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Gastroenterology > Gallstone > Flashcards

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.

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2
Q

What is the electrolyte composition of hepatic bile?

A

Hepatic bile is an isotonic fluid with an electrolyte composition resembling blood plasma.

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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.

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4
Q

What are the major solute components of bile by moles percent?

A
  • Bile acids (80%)
  • Phospholipids (16%)
  • Unesterified cholesterol (4%)
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5
Q

What is the total daily basal secretion of hepatic bile?

A

~500–600 mL.

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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
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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.

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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.

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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.

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10
Q

True or False: The cystic fibrosis transmembrane regulator (CFTR) is located on canalicular membranes.

A

False.

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11
Q

Fill in the blank: In the lithogenic state, the cholesterol value in bile can be as high as _______.

A

8–10%.

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12
Q

What condition is caused by mutations of MRP2 (ABCC2)?

A

Dubin-Johnson syndrome.

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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.

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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
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15
Q

What is the role of ABCG5/G8 in bile production?

A

They are canalicular half transporters for cholesterol and other neutral sterols.

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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.

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17
Q

What can a genetic defect in BSEP (ABCB11) lead to?

A

PFIC2 and BRIC2.

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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.

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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.

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20
Q

Which secondary bile acid is a stereoisomer of CDCA?

A

Ursodeoxycholic acid (UDCA)

UDCA is found in low concentration.

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21
Q

What is the typical ratio of glycine to taurine conjugates in bile?

A

~3:1

This ratio is observed in healthy subjects.

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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.

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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.

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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.

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25
Q

What role do bile acids play in dietary fat absorption?

A

Facilitate normal intestinal absorption via a micellar transport mechanism

They mainly aid in the absorption of cholesterol and fat-soluble vitamins.

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26
Q

How do bile acids aid in hepatic bile flow?

A

They serve as a major physiologic driving force

Bile acids also aid in water and electrolyte transport in the small bowel and colon.

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27
Q

What receptors do bile acids function as hormones by binding to?

A

Nuclear (farnesoid X receptor [FXR]) and G protein–coupled (TGR5) receptors

These receptors regulate bile acid metabolism and their enterohepatic circulation.

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28
Q

Fill in the blank: Bile acids are detergent-like molecules that form _______ in aqueous solutions.

A

micelles

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29
Q

True or False: Lithocholic acid is more efficiently absorbed from the colon than deoxycholic acid.

A

False

Lithocholic acid is much less efficiently absorbed.

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30
Q

What is the primary function of enterohepatic circulation?

A

Efficient conservation of bile acids

Bile acids are reabsorbed and recirculated to maintain their pool size.

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31
Q

How are unconjugated and conjugated bile acids absorbed in the gut?

A

Passive diffusion along the entire gut

Conjugated bile acids also utilize an active transport mechanism in the distal ileum.

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32
Q

What is the normal bile acid pool size?

A

~2–4 g

This size is maintained through synthesis and reabsorption.

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33
Q

How many times does the bile acid pool circulate daily under normal conditions?

A

~5–10 times

This frequency depends on meal size and composition.

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34
Q

What is the efficiency of intestinal reabsorption of bile acids?

A

~95%

This high efficiency limits daily fecal loss to 0.2–0.4 g.

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35
Q

What compensates for the daily fecal loss of bile acids?

A

Equal daily synthesis by the liver

This maintains the size of the bile acid pool.

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36
Q

What effect do bile acids have on fibroblast growth factor 19 (FGF19)?

A

Stimulate its release

FGF19 suppresses hepatic synthesis of bile acids from cholesterol.

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37
Q

Which enzyme is inhibited by FGF19 to suppress bile acid synthesis?

A

Cytochrome P450 7A1 (CYP7A1)

This enzyme is rate-limiting in bile acid synthesis from cholesterol.

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38
Q

What is the maximum rate of bile acid synthesis per day?

A

~5 g/d

This rate may be insufficient when intestinal reabsorption is impaired.

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39
Q

Which transporters are involved in the enterohepatic circulation of bile acids?

A

ABC transporters

They play a crucial role in the regulation of bile acid levels.

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40
Q

What regulates the expression of ABC transporters and rate-limiting enzymes in bile acid synthesis?

A

Nuclear receptors

These are ligand-activated transcription factors.

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41
Q

Which receptor upregulates the hepatic BSEP (ABCB11)?

A

Farnesoid X receptor (FXR)

FXR also represses bile acid synthesis.

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42
Q

What is the role of the liver X receptor (LXR) in cholesterol transport?

A

Upregulates the cholesterol transporter ABCG5/G8

LXR acts as an oxysterol sensor.

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43
Q

What is the function of the sphincter of Oddi (SOD) in the fasting state?

A

Offers a high-pressure zone of resistance to bile flow from the CBD into the duodenum

Prevents reflux of duodenal contents into the pancreatic and bile ducts and promotes filling of the gallbladder.

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44
Q

What hormone controls the evacuation of the gallbladder?

A

Cholecystokinin (CCK)

Released from the duodenal mucosa in response to the ingestion of fats and amino acids.

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45
Q

What are the effects of cholecystokinin (CCK) on the gallbladder?

A
  • Powerful contraction of the gallbladder
  • Decreased resistance of the SOD
  • Enhanced flow of biliary contents into the duodenum
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46
Q

How is hepatic bile concentrated within the gallbladder?

A

By energy-dependent transmucosal absorption of water and electrolytes

This process allows the gallbladder to store bile effectively.

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47
Q

What is the normal capacity of the gallbladder?

A

~30 mL

This volume indicates the typical storage capability of the gallbladder.

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48
Q

Fill in the blank: The major factor controlling gallbladder evacuation is the peptide hormone _______.

A

Cholecystokinin (CCK)

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49
Q

True or False: The sphincter of Oddi decreases resistance to bile flow during fasting.

A

False

The sphincter of Oddi offers a high-pressure zone of resistance during fasting.

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50
Q

What substances trigger the release of cholecystokinin (CCK)?

A
  • Fats
  • Amino acids
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51
Q

What happens to the bile acid pool during an overnight fast?

A

Almost the entire bile acid pool may be sequestered in the gallbladder for delivery into the duodenum with the first meal of the day.

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52
Q

What are congenital anomalies of the biliary tract?

