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Gastroenterology > Pancreatitis > Flashcards

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.

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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.

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3
Q

What stimulates the release of secretin from the duodenal mucosa?

A

Gastric acid

Secretin is released from S cells in the duodenum.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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12
Q

What is the ion of primary physiologic importance within pancreatic secretion?

A

Bicarbonate

Bicarbonate plays a crucial role in various digestive processes.

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13
Q

What percentage of bicarbonate in pancreatic secretion is derived from plasma?

A

93%

The remaining 7% comes from intracellular metabolism.

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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.

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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.

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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.

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17
Q

Which neurotransmitter plays an important role in ductal cell secretion?

A

Acetylcholine

Acetylcholine enhances the secretion process in ductal cells.

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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.

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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.

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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.

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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.

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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.

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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.

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24
Q

What is the role of amylolytic enzymes?

A

Hydrolyze starch to oligosaccharides and maltose

Amylase is a key enzyme in this process.

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25
Q

List the lipolytic enzymes secreted by the pancreas.

A
  • Lipase
  • Phospholipase A2
  • Cholesterol esterase

These enzymes are involved in lipid digestion.

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26
Q

How do bile salts affect lipase activity?

A

Inhibit lipase in isolation

Colipase binds to lipase to prevent this inhibition.

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27
Q

What are the two types of proteolytic enzymes found in pancreatic secretions?

A
  • Endopeptidases
  • Exopeptidases

Endopeptidases include trypsin and chymotrypsin; exopeptidases include carboxypeptidases and aminopeptidases.

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28
Q

What is the function of enterokinase?

A

Cleaves trypsinogen to form trypsin

Enterokinase is located in the duodenal mucosa and initiates the activation of proteolytic zymogens.

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29
Q

What triggers pancreatic enzyme secretion?

A

Neurologic stimulation

This stimulation is primarily cholinergic and involves the vagus nerve.

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30
Q

What neurotransmitters are involved in stimulating pancreatic enzyme secretion?

A
  • Acetylcholine
  • Gastrin-releasing peptides

These neurotransmitters activate calcium-dependent secondary messenger systems.

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31
Q

What is the role of VIP in pancreatic function?

A

Potentiates the effect of acetylcholine

VIP is present in intrapancreatic nerves.

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32
Q

True or False: Humans have CCK receptors on acinar cells.

A

False

In contrast to other species, humans lack CCK receptors on acinar cells.

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33
Q

What is the effect of CCK in physiological concentrations on pancreatic secretion?

A

Stimulates pancreatic secretion

CCK stimulates afferent vagal and intrapancreatic nerves.

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34
Q

What is the process that prevents autodigestion of the pancreas?

A

Autoprotection of the pancreas

Autoprotection mechanisms include packaging of pancreatic proteases, calcium homeostasis, acid-base balance, and synthesis of protease inhibitors.

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35
Q

Name one mechanism that prevents autodigestion of the pancreas.

A

Packaging of pancreatic proteases in the precursor form

This refers to the storage of enzymes in inactive forms to prevent premature activation.

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36
Q

What role does intracellular calcium homeostasis play in pancreatic protection?

A

Low intracellular calcium in acinar cells promotes destruction of spontaneously activated trypsin

This helps prevent the activation of digestive enzymes within the pancreas.

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37
Q

What is the function of pancreatic secretory trypsin inhibitor (PSTI)?

A

Binds and inactivates ~20% of intracellular trypsin activity

PSTI is crucial for preventing autodigestion by inhibiting activated trypsin.

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38
Q

What other protease can lyse and inactivate trypsin?

A

Chymotrypsin C

This protease also plays a role in protecting the pancreas by inactivating trypsin.

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39
Q

What happens if any of the protective mechanisms of the pancreas fail?

A

Leads to premature enzyme activation, autodigestion, and ultimately acute pancreatitis

This highlights the importance of these protective mechanisms in maintaining pancreatic health.

