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ALL YOU NEED TO KNOW ABOUT JAUNDICE AND LIVER FAILURE Harish Bavaand BartRosiński Reviewed by Kajal Aubeeluck Here’s whatwedo: ■ Weekly tutorialsopento all! 18:00 every Thursday ■ Focussed oncore presentationsand teaching diagnostictechniquefrom a If you’re new here… clinical perspective Welcome to ■ Raccuracyby doctorsto ensure Teaching ■ We’ll keepyouupdatedabout our Things! upcoming events viaemail and groupchats!Jaundice Harish BavaWhat is Jaundice ■ Hyperbilirubinemia ■ Excessbilirubinresultsinyellow discolouration, initially oftheeyes(scleral icterus),followedby theskin ■ Normal levelsof bilirubininthebody: 3-17𝜇mol/L ■ Bilirubinlevels to causescleral icterus: >30𝜇mol/L ■ Bilirubinlevels to causeyellow discolourationof theskin: >50𝜇mol/L ■ Excessbilirubinisaresult ofimpairedexcretionor increased production – Isthen deposited intheeyes andskinNormal physiologyNormal physiology ■ RBC broken downinto globin andhaem ■ Globin isbrokendownintoamino acids – Reusedforproteinsynthesis ■ Haem broken downinto ironcomponent andbiliverdin – Ironcomponent converted into ferritin – Biliverdin convertedintounconjugatedbilirubin(non-soluble) and transported to liver – Conjugatedby glucuronicacidby enzymeuridinediphosphate (UDP)- glucuronosyl transferase – Conjugatedbilirubin (soluble)secreted into bilecanaliculus,theninto duodenum – Convertedby bacteriainto urobilinogen – Excreted inthestool asstercobilin – Excreted intheurineasurobilin(10%)Causes of Jaundice ■ Thiscanbesplit into threecategories: – Pre-hepatic jaundice – Post-hepatic jaundice (ObstructiveCholestasis)Pre-hepatic Jaundice Anythingcausingincreased breakdownred blood cells,resultinginthe release/increaseof unconjugated bilirubinin the blood causingjaundice. ■ Autoimmunehaemolyticanaemia ■ Haemolysis ■ Sickle cell disease – whenincrisis ■ G6PD deficiency ■ Thalassaemia major ■ Gilbert’s syndrome ■ Crigler-Najjar syndromePre-hepatic Jaundice ■ Autoimmunehaemolyticanaemia – Canbe‘warm’ or ‘cold’ – Warm AIHA ■ IgGantibodies causes haemolysis atbody temperature in extravascular sites such as spleen ■ Caused by autoimmune diseases, neoplasia, can be idiopathic, drugs(e.g. methyldopa) ■ Treated usingsteroids and treating underlying disorder – Cold AIHA ■ IgMantibodies causinghaemolysisat4ºC. Haemolysismediated by complementand more commonly intravascular ■ Symptoms include Raynaud’s, anddo not respondwell to steroids ■ Caused by neoplasia, and infections(mycoplasma, EBV)Pre-hepatic Jaundice ■ Haemolysis – Acutebleeding leads to increased haemolysis – Thebody does not havethecapacity to conjugateand excretethis increased level ofbilirubin – ResultsinjaundicePre-hepatic Jaundice ■ Sickle cell disease – whenincrisis ■ G6PD deficiency ■ Thalassaemia major ■ Eachof theseresult inmisshaped cells, canlead to haemolysis and increased bilirubinPre-hepatic Jaundice ■ G6PD deficiency – Deficiency ofa key enzymewithinthebloodcell involvedinthepentose phosphatepathway – Adeficiency resultsin increased susceptibility to oxidativestress – Inneonates,thiscancausejaundice – It isexacerbatedby favabeans, infectionsand sulfa- drugs (sulfasalazine,sulfonylureas,sulphonamides)Pre-hepatic Jaundice ■ Gilbert’s syndrome isa lack of the UDP-glucuronosyl transferaseenzyme resulting in aninability to conjugatebilirubin – Doesnot present withany other symptomsgated bilirubin – It canbeexacerbatedby any stress onthebody,typically exercise, fastingor intercurrent illness – Thisrequiresno treatment asit isbenignPre-hepatic Jaundice ■ Crigler-Najjar syndrome – Autosomal recessive – Resultsinabsolutedeficiency ofUDP-glucuronosyl transferaseenzyme resulting in aninability to conjugatebilirubin – Type 1 ismoreseverethantype2 ■ Type 1 do not typically survive toadulthood ■ Type 2may improve with