.
Jaundice
- 1. Jaundice A Presentation bySS-32 Muhammad Shoyab Tahmina Sultana Rumi Asim Kumer Das 5th Year MBBS Sir Salimullah Medical College Mitford, Dhaka 15 June 2009
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- 4. Jaundice is shrouded inmisconceptions and superstitions
- 6. Definition Jaundice may bedefined as yellowish discoloration of the sclera, skin and mucous membranes. Guyton
- 7. Clinical jaundice >3 mg / dL (> 51 µmol / L) Latent jaundice 1 – 3 mg / dL (17 – 51 µmol / L) Normal serum bilirubin upto 1 mg / dL (17 µmol / L) Conjugated 0.1 – 0.4 mg / dL Unconjugated 0.2 – 0.7 mg / dL Clinical Classification Kumar & Clark | Samson Wright’s
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- 9. Mechanisms of Hyperbilirubinaemia Robbins Excess production Reducedhepatocellular uptake Impaired conjugation Decreased secretion from hepatocyte into bile canaliculi Impaired bile flow
- 10. Excess production Reduced hepatocellularuptake Impaired conjugation Decreased secretion from hepatocyte into bile canaliculi Impaired bile flow Classification of Jaundice Haemolytic / Pre-hepatic Hepatocellular Obstructive / Post-hepatic
- 11. Excess production Reduced hepatocellularuptake Impaired conjugation Decreased secretion from hepatocyte into bile canaliculi Impaired bile flow Classification of Jaundice CONJUGATED UNCONJUGATED
- 12. Excess production Reduced hepatocellularuptake Impaired conjugation Decreased secretion from hepatocyte into bile canaliculi Impaired bile flow Classification of Jaundice CONJUGATED UNCONJUGATED Haemolytic / Pre-hepatic Obstructive / Post-hepatic Hepatocellular
- 13. Bilirubin UNCONJUGATED CONJUGATED Insoluble inwater Tightly bound to albumin Cannot be excreted in urine Deposited in tissues, with special affinity to lipids (hence kernicterus) Soluble in water Weakly bound to albumin Can be excreted in urine Elevation for prolonged periods allows it to bind tightly with albumin Robbins | www.drsarma.in
- 14. Aetiology of Jaundice PRE-HEPATIC HaemolyticDisorders Spherocytosis Sickle cell anaemia Thalassaemia Haemolytic disease of the newborn Autoimmune haemolytic anaemia Microangiopathic haemolytic anaemia Paroxysmal nocturnal hemoglobinuria Cecil | Cuschieri | Harrison UNCONJUGATED
- 15. Aetiology of Jaundice HEPATOCELLULAR ViralHepatitis Hepatitis A, B, C, D, E Epstein-Barr virus Cytomegalovirus Herpes simplex virus Alcoholic Liver Disease Drug-induced Liver Disease Paracetamol, Alpha-methyldopa, Isoniazid Allopurinol, Ketoconazole, Chlorpromazine Methotrexate, Phenytoin, Halothane Harrison CONJUGATED
- 16. Aetiology of Jaundice HEPATOCELLULAR EnvironmentalToxins Aflatoxin Carbon tetrachloride Autoimmune Hepatitis Congenital Dubin-Johnson Syndrome Rotor’s Syndrome Gilbert's syndrome Crigler-Najjar Syndrome Neonatal jaundice Cecil | Cuschieri | Davidson CONJUGATED UNCONJUGATED
- 17. Aetiology of Jaundice POST-HEPATIC IntrahepaticCholestasis Primary biliary cirrhosis Primary sclerosing cholangitis Cholestasis of pregnancy Total parenteral nutrition Benign postoperative cholestasis Paraneoplastic syndrome Harrison CONJUGATED
- 18. Aetiology of Jaundice POST-HEPATIC ExtrahepaticCholestasis Gallstones Tumors of the head of the pancreas Gallbladder cancer Periampullary tumors Portal lymphadenopathy Congenital biliary atresia Choledochal cysts Infectious cholangiopathy (Leptospira, Clonorchis sinensis, Ascaris lumbricoides, Fasciola hepatica) Cecil CONJUGATED
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- 21. Haemolytic Jaundice Mild anaemia Recurrent, mildjaundice Positive family history History of recurrent blood transfusion Short Cases, ABM A | ACP Board Review
- 22. Haemolytic Jaundice Mongoloid facies ACPBoard Review Hepatosplenomegaly CONTD . . .
