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Jaundice and Hepatomegaly

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Jaundice and Hepatomegaly

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    1. Jaundice and Hepatomegaly Dr Mark A Aldersley Consultant Hepatologist UHCW NHS Trust

    2. Jaundice and Hepatomegaly Jaundice Hepatomegaly

    3. Hepatomegaly Common Causes: Congestive Cardiac Failure Cirrhosis (although end-stage typically small) Secondary cancers (liver metastases)

    4. Hepatomegaly Other Causes: Infections (Hepatitis A, B and C, EBV, amoebic abscess) Primary Tumours (Benign and malignant) Lymphoproliferative disorders Primary Biliary Cirrhosis Haemochromatosis

    5. Hepatomegaly Other Causes: Sarcoid Amyloid Hydatid Cyst Budd-Chiari Riedel’s Lobe Emphysema (apparent hepatomegaly)

    6. Hard and Knobbly Hepatomegaly Malignancy (Primary or Secondary) Polycystic Disease Macronodular Cirrhosis Hydatid Cysts Syphylitic Gummas

    7. Hepatosplenomegaly Myeloproliferative Disorders Lymphoproliferative Disorders Cirrhosis and Portal HT

    8. Hepatosplenomegaly and palpable Lymph Nodes Chronic Lymphocytic Leukaemia Lymphoma Others EBV, sarcoid

    9. Hepatosplenomegaly-other causes Brucellosis Weil’s Disease Toxoplasmosis CMV Storage Disorders (Gaucher’s) Amyloid Polycystic Disease

    10. Hepatosplenomegaly-other causes on worldwide basis Malaria Kala-azar Schistosomiasis

    11. Jaundice Investigation Liver Function tests Imaging techniques

    12. Jaundice Pre-hepatic Hepatic Post-hepatic

    13. Jaundice Pre-hepatic Haemolysis Gilbert’s Syndrome

    14. Jaundice Hepatic Hepatitis Alcohol Cholestatic liver disease Genetic Haemochromatosis Wilsons Alpha 1 Anti-trypsin deficiency

    15. Table 2-1. Human hepatitis viruses. The five known agents of viral hepatitis belong to distinct, and unrelated, classes of viruses. Four of the five viruses (hepatitis A virus 'HAV', hepatitis C virus 'HCV', hepatitis D virus 'HDV', and hepatitis E virus 'HEV') are RNA­containing viruses whereas the fifth virus, hepatitis B virus (HBV), is a DNA­containing agent. The two nonenveloped agents, HAV and HEV, are characteristically transmitted through enteric routes of spread, and neither is associated with a carrier state of chronic hepatitis. In contrast, the enveloped viruses (HBV, HDV, and HCV) may lead to persistent infection and chronic hepatitis. HBsAg­hepatitis B surface antigen. Table 2-1. Human hepatitis viruses. The five known agents of viral hepatitis belong to distinct, and unrelated, classes of viruses. Four of the five viruses (hepatitis A virus 'HAV', hepatitis C virus 'HCV', hepatitis D virus 'HDV', and hepatitis E virus 'HEV') are RNA­containing viruses whereas the fifth virus, hepatitis B virus (HBV), is a DNA­containing agent. The two nonenveloped agents, HAV and HEV, are characteristically transmitted through enteric routes of spread, and neither is associated with a carrier state of chronic hepatitis. In contrast, the enveloped viruses (HBV, HDV, and HCV) may lead to persistent infection and chronic hepatitis. HBsAg­hepatitis B surface antigen.

    16. Jaundice Post-hepatic Common bile duct stones Pancreatic cancer Cholangiocarcinoma Liver metastases

    18. Jaundice History Alcohol Drugs Weight Gain/Diabetes Blood Transfusion Past History IV Drug Use High risk sexual behaviour Complications of Chronic Liver disease Weight loss Appetite loss Abdo pain Fever

    19. Jaundice Examination Skin Palmar erythema Leuconychia Injection sites and tattoos Spider Naevi Eyes Nodes Liver Flap/Confusion

    20. Jaundice Examination Abdo exam: Ascites, Liver Spleen Abdo mass Caput medusa Peripheral oedema

    21. Investigations Blood Tests USS CT Scan MRI Scan ERCP MRCP EUS Liver Biopsy

    39. Other Investigations for Jaundice

    47. Large CBD Stones

    51. Endoscopic Ultrasound

    52. Summary Discussed causes of Hepatomegaly and Jaundice History features Examination features Basic investigations

    53. CASE STUDY JAUNDICE

    54. Presenting Complaint 61yr old retired lady Presented with:- Severe epigastric pain Jaundice Pale stools Dark urine Pruritus