A

Abnormalities in number, size, and shape of biliary structures

Examples include agenesis of the gallbladder, duplications, rudimentary or oversized gallbladders, and diverticula.

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53
Q

What is a Phrygian cap?

A

A clinically innocuous entity with a partial or complete septum separating the fundus from the body of the gallbladder

It is not associated with significant clinical symptoms.

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54
Q

List some anomalies of position or suspension of the gallbladder.

A
  • Left-sided gallbladder
  • Intrahepatic gallbladder
  • Retrodisplacement of the gallbladder
  • Floating gallbladder
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55
Q

True or False: A floating gallbladder can predispose to acute torsion.

A

True

Floating gallbladder can also lead to volvulus or herniation.

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56
Q

Fill in the blank: Anomalies of the biliary tract may include _______.

A

[agenesis of the gallbladder]

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57
Q

What is the clinical significance of a Phrygian cap?

A

It is clinically innocuous and typically does not require treatment

It can be identified incidentally on imaging studies.

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58
Q

What complications can arise from a floating gallbladder?

A
  • Acute torsion
  • Volvulus
  • Herniation
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59
Q

What are the two major types of gallstones?

A

Cholesterol stones and pigment stones

Cholesterol stones account for >90% of all gallstones in Western industrialized countries.

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60
Q

What is the primary composition of cholesterol stones?

A

Cholesterol monohydrate, calcium salts, bile pigments, proteins, and fatty acids

Cholesterol stones usually contain >50% cholesterol monohydrate.

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61
Q

What are the two types of pigment stones?

A

Black stones and brown stones

Brown stones form secondary to chronic biliary infection.

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62
Q

At what age does gallstone formation increase?

A

After age 50

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63
Q

What is the mechanism that leads to the formation of lithogenic bile?

A

Increased biliary secretion of cholesterol

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64
Q

What factors can increase biliary cholesterol secretion?

A

Obesity, metabolic syndrome, high-caloric diets, drugs

Example drugs include clofibrate.

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65
Q

What role do genetic factors play in gallstone disease?

A

Genetic factors account for 25% of phenotypic variation in gallstone pathogenesis

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66
Q

What gene variant is associated with gallstones in 21% of patients?

A

ABCG5/G8

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67
Q

What is the primary cause of cholesterol supersaturation in bile?

A

Hypersecretion of cholesterol

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68
Q

What is biliary sludge composed of?

A

Lecithin-cholesterol liquid crystals, cholesterol monohydrate crystals, calcium bilirubinate, mucin gels

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69
Q

True or False: Biliary sludge can be a precursor to gallstone disease.

A

True

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70
Q

What are the two key changes during pregnancy that contribute to gallstone formation?

A

Increased cholesterol saturation of bile, sluggish gallbladder contraction

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71
Q

What percentage of women develop gallbladder sludge during pregnancy?

A

20–30%

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72
Q

What is the effectiveness of UDCA in preventing gallstone formation during rapid weight reduction?

A

Highly effective; only 3% of UDCA recipients developed gallstones

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73
Q

What are the three defects that lead to cholesterol gallstone disease?

A

Bile supersaturation with cholesterol, nucleation of cholesterol monohydrate, abnormal gallbladder motor function

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74
Q

Fill in the blank: Cholesterol is essentially ______-insoluble.

A

water

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75
Q

What happens when there is an excess of cholesterol in bile?

A

Unstable cholesterol-rich vesicles aggregate into large multilamellar vesicles

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76
Q

What is the significance of the UGT1A1 gene variant in gallstone disease?

A

Associated with cholesterol stones and indicates the role of pigment particles in pathogenesis

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77
Q

What can cause gallbladder hypomotility?

A

Fasting, parenteral nutrition, pregnancy, certain drugs

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78
Q

What is the result of impaired gallbladder emptying?

A

Increased incidence of gallstones

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79
Q

What are black pigment stones composed of?

A

Pure calcium bilirubinate or polymer-like complexes with calcium and mucin glycoproteins

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80
Q

In which patient conditions are black pigment stones more common?

A
  • Chronic hemolytic states
  • Cirrhosis (especially related to alcohol)
  • Gilbert’s syndrome
  • Cystic fibrosis
  • Ileal diseases, ileal resection, or ileal bypass
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81
Q

What contributes to the pathogenesis of black pigment stones in ileal disease states?

A

Enterohepatic recycling of bilirubin

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82
Q

What are brown pigment stones composed of?

A

Calcium salts of unconjugated bilirubin with varying amounts of cholesterol and protein

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83
Q

What causes the formation of brown pigment stones?

A

Increased amounts of unconjugated, insoluble bilirubin in bile that precipitates to form stones

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84
Q

How may deconjugation of bilirubin occur in the formation of brown pigment stones?

A
  • Mediated by endogenous β-glucuronidase
  • Spontaneous hydrolysis
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85
Q

What can lead to the production of β-glucuronidase in cases of brown pigment stone formation?

A

Chronic infection of bile by bacteria

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86
Q

Where is pigment stone formation frequent?

A

Asia

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87
Q

What is often associated with pigment stone formation in the gallbladder and biliary tree?

A

Parasitic infections

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88
Q

What is the primary diagnostic procedure for cholelithiasis?

A

Ultrasonography of the gallbladder

It has replaced oral cholecystography (OCG) due to its accuracy.

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89
Q

What is the smallest size of stones that can be confidently identified using ultrasound?

A

1.5 mm in diameter

Identification relies on firm criteria such as acoustic shadowing.

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90
Q

What are the false-negative and false-positive rates for ultrasound in gallstone patients?

A

~2–4%

These rates are observed in major medical centers.

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91
Q

What is biliary sludge?

A

Material of low echogenic activity that forms a layer in the gallbladder

It shifts with postural changes and does not produce acoustic shadowing.

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92
Q

What may the plain abdominal film detect in relation to gallstones?

A

Gallstones containing sufficient calcium

Approximately 10–15% of cholesterol and ~50% of pigment stones are radiopaque.

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93
Q

What conditions can plain radiography help diagnose?

A
  • Emphysematous cholecystitis
  • Porcelain gallbladder
  • Limey bile
  • Gallstone ileus

These conditions may have specific radiographic features.

