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GI > Bile, gallbladder, gallstones > Flashcards

Bile, gallbladder, gallstones Flashcards

1
Q

Role of gallbladder?

A

Storage of bile for modifying fats to be digested

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2
Q

Why does gallbladder store concentrated bile?

A

active Na+ transport from gallbladder + H2O follows→ increased solid content

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3
Q

What does pancreatic juice contain?

A

bile salts, bile pigments + dissolved substances in alkaline electrolytes

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4
Q

pH of gall bladder bile?

A

7

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5
Q

Why does bile become more acidic?

A
  • Na+ exchanged for H + ,

- but [Na + ] increases as more Cl- and HCO3 - lost

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6
Q

Role of gall bladder secretions?

A

come together with pancreatic secretions, go into

duodenum to neutralise acidic chyme from stomach, especially HCO3- vital

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7
Q

Describe how bile is modified

A
  • bile formed in liver (from bile acids) moves through larger ductules + ducts and as composition is modified (by movement of Na+ and H+ )
  • water added by specific tight junctions within ductules
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8
Q

Role of cholangiocytes?

A

secretion of bile in healthy individuals via net release of HCO3 - and H2O

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9
Q

What contributes to secretions from cholangiocytes?

A

hormones + other locally acting mediators eg secretin, ACh, ATP

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10
Q

Watery secretions of pancreas?

A

HCO3-, Cl-

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11
Q

What are bile salts formed from?

A

bile acid + cation eg Na+

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12
Q

Role of ductules?

A
  • Remove glucose, AA, GSH is hydrolysed, due to too much glucose etc could result in bacteria.
  • Secrete IgA for mucosal protection + HCO3 - in response to secretin in postprandial period (after meal)
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13
Q

Role of ductules?

A
  • Remove glucose, AA, GSH is hydrolysed, due to too much glucose etc could result in bacteria.
  • Secrete IgA for mucosal protection + HCO3- in response to secretin in postprandial period (after meal)
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14
Q

Describe how bile flows

A
  • hepatocytes
  • bile canaliculi (merge to form ductules)
  • terminal bile ducts
  • hepatic ducts (left + right)
  • common bile duct
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15
Q

What are bile canaliculi?

A

bile capillaries, tube collects bile secreted by hepatocytes

small passageways that convey bile into larger bile ducts

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16
Q

What are The Canals of Hering?

A

part of outflow system of exocrine bile product from liver

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17
Q

What secretes components of bile + what are the components?

A
  • Hepatocytes = cholesterol, lectithin, bile acids, bile pigments (bilirubin, biliverdin, urobillin)
  • Epithelial cells of bile duct = bicarbonate rich salt solution
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18
Q

Role of sphincter of Oddi?

A
  • Contracts during fasting, so bile goes back up to gall bladder
  • Relaxes during + after meals
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19
Q

Role of secretin?

A

influences secretion of bicarbonate-rich solution + H2O

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20
Q

Describe how bile secretion into canaliculi is regulated by bile conc in blood

A

-↑bile during + after a meal to digest the food esp if fatty
meal
-↑bile salt conc in the blood
-↑bile salt secretion into the bile canaliculi

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21
Q

What’s sphincter of oddi?

A

hepatopancreatic sphincter

Lecithin helps to dissolve fat and cholesterol and can help regulate the functions of the liver, gallbladder and kidney
Biliverdin (bile pigment), green tetrapyrrolic; a product of haem catabolism. It is the pigment responsible for a greenish colour sometimes seen in bruises;
Urobilin = yellow colour of urine; also found in faeces; product of haem

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22
Q

What’s sphincter of oddi?

A

hepatopancreatic sphincter

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23
Q

Role of lecithin?

A

dissolve fat + cholesterol to regulate functions of liver, gallbladder, kidney
, ;
Urobilin = yellow colour of urine; also found in faeces; product of haem

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24
Q

Role of lecithin?

A

dissolve fat + cholesterol to regulate functions of liver, gallbladder, kidney

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25
Q

What’s urobilin?

A

yellow colour of urine; also found in faeces; product of haem

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26
Q

Substances secreted across bile canalicular membrane via transporters?

A 
Bile acids
Phosphatidylcholine
Conjugated bilirubin
Cholesterol
Xenobiotics (foreign chemicals/substances, e.g. drugs)
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27
Q

Substances secreted across bile canalicular membrane via diffusion?

