369: Diseases of the Gallbladder and Bile Ducts Flashcards
1
Q
Isotonic fluid with an electrolyte composition resembling blood plasma
A
Hepatic bile
2
Q
Total solute concentration of hepatic bile vs gallbladder bile
A
hepatic bile: 3-4g/dL
gallbladder bile: 10-15g/dL
3
Q
Components of bile
A
- Bile acids (80%)
- lecithin and traces of other phospholipids (16%)
- unesterified cholesterol (4%)
- Others: Conjugated bilirubin, protein (all Immunoglobulins, albumin, metabolites of hormones); electrolytes; mucus; drugs and their metabolites
4
Q
Total daily basal secretion of hepatic bile
A
500-600mL
5
Q
3 Mechanisms important in regulating bile flow
A
- Active transport of bile acids from hepatocytes into the bile canaliculi
- Active transport of other organic anions
- Cholangiocellular secretion (secretin-mediated secretion of sodium and bicarbonate-rich fluid into bile ducts
6
Q
An aminophospholipid transferase (“flippase”) essential for maintaining the lipid asymmetry of the canalicular membrane
A
F1C1 (ATP8B1)
7
Q
Important ATP-dependent canalicular transport proteins (“export pump”/ABC transporters)
A
- Bile salt export pump (BSEP, ABCB11)
- Anionic conjugate export pump (MRP2, ABCC2) - canalicular excretion of amphiphilic conjugates from phase II conjugation
- Multidrug export pump (MDR1, ABCB1) - hydrophobic cationic compounds
- Phospholipid export pump (MDR3, ABCB4)
8
Q
Other transporters
A
- Hemitransporters ABCG5/G8 - canalicular cholesterol and phytosterol transporter
- C1/HCO3 anion exchanger isoform 2 (AE2, SLC4A2) - canalicular bicarbonate secretion
- F1C1 (ATP8B1)
9
Q
Genetic defects associated with defect in F1C1
A
- Progressive familial intrahepatic cholestasis type 1 (PFIC1)
- Benign recurrent intrahepatic cholestasis type 1 (BRIC1)
10
Q
Genetic defects associated with defect in BSEP
A
- PFIC2
2. BRIC2
11
Q
Genetic defect associated with defect in MRP2(ABCC2)
A
Dubin-Johnson syndrome - CONJUGATED hyperbilirubinemia
12
Q
Genetic defects associated with defect in MDR3(ABCB4)
A
PFIC3
13
Q
Genetic defects associated with defect in ABCG5/G8
A
Sitosterolemia
14
Q
Genetic defects associated with defect in cystic fibrosis transmembrane regulator (CFTR, ABCC7)
A
Cystic fibrosis
Chronic cholestatic liver disease
15
Q
Review: The primary bile acids
A
- Cholic acid
2. Chenodeoxycholic acid (CDCA)
16
Q
Primary bile acids are conjugated with these amino acids then secreted into the bile
A
- Glycine OR
- Taurine
Ratio of glycine to taurine conjugates in bile: 3:1
17
Q
Secondary bile acids
A
- Deoxycholate
- Lithocholate
- Ursodeoxycholic acid (UDCA) : in low concentration
18
Q
Where do secondary bile acids form?
