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HPIM Gastro > 369: Diseases of the Gallbladder and Bile Ducts > Flashcards

369: Diseases of the Gallbladder and Bile Ducts Flashcards

1
Q

Isotonic fluid with an electrolyte composition resembling blood plasma

A

Hepatic bile

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2
Q

Total solute concentration of hepatic bile vs gallbladder bile

A

hepatic bile: 3-4g/dL

gallbladder bile: 10-15g/dL

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3
Q

Components of bile

A
  1. Bile acids (80%)
  2. lecithin and traces of other phospholipids (16%)
  3. unesterified cholesterol (4%)
  4. Others: Conjugated bilirubin, protein (all Immunoglobulins, albumin, metabolites of hormones); electrolytes; mucus; drugs and their metabolites
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4
Q

Total daily basal secretion of hepatic bile

A

500-600mL

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5
Q

3 Mechanisms important in regulating bile flow

A
  1. Active transport of bile acids from hepatocytes into the bile canaliculi
  2. Active transport of other organic anions
  3. Cholangiocellular secretion (secretin-mediated secretion of sodium and bicarbonate-rich fluid into bile ducts
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6
Q

An aminophospholipid transferase (“flippase”) essential for maintaining the lipid asymmetry of the canalicular membrane

A

F1C1 (ATP8B1)

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7
Q

Important ATP-dependent canalicular transport proteins (“export pump”/ABC transporters)

A
  1. Bile salt export pump (BSEP, ABCB11)
  2. Anionic conjugate export pump (MRP2, ABCC2) - canalicular excretion of amphiphilic conjugates from phase II conjugation
  3. Multidrug export pump (MDR1, ABCB1) - hydrophobic cationic compounds
  4. Phospholipid export pump (MDR3, ABCB4)
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8
Q

Other transporters

A
  1. Hemitransporters ABCG5/G8 - canalicular cholesterol and phytosterol transporter
  2. C1/HCO3 anion exchanger isoform 2 (AE2, SLC4A2) - canalicular bicarbonate secretion
  3. F1C1 (ATP8B1)
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9
Q

Genetic defects associated with defect in F1C1

A
  1. Progressive familial intrahepatic cholestasis type 1 (PFIC1)
  2. Benign recurrent intrahepatic cholestasis type 1 (BRIC1)
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10
Q

Genetic defects associated with defect in BSEP

A
  1. PFIC2

2. BRIC2

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11
Q

Genetic defect associated with defect in MRP2(ABCC2)

A

Dubin-Johnson syndrome - CONJUGATED hyperbilirubinemia

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12
Q

Genetic defects associated with defect in MDR3(ABCB4)

A

PFIC3

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13
Q

Genetic defects associated with defect in ABCG5/G8

A

Sitosterolemia

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14
Q

Genetic defects associated with defect in cystic fibrosis transmembrane regulator (CFTR, ABCC7)

A

Cystic fibrosis

Chronic cholestatic liver disease

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15
Q

Review: The primary bile acids

A
  1. Cholic acid

2. Chenodeoxycholic acid (CDCA)

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16
Q

Primary bile acids are conjugated with these amino acids then secreted into the bile

A
  1. Glycine OR
  2. Taurine

Ratio of glycine to taurine conjugates in bile: 3:1

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17
Q

Secondary bile acids

A
  1. Deoxycholate
  2. Lithocholate
  3. Ursodeoxycholic acid (UDCA) : in low concentration
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18
Q

Where do secondary bile acids form?