A

water, glucose, Ca2+, GSH, AA, urea

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28
Q

Composition of hepatic bile?

A

97% water, cholesterol, lecithin, bile acids, bile pigments

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29
Q

Composition of gallbladder bile?

A

89% water, HCO3-, Cl-, Ca2+, Mg2+, Na+, cholesterol, bilirubin, bile salts

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30
Q

Where does bile go between meals?

A

goes to gallbladder between meals when sphincter of Oddi is closed

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31
Q

Where do bile acids go after synthesis?

A
  • transported across canalicular membrane
  • bile canaliculi
  • gallbladder
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32
Q

Describe classic/neutral pathway for bile acid formation

A
  • hydroxylation of sterol nucleus by CYP7A1
  • saturation of double bond of sterol nucleus
  • epimerisation of the 3β-hydroxyl group + hydroxylations
  • shortening of side chain to 3C atoms
  • carboxylation of last C atom of side chain

Alternative pathway
Steps in the pathway
Side chain modification by 27-hydroxylase (CYP27A1)
Modification of sterol ring of oxysterols
7α-hydroxylation by CYP7B1
CYP7B1 is similar to CYP7A1, but CYP7B1 has a more broad substrate specificity than CYP7A1

Brief summary of the two major bile acid biosynthetic pathways
You do not need to learn/memorise the names of these enzymes and the products of the reactions
Classic/neutral pathway:
Cholesterol is converted to 7α-hydroxycholesterol by the rate-limiting enzyme CYP7A1 (located in ER)
The 3 -hydroxysteroid dehydrogenase (3- -HSD, HSD3B7) converts 7α-hydroxycholesterol to 7α-hydroxy-4-cholesten-3-one (C4), which is converted to 7 α,12α-dihydroxy-4-cholesten-3-one by a sterol 12α-hydroxylase (CYP8B1 (alternative symbol = CYP12) leading to synthesis of cholic acid
Without the action of by CYP8B1, C4 is eventually converted to chenodeoxycholic acid. Here, the mitochondrial sterol 27-hydroxylase (CYP27A1) catalyses the steroid side chain oxidation in both cholic acid and chenodeoxycholic acid syntheses from C4

In the alternative/”acidic” pathway:
Cholesterol is first converted to 27-hydroxycholesterol by CYP27A1
Oxysterol 7α-hydroxylase (CYP7B1) catalyses hydroxylation of 27-hydroxycholesterol to 3 ,7α-dihydroxy-5-cholestenoic acid, which eventually is converted to chenodeoxycholic acid.

Generation of secondary bile acids: In the large intestine, bacterial 7α-dehydroxylase removes a hydroxyl (from C7 position of the primary bile acids) which leads to the conversion of cholic acid to deoxycholic acid and chenodeoxycholic acid to lithocholic acid.

The activity of the enzymes are tightly regulated. Synthesis, transport and release are also tightly regulation for optimal physiological response. Unlike CYP7A1, the activity of CYP27A1 is not regulated by bile acids

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33
Q

Describe classic/neutral pathway for bile acid formation

A
  • hydroxylation of sterol nucleus by CYP7A1
  • saturation of double bond of sterol nucleus
  • epimerisation of the 3β-hydroxyl group + hydroxylations
  • shortening of side chain to 3C atoms
  • carboxylation of last C atom of side chain
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34
Q

Describe alternative pathway for bile acid formation

A
  • side chain modification by 27-hydroxylase (CYP27A1)
  • modification of sterol ring of oxysterols
  • 7α-hydroxylation by CYP7B1
  • CYP7B1 similar to CYP7A1 but CYP7B1 has broader substrate specificity than CYP7A1
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35
Q

Features of bile acids?

A
  • Vital in GI
  • Made from cholesterol
  • Secreted into bile
  • Conjugated to glycine or taurine in liver
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36
Q

Why conjugate bile acids?

A

helps to increase the ability of bile acids to be secreted + decreases their cytotoxicity

37
Q

Why conjugate bile acids?

A

↑ amphipathic nature of bile acids to increase ability of bile acids to be secreted + decreases their cytotoxicity

38
Q

What are bile salts?

A

sodium + potassium of conjugated bile acids

39
Q

What are primary bile acids?

A

synthesised by liver

40
Q

What are secondary bile acids?

A

result from deconjugation of primary bile acids by bacterial hydroxylase enzymes in colon

41
Q

Role of bacterial hydroxylase enzymes?