phenobarbitolHepatic Jaundice Anythingcausinginflammation/damagetotheliver. ■ Hepatitis – Viral hepatitis – Autoimmunehepatitis ■ Alcoholic Fatty Liver Disease ■ Non-alcoholicFatty LiverDisease ■ LiverCirrhosis ■ Malignancy- hepatocellular carcinoma,cholangiocarcinoma ■ Wilson’sdisease ■ Primary sclerosing cholangitis ■ Primary biliarycholangitisHepatic Jaundice ■ Wilson’sdisease – Thisischaracterisedby excesscopper inthebody – Abuild up of copper intheliver results inhepatitis andcirrhosis,both of whichresult injaundice ■ PSC– inflammationof theintraandextrahepaticducts – 96%of PSCpatientsalso have UC ■ PBC – autoimmunereactionof thebiliary tree,mediated byAnti- mitochondrial antibodies – Early presentationis pruritusPost-Hepatic Jaundice Anythingcausingobstructiontothebileducts resulting ina buildup of conjugated bilirubinthat cannot pass out or bereabsorbed. ■ PancreaticCancer ■ Cholecystitis ■ Ascending Cholangitis ■ GallstonesPost-Hepatic Jaundice ■ Pancreaticcancer – Oneof thehardest cancers to diagnoseasit typically presents at a very – Around80% are adenocarcinomasof theheadof thepancreas – Themost commoninitial presentationispainlessjaundicewithpale stools,dark urine,and pruritus – Followingthis, patients have abdominal massesdue to metastases – Investigated using abdominal ultrasound,high-resolutionCT – Canbemanaged using a‘Whipple’sprocedure’Post-Hepatic Jaundice ■ Cholecystitis – inflammationof thegallbladderusually dueto gallstones ■ Ascending Cholangitis – bacterial infection(E.coli)of thebiliary tree – ■ RUQpainly presentswithCharcot’s triad ■ Fever ■ Jaundice ■ Gallstones ■ All thesearedisordersof thebiliary tract ■ Inflammationor obstructionof thebiliary treeresults injaundicedueto blockageof bile – Bilirubinis absorbedinto thebody instead ofbeingexcreted resulting in jaundiceHistoryand presentation ■ History: – Discolourationof skin – Pruritus – Fevers/other infectivesymptoms – RUQpain – Recent travel history/risk factorsof hepatitis – Positivealcohol history – Weight loss/night sweats – History of ulcerativecolitis ■ On examination: – Proximal myopathy – Stigmataof liver cirrhosis – spidernaevi,caput medusae,palmar erythema,gynaecomastia,Dupuytren’scontracture, ascites, – Palpable lymphnodes – RaisedJVP – Hepatosplenomegaly – AscitesHistoryand PresentationSBA Apatient ispresentingwithjaundice.What investigationswill youconsider doing? A- LFTs,serum bilirubin, ERCP,urinedip, clotting times B - LFTs,serum bilirubin, MRCP,abdominal X-ray,viral serology C- LFTs,abdominal ultrasound, viral serology, MRCP D - LFTs,serum bilirubin, clotting times,abdominal CT, MRCP,viral serology E- LFTs,serum bilirubin, clotting times,abdominal ultrasound,MRCP, viral serology,antibody screenSBA Apatient ispresentingwithjaundice.What investigationswill youconsider doing? A- LFTs,serum bilirubin, ERCP,urinedip, clotting times B - LFTs,serum bilirubin, MRCP,abdominal X-ray,viral serology C- LFTs,abdominal ultrasound, viral serology, MRCP D - LFTs,serum bilirubin, clotting times,abdominal CT, MRCP,viral serology E- LFTs,serum bilirubin, clotting times,abdominal ultrasound,MRCP, viral serology,antibody screenLFTsand Investigations ■ LFTs are important at distinguishing betweena hepaticpicturevsabiliary picture ■ AST+ ALT – ariseintheseindicatea hepaticpicture ■ ALP+ Gamma-GT– ariseintheseindicatea biliary picture ■ Serum bilirubin – indicates ariseineither conjugated or unconjugated bilirubin ■ Clottingtimes ■ Viral serologies, antibody screen,serum ceruloplasmin ■ MRCP,abdominal ultrasoundTreatment ■ Treatingjaundiceisby treatingtheunderlying pathology ■ Pr– Mild– canbe treated withwarm baths – Antihistaminescanprovide relief – For cholestasis related pruritus – bileacid sequestrantssuchas cholestyraminecanbe effective ■ Severejaundicesecondary to liver cirrhosis