Pancreatitis Flashcards
1
Q
What is the daily volume of isosmotic alkaline fluid secreted by the pancreas?
A
1500–3000 mL
This fluid has a pH greater than 8 and contains approximately 20 enzymes.
2
Q
What is the primary function of pancreatic secretions?
A
To provide enzymes and bicarbonate for digestion
These secretions create an optimal pH for enzyme function in the gastrointestinal tract.
3
Q
What stimulates the release of secretin from the duodenal mucosa?
A
Gastric acid
Secretin is released from S cells in the duodenum.
4
Q
What role does secretin play in pancreatic secretion?
A
Stimulates secretion of water and electrolytes from pancreatic ductal cells
Secretin is crucial for maintaining the bicarbonate component of pancreatic secretions.
5
Q
Which substances trigger the release of cholecystokinin (CCK)?
A
Long-chain fatty acids and essential amino acids (tryptophan, phenylalanine, valine, methionine)
Gastric acid also triggers CCK release from Ito cells in the duodenum and proximal jejunum.
6
Q
What type of secretion does CCK evoke from pancreatic acinar cells?
A
Enzyme-rich secretion
CCK plays a crucial role in the digestive enzyme output of the pancreas.
7
Q
How does the parasympathetic nervous system influence pancreatic secretion?
A
Exerts significant control, especially during the cephalic phase
The vagus nerve is the primary pathway for this control.
8
Q
What are the permissive roles of vagal pathways in pancreatic secretion?
A
Essential for enzyme secretion; less so for water and bicarbonate
Hormonal effects of secretin and CCK are more critical for the latter.
9
Q
What is the role of vasoactive intestinal peptide (VIP) in pancreatic secretion?
A
Acts as a secretin agonist
Vagal stimulation can enhance the release of VIP.
10
Q
Name two inhibitory neuropeptides that influence pancreatic exocrine secretion.
A
Somatostatin and pancreatic polypeptide
Other inhibitory neuropeptides include peptide YY, neuropeptide Y, enkephalin, pancreastatin, calcitonin gene-related peptides, glucagon, and galanin.
11
Q
True or False: Somatostatin acts only at one site to inhibit pancreatic secretion.
A
False
Somatostatin acts at multiple sites throughout the body.
12
Q
What is the ion of primary physiologic importance within pancreatic secretion?
A
Bicarbonate
Bicarbonate plays a crucial role in various digestive processes.
13
Q
What percentage of bicarbonate in pancreatic secretion is derived from plasma?
A
93%
The remaining 7% comes from intracellular metabolism.
14
Q
How does bicarbonate enter the duct lumen?
A
Through the sodium bicarbonate cotransporter
This process is influenced by depolarization caused by chloride efflux.
15
Q
What role do secretin and VIP play in bicarbonate secretion?
A
They bind at the basolateral surface and increase intracellular cyclic AMP
This action opens the CFTR on the apical surface, promoting secretion.
16
Q
What is the effect of CCK on the secretion of bicarbonate?
A
It markedly potentiates the stimulatory effects of secretin
CCK acts as a neuromodulator in this process.
17
Q
Which neurotransmitter plays an important role in ductal cell secretion?
A
Acetylcholine
Acetylcholine enhances the secretion process in ductal cells.
18
Q
What is one of the functions of intraluminal bicarbonate secreted from ductal cells?
A
Helps neutralize gastric acid
This is crucial for maintaining a suitable environment for digestive enzymes.
19
Q
Name two additional functions of intraluminal bicarbonate.
A
- Increases the solubility of fatty acids and bile acids
- Maintains an optimal pH for pancreatic and brush border enzymes
Prevents intestinal mucosal damage as well.
20
Q
True or False: Bicarbonate secretion from ductal cells is only important for neutralizing gastric acid.
A
False
Bicarbonate also plays roles in solubility, pH maintenance, and mucosal protection.
21
Q
What is the primary function of the acinar cell in the pancreas?
A
Production and secretion of pancreatic enzymes
Acinar cells are specialized for synthesizing and secreting digestive enzymes.
22
Q
Where are proteins synthesized in acinar cells processed?
A
In the Golgi
Proteins synthesized by the rough endoplasmic reticulum are processed in the Golgi before secretion.
23
Q
What are the three main types of enzymes secreted by the pancreas?
A
Amylolytic, lipolytic, and proteolytic enzymes
These enzymes aid in the digestion of carbohydrates, fats, and proteins respectively.
24
Q
What is the role of amylolytic enzymes?
A
Hydrolyze starch to oligosaccharides and maltose
Amylase is a key enzyme in this process.
25
List the lipolytic enzymes secreted by the pancreas.
* Lipase
* Phospholipase A2
* Cholesterol esterase
## Footnote
These enzymes are involved in lipid digestion.
26
How do bile salts affect lipase activity?
Inhibit lipase in isolation
## Footnote
Colipase binds to lipase to prevent this inhibition.
27
What are the two types of proteolytic enzymes found in pancreatic secretions?
* Endopeptidases
* Exopeptidases
## Footnote
Endopeptidases include trypsin and chymotrypsin; exopeptidases include carboxypeptidases and aminopeptidases.
28
What is the function of enterokinase?
Cleaves trypsinogen to form trypsin
## Footnote
Enterokinase is located in the duodenal mucosa and initiates the activation of proteolytic zymogens.
29
What triggers pancreatic enzyme secretion?
Neurologic stimulation
## Footnote
This stimulation is primarily cholinergic and involves the vagus nerve.
30
What neurotransmitters are involved in stimulating pancreatic enzyme secretion?
* Acetylcholine
* Gastrin-releasing peptides
## Footnote
These neurotransmitters activate calcium-dependent secondary messenger systems.
31
What is the role of VIP in pancreatic function?
Potentiates the effect of acetylcholine
## Footnote
VIP is present in intrapancreatic nerves.
32
True or False: Humans have CCK receptors on acinar cells.
False
## Footnote
In contrast to other species, humans lack CCK receptors on acinar cells.
33
What is the effect of CCK in physiological concentrations on pancreatic secretion?
Stimulates pancreatic secretion
## Footnote
CCK stimulates afferent vagal and intrapancreatic nerves.
34
What is the process that prevents autodigestion of the pancreas?
Autoprotection of the pancreas
## Footnote
Autoprotection mechanisms include packaging of pancreatic proteases, calcium homeostasis, acid-base balance, and synthesis of protease inhibitors.
35
Name one mechanism that prevents autodigestion of the pancreas.
Packaging of pancreatic proteases in the precursor form
## Footnote
This refers to the storage of enzymes in inactive forms to prevent premature activation.
36
What role does intracellular calcium homeostasis play in pancreatic protection?
Low intracellular calcium in acinar cells promotes destruction of spontaneously activated trypsin
## Footnote
This helps prevent the activation of digestive enzymes within the pancreas.
37
What is the function of pancreatic secretory trypsin inhibitor (PSTI)?
Binds and inactivates ~20% of intracellular trypsin activity
## Footnote
PSTI is crucial for preventing autodigestion by inhibiting activated trypsin.
38
What other protease can lyse and inactivate trypsin?
Chymotrypsin C
## Footnote
This protease also plays a role in protecting the pancreas by inactivating trypsin.
39
What happens if any of the protective mechanisms of the pancreas fail?
Leads to premature enzyme activation, autodigestion, and ultimately acute pancreatitis
## Footnote
This highlights the importance of these protective mechanisms in maintaining pancreatic health.