A

in colon to deconjugate primary bile acids -> seoncdary

42
Q

Major bile acids found in humans?

A

Cholic acid: 50% = most important
Chenodeoxycholic acid: 30%
Deoxycholic acid: 15%
Lithocholic acid: 5%

43
Q

How secondary bile acids made?

A
  • in large intestine
  • bacterial 7α-dehydroxylase removes hydroxyl (from C7 of primary bile acids)
  • in intestine bacteria deconjugatebile acids
  • deconjugated bile acids are excreted or reabsorbed
  • anaerobic bacteria in colon modify primary bile acids to secondary bile acids

From liver bile move to bile canaliculi cells which join the bile ductules and then the bile ducts; following food intake bile acids are secreted by the gallbladder into the duodenum
CCK mediates the release of bile acids → emulsification of fats

44
Q

How secondary bile acids made?

A
  • in large intestine
  • bacterial 7α-dehydroxylase removes hydroxyl (from C7 of primary bile acids)
  • in intestine bacteria deconjugatebile acids
  • deconjugated bile acids are excreted or reabsorbed
  • anaerobic bacteria in colon modify primary bile acids to secondary bile acids
  • from liver bile
  • move to bile canaliculi cells
  • join bile ductules + bile ducts
  • food intake bile acids secreted by gallbladder into duodenum
45
Q

Role of CCK?

A

mediates release of bile acids → emulsification of fats

46
Q

eg of primary bile acids?

A

cholic acid

chenodeoxycholic acid

47
Q

eg of secondary bile acids?

A

cholic acid -> deoxycholic acid

chenodeoxycholic acid -> lithocholic + ursodeoxycholic acid

48
Q

Functions of bile/bile acids?

A

Metabolic regulators
-Elimination of cholesterol to bile acids (5% excreted in faeces)
-Synthesis + excretion of bile acids in faeces for elimination of excess cholesterol
-Reduce cholesterol ppt in gallbladder - bile acids + phospholipids solubilise cholesterol in bile
-Facilitate absorption of fat-soluble vitamins (ADEK)
-Regulate their own transport + metabolism via enterohepatic circulation
-Digestion of TG - work with phospholipids (licithin) + monoglycerides for emulsification of fats :
Digestion of dietary fats by acting as emulsifying agents that render fats accessible to pancreatic lipases

49
Q

Role of bile acid sequestrants (BASs)?

A
  • Manipulation of bile acid enterohepatic circulation with non-systemically absorbed resins modulating processes regulated by bile acids
  • Treatment of dyslipidemia
  • Treatment of dysglycemia in type 2 diabetes
50
Q

What causes release of bile/bile salts?

A

Contraction of gallbladder

  • Cephalic phase: taste, smell, food in mouth → impulses via vagus
  • Gastric phase: distension of stomach generates impulses in vagus
  • Intestinal phase: most gallbladder emptying; key mediators for increased release are : CCK + secretin
51
Q

Describe how vagus leads to emulsification of fats

A
  • vagus conveys info about state of body’s organs to CNS
  • conveys contents of duodenum to CNS
  • if contains lipids
  • release of CCK
  • stimulates bile release
  • emulsification of fats + prepares them for digestion by pancreatic lipases
52
Q

Describe mechanisms controlling the secretion of bile into duodenum

A
  • components of bile, pancreatic juices released + work
  • sphincter of Oddi relaxes
  • gallbladder contracts
  • pancreatic/gallbladder secretions into duodenum
  • neutralisation of acids + digestion will occur.
  • distension of duodenum
  • sends signals via vagal afferents to dorsal vagal complex
  • signals return via efferents
  • relaxation of sphincter of Oddi occurs via NO + VIP
  • gallbladder contracts under stimulation of Ach, CCK also mediating contraction
  • if fatty components stimulates CCK release
  • CCK stimulate afferent signals
  • act directly on gallbladder
  • motillin influence gallbladder motility + volume
53
Q

Role of motilin?

A

influence gallbladder motility + volume

54
Q

Effect of fatty foods on duodenum?