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40
Q

What mechanism controls pancreatic enzyme secretion?

A

A negative feedback mechanism induced by active serine proteases and nutrients in the distal small intestine

This mechanism ensures that enzyme secretion is appropriately regulated based on the digestive needs.

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41
Q

What effect does perfusion of the duodenal lumen with phenylalanine have?

A

It causes a prompt increase in plasma CCK levels and increased secretion of chymotrypsin and other pancreatic enzymes

Phenylalanine stimulates early digestion.

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42
Q

What effect does simultaneous perfusion with trypsin have on pancreatic enzyme secretion?

A

It blunts the responses induced by phenylalanine

Trypsin stimulates late digestion.

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43
Q

What happens when the duodenal lumen is perfused with protease inhibitors?

A

It leads to enzyme hypersecretion

This indicates that protease activity is important for regulating enzyme secretion.

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44
Q

What peptide is involved in stimulating CCK release in the duodenum?

A

CCK-releasing factor (CCK-RF)

CCK-RF is released in response to dietary proteins.

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45
Q

How do serine proteases inhibit pancreatic secretion?

A

By inactivating a CCK-releasing peptide in the lumen of the small intestine

This is part of the feedback mechanism that regulates enzyme secretion.

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46
Q

What is the role of secretin in pancreatic secretion?

A

It stimulates vagal and other neural pathways to activate pancreatic duct cells to secrete bicarbonate

Secretin is released in response to acidification of the duodenum.

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47
Q

What is the purpose of bicarbonate secretion in the duodenum?

A

To neutralize the duodenal acid

This is crucial for creating an optimal environment for enzyme activity.

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48
Q

What is the relationship between dietary proteins and CCK-RF?

A

Dietary proteins bind proteases, leading to an increase in free CCK-RF

This enhances CCK release into the blood.

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49
Q

How does CCK primarily act to mediate pancreatic enzyme secretion?

A

Through neural pathways (vagal-vagal)

This leads to acetylcholine-mediated secretion.

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50
Q

When is pancreatic protease secretion reduced?

A

When the protein within the duodenum is digested

This marks the completion of the feedback process for enzyme secretion.

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51
Q

What additional hormones provide feedback inhibition of pancreatic enzyme secretion?

A

Peptide YY and glucagon-like peptide-1

This occurs following lipid or carbohydrate exposure to the ileum.

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52
Q

What are the leading causes of acute pancreatitis in the United States?

A

Gallstones and alcohol account for 80–90% of identified cases

Gallstones: 30–60%, Alcohol: 15–30%

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53
Q

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?

A

Fourfold greater risk

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54
Q

What factors besides alcohol ingestion can affect a person’s susceptibility to pancreatic injury?

A
  • Cigarette smoking
  • Genetic predisposition
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55
Q

What percentage of patients experience acute pancreatitis following endoscopic retrograde cholangiopancreatography (ERCP)?

A

5–10%

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56
Q

How can the risk of post-ERCP pancreatitis be decreased?

A
  • Proper patient selection
  • Prophylactic pancreatic duct stent
  • Rectal NSAIDs (e.g., indomethacin)
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57
Q

What are some risk factors for post-ERCP pancreatitis?

A
  • 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
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58
Q

What percentage of acute pancreatitis cases is caused by hypertriglyceridemia?

A

1–4%

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59
Q

What are typical serum triglyceride levels in patients with hypertriglyceridemic pancreatitis?

A

> 1000 mg/dL

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60
Q

What underlying condition is most common in patients with hypertriglyceridemic pancreatitis?

A

Undiagnosed or uncontrolled diabetes mellitus

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61
Q

What can precipitate a bout of acute pancreatitis in patients with hypertriglyceridemia?

A
  • Alcohol
  • Medications (e.g., oral contraceptives)
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62
Q

What is the role of apolipoprotein CII in lipid metabolism?

