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FinalsEazy NISH DALAVAYEHEPATOLOGY FOR FINALS SESSION TIME – 1.5 HOURS Hepatology is a • The liver is a crucial organ that plays a major role in many life functions branch of gastroenterology • throughout the worldhe liver are common that is rapidly • Understanding the underlying basic evolving principles is key to understanding disease Q U E S T I O1N A 56-year-old man presents to the emergency A BRAIN department with palpitations. An ECG demonstrates a tachycardia with an irregularly irregular rhythm and B SPLEEN no p waves. An echocardiogram shows a thrombus in the left atrium. C LIVER Which of the following organs is most likely to D GALLBLADDER continue to function in the situation of an embolic event? E COLON ANSWER ON THE ZOOM POLL Q U E S T I 1 N A 56-year-old man presents to the emergency A BRAIN department with palpitations. An ECG demonstrates a tachycardia with an irregularly irregular rhythm and B SPLEEN no p waves. An echocardiogram shows a thrombus in the left atrium. C LIVER Which of the following organs is most likely to D GALLBLADDER continue to function in the situation of an embolic event? E COLON THE LIVER HAS DUAL BLOOD SUPPLY FROM THE PORTAL VEIN & THE HEPATIC ARTERY PROPER LIVER ANATOMY EMBRYOLOGICALLY, THE LIVER IS DERIVED FROM ENDODERM THE GLISSON’S CAPSULE COVERS THE LIVER MAJOR LIVER FUNCTIONS Medications (cytochrome system) Insulin-like growth factor (IGF-1) DETOXIFICATION Waste products e.g. ammonia HORMONE PRODUCTION Thrombopoietin Glucose metabolism Hepcidin METABOLISM Lipid metabolism Excrete bilirubin BILE FORMATION Protein metabolism Help emulsify lipids Plasma proteins e.g. albumin IN NEONATES Site of RBC production from 6 weeksbirth Clotting factors Bile acids, cholesterol SYNTHESIS Glucose (gluconeogenesis) Vitamin D Acute phase reactants Glycogen STORAGE Fat-soluble vitamins (A,D,E,K) Iron Copper Q U E S T I 2 N A 45-year-old man has a history of alcohol abuse, A SPIDER ANGIOMATA hepatitis C and HIV. He is disoriented and his friend confirms his heavy drinking habits. On examination, B SPLENOMEGALY there is palmar erythema, gynaecomastia and numerous spider angiomata. The abdomen is C DILATED PERIUMBILICAL VEINS severely distended and periumbilical veins are evident. There is ankle oedema as well as evidence of D ANKLE OEDEMA asterixis. A CT abdomen showed evidence of splenomegaly. E ALTERED MENTAL STATUS Which of these signs in the patient has the same ANSWER ON THE ZOOM POLL pathogenesis as his gynaecomastia? Q U E S T I O2N A 45-year-old man has a history of alcohol abuse, A SPIDER ANGIOMATA hepatitis C and HIV. He is disoriented and his friend confirms his heavy drinking habits. On examination, B SPLENOMEGALY there is palmar erythema, gynaecomastia and numerous spider angiomata. The abdomen is C DILATED PERIUMBILICAL VEINS severely distended and periumbilical veins are evident. There is ankle oedema as well as evidence of D ANKLE OEDEMA asterixis. A CT abdomen showed evidence of splenomegaly. E ALTERED MENTAL STATUS Which of these signs in the patient has the same SPIDER ANGIOMATA OFTEN APPEAR pathogenesis as his gynaecomastia? IN HIGH OESTROGEN STATES UNDERSTANDING LIVER DISEASE ALCOHOL METABOLIC HEPATITIS CAUSES INFLAMMATORY CAUSES IRREVERSIBLE STEATOSIS CHRONIC LIVER CIRHOSSIS DISEASE VASCULAR CAUSES MEDICATIONS FIBROSIS HEPATOCELLULAR CARCINOMA CRYPTOGENIC KEY DEFINITION CIRRHOSIS = IRREVERSIBLE REMODELLING OF THE LIVER DUE TO FIBROSIS CHRONIC LIVER DISEASE DECOMPENSATION COMPENSATED DECOMPENSATED LIVER CONTINUES LIVER NO LONGER ABLE TO TO FUNCTION MEET DEMANDS TYPICALLY LEADS TO COMPLICATIONS ASYMPTOMATIC CAUSES OF DECOMPENSATION BOTH CAN HAVE STIGMATA OF CHRONIC LIVER DISEASE • INFECTION • CONSTIPATION • ALCOHOL • GI BLEED • MEDICATIONS • DEHYDRATION • OFTEN IDIOPATHIC STIGMATA OF CHRONIC LIVER DISEASE LEUKONYCHIA PALMAR ERYTHEMA SPIDER NAEVI CAPUT MEDUSAE GYNECOMASTIA DUPUYTREN’S CONTRACTURE LACK OF CHEST HAIR! HIGH-VOLUME ASCITES FEATURES OF CHRONIC LIVER DISEASE RESULT SIGNIFICANCE GENERAL Fatigue, malaise , anorexia , weight loss Non-specific features Splenomegaly, caput medusae, varices Portal hypertension Palmar erythema, gynaecomastia, amenorrhea, STIGMATA OF loss of body hair, spider naevi Hyperoestrogenism CHRONIC LIVER DISEASE Leukonychia, peripheral oedema Hypoalbuminaemia Dupuytren's contracture, clubbing, pruritis Chronic liver disease Ascites Portal hypertension Jaundice Impaired conjugation & excretion of bilirubin SIGNS OF Hepatic encephalopathy Accumulation of neurotoxic metabolites (ammonia) DECOMPENSATION Coagulopathy Decreased liver function GI bleeding Rupture of varices OTHER Hepatorenal syndrome, hepatopulmonary syndrome, hepatocellular carcinoma, spontaneous bacterial peritonitis, diabetes mellitus, secondary hyperparathyroidism, hyponatraemia, portal vein thrombosis COMPLICATIONS CHILD-PUGH SCORE DETERMINES THE SEVERITY OF DECOMPENSATED CIRRHOSIS 1 2 3 ALBUMIN (g/L) >35 28-35 <28 ASCITES NONE CONTROLLED REFRACTORY BILIRUBIN (mg/dL) <2 2-3 >3 (JAUNDICED) NONE GRADE 1-2 