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94
Q

Why is oral cholecystography (OCG) regarded as obsolete?

A

It has been replaced by ultrasound

OCG may still assess cystic duct patency and gallbladder emptying.

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95
Q

What is the role of radiopharmaceuticals like 99m Tc-labeled N-substituted iminodiacetic acids?

A

They are used in imaging the biliary tree

They are excreted into the biliary tree even in the presence of serum bilirubin elevations.

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96
Q

What does failure to image the gallbladder during a radiopharmaceutical scan indicate?

A

Possible cystic duct obstruction, acute or chronic cholecystitis, or surgical absence of the organ

This finding is significant in diagnosing acute cholecystitis.

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97
Q

How can ultrasound be used in relation to gallbladder function?

A

To assess the emptying function of the gallbladder

This can provide insight into gallbladder health and functionality.

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98
Q

Fill in the blank: The _____ has historically been a useful procedure for the diagnosis of gallstones but is now regarded as obsolete.

A

oral cholecystography (OCG)

It has been replaced by ultrasound due to improved accuracy.

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99
Q

What is the most specific and characteristic symptom of gallstone disease?

A

Biliary colic

Biliary colic is characterized by a constant and often long-lasting pain.

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100
Q

What causes symptoms in gallstone disease?

A

Inflammation or obstruction following migration into the cystic duct or CBD

CBD refers to the common bile duct.

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101
Q

Describe the nature of pain associated with biliary colic.

A

Severe, steady ache or fullness in the epigastrium or right upper quadrant (RUQ)

Pain may radiate to the interscapular area, right scapula, or shoulder.

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102
Q

How long can biliary colic persist?

A

30 minutes to 5 hours

It may subside gradually or rapidly.

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103
Q

True or False: Biliary colic is characterized by intermittent pain.

A

False

Biliary colic is steady rather than intermittent.

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104
Q

What should raise suspicion of acute cholecystitis?

A

An episode of biliary pain persisting beyond 5 hours

Acute cholecystitis is a possible complication of gallstone disease.

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105
Q

What symptoms frequently accompany episodes of biliary pain?

A

Nausea and vomiting

These symptoms are common during biliary colic episodes.

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106
Q

What do elevated levels of serum bilirubin and/or alkaline phosphatase suggest?

A

A common duct stone

These laboratory findings can indicate complications from gallstones.

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107
Q

What do fever or chills (rigors) with biliary pain usually imply?

A

A complication such as cholecystitis, pancreatitis, or cholangitis

These complications are serious and require medical attention.

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108
Q

Fill in the blank: Complaints of short-lasting, vague epigastric fullness, dyspepsia, eructation, or flatulence should not be confused with _______.

A

Biliary pain

These symptoms are not specific for biliary calculi.

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109
Q

What can precipitate biliary colic?

A

Eating a fatty meal, consumption of a large meal after fasting, or eating a normal meal

Biliary colic may also frequently occur nocturnally.

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110
Q

What is the percentage of asymptomatic patients with gallstones who remain asymptomatic over 25 years?

A

60 to 80%

This statistic highlights the long-term stability of asymptomatic gallstones.

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111
Q

What is the probability of developing symptoms within 5 years after diagnosis of gallstones?

A

2–4% per year

This probability decreases to 1–2% in subsequent years.

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112
Q

What is the yearly incidence of complications in gallstone patients?

A

0.1–0.3%

This indicates the relatively low risk of complications annually.

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113
Q

What is the likelihood of patients remaining asymptomatic for 15 years developing symptoms later?

A

Unlikely

Most patients who develop complications had prior warning symptoms.

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114
Q

What conclusions can be drawn regarding diabetic patients with silent gallstones?

A

Similar conclusions apply as to asymptomatic patients

This indicates that the risk dynamics are comparable.

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115
Q

What does decision analysis suggest about the cumulative risk of death due to gallstone disease under expectant management?

A

The risk is small

This informs the management approach for asymptomatic patients.

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116
Q

Is prophylactic cholecystectomy warranted in asymptomatic gallstone patients according to decision analysis?

A

No

Prophylactic surgery is not recommended in these cases.

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117
Q

In gallstone patients, who is more likely to develop symptoms of biliary pain?

A

Patients diagnosed at a young age

This contrasts with patients over 60 years at initial diagnosis.

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118
Q

Are diabetic patients with gallstones more susceptible to septic complications?

A

Yes, somewhat more susceptible

The exact magnitude of this risk remains incompletely defined.

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119
Q

What is the risk of developing symptoms or complications requiring surgery in asymptomatic gallstone patients?

A

The risk is quite small.

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120
Q

What are the three factors to consider for recommending cholecystectomy in gallstone patients?

A
  • Presence of frequent or severe symptoms
  • History of prior complications of gallstone disease
  • Underlying condition predisposing to increased risk of complications
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121
Q

What are examples of prior complications of gallstone disease?

A
  • Acute cholecystitis
  • Pancreatitis
  • Gallstone fistula
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122
Q

In which patients might prophylactic cholecystectomy be considered?

A
  • Patients with very large gallstones (>3 cm)
  • Patients with gallstones in a congenitally anomalous gallbladder
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123
Q

Should routine cholecystectomy be recommended for young patients with asymptomatic gallstones?

A

Few authorities would now recommend it.

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124
Q

What is laparoscopic cholecystectomy?

A

A minimal-access approach for the removal of the gallbladder and its stones.

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125
Q

What are the advantages of laparoscopic cholecystectomy?

A
  • Markedly shortened hospital stay
  • Minimal disability
  • Decreased cost
126
Q

What are the complication rates for laparoscopic cholecystectomy?

A
  • 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
Q

What has laparoscopic cholecystectomy become the standard treatment for?

A

Symptomatic cholelithiasis.

128
Q

What is the medical therapy for gallstone dissolution?

A

UDCA therapy.

129
Q

What are the criteria for patients to be candidates for gallstone dissolution therapy?

A
  • Functioning gallbladder
  • Radiolucent stones <10 mm in diameter
130
Q

What is the expected success rate of complete dissolution of stones <10 mm in diameter?

A

~50% within 6 months to 2 years.

131
Q

What is the recommended size of stones for good results with UDCA therapy?

A

Stones <5 mm in diameter.