    55. History of Presenting Complaint Pain radiated into back No alleviating/exacerbating factors Recent diarrhoea and nausea Loss of appetite Generally feeling unwell

    56. Relevant History No known risk factors for jaundice Non-smoker Moderate alcohol intake NKDA Previous breast fibroadenoma Divorced

    57. Examination Vital signs normal Abdomen soft and non-distended No masses felt -ve Murphy’s sign Non palpable gall bladder Systems review normal

    58. Analysis Obstructive jaundice No signs of chronic liver disease Possible diagnosis:- Gallstones Peri-ampullary carcinoma

    59. Investigations and Results FBC, U + E’s, BM ECG, CXR, AXR Elevated total bilirubin 116µML-1 Raised ALT and Alk Phos INR and albumin levels normal Elevated CA19-9

    60. Imaging USS:- Dilated CBD and gallbladder No gallstones Focus in head of pancreas CT:- Attenuation area in pancreas head and uncinate process

    61. Management Pain relief Piriton Vitamin K Whipple’s procedure:- Gastrectomy/duodenectomy Pancreatectomy Cholecystectomy

    62. Histology Ductal adenocarcinoma of pancreas Local lymph node involvement No distant metastases Completely excised at all margins

    63. Post Surgery Jaundice disappeared Referred to dietician and cancer outreach team Discharged home 5 month follow up found:- Raised CA 19-9 Recurrent tumour encasing SMA Liver metastases

    64. Case Study: Hepatomegaly Mr A.H. 42 year old

    65. Presenting complaint Low Hb on recent blood test

    66. PMH – Admitted 10.2002 2 wk bleeding paraumbilical pustule bleeding gums swollen abdomen & ankles ? appetite; weight loss; nausea pruritis ? lethargy, weakness

    67. Social history Hx depression Recently divorced 25 yrs hx drinking at least 50 units per week smoking 20-40 cigarettes per week

    68. Hepatomegaly: Causes Likely causes: Other causes:

    69. Examination findings Gaunt appearance Alopecia Yellow sclera Raised JVP (+6-8cms) Spider naevi over neck & upper chest Tender abdomen; guarding? no other masses Paraumbilical scar Hepatomegaly (~3-4cm) Splenomegaly

    70. Investigations Blood tests (FBC, U&Es, LFTs) Abdominal U/S Gastroscopy Sigmoidoscopy?

    71. Significant Results Blood tests ?Hb, albumin; ?bilirubin, INR, Alk Phos Abdominal U/S irregular echogenic pattern ? cirrhosis Gastroscopy “barely noticeable” oesophageal varices

    72. Case Presentation A 75 year old woman presents with increasing jaundice. Her relatives have noticed very dark urine. How will you proceed? Causes? History and Examination? Investigation?

    73. Case Presentation Mrs HY is a 35 year old woman who presents to her GP with a 4 week history of tiredness and an ache in the right upper quadrant of the abdomen. Her GP finds a 5cm enlarged liver on examination and refers her to outpatients. Causes? History and Examination? Investigation?

    74. Figure 9-4. U.S. alcoholic cirrhosis mortality rates. Cirrhosis mortality in the United States between 1900 and 1957 compared with death from all causes per 100,000 population. Mortality rates from cirrhosis significantly dropped off during Prohibition and returned to previous levels after Prohibition was repealed [6]. Subsequently, the mortality rate reached 15/100,000 in 1973, and further decreased to 9.1/100,000 by 1988. This decrease paralleled a significant decrease in per capital alcohol consumption during the same period. Despite these decreasing trends, the mortality from alcoholic cirrhosis is still 20% over the mortality rate in the 1950s. References: [6]. Martini GA, Bode CH, In Alcoholic Cirrhosis and Other Toxic Hepatopathies. Edited by Engel A, Larrson T. Stockholm: Nordiska Bokhandelns Forlag; 1970 315-Figure 9-4. U.S. alcoholic cirrhosis mortality rates. Cirrhosis mortality in the United States between 1900 and 1957 compared with death from all causes per 100,000 population. Mortality rates from cirrhosis significantly dropped off during Prohibition and returned to previous levels after Prohibition was repealed [6]. Subsequently, the mortality rate reached 15/100,000 in 1973, and further decreased to 9.1/100,000 by 1988. This decrease paralleled a significant decrease in per capital alcohol consumption during the same period. Despite these decreasing trends, the mortality from alcoholic cirrhosis is still 20% over the mortality rate in the 1950s. References: [6]. Martini GA, Bode CH, In Alcoholic Cirrhosis and Other Toxic Hepatopathies. Edited by Engel A, Larrson T. Stockholm: Nordiska Bokhandelns Forlag; 1970 315-

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