- 23. Haemolytic Jaundice Serum bilirubinnot above 6 mg / dL Microcytic hypochromic anaemia Evidence of haemolysis Liver function tests normal No bilirubin in urine Harrison CONTD . . .
- 24. Haemolytic Jaundice Prolonged elevation of unconjugated bilirubinmay lead to kernicterus B&L CONTD . . .
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- 26. Anorexia, nausea vomiting Mild fever Moderatejaundice Hepatocellular Jaundice ACP Board Review | Macleod
- 27. Enlarged tender liver Signs ofchronic liver disease may be present Hepatocellular Jaundice CONTD . . .
- 28. Marked rise of serumalanine aminotransferase (ALT) Bilirubin appears in urine Hepatocellular Jaundice CONTD . . .
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- 30. Obstructive Jaundice Deep jaundice Pale, bulky, frothy,sticky, foul-smelling stool Dark urine Itching
- 31. Right hypochondriac tenderness Gall bladder may bepalpable Obstructive Jaundice CONTD . . .
- 32. Obstructive Jaundice Marked rise of serumalkaline phosphatase (ALP) Bilirubin appears in urine No urobilinogen in urine CONTD . . .
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- 34. Sequelae of HBVInfection Subclinical Disease (65%) Recovery Acute Hepatitis (25%) Healthy Carrier (5%) Fulminant Hepatitis Persistent Infection (4%) Chronic Hepatitis Recovery Cirrhosis HCC Death Robbins 100% 99% 1% 70-90% 10-33% 20-50% 10%
- 35. Prevention of HBVInfection • Screen blood donors • Health education • Use barrier contraceptive • Immunisation • Avoid sharing needles, razors, tooth brushes • Disinfection of surgical and laboratory articles
- 36. HBV Immunisation Active (pre- exposureHBsAg) • Patient requiring repeated blood transfusion • IV drug abuser • Homosexual male • Sex worker • Baby of HBV mother • Patient on dialysis • Medical, paramedical and laboratory staff • Spouse of HBV carrier Passive (post- exposure HBIg) • Surgeons, nurses • Laboratory technicians • Newborn of carrier mother • Sexual contacts of HBV patients
- 37. Why is HCVMore Dangerous? • Clinical features are less prominent • Hepatic enzyme levels unreliable • More chronicity • More chance of malignant transformation • No vaccine available
- 38. Jaundice alone isnot criteria for admission If liver failure present or suspected extrabiliary compression then admit Surgery consult if obstructive When to admit
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- 40. Approach to Jaundice Howto clinically evaluate the patient? What tests will help us in D.D? What imaging modalities will be useful? How to monitor the progress ? www.drsarma.in
- 41. Algorithm for Jaundice JAUNDICE History Examination YOUNG Riskof hepatitis OLDER No risk of hepatitis Weight Loss Liver Biochemistry VIRAL MARKER + ve Viral Hepatitis – ve CBD OK Re-check drug history Autoantibodies Liver biopsy CBD dilated Biliary Obstruction MRCP / ERCP ULTRASOUND SOL Biopsy Liver Biochemistry Viral marker + ve – ve Viral Hepatitis K&C
- 42. History • Pain • Fever •Confusion • Weight loss • Sex, drugs • Alcohol • Pruritus • Malaise, myalgias • Oedema • Dark urine • Abdominal girth • Other autoimmune disease • HIV status • Prior biliary surgery • Family history of liver disease
- 43. Important Clues From History Duration of jaundice – Acute / Chronic Abdominal pain vs painless jaundice Fever – Viral / bacterial / sepsis Arthralgia, rash, glands; Pruritus - obstructive Appetite – Hepatocellular / Malignancy Weight loss – Malignancy – CAH Colour of stools – chalky white – obstructive Family history – Hemolytic – Inherited dis. H/O transfusion, promiscuity, IDU Alcohol abuse, Medications – INH, EM, Largactil www.drsarma.in