132
Q

What is the daily dose of UDCA for gallstone dissolution?

A

10–15 mg/kg per day.

133
Q

What is the likelihood of stones >10 mm in size dissolving?

A

Rarely dissolve.

134
Q

What is the response of pigment stones to UDCA therapy?

A

Not responsive.

135
Q

What percentage of patients with symptomatic cholelithiasis are candidates for UDCA treatment?

A

Probably ≤10%.

136
Q

What is a significant issue with gallstone dissolution therapy?

A

Recurrent stones (30–50% over 3–5 years of follow-up).

137
Q

What is a consideration for patients taking UDCA therapy for gallstone dissolution?

A

Taking a drug for up to 2 years and perhaps indefinitely.

138
Q

For which patients should long-term treatment with UDCA be considered after cholecystectomy?

A

Patients with cholesterol gallstone disease who develop recurrent choledocholithiasis.

139
Q

What is acute cholecystitis?

A

Acute inflammation of the gallbladder wall

Usually follows obstruction of the cystic duct by a stone.

140
Q

What are the three factors that can evoke an inflammatory response in acute cholecystitis?

A
  • Mechanical inflammation
  • Chemical inflammation
  • Bacterial inflammation
141
Q

What is the role of bacterial inflammation in acute cholecystitis?

A

May play a role in 50–85% of patients

Organisms frequently isolated include Escherichia coli, Klebsiella spp., Streptococcus spp., and Clostridium spp.

142
Q

What are common symptoms experienced during an attack of acute cholecystitis?

A
  • Biliary pain
  • Anorexia
  • Nausea
  • Vomiting
143
Q

What percentage of patients report having experienced prior attacks of biliary pain that resolved spontaneously?

A

Approximately 60–70%

144
Q

What is Murphy’s sign?

A

Increased pain and inspiratory arrest during subcostal palpation of the RUQ

Indicates gallbladder inflammation.

145
Q

What are characteristic findings upon physical examination in acute cholecystitis?

A
  • Tenderness in the RUQ
  • Enlarged, tense gallbladder in 25–50% of patients
  • Localized rebound tenderness
  • Abdominal distention
  • Hypoactive bowel sounds
146
Q

What is the triad of symptoms highly suggestive of acute cholecystitis?

A
  • Sudden onset of RUQ tenderness
  • Fever
  • Leukocytosis
147
Q

What is the typical leukocyte count in patients with acute cholecystitis?

A

10,000–15,000 cells per microliter with a left shift on differential count

148
Q

What imaging technique is useful for diagnosing acute cholecystitis?

A

Ultrasound

Demonstrates calculi in 90–95% of cases and signs of gallbladder inflammation.

149
Q

What is the typical course of treatment for acute cholecystitis?

A

Early surgery whenever possible

Approximately 75% of patients treated medically have remission of acute symptoms within 2–7 days.

150
Q

What is Mirizzi’s syndrome?

A

A rare complication where a gallstone becomes impacted in the cystic duct causing compression of the CBD

Results in CBD obstruction and jaundice.

151
Q

What is the importance of preoperative diagnosis of Mirizzi’s syndrome?

A

To avoid CBD injury

152
Q

What imaging techniques can demonstrate extrinsic compression of the CBD in Mirizzi’s syndrome?

A
  • Endoscopic retrograde cholangiopancreatography (ERCP)
  • Percutaneous transhepatic cholangiography (PTC)
  • Magnetic resonance cholangiopancreatography (MRCP)
153
Q

What percentage of patients with acute cholecystitis experience recurrence within 1 year?

A

Approximately 25%

154
Q

True or False: Jaundice is a common early symptom of acute cholecystitis.

A

False

155
Q

Fill in the blank: The serum bilirubin is mildly elevated in fewer than _____ of patients with acute cholecystitis.

A

half

156
Q

What percentage of patients with acute cholecystitis do not have calculi found at surgery?

A

5–14%

This indicates that acalculous cholecystitis can occur without the presence of gallstones.

157
Q

What is a common underlying explanation for acalculous cholecystitis?

A

Not found in >50% of cases

This highlights the challenge in identifying specific causes for acalculous cholecystitis.

158
Q

Which conditions are associated with an increased risk for acalculous cholecystitis? List at least three.

A
  • Prolonged fasting
  • Serious trauma or burns
  • Postpartum period following prolonged labor

These conditions can lead to inflammation of the gallbladder without stones.

159
Q

What may complicate periods of prolonged parenteral hyperalimentation?

A

Acalculous cholecystitis

This indicates a potential risk for patients receiving long-term nutritional support intravenously.

160
Q

What might be responsible for some cases of acalculous cholecystitis?

A

Biliary sludge in the cystic duct

Biliary sludge can obstruct the cystic duct and lead to inflammation.

161
Q

Name two precipitating factors for acalculous cholecystitis.

A
  • Vasculitis
  • Obstructing adenocarcinoma of the gallbladder

These factors can lead to gallbladder inflammation in the absence of stones.

162
Q

True or False: The clinical manifestations of acalculous cholecystitis are distinguishable from those of calculous cholecystitis.

A

False

Both forms present similarly, complicating diagnosis.

163
Q

What imaging studies may be useful in diagnosing acalculous cholecystitis?

A

Ultrasound or computed tomography (CT)

These imaging techniques can show a large, tense, static gallbladder without stones.

164
Q

What is the complication rate for acalculous cholecystitis compared to calculous cholecystitis?

A

Exceeds that for calculous cholecystitis

This suggests that acalculous cholecystitis may have a worse prognosis.

165
Q

What is essential for the successful management of acute acalculous cholecystitis?

A

Early diagnosis and surgical intervention

Prompt treatment is crucial to improve outcomes.

166
Q

Fill in the blank: Acalculous cholecystitis may also be seen with a variety of other _______ processes.

A

systemic

Examples include sarcoidosis, cardiovascular disease, tuberculosis, and syphilis.

167
Q

What is acalculous cholecystopathy?

A

Disordered motility of the gallbladder producing recurrent biliary pain in patients without gallstones.

168
Q

What can be used to measure the gallbladder ejection fraction during cholescintigraphy?

A

Infusion of an octapeptide of CCK.

169
Q

What are some surgical findings associated with acalculous cholecystopathy?

