Liver And Biliary System Flashcards
What are the livers three main functions?
Storage:
Glycogen, vitamins, iron, copper
Synthesis:
Glucose, protein, lipids, cholesterol, bile, coagulation factors, albumin
Metabolism/ detoxification:
Bilirubin, ammonia, drugs, alcohol. Carbohydrates/ lipids
Vague symptoms of liver disease?
Nausea Vomiting Fatigue Anorexia Abdo pain
What are some more specific symptoms of liver disease? Link them to the deranged function
Jaundice -metabolism of bilirubin
Oedema/ ascites (portal hypertension-> build up of protein rich fluid) - synthesis albumin
Bleeding/ easy bruising - synthesis clotting factors
Confusion- metabolism of ammonia
Causes of acute liver failure
Rapid onset, no previous liver disease
Paracetamol overdose, other meds (tetracycline, aspiring children), acute viral infections (EBV, CMV, Hep A/B), acute excessive alcohol intake
How does cirrhosis of the liver happen?
Cirrhosis is the end rust of lots of conditions in chronic liver disease e.g. ongoing inflammation -> fibrosis, associated with hepatocyte necrosis, resulting in architectural changes (nodules)
Occurs over years -> irreversible impairment of liver function, distortion of architecture
What are some causes of liver cirrhosis?
Drugs - alcohol, Iatrogenic
Infection - HBV, HCV
Deposition - fat, iron, copper
Auto immune - hepatitis, PBC, PSC
Other - alpha1 antitrypsin, glycogen storage, Budd-Chiari
How does alcohol affect the liver?
Fatty changes (weeks) initially reversible -> hepatomegaly
Alcoholic hepatitis (years) initially reversible
Cirrhosis (years) - end stage, irreversible
Partly due to build up of acetaldehyde
Symptoms of alcoholic hepatitis
Rapid onset jaundice, tender helatomegaly (RUQ pain)
More severe:
Nausea, oedema, ascites, splenomegaly
How is viral hepatitis spread? What might it lead to? Does it have a cure or vaccine?
Blood borne
Poses risk for hepatocellular carcinoma
Hep B vaccine but no cure
Hep C cure but no vaccine (majority asymptomatic acute)
What is non- alcoholic fatty liver disease (NAFLD)? What are some risk factors, how can you reduce them?
Similar lathogensesis to alcoholic, linked with insulin resistance -> accumulation of triglycerides and other lipids in hepatocytes
Inflammation present = non-alcoholic steatohepatitis (NASH)
Risks: obesity, diabetes, metabolic syndrome (dyslipidaemia), familial hyperlipidaemia
Lose weight, oral hypoglycaemic agents
What is hereditary haemochromatosis?
Abnormal iron metabolism
Increased absorption iron from small intestine -> excess deposition
Autosomal recessive
Increased ferritin
Can -> hepatocellular carcinoma
What is Wilson’s disease?
Abnormal copper metabolism
Reduced secretion of copper from biliary system -> accumulation in tissues
Autosomal recessive
Low caeruloplasmin
What are some complications of liver cirrhosis?
-portal hypertension (build up of blood in portal venous system) fibrotic liver not very expansive -> compresses veins entering liver -> ascites (beet belly) and splenomegaly
PH -> Blood can shunt from portal system to systemic venous circulation via Portosystemic anastomoses which are not usually used -> distension of veins (varices)
PH -> arterial vasodilation splanchnic -> RAAS activated -> renal artery vasoconstriction (reduced blood flow to kidney) -> acute kidney injury
(Portal hypertension, varices, Ascites, splenomegaly, AKI)
What are the three important sites of varices?
- Oesophageal (upper 2/3 drains into oesophageal veins. Distal portion -> left gastric vein -> mucosal varices (if rupture -> haematemesis)
- Anorectal (between superior and middle/ inferior rental veins, typically painless, rarely bleed)
- Umbilical (rarer, ligamentum teres links liver to umbilicus), normally no blood flow, caput medusa (distended and engorged epigastric veins)
What’s the biliary tree?
Superficially:common hepatic duct & cystic duct join -> common bile duct
Inferiorly: pancreatic duct & ampulla of vater (from duodenum) join -> common bile duct