A

Colon

As bacterial metabolites of primary bile acids

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19
Q

Serve as major physiologic driving force for hepatic bile flow and aid in water and electrolyte transport in the small bowel and colon

A

Bile acids

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20
Q

Transport mechanism of bile acids in the gut

A

Passive diffusion (Unconjugated, some conjugated)

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21
Q

Transport mechanism for conjugated bile acids in the DISTAL ILEUM and important in bile salt recirculation

A

Active transport

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22
Q

Normal bile acid pool size

A

2-4g

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23
Q

of circulation of the bile acid pool daily

A

5-10 times daily

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24
Q

Percentage of bile that is reabsorbed in the intestine

A

95%

Fecal loss of bile acids: 0.2-0.4g/d

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25
Q

What growth factor is released by the bile acids in the intestine into the circulation that will suppress synthesis of bile acids (in liver) from cholesterol by inhibiting the RATE-LIMITING ENZYME cytochome P450 7A1 (CYP7A1) and PROMOTES GALLBLADDER RELAXATION

A

Fibroblast growth factor 19 (FGF19)

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26
Q

2 important mechanisms that maintain/balance bile salts in the body

A
  1. Hepatic synthesis (5%)
  2. Intestinal reabsorption (95%)

Maximum rate of hepatic synthesis is 5g/d

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27
Q

Nuclear receptor that upregulates the hepatic BSEP (ABCB11) and repress bile acid synthesis

A

Farnesoid X receptor (FXR)

A bile acid sensor

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28
Q

Nuclear receptor that upregulates the cholesterol transporter (ABCG5/G8)

A

Liver X receptor (LXR)

An oxysterol sensor

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29
Q

2 Functions of the tonic contraction of Sphincter of Oddi during the FASTING state

A
  1. Prevent reflux of duodenal contents into the pancreatic and bile ducts
  2. Promote filling of the gallbladder
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30
Q

Peptide hormone that is the major factor controlling the evacuation of the gallbladder

A

Cholecystokinin (CCK)

Released into the DUODENAL mucosa
Stimulant: Ingestion of fats and amino acids

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31
Q

Functions of CCK

A
  1. Powerful contraction of gallbladder
  2. Decreased resistance of the sphincter of Oddi
  3. Enhanced flow of biliary contents into the duodenum
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32
Q

Normal capacity of gallbladder

A

30mL of bile

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33
Q

Clinically innocuous entity in which a partial or complete septum (fold) separates the fundus from the body

A

Phrygian cap

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34
Q

T of F:

Gallstone formation increases after age 40.

A

False

After age 50

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35
Q

T or F:

Gallstones are more common among men

A

False

Women

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36
Q

Review: 2 Major Types of Gallstones

A
  1. Cholesterol stones (90%)

2. Pigment stones

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37
Q

Usually contain >50% cholesterol monohydrate plus admixture of calcium salts, bile pigments, proteins, and fatty acids.

A

Cholesterol gallstones

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38
Q

Composed primarily of calcium bilirubinate and contain <20% cholesterol;

A

Pigment stones

Classified into “black” and “brown” types

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39
Q

Type of pigment stone that forms secondary to chronic biliary infection

A

“brown” pigment stones

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40
Q

The most important mechanism in the formation of lithogenic (stone-forming) bile

A

Increased biliary secretion of cholesterol

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41
Q

T or F: Obesity, not metabolic syndrome, is associated with formation of lithogenic bile.

A

False

Obesity, Metabolic syndrome, high-caloric and cholesterol-rich diets, drug (clofibrate)

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42
Q

Rate limiting enzyme of hepatic cholesterol synthesis causing increased hepatic uptake of cholesterol from blood

A

Hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase

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43
Q

The 3 mechanisms that cause gallstone disease

A
  1. Bile supersaturation with cholesterol
  2. Nucleation of cholesterol monohydrate with subsequent crystal retention and stone growth
  3. Abnormal gallbladder motor function known to predispose to cholesterol-stone formation

See Table 369-1, p.2078

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44
Q

Mechanism by which ORAL CONTRACEPTIVES can cause gallstone disease

A

Decreased bile salt excretion

Effect: Decreased conversion of cholesterol to cholesteryl esters

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45
Q

Mechanism by which PREGNANCY can cause gallstone disease

A

Impaired GB emptying due to progesterone + estrogen

Effect: Increase biliary cholesterol secretion

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46
Q

GB hypomotility leading to stasis and formation of sludge are present in these conditions

