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GI: Clin Med IIA > Disorders of the Biliary Tract > Flashcards

Disorders of the Biliary Tract Flashcards

1
Q

what is calot’s triangle?

A
  1. Oriented so that its apex is directed at the liver
  2. The borders are:
    - Medial-common hepatic duct
    - Inferior-cystic duct
    - Superior-inferior surface of the liver
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2
Q

Calot’s triangle is of clinical iportance during what procedure?

A

laparoscopic cholecystectomy

  • triangle is carefully dissected
  • Contents and borders identified
  • This allows surgeon to take into account any anatomical variation and allows cystic duct/artery to be delineated
  • To allow safe ligation of both
  • If cannot be delineated, may have to switch to open
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3
Q

what is the gallbladder’s main function?

A

concentrate and store bile produced by the liber: release it after a meal that contains fats = helps with digestion

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4
Q

Secreted by liver, stored in gallbladder
Yellow/green fluid

what this be

A

bile

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5
Q

The presence of lipids in the duodenum stimulates the release of what?
The release of this substance results in what?

A

cholecystokinin (CCK)

stimulates gallbladder wall contraction and relaxation of Sphincter of Oddi
Results in the release of bile into cystic duct and common bile duct

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6
Q

besides bile released into the cystic duct and common bile duct, where else does it flow into?

A

the second part of the duodenum and causes emulsification of large fat droplets into small ones (Micelles) - The formation of micelles aid in the absorption of fat and fat-soluble particles.

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7
Q

composition of bile

A

water and electrolytes and other substances which include bile salts, cholesterol, bilirubin, lecithin, amino acids, drugs, toxins, heavy metals, and vitamins

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8
Q

5 main functions of bile

A
  1. Aids in the digestion of fat via fat emulsification
  2. Absorption of fat and fat-soluble vitamins
  3. Excretion of bilirubin and excess cholesterol
  4. Provides an alkaline fluid in the duodenum to neutralize the acidic pH of the chyme that comes from the stomach
  5. It provides bactericidal activity against microorganisms present in the ingested food
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9
Q

how does eating affect the release of bile?

A

When you eat, the gallbladder releases bile into the common bile duct, where it’s carried to the duodenum.
This helps break down fat in food

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10
Q

what hormone also acts as a hunger suppressant - Inhibits gastric emptying
Stimulates bile production in liver

A

CCK

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11
Q

This is also known as Gallstones

A

Cholelithiasis

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12
Q

Gallstones form from: (3)

A
  1. Ratio of cholesterol too high
  2. Ratio of bilirubin too high
  3. Gallbladder not emptying bile enough
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13
Q

types of gallstones and which is MC?

A
  1. Cholesterol gallstones - m/c
  2. Calcium Bilirubinate (pigmented) gallstones
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14
Q

RF for cholelithiasis

A
  1. “Western” cultures
  2. Genetics
    - Caucasians, Hispanics, & Native Americans
    - Genetics and diets
    - LITH gene in NA that promote fat and cholesterol storage
  3. women
  4. obesity
  5. pregnancy
  6. older age
  7. rapid wt loss
  8. genetic predisopsition
  9. medical conditions
    - Hemolytic anemias
    - HLD
    - DM
    - Cirrhosis
    - Hypertriglyceridemia
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15
Q

why do women have a higher risk for cholelithiasis

A

Increase cholesterol levels in bile and decrease emptying/movement
- Excess estrogen from pregnancy
- Excess estrogen from hormone replacement
- OCPs

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16
Q

how does obesity act as a RF for cholelithiasis?

A

Enhanced cholesterol synthesis

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17
Q

how is pregnancy a RF for cholelithiasis?

A

Change in bile composition and delayed emptying

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18
Q

what diet may help prevent gallstones?

A

low-carb diet and a Mediterranean diet as well as physical activity and cardiorespiratory fitness

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19
Q

what drink appears to protect against gallstones in women?

