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Alimentary > Liver > Flashcards

Liver Flashcards

1
Q

The five main functions of the liver are:

A
  • 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
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2
Q

How many segments is the liver divided into:

A

8

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3
Q

Name the four lobes of the liver

A

Left, right, caudate and quadrate

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4
Q

Liver blood supply

A

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

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5
Q

What are liver cells called

A

Hepatocytes

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6
Q

What are Kupffer cells?

A

The liver’s resident macrophages

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7
Q

What structures constitute the portal triad

A

Bile duct, hepatic artery and portal vein

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8
Q

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

A

Pre-hepatic jaundice (unconjugated dhyperbilirubinaemia)

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9
Q

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

A

Intrahepatic jaundice

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10
Q

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

A

Post-hepatic jaundice

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11
Q

Examples of enzymes which leak into the blood upon hepatocyte injury are:

A

ALT, AST, GGT

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12
Q

What enzyme level is raised in the blood during biliary obstruction

A

alkaline phosphatase

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13
Q

Major serum protein synthesised in the liver, It has a relatively long half-life, so low levels indicate long-tem insufficient liver function

A

Albumin

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14
Q

Liver cells synthesise most clotting factors, therefore a bleeding tendency results from hepatic insufficiency. This can be detected by measuring ………….

A

The prothrombin time

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15
Q

First imaging test to use in most circumstances to view the liver due to relatively low cost, mobility and no ionising radiation

A

Ultrasound

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16
Q

Name the three imaging techniques used to view the biliary tree

A

MRCP - only diagnostic
ERCP - should only use if therapeutic procedure planned
PTC - more invasive, only used if other methods do not work

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17
Q

Hepatocyte injury with cell death, inflammation and regeneration without structural change to the liver

A

Acute hepatitis

18
Q

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

A

Acute liver failure

19
Q

Infiltration of liver cells by fat

A

Steatosis

20
Q

Inflammation of the liver with concurrent fat accumulation

A

Steatohepatitis

21
Q

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

A

Cirrhosis

22
Q

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

A

Hepatocellular carcinoma

23
Q

What are the three histological changes seen in alcoholic liver injury:

A 
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
24
Q

How does alcohol injure the liver

A
  • 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
25
Q

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

A

Non-alcoholic fatty liver disease

26
Q

Similar to alcoholic steatohepatitis with less inflammation

A

non-alcoholic steatohepatitis(NASH)

27
Q

Hepatitis viruses spread by oral route

A

A, E

28
Q

Hepatitis viruses spread blood-borne route

A

B, C

29
Q

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

A

Autoimmune hepatitis

30
Q

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

A

Primary biliary cirrhosis

31
Q

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

A

Primary sclerosing cholangitis

32
Q

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

A

haemochromatosis

33
Q

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

A

Wilson’s disease

34
Q

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

A

Alpha-1 antitrypsin deficiency

35
Q

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

A

Portal hypertension

36
Q

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

A

Hepatocellular carcinoma

37
Q

Adenocarcinoma of bile ducts particularly associated with inflammatory conditions of the bile ducts(e.g. Primary sclerosing cholangitis)

A

Cholangiocarcinoma

38
Q

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

A

Metastatic tumours

39
Q

LOOK UP IN LETURE NOTES ABOUT LIVER TRANSPLANT

A

Liver transplantation

40
Q

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
A

Chronic liver failure

Alimentary (8 decks)

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