A
  1. Prolonged parenteral nutrition
  2. Fasting
  3. Pregnancy
  4. Drugs such as octreotide
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47
Q

Lipid-lowering agent that reduces VLDL however this increases biliary secretion of cholesterol

A

Clofibrate

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48
Q

Genetic defect in this gene causing gallstone disease; mechanism is decreased PHOSPHOLIPID secretion

A

MDR3 gene

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49
Q

Genetic defect in this gene causing gallstone disease; mechanism is decreased BILE ACID secretion

A

CYP7A1 gene

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50
Q

Characteristics of BILE sludge in studies

A
  1. Recurrent
  2. Can form gallstones (asymptomatic and symptomatic)
  3. Associated with severe biliary pain with/without pancreatitis
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51
Q

T or F: Biliary sludge in pregnancy is more frequent than gallstone formation

A

True

20-30% biliary sludge
5-12% gallstones

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52
Q

T or F: Biliary sludge in pregnancy is asymptomatic and resolves spontaneously after delivery

A

True

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53
Q

T or F: Gallstone formation in pregnancy are associated with biliary colic and will not disappear even after delivery

A

False

May have spontaneous dissolution after delivery

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54
Q

Stones that are composed of either pure calcium bilirubinate or polymer-like complexes with calcium and mucin glycoproteins

A

Black pigment stones

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55
Q

Conditions associated with BLACK pigment stones

A
  1. Chronic hemolytic state
  2. Liver cirrhosis
  3. Gilbert’s syndrome
  4. Cystic fibrosis
  5. Patients with ileal diseases, ileal resection, or ileal bypass
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56
Q

Stones that are composed of calcium salts of unconjugated bilirubin with varying amounts of cholesterol and protein

A

Brown pigment stones

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57
Q

Pigment stone associated when bile is chronically infected by bacteria

A

Brown pigment stones

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58
Q

Material of low echogenic acitivity that typically forms a layer in the most dependent position of the GB; it shifts with postural changes but fails to produce acoustic shadowing

A

Biliary sludge

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59
Q

Procedure of choice for detection of stones
A. GB ultrasound
B. Plain abd xray
C. Radioisotope scans (HIDA, DIDA)

A

A. GB ultrasound

See Table 369-2

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60
Q

Procedure that shows pathognomotic findings in porcelain gallbladder and emphysematous cholecystitis
A. GB ultrasound
B. Plain abd xray
C. Radioisotope scans (HIDA, DIDA)

A

B. Plain abd xray

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61
Q

T or F: Radioisotope scans are indicated for confirmation of suspected chronic cholecystitis

A

False

ACUTE cholecystitis
Less sensitive and less specific in chronic cholecystitis

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62
Q

Most specific and characteristic symptom of gallstone disease

A

Biliary colic

Constant and often long-lasting pain
30mins - 5hours

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63
Q

Characteristic pain caused by obstruction of the cystic duct or CBD by a stone

A

Visceral pain : Severe, steady ache or fullness
Location: Epigastrium or RUQ
Radiation: Interscapular area, right scapula, or shoulder

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64
Q

Biliary pain in the presence of this finding suggests a common duct stone

A

Elevated level of serum bilirubin AND/OR alkaline phosphatase

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65
Q

Biliary pain associated with fever or chills (rigors) suggests what?

A
  1. Cholecystitis
  2. Pancreatitis
  3. Cholangitis
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66
Q

T or F: Biliary colic is frequently nocturnal, occurring within a few hours of retiring

A

True

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67
Q

Decision analysis suggestions in asymptomatic patients with gallstone disease

A
  1. Cumulative risk of death due to gallstone disease while on expectant management is small
  2. prophylactic cholecystectomy is NOT warranted
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68
Q

T or F: Diabetic patients can have silent MI as well as silent gallstones.