A
  • FA in duodenum
  • CCK secretion
  • increased plasma CCK :
  • gallbladder contracts -> bile into common bile duct -> bile into duodenum
  • spincher of oddi relax -> bile into duodenum
55
Q

Describe how chyme causes release of bile into duodenum

A
  • bile with pancreatic secretions when chyme enters small intestine from stomach
  • chyme stimulates enteroendocrine cells of duodenum to secrete CCK + secretin
  • CCK + secretin absorbed intestinal mucosa into bloodstream
  • stimulate liver to synthesise + release bile into common bile duct
  • CCK stimulates gallbladder contraction
  • ejecting conc bile into cystic duct + common bile duct
  • sphincter of oddi relaxes
  • bile flow from common bile duct into duodenum
  • emulsifies fat droplets
  • fat further broken down by pancreatic lipases
56
Q

Role of chyme?

A

stimulates enteroendocrine cells of duodenum to secrete CCK + secretin

57
Q

Effect of excess bile production?

A

↑ bile production → diarrhoea, wt loss, gallbladder damage due to inflammation

58
Q

What’s enterohepatic circulation?

A

Recycling pathway from intestine to liver + back to intestine

  • Most of bile salts reabsorbed by Na+-bile salt coupled transporters
  • Bile salts returned to liver + secreted again into bile
  • Body’s content of bile acid pool (~3.5g) recycled ~twice per meal
  • 95% bile released to small intestine is recycled + 5% lost in faeces
59
Q

Where’s lecithin (phospholipids) synthesised?

A

liver

60
Q

Why are bile salts referred to as biological detergents?

A
  • Excrete cholesterol + potentially toxic compounds (bilirubin, xenobiotics, metabolites of drugs)
  • Solubilise ingested fat + fat-soluble vitamins facilitating their digestion by pancreatic lipases before being absorbed
61
Q

Effect of interruption of enterohepatic circulation + eg?

A

eg after ileal resection

  • Excess synthesis of bile salts by liver
  • Kidneys excrete synthesised bile salts (+ some cholesterol)
62
Q

What’s ileocaecal resection?

A

surgical removal of caecum along most distal portion of small bowel— terminal ileum
performed for Crohn’s disease.

63
Q

How’s primary + secondary bile acids removed?

A

by intestine into liver via portal circulation

64
Q

Describe how primary + secondary bile acids removed

A
  • specific transporters in terminal ileum transport bile salts from lumen of digestive tract to intestinal capillaries
  • bile salts transported directly to liver via hepatic portal vein
  • hepatocytes take up bile salts from blood, increase secretion of bile salts into bile canaliculi
65
Q

What causes the increased cholesterol?

A
  • Liver secretes excess into bile

- Reabsorption of salt + water

66
Q

What are gallstones composed of?

A

Cholesterol crystallises –> gallstones

Ppt of bile pigments

67
Q

Features of gallstones (cholelithiasis)

A
  • Ratio of incidence of gallstones = 2:1 in women vs men
  • Incidence increases with age
  • Higher the cholesterol content of bile, then greater conc of phospholipid + bile salts
  • Environmental factors : female sex, social class, reduced physical activity, high calorie + low in legumes diet, high polyunsaturated FA diet
  • Deviation from bile acids : phosphatidylcholine : cholesterol in canalicular bile of 10:3:1 → cholesterol gallstones
  • Supersaturation + rapid nucleation of cholesterol in bile vital in pathogenesis of cholesterol gallstones
  • Increasing phospholipid concin bile can prevent cholesterol gallstones than increasing bile acid conc
68
Q

Types of gallstones + composition?

A
  • Cholesterol stones (85%): obesity; ↓ bile acids vs ↓ phospholipids
  • Calcium bilirubinate stones : ↑unconjugated bilirubin
69
Q

Factors involved in gallstone formation?

A
  • Bile stasis: stones form in bile that stays in gallbladder rather than flowing bile into ducts into duodenum
  • Decreased bile acids due to malabsorption (in cystic fibrosis – dehydrated + acidic; 10% higher incidence)
  • Chronic infection : bacteria forms pigment stones
  • Super-saturation of bile with cholesterol
  • Nucleation factors or glycoprotein
70
Q

How long does gallstone form in normal vs patient?

A

Bile from gallstone sufferers: 2-3 days

Bile from normal individuals: 2 weeks (delay due to anti-nucleation factors)

71
Q

Features of calcium bilirubinate stones?

A
  • Small black and fragile

- If unconjugated bilirubin very high eg in haemolytic anaemia, hereditary spherocytosis

72
Q

Features of cholesterol stones?