A
Colon
As bacterial metabolites of primary bile acids
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
20
Q
Transport mechanism of bile acids in the gut
A
Passive diffusion (Unconjugated, some conjugated)
21
Q
Transport mechanism for conjugated bile acids in the DISTAL ILEUM and important in bile salt recirculation
A
Active transport
22
Q
Normal bile acid pool size
A
2-4g
23
Q
of circulation of the bile acid pool daily
A
5-10 times daily
24
Q
Percentage of bile that is reabsorbed in the intestine
A
95%
Fecal loss of bile acids: 0.2-0.4g/d
25
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
Fibroblast growth factor 19 (FGF19)
26
2 important mechanisms that maintain/balance bile salts in the body
1. Hepatic synthesis (5%)
2. Intestinal reabsorption (95%)
Maximum rate of hepatic synthesis is 5g/d
27
Nuclear receptor that upregulates the hepatic BSEP (ABCB11) and repress bile acid synthesis
Farnesoid X receptor (FXR)
A bile acid sensor
28
Nuclear receptor that upregulates the cholesterol transporter (ABCG5/G8)
Liver X receptor (LXR)
An oxysterol sensor
29
2 Functions of the tonic contraction of Sphincter of Oddi during the FASTING state
1. Prevent reflux of duodenal contents into the pancreatic and bile ducts
2. Promote filling of the gallbladder
30
Peptide hormone that is the major factor controlling the evacuation of the gallbladder
Cholecystokinin (CCK)
Released into the DUODENAL mucosa
Stimulant: Ingestion of fats and amino acids
31
Functions of CCK
1. Powerful contraction of gallbladder
2. Decreased resistance of the sphincter of Oddi
3. Enhanced flow of biliary contents into the duodenum
32
Normal capacity of gallbladder
30mL of bile
33
Clinically innocuous entity in which a partial or complete septum (fold) separates the fundus from the body
Phrygian cap
34
T of F:
| Gallstone formation increases after age 40.
False
After age 50
35
T or F:
| Gallstones are more common among men
False
Women
36
Review: 2 Major Types of Gallstones
1. Cholesterol stones (90%)
| 2. Pigment stones
37
Usually contain >50% cholesterol monohydrate plus admixture of calcium salts, bile pigments, proteins, and fatty acids.
Cholesterol gallstones
38
Composed primarily of calcium bilirubinate and contain <20% cholesterol;
Pigment stones
Classified into "black" and "brown" types
39
Type of pigment stone that forms secondary to chronic biliary infection
"brown" pigment stones
40
The most important mechanism in the formation of lithogenic (stone-forming) bile
Increased biliary secretion of cholesterol
41
T or F: Obesity, not metabolic syndrome, is associated with formation of lithogenic bile.
False
Obesity, Metabolic syndrome, high-caloric and cholesterol-rich diets, drug (clofibrate)
42
Rate limiting enzyme of hepatic cholesterol synthesis causing increased hepatic uptake of cholesterol from blood
Hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase
43
The 3 mechanisms that cause gallstone disease
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
44
Mechanism by which ORAL CONTRACEPTIVES can cause gallstone disease
Decreased bile salt excretion
Effect: Decreased conversion of cholesterol to cholesteryl esters
45
Mechanism by which PREGNANCY can cause gallstone disease
Impaired GB emptying due to progesterone + estrogen
Effect: Increase biliary cholesterol secretion
46
GB hypomotility leading to stasis and formation of sludge are present in these conditions
1. Prolonged parenteral nutrition
2. Fasting
3. Pregnancy
4. Drugs such as octreotide
47
Lipid-lowering agent that reduces VLDL however this increases biliary secretion of cholesterol
Clofibrate
48
Genetic defect in this gene causing gallstone disease; mechanism is decreased PHOSPHOLIPID secretion
MDR3 gene
49
Genetic defect in this gene causing gallstone disease; mechanism is decreased BILE ACID secretion
CYP7A1 gene
50
Characteristics of BILE sludge in studies
1. Recurrent
2. Can form gallstones (asymptomatic and symptomatic)
3. Associated with severe biliary pain with/without pancreatitis
51
T or F: Biliary sludge in pregnancy is more frequent than gallstone formation
True
20-30% biliary sludge
5-12% gallstones
52
T or F: Biliary sludge in pregnancy is asymptomatic and resolves spontaneously after delivery
True
53
T or F: Gallstone formation in pregnancy are associated with biliary colic and will not disappear even after delivery
False
May have spontaneous dissolution after delivery
54
Stones that are composed of either pure calcium bilirubinate or polymer-like complexes with calcium and mucin glycoproteins
Black pigment stones
55
Conditions associated with BLACK pigment stones
1. Chronic hemolytic state
2. Liver cirrhosis
3. Gilbert's syndrome
4. Cystic fibrosis
5. Patients with ileal diseases, ileal resection, or ileal bypass
56
Stones that are composed of calcium salts of unconjugated bilirubin with varying amounts of cholesterol and protein
Brown pigment stones
57
Pigment stone associated when bile is chronically infected by bacteria
Brown pigment stones
58
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
Biliary sludge
59
Procedure of choice for detection of stones
A. GB ultrasound
B. Plain abd xray
C. Radioisotope scans (HIDA, DIDA)
A. GB ultrasound
See Table 369-2
60
Procedure that shows pathognomotic findings in porcelain gallbladder and emphysematous cholecystitis
A. GB ultrasound
B. Plain abd xray
C. Radioisotope scans (HIDA, DIDA)
B. Plain abd xray
61
T or F: Radioisotope scans are indicated for confirmation of suspected chronic cholecystitis
False
ACUTE cholecystitis
Less sensitive and less specific in chronic cholecystitis
62
Most specific and characteristic symptom of gallstone disease
Biliary colic
Constant and often long-lasting pain
30mins - 5hours
63
Characteristic pain caused by obstruction of the cystic duct or CBD by a stone
Visceral pain : Severe, steady ache or fullness
Location: Epigastrium or RUQ
Radiation: Interscapular area, right scapula, or shoulder
64
Biliary pain in the presence of this finding suggests a common duct stone
Elevated level of serum bilirubin AND/OR alkaline phosphatase
65
Biliary pain associated with fever or chills (rigors) suggests what?