A

True

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69
Q

Recommendations for cholecystectomy

A
  1. Presence of symptoms that are frequent enough or severe enough to interfere with the patient’s general routine
  2. Presence of prior complication of gallstone disease (history of acute chole, pancreatitis, gallstone fistula)
  3. Presence of underlying condition predisposing the patient to increased risk of gallstone complications
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70
Q

Can be considered for prophylactic cholecystectomy

A

Very large gallstones (>3cm in diameter)

Gallstones in congenitally anomalous GB

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71
Q

Advantages of laparoscopic cholecystectomy

A
  1. Markedly shortened hospital stay
  2. Minimal disability
  3. Decreased cost

Procedure of choice for most patients referred for elective cholecystectomy

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72
Q

“Gold Standard” for treating symptomatic cholelithiasis

A

Laparoscopic cholecystectomy

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73
Q

Diameter of radiolucent stones that can have complete dissolution within 6 months to 2 years

A

<10mm in diameter

Achieved in 50% of patients
>10mm are rarely dissolve

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74
Q

Dose of UDCA for gallstone dissolution

A

10-15mg/kg per day

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75
Q

T or F: Pigment stones are not responsive to UDCA therapy.

76
Q

T or F: Patients with cholesterol gallstone disease who develop recurrent choledocholithiasis after cholecystectomy should be on a long-term treatment with UDCA.

77
Q

3 Factors responsible for the inflammatory response of the GB

A
  1. MECHANICAL inflammation produced by increased intraluminal pressure and distention with resulting ischemia of gallbladder mucosa and wall
  2. CHEMICAL inflammation caused by the release of lysolecithin and other local tissue factors
  3. BACTERIAL inflammation
78
Q

Organisms most frequently isolated by culture of gallbladder bile in acute cholecystitis

A
  1. Klebsiella spp.
  2. Escherichia coli
  3. Streptococcus spp.
  4. Clostridium spp.
79
Q

T or F: Jaundice is usually an early sign of acute cholecystitis

A

False

Unusual but may occur when edematous inflammatory changes involve the bile ducts and surrounding lymph nodes

80
Q

T or F: High grade fever, shaking chills and rigors are usually seen in acute cholecystitis

A

False

LOW grade fever
Shaking chills or rigors UNCOMMON

81
Q

T or F: An enlarged, tensed gallbladder is almost always palpable in patients with acute cholecystitis

A

False

25-50%

82
Q

Deep inspiration or cough during subcostal palpation of the RUQ usually produces increased pain and inspiratory arrest

A

Murphy’s sign

83
Q 
Common signs in acute cholecystitis except:
A. localized rebound tenderness
B. hypoactive bowel sounds
C. abdominal distention
D. abdominal rigidity
A

D. Abdominal rigidity

Abdominal rigidity and generalized peritoneal signs are lacking in the absence of perforation

84
Q

Triad of symptoms highly suggestive of acute cholecystitis

A
  1. Sudden onset RUQ tenderness
  2. Fever
  3. Leukocytosis (10,000-15,000 cells/mL) with left shift on differential count
85
Q

Relationship of bilirubin and aminotransferases in acute cholecystitis

A
  1. Serum bilirubin - mildly elevated

2. Serum aminotransferases - modest elevations (less than fivefold)

86
Q

Confirmatory imaging test if the bile duct imaging seen in ultrasound did not visualized the gallbladder

A

Radionuclide biliary scan (e.g. HIDA)

87
Q

T or F: Acute cholecystitis is best treated by early surgery whenever possible.