A

Abnormalities such as:
* Chronic cholecystitis
* Gallbladder muscle hypertrophy
* Markedly narrowed cystic duct

170
Q

What criteria can identify patients with acalculous cholecystopathy?

A
  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
Q

What additional clue can indicate acalculous cholecystopathy?

A

Identification of a large gallbladder on ultrasound examination.

172
Q

True or False: SOD dysfunction can cause recurrent RUQ pain.

A

True

173
Q

Fill in the blank: An abnormal CCK cholescintigraphy in acalculous cholecystopathy shows a gallbladder ejection fraction of _______.

A

<40%

174
Q

What is emphysematous cholecystitis thought to begin with?

A

Acute cholecystitis (calculous or acalculous)

Emphysematous cholecystitis is characterized by subsequent ischemia or gangrene of the gallbladder wall.

175
Q

What bacteria are most frequently cultured in emphysematous cholecystitis?

A
  • Clostridium welchii
  • C. perfringens
  • E. coli

These include both anaerobes and aerobes.

176
Q

In which demographic does emphysematous cholecystitis occur most frequently?

A

Elderly men and patients with diabetes mellitus

This condition is notably more prevalent in these populations.

177
Q

What are the clinical manifestations of emphysematous cholecystitis compared to?

A

Nongaseous cholecystitis

The symptoms are essentially indistinguishable.

178
Q

How is the diagnosis of emphysematous cholecystitis typically made?

A

On plain abdominal film

Diagnosis is confirmed by finding gas within the gallbladder lumen or wall.

179
Q

What indicates emphysematous cholecystitis on an abdominal film?

A

Gas within the gallbladder lumen, dissecting within the gallbladder wall, or in the pericholecystic tissues

These findings form a gaseous ring.

180
Q

What are the morbidity and mortality rates associated with emphysematous cholecystitis?

A

Considerable

The condition is serious and requires prompt attention.

181
Q

What is mandatory for the management of emphysematous cholecystitis?

A

Prompt surgical intervention and appropriate antibiotics

Timely treatment is crucial to reduce risks.

182
Q

True or False: The clinical manifestations of emphysematous cholecystitis are easily distinguishable from those of nongaseous cholecystitis.

A

False

They are essentially indistinguishable.

183
Q

Fill in the blank: Emphysematous cholecystitis is characterized by infection by _______.

A

[gas-producing organisms]

This leads to significant complications.

184
Q

What is chronic cholecystitis?

A

Chronic inflammation of the gallbladder wall

185
Q

What is chronic cholecystitis almost always associated with?

A

The presence of gallstones

186
Q

What causes chronic cholecystitis?

A

Repeated bouts of subacute or acute cholecystitis or persistent mechanical irritation by gallstones

187
Q

What percentage of patients with chronic cholecystitis have bacteria in their bile?

A

> 25%

188
Q

Does the presence of infected bile in chronic cholecystitis affect operative risk during elective cholecystectomy?

A

Probably adds little to the operative risk

189
Q

How long may chronic cholecystitis be asymptomatic?

A

For years

190
Q

What can chronic cholecystitis progress to?

A

Symptomatic gallbladder disease or acute cholecystitis

191
Q

What may chronic cholecystitis present with?

A

Complications

192
Q

What is empyema of the gallbladder?

A

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.

Clinical picture includes high fever, severe RUQ pain, marked leukocytosis, and often prostration.

193
Q

What are the risks associated with empyema of the gallbladder?

A

Empyema carries a high risk of gram-negative sepsis and/or perforation.

Emergency surgical intervention with proper antibiotic coverage is required as soon as the diagnosis is suspected.

194
Q

What is hydrops of the gallbladder?

A

Hydrops or mucocele of the gallbladder results from prolonged obstruction of the cystic duct, usually by a large solitary calculus.

The obstructed gallbladder lumen is distended by mucus or clear transudate produced by mucosal epithelial cells.

195
Q

What are the physical examination findings in a patient with hydrops of the gallbladder?

A

A visible, easily palpable, nontender mass sometimes extending from the RUQ into the right iliac fossa may be found.

The patient frequently remains asymptomatic, but chronic RUQ pain may occur.

196
Q

What is the recommended treatment for hydrops of the gallbladder?

A

Cholecystectomy is indicated.

This is necessary because empyema, perforation, or gangrene may complicate the condition.

197
Q

What causes gangrene of the gallbladder?

A

Gangrene results from ischemia of the wall and patchy or complete tissue necrosis.

Underlying conditions may include marked distention of the gallbladder, vasculitis, diabetes mellitus, empyema, or torsion.

198
Q

What may predispose gangrene of the gallbladder to perforation?

A

Gangrene usually predisposes to perforation, but perforation may also occur in chronic cholecystitis without premonitory warning symptoms.

Localized perforations are usually contained by the omentum or by adhesions.

199
Q

What are the consequences of bacterial superinfection in a gallbladder with localized perforation?

A

Bacterial superinfection results in abscess formation.

Most patients are treated with cholecystectomy, but some may require cholecystostomy and drainage of the abscess.

200
Q

What is the mortality rate associated with free perforation of the gallbladder?

A

The mortality rate is approximately 30%.

Free perforation is less common but associated with severe complications.

201
Q

What symptom may patients experience after free perforation of the gallbladder?

A

Patients may experience a sudden transient relief of RUQ pain as the distended gallbladder decompresses.

This is often followed by signs of generalized peritonitis.

202
Q

What may result from inflammation and adhesion formation in relation to the gallbladder?

A

Fistula formation into an adjacent organ

Fistulas commonly occur into the duodenum, hepatic flexure of the colon, stomach, jejunum, abdominal wall, and renal pelvis.

203
Q

What is the most common site for fistulas resulting from gallbladder issues?

A

Duodenum

Other sites include the hepatic flexure of the colon, stomach, jejunum, abdominal wall, and renal pelvis.

204
Q

What percentage of patients undergoing cholecystectomy may have clinically ‘silent’ biliary-enteric fistulas?

A

Up to 5%

These fistulas can occur as a complication of acute cholecystitis.

205
Q

How can asymptomatic cholecystoenteric fistulas sometimes be diagnosed?

A

Finding gas in the biliary tree on plain abdominal films

Barium contrast studies or endoscopy may also demonstrate the fistula.