40
What mechanism controls pancreatic enzyme secretion?
A negative feedback mechanism induced by active serine proteases and nutrients in the distal small intestine
## Footnote
This mechanism ensures that enzyme secretion is appropriately regulated based on the digestive needs.
41
What effect does perfusion of the duodenal lumen with phenylalanine have?
It causes a prompt increase in plasma CCK levels and increased secretion of chymotrypsin and other pancreatic enzymes
## Footnote
Phenylalanine stimulates early digestion.
42
What effect does simultaneous perfusion with trypsin have on pancreatic enzyme secretion?
It blunts the responses induced by phenylalanine
## Footnote
Trypsin stimulates late digestion.
43
What happens when the duodenal lumen is perfused with protease inhibitors?
It leads to enzyme hypersecretion
## Footnote
This indicates that protease activity is important for regulating enzyme secretion.
44
What peptide is involved in stimulating CCK release in the duodenum?
CCK-releasing factor (CCK-RF)
## Footnote
CCK-RF is released in response to dietary proteins.
45
How do serine proteases inhibit pancreatic secretion?
By inactivating a CCK-releasing peptide in the lumen of the small intestine
## Footnote
This is part of the feedback mechanism that regulates enzyme secretion.
46
What is the role of secretin in pancreatic secretion?
It stimulates vagal and other neural pathways to activate pancreatic duct cells to secrete bicarbonate
## Footnote
Secretin is released in response to acidification of the duodenum.
47
What is the purpose of bicarbonate secretion in the duodenum?
To neutralize the duodenal acid
## Footnote
This is crucial for creating an optimal environment for enzyme activity.
48
What is the relationship between dietary proteins and CCK-RF?
Dietary proteins bind proteases, leading to an increase in free CCK-RF
## Footnote
This enhances CCK release into the blood.
49
How does CCK primarily act to mediate pancreatic enzyme secretion?
Through neural pathways (vagal-vagal)
## Footnote
This leads to acetylcholine-mediated secretion.
50
When is pancreatic protease secretion reduced?
When the protein within the duodenum is digested
## Footnote
This marks the completion of the feedback process for enzyme secretion.
51
What additional hormones provide feedback inhibition of pancreatic enzyme secretion?
Peptide YY and glucagon-like peptide-1
## Footnote
This occurs following lipid or carbohydrate exposure to the ileum.
52
What are the leading causes of acute pancreatitis in the United States?
Gallstones and alcohol account for 80–90% of identified cases
## Footnote
Gallstones: 30–60%, Alcohol: 15–30%
53
What is the risk of acute pancreatitis in patients with at least one gallstone less than 5 mm in diameter compared to those with larger stones?
Fourfold greater risk
54
What factors besides alcohol ingestion can affect a person's susceptibility to pancreatic injury?
* Cigarette smoking
* Genetic predisposition
55
What percentage of patients experience acute pancreatitis following endoscopic retrograde cholangiopancreatography (ERCP)?
5–10%
56
How can the risk of post-ERCP pancreatitis be decreased?
* Proper patient selection
* Prophylactic pancreatic duct stent
* Rectal NSAIDs (e.g., indomethacin)
57
What are some risk factors for post-ERCP pancreatitis?
* Minor papilla sphincterotomy
* Suspected sphincter of Oddi dysfunction
* Prior history of post-ERCP pancreatitis
* Age <60 years
* More than two contrast injections into the pancreatic duct
* Endoscopist experience
58
What percentage of acute pancreatitis cases is caused by hypertriglyceridemia?
1–4%
59
What are typical serum triglyceride levels in patients with hypertriglyceridemic pancreatitis?
>1000 mg/dL
60
What underlying condition is most common in patients with hypertriglyceridemic pancreatitis?
Undiagnosed or uncontrolled diabetes mellitus
61
What can precipitate a bout of acute pancreatitis in patients with hypertriglyceridemia?
* Alcohol
* Medications (e.g., oral contraceptives)
62
What is the role of apolipoprotein CII in lipid metabolism?
Activates lipoprotein lipase, important for clearing chylomicrons from bloodstream
63
What percentage of acute pancreatitis cases are drug-related?
<2%
64
How do drugs typically cause pancreatitis?
* Hypersensitivity reaction
* Generation of a toxic metabolite
65
What are the two forms of acute pancreatitis based on pathology?
* Interstitial pancreatitis
* Necrotizing pancreatitis
66
What is the pathogenic theory of autodigestion in acute pancreatitis?
Activation of proteolytic enzymes in the pancreas acinar cell compartment rather than in the intestinal lumen
67
What factors are believed to facilitate premature activation of trypsin in acute pancreatitis?
* Endotoxins
* Exotoxins
* Viral infections
* Ischemia
* Oxidative stress
* Lysosomal calcium
* Direct trauma
68
What is the consequence of activated proteolytic enzymes in acute pancreatitis?
Digest pancreatic and peripancreatic tissues and activate other enzymes
69
What is a potential result of spontaneous activation of trypsin?
Autodigestion
70
What are the three phases of pancreatitis?
1. Intrapancreatic digestive enzyme activation and acinar cell injury
2. Activation, chemoattraction, and sequestration of leukocytes and macrophages
3. Effects of activated proteolytic enzymes and cytokines on distant organs
## Footnote
These phases illustrate the progression of the disease and its systemic effects.
71
What mediates trypsin activation in pancreatitis?
Lysosomal hydrolases such as cathepsin B
## Footnote
Cathepsin B colocalizes with digestive enzymes in intracellular organelles.
72
What is the consequence of trypsin activation in the pancreas?
Acinar cell injury
## Footnote
Trypsin activation leads to damage of pancreatic cells.
73
What happens in the second phase of pancreatitis?
Activation, chemoattraction, and sequestration of leukocytes and macrophages in the pancreas
## Footnote
This phase enhances the intrapancreatic inflammatory reaction.
74
What effect does neutrophil depletion have in experimental pancreatitis?
Reduces the severity of pancreatitis
## Footnote
Induced by prior administration of an antineutrophil serum.
75
What role do neutrophils play in trypsinogen activation?
Neutrophils can activate trypsinogen
## Footnote
Suggests a two-step activation process involving neutrophils.
76
What are the consequences of activated proteolytic enzymes in the third phase of pancreatitis?
Digest pancreatic and peripancreatic tissues, activate other enzymes, and cause cellular injury
## Footnote
This leads to vascular damage, coagulation necrosis, and fat necrosis.
77
What are the systemic effects of bradykinin peptides and vasoactive substances released during pancreatitis?
Vasodilation, increased vascular permeability, and edema
## Footnote
These effects can profoundly impact other organs.
78
What syndrome may occur as a result of the cascade of effects during pancreatitis?
Systemic inflammatory response syndrome (SIRS) and acute respiratory distress syndrome (ARDS)
## Footnote
These conditions may lead to multiorgan failure.
79
List the six genetic variants associated with susceptibility to pancreatitis.
* Cationic trypsinogen gene (PRSS1)
* Pancreatic secretory trypsin inhibitor (SPINK1)
* Cystic fibrosis transmembrane conductance regulator gene (CFTR)
* Chymotrypsin C gene (CTRC)
* Calcium-sensing receptor (CASR)
* Claudin-2 (CLDN2)
## Footnote
These variants are linked to the control of trypsin activity.
80
Which genetic variant is sufficient to precipitate acute pancreatitis without other risk factors?