A

Activates lipoprotein lipase, important for clearing chylomicrons from bloodstream

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63
Q

What percentage of acute pancreatitis cases are drug-related?

A

<2%

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64
Q

How do drugs typically cause pancreatitis?

A
  • Hypersensitivity reaction
  • Generation of a toxic metabolite
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65
Q

What are the two forms of acute pancreatitis based on pathology?

A
  • Interstitial pancreatitis
  • Necrotizing pancreatitis
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66
Q

What is the pathogenic theory of autodigestion in acute pancreatitis?

A

Activation of proteolytic enzymes in the pancreas acinar cell compartment rather than in the intestinal lumen

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67
Q

What factors are believed to facilitate premature activation of trypsin in acute pancreatitis?

A
  • Endotoxins
  • Exotoxins
  • Viral infections
  • Ischemia
  • Oxidative stress
  • Lysosomal calcium
  • Direct trauma
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68
Q

What is the consequence of activated proteolytic enzymes in acute pancreatitis?

A

Digest pancreatic and peripancreatic tissues and activate other enzymes

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69
Q

What is a potential result of spontaneous activation of trypsin?

A

Autodigestion

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70
Q

What are the three phases of pancreatitis?

A
  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

These phases illustrate the progression of the disease and its systemic effects.

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71
Q

What mediates trypsin activation in pancreatitis?

A

Lysosomal hydrolases such as cathepsin B

Cathepsin B colocalizes with digestive enzymes in intracellular organelles.

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72
Q

What is the consequence of trypsin activation in the pancreas?

A

Acinar cell injury

Trypsin activation leads to damage of pancreatic cells.

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73
Q

What happens in the second phase of pancreatitis?

A

Activation, chemoattraction, and sequestration of leukocytes and macrophages in the pancreas

This phase enhances the intrapancreatic inflammatory reaction.

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74
Q

What effect does neutrophil depletion have in experimental pancreatitis?

A

Reduces the severity of pancreatitis

Induced by prior administration of an antineutrophil serum.

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75
Q

What role do neutrophils play in trypsinogen activation?

A

Neutrophils can activate trypsinogen

Suggests a two-step activation process involving neutrophils.

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76
Q

What are the consequences of activated proteolytic enzymes in the third phase of pancreatitis?

A

Digest pancreatic and peripancreatic tissues, activate other enzymes, and cause cellular injury

This leads to vascular damage, coagulation necrosis, and fat necrosis.

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77
Q

What are the systemic effects of bradykinin peptides and vasoactive substances released during pancreatitis?

A

Vasodilation, increased vascular permeability, and edema

These effects can profoundly impact other organs.

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78
Q

What syndrome may occur as a result of the cascade of effects during pancreatitis?

A

Systemic inflammatory response syndrome (SIRS) and acute respiratory distress syndrome (ARDS)

These conditions may lead to multiorgan failure.

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79
Q

List the six genetic variants associated with susceptibility to pancreatitis.

A
  • 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)

These variants are linked to the control of trypsin activity.

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80
Q

Which genetic variant is sufficient to precipitate acute pancreatitis without other risk factors?

A

PRSS1 mutations

Other variants serve as disease modifiers.

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81
Q

What is the major symptom of acute pancreatitis?

A

Abdominal pain

Abdominal pain can vary from mild discomfort to severe, constant distress.

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82
Q

Describe the character and location of pain in acute pancreatitis.

A

Steady and boring in character, located in the epigastrium region

Pain may radiate to the back, chest, flanks, and lower abdomen.

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83
Q

What are common additional symptoms associated with abdominal pain in acute pancreatitis?

A
  • Nausea
  • Vomiting
  • Abdominal distention

Abdominal distention is due to gastric and intestinal hypomotility.

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84
Q

What physical examination findings may be observed in a patient with acute pancreatitis?

A
  • Distressed and anxious patient
  • Low-grade fever
  • Tachycardia
  • Hypotension

Shock may occur due to various factors.

