Liver Flashcards
The five main functions of the liver are:
- Metabolising, storing or excreting the absorbed products of digestion
- Makes and excretes bile
- Synthesises proteins
- Metabolises hormones and drugs
- Mounts an immune response to portal pathogens
How many segments is the liver divided into:
8
Name the four lobes of the liver
Left, right, caudate and quadrate
Liver blood supply
Arterial blood from right, middle and left hepatic arteries which are branches of the common hepatic artery arising from the coeliac axis.
Venous blood from the hepatic portal vein which drains the alimentary tract
What are liver cells called
Hepatocytes
What are Kupffer cells?
The liver’s resident macrophages
What structures constitute the portal triad
Bile duct, hepatic artery and portal vein
Increased breakdown of red blood cells(haemolysis) resulting in the production of bilirubin that exceeds the capacity of the liver to conjugate and excrete it
Pre-hepatic jaundice (unconjugated dhyperbilirubinaemia)
Failure of hepatocytes to conjugate and excrete bilirubin. The excess bilirubin is predominantly conjugated, reabsorbed into the blood and then excreted in the urine, causing darkening
Intrahepatic jaundice
Obstruction of the bile ducts so bilirubin can not be excreted in to the duodenal lumen. Excess bilirubin is conjugated and darkens the urine. Patients stools will be pale as bile pigment does not reach the intestines
Post-hepatic jaundice
Examples of enzymes which leak into the blood upon hepatocyte injury are:
ALT, AST, GGT
What enzyme level is raised in the blood during biliary obstruction
alkaline phosphatase
Major serum protein synthesised in the liver, It has a relatively long half-life, so low levels indicate long-tem insufficient liver function
Albumin
Liver cells synthesise most clotting factors, therefore a bleeding tendency results from hepatic insufficiency. This can be detected by measuring ………….
The prothrombin time
First imaging test to use in most circumstances to view the liver due to relatively low cost, mobility and no ionising radiation
Ultrasound
Name the three imaging techniques used to view the biliary tree
MRCP - only diagnostic
ERCP - should only use if therapeutic procedure planned
PTC - more invasive, only used if other methods do not work
Hepatocyte injury with cell death, inflammation and regeneration without structural change to the liver
Acute hepatitis
A result of acute severe liver cell injury with insufficient regeneration (massive necrosis). Result in vomiting, hypoglycaemia, encephalopathy, very high ALT and AST, jaundice and bruising
Acute liver failure
Infiltration of liver cells by fat
Steatosis
Inflammation of the liver with concurrent fat accumulation
Steatohepatitis
Diffuse and irreversible process, potential end stage of chronic liver disease of any cause. Characterised by fibrosis and nodular regeneration. Complications are liver failure, portal hypertension and liver cell carcinoma
Cirrhosis
The most common type of liver cancer. Most cases are as a result of either a viral hepatitis infection (hepatitis B or C), metabolic toxins such as alcohol or aflatoxin, conditions like hemochromatosis and alpha 1-antitrypsin deficiency or NASH
Hepatocellular carcinoma
What are the three histological changes seen in alcoholic liver injury:
Fatty change(steatosis) Alcoholic steahepatosis, combination of fatty changes and inflammation - leads to liver cell death and fibrosis Architectural damage ranging from pericellular fibrosis to cirrhosis
How does alcohol injure the liver
- Alcohol metabolism disturbs other metabolic pathways, such as fat and carbohydrate, so fat accumulates in liver cells
- Acetaldehyde, the main product of alcohol metabolism, binds to liver cell proteins, resulting in injured hepatocytes and an inflammatory reaction.
- Alcohol stimulates collagen synthesis in the liver, leading to fibrosis and eventually cirrhosis
Associated with obesity and excess calorie intake with little exercise. Usually asymptomatic but now recognised to be the commonest cause of persistent mild elevation of liver enzymes. In a proportion of patients it progresses to cirrhosis
Non-alcoholic fatty liver disease
Similar to alcoholic steatohepatitis with less inflammation
non-alcoholic steatohepatitis(NASH)
Hepatitis viruses spread by oral route
A, E
Hepatitis viruses spread blood-borne route
B, C
Occurs more commonly in females, is often a severe form of hepatitis that can cause acute liver failure. Liver biopsy shows chronic hepatitis often with plasma cells and liver cell rosettes. Raised serum IgG snd transaminases. Anti-smooth muscle, antinuclear or anti-LKM(liver-kidney microsomal) antibodies are often present. Treatment with long-term immunosuppression can prevent progression to cirrosis
Autoimmune hepatitis
Granulomatous inflammation surrounds and destroys bile ducts in early disease. Liver biopsy shows bile duct destruction, granulomas, ductular proliferation, fibrosis and eventual cirrhosis. Biopsy not now considered necessary for diagnosis in patients with anti-mitochondrial antibodies, high IgM and alkaline phosphatase. Clinical features include pruritus and xanthelasmas. Female > male
Primary biliary cirrhosis
Autoimmune disease that results in damage and destruction of the bile ducts. Associated with ulcerative colitis. Liver biopsy shows periductal ‘onion skin’ fibrosis, bile duct loss, progresses to cirrhosis. Males > females
Primary sclerosing cholangitis
A group of autosomal recessive disorders of iron metabolism. The defects result in excessive iron absorption from intestinal absorption. This excess iron accumulates in tissues causing a variety of signs and symptoms. Liver biopsy done to determine the degree of iron excess and fibrosis. Treatment is by venesection, removing units of blood until excess iron is depleted
haemochromatosis
Rare but treatable inherited autosomal recessive disorder in which copper accumulates in the liver causing hepatitis and cirrhosis, and in the basal ganglia of the brain, causing severe progressive neurological disability
Wilson’s disease
Genetic disorder of synthesis of a serum protein in the liver. The misfolded protein accumulates as globules in liver cells. Injury to these hepatocytes results in progressive fibrosis and cirrhosis. This disorder also predisposes to pulmonary emphysema due to unopposed action of neutrophil enzymes damaging alveolar walls
Alpha-1 antitrypsin deficiency
Increased blood pressure in the hepatic portal vein is due to a combination of:
-increased portal blood flow
-increased hepatic vascular resistance
-intrahepatic arteriovenous shunting
Leads to oesophageal varices, haemorrhoids, ascites, splenomegaly, caput medusae
Portal hypertension
Results mostly in livers with cirrhosis as a result of progression through a series of pre-malignant lesions. Presents as decompensating cirrhosis due to replacement of liver by cancer cells.
A small proportion occur in patients without cirrhosis, they tend to present late with a large intrahepatic mass. In these patients the remaining liver retains its regenerative capacity so surgical management is possible for early stage cancers
Hepatocellular carcinoma
Adenocarcinoma of bile ducts particularly associated with inflammatory conditions of the bile ducts(e.g. Primary sclerosing cholangitis)
Cholangiocarcinoma
Liver is common deposit site for metastases. Should assume that a tumour found in the liver is secondary until proved otherwise. Usually form multiple deposits from a few large tumours with central necrosis to numerous small metastases throughout the liver. Most often due to metastatic adenocarcinoma, especially from a primary in the pancreas, stomach, bowel, lung or breast
Metastatic tumours
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Liver transplantation
Functionally decompensated cirrhosis. Characterised clinically by:
- Hypoalbuminaemia causes oedema.
- Clotting factor deficiencies cause bruising.
- Ascites caused by low albumin, portal hypertension and a disturbance of aldosterone metabolism.
- Encephalopathy, sometimes leading to coma
- Fetor hepaticus, characteristic breath odour
Chronic liver failure
