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Alimentary system > 7. Liver failure and Jaundice > Flashcards

7. Liver failure and Jaundice Flashcards

1
Q

State 3 roles of bile.

A

Cholesterol homeostasis
Dietary lipid/vitamin absorption
Removal of xenobiotics, drugs and endogenous waste products (e.g. steroid hormones)

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2
Q

List the major components of bile.

A

WATER, Bile salts, Bile pigments, cholesterol, bilirubin, phospholipids, bicarbonate

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3
Q

How much bile is produced daily?

A

500 mL

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4
Q

What gives bile its green/ yellow colour?

A

glucoronides of bile pigments

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5
Q

Which cell types produce bile? State the relative proportions of bile produced by each cell type.

A

Hepatocytes: 60%
Cholangiocytes: 40%

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6
Q

How does bile change as it flows through the biliary tree?

A 
pH is altered
H2O is drawn into bile 
Glucose and organic acids are reabsorbed
HCO3- and Cl- are secreted into bile by CFTR
IgA is secreted into bile
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7
Q

What does bile flow depend on?

A

concentration of the bile (created by biliary transporters)

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8
Q

What regulates bile concentration?

A

Transporters on hepatocytes and cholangiocytes

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9
Q

State 4 of the main transporters that regulate bile concentration.

A

Bile Salt Excretory Protein (BSEP)
MDR related proteins (MRP1)
Multi-drug Resistance Genes (MDR1)
Familial Intrahepatic Cholestasis gene (FIC1)

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10
Q

Which transporter actively transports bile acids across hepatocyte canalicular membranes into bile?

A

BSEP

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11
Q

What is the function of bile salts?

A

Reduce surface tension of fats

Emulsify fat preparatory to its digestion/absorption

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12
Q

What percentage of bile is water?

A

97%

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13
Q

Why do Bile salts form micelles?

A

Amphipathic (1 hydrophilic surface facing out, 1 hydrophobic (fatty acid/cholesterol) surface facing in)

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14
Q

What makes bile salts potentially cytotoxic in high concentrations?

A

Their detergent like actions

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15
Q

Describe the effect of cholecystokinin (CCK) on bile release.

A

Causes contraction of the gallbladder and relaxation of the sphincter of Oddi

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16
Q

Where is bile stored between meals (when sphincter of odd is contracted), and what duct carries it to/ from this location?

A

Gall bladder

Cystic duct

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17
Q

What join to form the common bile duct?

A

Common hepatic duct

Cystic duct

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18
Q

What join to form the Common Hepatic Duct?

A

Right and left hepatic ducts

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19
Q

Describe the enterohepatic circulation

A

Some things that come from the liver in the bile enter the intestine and circulate back to the liver (portal system)

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20
Q

What is the consequence of drugs with high EH circulation?

A

Have prolonged effects

dose may need to be adjusted

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21
Q

What percentage of bile salts are reabsorbed in the terminal ileum? (and thus undergo enterohepatic circulation)

A

95%

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22
Q

What % of bile salts are converted to secondary bile acids?

A

5%

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23
Q

What happens to the 2 secondary bile acids?

A

Deoxycholate reabsorbed

99% lithocholate excreted in stool

24
Q

Describe how terminal ileal disease can cause steatorrhoea.

A

Less bile salts are reabsorbed, so less bile salts are released in the bile into the duodenum so there is less fat emulsification, digestion and absorption.
More fat passes through the small intestines, enters the colon and leaves the body.
Malabsorption of fat soluble vitamins

25
Q

State 3 important roles of the gallbladder.

A 
Stores bile (50ml)
Acidifies bile
Concentrates bile (can reduce volume by 90%)
26
Q

What are the effects of cholecystectomy?

A

Bile drips into the duodenum (can function normally)
Not able to produce a large release of bile due to gallbladder contraction so may result in discomfort after eating a fatty meal.

27
Q

What are the main sources of bilirubin?

A

75% Breakdown of haem group in haemoglobin
22% Breakdown of other haem proteins
3% from ineffective erythropoiesis

28
Q

What plasma protein carries bilirubin to the liver? Why is this required?

A

Albumin

Spleen is where most Br is released but is water insoluble

29
Q

What happens to bilirubin when it reaches the liver?

A

BR is conjugated with glucuronic acid to make it more water soluble by the action of UDPGA from smooth ER
(Forms BR diglucuronide)

30
Q

Equation for total BR

A

Free BR (unconjugated) + Conjugated BR

31
Q

What is UDPGA AKA?

A

UDPGT

32
Q

What 2 substances can bilirubin be converted to in the intestines and how are they excreted?