- 44. Examination • BP /HR / Temp • Mental status • Asterixis • Abdominal tenderness • Liver size • Splenomegaly • Ascites • Oedema • Spider angiomata • Hyperpigmentation • Kayser-Fleischer rings • Xanthomas • Gynecomastia • Virchow’s left supraclavicular lymphadenopathy
- 45. Investigations • AST, ALT,ALP • Serum bilirubin • Serum albumin • Prothrombin time • Blood glucose • Na-K-PO4, acid- base • Acetaminophen level • CBC / platelet • Ammonia • Viral serologies • ANA-ASMA-AMA • Quantitative Ig • Ceruloplasmin • Iron profile • Blood cultures
- 46. Imaging • Ultrasound • CT •ERCP • MRCP • PTC
- 47. Imaging : USG 98%specific, 90% sensitive for GB stones and dilated ducts Portable, cheap, no radiation, no IV contrast
- 48. Imaging : CT Betterimaging of the pancreas and abdomen
- 49. Imaging : MRCP Imagingof biliary tree Useful for duct stones
- 50. Imaging : ERCP Distalbiliary obstruction Brushing and biopsy for malignancy
- 51. Liver Function Tests(LFT) Liver function test Normal Range Bilirubin Total Conjugated 0.1 to 1.0 mg / dL < 0.2 mg / dL Alkaline phosphatase 25-112 IU / L Aspartate transaminase (AST) 5-31 IU / L Alanine transaminase (ALT) 5-35 IU / L Albumin 3.5-5.0 g / dL Prothrombin time (PT) 12-16 s www.drsarma.in
- 52. Utility of LFT TestUtility ALT ALT < AST in alcoholism Albumin Assess severity / chronicity Alkaline phosphatase Diagnosis of Obstructive Jaundice AST Early diagnosis of Liver disease, Follow-up Bilirubin Diagnose jaundice and its severity Gamma-globulin Diagnosis and follow-up of chronic hepatitis & cirrhosis GGT Diagnosis of alcohol abuse Prothrombin time (PT) Assess severity of disease www.drsarma.in
- 53. HBV Serology HBsAg HBcAb IgM HBcAb IgGHBsAb Acute HBV + + - - Resolved HBV - - + + Chronic HBV + - + - HBV vaccinated - - - +
- 54. Diagnosis of AlcoholicLiver Disease • The history is the key – 60 grams/day • Gynecomastia, parotids, Dupuytren’s • Lab clues: AST/ALT > 2, MCV > 94 AST < 300 • Anorexia, fever, jaundice, hepatomegaly
- 55. Diagnosis of Immune-Mediated Liver Diseases LFTSerology Ig Biopsy AIH ALT ANA ASMA IgG Portal inflammation Plasmacytes Piecemeal necrosis PBC ALP AMA IgM Bile duct destruction granulomas PSC ALP none normal Periductal concentric fibrosis
- 56. Diagnosis of Autoimmune Hepatitis •Widely variable clinical presentations – Asymptomatic LFT abnormality (ALT and AST) – Severe hepatitis with jaundice – Cirrhosis and complications of portal HTN • Often associated with other autoimmune diseases • Diagnosis: – Compatible clinical presentation – ANA or ASMA with titer 1:80 or greater – IgG > 1.5 upper limits of normal – Liver biopsy: portal lymphocytes + plasma cells
- 57. Diagnosis of PrimaryBiliary Cirrhosis • Compatible clinical presentation • AMA titer 1:80 or greater (95% sens/spec) • IgM > 1.5 upper limits of normal • Liver biopsy : bile duct destruction
- 58. Diagnosis of Primary SclerosingCholangitis • ERCP (now MRCP) • No autoantibodies, no elevated globulins • Biopsy: concentric fibrosis around bile ducts
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- 60. Principles of Treatment •No specific treatment • Hospitalised for early detection of fulminant hepatic failure, if at risk • Adequate protein and calorie in diet • Avoid hepatotoxic drugs (e.g. sedatives, hypnotics, alcohol)
- 61. Principles of Treatment •Bed rest : 3 – 5 weeks • If constipated : lactulose • If diarrhoea : avoid milk and milk products; maintain hydration • If severe vomiting : glucose and IV fluid • Psychological support CONTD . . .