88
Q

Rare complication in which gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the CBD, resulting in CBD obstruction and jaundice

A

Mirizzi’s syndrome

89
Q

Imagings used to demonstrate characteristic extrinsic compression of CBD in Mirizzi’s syndrome

A
  1. ERCP
  2. MRCP
  3. PTC
90
Q

Conditions that increases risk for ACALCULOUS cholecystitis

A
  1. Serious trauma or burns
  2. Postpartum period following prolonged labor
  3. Orthopedic and other nonbiliary major surgical operations in post-op period
91
Q

Precipitating factors for ACALCULOUS cholecystitis

A
  1. Biliary sludge in cystic duct
  2. Vasculitis
  3. Obstructing adenoCA of GB
  4. Diabetes mellitus
  5. Torsion of GB
  6. Unusual bacterial infections of GB (Leptospira, Streptococcus, Salmonella, Vibrio cholerae)
  7. Parasitic infestations of GB
  8. Others diseases: Sarcoidosis, cardiovascular dse, tuberculosis, syphilis, actinomycosis
92
Q

Management of ACALCULOUS cholecystitis

A
  1. Early diagnosis
  2. Early surgical intervention
  3. Meticulous attention to post-op care
93
Q

Infusion of this hormone can be used to measure gallbladder ejection fraction during cholescintigraphy

A

Octapeptide of CCK

94
Q

Progression of emphysematous cholecystitis

A
  1. Acute cholecystitis (calculous or acalculous)
  2. Ischemia or gangrene of gallbladder wall
  3. Infection by gas-producing organisms
95
Q

Bacteria most frequently cultured in emphysematous cholecystitis

A

Anaerobes: Clostridium welchii, Clostridium perfringens
Aerobes: E. coli

96
Q

Population where emphysematous cholecystitis occurs most frequently

A
  1. Elderly men

2. Diabetic patients

97
Q

Imaging used for diagnosis of emphysematous cholecystitis

A

Plain abdominal film

Gas within the GB lumen, dissecting within the GB wall to form a gaseous ring, or in pericholecystic tissues

98
Q

Management of emphysematous cholecystitis

A
  1. Prompt surgical intervention

2. Appropriate antibiotics

99
Q

Results from progression of acute cholecystitis with persistent cystic duct obstruction to superinfection of the stagnant bile with a pus-forming bacterial organism

A

Empyema of gallbladder

100
Q

Clinical picture of empyema of GB

A

Resembles cholangitis + high fever
Severe RUQ pain
Marked leukocytosis
Prostration

101
Q

Management of empyema of GB

A
  1. EMERGENCY surgical intervention

2. Proper antibiotic coverage

102
Q

Condition that results from prolonged obstruction of the cystic duct, usually by a large solitary calculus

A

Hydrops OR mucocele of gallbladder

103
Q

Management of hydrops of mucocele

A

Cholecystectomy is indicated to prevent complications: empyema, perforation, gangrene

104
Q

Most common locations of fistula formation

A
  1. into the duodenum
  2. hepatic flexure of colon
  3. stomach
  4. jejunum
  5. abdominal wall
  6. renal pelvis
105
Q

Imaging used to demonstrate fistula

A
  1. Barium contrast studies

2. Endoscopy of upper GI tract or colon

106
Q

Treatment for fistula in symptomatic patients

A

Cholecystectomy
CBD exploration
Closure of fistulous tract

107
Q

Mechanical intestinal obstruction resulting from the passage of a large gallstone into the bowel lumen

A

Gallstone ileus

108
Q

Most common site of obstruction by impacted gallstone

A

Ileocecal valve

109
Q

Diagnostic confirmation of gallstone ileus

A

Plain abdominal film (occasionally)

Upper GI series

110
Q

Management of gallstone ileus

A

Laparotomy with stone extraction/propulsion into the colon

111
Q

T or F: Cholecystectomy is advised in all patients with porcelain gallbladder due to development of carcinoma of the GB

112
Q

Drugs given in acute cholecystitis for analgesia that will produce less spasm of the sphincter of Oddi

A

Meperidine

NSAIDs

113
Q

Most common organisms present in acute cholecystitis

A

E. coli
Klebsiella spp.
Streptococcus spp.

114
Q

Antibiotic therapy for acute cholecystitis

A
  1. Piperacillin or Mezlocillin
  2. Ampicillin Sulbactam
  3. Ciprofloxacin
  4. Moxifloxacin
  5. 3rd generation cephalosporin
  6. Metronidazole : if gangrenous or emphysematous chole is suspected
115
Q

Antibiotic therapy in acute cholecystitis if ascending cholangitis is suspected

A

Imipenem

Meropenem

116
Q

Timing of surgery for uncomplicated acute cholecystitis

A

Early elective laparoscopic cholecystectomy = 48-72h

117
Q

T or F: Complication rate is not increased in patients undergoing early as opposed to delayed (>6 weeks after diagnosis) cholecystectomy

118
Q

When is delayed surgical intervention considered?