A

Urobilinogen (mainly in the intestines by bacterial action)
and excreted via the kidneys.
1/2 is reabsorbed and taken up via the portal vein to the liver, enters circulation and is excreted by the kidneys.
GIT mucosa is impermeable to conjugated BR but is permeable to unconjugated BR and urobilinogens.
So some unconjugated BR enters the enterohepatic circulation, and some forms urobilinogens.
20% of urobilinogens are reabsorbed into general circulation.
Some converted to stercobilinogen and then to stercobilin and excreted with the stools

33
Q

Why is Faeces brown?

A

Conjugated BR pumped into intestine
Enters colon
In colon, BR is reduced to stercobilinogen
Stercobilinogen is oxidized to stercobilin which is brown

34
Q

What concentration of bilirubin is considered jaundice?

A

> 34 mcmol/L

35
Q

What may be a cause of jaundice?

A

Cholestasis (slow/ cessation of bile flow)

36
Q

What are the 3 types of jaundice?

A

Pre-hepatic
Hepatic
Post-hepatic

37
Q

State 4 causes of pre-hepatic jaundice. What would be the expected conjugated: unconjugated ratio?

A

Increased unconjugated BR because there is too much BR being produced for the liver to conjugate it all
Caused by haemolysis, haematoma resorption, massive transfusion, ineffective erythropoiesis

38
Q

What characterises hepatic jaundice?

A

Defective uptake, conjugation and BR excretion

Blood test: predominantly unconjugated BR

39
Q

What causes hepatic jaundice?

A

Liver failure

Acute/ chronic

40
Q

How can you distinguish between pre-hepatic and hepatic jaundice?

A

Pre-hepatic have a normal liver

Hepatic: Lots of liver enzymes and history of cause of liver failure

41
Q

What can cause post-hepatic jaundice?

A

An obstruction to the biliary system, reduces bile flow into duodenum
Amount of BR entering gut is reduced, thus amount of BR in body increases
e.g. pancreatic carcinoma or a gallstone

42
Q

3 clinical features of post-hepatic jaundice?

A

Blood test: Most BR will be conjugated
Pale faeces: bile isn’t entering the colon so less stercobilin is produced
Dark urine: body is tries to excrete some BR via the urine, which would contain a lot of urobilinogen, which is dark
Dilated bile ducts on scan: bile back up causes swelling

43
Q

What is Gilbert’s Syndrome?

A

Most common hereditary cause of increased BR
Autosomal recessive
Elevated unconjugated BR in bloodstream
Caused by a 70-80% decrease in the glucuronidation activity of UDPGA.
Mild jaundice may occur when stressed, infected, fasting

44
Q

Liver Failure pathophysiology

A

Rate of hepatocyte death > regeneration

Could be caused by apoptosis or necrosis

45
Q

What are the 2 main types of liver failure and how are they different?

A

Acute: rapid development, occurs in a pre-existing normal liver (fulminant/ sub-fulminant)
Chronic: years/ cirrhosis, due to chronic liver disease

46
Q

List 4 causes of chronic liver failure

A

Viral hepatitis (B and C)
Alcohol excess
Fatty liver
Autoimmune disease

47
Q

List 3 toxins that cause acute liver failure

A

Paracetamol
Amanita phalloides
Bacillus cereus

48
Q

Prevalence of acute liver failure

A

Relatively uncommon

most common cause is paracetamol OD

49
Q

4 Acute liver failure causes (other than toxins)

A

Diseases of pregnancy (AFLOP, Hepatic infarction)
Idiosyncratic drug reactions (NSAID’s, Amoxicillin, rifampicin)
Vascular Diseases: (Ischaemic hepatitis, VOD)
Metabolic causes: (Wilson’s disease, Reye’s syndrome)

50
Q

How does aetiology of acute liver failure differ between west and developing world?

A

West: Usually drug induced

Developing world: Viral hepatitis

51
Q

State some of the functions of the liver.

A 
Detoxification
Glycogen storage
Production of clotting factors
Immune function and globulin production 
Maintenance of homeostasis
52
Q

What are the results of hepatocyte failure for liver function?

A

Encephalopathy and cerebral oedema (Rise in ammonia)
Hypoglycaemia
Coagulopathy and bleeding
Increased susceptibility to infection
Circulatory collapse, renal failure (not making albumin and low BP)

53
Q

7 Causes of death in acute liver failure

A 
Bacterial and fungal infections
Circulatory instability
Cerebral Oedema
Renal failure
Respiratory failure
Acid-base and electrolyte disturbance
Coagulopathy
54
Q

What is the only therapeutic intervention of proven benefit for acute liver failure?

A

Liver transplant

55
Q

Outcome of liver transplant

A

5 year survival rate between 60-80%

No recurrence of disease but patient will require life-long immunosuppression

Alimentary system (15 decks)

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