- 62. Acute Viral Hepatitis •Follow the principles of treatment • Special advice for HBV and HCV patients – Avoid blood donation – Use barrier contraceptive – Screen and vaccinate partner – Check HBsAg after 3 months
- 63. Treatment of ChronicHBV • No drug available to eradicate HBV completely • If HBeAg +ve : pegylated interferon for 6 months • If HBeAg –ve : 12 months • Other options : lamivudine, adefovir, liver transplantation
- 64. Treatment of HCVInfection • Follow the principles of treatment • α-interferon 3 M units thrice weekly for 1 year
- 65. Fulminant Hepatic Failure Hepaticencephalopathy characterised by mental changes, confusion, stupor and coma occurring within 8 weeks of the precipitating illness, in the absence of pre-existing liver disease. Davidson
- 66. Causes of FulminantHepatic Failure • Acute viral hepatitis • Hepatotoxic drugs • Toxins • Leptospirosis • Wilsons’ disease, Budd-Chiari syndrome • Hepatic malignancies
- 67. Clinical Features of FulminantHepatic Failure • Features of encephalopathy • Features of raised intracranial pressure • General features
- 68. Clinical Features of FulminantHepatic Failure • Features of encephalopathy • Features of raised intracranial pressure • General features • Confusion, disorientation, slurred speech • Flapping tremor • Exaggerated reflexes, extensor plantar response • Constructional apraxia
- 69. Clinical Features of FulminantHepatic Failure • Features of encephalopathy • Features of raised intracranial pressure • General features • Headache • Vomiting • Papilloedema • Fixed pupils • Myoclonus • Bradycardia • Profuse sweating
- 70. Clinical Features of FulminantHepatic Failure • Features of encephalopathy • Features of raised intracranial pressure • General features • Weakness, nausea, vomiting • Right hypochondriac pain • Jaundice • Foetor hepaticus • Liver : initially palpable, later not • Ascites, oedema
- 71. Treatment of Fulminant HepaticFailure • Admission into intensive care unit • Correct encephalopathy • No protein intake • Avoid sedatives, diuretics • High carbohydrate diet • For cerebral oedema : mannitol
- 72. • Correct hypokalaemiaand hypocalcaemia • To prevent GIT haemorrhage : tablet ranitidine 150 mg 12 hourly Treatment of Fulminant Hepatic Failure CONTD . . .
- 73. When to Referto Gastroenterologist Unexplained jaundice Suspected obstruction Acute hepatitis – severe or fulminant Unexplained abnormal LFTs persisting for 6 months or greater Unexplained cholestasis Cirrhosis (in non- alcoholic) for consideration of liver transplant Suspected hereditary hemochromatosis Suspected Wilson's disease Suspected autoimmune hepatitis Chronic hepatitis C for consideration of antiviral therapywww.drsarma.in
- 74. Treatment of AlcoholicLiver Disease • Abstinence • Nutrition • Prednisolone 40 mg/day x 28 days –contraindications: infection, renal failure, GI bleeding • Pentoxifylline 400 mg PO tid x 28 days
- 75. Hepatotoxic Drugs • Hepatocellular –Paracetamol, INH, methyldopa, MTX • Cholestatic – chlorpromazine, estradiol, antibiotics • Chronic Hepatitis – methyldopa, phenytoin • Hypersensitivity Reaction – Phenytoin, allopurinol
- 76. Paracetamol Toxicity • Dangerdosages (70 kg patient) –Toxicity possible > 10 gm –Severe toxicity certain > 25 gm –Lower doses potentially hepatotoxic in: • Chronic alcoholics • Malnutrition or fasting • Dilantin, Tegretol, phenobarbital, INH, rifampin • NOT in acute EtOH ingestion • NOT in non-alcoholic chr. liver disease
- 77. Features of Paracetamol Toxicity •Day 1: – Nausea, vomiting, malaise, or asymptomatic • Day 2 – 3: – Initial symptoms resolve – AST and ALT begin to rise by 36 hours – RUQ pain, tender enlarged liver on exam • Day 4 – AST and ALT peak > 3000 – Liver dysfunction: PT, encephalopathy, jaundice. Acute renal failure (ATN)
- 78. Treatment of Paracetamol Toxicity •Activated charcoal if < 4 hours from ingestion : single dose 1 mg/kg PO or NG • N-Acetylcysteine (NAC) – 140 mg/kg loading dose PO or NG – 70 mg/kg q 4 hours PO or NG X 17 doses • Continue longer until INR < 2.0 and improved • OK to DC if acetaminophen levels undetectable and normal AST at 36 hours CONTD . . .
