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Phase 2 1. Gastroenterology > Biliary tree and gallstones > Flashcards

Biliary tree and gallstones Flashcards

1
Q

Cholecystitis

A

inflammation of gallbladder

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2
Q

Cholelithiasis

A

gallstone (within gallbladder)

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3
Q

Cholecystectomy

A

removal of gallbladder

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4
Q

Choledocholithiasis

A

gallstone within bile duct

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5
Q

Cholangitis

A

infection of bile duct

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6
Q

MRCP

A

magnetic resonance cholangiopancreatography

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7
Q

ERCP

A

endoscopic retrograde cholangiopancreatography

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8
Q

PTC

A

percutaneous transhepatic cholangiography

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9
Q

What is the organisation of the biliary tree?

A 
> biliary canaliculi
> interlobular bile ducts
> septal bile ducts
> intrahepatic ducts
> R/L hepatic ducts
> common hepatic ducts
> common bile ducts
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10
Q

Describe the route of the common bile duct

A

Passes:
 Behind duodenum
 Last part of the bile duct through the head of the pancreas
o Joins with main pancreatic duct
o opens in to 2 nd part of duodenum (Ampulla of
Vater)
o flow of bile regulated by Sphincter of Oddi (smooth
muscle)

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11
Q

What is the main function of the gall bladder?

A

Reservoir for bile = there is a 30-50 ml capacity

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12
Q

Where is the gallbladder found?

A

Gall bladder lies in the gall bladder fossa on the inferior

surface of the right liver

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13
Q

What are the anatomical regions of the gall bladder?

A

fundus, body and neck

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14
Q

Describe the epithelium found in the gall bladder

A

Columnar epithelial lining throughout the duct and the gall bladder

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15
Q

How is bile concentrated?

A

Bile becomes concentrated as water and bile salts are reabsorbed

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16
Q

How is bile drained from the gallbladder?

A

Connected to the common hepatic duct/common bile duct by the cystic duct
o It’s usually 2.5 cm in length
o Variable length and positioning of the cystic duct

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17
Q

What are the components of bile?

A
  • bile acids
  • water
  • electrolytes
  • cholesterol
  • phospholipids
  • conjugated bilirubin
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18
Q

What is the main substrate for bile acid synthesis?

A

cholesterol

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19
Q

What enzymes are key in bile synthesis?

A

cholesterol 7alpha hydroxylase and the P450
enzymes catalyse the rate limiting step of bile
salt synthesis

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20
Q

What are the bile acids?

A

Cholic acid and chenodeoxycholic acid are

main “primary” bile acids

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21
Q

How are bile acids converted to bile salts?

A
  • Primary bile acids are conjugated to secondary
    bile acids by the addition of amino acid groups
    (taurine or glycine) before being actively
    exported from the hepatocyte
  • Action of intestinal bacteria can produce
    “secondary” bile salts by de-hydroxylation

Some bile acids remain in the acid state (not
converted into salt)

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22
Q

What are bile acids

A

contain 24 carbons, with two or three hydroxyl groups and a side chain that terminates in a
carboxyl group.
o Amphipathic  can act as emulsifying agents in the intestine, helping prepare dietary
triacylglycerol and other complex lipids for degradation by pancreatic digestive enzymes.
o E.g. cholic acid (a triol) and chenodeoxycholic acid (a diol), are called “primary” bile acids.

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23
Q

What are bile salts

A

Before the bile acids leave the liver, they are conjugated to a molecule of either glycine or
taurine (an end product of cysteine metabolism).
o These new structures are called bile salts
o E.g. glycocholic and glycochenodeoxycholic acids, and taurocholic and taurochenodeoxycholic
acids
o more effective detergents than bile acids because of their enhanced amphipathic nature.

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24
Q

List the principle bile acids

A 
 Cholic acid
 Chenodeoxycholic acid
 Glycocholic acid
 Taurocholic acid
 Deoxycholic acid
 Lithocholic acid
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25
Q

What are the promoting factors to bile secretion?

A
  • vagal stimulation

- cholecystokinin

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26
Q

How does vagal stimulation promote bile secretion?

A

promotes weak gall bladder

contraction

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27
Q

How does cholecystokinin promote bile secretion?

A

this hormone is secreted in
response to fat in the duodenum
- CCK causes the gall bladder to contract and the
relaxation of the sphincter of Oddi
- Promotes release of bile juice in to the duodenum

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28
Q

What indirectly promotes bile secretion?

A

SECRETIN – hormone is secreted in response to acid in the duodenum
 Stimulates biliary duct cells to secrete
bicarbonate and water
 This expands the volume of bile and increases its
flow out into the intestine

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29
Q

What inhibits bile secretion?

A

SYMPATHETIC NERVES & GUT HORMONE VASOACTIVE INTESTINAL POLYPEPTIDE (VIP) & SOMATOSTATIN (-)

30
Q

How is bile secretion inhibited?

