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    DCLD

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    Anonymous uoxEU3mk
    The document provides an overview of liver cirrhosis, including: - The liver has 5 functional domains, 4 lobes, 3 vascular structures, and 2 important ligaments. - Cirrhosis is a chronic reduction in liver function characterized by poor synthetic, metabolic, and immunological functions due to vascular compromise and fibrosis. - Causes include alcoholic liver disease, viral hepatitis, genetic disorders. Complications are portal hypertension, hepatic encephalopathy, and liver failure. - Investigations include blood tests of liver function, imaging like ultrasound and CT, and liver biopsy. Treatment focuses on managing complications and liver transplant for end-stage disease.

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    DCLD

    Uploaded by

    Anonymous uoxEU3mk
    3K views36 pages
    The document provides an overview of liver cirrhosis, including: - The liver has 5 functional domains, 4 lobes, 3 vascular structures, and 2 important ligaments. - Cirrhosis is a chronic reduction in liver function characterized by poor synthetic, metabolic, and immunological functions due to vascular compromise and fibrosis. - Causes include alcoholic liver disease, viral hepatitis, genetic disorders. Complications are portal hypertension, hepatic encephalopathy, and liver failure. - Investigations include blood tests of liver function, imaging like ultrasound and CT, and liver biopsy. Treatment focuses on managing complications and liver transplant for end-stage disease.

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    ,lkk

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    The document provides an overview of liver cirrhosis, including: - The liver has 5 functional domains, 4 lobes, 3 vascular structures, and 2 important ligaments. - Cirrhosis is a chronic reduction in liver function characterized by poor synthetic, metabolic, and immunological functions due to vascular compromise and fibrosis. - Causes include alcoholic liver disease, viral hepatitis, genetic disorders. Complications are portal hypertension, hepatic encephalopathy, and liver failure. - Investigations include blood tests of liver function, imaging like ultrasound and CT, and liver biopsy. Treatment focuses on managing complications and liver transplant for end-stage disease.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    3K views36 pages

    DCLD

    Uploaded by

    Anonymous uoxEU3mk
    The document provides an overview of liver cirrhosis, including: - The liver has 5 functional domains, 4 lobes, 3 vascular structures, and 2 important ligaments. - Cirrhosis is a chronic reduction in liver function characterized by poor synthetic, metabolic, and immunological functions due to vascular compromise and fibrosis. - Causes include alcoholic liver disease, viral hepatitis, genetic disorders. Complications are portal hypertension, hepatic encephalopathy, and liver failure. - Investigations include blood tests of liver function, imaging like ultrasound and CT, and liver biopsy. Treatment focuses on managing complications and liver transplant for end-stage disease.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 36
    At a glance
    Powered by AI
    The key takeaways are the functional domains, lobes, vascular structures, ligaments and biliary tree of the liver.

    The main functional domains of the liver are synthetic, metabolic, vascular, immunological and biliary.

    The main vascular structures that supply the liver are the hepatic portal vein, hepatic artery and hepatic veins.

    Tim Badcock

    FY1 Colorectal surgery


    21/10/13
    Plan
    • Introduction to the liver
    • Definition
    • Clinical Scenario
    • Presentation
    • Aetiology
    • Complications
    • Investigations
    • Management
    • Prognosis
    Introduction to the liver
     5 Functional
    domains
     4 lobes
     3 vascular
     2 important
    ligaments
     1 Biliary tree
    5.Domains
    • Synthetic
    – Albumin
    – Clotting factors (1972)
    • Metabolism
    – CYP350 drugs
    – Gluconeogenesis/glycogenesis/glycogenolysis
    – Homeostasis
    – Iron, copper, vitamin K
    • Vascular
    • Immunological
    – Kuppfer cells beside sinusoids
    • Biliary tree
    – Bilirubin
    – Left/right hepatic = common hepatic duct
    – Common hepatic + bile duct = common bile duct
    – Common bile duct + pancreatic duct
    4. Lobes
     Left
     Right
     Caudate
     Quadrate
    3. Vascular structures
     Hepatic portal vein (80%)
     Hepatic artery (18%)
     Hepatic vein (2%)
    2. Ligaments
     Falciform (developmental structure of liver, umbilical
    vein)
     Venosum (ductus venosus)
    1. Biliary tree
    2
    3
    4
    1
    5
    6

