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Alcoholic liver disease
- 2. Functions of the liver Alcohol metabolism ALD Signs and symptoms Liver Function tests Complications Prognosis
- 3. Storage – glycogen, vitamins, iron, copper Metabolism – Drugs (incl alcohol), carbohydrate, lipid, protein Production – Bile, albumin, clotting factors, hormones
- 4. Acetate then oxidised in peripheral tissues via citric acid cycle to CO2, fatty acids and water, producing energy
- 5. Three stages: Alcoholic fatty liver (Steatosis) Alcoholic hepatitis Cirrhosis
- 6. Over 90% of chronic heavy drinkers will develop steatosis 10-20% will develop alcoholic hepatitis ALD cause of death of 1 in 50 people in Scotland. 4 fold increase in deaths from ALD in past 30 years. Risks: alcohol quantity/pattern, gender (F), Hep C infection, haemochromatosis, genetic factors, malnutrition, deprivation.
- 8. Not just end result of alcoholism Non alcoholic fatty liver disease (NAFLD) Chronic Hepatitis B ± D or C PSC/PBC AI hepatitis Haemochromatosis Wilson’s disease
- 9. Steatosis: usually asymptomatic, hepatomegaly Alcoholic hepatitis: malaise, jaundice, tender hepatomegaly, fever, weight loss, abdominal discomfort Cirrhosis: Similar to other causes of cirrhosis. Hepatomegaly, splenomegaly, malaise, jaundi ce, weight loss, ascites, signs of CLD
- 11. History and Examination – Alcohol Bloods including FBC, U&Es LFTs, coagulation, cholesterol, glucose, liver screen Liver imaging – Ultrasound, CT/MRI
- 12. Synthetic function ◦ Albumin, INR Hepatic enzymes ◦ AST, ALT Cholestatic enzymes ◦ Alk Phos, Gamma GT Inducible enzymes ◦ Gamma GT Bilirubin ◦ if isolated consider Gilberts or Haemolysis
- 13. Hepatitis ◦ Increased ALT/AST, mild GGT mild Alk phos ◦ Serology Alcohol ◦ Increased ALT/AST, large GGT, moderate Alk phos ◦ Ethanol and MCV ◦ High AST:ALT (2:1) Gallstones/primary Biliary cirrhosis ◦ Large Alk Phos, Large GGT, mild ALT/AST
- 14. PBC ◦ IgM + Antimitochondrial antibodies Autoimmune Hepatitis ◦ Anti ds-DNA, SMA, IgG and IgA Sclerosing cholangitis ◦ ANCA
- 15. AST 4-50 77 27 1218 104 ALT 4-50 71 18 1055 114 ALK P 30-120 85 98 191 390 Bili <32 21 49 140 87 Albumin 36-46 41 43 31 39
- 17. Differntial of large transaminitis ◦ Ischaemic Injury ◦ Acute Viral Hepatitis ◦ Paracetamol overdose
- 18. Ascites Portal hypertensive bleeding Hepatic encephalopathy
- 19. Peritoneal fluid accumulation – transudate Portal hypertension - ↑ pressure on portal vein Sodium and water retention due to vasodilatation (RAAS) Hypoalbuminaemia due to ↓ synthetic function of liver – low plasma oncotic pressure
- 20. Engorged veins due to portal hypertension Develop in areas with collateral circulation Treatment: treat hypovolaemia, endoscopy, banding
- 21. Neuropsychiatric abnormalities in those with liver disease and no attributable brain disease Neurotoxic substances bypass liver metabolism (eg ammonia)
- 22. Child Pugh score – assesses the prognosis of chronic liver disease
- 23. One year Two year Points Class survival survival 5-6 A 100% 85% 7-9 B 81% 57% 10-15 C 45% 35%
- 24. Functions of the liver Alcohol metabolism ALD Signs and symptoms Liver Function tests Complications Prognosis
Editor's Notes
- Ethanol – acetaldehyde mostly catalysed by alcohol dehydrogenase with some input from the microsomal enzyme oxidising system (MEOS).Acetaldehyde – acetate catalysed by aldehyde dehydrogenase in liver mitochondriaAcetate then travels to peripheral tissues where it is activated to acetyl CoAWide variation between people as to how fast alcohol metabolism occurs – genetics, enzymesSmall amounts are eliminated unchanged in breath, sweat and urine – alcohol breath test In presence of high blood alcohol levels, drug metabolism (eg morphine) is slowed as they compete for the same cytochrome P450 enzymes
- Liver damage caused by alcohol misuse. Covers a range of conditions and associated symptoms.
