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*Medicine: Gastrointestinal > Gall stones > Flashcards

Gall stones Flashcards

1
Q

What are 3 different types of gallstone?

A
  • cholesterol stones (20%)
  • pigment stones (5%)
  • mixed stones (75%)
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2
Q

What are the risk factors for cholelithiasis/gallstone disease?

A
  • increasing age
  • female sex
  • hispanic + native-american ethnicity
  • FHx of gallstones
  • gene mutations
  • pregnancy/exog oestrogen
  • obesity, diabetes
  • non-alcoholic liver disease
  • TPN
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3
Q

What is the composition of bile?

A
  • bilirubin - by-prod of haem degradation
  • cholesterol - kept soluble by bile salts + lecithin
  • bile salts/acids - mostly reabsorbed in terminal ileum
  • lecithin - increases solubility of cholesterol
  • inorganic salts - sodium bicarb to keep bile alkaline to neutralise gastric acid in duodenum
  • water - makes up 97% of bile
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4
Q

What is the pathogenesis of cholesterol stones forming?

A
  • imbalance between bile salts/lecithin and cholesterol
  • allows cholesterol to precipitate out of solution and form stones
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5
Q

What is the pathogenesis of pigment stones forming?

A
  • occur due to excess of circulating bile pigment
  • eg. haemolytic anaemia
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6
Q

What other factors influence pathogenesis of gallstones?

A
  • stasis (eg. pregnancy)
  • ileal dysfunction (prevents re-absorption of bile salts)
  • obesity and hypercholesterolaemia
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7
Q

What are the clinical features of biliary colic?

A
  • intense RUQ/epigastric pain
    • radiates to right side
    • might radiate to tip of shoulder/back
  • nausea and vomiting
  • postprandial pain
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8
Q

What are complications of gallstones?

A
  • biliary colic
  • acute cholecystitis
    • GB empyema, gangrene, perforation
  • obstructive jaundice
  • ascending cholangitis
  • pancreatitis
  • gallstone ileus
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9
Q

What are differential diagnoses for RUQ pain?

A
  • gallstone disease (+ related complications)
  • gastritis/duodenitis
  • peptic ulcer disease/perforated peptic ulcer
  • acute pancreatitis
  • right lower lobe pneumonia
  • MI
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10
Q

How would you differentiate between the gallstone complications?

A
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11
Q

What link does Crohn’s disease have to gallstones?

A
  • Crohn’s predisposes to development of gallstones
  • Due to malabsorption of bile salts from terminal ileum
  • Affected individual becomes depleted in bile salts
  • They do not have enough bile to maintain the cholesterol dissolved in bile
  • Thus cholesterol stones form
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12
Q

What investigations can be done for gallstones?

A
  • Ultrasound of gallbladder -> identify 90% of gallstones
  • Liver function tests to assess liver fxn
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13
Q

What ducts meet to form the common bile duct?

A
  • Cystic duct from gallbladder
  • Common hepatic duct (from R + R hepatic ducts)
  • Come together to form common bile duct (outside the liver)
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14
Q

Remember, most patients with gallstones are asymptomatic. How might patients with symptomatic gallstones present?

A
  • Biliary colic or cholecystitis (>90% of symptomatic presentations)
  • Jaundice +/- ascending cholangitis
  • Acute pancreatitis
  • Gallstone ‘ileus’
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15
Q

How does a biliary colic come about and how does this present?

A
  • if a gallstone impacts in + obstructs the cystic duct
  • the gallbladder will contract against the acutely obstructed duct
  • resulting in symptoms of biliary colic:
    • upper abdo/RUQ pain, may radiate to back/tip of scapula, often nausea + vomiting

If imaging shows gallstones + history compatible then laparoscopic cholecystectomy

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16
Q

How does acute cholecystitis develop from a gallstone?

A
  • if the impacted stone occludes cystic duct for a prolonged period of time
  • it will rub + damage the mucosal lining
  • thereby inciting an acute inflammatory response in gallbladder wall
  • there is development of acute cholecystitis
  • presence of fever indicates acute cholecystitis (or cholangitis)

Imaging (USS) + cholecystectomy (ideally <48hrs of presentation)

17
Q

What is acute acalculous cholecystitis?