206
Q

What is the usual treatment for symptomatic patients with biliary-enteric fistulas?

A

Cholecystectomy, CBD exploration, and closure of the fistulous tract

This treatment addresses the underlying issues causing symptoms.

207
Q

What does gallstone ileus refer to?

A

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

The stone typically enters through a cholecystoenteric fistula.

208
Q

Where does the impacted gallstone usually cause obstruction in gallstone ileus?

A

Ileocecal valve

This is true provided that the more proximal small bowel is of normal caliber.

209
Q

What size of gallstones is thought to predispose to fistula formation?

A

> 2.5 cm in diameter

These larger stones can gradually erode through the gallbladder fundus.

210
Q

What diagnostic confirmation methods can be used for gallstone ileus?

A

Plain abdominal film or upper gastrointestinal series

These methods may show small-intestinal obstruction with gas in the biliary tree (pneumobilia) and a calcified, ectopic gallstone.

211
Q

What remains the procedure of choice to relieve obstruction in gallstone ileus?

A

Laparotomy with stone extraction

Propulsion of the stone into the colon is also an option.

212
Q

What should be done with large stones within the gallbladder during treatment?

A

Evacuation of large stones should be performed

This is important to prevent further complications.

213
Q

True or False: The gallbladder and its attachment to the intestines should typically be left alone during treatment.

A

True

This is a general guideline in managing gallstone ileus.

214
Q

What is limey bile?

A

Calcium salts in the lumen of the gallbladder that cause precipitation and opacification of bile

Limey bile is also referred to as milk of calcium bile.

215
Q

What is the typical clinical significance of limey bile?

A

Usually clinically innocuous

However, cholecystectomy is often performed, particularly in hydropic gallbladders.

216
Q

What is porcelain gallbladder?

A

Calcium salt deposition within the wall of a chronically inflamed gallbladder

It can be detected on plain abdominal films.

217
Q

What was the past recommendation for patients with porcelain gallbladder?

A

Cholecystectomy was advised for all patients

This was due to a perceived high incidence of carcinoma associated with this condition.

218
Q

What are the two patterns of gallbladder wall calcification?

A
  • Complete intramural calcification
  • Selective mucosal calcification

These patterns have implications for cancer risk associated with porcelain gallbladder.

219
Q

Which type of gallbladder wall calcification has a higher incidence of cancer?

A

Selective intramural calcification

The risk is still very small.

220
Q

Is cholecystectomy necessary for all patients with porcelain gallbladder?

A

No, close surveillance is also acceptable

The need for surgery is not absolute.

221
Q

What is the mainstay of therapy for acute cholecystitis?

A

Surgical intervention

Surgical intervention is considered the primary treatment for acute cholecystitis and its complications.

222
Q

What may be required before cholecystectomy in acute cholecystitis?

A

A period of in-hospital stabilization

Patients may need to be stabilized before undergoing surgery.

223
Q

What is the initial management for patients with acute cholecystitis?

A

Elimination of oral intake, nasogastric suction, electrolyte repair, analgesia

These steps are crucial in managing patients before surgery.

224
Q

What type of antibiotic therapy is indicated in severe acute cholecystitis?

A

Intravenous antibiotic therapy

Even if bacterial superinfection has not occurred, antibiotics are necessary.

225
Q

Which organisms are commonly targeted in antibiotic therapy for acute cholecystitis?

A
  • E. coli
  • Klebsiella
  • Enterococcus
  • Enterobacter
  • Streptococcus

These organisms are likely to be present in cases of acute cholecystitis.

226
Q

List effective antibiotics for treating acute cholecystitis.

A
  • Piperacillin plus tazobactam
  • Imipenem
  • Meropenem
  • Ceftriaxone plus metronidazole
  • Levofloxacin plus metronidazole

These antibiotics are effective against the common organisms in acute cholecystitis.

227
Q

What surgical options are appropriate for complicated acute cholecystitis?

A
  • Urgent cholecystectomy
  • Percutaneous cholecystostomy

These options are indicated when complications such as empyema or perforation are suspected.

228
Q

When should early elective laparoscopic cholecystectomy be performed?

A

Ideally within 48–72 hours after diagnosis

Early intervention reduces complications.

229
Q

What is the complication rate for early cholecystectomy compared to delayed cholecystectomy?

A

Not increased in early cholecystectomy

Early surgery does not increase risks compared to delayed surgery.

230
Q

What conditions may lead to delayed surgical intervention in acute cholecystitis?

A
  • Unacceptable risk for early surgery
  • Doubt about the diagnosis of acute cholecystitis

These conditions necessitate postponement of surgery.

231
Q

What are alternative management strategies for seriously ill patients with cholecystitis?

A
  • Percutaneous drainage
  • Transpapillary drainage
  • Transmural drainage

These strategies may be used before elective cholecystectomy.

232
Q

What are early complications following cholecystectomy?

A

Atelectasis, pulmonary disorders, abscess formation, hemorrhage, biliary-enteric fistula, bile leaks

Abscess formation is often subphrenic.

233
Q

What might jaundice indicate after cholecystectomy?

A

Absorption of bile from an intraabdominal collection or mechanical obstruction of the CBD

Causes include retained calculi, intraductal blood clots, or extrinsic compression.

234
Q

What percentage of patients experience total or near-total relief of preoperative symptoms after cholecystectomy?

A

75–90%

Cholecystectomy is considered a very successful operation.

235
Q

What is the most common cause of persistent postcholecystectomy symptoms?

A

An overlooked symptomatic nonbiliary disorder

Examples include reflux esophagitis, peptic ulceration, pancreatitis, or irritable bowel syndrome.

236
Q

What are the potential causes of postcholecystectomy syndromes?

A
  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

A small percentage of patients may have disorders of the extrahepatic bile ducts.

237
Q

True or False: Persistent postcholecystectomy symptoms are always due to biliary disorders.

A

False

The symptoms can be due to nonbiliary disorders as well.

238
Q

What is cystic duct stump syndrome?

A

A condition where symptoms resembling biliary pain or cholecystitis occur in postcholecystectomy patients due to a long (>1 cm) cystic duct remnant.

This syndrome is often misattributed when symptoms arise after gallbladder removal.