PRSS1 mutations
## Footnote
Other variants serve as disease modifiers.
81
What is the major symptom of acute pancreatitis?
Abdominal pain
## Footnote
Abdominal pain can vary from mild discomfort to severe, constant distress.
82
Describe the character and location of pain in acute pancreatitis.
Steady and boring in character, located in the epigastrium region
## Footnote
Pain may radiate to the back, chest, flanks, and lower abdomen.
83
What are common additional symptoms associated with abdominal pain in acute pancreatitis?
* Nausea
* Vomiting
* Abdominal distention
## Footnote
Abdominal distention is due to gastric and intestinal hypomotility.
84
What physical examination findings may be observed in a patient with acute pancreatitis?
* Distressed and anxious patient
* Low-grade fever
* Tachycardia
* Hypotension
## Footnote
Shock may occur due to various factors.
85
What are the potential causes of shock in acute pancreatitis?
* Hypovolemia from exudation of blood and plasma proteins
* Increased formation and release of kinin peptides
* Systemic effects of proteolytic and lipolytic enzymes
## Footnote
These factors contribute to vasodilation and increased vascular permeability.
86
Under what circumstances does jaundice occur in acute pancreatitis?
When there is extrinsic compression or intraductal obstruction
## Footnote
Compression may be due to peripancreatic edema or pancreatic head mass.
87
What rare skin manifestation can occur in acute pancreatitis?
Erythematous skin nodules due to subcutaneous fat necrosis
## Footnote
These occurrences are rare.
88
What pulmonary findings may be present in 10–20% of patients with acute pancreatitis?
* Basilar rales
* Atelectasis
* Pleural effusion
## Footnote
Pleural effusion is most frequently left-sided.
89
What abdominal signs are commonly observed in acute pancreatitis?
* Abdominal tenderness
* Muscle rigidity
## Footnote
These signs may be less impressive compared to the intense pain.
90
What changes in bowel sounds are typically noted in acute pancreatitis?
Diminished or absent bowel sounds
## Footnote
This is associated with the condition.
91
What might be palpable in the upper abdomen later in the course of acute pancreatitis?
An enlarged pancreas
## Footnote
This may be due to acute fluid collection, walled-off necrosis, or a pseudocyst.
92
What does Cullen’s sign indicate in the context of acute pancreatitis?
Faint blue discoloration around the umbilicus
## Footnote
This may result from hemoperitoneum.
93
What does Turner’s sign reflect in severe necrotizing pancreatitis?
Blue-red-purple or green-brown discoloration of the flanks
## Footnote
This indicates tissue breakdown of hemoglobin from hemorrhage.
94
True or False: Shock is a common occurrence in acute pancreatitis.
True
## Footnote
Shock may arise from various underlying causes.
95
What serum amylase and lipase values are strongly supportive of the diagnosis of pancreatitis?
Values threefold or more above normal
## Footnote
This is valid if alternate etiologies are excluded.
96
Is there a correlation between the severity of pancreatitis and the degree of serum lipase and amylase elevations?
No correlation exists
## Footnote
The severity of pancreatitis does not correlate with elevation levels.
97
How long may pancreatic lipase levels remain elevated in pancreatitis?
7–14 days
## Footnote
Total serum amylase values may return toward normal after 3–7 days.
98
What can cause spurious elevations in serum amylase?
Acidemia (arterial pH ≤7.32)
## Footnote
This is particularly relevant in patients with diabetic ketoacidosis.
99
What effect does severe hypertriglyceridemia have on serum amylase levels?
Serum amylase levels can be spuriously low
## Footnote
This can complicate the evaluation of pancreatitis.
100
Which enzyme is considered more specific for diagnosing pancreatitis, amylase or lipase?
Lipase
## Footnote
Serum lipase activity increases in parallel with amylase activity.
101
What leukocyte count is indicative of leukocytosis in pancreatitis?
15,000–20,000 leukocytes/μL
## Footnote
Leukocytosis is common in patients with pancreatitis.
102
What hematocrit value may indicate hemoconcentration and more severe disease?
>44%
## Footnote
Hemoconcentration is a harbinger of more severe disease.
103
What is a significant risk factor for mortality in pancreatitis patients?
Prerenal azotemia with BUN >22 mg/dL
## Footnote
This results from loss of plasma into the retroperitoneal space and peritoneal cavity.
104
What is a common metabolic change in pancreatitis patients related to blood glucose?
Hyperglycemia
## Footnote
Caused by decreased insulin release and increased glucagon release.
105
In what percentage of pancreatitis patients does hypocalcemia occur?
~25%
## Footnote
The pathogenesis of hypocalcemia is incompletely understood.
106
What is 'soap formation' in the context of pancreatitis?
Intraperitoneal saponification of calcium by fatty acids
## Footnote
Occurs occasionally with large amounts dissolved in ascitic fluid.
107
What serum bilirubin level is classified as hyperbilirubinemia in pancreatitis?
>4.0 mg/dL
## Footnote
Jaundice is typically transient and resolves in 4–7 days.
108
What alanine aminotransferase (ALT) elevation is associated with gallstone etiology in acute pancreatitis?
>3× the upper limit of normal
## Footnote
This elevation indicates a gallstone cause in acute pancreatitis.
109
What percentage of patients may experience hypoxemia in pancreatitis?
5–10%
## Footnote
Hypoxemia may herald the onset of ARDS.
110
What abnormalities may be seen on an electrocardiogram in acute pancreatitis?
ST-segment and T-wave abnormalities
## Footnote
These can simulate myocardial ischemia.
111
What is the recommended initial diagnostic imaging modality for pancreatitis?
Abdominal ultrasound
## Footnote
It is useful to evaluate for gallstones and common bile duct dilation.
112
What are the morphologic features of acute pancreatitis outlined in the Revised Atlanta Criteria?
1. Interstitial pancreatitis
* 2. Necrotizing pancreatitis
* 3. Acute pancreatic fluid collection
* 4. Pancreatic pseudocyst
* 5. Acute necrotic collection (ANC)
* 6. Walled-off necrosis (WON)
## Footnote
These features are assessed via computed tomography (CT) scan.
113
What should any severe acute pain in the abdomen or back suggest?
The possibility of acute pancreatitis
## Footnote
Severe acute pain can be indicative of various conditions, but in this context, acute pancreatitis is a key consideration.
114
What are the three criteria for diagnosing acute pancreatitis?
1. Typical abdominal pain in the epigastrium that may radiate to the back
2. Threefold or greater elevation in serum lipase and/or amylase
3. Confirmatory findings on cross-sectional abdominal imaging
## Footnote
At least two of these criteria must be met for a diagnosis of acute pancreatitis.
115
What are markers of severity in acute pancreatitis?
1. Hemoconcentration (hematocrit >44%)
2. Admission azotemia (BUN >22 mg/dL)
3. SIRS
4. Signs of organ failure
## Footnote
These markers may indicate a more severe case of acute pancreatitis.
116
List five disorders that should be included in the differential diagnosis of acute pancreatitis.
* Perforated viscus, especially peptic ulcer
* Acute cholecystitis and biliary colic
* Acute intestinal obstruction
* Mesenteric vascular occlusion
* Renal colic
## Footnote
The differential diagnosis is critical to rule out other potential causes of similar symptoms.
117
Which condition may be difficult to differentiate from acute pancreatitis due to elevated serum amylase?
Acute cholecystitis
## Footnote
Both acute pancreatitis and acute cholecystitis can present with elevated serum amylase, complicating diagnosis.