A

-85%
-Large, single or multiple
-Cross sectio : radiating from centre
-Predisposition arises in 2 situations :
↑ cholesterol in bile (obesity or diet)
decreased bile acids (malabsorption of bile acids in cystic fibrosis)

73
Q

Treatment of gallstones?

A

Oral administration of chenodeoxycholic acid (CDCA) + ursodeoxycholic acid ( UDCA) to enrich bile with these bile acids to decrease cholesterol supersaturation + dissolve stones

74
Q

Effect of cystic fibrosis on liver?

A
  • bile produced dehydrated so more acidic
  • less flow into small intestine
  • dehydrated bile collects in gallbladder –> gallstones
  • inflammation of gallbladder
  • pain, fevers, nausea, vomiting
  • gallbladder removal
  • dehydrated bile obstructs bile ducts
  • Doctor examines your liver at each clinic visit
  • Blood tests of liver function are checked annually
  • Radiographic tests performed to evaluate liver + gallbladder

-Babies have vomiting, dehydration, salty-tasting skin, intestinal blockages

75
Q

Effect of cirrhosis on liver?

A
  • destruction of liver cells
  • bile ducts blocked by dehydrated mucus + bile
  • inflammation + damage to liver
  • fibrosis of ducts affects blood flow to liver
  • blood redirected to other blood vessels
  • vessels cannot accommodate increased volume so swell + prone to bleeding
  • liver failure
  • toxic substances remain in bloodstream
76
Q

Treatment of gallbladder + liver disease?

A
  • Laparoscopic Cholecystectomy : removal of gallbladder.

- Oral Dissolution Therapy : consuming ursodeoxycholic acid/actigall to dissolve formations in liver

77
Q

Effect of small vs large gallstones?

A 
Small = easy passage via bile duct
Large = lodge in opening of gallbladder :
  • duct from pancreas joins bile duct before it joins duodenum
  • lodging at this point
  • stoppage of bile + pancreatic secretions
  • pressure builds up
  • nutritional deficiency
  • further pressure build up
  • decreased secretion of bile
  • jaundice
78
Q

What’s jaundice?

A

accumulation of bilirubin in blood

79
Q

Cause of yellow in urine?

A

bilirubin

80
Q

Cause of brown in faeces?

A

stercobilin

81
Q

Why do cholesterol stones form?

A
  • in gallbladder
  • altered hepatocellular + gallbladder function
  • overproduction of cholesterol by liver due to obesity, drugs
82
Q

Gallbladder factors which promote stone formation?

A

hypomotility + secretion of nucleating factors eg mucus glycoprotein mediated by increase in prostaglandin production by gallbladder mucosa

83
Q

Why do brown pigment stones form?

A

calcium bilirubinate due to biliary infection

84
Q

Why do black pigment stones form?

A

extremely hard bilirubin polymers found in gallbladder

85
Q

Role of biliary sludge?

A

necessary precedent of gallstones + comprises cholesterol monohydrate crystals, glycoproteins, granules of calcium bilirubinate

86
Q

Diagnoses of gallstones?

A
  • Explore right upper quadrant of gallbladder to detect gallstones: Ultrasonography + computer tomography
  • Image gallbladder + ducts: Cholescintigraphy - administer tecnetium-99m-labelled derivative of iminodiacetic acid (radioactive tracer) :
  • injected via any accessible vein
  • circulate to liver
  • excreted into biliary system
  • stored by gallbladder + biliary system
  • Visualise biliary tree by contrast media : Endoscope retrograde cholangiopancreotography (ERCP)
  • Insert device to remove gallstone fragments obstructing bile flow / pancreatic juice
87
Q

What’s cholescintigraphy scan?

A

=hepatobiliary iminodiacetic acid(HIDA),paraisopropyl iminodiacetic acid(PIPIDA),diisopropyl iminodiacetic acid(DISIDA) scan
-Nuclear imaging procedure to evaluate health + gallbladder function

88
Q

Clinical features of gallstones?

A
  • 85% asymptomatic (gallstones remain in gallbladder)
  • If neck of cystic duct impaired bile → cannot escape gallbladder so conc (chemical cholecystitis) → biliary pain ensues (acute cholecystitis)
  • Gallstones that impact common bile duct → obstruction of bile flow + cholestatic jaundice –> bacterial infections (cholangitis)
  • Gallbladder secretes mucus if inflamed + rupture (mucocele or hydrops)

GI (15 decks)

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