GRADE 3-4 ENCEPHALOPATHY INR <1.7 1.7 – 2.3 >2.3 Class A à 5-6, mild disease, one year survival 100% Class B à 7-9, moderate disease, one year survival 80% Class C à 10-15, severe disease, one year survival 45% Q U E S T I O N3 A 56-year-old presents to the hospital with jaundice that developed in the past 3 days. On examination, A ALCOHOL LIAISON SERVICE there is evidence of Dupuytren’s contracture and B PHYSIOTHERAPY palmar erythema. Blood tests are performed and are shown below. C DIETICIAN Based on the likely cause of the patient’s jaundice, which referral would the patient benefit most from? D HAEMATOLOGY MEAN CELL VOLUME 102 (80- 96 fL) HAEMOGLOBIN 11 (13.0- 17.0 g/dL) ALT 70 (10-50 IU/L) E OCCUPATIONAL THERAPY AST 500 (10-40 IU/L) ALP 65 (25-115 IU/L) ANSWER ON THE ZOOM POLL GGT 65 (9-40 IU/L) BILIRUBIN 40 (< 17µmol/L) Q U E S T I O N3 A 56-year-old presents to the hospital with jaundice that developed in the past 3 days. On examination, A ALCOHOL LIAISON SERVICE there is evidence of Dupuytren’s contracture and B PHYSIOTHERAPY palmar erythema. Blood tests are performed and are shown below. C DIETICIAN Based on the likely cause of the patient’s jaundice, which referral would the patient benefit most from? D HAEMATOLOGY MEAN CELL VOLUME 102 (80- 96 fL) HAEMOGLOBIN 11 (13.0- 17.0 g/dL) ALT 70 (10-50 IU/L) E OCCUPATIONAL THERAPY AST 500 (10-40 IU/L) ALP 65 (25-115 IU/L) AST: ALT > 2, ↑ GGT, JAUNDICE & GGT 65 (9-40 IU/L) A MACROCYTIC ANAEMIA ALL SUGGEST ALCOHOLIC HEPATITIS IN THIS PATIENT BILIRUBIN 40 (< 17µmol/L) ALCOHOLIC LIVER DISEASE ALCOHOLIC ALCOHOLIC FATTY CIRRHOSIS HEPATITIS LIVER DISEASE CHRONIC LIVER DISEASE Alcoholic hepatitis PATHOPHYSIOLOGY CLINICAL FEATURES • Jaundice • Fever • Symptomatic hepatitis due to heavy alcohol • Anorexia consumption • Weight loss • Tender hepatomegaly (RUQ pain) • Features of chronic liver disease • Alcohol withdrawal symptoms e.g. tremors DIAGNOSIS TREATMENT • Exclude other causes of hepatitis (non-invasive liver screen) • AST/ALT ratio > 2 • Alcohol cessation • ↑GGT • Supportive care • ↑ bilirubin • ↑ INR • Liver biopsy • Mallory-Denk bodies Q U E S T I O4N A 46-year-old man presents to the emergency department A LIVER CIRRHOSIS with a 3 week history of abdominal distension. On examination, there is evidence of cachexia, abdominal B TUBERCULOSIS distension and shifting dullness. There is also evidence of non-pitting oedema in both ankles. The ascitic albumin level is 2.7 g/dL and the serum albumin level is 3.6 g/dL. The C NEPHROTIC SYNDROME ascitic fluid is milky and triglycerides are elevated. The ascitic white cell count is 560/mm with lymphocytic D SPONTANEOUS BACTERIAL PERITONITIS predominance. E INTRA -ABDOMINAL LYMPHOMA What is the likely cause of the patient’s ascites? ANSWER ON THE ZOOM POLL Q U E S T I O4N A 46-year-old man presents to the emergency department A LIVER CIRRHOSIS with a 3 week history of abdominal distension. On examination, there is evidence ofachexia, abdominal B TUBERCULOSIS distension and shifting dullness. There is also evidence of non-pitting oedema in both ankles. The ascitic albumin level is 2.7 g/dL and the serum albumin level is 3.6 g/dL. The C NEPHROTIC SYNDROME ascitic fluid is milky and triglycerides are elevated. The ascitic white cell count is 560/mm with lymphocytic D SPONTANEOUS BACTERIAL PERITONITIS predominance. E INTRA -ABDOMINAL LYMPHOMA What is the likely cause of the patient’s ascites? THE MILKY ASCITIC FLUID, A SAAG < 1.1 & ELEVATED TRIGLYCERIDES INDICATES CHYLOUS ASCITES. NON - PITTING OEDEMA HERE SUGGESTS LYMPHOEDEMA. CIRHOSSIS PORTAL SALT & WATER HYPERTENSION RETENTION ASCITES SERUM ASCITES-ALBUMIN GRADIENT (SAAG) = serum albumin (g/dL) - ascitic fluid albumin (g/dL) ↑ Capillary hydrostatic pressure ↓ Oncotic pressure /↑ Capillary permeability BLOOD WATER WATER + ALBUMIN PERITONEAL CAVITY ↑ ↓ SAAG = serum albumin - ascitic fluid albumin SAAG = ↑serum albumin - asc↓tic fluid albumin HIGH SAAG ( >1.1g/dL) LOW SAAG (<1.1g/dL) LIVER CIRHOSSIS NEPHROTIC SYNDROME PANCREATITIS RIGHT HEART FAILURE HEPATIC MALIGNANCY PERITONEAL CARCINOMATOSIS TUBERCULOSIS Q U E S T I O5N A diagnostic paracentesis is performed to confirm if a A 225/ µl (40% NEUTROPHILS) patient has spontaneous bacterial peritonitis (SBP). B 225/ µl (40% LYMPHOCYTES) Which of the following values for the white cell count is diagnostic of SBP? C 625/ µl (40% LYMPHOCYTES) D 125/ µl (90% NEUTROPHILS) E 625/ µl (40% NEUTROPHILS) ANSWER ON THE ZOOM POLL Q U E S T I O5N A diagnostic paracentesis is performed to confirm if a A 225/ µl (40% NEUTROPHILS) patient has spontaneous bacterial peritonitis (SBP). B 225/ µl (40% LYMPHOCYTES) Which of the following values for the white cell count is diagnostic of SBP? C 625/ µl (40% LYMPHOCYTES) D 125/ µl (90% NEUTROPHILS) E 625/ µl (40% NEUTROPHILS) WCC > 250/mm 3& PREDOMINANTLY NEUTROPHILS IS DIAGNOSTIC OF SBP ASCITIC FLUID ANALYSIS RESULT SIGNIFICANCE BLOODY Trauma or malignancy COLOUR MILKY Chylous ascites TURBID/ CLOUDY Infection or malignancy TRANSPARENT/ STRAW COLOUR Uncomplicated ascites (cirrhosis) <250/mm 