118
How can pain of biliary tract origin be characterized compared to pancreatitis pain?
Pain of biliary tract origin is more right sided or epigastric than periumbilical or left upper quadrant and can be more severe; ileus is usually absent
## Footnote
Understanding the pain characteristics is essential for diagnosis.
119
What imaging technique is helpful in diagnosing cholelithiasis and cholecystitis?
Ultrasound
## Footnote
Ultrasound is a non-invasive method that can provide critical information for these conditions.
120
What differentiates intestinal obstruction due to mechanical factors from pancreatitis?
History of crescendo-decrescendo pain, findings on abdominal examination, and CT showing changes characteristic of mechanical obstruction
## Footnote
These diagnostic clues help in distinguishing between the two conditions.
121
What is usually suspected in elderly debilitated patients with leukocytosis, abdominal distention, and bloody diarrhea?
Acute mesenteric vascular occlusion
## Footnote
This condition often presents with specific symptoms that can lead to its identification.
122
Which vasculitides may be confused with pancreatitis?
1. Systemic lupus erythematosus
2. Polyarteritis nodosa
## Footnote
These systemic conditions can lead to pancreatitis as a complication.
123
True or False: Diabetic ketoacidosis is often accompanied by elevated serum lipase levels.
False
## Footnote
While diabetic ketoacidosis may present with abdominal pain and elevated serum amylase, serum lipase levels are usually not elevated.
124
What are the two phases of acute pancreatitis defined by the Revised Atlanta Criteria?
Early (<2 weeks) and late (>2 weeks)
## Footnote
These phases describe the hospital course of the disease.
125
How is severity defined in the early phase of acute pancreatitis?
By clinical parameters rather than morphologic findings
## Footnote
Most patients exhibit SIRS, and persistent SIRS predisposes to organ failure.
126
What are the three organ systems assessed to define organ failure in acute pancreatitis?
* Respiratory
* Cardiovascular
* Renal
## Footnote
Organ failure is defined as a score of 2 or more for one of these organ systems using the modified Marshall scoring system.
127
What is considered persistent organ failure in acute pancreatitis?
Organ failure lasting more than 48 hours
## Footnote
This is the most important clinical finding regarding the severity of the acute pancreatitis episode.
128
What constitutes multisystem organ failure in acute pancreatitis?
Organ failure affecting more than one organ
## Footnote
This indicates a more severe clinical condition.
129
Is CT imaging recommended during the first 48 hours of admission in acute pancreatitis?
No, it is usually not needed or recommended
## Footnote
This is especially true in the early phase.
130
What characterizes the late phase of acute pancreatitis?
A protracted course of illness requiring imaging to evaluate for local complications
## Footnote
The critical clinical parameter remains persistent organ failure.
131
What supportive measures may be required in the late phase of acute pancreatitis?
* Renal dialysis
* Ventilator support
* Supplemental nutrition via nasojejunal or parenteral route
## Footnote
These measures are critical for patient management during this phase.
132
What is the radiographic feature of greatest importance in the late phase of acute pancreatitis?
Development of necrotizing pancreatitis on CT imaging
## Footnote
Necrosis is associated with prolonged hospitalization and may require intervention if infected.
133
True or False: Infected necrosis in acute pancreatitis may require surgical intervention.
True
## Footnote
Intervention can be percutaneous, endoscopic, and/or surgical depending on the clinical scenario.
134
What are the three classes of severity defined for acute pancreatitis?
Mild, moderately severe, and severe
## Footnote
Each class has distinct characteristics and management strategies.
135
What defines mild acute pancreatitis?
Without local complications or organ failure
## Footnote
Most patients with interstitial acute pancreatitis have mild pancreatitis.
136
How long does mild acute pancreatitis typically last?
3–7 days after onset
## Footnote
The disease is self-limited and subsides spontaneously.
137
What dietary recommendations are given for patients recovering from mild acute pancreatitis?
Clear or full liquid diet; low-fat solid diet after recovery
## Footnote
Oral intake can resume if the patient is hungry and has normal bowel function.
138
What characterizes moderately severe acute pancreatitis?
Transient organ failure or local/systemic complications without persistent organ failure
## Footnote
Mortality rate remains low for these patients.
139
What is the duration of organ failure in severe acute pancreatitis?
Persistent organ failure for more than 48 hours
## Footnote
It can involve one or more organs.
140
What imaging studies should be obtained in severe acute pancreatitis?
CT scan or magnetic resonance imaging (MRI)
## Footnote
These help assess for necrosis and/or complications.
141
What management steps are taken if a local complication is encountered in severe acute pancreatitis?
Management is dictated by clinical symptoms, evidence of infection, maturity of fluid collection, and clinical stability
## Footnote
Each case may require a tailored approach.
142
True or False: Prophylactic antibiotics are recommended for severe acute pancreatitis.
False
## Footnote
Prophylactic antibiotics are no longer recommended.
143
What can happen to patients with moderately severe acute pancreatitis regarding hospitalization?
Prolonged hospitalization greater than 1 week
## Footnote
This may occur if local complications develop.
144
What are the two types of pancreatitis recognized on imaging?
Interstitial and necrotizing pancreatitis
145
When is CT imaging with IV contrast best evaluated for acute pancreatitis?
3–5 days into hospitalization if patients are not responding to supportive care
146
What does the Revised Atlanta Criteria outline?
Terminology for local complications and fluid collections along with a CT imaging template
147
What is the percentage of admissions for acute pancreatitis that are classified as interstitial pancreatitis?
90–95%
148
What are the characteristics of interstitial pancreatitis?
Diffuse gland enlargement, homogenous contrast enhancement, mild inflammatory changes or peripancreatic stranding
149
What is the typical resolution time for symptoms in interstitial pancreatitis?
Generally resolves within a week of hospitalization
150
What percentage of acute pancreatitis admissions are classified as necrotizing pancreatitis?
5–10%
151
What are the imaging characteristics of necrotizing pancreatitis?
Lack of pancreatic parenchymal enhancement by IV contrast and/or presence of peripancreatic necrosis
152
What is the natural history of pancreatic and peripancreatic necrosis?
Variable; may remain solid or liquefy, remain sterile or become infected, and persist or disappear over time
153
What is the prognosis for patients with only extrapancreatic necrosis compared to those with pancreatic necrosis?
More favorable prognosis
154
Why is CT identification of local complications critical in acute pancreatitis?
Patients with infected and sterile necrosis are at greatest risk of mortality
155
What is the median prevalence of organ failure in necrotizing pancreatitis?
>50%
156
What is the mortality rate with single-organ system failure in necrotizing pancreatitis?
3–10%
157
What is the mortality rate with multiorgan failure in necrotizing pancreatitis?
Nearly 50%
158
Fill in the blank: Interstitial pancreatitis is characterized by _______.
Diffuse gland enlargement, homogenous contrast enhancement, mild inflammatory changes or peripancreatic stranding
159
True or False: Necrotizing pancreatitis may not evolve until several days of hospitalization.
True
160
What is the typical duration for most cases of acute pancreatitis to subside?
3–7 days
## Footnote
85–90% of cases are self-limited and resolve spontaneously.
161
What is the first step in managing acute pancreatitis in the emergency ward?
Early and aggressive fluid resuscitation
## Footnote
This is critical after diagnosis confirmation.
162
What type of medication is administered to patients with acute pancreatitis for pain management?
