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Y2 GI block > Biliary System and Gallstones > Flashcards

Biliary System and Gallstones Flashcards

1
Q

Explain the anatomy of the biliary tree (smallest to biggest)

A

Biliary Canaliculi –> Interlobular Bile duct –> septal bile duct –> intrahepatic duct (in portal triad) –> R/L hepatic duct –> common HEPATIC duct

Common hepatic duct leaves the liver and joins the cystic duct from the gall bladder to form the –> Common BILE duct

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2
Q

Describe the anatomy of the common BILE duct (where it passes, what it joins with, where it opens)

A
  • Passes behind the duodenum
  • Passes through the head of the pancreas and joins with the PANCREATIC duct
  • Opens in to the 2nd part of the duodenum through the Ampulla of Vater
  • Flow of bile regulated by Sphincter of Oddi (smooth muscle)
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3
Q

Describe the anatomy of the gall bladder (the type of epithelium, role, anatomical parts, where it is found, relation of GB in accordance with other organs)

A
  • Gallbladder is reservoir for bile - 30-50ml capacity
  • Columnar epithelial lining
  • Concentrates bile (H2O and salts reabsorbed)
  • Has a neck, body and fundus
  • Lies in gall bladder fossa on the inferior surface of the R lobe of the liver
  • most anterior of visceral organs
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4
Q

What is the Hartmann’s pouch?

A

Outpouching/ dilatation of the gall bladder wall

Common site for Gallstones

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5
Q

What is the murphy’s point

A

GB fundus may be palpated between lateral border of rectus abdominus muscles and costal margin (9th costal cartilage)

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6
Q

What are the components of bile

A 
Conjugated bilirubin
Bile acids
Cholesterol
Water
Electrolytes
Phospholipids
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7
Q

What is Gilbert’s syndrome

A

(UGT enzyme is involved in converting unconjugated bilirubin to conjugated bilirubin)

  • It is a genetic defect on chromosome 2 for the locus coding for the UGT-1A1 protein.
  • These people may develop jaundice in times of fasting or stress
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8
Q

Describe the regulation of relaxation and contraction of the GB and secretion of bile

A

Normally, GB is relaxed and concentrating the bile
When a fatty meal is eaten:
- Vagal stimulation promotes GB contraction
- Cholecystokinin (CCK) released from duodenum in response to presence of luminal fat
- CCK mediated GB contraction and relaxation of sphincter of Oddi (SO) promotes release of bile juice into duodenum
- After bile is released, GB relaxation and closure of SO is mediated by sympathetic nerves, and gut hormones vasoactive intestinal polypeptide (VIP) and somatostatin

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9
Q

What percentage of bile salts recirculate via enterohepatic circulation? What happens to the remaining 5%?

A

Majority (95%) of bile salts recirculate via enterohepatic circulation
5% goes into colon and is lost in faeces everyday

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10
Q

What causes bile salt diarrhoea (greeny watery diarrhoea)

A

If the terminal ileum does not absorb bile acids then they reach the colon and cause diarrhoea. Can happen due to:

  • After surgery if the terminal ileum or ileocaecal valve is removed
  • Disease of the terminal ileum eg Crohn’s disease
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11
Q

What are the 5 Fs of gall stones (increased risk)

A 
female
fair
fertile
forty
fat
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12
Q

Give some risk factors for gall stones

A 
Increasing incidence with age
Family history
Caucasian>non-caucasian
Diet (low fibre)
Inflammatory bowel disease
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13
Q

What are the 3 main types of gallstones explain them

A

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

2) BILE PIGMENT STONE
Multiple, irregular, hard
Associated with chronic haemolysis (eg sickle cell)

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

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14
Q

What is the pathogenesis of gall stones

A

Three main events that often occur together

1) Cholesterol supersaturation
- Cholesterol is solubilised by bile but high levels of cholesterol lead to supersaturation
- (high cholesterol) Typically occurs when oestrogen levels high – eg obesity, pregnancy, OCP(oral contraceptive pill), liver disease
- Also when bile acid levels are LOW – eg following small bowel resection or in active Crohns when enterohepatic circulation is ineffective

2) Biliary Stasis
- Occurs during periods of fasting or starvation
- Observed during prolonged total parenteral nutrition

3) INCREASED SECRETION OF BILIRUBIN
- Bilirubin is soluble in bile following conjugation with glucuronide (ie conjugated bilirubin). Pigmented stones can develop when:-
- Increased RBC breakdown – esp haematological conditions (eg sickle cell), malaria, valvular heart disease, post chemotherapy
- Failure of hepatic conjugation

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15
Q

List some complications of gallstones

A

Gallbladder:

  • Biliary colic (sudden pain occurs due to a gallstone temporarily blocking the cystic duct)
  • Acute Cholecystitis (inflammation of gall bladder)
  • Empyema (pus)
  • Mucocoele (mucous cyst- forms a lump)
  • Cancer

Common bile duct

  • Obstructive jaundice
  • Cholangitis (infection of bile duct)
  • Pancreatitis

Small Intestine:
- Gall stone ileus (SI obstruction due to gall stone impaction)

