Presentation on theme: "glycogenolysis & gluconeogenesis"— Presentation transcript:
1 glycogenolysis & gluconeogenesis Catabolism of hormonesand other serum proteinsGlucose homeostasis;glycogenolysis & gluconeogenesisChronic Liver DiseaseSynthesis:AlbuminCoagulation factorsStorage:GlycogenIronCu, Iron, vitaminsBile excretionKatharine Brown
2 Objectives Causes and management of chronic liver disease Management of an UGI BleedKey features of less common types of chronic liver disease
3 A patient case…54 year old gentleman presents to his GP with increasing swelling of his abdomen and feet over the last 2 months. He has been increasing tired over this time and feels nauseous and is off his food. His wife has commented that his eyes have turned yellow over the last few days. He works in a warehouse and smokes 10 cigarettes a day. He admits to drinking 4 cans of lager a night. His wife says he drinks at least 8 cans a night and a bottle of whisky a week.On examination he is jaundiced but has no hepatic flap and is orientated in time, place and person. His abdomen is distended but soft and non-tender. There is no palpable organomegaly but there is shifting dullness.What are your main differential diagnoses for this gentleman?
4 Differential Diagnoses (Decompensated) Alcoholic liver diseaseViral liver diseaseAutoimmune liver disease, Wilson’s, HH etcHepatocellular CarcinomaPancreatic CancerCryptogenic Liver CirrhosisWhat further history would be needed?What signs would you look for on examination?
7 What is your management plan? ConservativeAlcohol abstinence, optimise nutrition, low salt diet, fluid restrictionMedicalVitamin B supplementation (IV/PO), chlordiazepoxideDiureticsParacentesis (give albumin)NG feedingAntibiotics (? SBP)Steroids + albumin (N.B. avoid NaCl)Lactulose (in hepatic encephalopathy)SurgicalTIPSSLiver transplantation
8 Complications of CLD Portal hypertension: oesophageal varices, ascites SBPHepatic encephalopathy (constipation, GI bleed, infection, renal failure)Hepatocellular carcinomaCoagulopathyHepato-renal syndromeLiver failure5 year survival rate in cirrhotic CLD 50%Child Pugh Score: bilirubin, INR, albumin, ascites, hepatic encephalopathy
9 Hepatic Encephalopathy Stage 1: shorted attention span, reversal of sleep-wake cycle, subtle personality changes (anxiety, irritability)Stage 2: lethargy, personality change, disorientation. Asterixis.Stage 3: stupor but responsive, severe confusion and disorientation, abnormal behaviour, incomprehensible speechStage 4: coma
12 Hepatitis B & C Hepatitis B Hepatitis C Virus DNA RNA Spread Blood, sexualBloodPresentationFever, malaise, anorexia, nausea, arthralgia, jaundice, RUQ painUsually asymptomatic early onInvestigationSee below. BiopsyAnti-HCV, HCV DNA. Biopsy.% Chronic5-10%85%TreatmentSupportive. Chronic: antivirals (nucleoside analogues). TransplantNucleoside analogues, protease inhibitors (anti-retroviral). Liver transplantHBV DNA = infectiousHBsAg = currently infectedAnti-HBs + Anti-HBc = past infectionAnti-HBs alone = vaccinated
13 Autoimmune Hepatitis Autoantibodies against hepatocytes Young/middle age, mainly womenPresentation: jaundice, RUQ pain, systemic symptomsMay be associated with other autoimmune conditionsInvestigations- Type 1: anti-smooth muscle antibodies (80%), anti-nuclear antibodies (10%)- Type 2 (children): anti-liver/kidney microsomal type 1 antibodies- Liver biopsyRx: immunosuppressant's (steroids, azathioprine), transplant
14 PBC and PSC Primary Biliary Cirrhosis Chronic granulomatous inflammation of interlobular bile ductsAutoimmune: anti-mitochrondrial antibody (98%)Associated with other autoimmune conditionsF:M 9:1, 50 y/oPrimary Sclerosing CholangitisInflammation, fibrosis and strictures (‘beading’)of intra and extra-hepatic bile ducts? Autoimmune: ANCA (80%)Associated with IBD20-30% develop cholangiocarcinoma
15 Wilson’s & α1AT Deficiency Wilson’s DiseaseAR defect in copper transporting ATPaseCopper accumulates in liver + CNS +Kayser-Fleischer ringsRx: penicillamine, transplantAlpha-1 Antitrypsin DeficiencyAR deficiency of α1ATSerine protease inhibitor produced by liverEmphysema + liver damage + HCC
17 SummaryAlcoholic liver disease is the most common type of CLDTreatment of ALD is mostly supportive with treatment of the complications; optimising nutrition and fluid balance is key.There are three autoimmune forms of CLDIn Wilson’s disease copper accumulates in the liver and CNSIn HH iron accumulates in the liver, skin, joints, pituitary, adrenals, pancreas, heart etc.Liver transplant is usually the only cure in chronic liver diseaseAny Questions?