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Jaundice-approach,DD,management,other investigation.pptx
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- 2. JAUNDICE ● Yellowish discolorationof body tissues resulting from the deposition of bilirubin ○ Sclera -High elastin -3mg/dL ○ 2nd Site - Under the tongue ○ Skin → Yellow → Long standing - Green ( Biliverdin)
- 3. JAundcie - scleral Undertongue biliverdin
- 4. Differential Diagnosis foryellowing ● Carotenoderma ○ Most commonly due to - Ingestion of excessive amount of vegetables - Carrots , leafy vegetables ○ Commonly associated with ■ Diabetes ■ Hypothyroidism ■ Anorexia Nervosa ● Drug induced ○ Quinacrine ○ Sunitinib ○ Sorafenib ○ Phenol exposure
- 5. Carotenoderma ● Pigment concentratedon ○ Palms ○ Soles ○ Forehead ○ Nasolabial folds ● Sclerae Spared
- 6. Bilirubin ● Prematurely destroyederythroid cells ● Myogolobin ● Cytochromes 80-85 % Breakdown of Senescent RBC Reticuloendothelial Cells Biliverdin CO Iron
- 7. Biliverdin Bilirubin Biliverdin Reductase ● Insolublein Water ● Bind to Albumin for transport Carrier Mediated Membrane transport to Hepatocytes
- 8. Unconjugated Bilirubin Glutathione -S- Transferase Superfamily Reduce Efflux back Endoplasmic Reticulum Conjugation to Glucouronic acid Uridine Diphosphate glucouronosyl transferase Bilirubin Monoglucouronide Bilirubin Diglucouronide Bile Canaliculi Sinusoid MRP 2 MRP 3 OATP1B1 / OATP1B3
- 10. Conjugated Bilirubin Small Intestine DistalIleum /Colon Unconjugated bilirubin Urobilinogen / Urobilins 80-90 % Excreted in Fecus 10-20 % Enterohepatic cycling Not absorbed due to ● Hydrophilicity ● Large molecular size Bacterial Beta-Glucuronidase Normal Gut Bacteria
- 11. Serum Bilirubin Direct =Conjugated Indirect = Unconjugated ● Diazotized sulfanilic acid → Stable compound absorbs maximally @ 540nm ● Accelerator - Alcohol
- 12. New Techniques ● 1)In Normal Persons /Gilbert Syndrome = almost 100% of Serum Bilirubin is Unconjugated : <3 % is Monoconjugated ● 2)Hepatobiliary disease = Monoconjugated predominance ● 3)Direct fraction also includes Delta Fraction ○ Delta fraction = delta Bilirubin = Biliprotein ○ Conjugated Bilirubin which covalently Bound to albumin ○ Important fraction in people with Hepatobiliary disorders / Cholestasis ○ This explains - Absence of Bilirubinuria and Serum bilirubin falls slowly
- 13. Urine Bilirubin ● Unconjugated= Bound to albumin = Not excreted in Urine ● Delta Bilirubin = Bound to albumin = Not excreted in Urine → ● Conjugated → Filtered in Glomerulus → Majority absorbed at PCT ● Presence of Bilirubinuria = Elevated Conjugated fraction = Hepatobiliary disease False Negative
- 15. Kumar and clark34.8 49-1 table harrison
- 16. Unconjugated Hyperbilirubinemia Hemolytic disorders Inherited ●Spherocytes ● Sickle cell anemia ● Thalasemia ● Pyruvate Kinase Deficiency ● G-6-PD deficiency Aquired ● Microangiopathic Hemolytic anaemia ● Paroxysmal nocturnal hemoglobinuria ● Spur cell anaemia ● Immune Hemolysis ● Parasitic Infections
- 19. Crigler Najjar Type 1 Exceptionallyrare Bilirubin > 20 mg/dL Neurological deficit Death at infancy / Childhood Absence of UDPGT Activity Type 2 Live into adulthood Bilirubin ~ 6-25 mg/dL <10% of Enzyme is active due to mutation UDPGT activity can induced by Phenobarbital Susceptible under illness
- 20. Gilbert Syndrome ● Impairedconjugation due to reduced Bilirubin UDPGT activity (10~35 %) ● Bilirubin ~ 6 mg/dL ● Intermittent Jaundice ● Incidence is 3-7 % ● Male : Female = 1.5-7
