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
Acute Cholecystitis tx (sx)
Pt presents w/in first few days of illness:
Laparoscopic cholecystectomy within 24hrs
Acute Cholecystitis tx (sx)
Pt presents >3-4 days after onset:
IVF, ABX, pain control, lap chole in 8 weeks
Acute Cholecystitis tx (sx)
Pt not a surgical candidate:
percutaneous cholecystostomy to drain infected GB
Ascending Cholangitis
Pathophysiology:
Epidemiology:
older, female
ascending bacterial infection of bile 2/2 biliary stasis and ascending infection from duodenum
Ascending Cholangitis MC bacterial isolation (4)
o E. Coli
o Klebsiella
o Enterobacter
o Bacteroides
Ascending Cholangitis RF
choledocholithiasis
Ascending Cholangitis
clinical presentation
Charcot’s triad –> Reynold’s pentad
N/V, + murphy’s, RUQ pain with guarding
V clinically ill
Charcot’s triad
RUQ pain, fever, jaundice
associated w/Ascending Cholangitis
Reynold’s pentad
RUQ pain, fever, jaundice, septic shock, disorientation
associated w/Ascending Cholangitis
Ascending Cholangitis
w/u
liver panel, ERCP
ERCP in Ascending Cholangitis
determines level and type of obstruction,
placement of biliary stent
culture,
removal of obstruction
Ascending Cholangitis
complications
: Gram negative septic shock
cardiac complications
renal failure
hepatic abscess
Ascending Cholangitis Treatment:
ICU placement and IVF, ERCP
ERCP for removal of obstruction
what if a. cholangitis pt is too sick for ERCP?
Decompression with cholesotomy and IV ABX
Choledocholithiasis
Pathophysiology, Risk Factors
Gallstones within common bile duct
RF: increasing age
Choledocholithiasis
clinical presentation
n/v, RUQ or epigastric pain and jaundice
Choledocholithiasis
liver panel labs
elevated alkphos, bilirubin AND transaminase
Choledocholithiasis test of choice
RUQ u/s
*unable to see stone due to bowel gas but can see dilated CBD
Choledocholithiasis confirmed w? gold standard?
MRCP to confirm
ERCP = gold standard bc can tx and diagnose
Choledocholithiasis Complications:
complete or incomplete CBD obstruction causing cholangitis or gallstone pancreatitis
Choledocholithiasis tx
ERCP + lap chole
Choledocholithiasis
Present and Known sx management
ERCP to remove stone followed by lap chole the next day
RF: pt could have stone that gets into different duct (retained ductal stone)
Choledocholithiasis found during cholangiogram sx management
explore
exploration of duct and removal of CBD stone
RF: Dye can push stone down (to pancreatic duct, causing pancreatitis) = Susceptible to surgeon damage
Choledocholithiasis found during cholangiogram sx management
complete
completion of cholecystectomy and ERCP to remove retained stones next day
o 2 procedures
Acalculous Cholecystitis
patho + epi
acute inflammation of GB w/o gallstones
Epidemiology: critically ill patients
Acalculous Cholecystitis w/u
liver panel u/s
Acalculous Cholecystitis clinical presentation
fever, elevated WBC, increased alkaline phosphatase and bilirubin
Acalculous Cholecystitis tx
Cholecystostomy (too ill for surgery)
cholangiogram
Preformed during cholecystectomy to assess for ductal stones
Injection of contrast to look for filling defects and free flow contrast
If stones are found: there will be a blockage of contrast
when would you do a cholangiogram
Significant change of biliary duct injury and subsequent stricture, bile leak, and need for biliary stent
U/S RUQ
Diagnostic study of choice to look for stones/sludge
Demonstrates thickening of GB wall, pericholecystic fluid, sonographic Murphy’s sign
Looks for acoustic shadowing (sludge has none)
HIDA scan
Evaluate for acute cholecystitis if RUQ u/s is non diagnostic
Injected IV and taken up selectively by hepatocytes and excreted into bile
picked up in response to CCK
positive HIDA =
gallbladder does not visualize (due to cystic duct obstruction (edema associated with cholecystitis or obstructing stone)
Also positive if HIDA does not enter the small intestine
Primary Biliary Cirrhosis
Autoimmune disorder causing immune mediated obliteration of SMALL/MEDIUM sized bile ducts in liver
Bile ducts are then destroyed and can no longer leave liver efficiently resulting in hepatitis in cirrhosis
PBC presentation
Women in their 40s, debilitating fatigue and severe pruritus
Early: increased ALT, AST, elevated bilirubin and alk phos
Late: development of thrombocytopenia and prolonged PT/INR
AMA is in the serum of 95% of pts w/PBC
PBC tx
ursodeoxycholic acid (slows progression in early phases)
liver transplant end stage dz
PBC prognosis
development of sicca complex (dry eyes/mouth), RUQ pain, hyperpigmentation or jaundice, signs of cirrhosis
Primary Sclerosing Cholangitis
Autoimmune process causing sclerosis of intra and extra-hepatic bile ducts of ALL SIZES, highly associated with IBD
PSC presentation
fatigue, pruritus, RUQ pain, repeated bouts of ascending cholangitis
MC in men 20s-40s
Elevated alk phos and bilirubin in cholestatic pattern
Auto-immune Abs: p-ANCA, ANA
tx of PSC
diagnosis confirmed with ERCP,
liver transplant, medical therapy ineffective
prognosis of PSC
time from diagnosis to death is 12 yrs, associated with CCC development
SURGICAL TREAMENT OF CHOICE
lap chole
due to reduced post op pain and LOS
triangle of Calot
cystic duct inferiorly
common hepatic duct medially,
inferior visceral surface of liver superiorly
used in lap chole
lap chole complications
increased pressure may cause internal organ injury
indications for open chole
complications to lap chole
pregnant
complications of open chole
increased infection
more pain
increased LOS
Cholecystostomy
Indications:
percutaneous drain place to relieve distended, inflamed, or purulent GB when surgery is contraindicated
