Bile, gall bladder, gall stones and Jaundice Flashcards

1
Q

Describe the path that bile takes from the liver

A
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2
Q

Label

A
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3
Q

How much bile made by liver per day?

A

600-1000ml

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4
Q

What is the capacity of the gallbladder?

A

30-50ml

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5
Q

Bile salts play a huge role in the digestion of fats. Explain what they do in this regard

A
  • Most dietary lipids are not water soluble
  • Pancreatic lipase is not lipid soluble funnily enough, so can only interact with lipids only at the surface of the lipid dropltet
  • The larger the droplet, the more lipids inside
  • Bile salts break apart the droplets, forming very tiny droplets, increasing the total surface area avaialble for enzymatic action
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6
Q

What type of the epitheium is found in the gall bladder?

A

Columnar

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7
Q

The gallbladder can store almost 12 hours worth of while. It does this by concentrating bile. How is this achieved?

A
  • Water, sodium, cholride and most other small electrolytes are continously absorbed through the gallbladder mucosa, concentrating the remaining components.
  • Most of this gallbladder absorption is caused by active transport of sodium, followed by secondary absorption of chloride ions, water and other components.
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8
Q
A
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9
Q

Where might you palpate the gallbladder?

A
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10
Q

State the man components of bile

A
  • Bile salts
  • Water
  • Biliurbin

Cholesterol

Fatty acids

Lecithin

Sodium

Potassium

Calcium

Cholride

Bicarbonate

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11
Q

Another function of bile salts apart from emulsification is:

A
  • Aid the absorption of fatty acids, monoglycerides, cholesterol and other lipids from the small intestine, by forming complexes with these lipids called MICELLES
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12
Q

Summarise how bilirubin is formed

A
  • red blood cells break down after 120 days in spleen, most components are recycled
  • Most parts are recycled
  • Haem from haemoglobin is broken down into biliverdin
  • Bilverdin is converted to uncojugated bilirubin
  • Unconjugated bilirubin is not not soluble in water, so is bound to albumin in blood
  • In the liver, bilirubin is conjugated to make it soluble, and is then excreted intotthe bile
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13
Q

Unconjugated bilirubin is conjugated through a two step process by which enzyme?

A

Uridine Diphosphatase Glucoronsyltransferase (UDT)

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14
Q

What disease is characterised by a mutation on chromosome two for the gene coding for the UGT enzyme?

A

Gilbert’s syndrome

  • People with this can develop jaundice during fasting or times of stress.
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15
Q

As far as I can tell, bile salts and bile acids are the same thing - NOT TRUE SEE OPPOSITE CARD

A

The liver hydroxylates cholesterol to produce the bile acids chenodeoxycholic acid and cholic acid ( Fig. 29.9 ); these bile acids are then conjugated with the amino acids glycine or taurine to yield primary bile salts .

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16
Q

The liver makes about 6g of bile salts daily. Outline how bile salts are formed, and also go onto discuss how secondary bile acids are formed

A
  • Bile salts are derived from cholesterol
  • Cholesterol is first converted to cholic acid or chenodeoxychloic acid.
  • These acids combine with either glycine or taurine, to form glyco and tauro-conjgated bile acids - the salts of these acids are then secreted into the bile

When these bile salts are secreted into the lumen of the intestine, bacterial partial dehydroxylation and removal of the glycine and taurine groups forms the secondary bile acids, deoxycholic acid and lithocholic acid. Cholic acid is converted into deoxycholic acid and chenodeoxycholic acid into lithocholic acid. All four of these bile acids can be taken back up into the blood stream, return to the liver, and be re-secreted in a process known as enterohepatic circulation

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17
Q

Explain the mechanisms by which gallbladder emptying is stimulated and inhibited

A
  • Emptying of the bladder is a result of contractions, along with relaxation of the sphincter of Oddi
  • The primary method for regulation of gallbladder contraction is Cholecystokinin
    • CCK is produced by the duodenal mucosa as a result of chyme (although fat is the primary driver) entering the duodenum, enters the blood and then activates the gallbladder, whilst also promoting relaxation of the sphincter of Oddi
    • The second way is Ach secreted by the vagus nerve and the inestinal enteric nervous system
  • GB relaxation and closure of SO mediated by sympathetic nerves, and gut hormones vasoactive intestinal polypeptide (VIP) and somatostatin
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18
Q

Explain what is meant by enterohepatic circulation of BIle salts

A
  • About 94% of bile salts are reabsorbed into the blood from the small intestine
  • This will be absorped throught the small intestine, and will primarily occur in the Illeum by active transport into the PORTAL CIRCULATION
  • Upon reaching the sinusoids, most are reabsorbed back into the hepatic cells and are re-secreted into the bile
  • Any not absorbed in the illeum will be excreted, however this will be replenished by the luver
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19
Q

The colon is not a fan of bile, and if lots of it gets there it can cause bile salt diarrhoea. When can this occur?