A

caffeinated coffee

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20
Q

pathophys of asx gallstones

A

Gallstones remaining in gallbladder
Most are asx
Found incidentally on abd imaging

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21
Q

pathophys of Symptomatic Cholelithiasis (Biliary Colic)

A
  1. Gallbladder contracts in response to stimulation
  2. Forces Gallstones to move blocking cystic duct opening/gallbladder outlet
    - Causes increased intra-gallbladder pressure and back up of bile resulting in pain
    - As gallbladder relaxes, stones often fall back from cystic duct, and pain slowly subsides
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22
Q

presentation of cholelithiasis

A
  1. asx
  2. sx (Biliary Colic)
    - RUQ pain - Hallmark
    - Intense, dull discomfort, associated w/ diaphoresis, N/V
    — constant
    — following “fatty” meals (gallbladder contraction)
    — Nocturnal pain
    — radiate to R shoulder blade
    — lasts about 30 mins - Plateaus in an hr, total 6 hrs

Pts with biliary colic not ill appearing - No fever or tachycardia!!
Abd exam is benign - Biliary colic is visceral pain; No peritoneal signs

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23
Q

labs for cholelithiasis

A

Lab results generally wnl
Cbc, LFTs, amylase/lipase, alkaline phosphatase

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24
Q

atypical sx of cholelithiasis

A
  1. Belching
  2. Early satiety
  3. Regurgitation
  4. Bloating
  5. flatulence
  6. Non Cardiac chest pain
  7. Nonspecific abdominal pain
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25
Q

diagnostic for cholelithiasis

A

Abdominal US (RUQ)
Other: CT, Abd. Xray

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26
Q

tx for Cholelithiasis - Biliary Colic

A

NSAIDS - pain control
Laparoscopic Cholecystectomy

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27
Q

do you need to tx asx cholelithaisis? prophylaxis?

A

no

No need for prophylactic cholecystectomy UNLESS:
1. gallbladder is calcified
1. stones >=3cm (diameter)
1. Native American (d/t higher rate of cholesterol stones)

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28
Q

Female pt who is in her 1st trimeter has cholelithiasis and wishes to get the definitive tx, what is your next step

A

nope can’t get it - Threat of harm during 1st trimester during organogenesis by anesthesia/abd surgery

can be performed in 2nd trimester preferably after conservative approach fails for repeated attacks

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29
Q

post-op education for cholelithiasis

A
  1. All can go home within 1 day of the procedure
  2. Return to work within days
    - Vs weeks undergoing open cholecystectomy
  3. Conversion to open may be necessary in 2-8% of cases
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30
Q

What is an intraoperative cholangiogram?

A

Xray of your bile ducts, usually done during a cholecystectomy. A dye is injected in common bile duct, then Xrays taken.

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31
Q

What if your patient is not a candidate for surgery to tx cholelithiasis?

A

Ursodeoxycholic acid (Ursodiol, Actigall)

PO bile salt given up to 2 yrs
dissolves cholesterol stones
may be considered in pts who refuse cholecystectomy

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32
Q

complications of cholelithiasis and which is MC?

A
  1. Acute Cholecystitis
    - Acute Calculous Cholecystitis: MC
    - Acute Acalculous Cholecystitis
    - chronic
  2. Choledocolithiasis
  3. Cholangitis
  4. Acute Pancreatitis
  5. Gallstone Ileus
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33
Q

cause and presentation of Acute Calculous Cholecystitis complication from cholelithasis

A
  • Due to gallstones
  • Sudden onset, severe
  • M/C d/t stone becomes lodged in cystic duct
34
Q

cause and presentation of acute acalculous cholecystitis complication from cholelithasis

A
  1. Results from gallbladder stasis and ischemia, which then causes a local inflammatory response in the gallbladder wall
  2. Generally seen in critically ill patients/post op after major surgery
    - Most have multiple RF/comorbidities
    - acalculous cholecystitis + endothelial injury + gallbladder ischemia + stasis = concentration of bile salts, gallbladder distension, and necrosis of gallbladder tissue
    - Once established, secondary infection is common (E. Coli m/c)
35
Q

cause of Chronic Cholecystitis

A
  1. Result of mechanical irritation or recurrent attacks of acute cholecystitis
  2. Episodes of biliary colic
  3. Stone becomes lodged, inflammation of gallbladder develops, stone moves, symptoms resolve
    - Fibrosis and Chronic thickening of gallbladder
    - Recurrent
36
Q

Acute Cholecystitis MCC by?

A
  1. > 90% d/t gallstones
  2. Stone becomes impacted at cystic duct
    - Inflammation at and behind the stone
    - Inflammation of the gallbladder
  3. Stones cause inflammation
  4. Inflammatory mediators
  5. released in response,
  6. specifically prostaglandins
  7. Small # d/t infectious agents
    - immunocompromised persons
37
Q

presentation of Acute Cholecystitis

A
  1. Ill appearing
  2. RUQ pain
    - Steady, sharp, severe pain
    - Precipitated by meal/fatty acid ingestion
    - epigastric or shoulder blade pain >4-6hrs, up to 18
  3. May have multiple “attacks” before seek treatment
  4. N/V, Fever, Tachycardia, Anorexia
  5. Patients lie still on examining table
    - due to peritoneal irritation
    - Aggravated by movement
    - Murphy Sign
38
Q

what is the murphy sign?