A
  1. Overall medical condition imposes an unacceptable risk for early surgery
  2. Diagnosis of acute cholecystitis is in doubt
119
Q

Treatment of choice for acute cholecystitis

A

Early cholecystectomy (within 72h)

120
Q

T or F: Mortality risk for early elective cholecystectomy is lower compared to mortality risk for emergency cholecystectomy in patients under age of 60.

121
Q

Early complications postcholecystectomy

A
  1. Atelectasis and other pulmonary disorders
  2. Abscess formation (often subphrenic)
  3. External or internal hemorrhage
  4. Biliary-enteric fistula
  5. Bile leaks
122
Q

Most common cause of persistent postcholecystectomy symptoms

A

Overlooked symptomatic nonbiliary disorder

e.g. reflux esophagitis, peptic ulceration, pancreatitis, irritable bowel syndrome

123
Q

Disorders of extrahepatic bile ducts (Postcholecystectomy syndromes) that may cause persistent symptomatology

A
  1. Biliary strictures
  2. Retained biliary calculi
  3. Cystic duct stump syndrome
  4. Stenosis or dyskinesia of the sphincter of Oddi
  5. Bile salt-induced diarrhea or gastritis
124
Q

5 criteria that defines papillary stenosis

A
  1. upper abdominal pain, RUQ or epigastric
  2. abnormal liver tests
  3. dilatation of the CBD upon ERCP examination
  4. delayed (>45min) drainage of contrast material from the duct
  5. increased basal pressure of the sphincter of Oddi

*more criteria present, greater likelihood of diagnosis

125
Q

Treatment for papillary stenosis

A

Endoscopic or surgical sphincteroplasty

126
Q

Indications for sphincterotomy in papillary stenosis

A
  1. Prolonged duration of symptoms
  2. Lack of response to symptomatic treatment
  3. Presence of severe disability
  4. Patient’s choice of sphincterotomy over surgery
127
Q

Procedure of choice for removing bile duct stones and other biliary and pancreatic problems

A

Endoscopic biliary sphincterotomy (EBS)

128
Q

T or F: Cholecystectomy shortens gut transit time by accelerating passage of fecal bolus through the colon with marked acceleration in the right colon producing the symptoms of dyspepsia

129
Q

Treatment for postcholecystectomy diarrhea

A

Bile-acid sequestering agents:
Cholestyramine
Colestipol

130
Q

Benign proliferation of gallbladder surface epithelium with glandlike formations, extramural sinuses, transverse strictures and/or fundal nodule (“adenoma” or “adenomyoma”) formation

A

Adenomyomatosis

131
Q

Abnormal deposition of lipid (cholesteryl esters) within macrophages in the lamina propria of the gallbladder wall

A

Cholesterolosis

132
Q

Diffuse form of cholesterolosis wherein the gallbladder mucosa is brick red and speckled with bright yellow flecks of lipid

A

“strawberry gallbladder”

133
Q

Treatment for adenomyomatosis and cholesterolosis

A

Cholecystectomy WHEN symptomatic OR cholelithiasis is present

134
Q

T or F: Gallbladder polyps is more common among male

135
Q

Treatment for gallbladder polyps

A

Cholecystectomy

If: 1. Symptomatic

  1. Asymptomatic >50 years old
  2. Polyps >10mm in diameter
  3. Associated with gallstones / polyp growth on utz
136
Q

Most common biliary anomalies in infancy

A

Atretic and hypoplastic lesions of extrahepatic and large intrahepatic bile ducts

