Jaundice and hepatomegaly.docx

1、Jaundice and hepatomegaly Jaundice and hepatomegaly 3.6 Jaundice and hepatomegaly 3.6.1 Distinguish between pre hepatic, hepatic and post-hepatic jaundice on clinical and biochemical grounds The basic cause of jaundice is production of bilirubin at a rate faster tha the liver can conjugate it. Prehe

2、patic Free (unconjugated) bilirubin is present in the blood at much higher concentrations. The liver works much harder than normal but cannot keep up enough to fully conjugate all the bilirubin the amount of unconjugated bilirubin remain high. The excess (above normal) amounts of conjugated bilirubi

3、n pass along the bile canaliculi and ends up as urobiligen in the gut. From here it is changed into water soluble urobilinogen (by bacteria) which is reabsorbed into the plasma and passed through the kidnet and into urine. Urobilinogen has no colour. Unconjugated bilirubin is not water soluble and s

4、o cannot be excreted in urine. Post-hepatic there is a fault or blockage somewhere downstream of conjugation. Conjugated bilirubin from the liver cant get to the gut (for example, because the bile duct is blocked), so spills over into the bloodstream. Conjugated bilirubin is water soluble, and can h

5、ence pass via the glomerulus into the urine, giving it a characteristic dark colour. Meanwhile, the drop in gut bilirubin leaves less substrate for bacteria so little or no urobilinogen can be formed; consequently none is found in the urine, and little stercobilin can be made. Cholestasis therefore

6、leads to pale stools and dark urine. Hepatic Damage to the hepatocytes themselves results in a mixed picture. Early on in the disease both types of bilirubin contribute to the jaundice, but as the disease progresses cholestasis often supervenes and conjugated hyperbilirubinaemia becomes the dominati

7、ng feature. In summary Pre-hepatic(Haemolytic) Dark Stool Haemoglobin Reticulocytosis N N N None N / Hepatic(toxins, infections)Post-hepatic(Cholestatic) Dark urine Pale stool N N / / None Clinical FBC LFT Unconjugated bilirubin Conjugated bilirubin ALP ALT Urine Bilirubin Urobiligen Tests: urine, F

8、BC, UE, LFT, Serology (HAV, HBV, HCV, EBV, CMV), clotting, blood film, reticulocyte count, Coombs test (used in the investigation of haemolytic anaemia. A positive Coombs test is found in cases of autoimmune haemolysis due to the presence of IgG, complement or both, on the surface of the patients re

9、d cells). Specific tests: serum copper ceruloplasmin ( in Wilsons), serum 1 antitrypsin, serum iron and TIBC ( in haemochromatosis) Imaging: USS, ERCP, MRCP, CT, Liver biopsy / N / N / N 3.6.2 Distinguish between infectious and mechanical causes of biliary obstruction; 3.6.3 Initiate appropriate inv

10、estigations for biliary obstruction Mechanical Gallstones Cancer head of pancreas Cancer hepatic Cancer cholecystic Strictures PSC Strictures PBS Infectious Cirrhosis - viral CT/ MRI 3.6.4 Distinguish the common causes of hepatomegaly on clinical grounds Cirrhosis Cardiac failureEarly Generally regu

11、lar surface No jaundice Late Generally irregular surface With jaundice Other causes: hepatitis, other infection, sarcoid, haemochromatosis, fatty liver, Riedels lobe, biliary tract disease 3.6.5 Initiate appropriate investigations for hepatomegaly CT / MRI FBC (with blood film) CXR / AXR ESR, UE, LF

12、T, Ca2+ InvestigationsLFTs: ALP in PSC CRP/ESR: in PSC / PBH WCC: in infection Serology: HAV, HBV, HCV, EBV, CMV USS: gallstones, cancer, cirrhosis ERCP / MRCP: strictures Secondary metastases Generally irregular No jaundice Generally regular No jaundice Tense, tender liver Peripheral oedema Increas

13、ed JVP Biopsy 3.6.6 Recognise the manifestations of chronic liver disease including encephalopathy and portal hypertension Liver Function albumin coagulation proteins Bile Complement oestrogen Ammonia urea Gluconeogenesis (amino acids glucose) Storage of glucose as glycogen Glycogenolysis Portal hyp

14、ertension A rise in pressure within the portal vein and its tributaries. Resultant from increased resistance to portal blood flow caused by cirrhosis: perisinusoidal collagen deposition, perivenular fibrosis, expansion of nodules. Consequences include porto-sytemic shunting in which some blood bypas

15、ses the liver through anastomoses with systemic circulation vessels this occurs at three sites: Between systemic and portal veins oesophageal vein and left gastric vein rectal/inferior rectal veins and superior rectal vein small epigastric v of anterior abdo wall and paraumbilical *Bleeding from thi

16、s site may occur through the rupture of delicate engorged vessels by eating this may result in haematemesis, melaena or death. Other results of portal hypertension: Ascites (can also be caused by congestive heart failure, malignancy or trauma) Transudate vs Exudate: A transudate is a fluid containing 25 mg of protein per ml of water. An exudate contains more than this. Transudates are typically caused by