    7
    8
    9
    Definition
    • Acute/chronic, organ system, key characteristics
    • A chronic reduction in hepatic function characterised
    by poor synthetic, metabolic, and immunological
    functions and vascular compromise associated with
    ascites and portal hypertension.
    • Also associated with acute decompensation events
    characterised by acute haemorrhage, severe abdominal
    infection, neurological impairment and oedema
    Timing
     Hyperacute (<1week)
     Acute liver failure (7-28 days)
     Fulminant liver failure
    (1 month-6 months)
     Chronic (>6 months)
    Presentation
    • Synthetic
    – Albumin – ascites, infection
    – Clotting - variceal bleed, haematemesis, meleana
    • Metabolism
    • Bilirubin – jaundice
    • CYP450 drugs – variable INR, toxicity
    • ODEVICES = inhibitor
    • PCBRAS – inducer
    • Hepatic encephalopathy
    • Hypoglycaemic
    • Hormones – high oestrogen
    • Syndromes
    Syndromes
     Autoantibodies against hepatocytes. Often young women with
    other autoimmune conditions. RUQ pain and jaundice
     α1- antitrypsin deficiency (early severe fibrosis)
     Primary biliary cirrhosis (AMA, young women autoimmune)
     Primary sclerosing choloangitis (ANA,
     Haemochromatosis – early onset jaundice, bronze diabetes
     Wilson’s disease – Keyser-Flescher, serum caeruloplasmin
     Gilbert Syndrome (UDP glucoronyl transferase, early mild
    jaundice)
     Crigler Nijjar syndrome (severe early, kernicterus)
    Presentation
     Vascular
     Hepatomegaly (RUQ pain)
     Splenomegaly
     Haematesis (oesophageal varices)
     Meleana
     Immunological
     Spontaneous bacterial peritonitis
    Biliary tree
     Jaundice
     Pre-hepatic (dark
    stools)
     Hepatic (dark urine,
    normal/pale stools)
     Obstructive (dark urine,
    pale stools)

    Urobilinogen/
    stercobilinogen
    Signs
    Aetiology
    • Alcoholic liver disease
    • Non-alcoholic fatty liver disease
    • Viral liver disease
    • Primiary biliary sclerosis, Primary sclerosing
    cholangitis, Wilson’s, HH etc
    • Hepatocellular Carcinoma (rare, UC)
    • Metastasis (common)/ Pancreatic cancer (rare)
    • Cryptogenic Liver Cirrhosis
    Pathophysiology
     Chronic inflammatory (swelling, fatty infiltraton,
    cytoplasm granulation)
     Eosinophil and macrophage invasion
     Lytic necrosis
     Fibrosis and contracture
     Loss of liver architecture
     Sinusoids
     Acinii
     Portal triad
    Alcoholic fatty liver disease
     High calorie intake in alcohol
     Fat droplets deposit in hepatocytes
     Ethanol directly affects cell membrane stability as does
    aldehyde
     Chronic necrosis of cells with fibrosis

     Later becomes small cirrhotic liver


    Non-alcoholic fatty liver disease
     5% population, asymptomatic
     Seen on US abdo/biopsy

     Diabetes Mellitus
     Metabolic syndrome (HTN, hypercholesteraemia,
    diabetes)
     Pregnancy (high oestrogen)
     Idiopathic

     Oxidative stress and steatohepatitis


    Hepatitis B & C
    Hepatitis B Hepatitis C
    Virus DNA RNA
    Spread Blood, sexual Blood
    Presentation Fever, malaise, anorexia, nausea, arthralgia, Usually asymptomatic early on
    jaundice, RUQ pain
    Investigation See below. Biopsy Anti-HCV, HCV DNA. Biopsy.

    % Chronic 5-10% 85%


    Treatment Supportive. Chronic: antivirals (nucleoside Nucleoside analogues, protease inhibitors
    analogues). Transplant (anti-retroviral). Liver transplant

    HbcAg = core antigen = replicating


    HBeAg = pre-core antigen = current infection
    HBsAg = surface antigen = acute/chronic
    HBV DNA = infectious

    Anti-HBc = active infection


    Anti-HBe = latent infection if HBeAg +ve
    vaccinated if HBeAg -ve
    Complications
     Portal hypertension
     Diabetes
     Spontaneous bacterial peritoneal
     Hepatic encephalopathy
     Liver transplant
     Malnutrition
     Renal failure
    Portal hypertension
     Oesophageal varices (azygous veins)
     Rectal varices (inferior rectal veins)
     Caput medusae (umbilical veins)
     Budd-Chiari syndrome (hepatic vein thrombosis)

     TIPSS (transjugular intrahepatic portosystemic shunt)


     OGD +/- Variceal banding, stent, sclerotherapy
     Massive haemorrhage protocol
    Diabetes
     Poor glucose storage
     Bronze diabetes

     Diabetic therapy
     Dietary modification
    Spontaneous bacterial peritoneal
     8% ascites
     Severe abdominal pain
     Severely unwell