Intravenous analgesics
## Footnote
Pain management is essential in the management process.
163
What should be assessed after confirming the diagnosis of acute pancreatitis?
Severity of the condition
## Footnote
Assessment of severity helps guide further management.
164
What should be done for patients who do not respond to aggressive fluid resuscitation?
Consider admission to a step-down or intensive care unit
## Footnote
This allows for further monitoring and management.
165
True or False: Most cases of acute pancreatitis exhibit organ failure or local complications.
False
## Footnote
Most cases are self-limited and do not exhibit organ failure.
166
What is the primary goal of the management of acute pancreatitis?
To ensure patient stability and prevent complications
## Footnote
Management focuses on supportive care.
167
Fill in the blank: 85–90% of acute pancreatitis cases are _______.
self-limited
## Footnote
These cases typically resolve without significant intervention.
168
What is the most important treatment intervention for acute pancreatitis?
Early, aggressive intravenous fluid resuscitation to prevent systemic complications from the secondary systemic inflammatory response.
169
What types of intravenous fluids are recommended for initial bolus in acute pancreatitis?
Lactated Ringer’s or normal saline.
170
What is the initial bolus amount of intravenous fluids for acute pancreatitis?
15–20 mL/kg (1050–1400 mL).
171
What is the recommended maintenance fluid rate after the initial bolus in acute pancreatitis?
2–3 mL/kg per hour (200–250 mL/h).
172
What is the target urine output to maintain during fluid resuscitation?
Urine output >0.5 mL/kg per hour.
173
How often should serial bedside evaluations be performed to assess fluid resuscitation?
Every 6–8 hours.
174
What two measurements are recommended every 8–12 hours to monitor response to therapy?
Hematocrit and BUN (blood urea nitrogen).
175
What is a strong indication that sufficient fluids are being administered during the first 12–24 hours?
A decrease in hematocrit and BUN.
176
What should be done if a rise in hematocrit or BUN is observed during serial measurement?
Treat with a repeat volume challenge with a 2-L crystalloid bolus followed by increasing the fluid rate by 1.5 mg/kg per hour.
177
True or False: A rising BUN during hospitalization is associated with inadequate hydration and higher in-hospital mortality.
True.
178
What should be considered if BUN or hematocrit fails to respond to the bolus challenge?
Transfer to an intensive care unit for hemodynamic monitoring.
179
What solution has been shown to decrease systemic inflammation in acute pancreatitis?
Lactated Ringer’s solution.
180
What should be determined in the emergency ward for acute pancreatitis patients?
Severity of acute pancreatitis to assist in patient triage
181
What is the Bedside Index of Severity in Acute Pancreatitis (BISAP)?
A scoring system incorporating five clinical and laboratory parameters
182
List the five parameters used in the BISAP score.
* BUN >25 mg/dL
* Impaired mental status (Glasgow coma scale score <15)
* SIRS
* Age >60 years
* Pleural effusion on radiography
183
What is the significance of having three or more BISAP factors present?
Associated with substantially increased risk for in-hospital mortality
184
What hematocrit level is associated with more severe acute pancreatitis?
Elevated hematocrit >44%
185
What admission BUN level is associated with more severe acute pancreatitis?
Admission BUN >22 mg/dL
186
How can the indices from BISAP and patient response to initial fluid resuscitation be used?
To triage patients to the appropriate hospital acute care setting
187
What is the expected response for patients with lower BISAP scores?
They tend to respond to initial management and can be safely triaged to a regular hospital ward
188
What does the absence of SIRS at 24 hours indicate?
The patient is unlikely to develop organ failure or necrosis
189
What should be considered for patients with persistent SIRS at 24 hours?
Consider for a step-down unit setting if available
190
What conditions should lead to consideration for direct admission to an intensive care unit?
Higher BISAP scores, elevations in hematocrit and admission BUN, lack of response to initial fluid resuscitation, and evidence of respiratory failure, hypotension, or organ failure
191
What is recommended in the emergency ward to assess for etiologies that may impact acute management?
A careful history, review of medications, selected laboratory studies, and an abdominal ultrasound
## Footnote
Laboratory studies include liver profile, serum triglycerides, and serum calcium. The abdominal ultrasound evaluates the gallbladder, common bile duct, and pancreatic head.
192
What is the initial imaging modality of choice for assessing gallstone pancreatitis?
Abdominal ultrasound
193
What should patients with evidence of ascending cholangitis undergo within 24–48 hours of admission?
ERCP
194
What procedure should be considered for patients with mild acute pancreatitis during the same admission?
Cholecystectomy
195
What is an alternative for patients who are not surgical candidates for gallstone pancreatitis?
Endoscopic biliary sphincterotomy
196
What serum triglyceride level is associated with acute pancreatitis?
>1000 mg/dL
197
What is the initial therapy for hypertriglyceridemia in acute pancreatitis?
Intravenous insulin
198
What adjunct therapies may be considered for hypertriglyceridemia, despite lacking compelling evidence of improved outcomes?
Heparin, plasmapheresis
199
What outpatient therapies are recommended for hypertriglyceridemia?
Control of diabetes, lipid-lowering agents, weight loss, avoidance of drugs that elevate lipid levels
200
What other potential etiologies may impact acute hospital care?
Hypercalcemia, post-ERCP pancreatitis
201
What methods are effective at decreasing pancreatitis after ERCP?
Pancreatic duct stenting, rectal indomethacin administration
202
True or False: There is compelling evidence that heparin or plasmapheresis improve clinical outcomes in hypertriglyceridemia.
False
203
What type of diet can be administered to subjects with mild acute pancreatitis once they are able to eat?
A low-fat solid diet
## Footnote
This diet is appropriate for individuals who have mild acute pancreatitis and can resume eating.
204
When should enteral nutrition be considered for subjects with more severe pancreatitis?
2–3 days after admission
## Footnote
This recommendation is made instead of total parenteral nutrition (TPN).
205
What are the advantages of enteral feeding over total parenteral nutrition (TPN)?
* Maintains gut barrier integrity
* Limits bacterial translocation
* Less expensive
* Fewer complications
## Footnote
Enteral feeding is preferred for patients with pancreatitis due to these benefits.
206
Is gastric feeding considered safe for patients with pancreatitis?
Yes
## Footnote
Gastric feeding is deemed safe; however, the advantages of nasojejunal enteral feeding over gastric feeding are still being researched.
207
True or False: Total parenteral nutrition (TPN) is preferred over enteral nutrition in severe pancreatitis cases.
False
## Footnote
Enteral nutrition is recommended over TPN for patients with severe pancreatitis.
208
What should be assessed in patients exhibiting signs of clinical deterioration despite aggressive fluid resuscitation?
Local complications, which may include necrosis, pseudocyst formation, pancreas duct disruption, peripancreatic vascular complications, and extrapancreatic infections.
## Footnote
A multidisciplinary team approach is recommended for assessment.
209
What is the recommended approach for managing necrosis?
A multidisciplinary team approach.
## Footnote
This includes specialists from gastroenterology, surgery, interventional radiology, and intensive care.
210
What diagnostic procedure was previously performed to evaluate infected pancreatic necrosis?
Percutaneous fine-needle aspiration of necrosis with Gram stain and culture.
## Footnote
This was typically done in patients with sustained leukocytosis, fever, or organ failure.
211
Why has the use of percutaneous fine-needle aspiration decreased in some institutions?
To avoid potentially contaminating an otherwise sterile collection.
