Session 6: Liver & Biliary System Pathology Flashcards
Broad liver functions.
Storage
Synthesis
Metabolism
Detoxification
Storage in liver
Glycogen
Vitamins
Iron
Copper
Synthesis in liver
Glucose Protein Lipids and cholesterol Bile Coagulation factors Albumin
Metabolism & detoxification in liver.
Bilirubin Ammonia Drugs Alcohol Carbs/lipids
General symptoms of liver disease.
Nausea
Fatigue
Anorexia
Abdo pain
Deranged function of jaundice
Faulty metabolism of bilirubin
Deranged function of oedema/ascites
Faulty synthesis of albumin
Deranged function of bleeding/easy bruising.
Faulty synthesis of clotting factors
Deranged function of confusion.
Faulty metabolism of ammonia.
Give examples of causes of acute liver failure.
Paracetamol overdose
Tetracycline, aspirin
Acute viral infections like EBV, CMV or Hep A/B
Acute excessive alcohol intake
Explain events leading up to cirrhosis.
Ongoing inflammation causing fibrosis of the liver.
This is associated with hepatocyte necrosis and result in architectural changes nodules.
Is cirrhosis reversible?
No
End result of cirrhosis.
Impairment of liver function
Distortion of architecture which can lead to hepatomegaly or sometimes even shrinkage.
Give broad causes of liver cirrhosis.
Drugs Infection Deposition Autoimmune Other
Give drugs which can cause cirrhosis.
Alcoholic liver disease
Iatrogenic
Give infections which can cause cirrhosis.
HBV and HCV
Give depositions that can cause cirrhosis.
Fat
Iron
Copper
Give autoimmune responses that can cause cirrhosis.
Autoimmune hepatitis which affects hepatocytes as due to ASMA (antismooth muscle antibody) or ANA (antinuclear antibody
PBC (primary biliary cirrhosis)
PSC (Primary sclerosing cholangitis)
Explain signs and symptoms of alcoholic liver disease.
Fatty liver leading to hepatomegaly
Alcoholic hepatitis leading to rapid onset of jaundice, tender hepatomegaly with RUQ pain.
Nausea, oedema, ascites and splenomegaly.
What an viral hepatitis lead to other than cirrhosis?
Hepatocellular carcinoma
Hep B has a vaccine but no cure.
Hep C has a cure but no vaccine.
Explain non alcoholic fatty liver disease (NAFLD)
A similar pathogenesis to alcoholic liver disease but without the alcohol.
Has a strong link to insulin resistance.
Due to an accumulation of triglycerides and other lipids in hepatocytes.
Risk factors of NAFLD.
Obesity
Diabetes
Metabolic syndrome like dyslipidaemia
Familial hyperlipidaemia
Explain Hereditary haemochromatosis.
Abnormal iron metabolism where there is an increase in absorption of iron in the small intestine leading to excess deposition.
Autosomal recessive disorder with increased ferritin.
Complications of hereditary haemochromatosis.
Liver cirrhosis
Hepatocellular carcinoma
Explain Wilson’s disease.
Abnormal copper metabolism with a reduced secretion of copper from the biliary system leading to accumulation of copper in tissues.
An autosomal recessive disorder with low ceruloplasmin which is supposed to transport copper in blood.
Give example of other less common conditions that can lead to cirrhosis.
Alpha1-antitrypsin deficiency
Glycogen storage abnormalities
Budd-Chiari
Complication of liver cirrhosis.
Portal hypertension
Hepatorenal syndrome
Explain how liver cirrhosis can cause portal hypertension.
Since the fibrotic liver is not very expansive there is compression of veins that enter the liver. This leads to a build up of blood in the portal venous system.
This leads to increased hydrostatic pressure in the portal venous system and ascites.
There is also an increase in pressure of the splenic circulation as the splenic vein feeds into the portal vein. This will cause splenomegaly as well.
