Gallstone Flashcards
1
Q
What is the pathway of bile secretion from hepatocytes?
A
Bile is secreted into canaliculi, small bile ductules, larger bile ducts, right and left hepatic ducts, common hepatic duct, cystic duct, and then the common bile duct into the duodenum.
2
Q
What is the electrolyte composition of hepatic bile?
A
Hepatic bile is an isotonic fluid with an electrolyte composition resembling blood plasma.
3
Q
How does gallbladder bile differ from hepatic bile?
A
Gallbladder bile has a higher total solute concentration (10–15 g/dL) due to reabsorption of inorganic anions and water.
4
Q
What are the major solute components of bile by moles percent?
A
- Bile acids (80%)
- Phospholipids (16%)
- Unesterified cholesterol (4%)
5
Q
What is the total daily basal secretion of hepatic bile?
A
~500–600 mL.
6
Q
What are the three mechanisms important in regulating bile flow?
A
- Active transport of bile acids from hepatocytes into bile canaliculi
- Active transport of other organic anions
- Cholangiocellular secretion
7
Q
What is the role of the Na+/taurocholate cotransporter (NTCP)?
A
It is a sinusoidal bile salt uptake system that transports bile salts from portal blood into hepatocytes.
8
Q
What is the function of ATP-binding cassette transport proteins in bile flow?
A
They are ATP-dependent canalicular transport systems known as ‘export pumps’ that facilitate the excretion of bile salts and other compounds.
9
Q
What happens in progressive familial intrahepatic cholestasis type 1 (PFIC1)?
A
Defective F1C1 (ATP8B1) results in the ablation of all other ATP-dependent transporter functions.
10
Q
True or False: The cystic fibrosis transmembrane regulator (CFTR) is located on canalicular membranes.
A
False.
11
Q
Fill in the blank: In the lithogenic state, the cholesterol value in bile can be as high as _______.
A
8–10%.
12
Q
What condition is caused by mutations of MRP2 (ABCC2)?
A
Dubin-Johnson syndrome.
13
Q
What is the main role of cholangiocellular secretion in bile production?
A
It involves secretin-mediated and cyclic AMP–dependent secretion of a bicarbonate-rich fluid into the bile ducts.
14
Q
What are the constituents of bile besides bile acids and phospholipids?
A
- Conjugated bilirubin
- Proteins (immunoglobulins, albumin, hormones)
- Electrolytes
- Mucus
- Heavy metals
- Drugs and their metabolites
15
Q
What is the role of ABCG5/G8 in bile production?
A
They are canalicular half transporters for cholesterol and other neutral sterols.
16
Q
What regulates the active transport of bile acids in hepatocytes?
A
A set of transport systems at the basolateral and canalicular apical plasma membrane domains.
17
Q
What can a genetic defect in BSEP (ABCB11) lead to?
A
PFIC2 and BRIC2.
18
Q
What are the primary bile acids synthesized from cholesterol?
A
Cholic acid and chenodeoxycholic acid (CDCA)
These acids are synthesized in hepatocytes and conjugated with glycine or taurine.
19
Q
How are secondary bile acids formed?
A
They are formed in the colon as bacterial metabolites of primary bile acids
Examples include deoxycholate and lithocholate.
20
Q
Which secondary bile acid is a stereoisomer of CDCA?
A
Ursodeoxycholic acid (UDCA)
UDCA is found in low concentration.
21
Q
What is the typical ratio of glycine to taurine conjugates in bile?
A
~3:1
This ratio is observed in healthy subjects.
22
Q
What do bile acids form in aqueous solutions above a critical concentration?
A
Molecular aggregates called micelles
The critical concentration is approximately ~2 mM.
23
Q
What is the solubility of cholesterol in bile dependent on?
A
Total lipid concentration and relative molar percentages of bile acids and lecithin
Normal ratios favor solubilizing mixed micelles.
24
Q
What do abnormal ratios of bile constituents promote?
A
Precipitation of cholesterol crystals in bile
This occurs via an intermediate liquid crystal phase.
25
What role do bile acids play in dietary fat absorption?
Facilitate normal intestinal absorption via a micellar transport mechanism
## Footnote
They mainly aid in the absorption of cholesterol and fat-soluble vitamins.
26
How do bile acids aid in hepatic bile flow?
They serve as a major physiologic driving force
## Footnote
Bile acids also aid in water and electrolyte transport in the small bowel and colon.
27
What receptors do bile acids function as hormones by binding to?
Nuclear (farnesoid X receptor [FXR]) and G protein–coupled (TGR5) receptors
## Footnote
These receptors regulate bile acid metabolism and their enterohepatic circulation.
28
Fill in the blank: Bile acids are detergent-like molecules that form _______ in aqueous solutions.
micelles
29
True or False: Lithocholic acid is more efficiently absorbed from the colon than deoxycholic acid.
False
## Footnote
Lithocholic acid is much less efficiently absorbed.
30
What is the primary function of enterohepatic circulation?
Efficient conservation of bile acids
## Footnote
Bile acids are reabsorbed and recirculated to maintain their pool size.
31
How are unconjugated and conjugated bile acids absorbed in the gut?
Passive diffusion along the entire gut
## Footnote
Conjugated bile acids also utilize an active transport mechanism in the distal ileum.
32
What is the normal bile acid pool size?
~2–4 g
## Footnote
This size is maintained through synthesis and reabsorption.
33
How many times does the bile acid pool circulate daily under normal conditions?
~5–10 times
## Footnote
This frequency depends on meal size and composition.
34
What is the efficiency of intestinal reabsorption of bile acids?
~95%
## Footnote
This high efficiency limits daily fecal loss to 0.2–0.4 g.
35
What compensates for the daily fecal loss of bile acids?
Equal daily synthesis by the liver
## Footnote
This maintains the size of the bile acid pool.
36
What effect do bile acids have on fibroblast growth factor 19 (FGF19)?
Stimulate its release
## Footnote
FGF19 suppresses hepatic synthesis of bile acids from cholesterol.
37
Which enzyme is inhibited by FGF19 to suppress bile acid synthesis?
Cytochrome P450 7A1 (CYP7A1)
## Footnote
This enzyme is rate-limiting in bile acid synthesis from cholesterol.
38
What is the maximum rate of bile acid synthesis per day?
~5 g/d
## Footnote
This rate may be insufficient when intestinal reabsorption is impaired.
39
Which transporters are involved in the enterohepatic circulation of bile acids?
ABC transporters
## Footnote
They play a crucial role in the regulation of bile acid levels.
