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LSS 2 > Alimentary System 7 - Jaundice and liver failure > Flashcards

Alimentary System 7 - Jaundice and liver failure Flashcards

1
Q

What percentage of bile is water?

A

97%

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2
Q

How much bile is produced daily, and where is it produced?

A
  • 500ml produced daily
  • 60% hepatocytes
  • 40% cholangiocytes
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3
Q

How to cholangiocytes affect bile composition?

A
  • Alter pH, fluidity, and modify bile
  • Water drawn in
  • Bicarbonate and chloride secreted into bile
  • Cholangiocytes introduce IgA by exocytosis
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4
Q

What moleules control bile flow and excretion of salts and toxins?

A
  • Biliary transporters
  • Bile salt excretory pump
  • MDR related proteins
  • Products of familial intrahepatic cholestasis gene and multidrug resistance gene
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5
Q

What is the function of the bile salt excretory pump (BESP)?

A
  • Active transport of bile acids into the bile

- Major determinant of bile flow

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6
Q

What is the function of MDR related proteins?

A
  • MDR1 mediates excretion of xenobiotics and cytotoxins
  • MDR 3 encodes a phospholipid transporter protein that translocates phosphatidylcholine from the inner to outer leaflet of the canalicular membrane
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7
Q

What are the two primary bile acids?

A
  • Cholic acid

- Chenodeoxycholic acid

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8
Q

How are secondary bile acids formed? List the two main acids.

A
  • Formed by conversion of primary acids via colonic bacteria
  • Cholic acid produces deoxycholic acid
  • Chenodeoxycholic acid forms lithocholic acid
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9
Q

What are bile salts?

A

Sodium and potassium salts of bile acids to glycine and taurine

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10
Q

List the functions of bile salts

A
  • Reduce surface tension of fats
  • Emulsify fat to prepare for digestion and absorption
  • Form micelles
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11
Q

Describe the composition of micelles

A
  • Hydrophilic domains face out

- Hydrophobic domains face in with free fatty acids and cholesterol inside

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12
Q

What is the issue with bile salts?

A

They are cytotoxic in high concentrations

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13
Q

List the pathway taken by bile in the biliary system

A
  • Produced in liver
  • Right+left hepatic duct form common hepatic duct
  • Enter the cystic duct to be stored in the gall bladder
  • Cystic duct unites with the common hepatic duct to form the common bile duct
  • Common bile duct joins with pancreatic duct to form ampulla of Vater
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14
Q

How is bile flow regulated?

A
  • Eating causes the sphincter of Oddi to relax
  • This is due to cholecystokinin
  • Cholecystokinin also causes the gall bladder to contract
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15
Q

Describe the circulation of bile salts between the stomach and liver

A
  • Called enterohepatic circulation
  • Bile salts travel to the GIT then back to the liver via blood, and the cycle continues
  • This also happens with some drugs present in the bile, and can prolong the action of drugs
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16
Q

What happens to the bile salts that are not absorbed by the ileum?

A
  • 95% absorbed - 5% enter the colon and form secondary bile ducts
  • Deoxycholate is absorbed
  • Lithocholate is excreted in the stool
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17
Q

How are bile salts absorbed in the ileum?

A

Using a sodium/bile salt co-transporter system with the sodium/potassium pump

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18
Q

What happens to bile salts in terminal ileal resection or disease?

A
  • Decreased bile salt reabsorption, and increased bile in the stool
  • This is because enterohepatic circulation is interrupted
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19
Q

What happens if bile is stopped from entering the gut?

A
  • Malabsorption of fat soluble vitamins (ADEK)

- 50% ingested fat appears in faeces

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20
Q

List the functions of the gall bladder

A
  • Stores bile
  • Acidifies bile
  • Concentrates bile (absorption of ions), reducing volume by 80-90%
21
Q

What are the effects of cholecystectomy?

A
  • Gall bladder is removed

- Digestion is mostly functional, but foods with high fat content need to be avoided

22
Q

What is bilirubin?

A

A water insoluble yellow pigment

23
Q

List the ways bilirubin is made and their relative proportions

A
  • 75% haemoglobin breakdown (spleen)
  • 22% catabolism of other haem proteins
  • 3% ineffective bone marrow erythropoiesis
24
Q

Describe the pathway taken by bilirubin to the gut

A
  • Bound to albumin from the spleen
  • Travels to the liver and dissociates
  • Conjugated to glucoronic acid by UDPGT to form diglucoronic acid
  • Transported into bile canaliculi to the GIT
25
Q

What does total bilirubin equal?