mayindicateevaluationforliver transplantationComplications ■ Unconjugatedbilirubin isinsolubleand is harmful to cells and cellular structures ■ Inadults, therearephysiological mechanismstoprotect against this, and therefore thereislimited toxiceffects ■ Inneonates,due to poorly developed blood-brain-barrier,highlevelsof bilirubincan beneurotoxicresulting inKernicterus – Thisisapermanent neurological injury Liver Failure Bart RosińskiNormal liver functions ■ Metabolic – Breaks down carbohydrates, fats and proteins – Drug metabolism – Conversion of glucose to glycogen – Conversion of ammonia to urea – Absorption of fat-soluble vitamins - A, D, E,K ■ Synthetic – Coagulation factors – II, VII, IX and X – Cholesterol – Albumin – Bile ■ Storage – Glycogen andsynthesisedvitamins Anatomy recap Dancygier, H. (2010). Hepatic Circulation. In: ClinicalHepatology. Springer,tps://www.hopkinsmedicine.org/health/conditions https://radiologykey.com/the-biliary-tree/ Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-93842-2_4 -and-diseases/liver-anatomy-and-functionsWhichof thefollowing best describestherole oftheliver in nitrogen metabolism? a) Conversionof ammoniainto ureafor excretion b) Direct excretionof ammoniathrough bile c) Breakdownof amino acidsexclusively in the kidneys d) Storage ofexcessnitrogeninhepatocytes e) Productionof ammoniaasa primary energy sourceWhichof thefollowing best describestherole oftheliver in nitrogen metabolism? a) Conversionof ammoniainto ureafor excretion b) Direct excretionof ammoniathrough bile c) Breakdownof amino acidsexclusively in the kidneys d) Storage ofexcessnitrogeninhepatocytes e) Productionof ammoniaasa primary energy sourceLFTs ■ AST(aspartateaminotransferase) Intrinsicenzymes – released during ■ ALT (alanineaminotransferase) hepatocellular injury ■ GGT (gamma-glutamyltransferase) Biliaryepithelial enzymes– released during ■ ALP(alkalinephosphatase) cholestasis ■ Bilirubin – ConjugatedvsunconjugatedWhich one of the following is least useful in assessing the severity of a patient with liver cirrhosis? a) ALT b) Prothrombin time c) Bilirubin d) Presence of ascites e) Presence of encephalopathyWhich one of the following is least useful in assessing the severity of a patient with liver cirrhosis? a) ALT b) Prothrombin time c) Bilirubin d) Presence of ascites e) Presence of encephalopathyAcute liver failure Inflammation Necrosis DecreaseinVolume ■ Not fibrotic Failure GetBetter ■ Acute process – often reversible ■ Onset of sx is <26w in student with previously healthy liver Symptoms ■ Look at synthetic fx in LFTs Bilirubin rise – Jaundice ■ Most often drug induced (hyperacute due to paracetamol OD) Dropped pH – TB drugs – Idiosyncratic hypersensitivity reactions Hepatic encephalopathy – Statins Renal Dysfunction Clotting pathology – Anti-epileptics – Cocaine/MDMA – ischaemic – Abx – flucloxacillin/amoxicillin– Cholestatic failure in 5% ■ Also seen in EtOH, viral hepatitis, toxin or pregnancyLeah is a 21-year-old university student who was brought in by ambulance to A&E. Her skin is yellow, and she is vomiting. She complains of abdominal pain, and says these symptoms began last night. Her LFT’s • ALT 710 U/L [3-40] • ALP 150 U/L [3-30] • Bilirubin, Albumin + INR were within the normal range What is the most likely cause? a) Alcoholic fatty liver disease b) Non-Alcoholic Fatty Liver Disease c) Paracetomol overdose d) Wilson’s disease e) Hepatitis BLeah is a 21-year-old university student who was brought in by ambulance to A&E. Her skin is yellow, and she is vomiting. She complains of abdominal pain, and says these symptoms began last night. Her LFT’s • ALT 710 U/L [3-40] • ALP 150 U/L [3-30] • Bilirubin, Albumin + INR were within the normal range What is the most likely cause? a) Alcoholic fatty liver disease b) Non-Alcoholic Fatty Liver Disease