40
What regulates the expression of ABC transporters and rate-limiting enzymes in bile acid synthesis?
Nuclear receptors
## Footnote
These are ligand-activated transcription factors.
41
Which receptor upregulates the hepatic BSEP (ABCB11)?
Farnesoid X receptor (FXR)
## Footnote
FXR also represses bile acid synthesis.
42
What is the role of the liver X receptor (LXR) in cholesterol transport?
Upregulates the cholesterol transporter ABCG5/G8
## Footnote
LXR acts as an oxysterol sensor.
43
What is the function of the sphincter of Oddi (SOD) in the fasting state?
Offers a high-pressure zone of resistance to bile flow from the CBD into the duodenum
## Footnote
Prevents reflux of duodenal contents into the pancreatic and bile ducts and promotes filling of the gallbladder.
44
What hormone controls the evacuation of the gallbladder?
Cholecystokinin (CCK)
## Footnote
Released from the duodenal mucosa in response to the ingestion of fats and amino acids.
45
What are the effects of cholecystokinin (CCK) on the gallbladder?
* Powerful contraction of the gallbladder
* Decreased resistance of the SOD
* Enhanced flow of biliary contents into the duodenum
46
How is hepatic bile concentrated within the gallbladder?
By energy-dependent transmucosal absorption of water and electrolytes
## Footnote
This process allows the gallbladder to store bile effectively.
47
What is the normal capacity of the gallbladder?
~30 mL
## Footnote
This volume indicates the typical storage capability of the gallbladder.
48
Fill in the blank: The major factor controlling gallbladder evacuation is the peptide hormone _______.
Cholecystokinin (CCK)
49
True or False: The sphincter of Oddi decreases resistance to bile flow during fasting.
False
## Footnote
The sphincter of Oddi offers a high-pressure zone of resistance during fasting.
50
What substances trigger the release of cholecystokinin (CCK)?
* Fats
* Amino acids
51
What happens to the bile acid pool during an overnight fast?
Almost the entire bile acid pool may be sequestered in the gallbladder for delivery into the duodenum with the first meal of the day.
52
What are congenital anomalies of the biliary tract?
Abnormalities in number, size, and shape of biliary structures
## Footnote
Examples include agenesis of the gallbladder, duplications, rudimentary or oversized gallbladders, and diverticula.
53
What is a Phrygian cap?
A clinically innocuous entity with a partial or complete septum separating the fundus from the body of the gallbladder
## Footnote
It is not associated with significant clinical symptoms.
54
List some anomalies of position or suspension of the gallbladder.
* Left-sided gallbladder
* Intrahepatic gallbladder
* Retrodisplacement of the gallbladder
* Floating gallbladder
55
True or False: A floating gallbladder can predispose to acute torsion.
True
## Footnote
Floating gallbladder can also lead to volvulus or herniation.
56
Fill in the blank: Anomalies of the biliary tract may include _______.
[agenesis of the gallbladder]
57
What is the clinical significance of a Phrygian cap?
It is clinically innocuous and typically does not require treatment
## Footnote
It can be identified incidentally on imaging studies.
58
What complications can arise from a floating gallbladder?
* Acute torsion
* Volvulus
* Herniation
59
What are the two major types of gallstones?
Cholesterol stones and pigment stones
## Footnote
Cholesterol stones account for >90% of all gallstones in Western industrialized countries.
60
What is the primary composition of cholesterol stones?
Cholesterol monohydrate, calcium salts, bile pigments, proteins, and fatty acids
## Footnote
Cholesterol stones usually contain >50% cholesterol monohydrate.
61
What are the two types of pigment stones?
Black stones and brown stones
## Footnote
Brown stones form secondary to chronic biliary infection.
62
At what age does gallstone formation increase?
After age 50
63
What is the mechanism that leads to the formation of lithogenic bile?
Increased biliary secretion of cholesterol
64
What factors can increase biliary cholesterol secretion?
Obesity, metabolic syndrome, high-caloric diets, drugs
## Footnote
Example drugs include clofibrate.
65
What role do genetic factors play in gallstone disease?
Genetic factors account for 25% of phenotypic variation in gallstone pathogenesis
66
What gene variant is associated with gallstones in 21% of patients?
ABCG5/G8
67
What is the primary cause of cholesterol supersaturation in bile?
Hypersecretion of cholesterol
68
What is biliary sludge composed of?
Lecithin-cholesterol liquid crystals, cholesterol monohydrate crystals, calcium bilirubinate, mucin gels
69
True or False: Biliary sludge can be a precursor to gallstone disease.
True
70
What are the two key changes during pregnancy that contribute to gallstone formation?
Increased cholesterol saturation of bile, sluggish gallbladder contraction
71
What percentage of women develop gallbladder sludge during pregnancy?
20–30%
72
What is the effectiveness of UDCA in preventing gallstone formation during rapid weight reduction?
Highly effective; only 3% of UDCA recipients developed gallstones
73
What are the three defects that lead to cholesterol gallstone disease?
Bile supersaturation with cholesterol, nucleation of cholesterol monohydrate, abnormal gallbladder motor function
74
Fill in the blank: Cholesterol is essentially ______-insoluble.
water
75
What happens when there is an excess of cholesterol in bile?
Unstable cholesterol-rich vesicles aggregate into large multilamellar vesicles
76
What is the significance of the UGT1A1 gene variant in gallstone disease?
Associated with cholesterol stones and indicates the role of pigment particles in pathogenesis
77
What can cause gallbladder hypomotility?
Fasting, parenteral nutrition, pregnancy, certain drugs
78
What is the result of impaired gallbladder emptying?
Increased incidence of gallstones
79
What are black pigment stones composed of?
Pure calcium bilirubinate or polymer-like complexes with calcium and mucin glycoproteins
80
In which patient conditions are black pigment stones more common?
* Chronic hemolytic states
* Cirrhosis (especially related to alcohol)
* Gilbert’s syndrome
* Cystic fibrosis
* Ileal diseases, ileal resection, or ileal bypass
81
What contributes to the pathogenesis of black pigment stones in ileal disease states?
Enterohepatic recycling of bilirubin
82
What are brown pigment stones composed of?
Calcium salts of unconjugated bilirubin with varying amounts of cholesterol and protein
83
What causes the formation of brown pigment stones?
Increased amounts of unconjugated, insoluble bilirubin in bile that precipitates to form stones
84
How may deconjugation of bilirubin occur in the formation of brown pigment stones?
