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PHGY 313 (3)
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18- Gallstone disease notes.docx

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Department
Physiology
Course
PHGY 313
Professor
Russell Jones
Semester
Winter

Description
Lecture 18 - 18/02/2013 Shouldn't be able to touch liver from under the ribs unless you have hepatitis. Common bile duct and pancreatic duct fuse and spill into the 2nd stage of duodenum through the ampulla of vater (controlled by sphincter of Oddi) Case Study: Gallstone disease  Pain after meal in upper R epigastric region. Urine became darker, stool floated. Jaundice in eyes. 1. How could the findings in the ultrasound explain the patient's pain?  After you eat food, CCK release is stimulated by fatty acids in the duodenum (APUD cells, specifically I cells). CCK causes gall bladder contraction and bile is secreted.  Stones block the duct, causing an increase in pressure. Pain receptors in wall of gall bladder you get gall bladder distension and pain.  Gall stones can be made of cholesterol, bile pigments, and Ca2+.  Stones are calcified and easily seen on the US. 2. How can you explain the yellowing of the sclera? Expand on the metabolism of the pigment causing the jaundice in this patient  Backflow in liver because of obstruction of common hepatic duct. Bilirubin enters the blood stream instead. The catabolism of heme makes biliverdin (greenish) via heme oxygenase. After a reduction you get bilirubin.  Bilirubin binds to glucoronic acid in 1:2 ratio.  Jaundice occurs when plasma bilirubin reaches 34μmoles/L.  Bilirubin glucoronide is deconjugated by bacteria.  Urobilinogen gives urine the yellow colour, and stercobilinogen gives colour to feces. o If secretion of stercobilinogen drops, feces
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