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sem 2 Liver and GI > Bile, Gallbladder and gall stones > Flashcards

Bile, Gallbladder and gall stones Flashcards

1
Q

main function of the gall bladder?

A

storage and concentration of bile

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2
Q

why is bile concentrated?

A

because of active Na+ transport from the gallbladder, and H2O follows sodium out as well.

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3
Q

what does pancreatic juice consist of?

A

Bile salts, bile pigments and dissolved substances in alkaline electrolytes
-some electrolytes come from the gall bladder and some come from the pancreas (gall bladder empties its contents and joins up with the pancreas)

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4
Q

where does bile come from?

A

liver

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5
Q

explain the flow of bile from hepatocytes:

A 
Hepatocytes
       ↓
Bile canaliculi (merge to form ductules)
        ↓
Terminal bile ducts
       ↓
Hepatic ducts (left and right)
       ↓
Common bile duct
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6
Q

where may water be added to bile?

A

Water is (may be) added via specific tight junctions within ductules

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7
Q

what are cholangiocytes?

A

epithelial cells of the bile duct

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8
Q

what do the ductule do?

A
  • scavenge glucose, amino acids
  • secrete IgA (for mucosal protection), HCO3- and H2O in response to secretin in the postprandial period
  • hydrolyse GSH
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9
Q

how many diff cell types can secrete bile? name them

A

2

  • hepatocytes
  • epithelial cells of bile ducts
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10
Q

what do hepatocytes secrete?

A
  • cholesterol
  • lecithin
  • bile acids
  • bile pigments
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11
Q

list the bile pigments secreted by the hepatocytes and their function

A
  • bilirubin (makes your skin a bit blue when bruised)
  • biliverdin (makes you yellow in terms of jaundice)
  • urobilin (colours the urine)
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12
Q

what do epithelial cells of bile ducts secrete?

A

bicarbonate-rich salt solution

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13
Q

which substance influences the release of bicarbonate-rich salt solution and H2O?

A

secretin

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14
Q

what is secretion of bile greatest

A

during and after a meal

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15
Q

an increase in [bile salt] in the blood leads to what?

A

an increase of bile salt secretion into bile canaliculi

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16
Q

what is enterohepatic circulation?

A

bile moving from the liver back into the GI tract as it gets reabsorbed into portal circulation

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17
Q

increased secretion leads to what?

A

increase in the flow of bile

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18
Q

what and where is the sphincter of Oddi?

A
  • hepatopancreatic sphincter

- controls when the fluid coming from the pancreas and gall bladder enters the second part of the duodenum

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19
Q

when does the sphincter of oddi contract?

A
  • Sphincter of Oddi contracts during periods of fasting. Whatever is secreted is back up and stored into the gall bladder.
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20
Q

when does the sphincter of oddi relax?

A
  • Sphincter of Oddi relaxes during and after meals. Squirted down into duodenum.
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21
Q

What happens during the interdigestive period (period between meals)?

A
  • sphincter of Oddi is contracted, which prevents bile from flowing out into the duodenum
  • this causes pressure to increase in the common bile duct –> bile flows into the gallbladder
  • in the gallbladder, the bile becomes concentrated because the epithelial cells reabsorb water and electrolytes
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22
Q

is bile/gall bladder essential for life?

A

no, you can cut it out and survive- cholecystectomised patients have a good quality of life. BUT, you have to be careful with what you eat- if you aren’t careful you may have problems with emulsification of fats

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23
Q

What substances are secreted across the bile canalicular membrane (into bile canaliculi) and how do they get across?

A
  • Bile acids
  • Phosphatidylcholine
  • Conjugated bilirubin
  • Cholesterol
  • Xenobiotics (foreign substance

– Specific transporters ferry the above into bile

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24
Q

what substances enter the bile via diffusion?

A 
-water
glucose
-Ca2+
-GSH
-amino acids
-urea
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25
Q

describe the composition of hepatic bile:

A

97% water

cholesterol, lecithin, bile acids, bile pigments, etc.

26
Q

describe the composition of gall bladder bile:

A

89% water

HCO3-, Cl-, Ca2+, Mg2+, Na+, cholesterol, bilirubin, bile salts, etc.

27
Q

the synthesis of bile starts from what?

so, the production of bile causes a reduction in what?

A

cholesterol breakdown

so, production of bile reduces cholesterol levels

28
Q

how many pathways are there are for bile acid/salt formation? name them and describe them

A

2 pathways

  • Classic/neutral pathway
  • Alternative/acidic pathway

in both pathways you can form deoxycholic acid and cholic acid (primary bile acids)

29
Q

bile acid + ? = bile salt

A

bile acid + sodium = bile salt

30
Q

what happens to bile acids after they enter bile?

A

-conjugated to glycine or taurine

31
Q

why are bile acids conjugated to glycine or taurine?

A
  • helps to increase the ability of bile acids to be secreted and reabsorbed
  • decreases their cytotoxicity (because they’re acidic, there is potential for them to cause damage to the cell)
32
Q

how can bile acids become deconjugated?

A

by the enzymes within anaerobic microbes located within the gut

33
Q

name the 4 major bile acids found in humans, and how they are categorised:

A

-Cholic acid: 50% = quantitatively more important
-Chenodeoxycholic acid: 30%
• principal primary bile acids formed in the liver

-Deoxycholic acid: 15%
-Lithocholic acid: 5%
• secondary bile acids that are formed in the colon

34
Q

what are the equations for the conversion of primary bile acids to secondary bile acids, via intestinal bacteria?