- 21. Conjugated Hyperbilirubinemia Patient presentswith asymptomatic jaundice Rotor Syndrome Dubin johnson Syndrome
- 22. History ● Exposure tochemicals/ medications/Alternative medicines ● Any transfusions/ IV drug intake/ ABuse ● Alcohol COnsumption ● Arthralgia / Myalgia preceding the jaundice →Drug induced / Viral Hepatitis ● Sudden onset of Right upper quadrant pain with Chills → CHoledocolithiasis ? Ascending cholangitis
- 23. Physical Examination ● Proximalmuscle wasting → Long standing disease ● Look for stigmata of Chronic Liver disease
- 26. Abdominal Examination ● Anydilated Veins ● Visible Organomegaly ● Abdominal distension ● Liver - Size and consistency → Look below xiphoid for enlarged Left lobe ● Ascites +/- ● Splenomegaly ● Murphy's sign
- 27. Laboratory Tests ● Totaland DIrect bilirubin Fraction ● SGOT,SGPT,ALP (49-1) ● Albumin levels → if low = Chronic Disease ● Prothrombin time → Vit K deficiency due to prolonged jaundice / Malabsorption ○ If the PT not corrected with Vitamin K supplementation → Hepatocellular Injury
- 28. ● Wilson -Young Patients ● Alcoholic -> Pattern of AST:ALT >2:1 ● Viral / Toxin → Enzyme > 500 u/L ○ ALT > AST ● Acute hepatocellular disease ○ 25 x Normal Value may be seen ● Hepatocellular / Cholestatic disease ○ < 8 x Normal Value
- 29. ACUTE VIRAL HEPATITIS Hepatitis A IgMAntibody Assay Hepatitis B Surface Antigen (HbSAg) Anti- HbC IgM Assay Hepatitis C Viral RNA test Hepatitis E IgM Antibody Assay Done depending on the circumstances Not Use full in Acute Hep C Takes 6 weeks to Positive EBV CMV Hep D WILSONS Ceruloplasmin Level Autoimmune Hepatitis ANA Anti - SMooth muscle Antibody
- 30. Drug Induced Predictable Acetaminophen Unpredictable Idiosyncratic reaction Environmental toxins VinylChloride Kava Amanita phalloides Jamaica bush tea
- 31. Cholestatic Conditions Intrahepatic Extra-hepatic USG Absence of biliary dilatation Presence of biliary dilatation ● CT ● MRCP -INITIAL DIAGNOSTIC TEST ● ERCP -GOLD STD -CHOLEDOCOLITHIASIS ● PTC ● EUS-Has comparable sensitivity to MRCP and can take Biopsy
- 33. Intrahepatic Hepatitis B Hepatitis C HepatitisA & E Alcoholic Hepatitis EBV CMV Anabolic Contraceptives Chlorpromazine Tolbutamide Primary biliary cholangitis ● Progressive destruction of interlobular bile ducts ● Anti-mitochondrial Ab Primary sclerosing cholangitis ● Fibrosis of larger bile duct ● Segmental sclerosis ● MRCP ● 75 % have inflammatory bowel disease TPN Malignancy Paraneoplastic stauffer syndrome - RCC Hodgkin,Medullary Carcinoma Thyroid Infection Sepsis Plasmodium falciparum Weil's disease - Jaundice + Renal failure + fever Other Ischemic hepatitis Heart failure - Congestion
- 35. Intrahepatic Familial forms Progressive familialintrahepatic cholestasis type 1-3 Benign recurrent cholestasis type 1&2 Benign recurrent cholestasis type 1&2 Episodic attacks of pruritus Cholestasis Jaundice - debilitating Serum bile acids = elevated GGT =Normal Doesn’t lead to chronic Liver disease Progressive familial intrahepatic cholestasis type 1-3 Begin at childhood Lead to CLD Progressive cholestasis Serum bile acids = Elevated Type 3 —> GGT = elevated
- 36. Extrahepatic Choledocolithiasis Mild right upperquadrant discomfort Cholangitis with jaundice Sepsis Circulatory collapse IgG4 associated cholangitis Responds to corticosteroids Chronic pancreatitis AIDS cholangiopathy Infection of epithelium with CMV / Cryptosporidium No jaundice Elevated ALP
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