A
  • Inhibition of inspiration by pain on palpation of RUQ
  • Ask pt to inspire deeply, which makes gallbladder descend toward and press against examining fingers = discomfort
  • Associated with muscle guarding and rebound tenderness
39
Q

labs for Acute Cholecystitis

A
  1. Leukocytosis - Left shift
  2. NO elevation in serum bilirubin, Aminotransferases, Alkaline Phosphatase - d/t blockage of cystic duct
    - If they are elevated, it’s generally d/t sludge passage into the common bile duct
40
Q

diagnostics for acute cholecystitis

A
  1. US - 1st Line
    - Stone lodged at cystic duct
    - Gallbladder wall thickening - >4-5mm
    - Pericholecystic fluid
  2. Sonographic Murphy’s sign
    - Similar to abdominal palpation
    - + response observed during palpation with US transducer
    - More accurate than hand palpation b/c it can confirm it is indeed the gallbladder
  3. HIDA scan
    - If U/S inconclusive
    - More sensitive
    - Useful in showing an obstructed cystic duct
41
Q

What is a HIDA scan?

A

Hepatobiliary Iminodiacetic Acid Scan (Cholescintigraphy)

  1. IV injection of Technetium-labeled iminodiacetic acid
  2. Liver takes up (in 10 minutes)
  3. hepatocytes take it up then travels with bile into gallbladder and bile ducts
  4. Watch move to gallbladder (15-30 minutes), biliary ducts, & duodenum (60 minutes)
  5. Watch for filling defects

Nonvisualized gallbladder = acute cholecystitis

42
Q

what other things does the HIDA scan measure?

A

gallbladder ejection fraction
- For Chronic cholecystitis, Acalculous cholecystitis

  1. Cholecystokinin (CCK) is injected
    - Stimulates contraction of gallbladder
    - pt with gallbladder disease often experience pain with administration

Normal = 35-75%
< 35% = gallbladder disease = Indication for cholecystectomy

43
Q

indications for HIDA scan

A
  • Gallbladder inflammation (cholecystitis)
  • Bile duct obstruction
  • Congenital abnormalities in the bile ducts, such as biliary atresia
  • Postoperative complications, such as bile leaks and fistulas
  • Assessment of liver transplant
44
Q

risks and pt education about HIDA Scan

A

Risk:

  • Allergic reaction to medications containing radioactive tracers used for the scan
  • Bruising at the injection site
  • Radiation exposure, which is small
  • NOT done in pregnancy

Pt Education:

  • Ordering doctor may want pt to fast for 4 hrs before - can have clear liquids
  • Have list of current medications
45
Q

complications with acute cholecystitis

A

Gangrenous Gallbladder
* Continuous or progression of RUQ abd pain, tenderness, muscle guarding, fever, leukocytosis after 24-48 hr
* Suggests severe inflammation and possible gangrene of the bladder
* Resulting from ischemia

Gallbladder perforation - 10% of cases
* Delay in dx
* Failure of tx

Hydrops of the gallbladder
* Results when acute cholecystitis subsides but cystic duct obstruction persists
* Producing distention of the gallbladder with a clear mucoid fluid

Mirizzi syndrome: Stone in neck of gallbladder may compress common hepatic duct and cause jaundice

Porcelain gallbladder
* Associated with cholelithiasis
* Calcification of gallbladder wall
* Chronic inflammation due to gallstones = scarring and calcification

46
Q

management for Acute Cholecystitis

A
  • Admit - NPO; NG tube if vomiting; IV fluids
  • Pip/Taz OR 2nd/3rd cephalo/Cipro + metronidazole
  • IV Meperidine (Demerol) for pain and or NSAIDS
  • Lap cholecystectomy within 24-48 hrs - Perform in same hospital stay; shorter lengths of stay, lower costs
  • Alt to surgery: Percutaneous cholecystostomy
47
Q

how does Choledocholithiasis happen

A

Gallstones in Common Bile Duct
* Passes = “Uncomplicated”
* May be asx
* MC RUQ pain
* Biliary pain d/t increase in CBD pressure
* Pain subsides when stone passes/removed

48
Q

how does cholangitis happen?