* Mediated by endogenous β-glucuronidase
* Spontaneous hydrolysis
85
What can lead to the production of β-glucuronidase in cases of brown pigment stone formation?
Chronic infection of bile by bacteria
86
Where is pigment stone formation frequent?
Asia
87
What is often associated with pigment stone formation in the gallbladder and biliary tree?
Parasitic infections
88
What is the primary diagnostic procedure for cholelithiasis?
Ultrasonography of the gallbladder
## Footnote
It has replaced oral cholecystography (OCG) due to its accuracy.
89
What is the smallest size of stones that can be confidently identified using ultrasound?
1.5 mm in diameter
## Footnote
Identification relies on firm criteria such as acoustic shadowing.
90
What are the false-negative and false-positive rates for ultrasound in gallstone patients?
~2–4%
## Footnote
These rates are observed in major medical centers.
91
What is biliary sludge?
Material of low echogenic activity that forms a layer in the gallbladder
## Footnote
It shifts with postural changes and does not produce acoustic shadowing.
92
What may the plain abdominal film detect in relation to gallstones?
Gallstones containing sufficient calcium
## Footnote
Approximately 10–15% of cholesterol and ~50% of pigment stones are radiopaque.
93
What conditions can plain radiography help diagnose?
* Emphysematous cholecystitis
* Porcelain gallbladder
* Limey bile
* Gallstone ileus
## Footnote
These conditions may have specific radiographic features.
94
Why is oral cholecystography (OCG) regarded as obsolete?
It has been replaced by ultrasound
## Footnote
OCG may still assess cystic duct patency and gallbladder emptying.
95
What is the role of radiopharmaceuticals like 99m Tc-labeled N-substituted iminodiacetic acids?
They are used in imaging the biliary tree
## Footnote
They are excreted into the biliary tree even in the presence of serum bilirubin elevations.
96
What does failure to image the gallbladder during a radiopharmaceutical scan indicate?
Possible cystic duct obstruction, acute or chronic cholecystitis, or surgical absence of the organ
## Footnote
This finding is significant in diagnosing acute cholecystitis.
97
How can ultrasound be used in relation to gallbladder function?
To assess the emptying function of the gallbladder
## Footnote
This can provide insight into gallbladder health and functionality.
98
Fill in the blank: The _____ has historically been a useful procedure for the diagnosis of gallstones but is now regarded as obsolete.
oral cholecystography (OCG)
## Footnote
It has been replaced by ultrasound due to improved accuracy.
99
What is the most specific and characteristic symptom of gallstone disease?
Biliary colic
## Footnote
Biliary colic is characterized by a constant and often long-lasting pain.
100
What causes symptoms in gallstone disease?
Inflammation or obstruction following migration into the cystic duct or CBD
## Footnote
CBD refers to the common bile duct.
101
Describe the nature of pain associated with biliary colic.
Severe, steady ache or fullness in the epigastrium or right upper quadrant (RUQ)
## Footnote
Pain may radiate to the interscapular area, right scapula, or shoulder.
102
How long can biliary colic persist?
30 minutes to 5 hours
## Footnote
It may subside gradually or rapidly.
103
True or False: Biliary colic is characterized by intermittent pain.
False
## Footnote
Biliary colic is steady rather than intermittent.
104
What should raise suspicion of acute cholecystitis?
An episode of biliary pain persisting beyond 5 hours
## Footnote
Acute cholecystitis is a possible complication of gallstone disease.
105
What symptoms frequently accompany episodes of biliary pain?
Nausea and vomiting
## Footnote
These symptoms are common during biliary colic episodes.
106
What do elevated levels of serum bilirubin and/or alkaline phosphatase suggest?
A common duct stone
## Footnote
These laboratory findings can indicate complications from gallstones.
107
What do fever or chills (rigors) with biliary pain usually imply?
A complication such as cholecystitis, pancreatitis, or cholangitis
## Footnote
These complications are serious and require medical attention.
108
Fill in the blank: Complaints of short-lasting, vague epigastric fullness, dyspepsia, eructation, or flatulence should not be confused with _______.
Biliary pain
## Footnote
These symptoms are not specific for biliary calculi.
109
What can precipitate biliary colic?
Eating a fatty meal, consumption of a large meal after fasting, or eating a normal meal
## Footnote
Biliary colic may also frequently occur nocturnally.
110
What is the percentage of asymptomatic patients with gallstones who remain asymptomatic over 25 years?
60 to 80%
## Footnote
This statistic highlights the long-term stability of asymptomatic gallstones.
111
What is the probability of developing symptoms within 5 years after diagnosis of gallstones?
2–4% per year
## Footnote
This probability decreases to 1–2% in subsequent years.
112
What is the yearly incidence of complications in gallstone patients?
0.1–0.3%
## Footnote
This indicates the relatively low risk of complications annually.
113
What is the likelihood of patients remaining asymptomatic for 15 years developing symptoms later?
Unlikely
## Footnote
Most patients who develop complications had prior warning symptoms.
114
What conclusions can be drawn regarding diabetic patients with silent gallstones?
Similar conclusions apply as to asymptomatic patients
## Footnote
This indicates that the risk dynamics are comparable.
115
What does decision analysis suggest about the cumulative risk of death due to gallstone disease under expectant management?
The risk is small
## Footnote
This informs the management approach for asymptomatic patients.
116
Is prophylactic cholecystectomy warranted in asymptomatic gallstone patients according to decision analysis?
No
## Footnote
Prophylactic surgery is not recommended in these cases.
117
In gallstone patients, who is more likely to develop symptoms of biliary pain?
Patients diagnosed at a young age
## Footnote
This contrasts with patients over 60 years at initial diagnosis.
118
Are diabetic patients with gallstones more susceptible to septic complications?
Yes, somewhat more susceptible
## Footnote
The exact magnitude of this risk remains incompletely defined.
119
What is the risk of developing symptoms or complications requiring surgery in asymptomatic gallstone patients?
The risk is quite small.
120
What are the three factors to consider for recommending cholecystectomy in gallstone patients?
* Presence of frequent or severe symptoms
* History of prior complications of gallstone disease
* Underlying condition predisposing to increased risk of complications
121
What are examples of prior complications of gallstone disease?
* Acute cholecystitis
* Pancreatitis
* Gallstone fistula
122
In which patients might prophylactic cholecystectomy be considered?
* Patients with very large gallstones (>3 cm)
* Patients with gallstones in a congenitally anomalous gallbladder
123
Should routine cholecystectomy be recommended for young patients with asymptomatic gallstones?
