PTS phase 2a - LIVER Annette - PowerPoint Presentation

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PTS phase 2a - LIVER

Annette chanzu and Shreya agrawal

The peer teaching society is not liable for false or misleading information

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What 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

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Functions 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

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Acute 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

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ACUTE

LIVER FAILURE

CHRONIC

LIVER FAILURE

RECOVERY

CIRRHOSIS

Viral – A / B / EBV

Drugs

Alcohol

Vascular

Obstruction

Congestion

Alcohol

Viral – B /C

Autoimmune

Metabolic

Iron

Copper

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Progression of chronic liver disease

Chronic liver condition

Liver

damage

Liver symptoms

Liver cirrhosis if prolonged

Liver failure ultimately + higher risk of hepatocellular carcinoma

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Bloods

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

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Liver 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

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Investigations

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

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A

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

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Hep 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

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PARACETAMOL 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

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NON-ALCOHOLIC LIVER DISEASE

Healthy - steatosis - steatohepatitis - fibrosis - cirrhosis Clinical presentation

Asymptomatic,

Nausea, vomiting, diarrhoea, hepatomegaly

DiagnosisImaging, biopsy (diagnostic)TreatmentReduce weight

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ALCOHOLIC 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

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CIRRHOSIS

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

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PORTAL HYPERTENSION

CausesPrehepaticPortal vein thrombosis

Intrahepatic

Schistosomiasis

CirrhosisBudd Chiari syndromePosthepaticRH failure

IVC obstructionUsually asymptomatic

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OESOPHAGEAL 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)

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Questions

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What signs / symptoms would you see in cirrhosis?

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What are the two most common causes of liver failure in the UK?

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What biomarker would be raised if a patient presented with Hepatocellular carcinoma?

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Calculate the number of units: A patient drinks 3 glasses of wine a week (each glass is 175ml, 13% strength)

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How would a patient present with Wernicke-Korsakoff encephalopathy?

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Case 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

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Case 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

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Any questions?