A
  • After surgery if the terminal illeum or ileocecal valve has been removed
  • disease of the terminal ileum , such as Chron’s
20
Q

How much of the population have gallstones on US scanning?

A

7-15%

21
Q

Risk factors for gallstones

A
  • Five F’s; Female, fat, forties, fair, fertile
  • •Increasing incidence with age
  • Family history
  • Caucasian>non-caucasian
  • Diet (low fibre)
  • Inflammatory bowel disease

Approx 80% asymptomatic and do not require treatment

22
Q

What are the main causes of gallstones

A
  • Cholesterol supersaturation
  • Accelerated nucleation of cholesterol “the initial process that occurs in the formation of a crystal from a solution, a liquid, or a vapour, in which a small number of ions, atoms, or molecules become arranged in a pattern characteristic of a crystalline solid,:
  • Biliary stasis - i.e. the flow of bile is impaired somehow , such as gallbladder hypomotility
  • When there is increased levels of bilirubin secretion
23
Q
  • Cholecystitis
  • Cholelithiasis
  • Cholecystectomy
  • Choledocholithiasis
  • Cholangitis

Define these terms

A
  • •Cholecystitis – inflammation of gallbladder
  • Cholelithiasis – gallstones (within gallbladder)
  • Cholecystectomy – removal of gallbladder
  • Choledocholithiasis – gallstone within bile duct
  • Cholangitis – infection of bile duct
24
Q

What are complications of gallastones that lodge in the gallbladder

A

Inside the gallbladder:

  • Biliary Colic (dull pain in the middle to upper right area of the abdomen. It occurs when a gallstone blocks the bile duct)
  • Acute Cholecystitis (Inflammation of the gallbladder as a result of stone being lodged in gallbladder or cystic duct)
  • Empyema (this usually occurs as a result of acute cholecystisis - the blockage means some bile is stangent, priming it for infection
  • Mucoceole - accumulation of mucus
25
Q

What are complications of gallstones that are in the common bile duct

A
  • obstructive jaundince - caused by build up bilirubin in the blood
  • Cholangitis - infection of the common bile duct
  • Pancreatitis - infection of the pancreas
26
Q

What are complications of gallstones in the small intestine?

A

Gallstone Ileus - A result of a fistula forming between the gall bladder and the small intestine

27
Q

Where would you expect biliary colic to occur? and under what circumstances (i.e when would it happen and what would be happening to cause this pain)

A
  • Epigastric region/Right hypochondrium, often through to back
  • Can occur after eating, which causes gallbladder contraction
  • A result of gallstone being lodged in gallbladder, often in the Hartman’s pouch or the neck, settles down if it moves back into the fundus or body.
  • LFT’s usually not affected
  • Can cause vomitting
  • Does not cause jaundice
28
Q

Treatment for recurrent biliary colic>

A

Cholecystectomy

29
Q

Acute cholecystitis is a complication of gallstones (typically ones in the gallbladder itself), leading to GB inflammation, oedoema and potential for bacterial infecction. What are the symptoms, and what would you expect to see in Bloodtests? How would you treat?

A
  • Pain, nausea, vomiting, fever, pain in abdomen
    • Gallbladder may be palpatebale
    • Murphy’s sign - Palpation of the right subcostal region reveals tenderness. During deep inspiration, the tenderness suddenly becomes worse and produces inspiratory arrest. Can also be elicited during ultrasound examination.
  • Raised inflammatory markers, Can be abnormal LFT with or without jaundice
  • Treat with antibiotics, analgesia, elective cholecystectomy when symptoms settle
30
Q
A
31
Q

People with galllstones may present either with biliary colic or Acute Cholecystitis. Symptoms are similar, but have slight differences. Outline them

A

Key difference is the inflammation

32
Q

Liver function tests - describe the main 3

A

AST/ALT - Hepatocyte enzymes (AST also found in muscle) - called the transaminses - markers of inflammation

ALP/GGT (enzymes associated with bile duct, but different enzyme of ALP also produced in bone

Bilirubin

33
Q

Another potential complication of gallstones is Obstructive Jaundice. What is this caused by?