c) Paracetomol overdose d) Wilson’s disease e) Hepatitis BParacetamol overdose - sx ■ Most commoncauseof acuteLF ■ Toxicity dependsonamount consumer,typeof exposure,timesince consumption ■ ALT >1000 First 24 hrs After 24-72 hrs Often asymptomatic, or vague symptoms When liver necrosis occurs -> acute liver failure Nausea & Vomiting Renal Failure, oliguria, metabolic acidosis Abdo pain, RUQ tenderness Liver necrosis causes: •Jaundice •Encephalopathy •HypoglycaemiaParacetamol overdose - mx ■ Use nomogram – cumulative dose + time take to decide if totreat ■ <1hr – activatedcharcoal ■ <4hrs – take level and treat with NAC ■ 4-8hrs – take level and treat with NAC ■ 8-24hrs – immediate NAC ■ Symptomatic/staggereddose - NACChronic Liver failure (cirrhosis) Normal Liver Steatosis Fibrosis Cirrhosis Failure ■ Process of inflammation with gradualcollagen deposition over many years ■ Failure with a background of cirrhosis ■ Steatosis (often driven by EtOH and metabolic syndromes) further drives more inflammation (steatohepatitis) – Fatty liver -> steatohepatitis Diagnosis – LFTs and imaging (with biopsies from level of steatohepatitis) ■ Hepatocytes will swell with globules of fat Transient elastography ■ Very often asymptomatic but changesto ALT and AST over time ■ Eventual complicationssuch as jaundice, ascites, varices orHE ■ Mx – nutrition, EtOH abstinence, NSAID avoidance, prophylactic lactulose/antibiotics, transplantYouarea doctor ontheacute medical ward.Oneof your patientsisa25-year- old manwhoisbeing treatedfor paracetamol poisoning.Your senior asksyou to order some blood tests to assesstheseverity of hiscondition,particularly if thereisanyevidence ofacute liver failure. Whichoneof thefollowingresultswould most support this diagnosis? a) Prothrombintime28s(10-14s) b) Albumin30g/L(35-50g/L) c) Creatinine250micromol/L(55-120micromol/L) d) Platelet count 500x10 /L(100-400x10 /L) 9 e) ALT 1465iu/L(3-40iu/L)Youarea doctor ontheacute medical ward.Oneof your patientsisa25-year- old manwhoisbeing treatedfor paracetamol poisoning.Your senior asksyou to order some blood tests to assesstheseverity of hiscondition,particularly if thereisanyevidence ofacute liver failure. Whichoneof thefollowingresultswould most support this diagnosis? a) Prothrombintime28s(10-14s) b) Albumin30g/L(35-50g/L) c) Creatinine250micromol/L(55-120micromol/L) d) Platelet count 500x10 /L(100-400x10 /L) 9 e) ALT 1465iu/L(3-40iu/L)Blood Tests to identifycauses Alcohol, PBC, Hemochromatosis, Wilson’s disease, AI hepatitis, alpha-11 trypsin, NAFLD, Malignancy, Budd-Chiari ■ INR– synthetic fxand coagulopathy ■ LFTs ■ FBC– infective cause?, thrombocytopaenia(chronic),anaemia (normocytic –haemolytic,Wilson’s, GI bleed; macrocytic – B12/folate, EtOH) ■ U&Es for baselineand HRS ■ CRP – infections are common infailure ■ Paracetamol levels,Hepatitisscreen,EBV, CMVserology, ɑ-1trypsin, caeruloplasmin, Fe-studies,auto-antibodies AHOY Ascites, Hepatic Encephalopathy, Cirrhosis side effects Oesophageal Varices, Yellow (Jaundice) PortalHypertension Sarcopenia Ascites Decreased Glycogen stores • Assess ascites with tap and microscopy • Could lead to SBP – broad spec pip-taz/cefIV 3 hits • Fluid restriction, low salt diet, diuretics • Portal HTN – decreased absorption Varices • EtOH – decreased absorption • Discussed in othertutorials • Ascites – high energy demand Encephalopathy SyntheticFailure Cancer Coagulopathy Regenerative nodules likely to be dysplastic • Prothrombic state with high INR 2-5% per year • Jaundice – low albumin, high INR Give vitamin K/FFP to aid factor production Hepato-renalsyndrome Portal Hypertension Resultingfrom portal HTN Widespread splanchnic vasodilation Reduction in effective CV which reducesrenal bloodflow This massreduction can leadtoAKI https://www.researchgate.net/figure/Symptomatology-of-portal-hypertension-5_fig1_375412646Whichof