Few authorities would now recommend it.
124
What is laparoscopic cholecystectomy?
A minimal-access approach for the removal of the gallbladder and its stones.
125
What are the advantages of laparoscopic cholecystectomy?
* Markedly shortened hospital stay
* Minimal disability
* Decreased cost
126
What are the complication rates for laparoscopic cholecystectomy?
* Complications develop in ~4%
* Conversion to laparotomy occurs in 5%
* Death rate is <0.1%
* Bile duct injury rate is 0.2–0.6%
127
What has laparoscopic cholecystectomy become the standard treatment for?
Symptomatic cholelithiasis.
128
What is the medical therapy for gallstone dissolution?
UDCA therapy.
129
What are the criteria for patients to be candidates for gallstone dissolution therapy?
* Functioning gallbladder
* Radiolucent stones <10 mm in diameter
130
What is the expected success rate of complete dissolution of stones <10 mm in diameter?
~50% within 6 months to 2 years.
131
What is the recommended size of stones for good results with UDCA therapy?
Stones <5 mm in diameter.
132
What is the daily dose of UDCA for gallstone dissolution?
10–15 mg/kg per day.
133
What is the likelihood of stones >10 mm in size dissolving?
Rarely dissolve.
134
What is the response of pigment stones to UDCA therapy?
Not responsive.
135
What percentage of patients with symptomatic cholelithiasis are candidates for UDCA treatment?
Probably ≤10%.
136
What is a significant issue with gallstone dissolution therapy?
Recurrent stones (30–50% over 3–5 years of follow-up).
137
What is a consideration for patients taking UDCA therapy for gallstone dissolution?
Taking a drug for up to 2 years and perhaps indefinitely.
138
For which patients should long-term treatment with UDCA be considered after cholecystectomy?
Patients with cholesterol gallstone disease who develop recurrent choledocholithiasis.
139
What is acute cholecystitis?
Acute inflammation of the gallbladder wall
## Footnote
Usually follows obstruction of the cystic duct by a stone.
140
What are the three factors that can evoke an inflammatory response in acute cholecystitis?
* Mechanical inflammation
* Chemical inflammation
* Bacterial inflammation
141
What is the role of bacterial inflammation in acute cholecystitis?
May play a role in 50–85% of patients
## Footnote
Organisms frequently isolated include Escherichia coli, Klebsiella spp., Streptococcus spp., and Clostridium spp.
142
What are common symptoms experienced during an attack of acute cholecystitis?
* Biliary pain
* Anorexia
* Nausea
* Vomiting
143
What percentage of patients report having experienced prior attacks of biliary pain that resolved spontaneously?
Approximately 60–70%
144
What is Murphy's sign?
Increased pain and inspiratory arrest during subcostal palpation of the RUQ
## Footnote
Indicates gallbladder inflammation.
145
What are characteristic findings upon physical examination in acute cholecystitis?
* Tenderness in the RUQ
* Enlarged, tense gallbladder in 25–50% of patients
* Localized rebound tenderness
* Abdominal distention
* Hypoactive bowel sounds
146
What is the triad of symptoms highly suggestive of acute cholecystitis?
* Sudden onset of RUQ tenderness
* Fever
* Leukocytosis
147
What is the typical leukocyte count in patients with acute cholecystitis?
10,000–15,000 cells per microliter with a left shift on differential count
148
What imaging technique is useful for diagnosing acute cholecystitis?
Ultrasound
## Footnote
Demonstrates calculi in 90–95% of cases and signs of gallbladder inflammation.
149
What is the typical course of treatment for acute cholecystitis?
Early surgery whenever possible
## Footnote
Approximately 75% of patients treated medically have remission of acute symptoms within 2–7 days.
150
What is Mirizzi's syndrome?
A rare complication where a gallstone becomes impacted in the cystic duct causing compression of the CBD
## Footnote
Results in CBD obstruction and jaundice.
151
What is the importance of preoperative diagnosis of Mirizzi's syndrome?
To avoid CBD injury
152
What imaging techniques can demonstrate extrinsic compression of the CBD in Mirizzi's syndrome?
* Endoscopic retrograde cholangiopancreatography (ERCP)
* Percutaneous transhepatic cholangiography (PTC)
* Magnetic resonance cholangiopancreatography (MRCP)
153
What percentage of patients with acute cholecystitis experience recurrence within 1 year?
Approximately 25%
154
True or False: Jaundice is a common early symptom of acute cholecystitis.
False
155
Fill in the blank: The serum bilirubin is mildly elevated in fewer than _____ of patients with acute cholecystitis.
half
156
What percentage of patients with acute cholecystitis do not have calculi found at surgery?
5–14%
## Footnote
This indicates that acalculous cholecystitis can occur without the presence of gallstones.
157
What is a common underlying explanation for acalculous cholecystitis?
Not found in >50% of cases
## Footnote
This highlights the challenge in identifying specific causes for acalculous cholecystitis.
158
Which conditions are associated with an increased risk for acalculous cholecystitis? List at least three.
* Prolonged fasting
* Serious trauma or burns
* Postpartum period following prolonged labor
## Footnote
These conditions can lead to inflammation of the gallbladder without stones.
159
What may complicate periods of prolonged parenteral hyperalimentation?
Acalculous cholecystitis
## Footnote
This indicates a potential risk for patients receiving long-term nutritional support intravenously.
160
What might be responsible for some cases of acalculous cholecystitis?
Biliary sludge in the cystic duct
## Footnote
Biliary sludge can obstruct the cystic duct and lead to inflammation.
161
Name two precipitating factors for acalculous cholecystitis.
* Vasculitis
* Obstructing adenocarcinoma of the gallbladder
## Footnote
These factors can lead to gallbladder inflammation in the absence of stones.
162
True or False: The clinical manifestations of acalculous cholecystitis are distinguishable from those of calculous cholecystitis.
False
## Footnote
Both forms present similarly, complicating diagnosis.
163
What imaging studies may be useful in diagnosing acalculous cholecystitis?
Ultrasound or computed tomography (CT)
## Footnote
These imaging techniques can show a large, tense, static gallbladder without stones.
164
What is the complication rate for acalculous cholecystitis compared to calculous cholecystitis?
Exceeds that for calculous cholecystitis
## Footnote
This suggests that acalculous cholecystitis may have a worse prognosis.
165
What is essential for the successful management of acute acalculous cholecystitis?
Early diagnosis and surgical intervention
## Footnote
Prompt treatment is crucial to improve outcomes.