## Footnote
Culture results may not lead to a clinical decision to de-escalate antimicrobial therapy.
212
Should prophylactic antibiotics be used in necrotizing pancreatitis?
No, prophylactic antibiotics do not lead to improved survival and may promote opportunistic fungal infections.
## Footnote
Empiric antibiotics should be considered in those with clinical decompensation.
213
What imaging should be considered with any change in clinical course for patients with necrosis?
Repeated CT or MRI imaging.
## Footnote
This is to monitor for complications such as thromboses, hemorrhage, or abdominal compartment syndrome.
214
How is sterile necrosis generally managed?
Conservatively, unless complications arise.
## Footnote
Targeted antibiotics should be instituted once infected necrosis is established.
215
What is the step-up approach in managing infected pancreatic necrosis?
Percutaneous or endoscopic transgastric/transduodenal drainage followed by surgical necrosectomy if necessary.
## Footnote
This approach has been successful in some pancreatic centers.
216
What is the outcome for one-third of patients treated with the step-up approach?
They did not require major abdominal surgery.
## Footnote
This highlights the effectiveness of the conservative management strategy.
217
What did a randomized trial report regarding the initial approach for symptomatic WON?
Advantages to an initial endoscopic approach compared to an initial surgical necrosectomy approach.
## Footnote
This is relevant for select patients requiring intervention.
218
For how long should conservative therapy be implemented before considering intervention?
4–6 weeks.
## Footnote
This allows pancreatic collections to resolve or develop a more organized boundary.
219
What should be assessed in patients exhibiting signs of clinical deterioration despite aggressive fluid resuscitation?
Local complications, which may include necrosis, pseudocyst formation, pancreas duct disruption, peripancreatic vascular complications, and extrapancreatic infections.
## Footnote
A multidisciplinary team approach is recommended for assessment.
220
What diagnostic procedure was previously performed to evaluate infected pancreatic necrosis?
Percutaneous fine-needle aspiration of necrosis with Gram stain and culture.
## Footnote
This was typically done in patients with sustained leukocytosis, fever, or organ failure.
221
Should prophylactic antibiotics be used in necrotizing pancreatitis?
No, prophylactic antibiotics do not lead to improved survival and may promote opportunistic fungal infections.
## Footnote
Empiric antibiotics should be considered in those with clinical decompensation.
222
What imaging should be considered with any change in clinical course for patients with necrosis?
Repeated CT or MRI imaging.
## Footnote
This is to monitor for complications such as thromboses, hemorrhage, or abdominal compartment syndrome.
223
How is sterile necrosis generally managed?
Conservatively, unless complications arise.
## Footnote
Targeted antibiotics should be instituted once infected necrosis is established.
224
What is the step-up approach in managing infected pancreatic necrosis?
Percutaneous or endoscopic transgastric/transduodenal drainage followed by surgical necrosectomy if necessary.
## Footnote
This approach has been successful in some pancreatic centers.
225
What is the outcome for one-third of patients treated with the step-up approach?
They did not require major abdominal surgery.
## Footnote
This highlights the effectiveness of the conservative management strategy.
226
For how long should conservative therapy be implemented before considering intervention?
4–6 weeks.
## Footnote
This allows pancreatic collections to resolve or develop a more organized boundary.
227
What is the incidence of pseudocyst in patients with acute pancreatitis?
Low; less than 10% of patients have persistent fluid collections after 4 weeks.
228
What percentage of patients with pseudocyst require intervention?
Only symptomatic collections require intervention.
229
What are the two main methods for draining symptomatic pseudocysts?
Endoscopic or surgical drainage.
230
What symptoms may indicate pancreatic duct disruption?
Increasing abdominal pain or shortness of breath.
231
What diagnostic imaging can confirm pancreatic duct disruption?
Magnetic resonance cholangiopancreatography (MRCP) or ERCP.
232
What is the effectiveness of a bridging pancreatic stent in resolving leaks?
>90% effective.
233
What is the effectiveness of nonbridging stents in resolving pancreatic duct leaks?
25–50% effective.
234
What complications can arise from perivascular issues in acute pancreatitis?
Splenic vein thrombosis, gastric varices, pseudoaneurysms, portal and superior mesenteric vein thromboses.
235
What is a potential life-threatening complication associated with gastric varices?
Bleeding.
236
How can a ruptured pseudoaneurysm be diagnosed and treated?
Mesenteric angiography and embolization.
237
What percentage of patients with acute pancreatitis develop hospital-acquired infections?
Up to 20%.
238
What types of infections should patients with acute pancreatitis be monitored for?
Pneumonia, urinary tract infection, and line infection.
239
What is important for the management of patients during hospitalization for acute pancreatitis?
Continued culturing of urine, monitoring of chest x-rays, and routine changing of intravenous lines.
240
What can follow-up care for patients with moderately severe and severe acute pancreatitis assess for?
Development of diabetes, exocrine pancreatic insufficiency, recurrent cholangitis, or infected fluid collections.
241
When should cholecystectomy be performed for acute gallstone pancreatitis?
During the initial hospitalization for mild clinical severity.
242
What needs to be considered for patients with necrotizing gallstone pancreatitis regarding cholecystectomy?
The timing of cholecystectomy needs to be individualized.
243
Fill in the blank: The presence of ascitic fluid in pancreatic duct disruption has a high _______ level.
amylase
244
What are the two most common etiologic factors for recurrent acute pancreatitis?
Alcohol and cholelithiasis
## Footnote
These factors are significant contributors to the recurrence of pancreatitis.
245
In patients with recurrent pancreatitis without an obvious cause, what differential diagnoses should be considered?
Occult biliary tract disease, including:
* Microlithiasis
* Hypertriglyceridemia
* Pancreatic cancer
* Hereditary pancreatitis
## Footnote
Identifying the underlying cause is crucial for effective management.
246
What percentage of patients diagnosed with idiopathic or recurrent acute pancreatitis were found to have occult gallstone disease?
Approximately two-thirds
## Footnote
This highlights the importance of investigating gallstone disease in recurrent cases.
247
What genetic defects can result in recurrent pancreatitis?
Hereditary pancreatitis and cystic fibrosis mutations
## Footnote
Genetic factors play a role in the predisposition to pancreatitis.
248
What are some other diseases of the biliary tree and pancreatic ducts that can cause acute pancreatitis?
Diseases include:
* Choledochocele
* Ampullary tumors
* Pancreas divisum
* Pancreatic duct stones, stricture, and tumor
## Footnote
These conditions can complicate the clinical picture of acute pancreatitis.
249
What two reasons theoretically increase the incidence of acute pancreatitis in patients with AIDS?
1. High incidence of infections involving the pancreas
2. Frequent use of certain medications
## Footnote
These factors can contribute to the development of pancreatitis in this population.
250
Name some infections that can affect the pancreas in patients with AIDS.
Infections include:
* Cytomegalovirus
* Cryptosporidium
* Mycobacterium avium complex
## Footnote
These infections are significant in the context of AIDS-related pancreatitis.
251
Which medications commonly used by patients with AIDS have been associated with an increased risk of acute pancreatitis?
Pentamidine, trimethoprim-sulfamethoxazole, and protease inhibitors
## Footnote
Awareness of these medications is important for managing potential side effects.
252
Has the incidence of acute pancreatitis in patients with AIDS changed, and if so, why?
Yes, it has been markedly reduced due to advances in therapy
## Footnote
The disuse of didanosine has contributed to this reduction.