thefollowing best describesthepathophysiology of hepato-renal syndrome(HRS)inpatients withadvanced liver disease? a) Direct toxicinjury to thekidneys from bilesalts b) Immune-mediateddestructionof renal glomeruli c) Severerenal ischemiadueto splanchnicvasodilationandreduced effectivearterial bloodvolume d) Primary renal tubular dysfunctionleading to salt wasting e) Obstructionof therenal arteriesdueto portal hypertensionWhichof thefollowing best describesthepathophysiology of hepato-renal syndrome(HRS)inpatients withadvanced liver disease? a) Direct toxicinjury to thekidneys from bilesalts b) Immune-mediateddestructionof renal glomeruli c) Severerenal ischemiadueto splanchnicvasodilationandreduced effectivearterial bloodvolume d) Primary renal tubular dysfunctionleading to salt wasting e) Obstructionof therenal arteriesdueto portal hypertension CP Score 1 2 3 Bilirubin <34 34-50 >50 Scoring (µmol/l) Albumin (g/l)>35 28-35 <28 Prothrombin <4 4-6 >6 time, ■ Child-Pugh score - estimates cirrhosisseverity prolonged by – A= 1-6 (best), B= 7-9, C= 10+ (worst) (s) – Bilirubin Encephalopa none mild marked – Albumin thy – INR Ascites none mild marked – Ascites – Encephalopathy ■ MELDscore – how urgently transplant is needed(mortality) – Dialysis – Creatinine MELD score 3-month mortality – Bilirubin – INR 40+ 71.3% 30-39 52.6% 20-29 19.6% 10-19 6% <9 1.9% Risk Factors Alcoholic disease Alcohol consumption Genetics Nutritional status Co-existing conditions (Hep C) ■ 3x subtypes – alcoholic fatty liver, alcoholic hepatitis and cirrhosis ■ Will occur in 30% of chronic drinkers ■ Increased AST:ALTration ■ Glucocorticoids can be given in acute alcoholic hepatitis (pentoxifylline as alternative) ■ Tvaccinationsclude EtOH abstinence, weight loss, high protein diet and ■ For delirium tremens use chlordiazepoxide (once free use acamprosate, baclofen and disulfiram) ■ Transplantation as main cure – MUST be 6mo EtOH free. Alcoholic disease - Symptoms IMPORTANT to screen chronic drinkers for Delerium tremens ■ Jaundice, RUQpain, hepatomegaly (common) ■ Palmar erythema,peripheral oedema,clubbing,dupuytren’scontracture, pruritis(cholestatsis),xanthomas, spider angiomas (multiple =cirrhosis) CIWA-AR and CAGE questionnaires an ■ Gynaecomastia,loss ofbody hair,amenorrhea,libido loss(estrogenic) be used to assess for dependency ■ Deliriumtremens ⟵keep patients this side of line 6-12h 24h 36h 48h 72h Drink delirium tremens tremulous, sweaty, aggressive peak seizure hallucinations coma, death tachycardic, agitated incidence (tactile)Hepatic Encephalopathy ■ Caused by increasedlevelsof ammoniawithinthebloodstream ■ Increased ammonia →astrocyteswelling from conversionof glutamateto glutamine →cerebral oedema – Increases also in ■ CO 2 ■ Urea ■ These willbuildup together in the liver, kidney and lung ■ Mx – Lactulose – increase nitrogenous wasteexcretion – Rifaximin – reduces intestinal nitrogenforming bacteria – IVmannitol– reducecerebral oedemaWest Haven Criteria Vilstrup et al.2014 https://cirrhosiscare.ca/treatment-provider/hepatic-encephalopathy-hcp/A 45-year-old female is seen in A&E having presented with worsening confusion. Her past medical history includes a diagnosis of alcohol-related liver disease with cirrhosis. She admits to still drinking 2 bottles of wine a day. She is very drowsy and disoriented to time and place. On examination, she has significant ascites with shifting dullness but does not report any abdominal pain. There is evidence of bilateral asterixis. She is afebrile with stable observations. ■ What grade of encephalopathy is she demonstrating? a) GradeI b) GradeII c) GradeIII d) GradeIV e) GradeVA 45-year-old female is seen in A&E having presented with worsening confusion. Her past medical history includes a diagnosis of