166
Fill in the blank: Acalculous cholecystitis may also be seen with a variety of other _______ processes.
systemic
## Footnote
Examples include sarcoidosis, cardiovascular disease, tuberculosis, and syphilis.
167
What is acalculous cholecystopathy?
Disordered motility of the gallbladder producing recurrent biliary pain in patients without gallstones.
168
What can be used to measure the gallbladder ejection fraction during cholescintigraphy?
Infusion of an octapeptide of CCK.
169
What are some surgical findings associated with acalculous cholecystopathy?
Abnormalities such as:
* Chronic cholecystitis
* Gallbladder muscle hypertrophy
* Markedly narrowed cystic duct
170
What criteria can identify patients with acalculous cholecystopathy?
1. Recurrent episodes of typical RUQ pain characteristic of biliary tract pain
2. Abnormal CCK cholescintigraphy demonstrating a gallbladder ejection fraction of <40%
3. Infusion of CCK reproducing the patient’s pain
171
What additional clue can indicate acalculous cholecystopathy?
Identification of a large gallbladder on ultrasound examination.
172
True or False: SOD dysfunction can cause recurrent RUQ pain.
True
173
Fill in the blank: An abnormal CCK cholescintigraphy in acalculous cholecystopathy shows a gallbladder ejection fraction of _______.
<40%
174
What is emphysematous cholecystitis thought to begin with?
Acute cholecystitis (calculous or acalculous)
## Footnote
Emphysematous cholecystitis is characterized by subsequent ischemia or gangrene of the gallbladder wall.
175
What bacteria are most frequently cultured in emphysematous cholecystitis?
* Clostridium welchii
* C. perfringens
* E. coli
## Footnote
These include both anaerobes and aerobes.
176
In which demographic does emphysematous cholecystitis occur most frequently?
Elderly men and patients with diabetes mellitus
## Footnote
This condition is notably more prevalent in these populations.
177
What are the clinical manifestations of emphysematous cholecystitis compared to?
Nongaseous cholecystitis
## Footnote
The symptoms are essentially indistinguishable.
178
How is the diagnosis of emphysematous cholecystitis typically made?
On plain abdominal film
## Footnote
Diagnosis is confirmed by finding gas within the gallbladder lumen or wall.
179
What indicates emphysematous cholecystitis on an abdominal film?
Gas within the gallbladder lumen, dissecting within the gallbladder wall, or in the pericholecystic tissues
## Footnote
These findings form a gaseous ring.
180
What are the morbidity and mortality rates associated with emphysematous cholecystitis?
Considerable
## Footnote
The condition is serious and requires prompt attention.
181
What is mandatory for the management of emphysematous cholecystitis?
Prompt surgical intervention and appropriate antibiotics
## Footnote
Timely treatment is crucial to reduce risks.
182
True or False: The clinical manifestations of emphysematous cholecystitis are easily distinguishable from those of nongaseous cholecystitis.
False
## Footnote
They are essentially indistinguishable.
183
Fill in the blank: Emphysematous cholecystitis is characterized by infection by _______.
[gas-producing organisms]
## Footnote
This leads to significant complications.
184
What is chronic cholecystitis?
Chronic inflammation of the gallbladder wall
185
What is chronic cholecystitis almost always associated with?
The presence of gallstones
186
What causes chronic cholecystitis?
Repeated bouts of subacute or acute cholecystitis or persistent mechanical irritation by gallstones
187
What percentage of patients with chronic cholecystitis have bacteria in their bile?
>25%
188
Does the presence of infected bile in chronic cholecystitis affect operative risk during elective cholecystectomy?
Probably adds little to the operative risk
189
How long may chronic cholecystitis be asymptomatic?
For years
190
What can chronic cholecystitis progress to?
Symptomatic gallbladder disease or acute cholecystitis
191
What may chronic cholecystitis present with?
Complications
192
What is empyema of the gallbladder?
Empyema of the gallbladder results from progression of acute cholecystitis with persistent cystic duct obstruction to superinfection of stagnant bile with a pus-forming bacterial organism.
## Footnote
Clinical picture includes high fever, severe RUQ pain, marked leukocytosis, and often prostration.
193
What are the risks associated with empyema of the gallbladder?
Empyema carries a high risk of gram-negative sepsis and/or perforation.
## Footnote
Emergency surgical intervention with proper antibiotic coverage is required as soon as the diagnosis is suspected.
194
What is hydrops of the gallbladder?
Hydrops or mucocele of the gallbladder results from prolonged obstruction of the cystic duct, usually by a large solitary calculus.
## Footnote
The obstructed gallbladder lumen is distended by mucus or clear transudate produced by mucosal epithelial cells.
195
What are the physical examination findings in a patient with hydrops of the gallbladder?
A visible, easily palpable, nontender mass sometimes extending from the RUQ into the right iliac fossa may be found.
## Footnote
The patient frequently remains asymptomatic, but chronic RUQ pain may occur.
196
What is the recommended treatment for hydrops of the gallbladder?
Cholecystectomy is indicated.
## Footnote
This is necessary because empyema, perforation, or gangrene may complicate the condition.
197
What causes gangrene of the gallbladder?
Gangrene results from ischemia of the wall and patchy or complete tissue necrosis.
## Footnote
Underlying conditions may include marked distention of the gallbladder, vasculitis, diabetes mellitus, empyema, or torsion.
198
What may predispose gangrene of the gallbladder to perforation?
Gangrene usually predisposes to perforation, but perforation may also occur in chronic cholecystitis without premonitory warning symptoms.
## Footnote
Localized perforations are usually contained by the omentum or by adhesions.
199
What are the consequences of bacterial superinfection in a gallbladder with localized perforation?
Bacterial superinfection results in abscess formation.
## Footnote
Most patients are treated with cholecystectomy, but some may require cholecystostomy and drainage of the abscess.
200
What is the mortality rate associated with free perforation of the gallbladder?
The mortality rate is approximately 30%.
## Footnote
Free perforation is less common but associated with severe complications.
201
What symptom may patients experience after free perforation of the gallbladder?
Patients may experience a sudden transient relief of RUQ pain as the distended gallbladder decompresses.
## Footnote
This is often followed by signs of generalized peritonitis.
202
What may result from inflammation and adhesion formation in relation to the gallbladder?
Fistula formation into an adjacent organ
## Footnote
Fistulas commonly occur into the duodenum, hepatic flexure of the colon, stomach, jejunum, abdominal wall, and renal pelvis.
203
What is the most common site for fistulas resulting from gallbladder issues?