A

Sympathetic nerve stimulation, VIP and somatostating:

Relaxes the gall bladder and tenses the sphincter
of Oddi
Limits bile release to the intestine

31
Q

What is the function of bile acids?

A
  • promote intestinal absorption of fats by emulsification and formation of micelles
  • enhance absorption of fat and soluble vitamins
  • facilitate excretion of cholesterol
  • exert hormone life effect to influence intestinal metabolic pathways
32
Q

How do bile acids facilitate excretion of cholesterol

A

by solubilising cholesterol within bile and by being a product of cholesterol metabolism

33
Q

How is bile reabsorbed from the gut?

A

Hormone like effect => promote expression of transporters which allow reabsorption from the gut

34
Q

What happens to secretion of bile in the presence of an obstruction?

A

Obstruction which limits bile flow results in reduced bile secretion
o As less fat is digested, less fat soluble vitamins are absorbed
o This causes low vitamins ADEK, resulting in increased INR => coagulopathy
o Standardised prothrombin is time increased => longer time to clot
(vitamin K essential in blood clotting)

35
Q

What is Post cholecystectomy syndrome?

A

o Describes presence of abdominal symptoms after (2 years) surgical removal of the gall bladder
o Bile leakage – causing pain and nausea etc.
o Flatulence,bloating, anddiarrhoea.
o Persistent pain in the upper right abdomen.

36
Q

Describe the enterohepatic circulation of bile

A

majority of reabsorption mainly occurs in the terminal
ileum by active transport into portal circulation

The bile acids are hydrophobic and enter systemic
circulation bound to albumin in the blood to facilitate
transport back to the liver

Venous blood from the ileum feeds into the portal
vein and then directly to the liver sinusoids => the
process of bile production and excretion begins again

37
Q

How much bile is lost and how is this replaced?

A

Total pool of bile acids circulates this way 6-8 times – 5% of these are not reabsorbed so they are excreted in the faeces

De novo synthesis from cholesterol is required to
replace the bile acids that are lost in faeces

38
Q

What factors increase incidence of gallstones?

A

o Age
o family history
o caucasians
o low fibre diets
o IBS: female, fair, fertile and fourty (risk factors)
o IBS can affect the terminal ileum and it will affect the reabsorption of bile acids
o Less bile acids available to mobilise cholesterol  cholesterol increases and forms stones

39
Q

What are the three main types of gallstones?

A
  • cholesterol stone
  • bile pigment stone
  • mixed stones
40
Q

Describe cholesterol stones

A

Usually solitary, oval and large (up to 3cm)

41
Q

Describe bile pigment stones

A

o Multiple, irregular, hard

o Associated with chronic haemolysis (e.g. sickle cell)

42
Q

Describe mixed stones

A

o Most common stone type (80%)
o Multiple, multi-faceted
o Laminated structure with layers of cholesterol, bile pigment and calcium salts

43
Q

What are the three main events that lead to gallstone formation

A
  1. cholesterol supersaturation
  2. biliary stasis
  3. increased secretion of bilirubin
44
Q

Describe cholesterol supersaturation

A

 Cholesterol is solubilised by bile, but high levels of cholesterol lead to supersaturation
 Typically occurs when oestrogen levels high – e.g. obesity, pregnancy, OCP, liver disease
 Also when bile acid levels are low – e.g. following small bowel resection or in active Crohns, when
enterohepatic circulation is ineffective
 When oestrogen levels are high there is an increase in the amount of HDL/LDL cholesterol
o the bile acids become overwhelmed with the large amount of cholesterol
o excess cholesterol will coalesce and form fatty stones
 Liver metabolises oestrogen
o NB: men with liver disease can’t metabolise the oestrogen  they are likely to have cholesterol
gallstones and secondary manifestations of oestrogen overload (gynecomastemia)

45
Q

Describe biliary stasis

A

 Occurs during periods of fasting or starvation

 Observed during prolonged total parenteral nutrition

46
Q

Describe increased secretion of bilirubin

A

 Bilirubin is soluble in bile following conjugation with glucuronide (i.e. conjugated bilirubin)  pigmented
stones can develop when:
o Increased red blood cell breakdown – especially in haematological conditions (e.g. sickle cell),
malaria, valvular heart disease and post chemotherapy
o Failure of hepatic conjugation

47
Q

What are the complications of gallstones within the gallbladder?

A
  • biliary colic
  • acute cholecystitis
  • empyema
  • mucocoele
  • cancer
48
Q

What are the complications of gallstones within the common bile duct?

A
  • obstructive jaundice
  • cholangitis
  • pancraetitis
49
Q

What are the complications of gallstones within the small intestine?

A
  • gallstone ileus
50
Q

What is biliary colic?