- Scotland's rates of ALD are increasing much faster than those of the rest of the UK. This is while deaths from other chronic disease are falling.Enough alcohol is sold in Scotland each year for each adult to exceed the recommended weekly limits.Those who drink alcohol out with meal times are more than twice as likely to develop ALD.Alcohol worsens the effects of hereditary haemochromatosis in liver damage.Those in the highest deprivation category are 16 times as likely to die of CLD as those in the most affluent areas.
- Steatosis – can also be seen in obesity and diabetes. Occurs in almost all heavy drinkers. Increased fatty acids are found in the liver, for which there are a number of causes. Decreased fatty acid oxidation in the mitochondria, increased transport of free fatty acids to the liver and increased production of fatty acids in the liver. Fatty change mainly occurs around central veins, where collagen is sometimes laid down too (perivenular fibrosis). If a patient stops drinking alcohol to excess, fatty liver may be reversed. Hepatitis – Liver cells damaged by excess alcohol and fatty change causing inflammation, infiltration of neutrophils, mallory bodies (proteinous substance found in cytoplasms in hepatitis, especially alcoholic) and hepatocyte necrosis. Reversible unless seen on top of a cirrhotic liverCirrhosis – 10 -20% of alcoholics progress to cirrhosis.. Characterised by inflammation, fibrosis, hepatocyte necrosis, Micronodular regeneration of the liver but with impaired architecture and function. Cirrhotic patients may have flares of hepatitis. Cirrhosis is ususally irreversible. May progress to hepatocellular carcinoma.
- NAFLD – similar to ALD except patient doesnt have an alcohol historyHep B±D, C – chronic inflammation causes liver damage leading to cirrhosis. Hep D accelerates the rate of progression of Hep B to cirrhosisPSC/PBC – autoimmune diseases that can cause cirrhosis. PSC affects larger bile ducts, blocking bile and causes scarring of ducts intra and post hepatic. PBC is destruction of the small bile ducts in the liver, causing cholestatsis and liver damage. AI hepatitis – autoimmune destruction of the liver architecture leading to fibrosis and cirrhosis. Haemochromatosis – iron overloadWilson’s – copper overload
- Signs of CLD including but not exclusively alcoholic liver disease. Spider naevi – central raised arteriole surrounded by smaller vessels. Due to high blood estrogen as liver cannot detoxify it. Palmar erythema – redness of thenar and hypothenar eminences due to high estrogenGynaecomastia – estrogen Finger clubbing Dupytrens contracture Ascites, caput medusaeHepatosplenomegalyJaundice, pruritis – increased bilirubin as not processed by liver AsterixisEasy bruising/bleeding – decreased production of clotting factors
- Seen in all causes of cirrhosis, not just alcoholic.
- Complex mechanism not completely understood.Ascites is an excess of total body water and sodium, but the cause of this is up for debate.The most recent hypothesis is that of peripheral arterial vasodilation. It says that portal hypertension, caused by a mechanical blockage of sinusoids (small hepatic vessels), decreasing radius of vessel and therefore increasing pressure, leads to vasodilation. Nitric oxide may be the vasodilator responsible. The vasodilation leads to a fall in the effective blood volume, causing the RAAS to retain sodium and water. Portal hypertension causes a locally increased hydrostatic pressure and therefore an increased hepatic and intestinal production of lymph which leaks (transudes) into the peritoneal cavity. The retention of sodium and water in turn increases the portal pressure further and forces more lymph out into the peritoneum. Hypoalbuminaemia aggravates as it reduces oncotic pressure, favouring the leakage of fluid from the sinusoids.
- Areas: oesophageal, gastric, rectal, abdominal wall (caput medusae) Backflow of blood into areas of lower pressure
- Bypass due to collateral circulation and the reduced function of the liver in metabolismAmmonia normally metabolised to urea in liver to become water soluble and is excreted in urineAmmonia and inflammation may cause morphologic changes to astrocytes, components of the BBB and cerebral oedema(seen in HE) HE can present with general confusion, disorientation or poor co-ordination. There is a chronic disorder of personality, mood and intellect. Asterixis (flapping tremor). Hypereflexia and increased tone.Management: identify and remove cause eg electrolyte imbalance or cerebral depressing drugs. Lactulose to empty bowels of nitrogenous substances. Treat any infection. Rifaximin to sterilise bowels long term. Protein should only be decreased in the short term.
- Which parameters would be used to assess prognosis?