253
What characterizes chronic pancreatitis?
Irreversible damage to the pancreas
## Footnote
In contrast to reversible changes seen in acute pancreatitis.
254
What leads to the inflammatory process in chronic pancreatitis?
Stellate cell activation leading to cytokine expression and extracellular matrix protein production
## Footnote
This contributes to acute and chronic inflammation and collagen deposition.
255
What histologic abnormalities are present in chronic pancreatitis?
Chronic inflammation, fibrosis, progressive destruction of exocrine and endocrine tissue
## Footnote
This includes atrophy of both tissue types.
256
What are the cardinal manifestations of chronic pancreatitis?
* Abdominal pain
* Steatorrhea
* Weight loss
* Diabetes mellitus
* Pancreatic cancer (less common)
## Footnote
These manifestations result from the underlying disease process.
257
What role does alcohol play in chronic pancreatitis?
Believed to be a primary cause, but other factors are likely required for disease development
## Footnote
This explains why not all heavy alcohol consumers develop pancreatic disease.
258
What is the association between smoking and chronic pancreatitis?
Increased susceptibility to pancreatic autodigestion and dysregulation of duct cell CFTR function
## Footnote
Smoking is an independent, dose-dependent risk factor.
259
Which proinflammatory cytokines are involved in chronic pancreatitis?
* Tumor necrosis factor α (TNF-α)
* Interleukin 1 (IL-1)
* Interleukin 6 (IL-6)
## Footnote
These can induce PSC activity and subsequent new collagen synthesis.
260
What is the role of transforming growth factor β (TGF-β) in chronic pancreatitis?
Stimulates self-activating autocrine pathways in PSCs
## Footnote
This may explain disease progression even after removal of noxious stimuli.
261
What is the most common cause of clinically apparent chronic pancreatitis among adults in the United States?
Alcoholism
## Footnote
Alcoholism is identified as the leading cause of chronic pancreatitis in adults, while cystic fibrosis is more common in children.
262
What is the prototypical genetic defect associated with chronic pancreatitis?
Cationic trypsinogen gene (PRSS1)
## Footnote
Mutations in this gene are linked to the pathogenesis of chronic pancreatitis.
263
What is the consequence of the PRSS1 gene defect?
Prevents destruction of prematurely activated trypsin
## Footnote
This leads to continual activation of digestive enzymes, resulting in acute injury and chronic pancreatitis.
264
What does the CFTR gene function as?
A cyclic AMP–regulated chloride channel
## Footnote
CFTR mutations can block pancreatic ducts and are associated with cystic fibrosis.
265
What is the risk of pancreatitis for patients with two CFTR mutations (compound heterozygotes)?
Fortyfold increased risk
## Footnote
This highlights the genetic risk factors associated with chronic pancreatitis.
266
What additional genetic mutation increases the risk of pancreatitis twentyfold?
N34S SPINK1 mutation
## Footnote
This mutation, in combination with CFTR mutations, significantly heightens the risk.
267
What is the combined risk of pancreatitis for patients with two CFTR mutations and an N34S SPINK1 mutation?
900-fold increased risk
## Footnote
This demonstrates the compounded risk associated with multiple genetic defects.
268
True or False: CFTR mutations are uncommon in the general population.
False
## Footnote
CFTR mutations are common, making it unclear if they alone can cause pancreatitis as an autosomal recessive disease.
269
Fill in the blank: The presence of CFTR mutations may reduce the frequency of _______ in heterozygous carriers.
acute pancreatitis
## Footnote
This suggests a potential protective effect of CFTR modulators.
270
What does autoimmune pancreatitis (AIP) refer to?
A form of chronic pancreatitis with distinct histopathology and unique clinical phenotype.
271
What are the two recognized subtypes of autoimmune pancreatitis?
Type 1 AIP and idiopathic duct-centric chronic pancreatitis (IDCP, type 2 AIP).
272
What is type 1 AIP associated with?
Pancreatic manifestation of IgG4-related disease.
273
What are the characteristic histopathologic findings of type 1 AIP?
* Lymphoplasmacytic infiltrate
* Storiform fibrosis
* Abundant IgG4 cells
274
How is IDCP histologically defined?
Presence of granulocytic infiltration of the duct wall without IgG4-positive cells.
275
What is a common association of type 1 AIP?
Involvement of other organs including bilateral submandibular gland enlargement and retroperitoneal fibrosis.
276
What is the association of IDCP with inflammatory bowel disease?
IDCP is associated with inflammatory bowel disease in ~10% of patients.
277
What are the most common presenting symptoms of AIP?
* Jaundice
* Weight loss
* New-onset diabetes
278
What laboratory finding supports the diagnosis of type 1 AIP?
Elevated serum IgG4 levels.
279
What imaging findings are typical in AIP?
Diffuse or focal enlargement of the pancreas.
280
What is the capsule sign in AIP?
Presence of an inflammatory rim that is highly specific for AIP.
281
What do ERCP or MRCP reveal in patients with AIP?
Strictures in the bile duct.
282
What mnemonic can help remember the key diagnostic features of AIP?
HISORt: Histology, Imaging, Serology, Other organ involvement, Response to glucocorticoid therapy.
283
What is the typical glucocorticoid treatment for AIP?
Prednisone at an initial dose of 40 mg/d for 4 weeks, followed by tapering.
284
What is the expected response time to glucocorticoid therapy in AIP patients?
Typically within a 2- to 4-week period.
285
What percentage of type 1 AIP patients achieve clinical remission with steroids?
99%.
286
What percentage of type 2 AIP patients achieve clinical remission with steroids?
92%.
287
What percentage of patients experience disease relapse after treatment for type 1 AIP?
31%.
288
What should a poor response to glucocorticoids raise suspicion for?
An alternate diagnosis, such as pancreatic cancer.
289
What are potential treatments for patients with multiple relapses of AIP?
* Immunomodulators (e.g., azathioprine)
* B-cell depletion therapy (e.g., rituximab)
290
True or False: The appearance of interval cancers following a diagnosis of AIP is common.
False.
291
What does autoimmune pancreatitis (AIP) refer to?
A form of chronic pancreatitis with distinct histopathology and unique clinical phenotype.
292
What are the two recognized subtypes of autoimmune pancreatitis?
Type 1 AIP and idiopathic duct-centric chronic pancreatitis (IDCP, type 2 AIP).
293
What is type 1 AIP associated with?
Pancreatic manifestation of IgG4-related disease.
294
What are the characteristic histopathologic findings of type 1 AIP?
* Lymphoplasmacytic infiltrate
* Storiform fibrosis
* Abundant IgG4 cells
295
How is IDCP histologically defined?
Presence of granulocytic infiltration of the duct wall without IgG4-positive cells.
296
What is a common association of type 1 AIP?
Involvement of other organs including bilateral submandibular gland enlargement and retroperitoneal fibrosis.
297
What is the association of IDCP with inflammatory bowel disease?
IDCP is associated with inflammatory bowel disease in ~10% of patients.
298
What are the most common presenting symptoms of AIP?
* Jaundice
* Weight loss
* New-onset diabetes
299
What laboratory finding supports the diagnosis of type 1 AIP?
Elevated serum IgG4 levels.
300
What imaging findings are typical in AIP?
Diffuse or focal enlargement of the pancreas.
301
What is the capsule sign in AIP?
Presence of an inflammatory rim that is highly specific for AIP.
302
What do ERCP or MRCP reveal in patients with AIP?
