Bile, Gall Bladder and Gall Stones Flashcards Preview

Physiology 1 - SGUL (Sem 2) > Bile, Gall Bladder and Gall Stones > Flashcards

Flashcards in Bile, Gall Bladder and Gall Stones Deck (25)
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1
Q

What is the ampulla of Vater?

A

The ampulla of Vater (hepatopancreatic duct/ampulla) is formed out of the union of the pancreatic duct and the common bile duct.
It is found near the duodenal papilla.

2
Q

What is the general function of the gallbladder?

A

It stores and concentrates bile.

The bile is concentrated because of active Na+ transport (and H2O) from the gallbladder.
The pH of the bile drops (becomes ‘acidic’) as Na+ is exchanged for H+.

3
Q

Describe bile acid synthesis.

A

Bile acid synthesis occurs in liver cells which synthesise primary bile acids (cholic acid and chenodeoxycholic acid in humans) via cytochrome P450-mediated oxidation of cholesterol in a multi-step process.

Approximately 600 mg of bile salts are synthesised daily to replace bile acids lost in faeces.

4
Q

Describe bile flow (as in what structures it goes through).

A
Hepatocytes
                  ⬇ 
       Bile Canaliculi
                  ⬇ 
    Terminal Bile ducts
                  ⬇ 
Hepatic ducts (left and right)
                  ⬇ 
     Common Bile duct
5
Q

What two components make up a bile acid?

A
  • bile

- a cation (eg. Na+)

6
Q

What two cells secrete bile salts (and what else)?

A
  • HEPATOCYTES: cholesterol, lecithin, bile acids, bile pigments (bilirubin, biliverdin, urobilin, etc.)
  • EPITHELIAL CELLS OF BILE DUCTS: bicarbonate-rich salt solution

[secretin influences the secretion of bicarbonate-rich salt solutions]

7
Q

Can cholecystomised patients have a good quality of life?

A

Yes, as long as they don’t eat too much fatty food.

8
Q

What substances are secreted across the canalicular membrane?

A
  • bile acids
  • phosphatidylcholine
  • conjugated bilirubin
  • cholesterol
  • xenobiotics (foreign chemical/ substance, e.g. drugs)

Specific transporters ferry the above into bile.
Substances such as water, glucose, Ca2+, GSH (glutathione), amino acids, and urea enter the bile by diffusion.

9
Q

Describe the composition of hepatic and gallbladder bile.

A

Hepatic bile: 97% water; cholesterol, lecithin, bile acids, bile pigments, etc.

Gallbladder bile: 89% water; HCP3-, Cl-, Ca2+, Mg2+, Na+, cholesterol, bilirubin, bile salts, etc.

Bile is concentrated in the gallbladder (NaCl and H2O loss means increased solid content)
Bile goes to the gallbladder between meals when the Sphincter of Oddi is closed.

10
Q

Briefly describe bile acids.

A

Bile acids are important in the GIT; they’re made from cholesterol and secreted into bile and conjugated to glycine or taurine.

Conjugation helps to increase the ability of bile acids to be secreted and also decrease their cytotoxicity.

11
Q

List and describe the 4 major bile acids found in humans.

A

PRIMARY BILE ACIDS:

  • Cholic Acid: 50% - quantitatively more important
  • Chenodeoxycholic Acid: 30%

SECONDARY BILE ACIDS:

  • Deoxycholic Acid: 15%
  • Lithocholic Acid: 5%

Primary bile acids are formed in the liver, while secondary bile acids are formed in the colon.

Cholesterol is converted to primary bile acids, then to secondary bile acids.

12
Q

List the main functions of bile/bile acids as metabolic regulators.

A
  • the elimination of cholesterol to bile acids (5% excreted in faeces) [excess cholesterol is synthesised into bile acids]
  • reduce the precipitation of cholesterol in the gallbladder (bile acids and phospholipids help solubilise cholesterol in bile)
  • facilitate the absorption of fat-soluble vitamins (ADEK)
  • regulate their own transport and metabolism via enterohepatic circulation (through the activation of various signalling pathways)
  • facilitate the digestion of triglycerides (work in cohort with phospholipids (lecithin) and monoglycerides to ensure the emulsification of fats)
    [they act as emulsifying agents that render fats accessible to pancreatic lipase]
13
Q

Describe the contraction of the gallbladder during the intestinal phase.

A

The vagus nerve conveys information about the state of the body’s organs to the CNS; here, it conveys the contents of the duodenum to the CNS.

If it contains lipids, this causes the release of CCK, which stimulates the release of bile which helps in the emulsification of fats and prepares them for digestion by pancreatic lipases.

14
Q

What are CCK and secretin released in response to?

A

CCK is released in response to lipids/fats.