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85
Q

What are the potential causes of shock in acute pancreatitis?

A
  • Hypovolemia from exudation of blood and plasma proteins
  • Increased formation and release of kinin peptides
  • Systemic effects of proteolytic and lipolytic enzymes

These factors contribute to vasodilation and increased vascular permeability.

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86
Q

Under what circumstances does jaundice occur in acute pancreatitis?

A

When there is extrinsic compression or intraductal obstruction

Compression may be due to peripancreatic edema or pancreatic head mass.

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87
Q

What rare skin manifestation can occur in acute pancreatitis?

A

Erythematous skin nodules due to subcutaneous fat necrosis

These occurrences are rare.

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88
Q

What pulmonary findings may be present in 10–20% of patients with acute pancreatitis?

A
  • Basilar rales
  • Atelectasis
  • Pleural effusion

Pleural effusion is most frequently left-sided.

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89
Q

What abdominal signs are commonly observed in acute pancreatitis?

A
  • Abdominal tenderness
  • Muscle rigidity

These signs may be less impressive compared to the intense pain.

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90
Q

What changes in bowel sounds are typically noted in acute pancreatitis?

A

Diminished or absent bowel sounds

This is associated with the condition.

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91
Q

What might be palpable in the upper abdomen later in the course of acute pancreatitis?

A

An enlarged pancreas

This may be due to acute fluid collection, walled-off necrosis, or a pseudocyst.

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92
Q

What does Cullen’s sign indicate in the context of acute pancreatitis?

A

Faint blue discoloration around the umbilicus

This may result from hemoperitoneum.

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93
Q

What does Turner’s sign reflect in severe necrotizing pancreatitis?

A

Blue-red-purple or green-brown discoloration of the flanks

This indicates tissue breakdown of hemoglobin from hemorrhage.

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94
Q

True or False: Shock is a common occurrence in acute pancreatitis.

A

True

Shock may arise from various underlying causes.

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95
Q

What serum amylase and lipase values are strongly supportive of the diagnosis of pancreatitis?

A

Values threefold or more above normal

This is valid if alternate etiologies are excluded.

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96
Q

Is there a correlation between the severity of pancreatitis and the degree of serum lipase and amylase elevations?

A

No correlation exists

The severity of pancreatitis does not correlate with elevation levels.

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97
Q

How long may pancreatic lipase levels remain elevated in pancreatitis?

A

7–14 days

Total serum amylase values may return toward normal after 3–7 days.

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98
Q

What can cause spurious elevations in serum amylase?

A

Acidemia (arterial pH ≤7.32)

This is particularly relevant in patients with diabetic ketoacidosis.

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99
Q

What effect does severe hypertriglyceridemia have on serum amylase levels?

A

Serum amylase levels can be spuriously low

This can complicate the evaluation of pancreatitis.

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100
Q

Which enzyme is considered more specific for diagnosing pancreatitis, amylase or lipase?

A

Lipase

Serum lipase activity increases in parallel with amylase activity.

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101
Q

What leukocyte count is indicative of leukocytosis in pancreatitis?

A

15,000–20,000 leukocytes/μL

Leukocytosis is common in patients with pancreatitis.

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102
Q

What hematocrit value may indicate hemoconcentration and more severe disease?

A

> 44%

Hemoconcentration is a harbinger of more severe disease.

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103
Q

What is a significant risk factor for mortality in pancreatitis patients?

A

Prerenal azotemia with BUN >22 mg/dL

This results from loss of plasma into the retroperitoneal space and peritoneal cavity.

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104
Q

What is a common metabolic change in pancreatitis patients related to blood glucose?

A

Hyperglycemia

Caused by decreased insulin release and increased glucagon release.

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105
Q

In what percentage of pancreatitis patients does hypocalcemia occur?

A

~25%

The pathogenesis of hypocalcemia is incompletely understood.