239
Q

What are the symptoms associated with cystic duct stump syndrome?

A

Symptoms resemble biliary pain or cholecystitis.

These symptoms can occur in patients even without demonstrable retained stones.

240
Q

True or False: Almost all patients with postcholecystectomy symptoms have cystic duct stump syndrome.

A

False.

Analysis shows that most symptoms are attributable to other causes.

241
Q

Fill in the blank: Cystic duct stump syndrome is associated with a cystic duct remnant longer than _______.

A

> 1 cm.

This length is significant in diagnosing the syndrome.

242
Q

What are the potential causes of symptoms of biliary colic with intermittent biliary obstruction?

A

Acalculous cholecystopathy, SOD stenosis, SOD dyskinesia

SOD refers to sphincter of Oddi.

243
Q

What is SOD stenosis thought to result from?

A

Acute or chronic inflammation of the papilla of Vater, glandular hyperplasia of the papillary segment

244
Q

List the five criteria used to define SOD stenosis.

A
  • 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
Q

What is the treatment for SOD stenosis after excluding acalculous cholecystopathy?

A

Endoscopic or surgical sphincteroplasty

246
Q

What factors are considered indications for sphincterotomy?

A
  • Prolonged duration of symptoms
  • Lack of response to symptomatic treatment
  • Presence of severe disability
  • Patient’s choice of sphincterotomy over surgery
247
Q

What are the three criteria that characterize biliary SOD disorders?

A
  • Biliary pain
  • Absence of bile duct stones or other abnormalities
  • Elevated liver enzymes or a dilated CBD, but not both
248
Q

What diagnostic tools can support the diagnosis of biliary SOD disorders?

A

Hepatobiliary scintigraphy, SOD manometry

249
Q

What should the presence of both elevated liver enzymes and a dilated CBD indicate?

A

The possibility of obstruction

250
Q

What are the proposed mechanisms for SOD dysfunction?

A
  • Spasm of the sphincter
  • Denervation sensitivity resulting in hypertonicity
  • Abnormalities in the sequencing or frequency rates of sphincteric contraction waves
251
Q

What medical treatments have been proposed for SOD dyskinesia?

A

Nitrites or anticholinergics

252
Q

What are the indications for endoscopic biliary sphincterotomy (EBS) or surgical sphincterotomy?

A

Failure to respond to a 2- to 3-month trial of medical therapy, especially if SOD pressures are elevated

253
Q

What percentage of patients experience long-term pain relief after EBS?

A

Approximately 45%

254
Q

What effect does cholecystectomy have on gut transit?

A

Cholecystectomy induces persistent changes in gut transit

These changes lead to noticeable modifications in bowel habits.

255
Q

How does cholecystectomy affect gut transit time?

A

It shortens gut transit time

This is due to the accelerated passage of the fecal bolus through the colon.

256
Q

What specific change occurs in the right colon after cholecystectomy?

A

Marked acceleration in the right colon

This contributes to changes in bowel habits.

257
Q

What happens to colonic bile acid output after cholecystectomy?

A

Increase in colonic bile acid output

This leads to a shift towards more diarrheagenic secondary bile acids.

258
Q

What is the most diarrheagenic secondary bile acid that increases after cholecystectomy?

A

Deoxycholic acid

Deoxycholic acid is associated with increased diarrhea.

259
Q

How is postcholecystectomy diarrhea classified?

A

Three or more watery movements per day

This occurs in 5-10% of patients undergoing elective cholecystectomy.

260
Q

What treatment is often effective for troublesome diarrhea postcholecystectomy?

A

Bile acid–sequestering agents

Examples include cholestyramine or colestipol.

261
Q

What does the term hyperplastic cholecystoses refer to?

A

A group of disorders of the gallbladder characterized by excessive proliferation of normal tissue components.

262
Q

What is adenomyomatosis?

A

A benign proliferation of gallbladder surface epithelium with glandlike formations, extramural sinuses, transverse strictures, and/or fundal nodule formation.

263
Q

What characterizes cholesterolosis?

A

Abnormal deposition of lipid, especially cholesteryl esters, within macrophages in the lamina propria of the gallbladder wall.

264
Q

What is the appearance of the gallbladder mucosa in its diffuse form known as ‘strawberry gallbladder’?

A

Brick red and speckled with bright yellow flecks of lipid.

265
Q

In cholesterolosis, what does the localized form show?

A

Solitary or multiple ‘cholesterol polyps’ studding the gallbladder wall.

266
Q

What is the relationship between cholesterol stones and cholesterolosis?

A

Cholesterol stones of the gallbladder are found in nearly half the cases.

267
Q

When is cholecystectomy indicated in cases of adenomyomatosis or cholesterolosis?

A

When biliary symptoms are present.

268
Q

What is the prevalence of gallbladder polyps in the adult population?

A

1–4% with a marked male predominance.

269
Q

List the types of gallbladder polyps.

A
  • Cholesterol polyps
  • Adenomyomas
  • Inflammatory polyps
  • Adenomas (rare)
270
Q

What significant changes have been found over a 5-year period in asymptomatic patients with gallbladder polyps <6 mm?

A

No significant changes.

271
Q

What is recommended for asymptomatic patients >50 years with gallbladder polyps >10 mm?

A

Cholecystectomy.

272
Q

True or False: Cholecystectomy is recommended for all patients with gallbladder polyps.

A

False.

273
Q

Fill in the blank: The gallbladder polyps that show few changes over a 5-year period are those measuring ________.

A

<6 mm or 7–9 mm.

274
Q

What should be done for symptomatic patients with gallbladder polyps?

A

Cholecystectomy is recommended.

275
Q

What does the term hyperplastic cholecystoses refer to?

A

A group of disorders of the gallbladder characterized by excessive proliferation of normal tissue components.

276
Q

What is adenomyomatosis?

A

A benign proliferation of gallbladder surface epithelium with glandlike formations, extramural sinuses, transverse strictures, and/or fundal nodule formation.

277
Q

What characterizes cholesterolosis?

A

Abnormal deposition of lipid, especially cholesteryl esters, within macrophages in the lamina propria of the gallbladder wall.

278
Q

What is the appearance of the gallbladder mucosa in its diffuse form known as ‘strawberry gallbladder’?