3 No peritonitis WHITE CELL COUNT > 250/ mm & predominantly neutrophilsSpontaneous bacterial peritonitis > 2.5 g/L Right heart failure, Peritoneal carcinomatosis, Tuberculosis, Budd Chiari (early) TOTAL PROTEIN < 2.5 g/L Cirrhosis, nephrotic syndrome, Budd Chiari (late) ALBUMIN DETERMINE THE SAAG Helps determine the likely cause of ascites (previous slide) AMYLASE Pancreatitis CYTOLOGY Malignancy CULTURES Infection ACID-FAST BACILLI Tuberculosis TRIGLYCERIDES Chylous ascitesBASED ON BSG GUIDELINES ASCITES MANAGEMENT PARACENTESIS SALT & FLUID DIURETICS TIPS RESTRICTION Diagnostic paracentesis is st Daily salt intake of Spironolactone 1 line For refractory ascites recommended in all patients no more than 5 – 6.5 g with new-onset ascites Can be combined with furosemide Serial paracentesis to remove large volume ascites if refractory to medical therapy SPONTANEOUS BACTERIAL PERITONITIS PATHOPHYSIOLOGY CLINICAL FEATURES • Infection of ascites • Sudden peritonitis • Infection without a perforation of the bowel • Often no signs of peritonism • ‘Spontaneous’à source of infection is not • Fever and chills known • Worsening ascites • Usually occurs in severe cirrhosis (Child-Pugh C) • New-onset/ worsening encephalopathy • Nausea/ vomiting DIAGNOSIS TREATMENT 3 • Ascitic fluid white cell count ≥ 250/mm and • Empirical antibiotic therapy initiated immediately after predominantly neutrophils the diagnosis • Ascites culturesoften negative Q U E S T I O6N A 65-year-old man presents to the emergency department A GIVE POTASSIUM CHLORIDE because of persistent somnolence for the past 2 weeks. The patient’s wife says he has been sleeping much more than B GIVE IV LACTULOSE usual but no other symptoms. He has a past medical history of liver cirrhosis due to long term alcohol abuse. On examination, shifting dullness and asterixis are noted. He is C GIVE IV RIFAXIMIN on Spironolactone and was recently started on Bendroflumethiazide. An arterial blood gas shows a D STOP SPIRONALACTONE metabolic alkalosis with a low potassium. TRANSJUGULAR INTRA -HEPATIC E PORTO -SYSTEMIC SHUNT (TIPS) In addition to fluids, what is the most appropriate next step? ANSWER ON THE ZOOM POLL Q U E S T I O6N A 65-year-old man presents to the emergency department A GIVE POTASSIUM CHLORIDE because of persistent somnolence for the past 2 weeks. The patient’s wife says he has beensleeping much more than B GIVE IV LACTULOSE usual but no other symptoms. He has a past medical history of liver cirrhosis due to long term alcohol abuse. On examination,shifting dullness and asterixis are noted. He is C GIVE IV RIFAXIMIN on Spironolactone and wasrecently started on Bendroflumethiazide. An arterial blood gas shows a D STOP SPIRONALACTONE metabolic alkalosis with a low potassium. E TRANSJUGULAR INTRA -HEPATIC PORTO -SYSTEMIC SHUNT (TIPS) In addition to fluids, what is the most appropriate next step? SLEEP DISTURBANCES IS ONE OF THE EARLIEST SIGNS OF HEPATIC ENCEPHALOPATHY. HYPOKALAEMIA IS ONE OF THE KEY PRECIPITATING FACTORS Hepatic encephalopathy PATHOPHYSIOLOGY CLINICAL FEATURES • Cirrhosis → ↓ hepatic metabolism → accumulation of • Diurnal sleeping disturbance earliest sign neurotoxic metabolites, especiallyammonia → cerebral oedema and ↑ intracranial pressure → • Asterixisà loss of motor control neurological symptoms • Fatigue • Neurological disturbances • Precipitated by situations of ↑ ammonia • Infections (SBP) • GI Bleeding • Hypovolemia (dehydration) DIAGNOSIS • Metabolic alkalosis, hypokalaemia • Portal vein thrombosis • Clinical diagnosis • Serum ammonia not useful acutely TREATMENT • Correct precipitating factors • Lactuloseà 1 line medical therapy • decreases absorption of ammonia • Rifaximin • Reduces ammoniaproducing bacteria Q U E S T I 7 N A 75-year-old man with known cirrhosis is admitted A PROPANOLOL to the Emergency Department with haematemesis. He is haemodynamically unstable with a heart rate of B TERLIPRESSIN 120bpm and a blood pressure of 100/60 mmHg. He is treated for a variceal bleed and has been stabilised C OMEPRAZOLE with intravenous fluids, blood transfusions and has been started on antibiotics. He is listed for an D PABRINEX endoscopy later that day. E IBUPROFEN What else should be given before his endoscopy? ANSWER ON THE ZOOM POLL Q1 Q2 Q U E S T I 7 N A 75-year-old man with known cirrhosis is admitted A PROPANOLOL to the Emergency Department with haematemesis. He is haemodynamically unstable with a heart rate of B TERLIPRESSIN 120bpm and a blood pressure of 100/60 mmHg. He is treated for a variceal bleedand has been stabilised C OMEPRAZOLE with intravenous fluids, blood transfusions and has been started on antibiotics. He is listed for an D PABRINEX endoscopy later that day. E IBUPROFEN What else should be given before his endoscopy? TERLIPRESSIN WILL REDUCE PORTAL PRESSURES AND IS GIVEN BEFORE ENDOSCOPY Q1 Q2 Q U E S T I 7 N An endoscopy is performed and confirmed A PROPANOLOL oesophageal varices. Band ligation is performed to control the bleeding. B TERLIPRESSIN What should be given as secondary prophylaxis for C