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106
Q

What is ‘soap formation’ in the context of pancreatitis?

A

Intraperitoneal saponification of calcium by fatty acids

Occurs occasionally with large amounts dissolved in ascitic fluid.

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107
Q

What serum bilirubin level is classified as hyperbilirubinemia in pancreatitis?

A

> 4.0 mg/dL

Jaundice is typically transient and resolves in 4–7 days.

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108
Q

What alanine aminotransferase (ALT) elevation is associated with gallstone etiology in acute pancreatitis?

A

> 3× the upper limit of normal

This elevation indicates a gallstone cause in acute pancreatitis.

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109
Q

What percentage of patients may experience hypoxemia in pancreatitis?

A

5–10%

Hypoxemia may herald the onset of ARDS.

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110
Q

What abnormalities may be seen on an electrocardiogram in acute pancreatitis?

A

ST-segment and T-wave abnormalities

These can simulate myocardial ischemia.

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111
Q

What is the recommended initial diagnostic imaging modality for pancreatitis?

A

Abdominal ultrasound

It is useful to evaluate for gallstones and common bile duct dilation.

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112
Q

What are the morphologic features of acute pancreatitis outlined in the Revised Atlanta Criteria?

A
  1. Interstitial pancreatitis
    * 2. Necrotizing pancreatitis
    * 3. Acute pancreatic fluid collection
    * 4. Pancreatic pseudocyst
    * 5. Acute necrotic collection (ANC)
    * 6. Walled-off necrosis (WON)

These features are assessed via computed tomography (CT) scan.

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113
Q

What should any severe acute pain in the abdomen or back suggest?

A

The possibility of acute pancreatitis

Severe acute pain can be indicative of various conditions, but in this context, acute pancreatitis is a key consideration.

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114
Q

What are the three criteria for diagnosing acute pancreatitis?

A
  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

At least two of these criteria must be met for a diagnosis of acute pancreatitis.

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115
Q

What are markers of severity in acute pancreatitis?

A
  1. Hemoconcentration (hematocrit >44%)
  2. Admission azotemia (BUN >22 mg/dL)
  3. SIRS
  4. Signs of organ failure

These markers may indicate a more severe case of acute pancreatitis.

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116
Q

List five disorders that should be included in the differential diagnosis of acute pancreatitis.

A
  • Perforated viscus, especially peptic ulcer
  • Acute cholecystitis and biliary colic
  • Acute intestinal obstruction
  • Mesenteric vascular occlusion
  • Renal colic

The differential diagnosis is critical to rule out other potential causes of similar symptoms.

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117
Q

Which condition may be difficult to differentiate from acute pancreatitis due to elevated serum amylase?

A

Acute cholecystitis

Both acute pancreatitis and acute cholecystitis can present with elevated serum amylase, complicating diagnosis.

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118
Q

How can pain of biliary tract origin be characterized compared to pancreatitis pain?

A

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

Understanding the pain characteristics is essential for diagnosis.

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119
Q

What imaging technique is helpful in diagnosing cholelithiasis and cholecystitis?

A

Ultrasound

Ultrasound is a non-invasive method that can provide critical information for these conditions.

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120
Q

What differentiates intestinal obstruction due to mechanical factors from pancreatitis?

A

History of crescendo-decrescendo pain, findings on abdominal examination, and CT showing changes characteristic of mechanical obstruction

These diagnostic clues help in distinguishing between the two conditions.

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121
Q

What is usually suspected in elderly debilitated patients with leukocytosis, abdominal distention, and bloody diarrhea?

A

Acute mesenteric vascular occlusion

This condition often presents with specific symptoms that can lead to its identification.

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122
Q

Which vasculitides may be confused with pancreatitis?

A
  1. Systemic lupus erythematosus
  2. Polyarteritis nodosa

These systemic conditions can lead to pancreatitis as a complication.

