GB Flashcards
GB - Duodenum path
Cystic Duct Common Hepatic Duct Common Bile Duct Pancreatic Duct Duodenum
Ampulla of vater location + fxn
between the pancreatic duct and the duodenum
`Controls the flow of bile and pancreatic juices via the sphincter of Oddi
- Bilirubin is formed by
breakdown of heme in hemoglobin, myoglobin
Poorly soluble in water
unbound = toxic to nervous system
where does bilirubin become conjugate
in liver via glucuronidation
combined with lecithin and cholesterol
bile composition
Detergent like substance that contains cholesterol, lecithin, bile acids, conjugated bilirubin and protein
bile stored + stimulus
GB
released in response to CCK and vagal stimulation when food enters duodenum
bile fxn (3)
Facilitate fat digestion and absorption
Alkalinize acidic gastric chyme
Facilitates absorption of fat soluble vitamins (A, D, E, K)
BILE ACIDS metabolism
Pass thru small intestine and are actively reabsorbed in the terminal ileum and returned to liver via enterohepatic circulation
Re-conjugated and re-excreted by hepatocytes
risk factors for gall stone formation
5 Fs
Female Forty Fat (high fat diet/obese) Fertile (multiple pregnancies) Family history
ALSO: crohn’s/ileum resection, TPN, DM
pathophys of cholelithiasis
Increase biliary cholesterol saturation = estrogen, obesity and rapid weight loss
Nucleation= increased by bacterial infection of biliary system, ABX (Ceftriaxone) and TPN
Biliary stasis 2/2 TPN, pregnancy, fasting
Cholesterol Stones:
supersaturation of cholesterol causes cholesterol to precipitated out of solution
YELLOW cholesterol stones
cause of Cholesterol Stones:
GB hypomotility and diets high in cholesterol will contribute to this process
Bilirubin Stones:
too much bilirubin secreted,
BLACK stones
causes of bilirubin stones
Hemolytic anemia (G6PD, Spherocytosis, Sickle Cell anemia)
infected Stones: color + location
BROWN stones, infected bile, soft;
MC found in cystic and common bile ducts
Biliary Sludge:
thick mucous in the GB that is a precursor to gall stones
mucous + proteins +cholesterol crystals + calcium
biliary sludge
Associated with
TPN, rapid weight loss, starvation
chronic cholecystitis AKA
biliary colic
biliary colic path
pain when gallstone lodges in cystic duct causing increasing tension in GB that is later relieved
Causes GB hypertrophy, inflammation and eventual atrophy/fibrosis
biliary colic epidemiology + risk factors
65% of symptomatic gall stone dz
fatty meals, preexisting dz
clinical présentation chronic cholecystitis
quick, rapid onset of pain in RUQ/epigastrium
***pain free after 1-4 hrs
+/-Bloating, belching, flatulence
chronic cholecystitis w/u
U/S RUQ
Labs are normal
MUST consider different diagnosis IF atypical presentation
chronic cholecystitis tx
elective laparoscopic Cholecystectomy
management before sx for biliary colic + timing
Avoid fatty foods and large meals
DM should not wait long bc prone to complications
Pregnant women can undergo lap chole in 2nd trimester if diet fails
Acute Cholecystitis
Pathophysiology:
stone becomes lodged in cystic duct causing a significant inflammatory response and mucosal thickening with sub serosal hemorrhage of GB
Acute Cholecystitis
Epidemiology + RF
95% due to gallstones, 5% caused by acalculous cholecystitis
hx of biliary colic
Acute Cholecystitis Clinical presentation
typical colic symptoms
pain doesn’t subside after 1-5 hours and lasts several days if untx
Pain more severe than usual colic
Febrile and systemically ill with anorexia, n/v
Pain located in RUQ, Murphy’s sign positive
Guarding and rebound tenderness
Acute Cholecystitis Work-up:
CBC, Liver panel, RUQ u/s, HIDA scan
LEUKOCYTOSIS (12-15k, >20k suggests perforation(
Mild elevation in bilirubin, rest of liver panel is WNL
Acute Cholecystitis Complications:
bacterial contamination of bile, acute gangrenous cholecystitis = GB abscess or GB
Acute Cholecystitis tx (medical)
IVF
ABX (GN and anaerobic coverage – Rocephin + flagyl, unasyn, zosyn)
pain control