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4 Liver, Biliary System and Pancreas 4.1 Presenting Problems 4.1.1 Jaundice Ref: Davidson P

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4 Liver, Biliary System and Pancreas 4.1 Presenting Problems 4.1.1 Jaundice Ref: Davidson P. 936, Andre Tan Ch10, JC56, GIL17, Block A TC (jaundice), Uptodate A. Physiology of Bilirubin Excretion Bilirubin: non-toxic breakdown product of heme □ Formed in reticuloendothelial system (RES) □ Two forms: → Unconjugated (indirect) bilirubin: - Not water soluble → bound to plasma protein - Cannot be excreted directly in urine → Conjugated (direct) bilirubin: - Water soluble - Can be excreted directly in urine Hepatic handling: □ Unconjugated bilirubin taken up by hepatocytes □ Bilirubin conjugated by UDP-glucuronyl transferase □ Secreted into bile canaliculi into duodenum Enterohepatic circulation: □ Conjugated bilirubin reduced into urobilinogen by intestinal flora → 10% reabsorbed into portal circulation → secreted in kidney as urobilin → confers straw colour of urine □ Unabsorbed urobilinogen oxidized into stercobilinogen and then stercobilin → confers brown colour of faeces Features of cholestatic jaundice: □ Tea-coloured urine: excretion of conjugated bilirubin in urine (bilirubinuria) □ Pale stools: reduced stercobilin content in stools □ Pruritus: retention of bile acid in blood - Page 171 of 335 - B. Causes of Jaundice Pre-hepatic Hepatic Post-hepatic Suggestive - Lemon yellow jaundice - Yellow jaundice - Greenish jaundice features - Dark stools (↑stercobilin) - Normal stools - Pale stools - Normal urine - Tea-coloured urine - Tea-coloured urine - Pruritus ± scratch marks LFT - ↑unconj. bilirubin - ↑conj. bilirubin - ↑conj. Bilirubin - AST/ALT normal - ↑↑↑AST/ALT - ↑AST/ALT - ALP/GGT normal (AST>ALT = toxins) - ↑↑↑ALP/GGT (ALT>AST = viral) - Albumin normal - Albumin normal - ↑ALP/GGT - ↓albumin (if subacute) Causes Haemolytic anaemia Acute liver injury Cholangitis/RPC - Congenital: - Viral hepatitis: A, B, E Choledocholithiasis Membrane - Alcoholic hepatitis Malignant biliary (spherocytosis) - Drug-induced hepatitis obstruction (MBO) Metabolic (G6PD) - Autoimmune hepatitis - Cholangiocarcinoma: hilar Hb (thalassaemia) Chronic liver disease (Klatskin tumour), CBD - Acquired: - Viral hepatitis: B, C - LNs: HCC, gallbladder, lymphoma, stomach Immune (auto-, allo-, - Alcoholic liver disease drug-induced) - Non-alcoholic fatty liver - CA head of pancreas - CA ampulla or duodenum Fragmentation disease (microangiopathic) - Metabolic: Wilson’s disease, Benign strictures haemochromatosis, Infection (parasitic, - Post-ERCP α -antitrypsin deficiency bacterial) 1 - Stones, chronic pancreatitis - Autoimmune: autoimmune Drugs and toxins hepatitis Other obstruction Congenital causes - HCC - Mirizzi syndrome - Gilbert syndrome Congenital causes - Choledochal cyst - Crigler-Najjar syndrome - Dubin-Johnson syndrome - Biliary atresia (very rare) - Rotor syndrome Medical causes - PBC - PSC - Intrahepatic cholestasis Ix CBC with reticulocyte Clotting profile U/S of HBP Peripheral blood smear AFP ERCP/MRCP if dilated LDH, haptoglobin Hepatitis serology: biliary system Direct Coomb’s test Acute: anti-HBc + anti-HAV IgM Contrast CT abdomen Chronic: HBsAg, anti-HCV if highly likely to be MBO Autoimmune panel: Autoimmune panel ± liver ANA, anti-smooth muscle, biopsy if no dilated biliary anti-LKM1 (for AI hepatitis) system Metabolic screen: AMA for PBC Cu: ceruloplasmin, 24h urine Cu p-ANCA for PSC (if segmental Fe: iron profile dilatation on ERCP) Abdominal USG: Cirrhosis, splenomegaly, ascites *Cannot distinguish between hepatic vs post-hepatic by direct:indirect ratio (both ~2:1). - Page 172 of 335 - C. Approach to Jaundice 1. History Is it truly jaundice? – r/o other causes of yellow skin □ Inspect the mucous membrane of sclera, mouth, palms and soles under natural light → Protected from the sun → minimizes photodegradation of bilirubin □ Other causes of yellow skin: → Diet: consumption of large quantity of food with lycopene or carotene139 → Drugs: rifampicin, quinacrine, TCMs Is it conjugated or unconjugated hyperbilirubinaemia? □ Conjugated (direct): → Tea-coloured urine → Pale stools → Pruritus ± scratch marks □ Unconjugated (indirect): none Is it hepatic jaundice? Hepatic causes of jaundice: □ Chronic liver disease: Hx of chronic liver disease and its All medical doctors aren’t very happy complications Alcohol, Metabolic, Drugs, □ Alcoholic: Hx of alcohol abuse Autoimmune, Virus, HCC □ (Metabolic) □ Drugs: recent drug Hx, TCM intake □ (Autoimmune: Hx of autoimmune diseases) □ Virus: → Feco-oral (A/E): travel Hx, ingestion of seafood → Blood-borne (B/C): hep B/C status, FHx of hepatitis and HCC, blood transfusion, risk factors for blood-borne transmission (transfusion, IVDU, needle stick injury, MSM) □ (HCC): usually late with replacement