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GB Flashcards

1
Q

GB - Duodenum path

A 
Cystic Duct 
Common Hepatic Duct  
Common Bile Duct 
Pancreatic Duct 
Duodenum
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2
Q

Ampulla of vater location + fxn

A

between the pancreatic duct and the duodenum

`Controls the flow of bile and pancreatic juices via the sphincter of Oddi

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3
Q
  • Bilirubin is formed by
A

breakdown of heme in hemoglobin, myoglobin

Poorly soluble in water
unbound = toxic to nervous system

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4
Q

where does bilirubin become conjugate

A

in liver via glucuronidation

combined with lecithin and cholesterol

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5
Q

bile composition

A

Detergent like substance that contains cholesterol, lecithin, bile acids, conjugated bilirubin and protein

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6
Q

bile stored + stimulus

A

GB

released in response to CCK and vagal stimulation when food enters duodenum

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7
Q

bile fxn (3)

A

Facilitate fat digestion and absorption

Alkalinize acidic gastric chyme

Facilitates absorption of fat soluble vitamins (A, D, E, K)

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8
Q

BILE ACIDS metabolism

A

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

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9
Q

risk factors for gall stone formation

A

5 Fs

Female
Forty 
Fat (high fat diet/obese) 
Fertile (multiple pregnancies)
Family history

ALSO: crohn’s/ileum resection, TPN, DM

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10
Q

pathophys of cholelithiasis

A

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

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11
Q

Cholesterol Stones:

A

supersaturation of cholesterol causes cholesterol to precipitated out of solution

YELLOW cholesterol stones

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12
Q

cause of Cholesterol Stones:

A

GB hypomotility and diets high in cholesterol will contribute to this process

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13
Q

Bilirubin Stones:

A

too much bilirubin secreted,

BLACK stones

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14
Q

causes of bilirubin stones

A

Hemolytic anemia (G6PD, Spherocytosis, Sickle Cell anemia)

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15
Q

infected Stones: color + location

A

BROWN stones, infected bile, soft;

MC found in cystic and common bile ducts

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16
Q

Biliary Sludge:

A

thick mucous in the GB that is a precursor to gall stones

mucous + proteins +cholesterol crystals + calcium

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17
Q

biliary sludge

Associated with

A

TPN, rapid weight loss, starvation

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18
Q

chronic cholecystitis AKA

A

biliary colic

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19
Q

biliary colic path

A

pain when gallstone lodges in cystic duct causing increasing tension in GB that is later relieved