Strictures in the bile duct.
303
What mnemonic can help remember the key diagnostic features of AIP?
HISORt: Histology, Imaging, Serology, Other organ involvement, Response to glucocorticoid therapy.
304
What is the typical glucocorticoid treatment for AIP?
Prednisone at an initial dose of 40 mg/d for 4 weeks, followed by tapering.
305
What is the expected response time to glucocorticoid therapy in AIP patients?
Typically within a 2- to 4-week period.
306
What percentage of type 1 AIP patients achieve clinical remission with steroids?
99%.
307
What percentage of type 2 AIP patients achieve clinical remission with steroids?
92%.
308
What percentage of patients experience disease relapse after treatment for type 1 AIP?
31%.
309
What should a poor response to glucocorticoids raise suspicion for?
An alternate diagnosis, such as pancreatic cancer.
310
What are potential treatments for patients with multiple relapses of AIP?
* Immunomodulators (e.g., azathioprine)
* B-cell depletion therapy (e.g., rituximab)
311
True or False: The appearance of interval cancers following a diagnosis of AIP is common.
False.
312
What is the primary reason patients with chronic pancreatitis seek medical attention?
Abdominal pain or symptoms of maldigestion
## Footnote
Symptoms of maldigestion include chronic diarrhea, steatorrhea, and weight loss.
313
What is a common consequence of severe abdominal pain in chronic pancreatitis patients?
Narcotic dependence
## Footnote
There is often a disparity between reported pain severity and physical findings.
314
What are some symptoms of maldigestion associated with chronic pancreatitis?
Chronic diarrhea, steatorrhea, weight loss
## Footnote
Fat-soluble vitamin deficiencies are also increasingly recognized.
315
What percentage of patients with chronic pancreatitis have metabolic bone disease?
~65%
## Footnote
This includes conditions like osteopenia or osteoporosis.
316
What serum enzyme levels are moderately specific but poorly sensitive for chronic pancreatitis?
Low serum pancreatic enzyme levels
## Footnote
Elevated serum bilirubin and alkaline phosphatase may indicate cholestasis.
317
What cumulative prevalence is associated with exocrine pancreatic insufficiency in chronic pancreatitis?
>80%
## Footnote
Overt steatorrhea is highly suggestive of this complication.
318
What test may be needed to confirm exocrine pancreatic insufficiency in milder cases?
Random fecal elastase-1 level
## Footnote
This test is conducted on a formed stool specimen.
319
What is the initial imaging modality of choice for suspected chronic pancreatitis?
Abdominal CT imaging
## Footnote
This is followed by MRI, endoscopic ultrasound, and pancreas function testing.
320
What features may be seen on CT imaging in chronic pancreatitis?
Calcifications, dilated pancreatic or biliary ducts, atrophic pancreas
## Footnote
CT also helps exclude pseudocyst and pancreatic cancer.
321
What diagnostic test has the best sensitivity for pancreatic disease?
Hormone stimulation test using secretin
## Footnote
The secretin test becomes abnormal when ≥60% of pancreatic exocrine function is lost.
322
True or False: EUS alone is specific enough for detecting early chronic pancreatitis.
False
## Footnote
EUS may show positive features in patients with diabetes or normal aging.
323
What does diffuse calcifications on plain film of the abdomen indicate?
Significant damage to the pancreas
## Footnote
This is pathognomic for chronic pancreatitis.
324
What is the most common cause of pancreatic calcification?
Alcohol
## Footnote
Other causes include hereditary pancreatitis, posttraumatic pancreatitis, idiopathic chronic pancreatitis, and tropical pancreatitis.
325
What is the lifetime prevalence of chronic pancreatitis–related diabetes?
Exceeds 80%
## Footnote
This indicates that a significant majority of patients with chronic pancreatitis will develop diabetes over their lifetime.
326
What causes hyperglycemia in chronic pancreatitis patients?
Insulin deficiency due to loss of islet cells
## Footnote
The loss of islet cells impairs insulin production, leading to elevated blood sugar levels.
327
Are diabetic ketoacidosis and diabetic coma common in chronic pancreatitis?
Uncommon
## Footnote
Despite the prevalence of diabetes, severe complications like ketoacidosis are rare.
328
What type of retinopathy may occur in chronic pancreatitis?
Nondiabetic retinopathy
## Footnote
This may be associated with deficiencies in vitamin A and/or zinc.
329
What bone conditions are increasingly recognized in chronic pancreatitis?
Osteoporosis and osteopenia
## Footnote
These conditions may be linked to factors like alcohol use, cigarette smoking, and vitamin D deficiency.
330
What are potential causes of gastrointestinal bleeding in chronic pancreatitis?
* Peptic ulceration
* Gastritis
* Pseudocyst eroding into the duodenum
* Arterial bleeding into the pancreatic duct (hemosuccus pancreaticus)
* Ruptured varices secondary to splenic vein thrombosis
## Footnote
These complications arise from various pathophysiological processes associated with chronic pancreatitis.
331
What complications can arise from chronic inflammation around the intrapancreatic portion of the common bile duct?
* Jaundice
* Cholestasis
* Biliary cirrhosis
## Footnote
These complications result from the obstruction and damage associated with chronic pancreatitis.
332
Which genetic conditions increase the risk of pancreatic cancer in chronic pancreatitis?
* Hereditary PRSS1
* Tropical pancreatitis
## Footnote
These conditions are associated with a higher incidence of pancreatic cancer compared to other forms of chronic pancreatitis.
333
What is the cornerstone of therapy for steatorrhea in chronic pancreatitis?
Pancreatic enzyme replacement therapy
## Footnote
Complete correction of steatorrhea is uncommon, but enzyme therapy helps control diarrhea and restore fat absorption.
334
What dosage of lipase is generally recommended for adult patients with exocrine pancreatic insufficiency?
25,000–50,000 units of lipase taken during each meal
## Footnote
The dose may need to be increased up to 100,000 units based on symptoms and pancreatic function test results.
335
What additional therapy may some patients require to optimize the response to pancreatic enzymes?
Acid suppression with proton pump inhibitors
## Footnote
This helps improve the effectiveness of pancreatic enzyme replacement therapy.
336
What effect did pregabalin have in a short-term randomized trial for chronic pancreatitis?
Decreased pain and lowered pain medication requirement
## Footnote
This suggests a potential option for managing pain in these patients.
337
What endoscopic treatments may be employed for pain management in chronic pancreatitis?
Sphincterotomy, pancreatic duct stenting, stone extraction, drainage of a pancreatic pseudocyst
## Footnote
These interventions are most appropriate in the setting of a dominant stricture.
338
What are some complications that can occur from endoscopic stenting?
Stent migration, stent occlusion, stent-induced pancreatic duct strictures
## Footnote
These complications raise concerns about the use of endoscopic stenting.
339
What is the therapy of choice for patients with pancreatic duct dilation?
Ductal decompression with surgical therapy
## Footnote
80% of such patients obtain immediate relief, but pain recurrence occurs in half by 3 years.
340
What did randomized trials compare regarding endoscopic and surgical therapy for chronic pancreatitis?
Surgical therapy was superior to endoscopy at decreasing pain and improving quality of life
## Footnote
This applies particularly to selected patients with dilated ducts and abdominal pain.
341
What is total pancreatectomy used for in chronic pancreatitis patients?
In highly selected patients with abdominal pain refractory to conventional therapy
## Footnote
Some patients may continue to experience pain postoperatively.