137
Q

Confirmatory diagnosis of biliary atresia

A

Surgical exploration

Operative cholangiography

138
Q

Treatment for biliary atresia

A

Roux-en-Y choledochojejunostomy with Kasai procedure

139
Q

Triad of choledochal cyst (1/3 of patients)

A

Abdominal pain
Jaundice
Abdominal mass

140
Q

Suggestive finding for choledochal cyst via ultrasound

A

Cyst separate from the gallbladder

141
Q

Confirmatory diagnosis for choledochal cyst

A

Demonstrate the entrance of extrahepatic bile ducts into the cyst

142
Q

Surgical treatment of choledochal cysts

A

Excision of “cyst” and biliary-enteric anastomosis

143
Q

T or F: Patients with choledochal cysts are at increased risk for cholangiocarcinoma

144
Q

Dilation of intrahepatic bile ducts involving the major intrahepatic radicles

A

Caroli’s disease

145
Q

Clinical manifestations of Caroli’s disease

A
  1. Recurrent cholangitis
  2. Abscess formation in and around the affected ducts
  3. Brown pigment gallstone formation within portions of ectatic intrahepatic biliary radicles
146
Q

Passage of gallstones into the CBD occurs in what percentage of patients with cholelithiasis

147
Q

T or F: Incidence of common duct stones increases with increasing age of patient

148
Q

Majority of the bile duct stones are of what type?

A

Cholesterol stones

149
Q

Brown pigment stones in CBD are common in what conditions?

A
  1. hepatobiliary parasitism or chronic, recurrent cholangitis
  2. congenital anomalies of the bile ducts (e.g. Caroli’s disease)
  3. dilated, sclerosed, or strictured ducts
  4. MDR3 (ABCB4) gene defects (impaired phospholipid secretion)
150
Q

T or F: Common duct stones are always symptomatic.

A

False

They can be asymptomatic for years and pass spontaneously into the duodenum

Most often: Symptomatic

151
Q

Characteristic presentation of acute cholangitis

A

Biliary pain
Jaundice
Spiking fevers with chills

CHARCOT’S TRIAD

152
Q

Type of acute cholangitis producing severe toxicity presenting with multiple hepatic abscesses and mortality rate approaching 100%

A

Suppurative acute cholangitis

153
Q

Safe and preferred initial procedure in acute cholangitis for both establishing a definitive diagnosis and providing effective therapy

A

ERCP with endoscopic sphincterotomy

154
Q

Differentials for painless jaundice

A
  1. Choledocholithiasis

2. Biliary obstruction secondary to malignancy of head of pancreas, bile ducts, or ampulla of Vater

155
Q

Law that states: presence of a palpably enlarged gallbladder suggests that biliary obstruction is secondary to an underlying malignancy rather than to calculous disease

A

Courvoisier’s Law

156
Q

Bilirubin level that gives suspicion of CBD stones in any patient with cholecystitis

A

> 85.5umol/L (5mg/dL)

157
Q

Bilirubin level that suggests neoplastic obstruction

A

> /=342 umol/L (20mg/dL)

158
Q

Order at which these parameters normalize after removing the CBD stones (starting from the most rapid)

A
  1. aminotransferases
  2. bilirubin (1-2 weeks)
  3. alkaline phosphatase
159
Q

When should you suspect coexisting pancreatitis in cases of cholecystitis?

A
  1. Back pain / pain to the left of the abdominal midline
  2. Prolonged vomiting with paralytic ileus
  3. Pleural effusion (left side)
160
Q

Treatment for coexisting pancreatitis in cholecystitis

A

Surgical treatment of gallstone disease

Resolution of pancreatitis follows

161
Q

Diagnosis of choledocholithiasis

A

Cholangiography, preop or intraop

162
Q

Next step when CBD stones are suspected prior to laparoscopic cholecystectomy

A

Do preoperative ERCP with endoscopic papillotomy and stone extraction

163
Q

When is CBD stones suspected in gallstone patients?