OMEPRAZOLE the variceal bleeding? D PABRINEX E BISOPROLOL ANSWER ON THE ZOOM POLL Q1 Q2 Q U E S T I 7 N An endoscopy is performed and confirmed A PROPANOLOL oesophageal varices. Band ligation is performed to control the bleeding. B TERLIPRESSIN What should be given as secondary prophylaxis for C OMEPRAZOLE the variceal bleeding? D PABRINEX E BISOPROLOL A NON -SELECTIVE BETA BLOCKER IS GIVEN Q1 Q2 FOR SECONDARY PROPHYLAXIS OF VARICES UPPER GI BLEED PATHOPHYSIOLOGY CLINICAL FEATURES • Important causes • Haematemesis • Bleeding peptic ulcer • e.g. Variceal bleed or Mallory-Weiss tear • Oesophageal/ Gastric varices • Coffee ground vomit • Mallory-Weiss Tear • E.g. Bleeding peptic ulcer • Oesophagitis • Melaena • Gastritis • ‘Black, tarry stool’, with an offensive odour • Aortoenteric fistula • Anaemia • Hereditary haemorrhagic telangiectasia • Fresh blood stool due to fast transit • Many other causes • Shock • Other features based on the cause of UGIB TREATMENT DIAGNOSIS • ABCDE Assessment • Calculate Glasgow-Blatchford Score • High Urea is common • See next slide • Upper GI endoscopy à diagnostic & therapeutic BASED ON BSG GUIDELINES VARICEAL HAEMORRHAGE IN CIRRHOSIS ABCDE ASSESSMENT PATIENTS SHOULD BE STARTED ON A NON- GIVE TERLIPRESSIN & ANTIBIOTICS SELECTIVE BETA BLOCKER (e.g. PROPANOLOL) FORCALCULATE GLASGOW BLATCHFORD SCORE SECONDARY PROPHYLAXIS OF VARICEAL BLEEDS ENDOSCOPY WITHIN 24 HOURS OESOPHAGEAL VARICES GASTRIC VARICES FAILURE TO CONTROL BLEEDING CYANOACRYLATE/ BAND LIGATION THROMBIN INJECTION REBLEEDING DESPITE RESUSCITATION +/- REBLEEDING DESPITE BALLOON TAMPONADE PROPHYLAXIS PROPHYLAXIS TRANSJUGULAR INTRA-HEPATIC PORTOSYSTEMIC SHUNT UPPER GI BLEED ABCDE ASSESSMENT CALCULATE GLASGOW BLATCHFORD SCORE VARICEAL BLEED BLEEDING PEPTIC ULCER UPPER GI ENDOSCOPY: • GIVE TERLIPRESSIN • GIVE BROAD SPECTRUM ANTIBIOTICS • ENDOSCOPIC CLIPPING +/- ADRENALINE • SCLEROTHERAPY WITH ADRENALINE UPPER GI ENDOSCOPY: • THERMAL COAGULATION WITH ADRENALINE • OESOPHAGEAL VARICESà BAND LIGATION • GASTRIC VARICES CYANOACRYLATE/ THROMBIN ADRENALINE IS NEVER GIVEN AS MONOTHERAPY IV PPI GIVEN AFTER ENDOSCOPY IF ENDOSCOPIC TREATMENT FAILS, TIPSS CAN BE PERFORMED PATIENTS SHOULD BE STARTED ON PROPANOLOL FOR SECONDARY PREVENTION TIPSS CONTRAINDICATIONS • Pre-existing hepatic encephalopathy • Severe heart failure • Severe pulmonary hypertension Q U E S T I O8N A 39-year old man presents to the GP with fatigue, A HEPATITIS A INFECTION fever and joint pain. He is unmarried and he has a history of multiple heterosexual partners. He does not B HEPATITIS B INFECTION use drugs illicitly. On examination, an urticarial vasculitic rash is noted and no jaundice is seen. Liver C HEPATITIS C INFECTION function tests show significantly raised ALT and AST. D INFECTIOUS MONONUCLEOSIS What is the likely diagnosis? E CYTOMEGALOVIRUS INFECTION ANSWER ON THE ZOOM POLL Q U E S T I O8N A 39-year old man presents to the GP with fatigue, A HEPATITIS A INFECTION fever and joint pain. He is unmarried and he has a history of multiple heterosexual partners. He does not B HEPATITIS B INFECTION use drugs illicitly. On examination, an urticarial vasculitic rashis noted and no jaundice is seen. Liver C HEPATITIS C INFECTION function tests show significantly raised ALT and AST. D INFECTIOUS MONONUCLEOSIS What is the likely diagnosis? E CYTOMEGALOVIRUS INFECTION SEXUAL CONTACT IS A MUCH STRONGER RISK FACTOR FOR HEPATITIS B INFECTION COMPARED TO HEPATITIS C INFECTION. HEPATITIS A HEPATITIS B HEPATITIS C HEPATITIS D HEPATITIS E VIRUS Non-enveloped RNA Virus Enveloped DNA virus Enveloped RNA virus Enveloped RNA virus Non-enveloped RNA virus Bodily fluids Bodily fluids Bodily fluids Faeco-oral (e.g. shellfish, ice) Faeco-oral TRANSMISSION Infected blood Infected blood Infected blood Perinatal Travel Sexual contact IV drug use, tattooing Can ONLY be transmitted to Travel RISK FACTORS Drinking contaminated water Blood transfusions Blood transfusions patients infected with Drinking contaminated water IV drug use, tattooing Sexual contact (uncommon) hepatitis B virus SEVERITY Severe when co-infection Causes severe fulminant Mild Sometimes severe Usually subclinical with hepatitis B hepatitis in pregnant woman CLINICAL FEATURES Fever, malaise, loss of appetite, RUQ pain, jaundice CHRONICITY NO YES YES (HIGH) YES NO Acute hepatitis Chronic hepatitis LIVER Chronic hepatitis Cirrhosis Acute hepatitis Cirrhosis Hepatocellular carcinoma (Same as Hepatitis B) Acute hepatitis DISEASES Hepatocellular carcinoma Vasculitis EXTRA-HEPATIC Polyarteritis nodosa Membranoproliferative GN MANIFESTATIONS NONE Membranous GN Cryoglobulinemia (Same as Hepatitis B) NONE Non-Hodgkin’s lymphoma Acuteà supportive care Requires combination of drugs TREATMENT Supportive care Pegylated interferon alfa Supportive care Chronicà antivirals End stageà transplantation Vaccine available Hepatitis B vaccine Vaccine available in China VACCINATION Vaccine available No vaccine available = HBIG à certain situations Protective against HDV (Not UK) Q U E S T I O9N A 35-year old woman is due for her