A

conjugated + unconjugated bilirubin

26
Q

What are urobilinogens and where are they formed?

A
  • Water soluble colourless derivatives of bilirubin formed by action of GIT bacteria
  • Mainly formed in the intestines and reabsorbed to be excreted in the kidney
27
Q

What is GIT mucosa permeable to with relation to bilirubin?

A
  • Permeable to unconjugated bilirubin and urobilinogens

- Impermeable to conjugated bilirubins

28
Q

How is urobilinogen excreted in the stool?

A
  • As stercobilinogen

- Oxidised to sercobilin which makes faeces brown

29
Q

What is jaundice?

A
  • A disease characterised by yellowing of the eyeballs (first) and the skin
  • Can be caused by cholestasis (slow bile flow) and resulting buildup of bilirubin in the blood
  • Bilirubin over 40-50microM/L
30
Q

List the causes of prehepatic jaundice

A
  • Haemolysis
  • Massive Transfusion
  • Haematoma resorption
  • Ineffective erythropoiesis
31
Q

List the causes of hepatic jaundice

A
  • Defective uptake, conjugation or bilirubin excretion

- Caused by liver failure (acute/chronic)

32
Q

List the posthepatic causes of jaundice

A
  • Defective transport due to blockage of the biliary duct system
  • Bile duct stones
  • Malignancy
  • Causes pale faeces due to decreased sercobilin and darker urine
33
Q

How can the three types of jaundice be distinguished?

A
  • Post hepatic will have high conjugated bilirubin and dilated bile ducts
  • Pre/hepatic jaundice have high unconjugated bilirubin, so ask about history of liver function to distinguish
34
Q

What is Gilberts syndrome?

A
  • Commonest hereditory cause of jaundice
  • Relatively asymptomatic except in times of stress
  • Affects 5% of the population
  • Caused by a reduction in activity of the UDPGT enzyme
35
Q

What is liver failure?

A

When the rate of hepatocyte death is higher than rate of regeneration

36
Q

Compare acute and chronic liver failure

A
  • Acute caused by paracetamol, as well as some diseases of pregnancy
  • Chronic caused by viral hepatitis, alcohol excess, and autoimmune diseases
37
Q

List the consequences of hepatocyte failure

A
  • Encephalopathy and cerebral oedema
  • Hypoglycaemia
  • Bleeding
  • Increased suseptability to infection
  • Renal failure
38
Q

What are the issues with liver transplants?

A
  • 10% mortality in 1 year
  • Lifelong immunosuppression
  • Expensive
  • Lack of donors
39
Q

List the early symptoms of liver disease

A
  • Lethargy
  • Anorexia
  • Malaise
  • Pruritus (itchy skin)
  • Right upper quadrant pain
40
Q

List the late symptoms of liver disease

A
  • Peripheral swelling
  • Abdominal bloating
  • Bruising
  • Vomiting of blood
  • Confusion and somnolence
41
Q

List the physical signs of liver disease

A
  • Jaundice
  • Gynaecomastia, testicular atrophy
  • Spider naevi
  • Loss of body hair
  • Palmar erythema
  • Xanthelasma
  • Finger clubbing
  • Ascites
  • Oedema
42
Q

Define liver cirrhosis

A
  • Necrosis of liver cells followed by progressive fibrosis and nodule formation
  • Leads to impairment of liver cell function, and distortion of the liver architecture
43
Q

List the common causes of cirrhosis

A
  • Alcohol (western world)
  • Hepatitis B and C world wide
  • Response to chronic liver injury
44
Q

Compare the two types of cirrhosis

A
  • Micronodular (uniform, small nodules up to 3mm in diameter, caused by ongoing alcohol damage)
  • Macronodular cirrhosis (varying size, seein in hepatitis)
  • Can be mixed
45
Q

Define acute liver failure

A

Severe hepatic dysfunction occuring within 6 months of the onset of symptoms of liver disease

46
Q

Describe the classification of acute liver failure

A
  • Hyperacute is where encephalopathy occurs within 7 days of jaundice
  • Acute is 8-28 days after jaundice
  • Subacute is 5-12 weeks after onset of jaundice
47
Q

List the clinical features of acute liver failure

A
  • CNS complications (hepatic encephalopathy)
  • Jaundice
  • Coagulopathy (bleeding and easy bruising)
  • Renal failure
  • Sepsis
  • Cardiovascular complications
  • Metabolic complications
48
Q

Define chronic liverfailure

A
  • Deterioration in liver function superimposed on chronic liver disease
  • Also called decompensation

LSS 2 (32 decks)

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