1. Cholecystitis
2. Pancreatitis
3. Cholangitis
66
T or F: Biliary colic is frequently nocturnal, occurring within a few hours of retiring
True
67
Decision analysis suggestions in asymptomatic patients with gallstone disease
1. Cumulative risk of death due to gallstone disease while on expectant management is small
2. prophylactic cholecystectomy is NOT warranted
68
T or F: Diabetic patients can have silent MI as well as silent gallstones.
True
69
Recommendations for cholecystectomy
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
70
Can be considered for prophylactic cholecystectomy
Very large gallstones (>3cm in diameter)
| Gallstones in congenitally anomalous GB
71
Advantages of laparoscopic cholecystectomy
1. Markedly shortened hospital stay
2. Minimal disability
3. Decreased cost
Procedure of choice for most patients referred for elective cholecystectomy
72
"Gold Standard" for treating symptomatic cholelithiasis
Laparoscopic cholecystectomy
73
Diameter of radiolucent stones that can have complete dissolution within 6 months to 2 years
<10mm in diameter
Achieved in 50% of patients
>10mm are rarely dissolve
74
Dose of UDCA for gallstone dissolution
10-15mg/kg per day
75
T or F: Pigment stones are not responsive to UDCA therapy.
True
76
T or F: Patients with cholesterol gallstone disease who develop recurrent choledocholithiasis after cholecystectomy should be on a long-term treatment with UDCA.
True
77
3 Factors responsible for the inflammatory response of the GB
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
Organisms most frequently isolated by culture of gallbladder bile in acute cholecystitis
1. Klebsiella spp.
2. Escherichia coli
3. Streptococcus spp.
4. Clostridium spp.
79
T or F: Jaundice is usually an early sign of acute cholecystitis
False
Unusual but may occur when edematous inflammatory changes involve the bile ducts and surrounding lymph nodes
80
T or F: High grade fever, shaking chills and rigors are usually seen in acute cholecystitis
False
LOW grade fever
Shaking chills or rigors UNCOMMON
81
T or F: An enlarged, tensed gallbladder is almost always palpable in patients with acute cholecystitis
False
25-50%
82
Deep inspiration or cough during subcostal palpation of the RUQ usually produces increased pain and inspiratory arrest
Murphy's sign
83
```
Common signs in acute cholecystitis except:
A. localized rebound tenderness
B. hypoactive bowel sounds
C. abdominal distention
D. abdominal rigidity
```
D. Abdominal rigidity
Abdominal rigidity and generalized peritoneal signs are lacking in the absence of perforation
84
Triad of symptoms highly suggestive of acute cholecystitis
1. Sudden onset RUQ tenderness
2. Fever
3. Leukocytosis (10,000-15,000 cells/mL) with left shift on differential count
85
Relationship of bilirubin and aminotransferases in acute cholecystitis
1. Serum bilirubin - mildly elevated
| 2. Serum aminotransferases - modest elevations (less than fivefold)
86
Confirmatory imaging test if the bile duct imaging seen in ultrasound did not visualized the gallbladder
Radionuclide biliary scan (e.g. HIDA)
87
T or F: Acute cholecystitis is best treated by early surgery whenever possible.
