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Path: Liver 6 - Gallstones + Pancreatitis (i) (biliary colic (most common…
Path: Liver 6 - Gallstones + Pancreatitis (i)
Normal GB
stores + concentrates bile
liver actually makes bile hence GB not vital
elective cholecystectomies v common - significant part of workload for general surgeon
anatomical variants regarding where the cystic duct becomes the CBD + vessels
bile contents
bile salts + phospholipids
detergent action for fat digestion
emulsify fats in distal DI so they can be absorbed
excretory: bili, chol, Ca salts, copper
chol not water soluble, hence remains in solution by forming micelle with bile salts - often may be an unstable solution - ! gallstones
bile secretion blocked - obstructive jaundice
Gallstones
common
easily identified with US
formed from bile constituents (+/- Ca)
predominantly chol >90% of cases, may be mixed
predominantly bili < 10% of cases (small, fragments pigment gallstones)
only 10% are radio-opaque (have Ca) on plain film X-ray
cholelithiasis = stones in GB
choledocholithiasis = stones in CBD
typically pass from GB to CBD via cystic duct
less commonly primarily form in CBD - harder to tx
stone in cystic duct: normally no obstructive jaundice as main secretion path (CHD -> CBD) still functional
rare exception = Mirizzi syndrome (big stone in cystic duct compresses CBD externally)
predisposing factors
female (stones in 16% of US women vs 9% of US men)
increasing age
obesity
high fat/low fibre western diet
high lipids
insulin resistant type 2 DM
geography, ethnic distribution (Native Americans, hispanic)
high dose oestrogen: pregnancy, OCP, HRT
GB hypomotility/stasis: rapid weightloss (bariatric surgery), fasting, TPN (removes stimulus)
for pigment stones specifically: bile salt depletion (Crohn's ileitis, ileal surgery), cirrhosis, haemolysis, parasites
pathogenesis
altered bile composition
lithogenic bile, promotes formation of calculi as well as microlithiasis + bile sludge
precise mechanism unexplained (possibly chol supersaturation?)
GB hypomotility (sluggish/static)
stones form in sequential episodes over long period
infection not a primary event (secondary infection = acute cholecystitis)
biliary colic
most common symptom related to gallstones
may be difficult to confidently dx
sudden steady severe pain in RUQ/epigastric region
lasts 30mins - 4hrs
will recur in 70%
increases risk of gallstone complications (1-2% with biliary colic will get complications)
may radiate to back/right shoulder via the flank
usually crescendo pattern/persistent
visceral pain due to GB distension following transient obstruction of cystic duct
aka GB attack
no fever/raised WCC/tenderness
dDx: dyspepsia, PUD, acute pancreatitis, oeso pain, MI
once dxed, do cholecystectomy to avert complications
Gallstone symptoms
most asymptomatic
incidental finding
tx not indicated
won't benefit from cholecystectomy
surgery puts them @ risk of postcholecystectomy syndrome (PCS) - presence of abdo symptoms 2 yrs after procedure
only 20% cause symptoms if followed up for 15 yrs
biliary colic develops in 1-4% annually
other symptoms are vague upper GI symptoms
vague abdo pain
dyspepsia
fatty food intolerance
early satiety
case selection for surgery not precise with vague symptoms, as these symptoms are not always relieved after
distinction between asymptomatic + symptomatic can be difficult
CBD obstruction a/w gallstones
obstructive jaundice
intermittent colicky pain
elevated ALP + gGT
dilated ducts (US)
risk of secondary infection
ascending cholangitis
acute pancreatitis