A

Brick red and speckled with bright yellow flecks of lipid.

279
Q

In cholesterolosis, what does the localized form show?

A

Solitary or multiple ‘cholesterol polyps’ studding the gallbladder wall.

280
Q

What is the relationship between cholesterol stones and cholesterolosis?

A

Cholesterol stones of the gallbladder are found in nearly half the cases.

281
Q

When is cholecystectomy indicated in cases of adenomyomatosis or cholesterolosis?

A

When biliary symptoms are present.

282
Q

List the types of gallbladder polyps.

A
  • Cholesterol polyps
  • Adenomyomas
  • Inflammatory polyps
  • Adenomas (rare)
283
Q

What is recommended for asymptomatic patients >50 years with gallbladder polyps >10 mm?

A

Cholecystectomy.

284
Q

True or False: Cholecystectomy is recommended for all patients with gallbladder polyps.

A

False.

285
Q

What should be done for symptomatic patients with gallbladder polyps?

A

Cholecystectomy is recommended.

286
Q

What are the most common biliary anomalies encountered in infancy?

A

Atretic and hypoplastic lesions of the extrahepatic and large intrahepatic bile ducts

These anomalies lead to severe obstructive jaundice during the first month of life.

287
Q

What is the typical clinical presentation of biliary atresia in infants?

A

Severe obstructive jaundice and pale stools during the first month of life

These symptoms are critical for early diagnosis.

288
Q

How is the diagnosis of biliary atresia confirmed?

A

Surgical exploration and operative cholangiography

Clinical, laboratory, and imaging findings can suggest biliary atresia.

289
Q

What percentage of biliary atresia cases are treatable with Roux-en-Y choledochojejunostomy?

A

Approximately 10%

The remainder are usually treated with the Kasai procedure.

290
Q

What are common long-term complications for patients with biliary atresia?

A

Chronic cholangitis, extensive hepatic fibrosis, and portal hypertension

These complications can occur even after successful biliary-enteric anastomoses.

291
Q

What is a choledochal cyst?

A

Cystic dilatation of the common bile duct (CBD)

It may also present as diverticulum formation in the intraduodenal segment.

292
Q

What can chronic reflux of pancreatic juice into the biliary tree lead to?

A

Inflammation and stenosis of the extrahepatic bile ducts

This can result in cholangitis or biliary obstruction.

293
Q

At what age do approximately 50% of patients with choledochal cysts present symptoms?

A

After age 10

The onset of symptoms may be gradual.

294
Q

What are the classic triad symptoms of choledochal cysts?

A

Abdominal pain, jaundice, and an abdominal mass

Only one-third of patients exhibit this classic triad.

295
Q

What imaging techniques can diagnose choledochal cysts?

A

Ultrasound, abdominal CT, MRCP, or cholangiography

Ultrasonographic detection of a cyst separate from the gallbladder suggests the diagnosis.

296
Q

What is the surgical treatment for choledochal cysts?

A

Excision of the cyst and biliary-enteric anastomosis

This is necessary to restore normal bile flow.

297
Q

What risk do patients with choledochal cysts face?

A

Increased risk for the subsequent development of cholangiocarcinoma

Regular monitoring is advised due to this risk.

298
Q

What is Caroli’s disease?

A

Dilatation of major intrahepatic bile ducts

It is one of the forms of congenital biliary ectasia.

299
Q

What are common clinical manifestations of Caroli’s disease?

A

Recurrent cholangitis, abscess formation, and brown pigment gallstone formation

These symptoms arise from ectatic intrahepatic biliary radicles.

300
Q

What imaging techniques are useful in diagnosing congenital biliary ectasia?

A

Ultrasound, MRCP, and CT

These methods demonstrate cystic dilatation of the intrahepatic bile ducts.

301
Q

What is Sclerosing Cholangitis (PSC)?

A

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

PSC is strongly associated with inflammatory bowel disease, especially ulcerative colitis.

302
Q

What is the association between IgG4-associated cholangitis and PSC?

A

It presents with biochemical and cholangiographic features indistinguishable from PSC and is often associated with autoimmune pancreatitis

Characterized by elevated serum IgG4 and infiltration of IgG4-positive plasma cells in bile ducts and liver tissue.

303
Q

What should be checked in all patients diagnosed with sclerosing cholangitis?

A

Serum IgG4 level

This is to rule out IgG4 disease as a cause of secondary sclerosing cholangitis, especially if they do not have inflammatory bowel disease.

304
Q

What is the initial treatment of choice for IgG4-associated cholangitis?

A

Glucocorticoids

Relapse is common after steroid withdrawal, especially with proximal strictures.

305
Q

What signs and symptoms do patients with PSC often present with?

A

RUQ abdominal pain, pruritus, jaundice, or acute cholangitis

Late in the course, complications may include complete biliary obstruction, secondary biliary cirrhosis, hepatic failure, or portal hypertension.

306
Q

How is the diagnosis of PSC established?

A

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

This produces a beaded appearance.

307
Q

What are the cholangiographic techniques of choice in suspected cases of PSC?

A

MRCP and ERCP

These techniques help visualize the bile ducts.

308
Q

What is Small Duct PSC?

A

Defined by chronic cholestasis and hepatic histology consistent with PSC in a patient with IBD, but with normal findings on cholangiography

Found in ~5% of patients with PSC, may represent an earlier stage with a better long-term prognosis.

309
Q

What complications can arise from Small Duct PSC?

A

Progression to classic PSC and/or end-stage liver disease

This may necessitate liver transplantation.

310
Q

What biliary tract changes may be seen in patients with AIDS?

A

A broad range of biliary tract changes including pancreatic duct obstruction and occasionally pancreatitis

Associated changes include diffuse intrahepatic bile duct involvement and ampullary stenosis.

311
Q

What are some infectious organisms associated with biliary tract lesions in AIDS?

A
  • Cryptosporidium
  • Mycobacterium avium-intracellulare
  • Cytomegalovirus
  • Microsporidia
  • Isospora

These organisms can cause various biliary tract infections.

312
Q

What procedure can provide significant pain reduction in patients with AIDS-associated papillary stenosis?

A

ERCP sphincterotomy

This procedure helps alleviate pain caused by stenosis.

Gastroenterology (14 decks)

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