occupational A ACUTE HEPATITIS B INFECTION health visit before she works in the hospital. She recently immigrated from China and has no significant B CHRONIC HEPATITIS B INFECTION past medical history. She brings a report with her to the appointment and the results are shown below: C RESOLVED HEPATITIS B INFECTION HBsAg: Negative Anti-HBs: Positive D VACCINATION AGAINST HEPATITIS B VIRUS Anti-HBc: Positive HBeAg: Negative E WINDOW PERIOD OF INFECTION Anti-HBe: Negative ANSWER ON THE ZOOM POLL How should the findings of the report be reported? Q U E S T I O9N A 35-year old woman is due for her occupational A ACUTE HEPATITIS B INFECTION health visit before she works in the hospital. She recently immigrated from China and has no significant B CHRONIC HEPATITIS B INFECTION past medical history. She brings a report with her to the appointment and the results are shown below: C RESOLVED HEPATITIS B INFECTION HBsAg: Negative Anti-HBs: Positive D VACCINATION AGAINST HEPATITIS B VIRUS Anti-HBc: Positive HBeAg: Negative E WINDOW PERIOD OF INFECTION Anti-HBe: Negative PRESENCE OF ANTI -HBs INDICATES IMMUNITY. THE HEPATITIS B VACCINE ONLY CONTAINS How should the findings of the report be reported? THE SURFACE ANTIGEN. HBsAg INDICATES INFECTION Hepatitis B Serology HBeAg INDICATES INCREASED REPLICATION / INFECTIVITY can be used to determine the stage Anti-HBc(IgM) INDICATES ACUTE INFECTION of Hepatitis B Anti-HBc(IgG) INDICATES CHRONIC INFECTION OR RESOLVED infection Anti-HBe INDICATES REDUCED REPLICATION / INFECTIVITY Anti-HBs (due to resolved infection or vaccination) HEPATITIS B SEROLOGY HEALTHY CHRONIC CHRONIC CURED DUE TO CURED DUE TO (no exposure or ACUTE ‘WINDOW INFECTION INFECTION PRIOR PRIOR INFECTION PERIOD’ (ACTIVE) (INACTIVE) INFECTION VACCINATION vaccination) HBsAg ACTIVE = HBeAg INACTIVE = Anti-HBc(IgM) Anti-HBc(IgG) VARIABLE Anti-HBe VARIABLE Anti-HBs Q U E S T I 10N A 43-year old woman presents to the emergency A PRIMARY SCLEROSING CHOLANGITIS department with right upper quadrant pain. She had an ileocecal resection last year due to Crohn’s Disease B AUTOIMMUNE HEPATITIS and has been receiving total parenteral nutrition ever since. Her ALT, AST, amylase and lipase levels are C GALLSTONE DISEASE normal. The ALP and GGT levels are both elevated. D SHORT GUT SYNDROME What is the most likely diagnosis? E LIVER METASTASIS FROM BONE CANCER ANSWER ON THE ZOOM POLL Q U E S T I O10 A 43-year old woman presents to the emergency A PRIMARY SCLEROSING CHOLANGITIS department with right upper quadrant pain. She had an ileocecal resection last year due to Crohn’s Disease B AUTOIMMUNE HEPATITIS and has been receiving total parenteral nutrition ever since. Her ALT, AST, amylase and lipase levels are C GALLSTONE DISEASE normal. The ALP and GGT levels are both elevated. D SHORT GUT SYNDROME What is the most likely diagnosis? E LIVER METASTASIS FROM BONE CANCER INCREASE IN BOTH ALP & GGT IS INDICATIVE OF CHOLESTASIS. ENTEROHEPATIC CIRCULATION OF BILE ACIDS IS LIKELY IMPAIRED HERE LIVER FUNCTION TESTS ↑ALT ↑ AST ↑ ALP ↑ GGT HEPATOCELLULAR CHOLESTASIS/ DAMAGE OBSTRUCTION ALP IS ALSO FOUND IN BONE TISSUE & PLACENTA ISCHAEMIC TRUE MEASURES OF LIVER FUNCTION HEPATITIS PROTHROMBIN TIME/ INR BILIRUBIN ALT > 1000 IU/L ALBUMIN PLATELETS CAN SOMETIMES OCCUR WITH ACUTE VIRAL HEPATITIS & AUTOIMMUNE HEPATITS PARACETAMOL GLUCOSE OVERDOSE Q U E S T I O 11 A 44-year old woman presents with fatigue and dark ENDOSCOPIC RETROGRADE A CHOLANGIOPANCREATOGRAPHY (ERCP) urine. She says her stools have also gotten lighter in colour. She takes ferrous sulphate to manage her iron B PERIPHERAL BLOOD FILM deficiency anaemia. On examination, she has scleral icterus but her abdomen is not distended. A liver C ABDOMINAL ULTRASOUND function test is performed and is shown below. What is the most appropriate next step? D HEPATITIS B SEROLOGY ALBUMIN 3.8 (35 - 50 g/L) BILIRUBIN 110 (< 17 µmol/L) E IRON STUDIES ALT 40 (10-50 IU/L) AST 56 (10-40 IU/L) ALP 822 (25-115 IU/L) ANSWER ON THE ZOOM POLL GGT 300 (9-40 IU/L) Q U E S T I O 11 A 44-year old woman presents with fatigue and dark ENDOSCOPIC RETROGRADE A CHOLANGIOPANCREATOGRAPHY (ERCP) urine. She says her stools have also gotten lighter in colour. She takes ferrous sulphate to manage her iron B PERIPHERAL BLOOD FILM deficiency anaemia. On examination, she has scleral icterus but her abdomen is not distended. A liver C ABDOMINAL ULTRASOUND function test is performed and is shown below. What is the most appropriate next step? D HEPATITIS B SEROLOGY ALBUMIN 3.8 (35 - 50 g/L) BILIRUBIN 110 (< 17 µmol/L) E IRON STUDIES ALT 40 (10-50 IU/L) AST 56 (10-40 IU/L) AN ABDOMINAL ULTRASOUND IS THE FIRST STEP ALP 822 (25-115 IU/L) IN EVALUATING BILIARY OBSTRUCTION GGT 300 (9-40 IU/L) Q U E S T I O12 A 45-year-old man presents with a one-month history A CHOLESTEROL GALLSTONES of RUQ pain. He notices the pain more after eating fatty foods. He has a history of Hereditary B ASCENDING CHOLANGITIS Spherocytosis. On examination, there is pronounced splenomegaly and he is Murphy's Sign negative. His C ACUTE LEUKEMIA ALP and