Liver and gall disease Flashcards
The normal liver
Right lobe
Left lobe
The portal circulation ‘the third arm’
Portal vein Umbilical vein Pancreas Spleen Inferior mesenteric vein Superior mesenteric vein -nutrients from gut into liver
Bile flow
Produced in liver as primary bile acids –> bile salts
Helps to digest food
Primary and secondary bile acids
Functions of liver
Approx 500 different functions Detoxification -filters and cleans blood of waste products -drugs, hormones Immune functions -fights infections and diseases -RE system Iinvolved in synthesis of clotting factors, proteins, enzymes, glycogen and fats Production of bile and breakdown of bilirubin Energy storage (glycogen and fats) Regulation of fat metabolism Ability to regenerate
Microanatomy
Organised in lobules with central (hepatic vein)
Hexagon - portal triads in the “corner”
Types of liver injury
Acute
–>viral (A,B, EBV), drugs, alcohol, vascular –> liver failure
–> recovery
Chronic
–>recovery
–>cirrhosis –> liver failure (varices, hepatoma)
–> alcohol, viral (B, C), autoimmune, metabolic (iron, copper) –> liver failure (varices, hepatoma)
Presentation of acute liver injury
Asymptomatic abnormal LFTs Malaise, nausea, anorexia Jaundice Confusion - think ALF *rarer*: Bleeding Liver pain
Presentation of chronic liver injury
Ascites, oedema Haematemesis (varices) Malaise, anorexia, wasting Easy bruising Itching Hepatomegaly, Abnormal LFTs *rarer*: Jaundice Confusion
Serum “liver function tests” (LFTs)
Albumin ALP – Alkaline phosphatase GGT – gamma GT ALT – Alanine Aminotransferase AST – Aspartate Aminotransferase Bilirubin Globulin
Prothrombin time (PT)/ INR Platelet count -normal LFTs and normal PT and platelet count do not exclude liver disease/ cirrhosis, but while normal the function is relatively preserved
Albumin
Bilirubin
Prothrombin time (PT)
Give some index of liver function
-if normal would suggest a “preserved” liver function
ALP – Alkaline phosphatase
GGT – gamma GT
AST – Alanine Aminotransferase
ALT – Aspartate Aminotransferase
Give no index of liver function
Jaundice causes
Pre-hepatic
-haemolysis
Hepatic
-cirrhosis
-acute hepatitis (viral, alcoholic, autoimmune, drug-induced)
-infiltration of the liver by tumours
Post-hepatic (obstruction of biliary outflow)
-gallstones
-external compression: pancreatitis, lymphadenopathy, pancreatic tumour, ampullary tumour
Bilirubin metabolism and excretion
Breakdown product of haemoglobin
Metabolised in liver
Excreted via intestine (and renally)
If bilirubin rises and is not excreted the motion turns pale
Bilirubin metabolism can be interrupted at various points
Cirrhosis of the liver
Scarring of the liver
Result of chronic longstanding damage to the liver
Scar tissue replaces healthy tissue (exceed healing capacity of liver) –> leading to disruption of liver architecture
> resistance to blood flow through the liver, leading to portal hypertension and its complication
Causes of chronic liver disease: most common
Alcohol
Non Alcoholic Steatohepatitis (NASH)
Viral hepatitis (B, C)
Jaundice
Mild can be difficult to spot (light; skin tone)
Scleral jaundice usually first noted
Due to > bilirubin
Less common causes of chronic liver disease
Immune -autoimmune hepatitis -primary biliary cirrhosis -primary sclerosing cholangitis Metabolic -haemochromatosis -Wilson’s -alpha 1 antitrypsin deficiency… Vascular -Budd-Chiari Drugs -amiodarone
Alcoholic liver disease
Commonest cause of cirrhosis in the UK
Deaths from ALD rising dramatically
Weekly safe limits
14 units
Harmful drinking
15-28 units
Hazardous drinking (very heavy)
> 28 units
Binge drinker
Men = >10 units in one session Women = >7 units in one session
The burden of alcohol
9 million adults in the UK who are drinking over the recommended daily limits
People aged 16-24 are the heaviest drinkers
In inner city A&E departments approximately 75% of patients attending after midnight are drunk
20% of patients admitted to hospital for illnesses unrelated to alcohol, are drinking at hazardous levels
Taking an alcohol history
1 unit = 8g EtOH
= half pint normal beer/ lager
= small glass of wine
= pub measure of spirits
Hepatitis B
DNA virus Reads in hepatocyte genome Persists in liver even if no longer in blood Can reactivate Mainly transmitted via intercourse/ vertically Early infection: chronicity Vaccination available Longterm treatment
