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
What are gallstones made from? How do they show up on an X-Ray? What are some risk factors?
Formed from bile contents (cholesterol, bile ligaments, mixed)
Most are radiolucent (compared to Renal calculi)
Diet, lifestyle, gender, age, pregnancy, pre-existing liver disease
What are some complications of gallstones? describe each
- biliary colic (RUQ pain typically few hrs after eating fatty meal), temporary obstruction of a gallstone usually in cystic duct, seen US, no inflammation ✅analgesia, elective cholecystectomy
- acute cholecystitis (presentation similar to above, Impaction of stone in cystic duct, inflammatory features, seen Us thick wall gallbladder, Murphy’s sign positive ✅ conservative, then cholecystectomy
- acute (ascending) cholangitis, infection of biliary tree (pain, inflammation, jaundice = Charot’s triad), impacted CBD stone or other obstructive causes ✅ IV antibiotics, fluids, relieve obstruction
- acute pancreatitis (acinar cell injury and necrosis, blockage of pancreatic duct, inflammation, autodigestion, epigastric pain radiates to back, vomiting, Cullen’s and Grey Turner’s sign), release of amylase and lipase (CT/ MRI). Depends severity: ✅ fluids, manage gallstones, organ support
What is Murphy’s sign?
Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.
What is Cullen’s and Grey Turner’s sign?
Discolouration of the flanks (side) from bleeding underneath
Sign of acute pancreatitis
Pneumonic to remember causes of pancreatitis
GET SMASHED
Gallstones
Ethanol
Trauma
Steroids Mumps Autoimmune Scorpion bite Hyperlipidemia ERCP Drugs