What is the physiological response to the portal hypertension?
The blood can shunt from the portal system to the systemic venous circulation by anastomoses which are usually not in use.
This leads to distension of the veins at the site of the anastomoses i.e. varices.
What are the three important sites where varices may arise due to portal hypertension?
Oesophageal varices
Anorectal varices
Umbilical varices
Explain how oesophageal varices come about.
The upper 2/3 of the portal vein will start to drain into the oesophageal veins. The distal portion of the portal vein will drain into the left gastric vein.
This can lead to mucosal varices.
Why might oesophageal varices be a problem?
Because they are fragile and easily rupture.
If they rupture they can cause significant haematemesis.
Explain how anorectal varices come about.
There are anastomoses between the superior and middle/inferior rectal veins.
The superior rectal vein feeds into the inferior mesenteric which will feed into the portal vein.
Instead the superior rectal vein will start to drain into the middle and inferior rectal veins and cause varcies here.
They are typically painless as they are above the pectinate line and rarely bleed.
Explain how umbilical varices come about.
They are not very common but the ligamentum teres is linked with the liver to the umbilicus. There is normally no blood flow here but because of portal vein hypertension there can be.
This is known as caput medusa.
Explain how liver cirrhosis can lead to hepatorenal syndrome.
Portal hypertension leading to arterial vasodilation of the splanchnic vessels.
This activates RAAS and leads to renal artery vasoconstriction even though there no problem in blood flow. This leads to reduced blood flow to kidney and reduced kidney function.
What are gallstones formed from?
Either:
Cholesterol
Bile pigments
Or a mix of them both
Can gallstones be seen on x-ray?
No, usually not as most of them are radiolucent.
Risk factors for developing gallstones.
Diet and lifestyle like high fat diet.
Age
Gender (female)
Pregnancy
Pre-existing liver disease
Give examples of complications of gallstones.
Biliary colic
Acute cholecystitis
Acute ascending cholangitis
Acute pancreatitis
Specific symptoms of biliary colic.
RUQ pain typically after a few hours after eating a fatty meal due to contraction of gallbladder due to CCK.
There are no features of inflammation.
What is biliary colic usually caused by?
Temporary obstruction of a gallstone usually in the cystic duct.
How to investigate biliary colic?
Ultrasound
Management of biliary colic.
Analgesia
Elective cholecystectomy
Specific symptoms and signs of acute cholecystitis.
Initial presentation is very similar to biliary colic although there are inflammatory features of acute cholecystitis.
What is acute cholecystitis caused by?
Impaction of a stone in the cystic duct.
Investigations of acute cholecystitis.
Ultrasound to find stone and thick wall gallbladder.
Positive Murphy’s sign which is painful gallbladder on ventilation.
Management of acute cholecystitis.
Initially conservative with analgesia.
Cholecystectomy
Specific signs and symptoms of acute ascending cholangitis.
An infection of the biliary tree
Charcot’s triad
What is Charcot’s triad?
Pain
Features of inflammation
Jaundice
What is acute ascending cholangitis caused by?
Typically an impacted CBD stone or other obstructive causes.
Management of acute ascending cholangitis.
IV antibiotics, fluids and relieve obstruction.
Explain acute pancreatitis.
Acinar cell injury and necrosis due to blockage of pancreatic duct.
This leads to an inflammatory response and autodigestion of pancreas.
Symptoms and signs of acute pancreatitis.
Epigastric pain radiating to the back.
It is often associated with vomiting.
Cullen’s and Grey Turner’s sign
What is Cullen’s sign?
Superficial oedema and bruising around the umbilicus
What is Grey Turner’s sign?
Bruising on the flanks below the 12th rib and above the anterior superior iliac spine.
Investigations of acute pancreatitis.
Amylase and Lipase release
CT/MRI to identify necrosis
Management of acute pancreatitis.
Fluids
Manage gallstones
Organ support.