- 79. Treatment of Paracetamol Toxicity Indicationsfor NAC therapy: • Above the line on the nomogram • Serum concentration > 10 mcg/ml and unknown time of ingestion • Repeated excessive doses, risk factors for acetaminophen hepatoxicity, and serum concentration > 10 mcg/ml • Evidence of hepatoxicity and a history of excessive acetaminophen dosing CONTD . . .
- 80. Primary Biliary Cirrhosis •Cholestatic liver disease (ALP) – Most common symptoms: pruritus and fatigue – Many patients asymptomatic, and dx by abnormal LFT • Female : male ratio = 9:1 • Treatment : Urodeoxycholic acid 15 mg/kg
- 81. Primary Sclerosing Cholangitis • Cholestaticliver disease (ALP) • Inflammation of large bile ducts • 90% associated with IBD – but only 5% of IBD patients get PSC • Cholangiocarcinoma : 10-15% lifetime risk • Treatment : Liver Transplantation
- 82. Manifestations of Wilson's Disease HEPATICPSYCHIATRIC CAH, Cirrhosis, Fulminant hepatitis Behavioral, organic dementia, EARLY NEUROLOGICAL Psychoneurosis, manic-depressive Incoordination, dysarthria, Schizophrenic psychosis Resting and intention tremors OPHTHALMIC Excessive salivation, dysphagia KF ring, sunflower cataract Mask-like facies, ataxia HEMATOLOGIC AND OTHERS LATE NEUROLOGICAL IV hemolysis, Hypersplenism Dystonia, spasticity, Rigidity, TCS Distal RTA, Osteomalacia, OS
- 84. Wilson’s Disease • Autosomalrecessive – Cu metabolism • Chronic hepatitis or fulminant hepatitis • Diagnosis : ceruloplasmin↓, urinary Cu↑ • Treatment : d-penicillamine
- 85. Neonatal Jaundice • Neonataljaundice is common • 50% healthy term infants • Re-emergence of kernicterus • In utero bilirubin is handled by placenta and mother’s liver • After birth, neonate to has cope with increase in bilirubin production and the immature liver cannot handle for a few days www.drsarma.in
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- 87. Basis of Phototherapy •Unconjugated bilirubin is not water soluble • Blue light converts the unconjugated bilirubin into its photoisomers • The photoisomers are water soluble • The soluble photoisomers pass through the glomerular filter and get excreted • Thus conjugation in liver is by passed www.drsarma.in
- 88. Agent : Leptospirainterrogens Host : Rodents Route of entry : intact skin, mucous membrane, cuts and abrasions Organs affected : kidneys, liver, meninges, brain Icteric Leptospirosis (Weil’s Disease)
- 89. Clinical Features ofIcteric Leptospirosis • Deep jaundice • Fever • Haemorrhage • Epistaxis, purpura, erythema • Haematemesis, melaena • Pleural, pericardial and subarachnoid haemorrhage
- 90. Clinical Features ofIcteric Leptospirosis • Renal impairment • Oliguria, anuria • Albumin, blood and casts in urine • Associated uveitis, iritis, myocarditis, encephalitis, aseptic meningitis
- 91. Diagnosis of Icteric Leptospirosis •Blood – polymorphonuclear leukocytosis • Liver function tests – elevated transaminases and prothrombin time • Definitive : culture of blood (1st week), urine (2nd week), ELISA, PCR
- 92. Treatment of Icteric Leptospirosis •Oral doxycycline • Intravenous penicillin • Treatment of renal impairment • Control haemorrhage
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Editor's Notes
- #2 Honourable Principal, Honourable Head of the Dept of Medicine, Professors, Senior Doctors and my fellow students, I welcome all of you to this session of integrated teaching on the topic : JAUNDICE. But . . .