A
  • Interuption in the delivery of bile somwhere in the biliary system
  • Prevents passage of bile into the duodenum
34
Q

What other causes are the of Obstructive jaundice aside from Gallstones?

A

Pancreatic cancer - tumour growth in pancreas can block biliary tree

Pancreatitis - Inflammation and swelling of pancreas can block biliary tree

35
Q

Signs and symptoms of obstructive jaundice?

A
  • Pale stools (due to insufficient bilirubin in small intestine - which later goes onto to form Stercobillin (which is what gives poo it’s colour)
  • Dark urine
  • Yellow sclerae
  • Pruritus - bile build up in the skin causes itchiness
  • Featurs of chronic liver disease
  • Hepatomegaly
  • Abdominal tenderness/palpable gallbladder
36
Q

What is Curvoisier’s law?

A
  • If the abdomen is not painful in the presence of a palpable, enlarged gallbladder and is accompanied with mild, painless jaundice, the cause is unlikely to be Gallstones.
  • Simply stated, if the gallbladder is palpable in the presence of jaundice, the jaundice is unlikely to be due to stone and one should think of a malignant cause of the lower extrahepatic biliary tree.
37
Q

What changes woud you expect to see in LFT in post hepatic jaundice ?

A
  • ALP increased significantly early on, associated with rise in GGT
  • Bilirubin rises steadily - level of bilirubin is indicative of how long the obstruction has been going on
  • In prolonged obstructive jaundice, you would expect coagulopathy
  • AST/ALT can be elevated in early obstructive jaudnice, but is much less prominent and more transient
38
Q

What would expect LFTs to be in Hepatic pathology such as viral hepatitis, paracetamol

A
  • Significantly elevated ALTs and ASTs
  • ALP/GGT would be normaly/slightly elevated
  • Bilrubin would be moderately increased
39
Q

BIlirbubin levels in a blood test are raised in obstructuve jaundice. Why is this?

A
  • Due to the blockage that is occuring, gallbladder pressure is increased, causing Conjugated bilirubin to be forced out into blood vessels.
40
Q

What are the 3 ways in which the biliary tree can be blocked

A
  • External compressoin
  • Inside the walls of the bile ducts
  • In the lumen of the bile ducts
41
Q

Why is there dark urine in obstructive jaundice

A

Since there is excessive Conjugated-Bilirubin circulating in the blood, it gets filtered by the kidney and we see a marked increase in Conjugated-Bilirubin in the urine, forming a dark urine

42
Q

What imaging tests can used for looking at biliary obstruction?

A
  • Go to is ultrasound (good for liver, gallbladder, biliary system)
  • CT
  • MRI
43
Q

What are potential causes of extrinsic compression of biliary structures

A
  • Tumours of the pancreas and of lymph nodes
  • Inflmammation - pancreatitis in particular
  • Mirizzi syndrome (Mirizzi syndrome is a rare complication of prolonged cholelithiasis with presence of large, impacted gallstone into the Hartman’s pouch, causing chronic extrinsic compression of common bile duct (CBD))
44
Q

Treatment for pancreatic cancer that compresses

A
  • ERCP and place of a stent provides draininge of bile, relief of jaundice, bridge to therapy.
45
Q

Causes of intramural biliary obstruction

A
  • Cholangiocarcinoma - cancer of the bile duct vessels
  • primary sclerosing cholangitis - inflamation that results in stricturing and hardening of the bile ducts ducts due to scar formation - thereby obstructing bile flow
  • IgG4 isease - autoimmune disease, ultimately causes scarring
  • Fibrosis from surgery or post inflammation
46
Q

Causes of intra luminal bile duct blockage

A
  • Stones
  • Sludge
  • Polyps
47
Q

What is ERCP and how does it work?

A
  • Endoscopic retrograde cholangiopancreatograhy
  • Procedure used to diagnose diseases of the gallbladder, biliary system, pancreas and liver
  • Starts with endoscope used to transverse GI tract, to identify bile Ampula of Vater and to feed catheter into the duct, and squirting a contrast agent while X-rays are taken
  • Can be used to:
    • Place a stent
    • Remove gallstones from bile duct