A
  1. History of jaundice or pancreatitis
  2. Abnormal tests of liver function
  3. Ultrasonographic or MRCP evidence of dilated CBD or stones in the duct
164
Q

Treatment of choice in elderly or poor-risk patients with common duct stones

A

EBS followed by spontaneous passage or stone extraction

165
Q

Most common cause of benign strictures of extrahepatic bile ducts

A

Surgical trauma

1 in 500

166
Q

Diagnostic of strictures in extrahepatic bile ducts

A

Percutaneous or endoscopic cholangiography

167
Q

Classic triad of hemobilia

A
  1. Biliary pain
  2. Obstructive jaundice
  3. Melena or occult blood in the stools
168
Q

Management of hemobilia

A

Minor episodes spontaneously resolve

Most often: Surgical ligation of bleeding vessel

169
Q

Most common cause of obstructive jaundice secondary to extrinsic compression of the ducts

A

Carcinoma of head of pancreas

170
Q

Organisms that most commonly cause infestation of the biliary tract

A
  1. Clonorchis sinensis
  2. Opisthorchis viverrini / Opisthorchis felineus
  3. Fasciola hepatica
  4. Ascaris lumbricoides
  5. Echinococcus spp.
171
Q

Diagnostic of hepatobiliary parasitism

A

Cholangiography AND presence of characteristic ova on stool examination

172
Q

Treatment of choice for hepatobiliary parasitism

A

Laparotomy with common duct exploration and biliary drainage procedure
Antibiotic coverage

173
Q

Progressive, inflammatory, sclerosing, and obliterative process affecting the extrahepatic and/or intrahepatic bile ducts

A

Primary or idiopathic sclerosing cholangitis

174
Q

Primary or idiopathic sclerosing cholangitis is associated with these conditions

A
  1. Inflammatory bowel disease (75%) (e.g.ulcerative colitis)
  2. Autoimmune pancreatitis
  3. Multifocal fibrosclerosis syndromes
  4. Riedel’s struma
  5. Pseudotumor of the orbit
175
Q

Recently described biliary disease of unknown etiology that presents with biochemical and cholagiographic features indistinguishable from PSC; often associated with autoimmune pancreatitis; characterized by elevated serum IgG4 and infiltration of IgG4-positive plasma cells in bile duts and liver tissue

A

Immunoglobulin G4 (IgG4)-associated cholangitis

176
Q

Initial treatment of choice for IgG4-associated cholangitis

A

Glucocorticoids

Relapse: Glucocorticoids and/or Azathioprine

177
Q

Diagnostic of sclerosing cholangitis

A

Finding multifocal, diffusely distributed strictures with intervening segments of normal or dilated ducts, producing a beaded appearance on cholangiography

178
Q

Cholangiographic techniques of choice for sclerosing cholangitis

179
Q

Independent predictors of bad prognosis in sclerosing cholangitis

A
  1. Advanced age
  2. Serum bilirubin concentration
  3. Liver histologic changes
180
Q

Associated infectious organisms infecting the biliary tract in patients with AIDS

A
  1. Cryptosporidium
  2. Mycobacterium avium-intracellulare
  3. Cytomegalovirus
  4. Microsporidia
  5. Isospora
181
Q

Treatment for AIDS-associated papillary stenosis

A

ERCP sphincterotomy

182
Q

Treatment of sclerosing cholangitis that may help symptoms of pruritus

A

Cholestyramine

183
Q

Prognosis of primary sclerosing cholangitis

A

Unfavorable

Media survival: 9-12 years

184
Q

Treatment of primary sclerosing cholangitis

A

Balloon dilatation or stenting may be appropriate

Rarely is surgical intervention indicated

185
Q

One of the most common indications for liver transplantation

A

Primary sclerosing cholangitis

HPIM Gastro (7 decks)

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