BILE LITHOGENITICY increased with
--low bile salt concentration
--low lecithin
--high cholesterol
THE FIVE F's: who is most likely to present with gall bladder concerns
--female
--fat
--forty
--fertile (has had children)
--fair
--the sixth F: feathers or first nation (natives)
SAD causes of gall stones:
--stasis, acids, diet
--stasis increases concentration & lithogenicity of bild, mbdt preg, fasting, pareneteral nutrit, spinal cord injury, pritikin diet
--acids: ileal resection or bypass, Crohn's dz, decrease bile acid levels, if low or absent dt bile salts reabsorbed in terminal ileum, if not lost then chol precipitates ??? this not make sense yet
--diet: high caloric intake, refined carbs, high sat: unsat fat ratio, decreased frequency of meals, low fiber-->decreased bile production, increase conversion to deoxycholic acid, decrease removal of deoxycholic acid in stool
CHOLELITHIASIS
--vegetarian diet protective? debatable.
--food allergy theory per Breneman 1948: avoid pork, onions & eggs to avoid attacks of biliary pain
--PATHOGENESIS: supersaturated bile (high chol) precipitates cholesterol monohydrate slude, gravel & stones
--MORPH:
----pure chol stones are oval/round and pale yellow, more common in the west
----stones mixed with calcium carbonate, phosphate and bilirubin get gray-white to black stone
----pigment stones made of calcium bilirubinate more in Asian pops
----more stones jammed in there they get facets from rubbing on each other
--SX: 70-80% ASx for decades, if Sx then bilicary "colic" pain, severe or excrutiating spasmodic or continuous in upper abdomen, pain in episodes, months/years apart
--Tx: allopathic: laparoscopic cholecystectomy
--COMPLICations: rare: empyema, perforation, fistula, cholangitis, extrahepatic cholestasis, pancreatitis, "gallstone ileus", hydrops or mucocele of the gallbladder
--Dx: HIDA scan, get gall bladder ejection fraction
PIGMENT STONES
--ETIO:
----chronic hemolysis
----GI dz-->unconj in GB (Crohn, cystic fibrosis
----ileal bypass/resection
----biliary infx
----statis from TPN
----periampullary diverticula (ampulla of vater)
----Giardia, H. Pylori
--MORPH:
----if GB sterile, stones black, multiple, crumbly
----if ducts infected, stone brown, soft, greasy
CHOLECYSTITIS
--inflam of the GB
--types: acute calculus and acute acalculus (w/ & w/o stones)
--measure wall thickness with US
--PATHOGENESIS: stone obstruction-->stasis-->mucosal phosphlipases hydrolyze lecithin to lysolecithin (toxic), mucus layer disrupted, bile salts and prostaglandins induce inflam of mucosa
--variable onset and course
--Sx: RUQ or epigastric pain, lowgrade fever, anorexia, tachycardia, diaphoresis, N = V.
--LABS: leukocytosis, increased ALP
--PROG: usu resolves in 1-7 days w/o intervention
--COMPLIC: empyema, gangrenous cholecystitis (esp w/ DM), sepsis, perforation and abscess, rupture and peritonitis, fistula to bowel
--ACALCULUS ETIO same as gastritis: ischemic compromise to GB from surgery, trauma, burns, sepsis, prolonged TPN, postpartum, multi-organ failure, multi-transfusions. Acalc mb just sludge, gangrene and perforation are more common, 50% fatality rate in critically ill pts.
CHRONIC CHOLECYSTITIS
--ETIO: usu stones
--MORPH:
--Rokitansky-Ashoff sinuses = diverticuli of GB
--porcelain gallbladder dt extensive calcification, risk factor for CA (5th mc GI CA, ASx)
--hydrops with chronic obstruction (edema)
CHOLEDOCHOLITHIASIS AND INFX
--stone in common bile duct
--clinical signs mb jaundice only
--if ascending cholangitis (infx) then fever, chills, abdom pain and jaundice
NEOPLASMS
--adenoma
--carcinoma = 5th mc GA CA, most in women 60-70
--ETIO: carcinogenic bile, chronic cholecystitis
--MORPH: porcelain GB, late dx, mets to liver at Dx, also ducts, local nodes, peritoneum, GI tract and lungs
--Sx: Asx or like cholecystitis
--1% 5 year survival
LIVER/GALL BLADDER FLUSH
--2 TSP olive oil, clove garlic and juice of one lemon, blend with a touch of cayenne, drink