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L21. Gallstone Disease
L21. Gallstone Disease
(1.5 hours)
• At the junction of the neck of the gallbladder and the cystic duct, there
is an out-pouching of the gallbladder wall forming a mucosal fold
known as "Hartmann's pouch“.
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Anatomy of the biliary tree
• Concentration
• Mucus secretion
Bile
• Secreted from hepatocytes 250-1000/day, 98% water, inorganic ions,
cholesterol, bile acid(maintain cholesterol in solution).
• Fatty food stimulate GB to contract(CCK) and relax of Sphincter of Oddi.
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Gallstone
• This is a crystalline concretion formed within the gallbladder by
accretion of bile components.
• These calculi are formed in the gallbladder but may distally pass
into other parts of the billiary tract.
• Migration of a gallstone into the opening of the cystic duct may block
the outflow of bile during gallbladder contraction.
• Metabolic
o Bile Acid : Cholesterol ratio
o Normal 25:1 but <13:1(critical ratio)-GS Risk
o Obesity BMI>30 kg/m2, ↑calorie diet, medication-steroids
• Bile Stasis:
o Pregnancy, Oral Contraceptives, Vagotomy
• Parasitic Infestation;
• clonorchis sinensis,
• Liver Flukes
• ascaris lumbricoides
• The presence of free fatty acids, deconjugated bilirubin, and bile acids
leads to the formation of insoluble calcium bilirubinate particles.
Biliary colic
• The pain begins postprandial (usually within an hour after a fatty meal),
is often described as intense and dull, and may last from 1-5 hours.
• From onset, the pain increases steadily over about 10 to 20 minutes and
then gradually wanes when the gallbladder stops contracting and the
stone falls back into the gallbladder.
Pathogenesis
• Grossly thickened
• Reddish with subserosal hemorrhages
• Pericholecystic fluid
• Hyperemic mucosa
• Patchy necrosis.
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Acute Cholecystitis cont.
• In severe cases 5% to 10%, the inflammatory process progresses and leads
to ischemia and necrosis of the gallbladder wall.
• Febrile
• Complains of anorexia, nausea, and vomiting
• Reluctant to move
• The Gallbladder distention with bile stasis and ischemia has been
implicated as causative factors.
1. Double impaction: One stone in the CBD and one stone in the cystic
duct.
6. Mucocele
• stone block CD with sterile bile
• Bile absorbed replaced by Over production of mucus by GB
epithelium.
7. Gallbladder empyema
• Overgrowth of colonizing bacteria in the gallbladder often occurs, and,
in severe cases, accumulation of pus in the gallbladder.
• The gallbladder wall may become necrotic, resulting in perforation and
pericholecystic abscess.
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Differential Diagnoses for GS.
• Acute Pancreatitis
• Appendicitis
• Bile Duct Strictures
• Bile Duct Tumors
• Cholangiocarcinoma
• Cholecystitis
• Gallbladder Cancer
• Pancreatic Cancer
• Peptic Ulcer Disease
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Investigations for GSD
• Patients with uncomplicated cholelithiasis or simple biliary colic
typically have normal laboratory test results.
Drawbacks
• Recurrence of stones once treatment is stopped
• Life-long maintenance is needed.
• After dissolution of the stones, lithotripsy or extracorporeal shock
wave Iithotripsy should be done.
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Types of medical treatment
• Cholecystectomy
• indicated in patients who have experienced symptoms or
complications of gallstones.
• Cholecystostomy
• Temporary drainage of pus from the gallbladder preferred to allow
stabilization and to permit later cholecystectomy under elective
circumstances.
• The relevant anatomy involves; the gall bladder, cystic duct, common bile
duct, ampulla of vater and sphincter of Oddi.
• Risks of GSD are; age, sex, pregnancy, obesity, rapid weight loss, cirrhosis,
hemolytic anemias.
• Gallstones can be; cholesterol stones, pigment stones, mixed stones and
brown pigment stones.
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Summary cont.
• Gall stone disease has a; lithogenic, asymptomatic, symptomatic &
complications stage.