     Ascitic tap
     Peritoneal lavage
     Intravenous antibiotics
     Liver transplant
    Hepatic encephalopathy
     Increased ammonia from bacterial activity on protein in faeces
     Liver bypass (TIPSS)
     Haemorrhage

     Foetor hepaticus
     Hepatic flap (asterix)
     Decreased mental capacity e.g. Constructional apraxia

     West Haven Criteria


     Grade I altered mood/behaviour
     Grade II reduced consciousness
     Grade III Stupor
     Grade IV Coma

     Enemas, lactulose, niacin, IV fluids


    Liver transplant
    End stage liver failure
    SBP
    Congenital syndromes

    Strict criteria for transplant

    Long term immunosuppresants (azathioprine,


    ciclosporin)
    Avoid alcohol
    Malnutrition
     Encourage highest possible protein intake
     High calorie intake
     Avoid alcohol
     Chlordiazepoxide
     Acamprosate
     Disulfiram
    Renal failure
     Increased vascular pressure from portal hypertension
    into splenic and renal veins
     Diabetic nephrotic syndrome – minimal change
     Hepatorenal syndrome – low oncotic pressure triggers
    peripheral hypovolaemia, neuropepetide Y and RAAS
    activation leads to constriction of afferent and
    dilatation of efferent arterioles leading to renal
    hypoperfusion
    Investigations
     Biological
     Bedside
     Bloods
     Imaging
     Special
     Psychological
     Alcohol addiction
     Depression
     Social
     Unemployment
     Supportive housing
    Biological • Imaging
     Bedside
     Observations (BP, pyrexia, BM) • US Abdomen
     ECG • CT abdomen
     ABG • CT angiography
     GCS/West Haven
    • CXR
     Bloods
    • ERCP
     FBC (anaemia, WCC)
    • Special
     U&Es (urea, creatinine)
     LFTs (all important) • Drugs e.g. paracetemol
     Clotting (intrinsic and extrinsic) • OGD (varices)
     CRP (infective) • Hepatitis screen/leptospirosis
     Cholesterol (fatty) • Ascitic tap
     HbA1c
    • Liver biopsy (cancer, severity)
     Gamma GT (alcohol)
    • PET scan (mets)
     Antibodies
    • Colnoscopy (ulcerative colitis)
    Liver function tests
     Total protein = albumin + globins
     Albumin – long term synthetic
     Bilirubin – bile production/retention, Gilberts/Crigler
    Nijjar, Sickle cell, Iatrogenic - carbimazole
     ALP – bile duct inflammation + bone + hyperoestrogenic
    states, drugs
     ALT – hepatocyte inflammaion + thyroid dysregulation +
    coeliac + exercise

     Clotting – INR, APTT


     Extras – amylase, gGT, paracetemol (NAC)
    Acute Management
    Personal • Hepatic encephlopathy –
     Alcohol abstinence laxatives, antibiotics, IV fluids
     Fluid restriction (avoid NaCl), mannitol
     10% dextrose infusion/sliding scale • SBP – antibiotics e.g. tazocin
     Raise head of bed Surgical
    Medical • TIPSS
     Jaundice – urseodoexycholic acid , • Peritoneal lavage/ascitic tap
    colystyramine reduces pruritus
     Alcohol complications - Pabrinex
    (IV/PO), chlordiazepoxide
     Ascites – Diuretics, Paracentesis, NG
    feeding
     Ulceration – omeprazole
     Bleeding – vitamin K/octaplex
     Wilsons’s - penicillamine
    Chronic management
    Personal Surgical
     Alcohol abstinence • TIPSS
     Optimise nutrition • Liver transplantation
     Low salt diet

    Medical
     Jaundice – urseodoexycholic acid ,
     Ascites – Diuretics
     Hepatic encephlopathy – laxatives,
     Autoimmune – steroids
     Renal failure - Haemodialysis
     Rastionalise pharmacy
     Omeprazole
    Prognosis
     5 year survival rate is 50%
     Post-transplant 5 year survival 65%
    References
     Kumar and Clarke, Clinical Medicine
     Oxford Clinical Handbook of Medicine
     Washington Hepatitis Study
     NICE guidelines albumen dialysis
     NICE guidance living donor liver transplant
     Review article: the modern management of hepatic encephalopathy by Bhajaj
     Netters anatomy
     Child-Pugh scoring article by Child and Pugh
     BMJ learning – liver disease module
     Doctors
     Consultant S Ramcharan, M Osborne, Dr Gelsthorpe
     Reg. K McArdle, J. Barnes
     SHO T. Nash
    THANK YOU
     Any questions?

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