A
  • acute cholecystitis without gallstones
  • thought to result from ischaemia
  • the cystic artery is an end artery w/ no collateral circulation
  • it occurs in pts who are hospitalised for conditions unrelated to gallbladder eg. hypotension + multiorgan failure; major trauma/burns; infections
  • clinical symptoms tend to be insidious since they are obscured by underlying condition
  • a high % of pts have no symptoms referable to gallbladder; diagnosis therefore rests on a high index of suspicion
  • as a result of either delay in dx or disease itself, incidence of gangrene + perforation is much higher in acalculous cholecystitis than cholecystitis due to gallstones

Rx → if pt fit then cholecystectomy, if unfit then percutaneous cholecystectomy

18
Q

What is chronic cholecystitis?

A
  • repeated episodes of biliary colic + acute cholecystitis
  • results in chronic inflammation w/ healing by fibrosis
  • as a consequence, gallbladder wall becomes thickened + the gallbladder shrinks in size
19
Q

How do gallstones cause jaundice?

A
  • if a gallstone impacts + obstructs the common bile duct (choledocholithasis), it will cause obstructive jaundice
  • the jaundice develops bc bile is unable to drain into the duodenum for excretion
20
Q

A serious complication of a gallstone obstructing the common bile duct is the development of ascending cholangitis. What is this?

A
  • inflammation of common bile duct
  • the biliary obstruction causes stasis
  • predisposes to superimposed infection: gut bacteria (usually gram negative eg. E coli, Klebsiella) gain entry to biliary tree via ampulla of Vater

Rx → fluids, broad-spectrum IV Abx, correct coagulopathy, early ERCP

21
Q

How does ascending chlangitis typically present clinically?

A
  • Charcot’s triad
  • jaundice, fever (usually w rigors) + RUQ pain
22
Q

What happens if ascending cholangitis is left untreated?

A
  • infection may ascend up to the liver
  • causing abscesses
  • and/or cause sepsis
  • serious condition if left untreated has a high mortality
23
Q

Gallstones are the commonest cause of acute pancreatitis. How do gallstones cause acute pancreatitis?

A
  • if gallstone passes down common bile duct
  • obstructs Ampulla of Vater
  • results in pancreatitis
  • there is reflux of pancreatic secretions back up the pancreatic duct -> pancreatic autodigestion -> pancreatitis
24
Q

What is gallstone ‘ileus’?

A
  • When a large gallstone causes small bowel obstruction
  • Stone erodes through gallbladder into duodenum; then obstructs terminal ileum
  • Gallstone enters the small bowel via a fistula, which forms between the inflamed wall of GB and a loop of small bowel

Rx → laparotomy + removal of gallstone from small bowel: enterotomy must be made proximal to site of obstruction + not at site of obstruction. Fistula between gallbaldder + duodenum should not be interfered with

25
Q

Why is gallstone ‘ileus’ a misnomer?

A
  • Ileus is characterised by cessation of normal peristaltic movements of bowel, typically a rxn of the bowel to any form of irritation around it (eg. post-op, peritonitis)
  • If a gallstone obstructs the small bowel, the small bowel proximal to the obstruction will attempt to overcome the blocokage by vigorous peristalsis

Hence, the term gallstone ‘ileus’ is incorrect

26
Q

What is cholangiocarcinoma?

A
  • second most common type of liver malignancy
  • arise in bile ducts
  • 80% arise in extra hepatic biliary tree
  • most pts present w/ jaundice + majority of these pts are late-stage
  • primary sclerosing cholangitis is main risk factor
  • in deprived countries → typhoid + liver flukes major risk factors
27
Q

How is diagnosis of cholangiocarcinoma made?

A
  • LFTs → obstructive picture
  • CA 19-9, CEA + CA 125 → elevated
  • CT/MRI + MRCP imaging methods of choice
28
Q

What is the treatment of cholangiocarcinoma and its prognosis?

A
  • best chance of cure = surgical resection
  • local invasion of peri hilar tumours is a particular problem + this coupled with lobar atrophy will often contraindicate surgical resection
  • palliation of jaundice important, although metallic stents should be avoided in those considered for resection

Prognosis is poor, 5-10% 5 year survival

*Medicine: Gastrointestinal (29 decks)

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