of hepatic parenchyma (unless underlying cirrhosis) or compression of bilateral bile ducts or porta hepatis LN mets Is it post-hepatic jaundice? □ Cholangitis: → Charcot’s triad: jaundice, fever, RUQ pain → Reynold’s pentad: jaundice, fever, RUQ tenderness, hypotension, confusion → Past episode (recurrent pyogenic cholangitis) □ Choledocholithiasis (CBD stone): → Episodic, painful jaundice in young individuals → Biliary colic symptoms: episodes of severe RUQ pain → Hx of gallstone diseases, past surgery, ERCP □ Malignant biliary obstruction: → New onset, painless, progressive jaundice in old individuals → CA pancreas: constant, dull, boring epigastric pain radiating to back (usually late feature) → Constitutional symptoms: LOA, LOW, malaise → Metastatic symptoms: bone pain, dyspnoea, neck lump □ Post-ERCP jaundice 139 Lycopene = 茄紅素. Carotene = 胡蘿蔔素. - Page 173 of 335 - Are there any complications? □ Liver decompensation: encephalopathy, hepatic fetor, worsening ascites □ Acute pancreatitis: abdominal pain radiating to the back with nausea and vomiting → Due to stone disease □ Fat malabsorption: → Steatorrhoea: fatty, loose stools (floaters) → Vitamin deficiency (A, D, E, K): coagulopathy 2. Physical Examination General examination □ Vitals: fever, haemodynamic stability □ General inspection: jaundice, distension, ankle oedema □ Specific signs: xanthomata (PBC), Kayser-Fleischer rings (Wilson’s disease), hyperpigmentation (haemochromatosis) Abdominal examination □ Scars: previous HBP surgeries □ Stigmata of chronic liver disease: ascites, caput medusae, gynaecomastia □ Generalized distension: ascites can be due to malnutrition, peritoneal malignancy, malignant portal vein obstruction □ Palpable masses: → Hepatomegaly: primary liver tumour, metastatic disease, biliary obstruction (usually mild) → Enlarged palpable gallbladder: indicates MBO if a/w painless jaundice → Splenomegaly: portal hypertension Digital rectal examination for pale stools Metastatic screen: LNs, bony tenderness, respiratory examination D/dx of epigastric mass + jaundice can be: □ Hepatomegaly (mild) due to biliary obstruction □ Hepatomegaly due to metastasis or HCC □ LN metastasis to coeliac axis and porta hepatis □ CA stomach with metastatic LN in porta hepatis □ Tumour obstructing both duodenum and bile duct → distended stomach + jaundice 3. Investigations Bilirubin level and type of bilirubin → conjugated vs unconjugated hyperbilirubinaemia Liver enzymes: □ Parenchymal pattern: indicates hepatocellular diseases, eg. hepatitis, cirrhosis… □ Ductal pattern: indicates obstructive jaundice □ Normal: consider possibility of prehepatic jaundice (haemolytic anaemia, Gilbert) Clotting profile: ↑INR may be due to hepatocellular dysfunction (unresponsive to vitamin K) or cholestasis (responsive to IV vitamin K) Subsequent Ix based on type of jaundice - Page 174 of 335 - 4.1.2 Malignant Biliary Obstruction Ref: Davidson P. 936, Andre Tan Ch10, JC56, Uptodate D/dx for obstructive jaundice: (red = malignant causes) Intrahepatic Extrahepatic Hepatocyte dysfunction (hepatitis of any Intraluminal cause, end-stage liver disease) CBD stones (hepatocyte dysfx → ↓excretion) Cholangitis (or RPC) Drugs: anabolic steroids, OC pills, chlorpromazine, arsenic Parasitic (eg. Ascaris lumbricoides, liver flukes) Mural Primary biliary cholangitis (A/I destruction of small ducts) Benign strictures: post-instrumentation, gallstones, No enteric intake (TPN, post-operative) chronic pancreatitis (↓CCK secretion → ↓GB contraction) Primary sclerosing cholangitis Intrahepatic cholestasis of pregnancy Sphincter of Oddi dysfunction (intermittent) (a/w ↑oestrogen levels) Cholangiocarcinoma Intrahepatic compression of bilateral Extramural bile ducts due to massive liver SOL (very uncommon) Gallbladder stone in Mirizzi syndrome Acute and chronic pancreatitis (uncommon) Carcinoma of head of pancreas Carcinoma of Ampulla of Vater or duodenum140 Porta hepatis LN (CA stomach, gallbladder, HCC) Clinical presentation: Courvoisier’s law (sign): □ Symptom: painless progressive obstructive jaundice Presence of palpable gallbladder in a → Jaundice: indicates bilirubin ≥2× ULN (~40-50) patient with painless obstructive → Stool/urinary changes: pale/clay-coloured stools jaundice is unlikely to be due to stone + tea-coloured urine (普洱茶咁深色) disease. Reason: a gallbladder that gives rise to CBD → Generalized pruritus (non-specific, not reliable) stone is likely to have been chronically □ Signs: painless enlargement of GB with jaundice inflamed leading to fibrosis and therefore (Courvoisier sign) would not be palpable. Blood tests: Exceptions: (1) Double stone (CBD + cystic duct) □ LFT showing classical obstructive pattern (2) Recurrent pyogenic cholangitis → ↑bilirubin (3) In situ CBD stones → ↑ALP (± GGT) > AST/ALT (mildly ↑) (4) Mirizzi
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