Duodenum
## Footnote
Other sites include the hepatic flexure of the colon, stomach, jejunum, abdominal wall, and renal pelvis.
204
What percentage of patients undergoing cholecystectomy may have clinically 'silent' biliary-enteric fistulas?
Up to 5%
## Footnote
These fistulas can occur as a complication of acute cholecystitis.
205
How can asymptomatic cholecystoenteric fistulas sometimes be diagnosed?
Finding gas in the biliary tree on plain abdominal films
## Footnote
Barium contrast studies or endoscopy may also demonstrate the fistula.
206
What is the usual treatment for symptomatic patients with biliary-enteric fistulas?
Cholecystectomy, CBD exploration, and closure of the fistulous tract
## Footnote
This treatment addresses the underlying issues causing symptoms.
207
What does gallstone ileus refer to?
Mechanical intestinal obstruction resulting from the passage of a large gallstone into the bowel lumen
## Footnote
The stone typically enters through a cholecystoenteric fistula.
208
Where does the impacted gallstone usually cause obstruction in gallstone ileus?
Ileocecal valve
## Footnote
This is true provided that the more proximal small bowel is of normal caliber.
209
What size of gallstones is thought to predispose to fistula formation?
>2.5 cm in diameter
## Footnote
These larger stones can gradually erode through the gallbladder fundus.
210
What diagnostic confirmation methods can be used for gallstone ileus?
Plain abdominal film or upper gastrointestinal series
## Footnote
These methods may show small-intestinal obstruction with gas in the biliary tree (pneumobilia) and a calcified, ectopic gallstone.
211
What remains the procedure of choice to relieve obstruction in gallstone ileus?
Laparotomy with stone extraction
## Footnote
Propulsion of the stone into the colon is also an option.
212
What should be done with large stones within the gallbladder during treatment?
Evacuation of large stones should be performed
## Footnote
This is important to prevent further complications.
213
True or False: The gallbladder and its attachment to the intestines should typically be left alone during treatment.
True
## Footnote
This is a general guideline in managing gallstone ileus.
214
What is limey bile?
Calcium salts in the lumen of the gallbladder that cause precipitation and opacification of bile
## Footnote
Limey bile is also referred to as milk of calcium bile.
215
What is the typical clinical significance of limey bile?
Usually clinically innocuous
## Footnote
However, cholecystectomy is often performed, particularly in hydropic gallbladders.
216
What is porcelain gallbladder?
Calcium salt deposition within the wall of a chronically inflamed gallbladder
## Footnote
It can be detected on plain abdominal films.
217
What was the past recommendation for patients with porcelain gallbladder?
Cholecystectomy was advised for all patients
## Footnote
This was due to a perceived high incidence of carcinoma associated with this condition.
218
What are the two patterns of gallbladder wall calcification?
* Complete intramural calcification
* Selective mucosal calcification
## Footnote
These patterns have implications for cancer risk associated with porcelain gallbladder.
219
Which type of gallbladder wall calcification has a higher incidence of cancer?
Selective intramural calcification
## Footnote
The risk is still very small.
220
Is cholecystectomy necessary for all patients with porcelain gallbladder?
No, close surveillance is also acceptable
## Footnote
The need for surgery is not absolute.
221
What is the mainstay of therapy for acute cholecystitis?
Surgical intervention
## Footnote
Surgical intervention is considered the primary treatment for acute cholecystitis and its complications.
222
What may be required before cholecystectomy in acute cholecystitis?
A period of in-hospital stabilization
## Footnote
Patients may need to be stabilized before undergoing surgery.
223
What is the initial management for patients with acute cholecystitis?
Elimination of oral intake, nasogastric suction, electrolyte repair, analgesia
## Footnote
These steps are crucial in managing patients before surgery.
224
What type of antibiotic therapy is indicated in severe acute cholecystitis?
Intravenous antibiotic therapy
## Footnote
Even if bacterial superinfection has not occurred, antibiotics are necessary.
225
Which organisms are commonly targeted in antibiotic therapy for acute cholecystitis?
* E. coli
* Klebsiella
* Enterococcus
* Enterobacter
* Streptococcus
## Footnote
These organisms are likely to be present in cases of acute cholecystitis.
226
List effective antibiotics for treating acute cholecystitis.
* Piperacillin plus tazobactam
* Imipenem
* Meropenem
* Ceftriaxone plus metronidazole
* Levofloxacin plus metronidazole
## Footnote
These antibiotics are effective against the common organisms in acute cholecystitis.
227
What surgical options are appropriate for complicated acute cholecystitis?
* Urgent cholecystectomy
* Percutaneous cholecystostomy
## Footnote
These options are indicated when complications such as empyema or perforation are suspected.
228
When should early elective laparoscopic cholecystectomy be performed?
Ideally within 48–72 hours after diagnosis
## Footnote
Early intervention reduces complications.
229
What is the complication rate for early cholecystectomy compared to delayed cholecystectomy?
Not increased in early cholecystectomy
## Footnote
Early surgery does not increase risks compared to delayed surgery.
230
What conditions may lead to delayed surgical intervention in acute cholecystitis?
* Unacceptable risk for early surgery
* Doubt about the diagnosis of acute cholecystitis
## Footnote
These conditions necessitate postponement of surgery.
231
What are alternative management strategies for seriously ill patients with cholecystitis?
* Percutaneous drainage
* Transpapillary drainage
* Transmural drainage
## Footnote
These strategies may be used before elective cholecystectomy.
232
What are early complications following cholecystectomy?
Atelectasis, pulmonary disorders, abscess formation, hemorrhage, biliary-enteric fistula, bile leaks
## Footnote
Abscess formation is often subphrenic.
233
What might jaundice indicate after cholecystectomy?
Absorption of bile from an intraabdominal collection or mechanical obstruction of the CBD
## Footnote
Causes include retained calculi, intraductal blood clots, or extrinsic compression.
234
What percentage of patients experience total or near-total relief of preoperative symptoms after cholecystectomy?
75–90%
## Footnote
Cholecystectomy is considered a very successful operation.
235
What is the most common cause of persistent postcholecystectomy symptoms?
An overlooked symptomatic nonbiliary disorder
## Footnote
Examples include reflux esophagitis, peptic ulceration, pancreatitis, or irritable bowel syndrome.
236
What are the potential causes of postcholecystectomy syndromes?
1. Biliary strictures
2. Retained biliary calculi
3. Cystic duct stump syndrome
4. Stenosis or dyskinesia of the SOD
5. Bile salt–induced diarrhea or gastritis
## Footnote
A small percentage of patients may have disorders of the extrahepatic bile ducts.