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16
Q

Describe Biliary Colic as a complication

stone location, pain location, what provokes the pain, symptoms, LFT, treatment

A
  • Stone location: usually neck/Hartmann’s pouch
  • Pain location: Pain epigastrium/RUQ/through to back
  • Usually provoked by eating –> GB contraction
  • Symptoms: Vomiting common, Does not cause jaundice or fever
  • LFT commonly normal
    Treatment:
  • Often settles if stone moves back in to GB body/fundus
  • If recurrent then cholecsytectomy
17
Q

Describe acute cholecystitis (pathogenesis, symptoms, diagnosis, treatment)

A
  • Impacted stone in GB leading to GB wall oedema/inflammation and development of bacterial infection within GB wall
  • Pain, nausea, vomiting, fever, abdominal tenderness
  • Raised inflammatory markers, sometimes abnormal LFT +/- jaundice
  • Treat with antibiotics, analgesia, elective cholecystectomy when symptoms settle
18
Q

What is palpated on the body to diagnose acute cholecystitis

A

Murphy’s sign
extreme tenderness over GB fundus – elicited by palpating fingers up towards costal margin as patient takes deep inhalation

19
Q

What are the signs and symptoms in obstructive jaundice

A
  • Pale stools- bile is not getting to the duct and fat is not being absorbed.
  • Dark urine- bilirubin is conjugated
  • Yellow sclerae
  • Pruritus (and scratch marks)- itchy, bile salt is depositing in the skin
20
Q

What is obstructive jaundice

A

a condition where normal drainage of bile from the liver to the small intestines is blocked.
Causes yellowing of the skin and eyes

21
Q

What is Curvoisier’s Law

A

in the presence of a palpable enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones (mostly due to scarring of the gall bladder caused by chronic inflammation)

22
Q

Describe LFTs in biliary obstruction

A
  • ALP is increased early – often up to 10x normal. Often associated with rise in GGT
  • Bilirubin rises steadily (as it isn’t being excreted) and level of bilirubin is indicative of duration of obstructive process
  • In prolonged obstructive jaundice, coagulopathy is common (blood is not clotting because bile is not reaching duodenum so Vitamin K is not being absorbed and Vit K is required for blood clotting factors) –> more likely to bleed
  • AST/ALT can be elevated in obstructive jaundice but much less prominent and often more transient
23
Q

What investigations will be carried out for someone with obstructive jaundice

A

Transabdominal ultrasound – first line

  • Info about liver, gallbladder and biliary system
  • Cheap, easily available

CT scan

  • Info about liver, pancreas and other organs,
  • Not so good for gallbladder or gallstones in general

MRCP
Magnetic Resonance Cholangiopancreaticogram
Good for biliary tree and pancreatic ducts
Good for telling of stones in duct

24
Q

What are the extrinsic compression reasons that cause obstructive jaundice

A

Tumours

  • Most commonly pancreatic cancer
  • Lymph nodes from other cancers

Inflammation
- Esp pancreatitis

Mirizzi Syndrome- gall stones in the gall bladder

25
Q

Describe Pancreatic cancer (location, compression, pain?, presentation, epidemiology, treatment)

A
  • Most commonly in head of pancreas gland
  • Compresses CBD as it passes through pancreatic - tissue
  • Painless jaundice
  • Often presents late with incurable disease
  • Only 5% of people with pancreatic cancer get a good curative operation
  • ERCP and stent provides drainage of bile, relief of
    jaundice, bridge to chemotherapy
26
Q

What are the intramural (wall of bile duct) reasons that cause obstructive jaundice

A

Tumours
- Cholangiocarcinoma

Inflammation

  • Primary Sclerosing Cholangitis (PSC)- also associated with IBD
  • IgG4 disease

Scarring / fibrosis

  • Post inflammatory
  • Post surgical
27
Q

What are the intraLUMINAL reasons that cause obstructive jaundice

A

Stones (most common)
Sludge
Polyps

28
Q

What are the 3 types of biliary obstruction

A

EXTRINSIC COMPRESSION- outside the wall
INTRAMURAL- in the wall
INTRALUMINAL- in the lumen

29
Q

Why is urine NOT DARK in pre-hepatic jaundice

A

In prehepatic jaundice the bilirubin is bound to albumin and therefore it is not filtered in the kidney, so the urine is not dark

30
Q

Why is urine DARK in hepatic and post-hepatic jaundice

A

the bilirubin is water soluble and therefore is filtered in the kidney and the urine is dark

31
Q

What are stools like in biliary obstruction

A

the stools are pale, fatty, offensive and difficult to flush

32
Q

Why is bile important

A

If you don’t have bile- causes Vitamin A deficiency so can cause night blindness
Vitamin D- important for bone development.
Vitamin K- important for coagulation factors
Vitamin E- important for immune system
Toxic metabolites and drug metabolites go into bile so if someone doesn’t have a functional biliary system- build up can be harmful

33
Q

How many times a day does bile acid circulate in a day

A
  • Total pool of bile acids circulates 6-8x/day
34
Q

Where does re absorption of bile mainly occur

A
  • Reabsorption mainly in ileum/terminal ileum by active transport into portal circulation
35
Q

How does liver compensate for bile loss in faeces

A

Synthesis of new bile acids in the liver compensates for faecal loss

36
Q

through what veins do bile salts return to the liver?

A

Portal veins

Y2 GI block (25 decks)

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