- #3 But . . . Why jaundice? Or you may very well have the question in your mind . . .
- #4 Why again jaundice? Haven’t we learned enough about it? The reason is this . . .
- #5 Despite advancements in medical knowledge and increasing awareness about health among the common mass, jaundice is an entity that has remained shrouded in misconceptions and superstitions, not only among the uneducated and the illiterate – but, alarmingly, even medically educated individuals have been found to refer friends and relatives for treatments based on drinking or washing in enchanted water, or placing a garland of plant roots and branches on the head, extracting bile from the body by scratching the scalp or applying heat on the abdomen, and so on – none of which have any scientific explanation nor do they have any beneficial effect on the patient. And that is why our presentation is aimed at
- #6 Enlightening all with science and to eliminate misconceptions.
- #7 We all know this definition of jaundice, and we also know that the yellowish discoloration is caused by deposition of bile pigments due to elevated levels of bilirubin in blood. The point of emphasis here is that the sclera is the most important site for examining jaundice. Why? – Being rich in elastic tissue, the sclera is the site of first manifestation (BLACK’S Dict). Also, there are certain other situations presenting with yellowish discoloration, and the sclera is the point of distinction between those non-icteric conditions and jaundice. For example, hyperbetacarotenemia manifests as generalised discoloration of the skin as well as urine, but the sclera is spared. Likewise, a dehydrated patient may complain of dark urine, and we can easily distiguish this from jaundice by examining the sclera.
- #8 Clinically, jaundice is not manifested before serum bilirubin is more than 3 mg / dL Although normal values are less than 1. In
- #9 Bilirubin is made in the reticulendothelial system Once broken down, it is released into plasma and bound to albumin Hepatocytes conjugate the bilirubin On the smooth ER, bilirubin is conjugated with glucoronic acid, xylose, or ribose Glucoronic acid is the major conjugate - catalyzed by UDP glucuronyl tranferase “Conjugated” bilirubin is water soluble and is secreted by the hepatocytes into the biliary canaliculi Converted to stercobilinogen (urobilinogen) (colorless) by bacteria in the gut Oxidized to stercobilin which is colored Excreted in feces Some stercobilin may be re-adsorbed by the gut and re-excreted by either the liver or kidney
- #10 Decide on which picture to keep and which to omit.
- #11 Production of bilirubin, i.e. unconjugated, more than the liver’s capacity to conjugate. We know that a healthy liver can handle six times the normal level of bilirubin Reduced uptake of unconjugated bilirubin by the liver cells Impaired conjugation inside the liver cells These mechanisms would result in a rise of unconjugated bilirubin. Bilirubin levels can also rise by Decreased ability of hepatocytes to secrete the conjugated bilirubin into the bile canaliculi, and Any impairment in the flow and drainage of bile through the biliary channels into the intestines. In the last two cases, the increase occurs in the levels of conjugated bilirubin. And as soon as the bilirubin builds up inside the hepatocyte and cannot be excreted, it regurgitates into the circulation, leading to hyperbilirubinaemia, which is clinically manifested as jaundice.
- #12 Production of bilirubin, i.e. unconjugated, more than the liver’s capacity to conjugate. We know that a healthy liver can handle six times the normal level of bilirubin Reduced uptake of unconjugated bilirubin by the liver cells Impaired conjugation inside the liver cells These mechanisms would result in a rise of unconjugated bilirubin. Bilirubin levels can also rise by Decreased ability of hepatocytes to excrete the conjugated bilirubin into the bile canaliculi, and Any impairment in the flow and drainage of bile through the biliary channels into the intestines. In the last two cases, the increase occurs in the levels of conjugated bilirubin. And as soon as the bilirubin builds up inside the hepatocyte and cannot be excreted, it returns to the circulation, leading to hyperbilirubinaemia, which is clinically manifested as jaundice.
