chanzu and Shreya agrawal The peer teaching society is not liable for false or misleading information What will be going over Functions of the liver Acute and chronic presentations Important blood results ID: 930200
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Slide1
PTS phase 2a - LIVER
Annette chanzu and Shreya agrawal
The peer teaching society is not liable for false or misleading information
Slide2What will be going over
Functions of the liver
Acute and chronic presentations
Important blood results
Conditions
Liver failure
Hepatitis
Paracetamol overdose
Alcoholic / non-alcoholic liver disease
Cirrhosis and complicationsQuestions
Slide3Functions of the liver
Function
What happens when it goes wrong
Oestrogen regulation
Gynecomastia – Men Spider naevi
Palmar erythema Detoxification Hepatic encephalopathy Metabolises carbohydrates
Hypoglycaemia Albumin production Oedema Ascites Leukonychia Clotting factor production Easy bruising Easy bleeding
Bilirubin regulation Jaundice – stool and urine changes Pruritus
Immunity – Kupffer cells in reticuloendothelial system Spontaneous bacterial infection can occur
Slide4Acute vs chronic presentation
ACUTE Malaise
Nausea
Anorexia
Jaundice
Rare Confusion Bleeding Pain
Hypoglycaemia CHRONIC Ascites
Oedema Dupuytren’s contracture
Malaise Anorexia Pruritus ClubbingPalmar erythema
XanthelasmaSpider naeviHepatomegaly Bleeding Haematemesis Easy bruising
Slide5ACUTE
LIVER FAILURE
CHRONIC
LIVER FAILURE
RECOVERY
CIRRHOSIS
Viral – A / B / EBV
Drugs
Alcohol
Vascular
Obstruction
Congestion
Alcohol
Viral – B /C
Autoimmune
Metabolic
Iron
Copper
Slide6Progression of chronic liver disease
Chronic liver condition
Liver
damage
Liver symptoms
Liver cirrhosis if prolonged
Liver failure ultimately + higher risk of hepatocellular carcinoma
Slide7Bloods
LFTs – Liver function tests Serum bilirubin Serum albumin
Prothrombin time – INR
Liver hepatic enzymes
Aminotransferases – Leak into blood when hepatocytes are damaged
AST ALT – More specific in hepatocellular disease
ALP – Alkaline phosphate Raised in intra/extra hepatic cholestatic disease of any cause Biliary tree GGT
Slide8Liver failure
Definition – Liver looses its ability to repair and regenerate leading to decompensation Causes
Infection – viral hepatitis
Metabolic – Wilsons / Alpha 1 antitrypsin
Autoimmune
PBC – Interlobular ducts PSC – Intra and extra hepatic Neoplastic HCC
Metastatic disease Vascular Budd Chiari – occlusion of hepatic veins Ischaemia Toxins
Paracetamol Alcohol
Presentation Symptoms Same as acute presentationSigns
Jaundice Coagulopathy Hepatic encephalopathy Altered mood / dyspraxia Liver flap / AsterixisFetor hepaticus Sweet and musty breath / urine
Slide9Investigations
Clinical examination Bloods
Increased PT
Increased AST / ALT
Toxicology screen
FBC, U&EIf ascites present – Peritoneal tap with microscopy and culture
ManagementConservative Fluids Analgesia
Medical Treat complications
Ascites - Diuretics Cerebral oedema - Mannitol Bleeding – Vitamin K
Encephalopathy - LactuloseSepsis - sepsis 6, antibioticsHypoglycaemia - dextroseSurgical Transplant Liver failure
Slide10A
B
C
D
E
Spread
Faeco-oral
Blood products and bodily fluids
Blood products and bodily fluids
Blood products and bodily fluids
Faeco
-oral route
Virus
RNA
DNA
RNA
RNA – requires Hep B
RNA
Infection
Acute & mild
Can be severe
Very slow progressing
Makes HBV worse- likely to progress to Cirrhosis or HCC
Normally mild
Test
Bloods
AST/ALT raised
Raised IgG and IgM
HBV ‘assay’
HBs-Ag
HBe
-Ag
Anti-HBs
Anti-HBc
HCV RNA
Anti-HCV serology
HDV- RNA
Anti- HDV
HVE RNA
Anti-HVE
Management
Generally supportive
Vaccine available
Vaccination.