True
88
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
Mirizzi's syndrome
89
Imagings used to demonstrate characteristic extrinsic compression of CBD in Mirizzi's syndrome
1. ERCP
2. MRCP
3. PTC
90
Conditions that increases risk for ACALCULOUS cholecystitis
1. Serious trauma or burns
2. Postpartum period following prolonged labor
3. Orthopedic and other nonbiliary major surgical operations in post-op period
91
Precipitating factors for ACALCULOUS cholecystitis
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
Management of ACALCULOUS cholecystitis
1. Early diagnosis
2. Early surgical intervention
3. Meticulous attention to post-op care
93
Infusion of this hormone can be used to measure gallbladder ejection fraction during cholescintigraphy
Octapeptide of CCK
94
Progression of emphysematous cholecystitis
1. Acute cholecystitis (calculous or acalculous)
2. Ischemia or gangrene of gallbladder wall
3. Infection by gas-producing organisms
95
Bacteria most frequently cultured in emphysematous cholecystitis
Anaerobes: Clostridium welchii, Clostridium perfringens
Aerobes: E. coli
96
Population where emphysematous cholecystitis occurs most frequently
1. Elderly men
| 2. Diabetic patients
97
Imaging used for diagnosis of emphysematous cholecystitis
Plain abdominal film
Gas within the GB lumen, dissecting within the GB wall to form a gaseous ring, or in pericholecystic tissues
98
Management of emphysematous cholecystitis
1. Prompt surgical intervention
| 2. Appropriate antibiotics
99
Results from progression of acute cholecystitis with persistent cystic duct obstruction to superinfection of the stagnant bile with a pus-forming bacterial organism
Empyema of gallbladder
100
Clinical picture of empyema of GB
Resembles cholangitis + high fever
Severe RUQ pain
Marked leukocytosis
Prostration
101
Management of empyema of GB
1. EMERGENCY surgical intervention
| 2. Proper antibiotic coverage
102
Condition that results from prolonged obstruction of the cystic duct, usually by a large solitary calculus
Hydrops OR mucocele of gallbladder
103
Management of hydrops of mucocele
Cholecystectomy is indicated to prevent complications: empyema, perforation, gangrene
104
Most common locations of fistula formation
1. into the duodenum
2. hepatic flexure of colon
3. stomach
4. jejunum
5. abdominal wall
6. renal pelvis
105
Imaging used to demonstrate fistula
1. Barium contrast studies
| 2. Endoscopy of upper GI tract or colon
106
Treatment for fistula in symptomatic patients
Cholecystectomy
CBD exploration
Closure of fistulous tract
107
Mechanical intestinal obstruction resulting from the passage of a large gallstone into the bowel lumen
Gallstone ileus
108
Most common site of obstruction by impacted gallstone
Ileocecal valve
109
Diagnostic confirmation of gallstone ileus
Plain abdominal film (occasionally)
| Upper GI series
110
Management of gallstone ileus
Laparotomy with stone extraction/propulsion into the colon
111
T or F: Cholecystectomy is advised in all patients with porcelain gallbladder due to development of carcinoma of the GB
True
112
Drugs given in acute cholecystitis for analgesia that will produce less spasm of the sphincter of Oddi
Meperidine
| NSAIDs
113
Most common organisms present in acute cholecystitis
E. coli
Klebsiella spp.
Streptococcus spp.
114
Antibiotic therapy for acute cholecystitis
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
Antibiotic therapy in acute cholecystitis if ascending cholangitis is suspected
Imipenem
| Meropenem
116
Timing of surgery for uncomplicated acute cholecystitis
Early elective laparoscopic cholecystectomy = 48-72h
117
T or F: Complication rate is not increased in patients undergoing early as opposed to delayed (>6 weeks after diagnosis) cholecystectomy
True
118
When is delayed surgical intervention considered?