A

Stone is impacted in the gall bladder – usually located in the neck/Hartmann’s pouch
o The gall bladder senses this and contracts to remove the gall stones
 The gall stone may fall back down (which doesn’t cause any problems) but if it’s stuck, it will cause pain in
the right upper quadrant through the back

51
Q

What are the symptoms of biliary colic?

A

Pain is provoked by eating as release of CCK triggers contraction of gall bladder
o This causes movement of the stone, resulting in pain
 Vomiting is common
 Doesn’t cause jaundice or fever
- LFT commonly normal
 Pain only settles if the stone moves back into the gall bladder body or fundus

52
Q

How is biliary colic treated?

A

 If this it is a recurrent problem, then cholecystectomy can be done

53
Q

What is ACUTE CHOLECYSTITIS?

A

Impacted stone in the gall bladder leading to GB wall oedema/inflammation and development of
bacterial infection within the GB wall

54
Q

What are the symptoms of acute cholecystitis?

A

inflammatory nature means that there is fever and vomiting (as well as abdominal tenderness, pain and nausea)

55
Q

What effect does acute cholecystitis have on blood tests?

A

Raised inflammatory markers, sometimes abnormal LFT +/- jaundice
o If the stone is mobile – the lining of gall bladder and bile duct can become inflamed causing
jaundice

56
Q

How is acute cholecystitis treated?

A

Treat with antibiotics, analgesia, elective cholecystectomy when symptoms settle
o Likely to resurface after treatment

57
Q

EMPYEME

A

pus filled gall bladder can arise after acute cholecystitis

58
Q

MUCOCOLE

A

distended gall bladder with lots of fluid (doesn’t advance)

59
Q

What are the signs and symptoms of obstructive jaundice?

A

 Pale stools
 Dark urine – spills of conjugated urine (backflow causes leakage of bilirubin)
 Yellow sclera
 Itch (and scratch marks)
 Features of chronic liver disease
o Hepatomegaly?
o Abdominal tenderness/palpable gallbladder?

60
Q

What is CHOLEDOCHOLITHIASIS:

A

“migration of one or more stone from GB to bile duct eventually causing obstruction”

These stones commonly impact above hepato-pancreatic ampulla where the duct narrows significantly

61
Q

How may Choledocholithiasis present?

A
  • obstructive jaundice
  • cholangitis
  • acute pancreatitis
62
Q

Describe obstructive jaundice in Choledocholithiasis

A

(usually with pain)
the obstruction causes backflow of bile into the liver, conjugated bilirubin then leaks out into circulation causing jaundice

Highlighted by changes in liver function tests

63
Q

Describe cholangitis in Choledocholithiasis

A

infection of the bile duct caused by bacteria (ascending from the duodenum)
 Bile flow normally flushes bacteria out of the biliary tree
 Obstruction will mean that bile cannot flow to flush out the pathogens

64
Q

describe acute pancreatitis in Choledocholithiasis

A

can arise as the narrow part of the CBT passes through the head – so things
get stuck there and generate an inflammatory process (as the pancreas is a very sensitive organ)

It will release of powerful enzymes as a result of inflammation, leading to autodigestion

65
Q

How is Choledocholithiasis diagnosed?

A

Diagnosis is through ultrasound -/+ MRCP confirms the diagnosis
 the normal diameter of the bile duct is 7mm; in case of choledocholithiasis the diameter increases

66
Q

How is Choledocholithiasis treated

A

antibiotics/ERCP stone removal/cholecystectomy
o The ERCP can be used to attempt stone removal
 An incision is made at the sphincter of Oddi to increase duct diameter, extract stones
with a balloon which pushes stone to the duodenum

o Cholecystectomy to prevent recurrence

67
Q

Describe the features of pancreatic cancer

A

Most commonly in the head of pancreas

Compresses common bile duct as it passes through
pancreatic tissue

Leads to painless jaundice - can’t give chemotherapy – need to eliminate jaundice before

Often presents late with incurable disease

68
Q

How is pancreatic cancer managed?

A

Stent is placed using ERCP
- provides the drainage of bile, relief of jaundice
and bridge to chemotherapy

69
Q

Describe the LFTs in obstructive jaundice

A

 ALP is increased early – often up to 10x ULN
 Often associated with rise in GGT
 Bilirubin rises steadily and level of bilirubin is indicative of duration of obstructive process
 AST/ALT can be elevated in obstructive jaundice but much less prominent and often more transient
 coagulopathy is common in prolonged obstructive jaundice

70
Q

What other factors can cause obstructive jaundice?

A

 Cancer of bile tube – painless jaundice
 Lymph glands around bile tubes – with intra-abdominal cancer and breast cancer metastasis
o lymph nodes enlarge and put pressure on the BD causing obstructive jaundice

Phase 2 1. Gastroenterology (20 decks)

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