alcohol-related liver disease with cirrhosis. She admits to still drinking 2 bottles of wine a day. She is very drowsy and disoriented to time and place. On examination, she has significant ascites with shifting dullness but does not report any abdominal pain. There is evidence of bilateral asterixis. She is afebrile with stable observations. ■ What grade of encephalopathy is she demonstrating? a) GradeI b) GradeII c) GradeIII d) GradeIV e) GradeVTransplantation ■ Mainanddefinitive treatment for liverfailure ■ UseKing’s CollegeCriteria to assessneed Paracetamol induced liver failure Non-paracetamol induced liver failure • Arterial pH <7.3 24h after ingestion • Prothrombin time >100s OR OR Any three of: • Pro-thrombin time >100s • Drug-induced liver failure • AND creatinine >300µmol/L • Age under 10 or over 40 years • AND grade III or IV encephalopathy. • 1 week from 1st jaundice to encephalopathy • Prothrombin time >50s • Bilirubin ≥300µmol/L.An 18-year-old female presents to the Emergency Department having ingested a staggered overdose of 100 paracetamol tablets over a 24-hour period. ■ Which single result below indicates severe paracetamol-induced liver failure and warrants discussion with a transplant centre? a) Aspartateaminotransferase1000units/L (0-35units/L) a) Arterial pH7.20 a) Lactate10mmol/L a) Pro-thrombintime150s a) Creatinine350micromole/LAn 18-year-old female presents to the Emergency Department having ingested a staggered overdose of 100 paracetamol tablets over a 24-hour period. ■ Which single result below indicates severe paracetamol-induced liver failure and warrants discussion with a transplant centre? a) Aspartateaminotransferase1000units/L (0-35units/L) a) Arterial pH7.20 a) Lactate10mmol/L a) Pro-thrombintime150s a) Creatinine350micromole/L Condition Definition Presentation Investigations Management Liverdisorders caused Often asymptomatic, Alcoholcessation, Lifestyle Alcoholic Fatty Liver by excessive alcohol fatigue, hepatomegaly.May Raised LFT, Ultrasound, modifications (weight loss, Disease consumption, causing progressto alcoholic CT, Liver biopsy exercise). Manage comorbid fat accumulation in hepatitis +cirrhosis conditions liver. Excessive fat Often asymptomatic, Alcoholcessation, Lifestyle Non-Alcoholic Fatty accumulation in the fatigue, hepatomegaly.May Raised LFT, Ultrasound, modifications (weight loss, LiverDisease (NAFLD) liver, not dueto progressto Non-alcoholic CT, Liver biopsy exercise). Manage comorbid alcoholconsumption. steatohepatitis +cirrhosis conditions Fever, fatigue, jaundice, HepatitisB Viral infection that abdominal pain, HBsAg,Anti-HBc, anti- Antiviralmedications (interferon, affects liver nausea/vomiting, darkurine, HBs, LFT tenofovir, entecavir) pale stools Autoimmune hepatitis is a chronic Fever, fatigue , jaundice, Raised LFT, Prednisolone, azathioprine, Autoimmune autoimmuneliver hepatomegaly,abdominal autoantibodies (e.g., monitoring and managing Hepatitis disease characterized discomfort,rash, ANA,SMA, anti-LKM), symptoms +side effects, liver by inflammation and polyarthritis, anorexia Liverbiopsy transplant damageto livercells. Genetic disorder Hepatic dysfunction (e.g., Serum ceruloplasmin characterized by hepatomegaly,jaundice), levels, 24-hour urinary excessive copper Copper chelators, Zinc Wilson's Disease accumulation in body, neurological symptoms copperexcretion,liver supplements, low copper diet particularly liver and (e.g., tremors, dystonia, biopsy (to assess copper dysarthria) content), genetic testing brain. ■ Useful tableoutlining core pointsfrom last year’s tutorialNOT covered in major detail ■ Viral hepatitis ■ Pregnancy relatedfatty liver ■ TIPS procedures ■ Varices ■ Ascites THANKS FOR WATCHING! Tutor1: HarishBava Tutor2: BartRosiński Pleasefill outthe feedback form on Medall and see you next week!