A
  • Gallstone becomes lodged and causes obstruction in CBD = “Complicated”
  • Bacterial infection: organisms, m/c E. Coli, ascend from the duodenum
  • Hepatic Injury
49
Q

presentation of choledocholithiasis

A
  • Intermittent biliary colic symptoms (RUQ pain); severe and persists for hours
  • Resulting from rapid increases in bile duct pressure
  • Jaundice (sometimes without pain)
  • Intermittent N/V
  • Epigastric tenderness
50
Q

work-up for Choledocholithiasis

A
  1. AST/ALT elevated early in course, followed by Alkaline Phosphatase, Gamma-glutamyl Transpeptidase (GGT)
    - GGT: Another enzyme found in liver that raises in response to liver damage/bile duct damage
  2. Hyperbilirubinemia
  3. transabdominal US - CBD dilation and impaired flow with stones
51
Q

Patients are often suspected of having choledocholithiasis when they present with ?

A

RUQ pain
elevated liver enzymes with elevation of alkaline phosphatase, GGT, and bilirubin

52
Q

T/F transabdominal US is helpful to visualize stones in the distal CBD for choledocholithiasis

A

F
Has poor sensitivity for stones in the distal CBD
b/c distal CBD is often obscured by bowel gas in imaging field

53
Q

tx for Choledocholilithiasis

A

ERCP + sphincterotomy and stone extraction/stent replacement
* CBD stone on Abd U/S
* Acute Cholangitis
* Hyperbilirubinemia (>4mg/dL) and CBD dilation
* >50% chance of CBD stone
Go directly to ERCP with cholecystectomy

54
Q

management for intermediate risk Choledocholilithiasis

A

Abnormal LFTs
Age >55
Dilated CBD on US

  • Go to MRCP/EUS for confirmation
  • Then removal with ERCP if stone noted
  • If no stone noted, still proceed to laparoscopic cholecystectomy
55
Q

Cholangitis is caused by bacterial infection in pt with CBD obstruction, what is the MC pathogen?

A

E. coli

56
Q

MOA of cholangitis?

A
  • Translocation from duodenum
  • Bacteria enter biliary tract when normal barrier mechanisms are disrupted
  • Resulting in stasis and infection
57
Q

Mechanisms to prevent entry include

Cholangitis

A

Sphincter of Oddi - Acts as mechanical barrier
Continuous flushing action of bile
Bacteriostatic activity of bile salts

58
Q

presentation of acute Cholangitis

A
  • Charcot Triad: RUQ Pain, Fever (+ chills), Jaundice
  • N/V
  • Reynolds Pentad: Charcot + hypotension and mental status change
  • RUQ tenderness
  • Hepatomegaly possible

Medical Emergency

59
Q

labs for acute cholangitis

A
  • CBC - Leukocytosis
  • Elevated inflammatory markers (CRP)
  • Blood cultures
  • Hepatic panel - Elevated Alkaline phosphatase (ALP) and bilirubin - possible mildly elevated AST/ALT
  • PTT
60
Q

imaging for cholangitis

A
  • US/CT - reveal stones & dilated ducts = CBD dilation > 6mm
  • MR cholangiography
  • DX: ERCP - Direct visualization, allows for stone extraction
61
Q

complications with cholangitis from ERCP?

A

Pancreatitis
d/t mechanical injury of pancreatic duct and hydrostatic injury from contrast injection

62
Q

complications from cholangitis

A
  • Liver damage - Cirrhosis & Liver failure if untreated
  • Septic shock with acute cholangitis if not treated promptly
63
Q

tx for acute cholangitis

A
  • ADMIT, IV fluids, pain control, NPO
  • ERCP w/ stone extraction & sphincterotomy within 48 hours - Liver function checked and vit. K if needed; Perform urgently with acute cholangitis; May leave stent temporarily
  • If pt still has gallbladder - lap chole performed AFTER ERCP
  • Mild - moderate = Cipro + flagyl
  • Severe (organ damage) = IV Zosyn + Flagyl

Metronidazole = flagyl; zosyn = pip/taz

64
Q

cause of Primary Sclerosing Cholangitis

A
  1. Chronic inflammatory disease of biliary tract
  2. From increased immune response to intestinal endotoxins - UC > CD - ⅔ have IBD
    - NO CURE
  3. Inflammation = obstructive symptoms and cholestasis
    - Fibrosis
    - Strictures of biliary system - Medium and large ducts; Intra/extra hepatic biliary tree
  4. Hereditary - MC men 20-50 y/o
65
Q

what can decrease the risk/improve outcomes of Primary Sclerosing Cholangitis

A

Coffee consumption is associated with a decreased risk
Statin associated with improved outcomes