Secretin is released in response to HCl in the duodenum. It will then go to stimulate duct cells in the liver (to release a bicarbonate-rich solution).

15
Q

Describe the mechanisms controlling the secretion of bile into the duodenum.

A

When the nutrients (lipids) are sensed in the duodenum, they trigger the release of CCK, which acts directly and indirectly.

Directly, it contracts the gallbladder.
Indirectly, it sends a signal to the dorsal vagal complex, which then sends a signal back down to contract the gallbladder (via ACh) and relax the Sphincter of Oddi (via NO/VIP).

There are also other levels of control - motilin, for example, induces gallbladder emptying and antral contractions in the fasting state of humans.

All this is mediated by distention, the neuronal signals and hormonal signals.

16
Q

In a near all-embracing manner, explain the release of bile into the duodenum.

A

1) Chyme enters the duodenum causing the release of cholecystokinin (CCK) and secretin from the duodenal enteroendocrine cells.
2) CCK and secretin enter the bloodstream, absorbed by the intestinal mucosa.
3) CCK induces the secretion of enzyme-rich pancreatic juice. Secretin causes the secretion of bicarbonate-rich pancreatic juice.
4) Bile salts and, to a lesser extent, secretin, is transported via the bloodstream and stimulates the liver to produce bile more rapidly.
5) CCK (via the bloodstream) causes the gallbladder to contract and the hepatopancreatic sphincter to relax; bile enters the duodenum.
6) During the cephalic and gastric phases, vagal nerve stimulation causes weak contractions of the gallbladder.

[note, the role of ACh, NO, VIP, etc. are omitted here]

17
Q

Describe how bile salts are ‘recycled’.

A

Most of the bile salts are reabsorbed by Na+-bile salt coupled transporters.
The bile salts are returned to the liver and secreted gain into the bile.

The recycling pathway from the intestine to the liver and back to the intestine is the enterohepatic circulation (via the hepatic portal vein).

18
Q

Both primary and secondary bile acids are removed by the intestine into the liver via the portal circulation.

A
  • There are specific transporters in the terminal ileum that transport bile salts from the lumen of the digestive tract to the intestinal capillaries.
  • The bile salts are transported directly to the liver via the hepatic portal vein.
  • The hepatocytes take up bile salts from the blood, and increase the secretion of bile salts into the bile canaliculi – these are the small passageways that convey bile into the larger bile ducts.

It is estimated that 95% of the bile that is released into the small intestine is recycled via the enterohepatic circulation, 5% is lost in the faeces.

19
Q

What will interruption of the enterohepatic circulation cause?

A
  • excess synthesis of bile salts by the liver (as you would be losing bile salts)
  • the kidneys will excrete the synthesised bile salts (and some cholesterol)
20
Q

Describe the formation of gallstones.

A

Changes in the composition of bile may cause cholesterol to precipitate out to form gallstones. There may also be precipitation of the pigments.

21
Q

What causes the increased cholesterol that could cause gallstones?

A
  • the liver excretes it in excess

The reabsorption of water and salt provides an environment for gallstones to form.

22
Q

What are the two types of gallstones?

A
  • cholesterol stones (85%)

- calcium bilirubinate (15%)

23
Q

List some factors involved in gallstone formation.

A
  • Bile Stasis: stones form in bile that is sequestered in the gallbladder rather than bile that is flowing in the bile ducts into the duodenum
  • decreased amount of bile acids due to malabsorption (in cystic fibrosis - dehydrated and acidic; 10% incidence); problems with bile production
  • chronic infection - bacteria help in the formation of pigment stones
  • supersaturation of bile with cholesterol
  • presence of nucleation factors or glycoprotein (possibly?)
24
Q

How would you visualise the gallbladder in a case of gallstones?

A
  • ultrasonography and computer tomography: explore the upper right quadrant of the gallbladder to detect gallstones
  • cholescintigraphy: administer technetium-99m-labelled derivative of iminodiacetic acid (radioactive tracer), to show images of the gallbladder and its ducts (we can then inject CCK to see how the gallbladder behaves)
  • endoscope retrograde cholangiopancreatography (ERCP): can visualise the biliary tree by injecting contrast media from an endoscope channel
25
Q

What symptoms will you end up with if a gallstone got stuck in each of the three possible places it could form?

A

1) gallstone in the cystic bile duct:
- painful gallbladder contractions
- inflammation of the gallbladder (acute cholecystitis)

2) gallstone blocking the common bile duct:
- pain and nausea
- lack of bile release
- failure to excrete bilirubin leads to jaundice
- can cause bacterial infection (cholangitis)

3) gallstone blocking the duodenal papilla
- inappropriate activation of pancreatic enzymes
- acute pancreatitis

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