GGT is increased. Urinary urobilinogen is negative. D PANCREATIC CANCER What is the likely cause of his symptoms? E CHRONIC HAEMOLYSIS ANSWER ON THE ZOOM POLL Q U E S T I O12 A 45-year-old man presents with a one-month history A CHOLESTEROL GALLSTONES of RUQ pain . He notices the pain more after eating fatty foods. He has a history of Hereditary B ASCENDING CHOLANGITIS Spherocytosis. On examination, there is pronounced splenomegaly and he is Murphy's Sign negative. His C ACUTE LEUKEMIA ALP and GGT is increased. Urinary urobilinogen is negative. D PANCREATIC CANCER What is the likely cause of his symptoms? E CHRONIC HAEMOLYSIS CHRONIC HAEMOLYSIS CAN LEAD TO PATIENTS DEVELOPING PIGMENTED ‘BILIRUBIN’ GALLSTONES. BILIRUBIN PATHWA Y MACROPHAGES BLOOD LIVER PORTAL INTESTINE (SPLEEN) VEIN RBC UROBILINOGENKIDNEYS IN URINE HAEM BILIARY recycled UDP- SYSTEM glucuronosyl- UNCONJUGATED UNCONJUGATED transferasCONJUGATED UROBILINOGEN BILIRUBIN BILIRUBIN BILIRUBIN (water insoluble) (water soluble) excreted ALBUMIN STERCOBILIN PRE-HEPATIC HEPATOCELLULAR POST-HEPATIC (HAEMOLYTIC) (CHOLESTATIC) ! HAEMOLYTIC JAUNDICE IMPAIRED CONJUGATION JAUNDICE HEPATOCELLULAR JAUNDICE OBSTRUCTIVE JAUNDICE PRE-HEPATIC JAUNDICE HEPATOCELLULAR JAUNDICE POST-HEPATIC JAUNDICE HYPERBILIRUBINAEMIA CAUSE Excess unconjugated bilirubinImpaired conjugation of Damage to hepatocytesimpaired Biliary obstruction production unconjugated bilirubin conjugation & reduced bilirubin excretion Haemolytic anaemia Gilbert’s syndrome Gallstone disease EXAMPLES Erythropoiesis disorders Crigler–Najjar syndrome Hepatocellular disease (e.g. hepatitis)PBC, PSC, Pancreatic cancer Biliary atresia UNCONJUGATED BILIRUBIN ↑↑ NORMAL ↑ CONJUGATED BILIRUBIN NORMAL ↑↑ URINARY BILIRUBIN NORMAL ↑ ↑↑ URINARY UROBILINOGEN ↑↑ NORMAL/ ↑ NEGATIVE URINE COLOUR NORMAL DARK URINE VERY DARK URINE STOOL COLOUR NORMAL NORMAL/ CLAY COLOURED STOOLS CLAY COLOURED STOOLS ALT, AST NORMAL ↑↑ NORMAL INITALLY (CAN↑ LATER ON) ALP, GGT NORMAL ↑ ↑↑ OTHER ↓ Hb , ↑ LDH, ↑ reticulocytes, ABDOMINAL ULTRASOUND ABDOMINAL ULTRASOUND INVESTIGATIONS ↓ haptoglobins Haemosiderinuria Gilbert ‘s Syndrome FEATURES OF LIVER DISEASE PANCREATIC CANCE à painless (intravascular haemolysisTransient jaundice triggered by stress, infection, fasting etc. jaundice, CA 19-9 Haemoglobinuria benign OTHER (intravascular haemolysis) FEATURES Crigler–Najjar Syndrome PBC à anti-mitochondrial antibodies Splenomegaly Persistent jaundice in first few (extravascular haemolysisdays of life. Kernicterus. PSC à P-ANCA Treatment needed. Pigmented gallstones Q U E S T I 14N A 44-year old woman presents with generalised A HAEMOLYTIC ANAEMIA pruritus. She also says that he has had several ‘near-collisions’ when she drives at night. She has B VEGAN DIET no significant medical history and examination is unremarkable. C BILIARY OBSTRUCTION What is the likely mechanism of her symptoms? D REDUCED BLOOD SUPPLY TO THE RETINA E RETINITIS PIGMENTOSA ANSWER ON THE ZOOM POLL Q U E S T I O14 A 44-year old woman presents with generalised A HAEMOLYTIC ANAEMIA pruritus. She also says that he has had several ‘near-collisions’ when she drives at night. She has B VEGAN DIET no significant medical history and examination is unremarkable. C BILIARY OBSTRUCTION What is the likely mechanism of her symptoms? D REDUCED BLOOD SUPPLY TO THE RETINA E RETINITIS PIGMENTOSA VITAMIN A IS FAT -SOLUBLE VITAMIN & IN BILIARY OBSTRUCTION, IT CAN BE MALABSORBED. DEFICIENCY CAN LEAD TO NIGHT -BLINDNESS AUTOIMMUNE LIVER DISEASES AUTOIMMUNE HEPATITIS TYPE 1 PRIMARY BILIARY CHOLANGITIS PRIMARY SCLEROSING CHOLANGITIS EPIDEMIOLOGY FEMALES > MALES FEMALES >> MALES MALES > FEMALES DESTRUCTION OF ONLY DESTRUCTION OF BOTH INTRAHEPATIC PATHOPHYSIOLOGY CHRONIC RELAPSING HEPATITIS INTRAHEPATIC BILE DUCTS BILE DUCTS & EXTRAHEPATIC BILE DUCTS ASSOCIATIONS OTHER AUTOIMMUNE DISEASES OTHER AUTOIMMUNE DISEASES INFLAMMATORY BOWEL DISEASE Often asymptomatic, fatigue, arthralgia, RUQ CLINICAL FEATURES pain, weight loss, nausea, amenorrhoeaPRURITUS, fatigue, jaundice, often asymptomPruritus, fatigue, Charcot’s triad (cholangitis) LIVER FUNCTION TESTS HEPATOCELLULAR PATTERN OF INJURY CHOLESTATIC PATTERN OF INJURY CHOLESTATIC PATTERN OF INJURY IMMUNOGLOBULINS IgG IgM - AUTOANTIBODIES ANA,ASMA, ANTI-SLA/LP ANTI-MITOCHONDRIAL ANTIBODIES P-ANCA Hepatocellular LFTS, autoantibodiesCholestatic LFTS + AMA positive + Abdominal USS DIAGNOSIS Liver biopsy +/- liver biopsy Cholestatic LFTS + MRCP (‘string of beads sign’) Prednisolone & Azathioprine Ursodeoxycholic Acid NOT Ursodeoxycholic acids Hepatitis A & Hepatitis B vaccination Pruritus Cholestyramine Pruritus Cholestyramine TREATMENT End stage liver disetransplantation Fat malabsorptionFat-soluble vitamins Fat malabsorptionFat-soluble vitamins End stage liver diseatransplantation End stage liver diseatransplantation RECURRENT CHOLANGITIS, STRICTURES, MAJOR COMPLICATION CIRRHOSIS CIRRHOSIS, HIGH CHOLESTEROL, OSTEOMALACIA CHOLANGIOCARCINOMA, CIRRHOSIS PROGNOSIS EXCELLENT EXCELLENT if responds to treatment POOR (most patients need a transplant) PBC à