Pegylated interferon alpha 2a
Tenofovir – Inhibits viral replication
Direct acting anti-
virals
Ribavirin
Sofusbuvir
Treat HBV
Supportive treatment
Complications
Cirrhosis
HCC
Cirrhosis HCC Cirrhosis HCC
Cirrhosis HCC
Slide11Hep B serology
Never had HBV
Vaccinated
Previous HBV
Chronic HBV
HB core Ab
-ve
-ve
+ve
+ve
HB envelope Ab
n/a
n/a
n/a
+/-ve
HB surface Ab
-ve
+ve
+ve
-ve
HB surface Ag
-ve
-ve
-ve
+
ve
Slide12Slide13Slide14PARACETAMOL OVERDOSE
In an overdose, there is not enough glutathione stores in the liver so toxic NAPQI builds up and leads to liver damageClinical presentationNausea, vomiting, anorexia, RUQ painTreatmentActivated charcoal – within 1 hour of ingestion
N-acetylcysteine
Slide15NON-ALCOHOLIC LIVER DISEASE
Healthy - steatosis - steatohepatitis - fibrosis - cirrhosis Clinical presentation
Asymptomatic,
Nausea, vomiting, diarrhoea, hepatomegaly
DiagnosisImaging, biopsy (diagnostic)TreatmentReduce weight
Slide16ALCOHOLIC LIVER DISEASE
Fatty liver - alcoholic hepatitis - cirrhosisStrength (ABV) x volume (ml) ÷ 1,000 = unitsInvestigations
GGT very raised; AST and ALT mildly raised.
FBC - Macrocytic anaemia
ComplicationsWernicke-Korsakoff encephalopathyPresents with ataxia, confusion, nystagmus, memory impairmentTreat with IV thiamineAcute/chronic pancreatitisMallory-Weiss tear
Slide17CIRRHOSIS
Loss of normal hepatic architecture with fibrosis - liver injury causes necrosis and apoptosisCauses
Common – chronic alcohol abuse, non-alcoholic fatty liver disease, Hepatitis
Others – Haemochromatosis, Wilson’s disease, Alpha-Antitrypsin deficiency
Clinical presentationAscites, clubbing, palmar erythema, xanthelasma, spider naevi, hepatomegaly, peripheral oedemaDiagnosis / Investigations
Low platelets, high INR, low albuminUS and CT – hepatomegalyLiver biopsyTreatmentAlcohol abstinence and good nutrition
Liver transplantationScreen for hepatocellular carcinoma every 6 months
Slide18PORTAL HYPERTENSION
CausesPrehepaticPortal vein thrombosis
Intrahepatic
Schistosomiasis
CirrhosisBudd Chiari syndromePosthepaticRH failure
IVC obstructionUsually asymptomatic
Slide19OESOPHAGEAL VARICES
These vessels are thin and not meant to transport higher pressure blood so they can easily ruptureRupture haematemesis blood digested melaenaInvestigate with upper GI endoscopy
Treatment
Medical
Beta blocker to reduce cardiac output – reduce portal pressureNitrate to reduce portal pressureSurgical
Band ligationTrans jugular intrahepatic portosystemic shunt (TIPSS)
Slide20Questions
Slide21What signs / symptoms would you see in cirrhosis?
Slide22What are the two most common causes of liver failure in the UK?
Slide23What biomarker would be raised if a patient presented with Hepatocellular carcinoma?
Slide24Calculate the number of units: A patient drinks 3 glasses of wine a week (each glass is 175ml, 13% strength)
Slide25How would a patient present with Wernicke-Korsakoff encephalopathy?
Slide26Case 1
You are reviewing a 48-year-old man who was admitted with sudden severe abdominal pain, confusion and pyrexia. He has a background of alcoholic cirrhosis and known ascites which is normally asymptomatic. An ascitic tap was done overnight which showed a raised neutrophil count and was sent for urgent microscopy & culture.What organism is most likely to grow from the ascitic tap?E- coli Staph aureus
Klebsiella
Streptococcus
Slide27Case 2
A patient presents with history of drinking with dark sticky faeces and blood in her vomit. Which drug would you use to treat her?SpironolactoneCiprofloxacinPropranolol
Amlodipine
Slide28Any questions?