1. Overall medical condition imposes an unacceptable risk for early surgery
2. Diagnosis of acute cholecystitis is in doubt
119
Treatment of choice for acute cholecystitis
Early cholecystectomy (within 72h)
120
T or F: Mortality risk for early elective cholecystectomy is lower compared to mortality risk for emergency cholecystectomy in patients under age of 60.
True
121
Early complications postcholecystectomy
1. Atelectasis and other pulmonary disorders
2. Abscess formation (often subphrenic)
3. External or internal hemorrhage
4. Biliary-enteric fistula
5. Bile leaks
122
Most common cause of persistent postcholecystectomy symptoms
Overlooked symptomatic nonbiliary disorder
e.g. reflux esophagitis, peptic ulceration, pancreatitis, irritable bowel syndrome
123
Disorders of extrahepatic bile ducts (Postcholecystectomy syndromes) that may cause persistent symptomatology
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
5 criteria that defines papillary stenosis
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
Treatment for papillary stenosis
Endoscopic or surgical sphincteroplasty
126
Indications for sphincterotomy in papillary stenosis
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
Procedure of choice for removing bile duct stones and other biliary and pancreatic problems
Endoscopic biliary sphincterotomy (EBS)
128
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
True
129
Treatment for postcholecystectomy diarrhea
Bile-acid sequestering agents:
Cholestyramine
Colestipol
130
Benign proliferation of gallbladder surface epithelium with glandlike formations, extramural sinuses, transverse strictures and/or fundal nodule ("adenoma" or "adenomyoma") formation
Adenomyomatosis
131
Abnormal deposition of lipid (cholesteryl esters) within macrophages in the lamina propria of the gallbladder wall
Cholesterolosis
132
Diffuse form of cholesterolosis wherein the gallbladder mucosa is brick red and speckled with bright yellow flecks of lipid
"strawberry gallbladder"
133
Treatment for adenomyomatosis and cholesterolosis
Cholecystectomy WHEN symptomatic OR cholelithiasis is present
134
T or F: Gallbladder polyps is more common among male
True
135
Treatment for gallbladder polyps
Cholecystectomy
If: 1. Symptomatic
2. Asymptomatic >50 years old
3. Polyps >10mm in diameter
4. Associated with gallstones / polyp growth on utz
136
Most common biliary anomalies in infancy
Atretic and hypoplastic lesions of extrahepatic and large intrahepatic bile ducts
137
Confirmatory diagnosis of biliary atresia
Surgical exploration
| Operative cholangiography
138
Treatment for biliary atresia
Roux-en-Y choledochojejunostomy with Kasai procedure
139
Triad of choledochal cyst (1/3 of patients)
Abdominal pain
Jaundice
Abdominal mass
140
Suggestive finding for choledochal cyst via ultrasound
Cyst separate from the gallbladder
141
Confirmatory diagnosis for choledochal cyst
Demonstrate the entrance of extrahepatic bile ducts into the cyst
142
Surgical treatment of choledochal cysts
Excision of "cyst" and biliary-enteric anastomosis
143
T or F: Patients with choledochal cysts are at increased risk for cholangiocarcinoma
True
144
Dilation of intrahepatic bile ducts involving the major intrahepatic radicles
Caroli's disease
145
Clinical manifestations of Caroli's disease
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
Passage of gallstones into the CBD occurs in what percentage of patients with cholelithiasis
10-15%
147
T or F: Incidence of common duct stones increases with increasing age of patient
True
148
Majority of the bile duct stones are of what type?
Cholesterol stones
149
Brown pigment stones in CBD are common in what conditions?
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
T or F: Common duct stones are always symptomatic.