Breast (more common in females) PSCà Sperm (more common in males) RULE OFMs: IgM, AMA, Middle aged female Q U E S T I O15 th A 23-year-old woman is in her 29 week of A INTRAHEPATIC CHOLESTASIS OF PREGNANCY pregnancy. She has been suffering from itching for the past 3 weeks. She has now developed mild B PRIMARY BILIARY CHOLANGITIS jaundice. Her total bilirubin and ALP are mildly elevated. The ALT and AST are also mildly elevated. C ACUTE FATTY LIVER OF PREGNANCY A full blood count is normal. D HELLP SYNDROME What is the most likely diagnosis? E HYPEREMESIS GRAVIDARUM ANSWER ON THE ZOOM POLL Q U E S T I O15 th A 23-year-old woman is in her 29 week of A INTRAHEPATIC CHOLESTASIS OF PREGNANCY pregnancy. She has been suffering from itching for the past 3 weeks. She has now developed mild B PRIMARY BILIARY CHOLANGITIS jaundice. Her total bilirubin and ALP are mildly elevated. The ALT and AST are also mildly elevated. C ACUTE FATTY LIVER OF PREGNANCY A full blood count is normal. D HELLP SYNDROME What is the most likely diagnosis? E HYPEREMESIS GRAVIDARUM PRURITUS & JAUNDICE IN THE THIRD TRIMESTER OF PREGNANCY IS VERY SUGGESTIVE OF INTRAHEPATIC CHOLESTASIS • Most common pregnancy-associated liver disease, usually occurs in third trimester • Pruritus, jaundice INTRAHEPATIC • ↑ bile acids, ↑ ALP, ↑ ALT, ↑ AST, ↑ conjugated bilirubin CHOLESTASIS OF • Ursodeoxycholic acid to manage symptoms & reduce bile acids PREGNANCY • Increased risk of stillbirth • Bile acids ≥ 100 micromol/consider delivery at 36 weeks gestations • Bile acids < 100 micromol/L: consider delivery at 36-39 weeks gestation LIVER DISEASES • Severe complication of pregnancy that usually occurs in the third trimester • Occurs usually in patients with pre-eclampsia UNIQUE TO HELLP SYNDROME • RUQ pain, nausea, vomiting, no signs of liver failure • Characterised by haemolysis, elevated liver enzymes & low platelets • Risk of rapid deterioration (e.g. DIC, pulmonary oedemulti-organ failure PREGNANCY • Life threatening, rare disease that usually occurs in the third trimester • Extensive fatty infiltration of tacute liver failure • Pre-eclampsia, multiple gestations, nulliparity are risk factors ACUTE FATTY LIVER • Jaundice, RUQ pain, coagulopathy, hypoalbuminaemiaascites OF PREGNANCY • Risk of disseminated intravascular coagulation, hypoglycaemia, high serum ammonia • ↑ ALT, ↑ AST, ↑ bilirubin • Liver biopsy can confirm diagnosis but should not be performed in pregnancy • Requires immediate delivery only treatment Q U E S T I 16N An 18-year-old male presents to the emergency A GIVE ACTIVATED CHARCOAL department after consuming 40 tablets of paracetamol, all at once, 2 hours ago. He is B MEASURE PARACETAMOL LEVELS IN 2 HOURS nauseous and has vomited multiple times. C GIVE N -ACETYLCYSTEINE IMMEDIATELY What is the most appropriate next step? D GIVE FLUMAZENIL E GIVE INTRAVENOUS BICARBONATE ANSWER ON THE ZOOM POLL Q U E S T I O16 An 18-year-old male presents to the emergency A GIVE ACTIVATED CHARCOAL department after consuming 40 tablets of paracetamol, all at once, 2 hours ago. He is B MEASURE PARACETAMOL LEVELS IN 2 HOURS nauseous and has vomited multiple times. C GIVE N -ACETYLCYSTEINE IMMEDIATELY What is the most appropriate next step? D GIVE FLUMAZENIL E GIVE INTRAVENOUS BICARBONATE IF PATIENTS PRESENT BETWEEN 1 -4 HOURS POST -INGESTION, MEASURE PARACETAMOL LEVELS AT 4 HOURS POST -INGESTION ANABOLIC AZATHIOPURINE TETRACYCLINES SALICYLATES ALLOPURINOL STEROIDS IMPORTANT MEDICATIONS ASSOCIATED WITH LIVER INJURY PARACETAMOL ISONIAZID CO-AMOXICLAV METHOTREXATE AMIODARONE Acute liver failure PATHOPHYSIOLOGY CLINICAL FEATURES • Jaundice • Acute liver dysfunction in the absence of underlying • Hepatic encephalopathy chronic liver disease • Coagulopathy • Hepatomegaly • Paracetamol overdosie the most common cause in Europe • Ascites • Viral hepatitis (A,B & E)is the most common cause • GI bleeding worldwide • Increased risk of infection & sepsis • Increased risk of metabolic abnormalities • Increased risk of multi-organ failure TREATMENT DIAGNOSIS • Must be managed in intensive care setting • ABCDE assessment • Supportive care & manage complications • Urgent blood tests (e.g. coagulation, LFTs, cultures) • Must consider early referral to transplant centre if • Non-invasive liver screen suitable (King’s college criteria) • Abdominal ultrasound PARACETAMOL SULFATION & CYP450 GLUCURONIDATION (≈8%) (≈90%) Non-toxic NAPQI metabolites GLUTHATHIONE NO GLUTHATHIONE EXCRETED IN URINE Conjugated NAPQI Unconjugated NAPQI (hepatotoxic) EXCRETED IN URINE N-acetylcysteine (≈2% excreted naturally in urine)ADAPTED FROM BMJ FLOWCHART KING’S COLLEGE CRITERIA FOR LIVER TRANSPLANTATION PARACETAMOL OVERDOSE = Arterial pH < 7.3 after 24 hours of STAGGERED OVERDOSE/ DOUBT OVER ingestion TIME OF INGESTION = ABCDE ASSESSMENT GIVE NAC IMMEDIATELLY OR All three of: • Hepatic encephalopathy > grade 3 • Serum creatinine >300 umol/L ACTIVATED PRESENTS < 1 HOUR • INR >6.5 POST INGESTION CHARCOAL >24 1-4 HOURS 4-8 HOURS 8-24 HOURS HOURS MEASURE SERUM MEASURE SERUM MEASURE SERUM