66
Q

presentation of Primary Sclerosing Cholangitis

A
  • Asymptomatic phase
  • Obstructive jaundice
  • Progressive jaundice
  • Pruritus
  • Fatigue, anorexia, indigestion
  • Hepatomegaly/splenomegaly
67
Q

lab findings of Primary Sclerosing Cholangitis

A
  • Elevated LFTs (AST, ALT,), hyperbilirubinemia and Alk Phos
  • Hypergammglobulinemia
  • Increased IgM levels
  • Atypical Perinuclear Antineutrophil cytoplasmic Antibodies (P-ANCA)
68
Q

imaging for Primary Sclerosing Cholangitis

A
  1. MRCP = “beads on a string”;
    - Less invasive than ERCP
    - See adjacent soft tissue and organs
    - Uses Magnetic Resonance Imaging to produce detailed pictures of gallbladder, liver, pancreas, and bile ducts
    - Segmental fibrosis of bile ducts with saccular dilations between strictures
  2. if MRCP inconclusive = ERCP
  3. If MRCP/ERCP inconclusive = Liver bx
    - Periductal fibrosis “onion skinning”
69
Q

complications with Primary Sclerosing Cholangitis

A
  1. Cirrhosis/Liver Failure- Ultimate cause of death
  2. Cholangiocarcinoma (10%)
  3. Cholelithiasis, Cholecystitis
  4. Acute Cholangitis
70
Q

tx for Primary Sclerosing Cholangitis

A

Goal: sx relief and mgmt of progressive disease
NO CURE

  1. ABX for acute episodes - Cipro
  2. A variety of immunosuppressive and anti-inflammatory agents have been studied
  3. Ursodeoxycholic acid - Currently TESTING this (not yet recommended)
    - Hydrophilic Bile Acid - Protects cholangiocytes against cytotoxic bile acids, stimulates hepatobiliary secretion, and protects hepatocytes against bile acid induced apoptosis
  4. ERCP with dilation (recurrent), stenting
  5. Liver transplant if advanced disease d/t PSC
  6. If progresses to carcinoma - resection of tumor, if possible, can improve survival time
71
Q

MC carcinoma of the biliary tract?

A

Carcinoma of the gallbladder

72
Q

which carcinoma of the biliary tract is the most deadly?

A

Cholangiocarcinoma (bile ducts)

73
Q

typical co-existing factors of Gallbladder Carcinoma

A
  • Chronic infection of gallbladder (Salmonella typhi)
  • Gallbladder polyp (growths that protrude from lining of gallbladder); can be cancerous, but rare
  • Calcification of the gallbladder (porcelain gallbladder)
74
Q

gallbladder carcinoma often invades what other organ?

A

liver - direct extension

75
Q

possible locations of Cholangiocarcinoma

A
  • ⅔ arise at confluence of right and left hepatic ducts - Klatskin tumor (hilar cholangiocarcinoma)
  • ¼ arise in common bile duct
  • Rest are intrahepatic ducts
76
Q

Cholangiocarcinoma incidence increases with what other conditions/states?

A
  • Primary sclerosing cholangitis
  • Biliary cirrhosis (chronic obstruction)
  • immunocompromised states
77
Q

presentation of biliary tract carcinoma

A
  1. Progressive jaundice - often first sign
    - Esp. in Cholangiocarcinoma
  2. RUQ pain - Esp. gallbladder carcinoma, may not have pain with cholangiocarcinoma
  3. Anorexia, wt loss
  4. Acute cholangitis - Fever, chills
  5. Pruritus
  6. RUQ tenderness
  7. Hepatomegaly
  8. Distended, palpable gallbladder - Courvoisier sign
  9. Ascites - Biliary cirrhosis
78
Q

labs for biliary tract carcinoma

A

Elevated LFT’s
Elevated CA 19-9
Hyperbilirubinemia

79
Q

imaging for biliary tract carcinoma

A
  • US/CT/MRCP - may reveal mass or biliary dilatation
  • ERCP + bx or US guided percutaneous biopsy required for dx
80
Q

tx for biliary tract carcinoma (resectable & unresectable)

A
  1. Surgical Resection
    - Curative if well localized
    - 85% 5 year survival
  2. Unresectable
    - Biliary-enteric bypass surgery (roux-en-Y hepaticojejunostomy)
81
Q

what is Roux-en-Y

A

Biliary stent placement helps reduce stricture at the anastomosis.
Once stent has been positioned, the small bowel is divided and distal small bowel brought up and sutured to the bile duct.
An end-to-side bowel-bowel anastomosis completes the reconstruction.

Bypasses the bile duct to allow digestive juices to drain from liver directly to jejunum

GI: Clin Med IIA (12 decks)

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