Hepatitis C
RNA virus
Mainly transmitted through IVDA; needles blood products
Once cleared = cleared
Reinfection possible - no immunity
Time limited treatment - well tolerated, 90% cure
No vaccination
Non-alcoholic fatty liver disease
On the rise; often unrecognised Risk factors -diabetes -obesity -hypertension -dyslipidaemia = metabolic syndrome LFTs may be normal; even in advanced disease Affecting 20% of Western population
Iceberg of fatty liver disease
HCC NASH CirrhosisNASH NAFLD with abnormal LFT NAFLD normal LFT Normal liver
UK HCV prevalence
<1% 2-400,000 IV drug use Medical treatment abroad Blood donation screening 1991
Complications of cirrhosis
Portal hypertension -ascites -varices ± haemorrhage -hypersplenism → thrombocytopenia (↓ platelets) Hepato-renal syndrome Encephalopathy Hepatocellular carcinoma
Portal hypertension
< platelets (thrombocytopenia)
Signs of chronic liver disease
Jaundice
-sign of decompensation in chronic liver disease
Leuconchia
-white nails fro hypoalbuminaemia (not liver disease specific)
Palmar erythema
Spider naevi
-sign of advanced liver disease but does not imply decompensation
Gynaecomastia
-sign of liver disease (related to low testosterone) but can also be drug related (spironolactone)
Finger clubbing
-not liver specific
Ascites
-advanced liver disease - decompensation
Dental considerations for pts with liver disease
Potential for increased bleeding in patients with liver disease
-coagulopathy
-thrombocytopenia
Potential for increased drug toxicity in patients with advanced liver disease
-caution should be used in prescribing medications metabolized in the liver
Infection risk, consider extra precautions if higher risk of injury (double gloves)
Hep B vaccination
HCV now very treatable
Dental considerations in practice in liver disease
Comprehensive medical and dental histories
Appropriate laboratory investigations
-full blood count (FBC)
-prothrombin Time (PT)
-LFTs
Consultation with and/or referral to treating physician(s) prior to dental treatment
Minimization of soft tissue trauma during dental procedures
Consideration of hospital setting for advanced surgical procedures or severely coagulopathic pts
Stages of (chronic) liver disease
NCPH = non-cirrhotic portal hypertension -often due to vacular problems in liver -tolerating bleeding well and clotting generally intact -relatively rare (pts generally aware) Pre-cirrhotic -no effect on dental work -may be asymptomatic Liver cirrhosis
Dental considerations in liver disease - medications
Caution in prescribing meds metabolised in liver and/ or impair haemostasis
-anaesthetics: local (amides) and general (halothane)
-spot antiplatelet (aspirin) 7 days before
-increased DILI with flucoloxacillin and co-amoxylav
-sedatives
Potential for increased drug toxicity in pts with advanced liver disease
-avoid NSAIDs
-paracetamol is safest pain killer in liver disease
-opiates: slow and low
Spotting liver cirrhosis
Compensated -invisible -blood can be normal -risk low Decompensated -visible -abnormal blood tests -risks high
Prognosis in cirrhosis (diagram)
Time (big to small) Bilirubin (small to big) Albumin (big to small) -as it gets lower ascites develops INR small to big Encepalopathy over time
Complications of chronic liver disease: chronic
Malnutrition
Bone disease
Complications of chronic liver disease: acute
GI bleeding and ascites (due to portal hypertension) Jaundice Hepatic encepalopathy Renal impairment Coagulopathy Infection
Treatment of liver disease: symptomatic
Diuretics
Nutrition support
Supplements
Propanolol
Treatment of liver disease: specific
Antiviral Immunosuppression Relieving obstruction Venesection Detox from alcohol
Hepatic encephalopathy
One of several features of decompensation
Difficult to spot if subtle
Can present as overt confusion in patient with CLD
Often more troublesome for other than pt, but can be disabling
Indicates underlying problem
-bleed
-infection
-compensation
-worsening chronic disease
Collateral history
Recognising hepatic encephalopathy
Confusion
Altered behaviour
Coma
Collateral history
How to test for hepatic encephalopathy
Serial 7s from 100 "baby hippopotamus" 5-star drawing Number connection test Ammonia level >50 (poor correlation)