- #13 If bilirubin levels exceed liver conjugation capabilities indirect levels will rise If excretion is altered, conjugated bilirubin levels rise
- #14 Production of bilirubin, i.e. unconjugated, more than the liver’s capacity to conjugate. We know that a healthy liver can handle six times the normal level of bilirubin Reduced uptake of unconjugated bilirubin by the liver cells Impaired conjugation inside the liver cells These mechanisms would result in a rise of unconjugated bilirubin. Bilirubin levels can also rise by Decreased ability of hepatocytes to excrete the conjugated bilirubin into the bile canaliculi, and Any impairment in the flow and drainage of bile through the biliary channels into the intestines. In the last two cases, the increase occurs in the levels of conjugated bilirubin. And as soon as the bilirubin builds up inside the hepatocyte and cannot be excreted, it returns to the circulation, leading to hyperbilirubinaemia, which is clinically manifested as jaundice.
- #15 Vanden Berg Reaction Indirect Direct
- #16 All of these are unconjugated hyperbilirubinaemias.
- #22 In haemolytic jaundice, there is an increased load on the liver for conjugation of the bilirubin produced by the excess haemolysis. The healthy liver is able to handle upto six times the normal load of bilirubin. So, hyperbilirubinaemia occurs only when the load of unconjugated bilirubin is more than the liver’s conjugation capacity. As such, haemolytic jaundice is often mild (i.e. not more than 6 mg / dL) and recurrent. And since the bone marrows can produce upto six to eight times their normal load of blood cells, the anaemia is also mild. In case of hereditary causes of haemolytic jaundice, like hereditary spherocytosis or thalassaemia, there may even be a positive family history. And the patient may be undergoing recurrent blood transfusion.
- #23 In haemolytic jaundice, there is an increased load on the liver for conjugation of the bilirubin produced by the excess haemolysis. The healthy liver is able to handle upto six times the normal load of bilirubin. So, hyperbilirubinaemia occurs only when the load of unconjugated bilirubin is more than the liver’s conjugation capacity. As such, haemolytic jaundice is often mild (i.e. not more than 6 mg / dL) and recurrent. And since the bone marrows can produce upto six to eight times their normal load of blood cells, the anaemia is also mild. In case of hereditary causes of haemolytic jaundice, like hereditary spherocytosis or thalassaemia, there may even be a positive family history. And the patient may be undergoing recurrent blood transfusion.
- #24 Why mongoloid facies? ------- The liver and spleen are enlarged due to the increased act of haemolysis taking place in the RE system.
- #25 The liver is perfectly healthy, so liver function tests are normal. No bilirubin in urine because of being uncojugated, but urobilinogen is elevated as more bilirubin is being conjugated and excreted.
- #26 Kernicterus due to deposition in basal ganglia because of lipid affinity.
- #27 Mild fever due to infectious process. ANV due to stretching of the liver capsule leading to upper GI discomfort.
- #28 Mild fever due to infectious process. ANV due to stretching of the liver capsule leading to upper GI discomfort.
- #29 Liver tender due to stretching of its capsule.
- #30 Liver enzymes are released into the circulation due to disintegration of necrotic liver cells due to the inflammatory process. And since there is an increased level of conjugated bilirubin circulating in the blood, bilirubin also appears in urine.
- #31 Obstruction prevents bile from reaching the intestine and thus impairs fat digestion. Thus, the ingested fatty food is excreted in stool, making it frothy, sticky, foul smelling. Lack of bile pigments makes the stool pale. Conjugated Bilirubin is excreted in urine, making it dark. Bile acids are deposited in skin, leading to pruritus.
- #32 Obstruction prevents bile from reaching the intestine and thus impairs fat digestion. Thus, the ingested fatty food is excreted in stool, making it frothy, sticky, foul smelling. Lack of bile pigments makes the stool pale. Conjugated Bilirubin is excreted in urine, making it dark. Bile acids are deposited in skin, leading to pruritus.
- #33 Since the obstructive process involves the hepatobiliary system . . .
- #34 The bile stagnant in the biliary channels exerts a detergent action on the epithelium of the channels, dissolving the enzymes in their membranes and releasing them into the circulation.
- #39 Jaundice is rarely manifested. Patient usually presents with jaundice. Diagnosis is tough. Hepatic enzyme levels are unreliable