Causes GB hypertrophy, inflammation and eventual atrophy/fibrosis

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20
Q

biliary colic epidemiology + risk factors

A

65% of symptomatic gall stone dz

fatty meals, preexisting dz

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21
Q

clinical présentation chronic cholecystitis

A

quick, rapid onset of pain in RUQ/epigastrium

***pain free after 1-4 hrs

+/-Bloating, belching, flatulence

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22
Q

chronic cholecystitis w/u

A

U/S RUQ

Labs are normal

MUST consider different diagnosis IF atypical presentation

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23
Q

chronic cholecystitis tx

A

elective laparoscopic Cholecystectomy

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24
Q

management before sx for biliary colic + timing

A

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

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25
Acute Cholecystitis | Pathophysiology:
stone becomes lodged in cystic duct causing a significant inflammatory response and mucosal thickening with sub serosal hemorrhage of GB
26
Acute Cholecystitis | Epidemiology + RF
95% due to gallstones, 5% caused by acalculous cholecystitis hx of biliary colic
27
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
28
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
29
Acute Cholecystitis Complications:
bacterial contamination of bile, acute gangrenous cholecystitis = GB abscess or GB
30
Acute Cholecystitis tx (medical)
IVF ABX (GN and anaerobic coverage – Rocephin + flagyl, unasyn, zosyn) pain control
31
Acute Cholecystitis tx (sx) Pt presents w/in first few days of illness:
Laparoscopic cholecystectomy within 24hrs
32
Acute Cholecystitis tx (sx) Pt presents >3-4 days after onset:
IVF, ABX, pain control, lap chole in 8 weeks
33
Acute Cholecystitis tx (sx) | Pt not a surgical candidate:
percutaneous cholecystostomy to drain infected GB
34
Ascending Cholangitis Pathophysiology: Epidemiology:
older, female ascending bacterial infection of bile 2/2 biliary stasis and ascending infection from duodenum
35
Ascending Cholangitis MC bacterial isolation (4)
o E. Coli o Klebsiella o Enterobacter o Bacteroides
36
Ascending Cholangitis RF
choledocholithiasis
37
Ascending Cholangitis clinical presentation
Charcot's triad --> Reynold's pentad N/V, + murphy's, RUQ pain with guarding V clinically ill
38
Charcot's triad
RUQ pain, fever, jaundice associated w/Ascending Cholangitis
39
Reynold's pentad
RUQ pain, fever, jaundice, septic shock, disorientation associated w/Ascending Cholangitis
40
Ascending Cholangitis w/u
liver panel, ERCP
41
ERCP in Ascending Cholangitis
determines level and type of obstruction, placement of biliary stent culture, removal of obstruction
42
Ascending Cholangitis complications
: Gram negative septic shock cardiac complications renal failure hepatic abscess
43
Ascending Cholangitis Treatment:
ICU placement and IVF, ERCP ERCP for removal of obstruction
44
what if a. cholangitis pt is too sick for ERCP?
Decompression with cholesotomy and IV ABX
45
Choledocholithiasis | Pathophysiology, Risk Factors
Gallstones within common bile duct RF: increasing age
46
Choledocholithiasis | clinical presentation
n/v, RUQ or epigastric pain and jaundice
47
Choledocholithiasis | liver panel labs
elevated alkphos, bilirubin AND transaminase
48
Choledocholithiasis test of choice
RUQ u/s *unable to see stone due to bowel gas but can see dilated CBD
49
Choledocholithiasis confirmed w? gold standard?
MRCP to confirm ERCP = gold standard bc can tx and diagnose
50
Choledocholithiasis Complications:
complete or incomplete CBD obstruction causing cholangitis or gallstone pancreatitis
51
Choledocholithiasis tx
ERCP + lap chole
52
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)
53
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
54
Choledocholithiasis found during cholangiogram sx management complete
completion of cholecystectomy and ERCP to remove retained stones next day o 2 procedures
55
Acalculous Cholecystitis | patho + epi
acute inflammation of GB w/o gallstones Epidemiology: critically ill patients
56
Acalculous Cholecystitis w/u
liver panel u/s
57
Acalculous Cholecystitis clinical presentation
fever, elevated WBC, increased alkaline phosphatase and bilirubin
58
Acalculous Cholecystitis tx
Cholecystostomy (too ill for surgery)
59
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
60
when would you do a cholangiogram
Significant change of biliary duct injury and subsequent stricture, bile leak, and need for biliary stent
61
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)
62
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
63
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
64
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
65
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
66
PBC tx
ursodeoxycholic acid (slows progression in early phases) liver transplant end stage dz
67
PBC prognosis
development of sicca complex (dry eyes/mouth), RUQ pain, hyperpigmentation or jaundice, signs of cirrhosis
68
Primary Sclerosing Cholangitis
Autoimmune process causing sclerosis of intra and extra-hepatic bile ducts of ALL SIZES, highly associated with IBD
69
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
70
tx of PSC
diagnosis confirmed with ERCP, liver transplant, medical therapy ineffective
71
prognosis of PSC
time from diagnosis to death is 12 yrs, associated with CCC development
72
SURGICAL TREAMENT OF CHOICE
lap chole due to reduced post op pain and LOS
73
triangle of Calot
cystic duct inferiorly common hepatic duct medially, inferior visceral surface of liver superiorly used in lap chole
74
lap chole complications
increased pressure may cause internal organ injury
75
indications for open chole
complications to lap chole | pregnant
76
complications of open chole
increased infection more pain increased LOS
77
Cholecystostomy | Indications:
percutaneous drain place to relieve distended, inflamed, or purulent GB when surgery is contraindicated

GI2 (6 decks)

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