237
True or False: Persistent postcholecystectomy symptoms are always due to biliary disorders.
False
## Footnote
The symptoms can be due to nonbiliary disorders as well.
238
What is cystic duct stump syndrome?
A condition where symptoms resembling biliary pain or cholecystitis occur in postcholecystectomy patients due to a long (>1 cm) cystic duct remnant.
## Footnote
This syndrome is often misattributed when symptoms arise after gallbladder removal.
239
What are the symptoms associated with cystic duct stump syndrome?
Symptoms resemble biliary pain or cholecystitis.
## Footnote
These symptoms can occur in patients even without demonstrable retained stones.
240
True or False: Almost all patients with postcholecystectomy symptoms have cystic duct stump syndrome.
False.
## Footnote
Analysis shows that most symptoms are attributable to other causes.
241
Fill in the blank: Cystic duct stump syndrome is associated with a cystic duct remnant longer than _______.
>1 cm.
## Footnote
This length is significant in diagnosing the syndrome.
242
What are the potential causes of symptoms of biliary colic with intermittent biliary obstruction?
Acalculous cholecystopathy, SOD stenosis, SOD dyskinesia
## Footnote
SOD refers to sphincter of Oddi.
243
What is SOD stenosis thought to result from?
Acute or chronic inflammation of the papilla of Vater, glandular hyperplasia of the papillary segment
244
List the five criteria used to define SOD stenosis.
* Upper abdominal pain, usually RUQ or epigastric
* Abnormal liver tests
* Dilatation of the CBD upon MRCP or ERCP examination
* Delayed (>45 min) drainage of contrast material from the duct
* Increased basal pressure of the SOD
245
What is the treatment for SOD stenosis after excluding acalculous cholecystopathy?
Endoscopic or surgical sphincteroplasty
246
What factors are considered indications for sphincterotomy?
* Prolonged duration of symptoms
* Lack of response to symptomatic treatment
* Presence of severe disability
* Patient’s choice of sphincterotomy over surgery
247
What are the three criteria that characterize biliary SOD disorders?
* Biliary pain
* Absence of bile duct stones or other abnormalities
* Elevated liver enzymes or a dilated CBD, but not both
248
What diagnostic tools can support the diagnosis of biliary SOD disorders?
Hepatobiliary scintigraphy, SOD manometry
249
What should the presence of both elevated liver enzymes and a dilated CBD indicate?
The possibility of obstruction
250
What are the proposed mechanisms for SOD dysfunction?
* Spasm of the sphincter
* Denervation sensitivity resulting in hypertonicity
* Abnormalities in the sequencing or frequency rates of sphincteric contraction waves
251
What medical treatments have been proposed for SOD dyskinesia?
Nitrites or anticholinergics
252
What are the indications for endoscopic biliary sphincterotomy (EBS) or surgical sphincterotomy?
Failure to respond to a 2- to 3-month trial of medical therapy, especially if SOD pressures are elevated
253
What percentage of patients experience long-term pain relief after EBS?
Approximately 45%
254
What effect does cholecystectomy have on gut transit?
Cholecystectomy induces persistent changes in gut transit
## Footnote
These changes lead to noticeable modifications in bowel habits.
255
How does cholecystectomy affect gut transit time?
It shortens gut transit time
## Footnote
This is due to the accelerated passage of the fecal bolus through the colon.
256
What specific change occurs in the right colon after cholecystectomy?
Marked acceleration in the right colon
## Footnote
This contributes to changes in bowel habits.
257
What happens to colonic bile acid output after cholecystectomy?
Increase in colonic bile acid output
## Footnote
This leads to a shift towards more diarrheagenic secondary bile acids.
258
What is the most diarrheagenic secondary bile acid that increases after cholecystectomy?
Deoxycholic acid
## Footnote
Deoxycholic acid is associated with increased diarrhea.
259
How is postcholecystectomy diarrhea classified?
Three or more watery movements per day
## Footnote
This occurs in 5-10% of patients undergoing elective cholecystectomy.
260
What treatment is often effective for troublesome diarrhea postcholecystectomy?
Bile acid–sequestering agents
## Footnote
Examples include cholestyramine or colestipol.
261
What does the term hyperplastic cholecystoses refer to?
A group of disorders of the gallbladder characterized by excessive proliferation of normal tissue components.
262
What is adenomyomatosis?
A benign proliferation of gallbladder surface epithelium with glandlike formations, extramural sinuses, transverse strictures, and/or fundal nodule formation.
263
What characterizes cholesterolosis?
Abnormal deposition of lipid, especially cholesteryl esters, within macrophages in the lamina propria of the gallbladder wall.
264
What is the appearance of the gallbladder mucosa in its diffuse form known as 'strawberry gallbladder'?
Brick red and speckled with bright yellow flecks of lipid.
265
In cholesterolosis, what does the localized form show?
Solitary or multiple 'cholesterol polyps' studding the gallbladder wall.
266
What is the relationship between cholesterol stones and cholesterolosis?
Cholesterol stones of the gallbladder are found in nearly half the cases.
267
When is cholecystectomy indicated in cases of adenomyomatosis or cholesterolosis?
When biliary symptoms are present.
268
What is the prevalence of gallbladder polyps in the adult population?
1–4% with a marked male predominance.
269
List the types of gallbladder polyps.
* Cholesterol polyps
* Adenomyomas
* Inflammatory polyps
* Adenomas (rare)
270
What significant changes have been found over a 5-year period in asymptomatic patients with gallbladder polyps <6 mm?
No significant changes.
271
What is recommended for asymptomatic patients >50 years with gallbladder polyps >10 mm?
Cholecystectomy.
272
True or False: Cholecystectomy is recommended for all patients with gallbladder polyps.
False.
273
Fill in the blank: The gallbladder polyps that show few changes over a 5-year period are those measuring ________.
<6 mm or 7–9 mm.
274
What should be done for symptomatic patients with gallbladder polyps?
Cholecystectomy is recommended.
275
What does the term hyperplastic cholecystoses refer to?
A group of disorders of the gallbladder characterized by excessive proliferation of normal tissue components.
276
What is adenomyomatosis?
A benign proliferation of gallbladder surface epithelium with glandlike formations, extramural sinuses, transverse strictures, and/or fundal nodule formation.
277
What characterizes cholesterolosis?
Abnormal deposition of lipid, especially cholesteryl esters, within macrophages in the lamina propria of the gallbladder wall.