False
They can be asymptomatic for years and pass spontaneously into the duodenum
Most often: Symptomatic
151
Characteristic presentation of acute cholangitis
Biliary pain
Jaundice
Spiking fevers with chills
CHARCOT'S TRIAD
152
Type of acute cholangitis producing severe toxicity presenting with multiple hepatic abscesses and mortality rate approaching 100%
Suppurative acute cholangitis
153
Safe and preferred initial procedure in acute cholangitis for both establishing a definitive diagnosis and providing effective therapy
ERCP with endoscopic sphincterotomy
154
Differentials for painless jaundice
1. Choledocholithiasis
| 2. Biliary obstruction secondary to malignancy of head of pancreas, bile ducts, or ampulla of Vater
155
Law that states: presence of a palpably enlarged gallbladder suggests that biliary obstruction is secondary to an underlying malignancy rather than to calculous disease
Courvoisier's Law
156
Bilirubin level that gives suspicion of CBD stones in any patient with cholecystitis
>85.5umol/L (5mg/dL)
157
Bilirubin level that suggests neoplastic obstruction
>/=342 umol/L (20mg/dL)
158
Order at which these parameters normalize after removing the CBD stones (starting from the most rapid)
1. aminotransferases
2. bilirubin (1-2 weeks)
3. alkaline phosphatase
159
When should you suspect coexisting pancreatitis in cases of cholecystitis?
1. Back pain / pain to the left of the abdominal midline
2. Prolonged vomiting with paralytic ileus
3. Pleural effusion (left side)
160
Treatment for coexisting pancreatitis in cholecystitis
Surgical treatment of gallstone disease
Resolution of pancreatitis follows
161
Diagnosis of choledocholithiasis
Cholangiography, preop or intraop
162
Next step when CBD stones are suspected prior to laparoscopic cholecystectomy
Do preoperative ERCP with endoscopic papillotomy and stone extraction
163
When is CBD stones suspected in gallstone patients?
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
Treatment of choice in elderly or poor-risk patients with common duct stones
EBS followed by spontaneous passage or stone extraction
165
Most common cause of benign strictures of extrahepatic bile ducts
Surgical trauma
1 in 500
166
Diagnostic of strictures in extrahepatic bile ducts
Percutaneous or endoscopic cholangiography
167
Classic triad of hemobilia
1. Biliary pain
2. Obstructive jaundice
3. Melena or occult blood in the stools
168
Management of hemobilia
Minor episodes spontaneously resolve
| Most often: Surgical ligation of bleeding vessel
169
Most common cause of obstructive jaundice secondary to extrinsic compression of the ducts
Carcinoma of head of pancreas
170
Organisms that most commonly cause infestation of the biliary tract
1. Clonorchis sinensis
2. Opisthorchis viverrini / Opisthorchis felineus
3. Fasciola hepatica
4. Ascaris lumbricoides
5. Echinococcus spp.
171
Diagnostic of hepatobiliary parasitism
Cholangiography AND presence of characteristic ova on stool examination
172
Treatment of choice for hepatobiliary parasitism
Laparotomy with common duct exploration and biliary drainage procedure
Antibiotic coverage
173
Progressive, inflammatory, sclerosing, and obliterative process affecting the extrahepatic and/or intrahepatic bile ducts
Primary or idiopathic sclerosing cholangitis
174
Primary or idiopathic sclerosing cholangitis is associated with these conditions
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
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
Immunoglobulin G4 (IgG4)-associated cholangitis
176
Initial treatment of choice for IgG4-associated cholangitis
Glucocorticoids
Relapse: Glucocorticoids and/or Azathioprine
177
Diagnostic of sclerosing cholangitis
Finding multifocal, diffusely distributed strictures with intervening segments of normal or dilated ducts, producing a beaded appearance on cholangiography
178
Cholangiographic techniques of choice for sclerosing cholangitis
MRCP
| ERCP
179
Independent predictors of bad prognosis in sclerosing cholangitis
1. Advanced age
2. Serum bilirubin concentration
3. Liver histologic changes
180
Associated infectious organisms infecting the biliary tract in patients with AIDS
1. Cryptosporidium
2. Mycobacterium avium-intracellulare
3. Cytomegalovirus
4. Microsporidia
5. Isospora
181
Treatment for AIDS-associated papillary stenosis
ERCP sphincterotomy
182
Treatment of sclerosing cholangitis that may help symptoms of pruritus
Cholestyramine
183
Prognosis of primary sclerosing cholangitis
Unfavorable
| Media survival: 9-12 years
184
Treatment of primary sclerosing cholangitis
Balloon dilatation or stenting may be appropriate
| Rarely is surgical intervention indicated
185
One of the most common indications for liver transplantation
Primary sclerosing cholangitis