PARACETAMOL PARACETAMOL PARACETAMOL 4 HOURS POST INGESTION IMMEDIATELY IMMEDIATELY IS THE PATIENT SYMPTOMATIC/ ABNORMAL IF ABOVE TREATMENT LINE GIVE IV BLOOD TESTS? ON NOMOGRAM N-ACETYLCYSTEINE (NAC)TAKEN FROM BARTS NHS TRUST ED GUIDELINESPOST-LECTURE NOTES Hereditary Haemochromatosis PATHOPHYSIOLOGY CLINICAL FEATURES • Often asymptomatic or non-specific (e.g. lethargy) • Hepatomegaly • Autosomal recessivecondition affecting iron • Arthralgia metabolism • Pseudogout • HFE gene defect à ↑ intestinal iron absorption iron overload • Skin hyperpigmentationà bronze skin • Diabetes mellitus • Iron commonly accumulates in liver, pancreas & • Hypogonadism, erectile dysfunction, amenorrhea heart, joints • Cardiomyopathies (restrictive/ dilated) • Symptoms usually start at 40-60 years old • Heart failure, arrhythmias • Delayed presentation in pre-menopausal woman • Increased risk of cirrhosis • Increased risk of HCC (even without cirrhosis) DIAGNOSIS TREATMENT • Iron studies • ↑ ferritin (1 step) • Reduce iron & vitamin C consumption • ↑ transferrin • Phlebotomy à 1 line treatment • ↑ serum iron • Desferrioxamine • Liver biopsy • Used if phlebotomy contraindicated e.g. • Prussian blue stain shows iron overload severe anaemia • Genetic testing Wilson’ s disease PATHOPHYSIOLOGY CLINICAL FEATURES • Autosomal recessivedisorder affecting copper • Liver metabolism • Acute liver failure • ATP7B gene mutation on chromosome 13 • Chronic liver disease/ cirrhosis • ↓ hepatic copper excretion • Ocular • ↓ serum caeruloplasmin • Kayser-Fleischer rings • ↑ copper absorption from the small intestine • Copper coloured rings around the • ↑ free serum copperà accumulates in tissues periphery of the cornea • Neuropsychiatric DIAGNOSIS • Personality changes • Copper studies • Parkinsonism • ↓ serum caeruloplasmin • Tremor (‘’wing-beating’’) • ↑ free serum copper • Dystonia • ↓ total serum copper • ↑ 24 hour urinary copper • Slit-lamp examination • Genetic studies TREATMENT • Reduce copper intake e.g. shellfish, nuts, organ meat • Copper chelators e.g. Penicillamine • Must be titrated carefully, lot of side effects BUDD-CHIARI SYNDROME PATHOPHYSIOLOGY CLINICAL FEATURES • Obstruction of hepatic venous outflow • Hepatomegaly, • Associated with hypercoagulable states • Abdominal pain • Myeloproliferative disorders e.g. PRV • Ascites • Malignancy • Oral contraceptives • Pregnancy • Risk of acute liver failure DIAGNOSIS TREATMENT • Systemic anticoagulation • Abdominal ultrasoundà first line • Angioplasty • CT à if ultrasound unavailable • TIPS Hepatocellular carcinoma PATHOPHYSIOLOGY CLINICAL FEATURES • Often asymptomatic • Primary malignancy of the liver, rare • Picked up during surveillance • Major complications of cirrhosis • Constitutional symptoms e.g. weight loss • RUQ pain, hepatomegaly, palpable mass • HCC can occur in chronic hepatitis B without cirrhosis • Paraneoplastic syndromes • Very poor prognosis • Hypoglycaemia • REMEMBER à the most common malignant lesion of • Erythrocytosis the liver is liver metastasis (NOT primary HCC) • Hypercalcaemia • Stigmata of chronic liver disease TREATMENT DIAGNOSIS • ↑ serum alpha-fetoprotein (AFP) • CT abdomen • Liver biopsy • Many options available e.g. resection • Often contraindicated due to risk of bleeding • Strict criteria for transplantation • Patients with cirrhosis are offereCC surveillance • Abdominal ultrasound every 6 months LIVER MASSES HEPATIC HAEMANGIOMA Most common benign mass, often found incidentally, avoid biopsy, no malignant potential BENIGN FOCAL NODULAR HYPERPLASIA Central stellate scarring on ultrasound, no malignant potential HEPATOCELLULAR ADENOMA Grows with oestrogeassociated with oral contraceptive pill use, some malignant potential HEPATOCELLULAR CARCINOMA Develops in patients with cirrhosis, ↑ serum alpha-fetoprotein (AFP) , very uncommon MALIGNANT CHOLANGIOCARCINOMA (intrahepatiAssociated usually with chronic gallbladder inflammation (e.g. PSRUQ mass & jaundicen LIVER METASTASIS Most common malignant lesion of the liver, usually from the GIT (e.g. colon), lungs and breasts TUMOUR MARKER ASSOCIATIONS MARKER TUMOUR TYPE OF CLINICAL ASSOCIATIONS SAMPLE SIGNIFICANCE HEPATOCELLULAR CARCINOMA PART OF SCREENING FOR ALPHA-FETOPROTEIN (AFP) BLOOD YOLK SAC TUMOUR HEPATOCELLULAR CARCINOMA MONITOR TREATMENT RESPONSE CANCER ANTIGEN 19-9 (CA 19-9) PANCREATIC CANCER BLOOD & RECURRENCE PART OF SCREENING FOR CANCER ANTIGEN 125 (CA 125) OVARIAN CANCER BLOOD OVARIAN CANCER COLORECTAL CANCER MONITOR TREATMENT RESPONSE CARCINOEMBRYONIC ANTIGEN (CEA) BLOOD PANCREATIC CANCER & RECURRENCE MONITOR TREATMENT RESPONSE CANCER ANTIGEN 15-3 (CA 15-3) BREAST CANCER BLOOD & RECURRENCE PART OF SCREENING FOR PSA (prostate specific antigen) PROSTATE CANCER BLOOD PROSTATE CANCER BREAST CANCER GUIDE TREATMENT PLAN HUMAN EPIDERMAL GROWTH FACTOR-2 (HER-2) TUMOUR TISSUE OESOPHAGEAL CANCER & PROGNOSIS PLEASE FILL OUT THE FEEDBACK FORM FOLLOW OUR SOCIALS TO STAY UP TO DATE WITH ALL EVENTS Image credits – Wikimedia Commons, Ra, Dermnet NZ @OSCEazyOfficial @osceazyofficial OSCEazy Osceazy@outlook.com