278
What is the appearance of the gallbladder mucosa in its diffuse form known as 'strawberry gallbladder'?
Brick red and speckled with bright yellow flecks of lipid.
279
In cholesterolosis, what does the localized form show?
Solitary or multiple 'cholesterol polyps' studding the gallbladder wall.
280
What is the relationship between cholesterol stones and cholesterolosis?
Cholesterol stones of the gallbladder are found in nearly half the cases.
281
When is cholecystectomy indicated in cases of adenomyomatosis or cholesterolosis?
When biliary symptoms are present.
282
List the types of gallbladder polyps.
* Cholesterol polyps
* Adenomyomas
* Inflammatory polyps
* Adenomas (rare)
283
What is recommended for asymptomatic patients >50 years with gallbladder polyps >10 mm?
Cholecystectomy.
284
True or False: Cholecystectomy is recommended for all patients with gallbladder polyps.
False.
285
What should be done for symptomatic patients with gallbladder polyps?
Cholecystectomy is recommended.
286
What are the most common biliary anomalies encountered in infancy?
Atretic and hypoplastic lesions of the extrahepatic and large intrahepatic bile ducts
## Footnote
These anomalies lead to severe obstructive jaundice during the first month of life.
287
What is the typical clinical presentation of biliary atresia in infants?
Severe obstructive jaundice and pale stools during the first month of life
## Footnote
These symptoms are critical for early diagnosis.
288
How is the diagnosis of biliary atresia confirmed?
Surgical exploration and operative cholangiography
## Footnote
Clinical, laboratory, and imaging findings can suggest biliary atresia.
289
What percentage of biliary atresia cases are treatable with Roux-en-Y choledochojejunostomy?
Approximately 10%
## Footnote
The remainder are usually treated with the Kasai procedure.
290
What are common long-term complications for patients with biliary atresia?
Chronic cholangitis, extensive hepatic fibrosis, and portal hypertension
## Footnote
These complications can occur even after successful biliary-enteric anastomoses.
291
What is a choledochal cyst?
Cystic dilatation of the common bile duct (CBD)
## Footnote
It may also present as diverticulum formation in the intraduodenal segment.
292
What can chronic reflux of pancreatic juice into the biliary tree lead to?
Inflammation and stenosis of the extrahepatic bile ducts
## Footnote
This can result in cholangitis or biliary obstruction.
293
At what age do approximately 50% of patients with choledochal cysts present symptoms?
After age 10
## Footnote
The onset of symptoms may be gradual.
294
What are the classic triad symptoms of choledochal cysts?
Abdominal pain, jaundice, and an abdominal mass
## Footnote
Only one-third of patients exhibit this classic triad.
295
What imaging techniques can diagnose choledochal cysts?
Ultrasound, abdominal CT, MRCP, or cholangiography
## Footnote
Ultrasonographic detection of a cyst separate from the gallbladder suggests the diagnosis.
296
What is the surgical treatment for choledochal cysts?
Excision of the cyst and biliary-enteric anastomosis
## Footnote
This is necessary to restore normal bile flow.
297
What risk do patients with choledochal cysts face?
Increased risk for the subsequent development of cholangiocarcinoma
## Footnote
Regular monitoring is advised due to this risk.
298
What is Caroli's disease?
Dilatation of major intrahepatic bile ducts
## Footnote
It is one of the forms of congenital biliary ectasia.
299
What are common clinical manifestations of Caroli's disease?
Recurrent cholangitis, abscess formation, and brown pigment gallstone formation
## Footnote
These symptoms arise from ectatic intrahepatic biliary radicles.
300
What imaging techniques are useful in diagnosing congenital biliary ectasia?
Ultrasound, MRCP, and CT
## Footnote
These methods demonstrate cystic dilatation of the intrahepatic bile ducts.
301
What is Sclerosing Cholangitis (PSC)?
A progressive, inflammatory, sclerosing, and obliterative process affecting the extrahepatic and/or intrahepatic bile ducts
## Footnote
PSC is strongly associated with inflammatory bowel disease, especially ulcerative colitis.
302
What is the association between IgG4-associated cholangitis and PSC?
It presents with biochemical and cholangiographic features indistinguishable from PSC and is often associated with autoimmune pancreatitis
## Footnote
Characterized by elevated serum IgG4 and infiltration of IgG4-positive plasma cells in bile ducts and liver tissue.
303
What should be checked in all patients diagnosed with sclerosing cholangitis?
Serum IgG4 level
## Footnote
This is to rule out IgG4 disease as a cause of secondary sclerosing cholangitis, especially if they do not have inflammatory bowel disease.
304
What is the initial treatment of choice for IgG4-associated cholangitis?
Glucocorticoids
## Footnote
Relapse is common after steroid withdrawal, especially with proximal strictures.
305
What signs and symptoms do patients with PSC often present with?
RUQ abdominal pain, pruritus, jaundice, or acute cholangitis
## Footnote
Late in the course, complications may include complete biliary obstruction, secondary biliary cirrhosis, hepatic failure, or portal hypertension.
306
How is the diagnosis of PSC established?
Finding multifocal, diffusely distributed strictures with intervening segments of normal or dilated ducts on cholangiography
## Footnote
This produces a beaded appearance.
307
What are the cholangiographic techniques of choice in suspected cases of PSC?
MRCP and ERCP
## Footnote
These techniques help visualize the bile ducts.
308
What is Small Duct PSC?
Defined by chronic cholestasis and hepatic histology consistent with PSC in a patient with IBD, but with normal findings on cholangiography
## Footnote
Found in ~5% of patients with PSC, may represent an earlier stage with a better long-term prognosis.
309
What complications can arise from Small Duct PSC?
Progression to classic PSC and/or end-stage liver disease
## Footnote
This may necessitate liver transplantation.
310
What biliary tract changes may be seen in patients with AIDS?
A broad range of biliary tract changes including pancreatic duct obstruction and occasionally pancreatitis
## Footnote
Associated changes include diffuse intrahepatic bile duct involvement and ampullary stenosis.
311
What are some infectious organisms associated with biliary tract lesions in AIDS?
* Cryptosporidium
* Mycobacterium avium-intracellulare
* Cytomegalovirus
* Microsporidia
* Isospora
## Footnote
These organisms can cause various biliary tract infections.
312
What procedure can provide significant pain reduction in patients with AIDS-associated papillary stenosis?
ERCP sphincterotomy
## Footnote
This procedure helps alleviate pain caused by stenosis.