A

chenodeoxycholic acid –> lithocholic acid and ursodeoxycholic acid

cholic acid –> deoxycholic acid

35
Q

list the main functions of Bile/Bile Acids:

A

Metabolic Regulators

  1. Elimination of cholesterol to bile acids (5% excreted in faeces)
    – Synthesis and subsequent excretion of bile acids in the faeces represents a significant mechanism for the elimination of excess cholesterol
  2. Reduce the precipitation of cholesterol in gallbladder; bile acids and phospholipids help solubilise cholesterol in the bile
  3. Facilitate the absorption of fat-soluble vitamins (ADEK)
  4. Regulate their own transport and metabolism via enterohepatic circulation
  5. Facilitate the digestion of triglycerides - work in concert with phospholipids (licithin) and monoglycerides to ensure the emulsification of fats
36
Q

why is emulsification of fats good?

A

makes them more accessible to pancreatic lipases

37
Q

3 phases of digestion (recap)

A
  • Cephalic phase: taste, smell and presence of food in the mouth → initiate impulses via vagus nerve and initiate secretion
  • Gastric phase: distension of stomach generates impulses in vagus nerve
  • Intestinal phase: period of most gallbladder emptying
38
Q

in the intestinal phase, what are the key mediators involved in mechanism for increased release?

A
  1. CCK in response to lipids; can also stimulate pancreatic secretions that are rich in bicarbonate
  2. Secretin in response to acidic chyme, stimulates duct cells
    - both released by duodenum
39
Q

effects of CCK

A
  • secreted from duodenum
  • causes sphincter of oddi to relax
  • triggers contraction of gall bladder
40
Q

what is the role of the vagus nerve?

A

conveys the contents of the duodenum to the CNS

-eg. 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

41
Q

describe some mechanisms of controlling the secretion of bile into the duodenum:

A

Motilin → gallbladder motility and volume
- Motilin induces gall bladder emptying and antral contractions in the fasted state in humans

CCK causes contraction of the gall bladder
- secretion of secretin, which will have an effect on the gall bladder and pancreas

efferent effect ofNO and VIP
- relaxation of Sphincter of Oddi

42
Q

what stimulates secretion of CCK (cholecytoskinin)?

A

presence of a fatty meal

LOOK AT 6 PART DIAGRAM IN NOTES!

43
Q

what is bile essential for?

A

chemical digestion of fat

44
Q

when and where is bile secreted?

A

from the pancreas when chyme enters the small intestine from the stomach

45
Q

chyme stimulates what?

A

stimulates enteroendocrine cells of the duodenum to secrete CCK and secretin
• CCK and secretin are absorbed intestinal mucosa into the bloodstream

46
Q

CCK and secretion summary of action

A
  1. Stimulate the liver to synthesise and release bile into the common bile duct.
  2. CCK stimulates the gallbladder to contract, ejecting concentrated bile into the cystic duct and common bile duct.
  3. Hepatopancreatic sphincter (Sphincter of Oddi) relaxes, allowing bile to flow from the common bile duct into the duodenum
47
Q

what percentage of bile salts are reabsorbed and how does this occur?

A

Most of bile salts are reabsorbed (95%) by Na+-bile salt coupled transporters

48
Q

what happens when there is excess synthesis of bile salts?

A

Kidneys will excrete the synthesised bile salts (and some cholesterol)

49
Q

the rate of incidence of gall stones increases with what?

A

age

50
Q

having a higher cholesterol content of bile means what?

A

greater concentrations of phospholipid and bile salts

51
Q

What causes the increased cholesterol in bile?

A

• Liver secretes excess
• Reabsorption of salt and water
• The cholesterol crystallises and forms gallstones
– Precipitation of bile pigments

52
Q

what are the 2 types of gall stones?

A
  • Cholesterol stones (85%): obesity, decreased bile acids compared to phospholipids
  • Calcium bilirubinate stones- due to increased conjugated bilirubin (usually associated with haemolytic anaemia)
53
Q

list some factors involved in gallstone formation:

A
  1. 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
  2. Decreased amount of bile acids and phospholipids due to malabsorption (GI tract blocked by a lot of mucus like in cystic fibrosis – dehydrated and acidic; 10% higher incidence); problems with bile production
  3. Chronic infection – bacteria help in the formation of pigment stones
  4. Super-saturation of bile with cholesterol
  5. Presence of nucleation factors?? (anti-nucleation factors may increase time taken for stone to form which is good, more research needs to be done)
54
Q

small gallstones:

A

easy passage via bile duct, not too bad

55
Q

larger gall stones:

A
  • Larger gallstones lodge in the opening of gallbladder
  • Duct from pancreas joins the bile duct before it joins the duodenum
  • Lodging of gallstones at this point causes the stoppage of bile and pancreatic secretions (pressure builds up, can impact the cystic duct or common bile duct)
  • Further pressure build up causes decreased secretion of bile
56
Q

consequence of gall stone lodging

A
  • nutritional deficiency
  • infection and fevers as a result
  • individuals can complain of upper right quadrant pain
57
Q

what is jaundice?

A

increased accumulation of bilirubin in blood, yellowing of skin

58
Q

how can we visualise the gallbladder?

A

– Ultrasonography and computer tomography: explore the right upper quadrant of gallbladder to detect gallstones

– Insert device(s) and remove gallstone fragments that may be obstructing the bile flow, pancreatic juice or both

59
Q

Clinical Features of Gallstones

A

If the neck of the cystic duct is impaired → biliary pain ensues (acute cholecystitis)

• Gallstones that impact common bile duct
→ obstruction of bile flow and cholestatic jaundice which can cause bacterial infections (cholangitis)

  • Gallbladder will secrete mucus if inflamed and rupture
  • jaundice due to bilirubin build up
60
Q

what % of are asymptomatic (gallstones remain in gallbladder)?

A

85%

sem 2 Liver and GI (11 decks)

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