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123
Q

True or False: Diabetic ketoacidosis is often accompanied by elevated serum lipase levels.

A

False

While diabetic ketoacidosis may present with abdominal pain and elevated serum amylase, serum lipase levels are usually not elevated.

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124
Q

What are the two phases of acute pancreatitis defined by the Revised Atlanta Criteria?

A

Early (<2 weeks) and late (>2 weeks)

These phases describe the hospital course of the disease.

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125
Q

How is severity defined in the early phase of acute pancreatitis?

A

By clinical parameters rather than morphologic findings

Most patients exhibit SIRS, and persistent SIRS predisposes to organ failure.

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126
Q

What are the three organ systems assessed to define organ failure in acute pancreatitis?

A
  • Respiratory
  • Cardiovascular
  • Renal

Organ failure is defined as a score of 2 or more for one of these organ systems using the modified Marshall scoring system.

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127
Q

What is considered persistent organ failure in acute pancreatitis?

A

Organ failure lasting more than 48 hours

This is the most important clinical finding regarding the severity of the acute pancreatitis episode.

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128
Q

What constitutes multisystem organ failure in acute pancreatitis?

A

Organ failure affecting more than one organ

This indicates a more severe clinical condition.

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129
Q

Is CT imaging recommended during the first 48 hours of admission in acute pancreatitis?

A

No, it is usually not needed or recommended

This is especially true in the early phase.

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130
Q

What characterizes the late phase of acute pancreatitis?

A

A protracted course of illness requiring imaging to evaluate for local complications

The critical clinical parameter remains persistent organ failure.

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131
Q

What supportive measures may be required in the late phase of acute pancreatitis?

A
  • Renal dialysis
  • Ventilator support
  • Supplemental nutrition via nasojejunal or parenteral route

These measures are critical for patient management during this phase.

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132
Q

What is the radiographic feature of greatest importance in the late phase of acute pancreatitis?

A

Development of necrotizing pancreatitis on CT imaging

Necrosis is associated with prolonged hospitalization and may require intervention if infected.

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133
Q

True or False: Infected necrosis in acute pancreatitis may require surgical intervention.

A

True

Intervention can be percutaneous, endoscopic, and/or surgical depending on the clinical scenario.

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134
Q

What are the three classes of severity defined for acute pancreatitis?

A

Mild, moderately severe, and severe

Each class has distinct characteristics and management strategies.

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135
Q

What defines mild acute pancreatitis?

A

Without local complications or organ failure

Most patients with interstitial acute pancreatitis have mild pancreatitis.

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136
Q

How long does mild acute pancreatitis typically last?

A

3–7 days after onset

The disease is self-limited and subsides spontaneously.

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137
Q

What dietary recommendations are given for patients recovering from mild acute pancreatitis?

A

Clear or full liquid diet; low-fat solid diet after recovery

Oral intake can resume if the patient is hungry and has normal bowel function.

138
Q

What characterizes moderately severe acute pancreatitis?

A

Transient organ failure or local/systemic complications without persistent organ failure

Mortality rate remains low for these patients.

139
Q

What is the duration of organ failure in severe acute pancreatitis?

A

Persistent organ failure for more than 48 hours

It can involve one or more organs.

140
Q

What imaging studies should be obtained in severe acute pancreatitis?

A

CT scan or magnetic resonance imaging (MRI)

These help assess for necrosis and/or complications.

141
Q

What management steps are taken if a local complication is encountered in severe acute pancreatitis?

A

Management is dictated by clinical symptoms, evidence of infection, maturity of fluid collection, and clinical stability

Each case may require a tailored approach.

142
Q

True or False: Prophylactic antibiotics are recommended for severe acute pancreatitis.

A

False

Prophylactic antibiotics are no longer recommended.

143
Q

What can happen to patients with moderately severe acute pancreatitis regarding hospitalization?

A

Prolonged hospitalization greater than 1 week

This may occur if local complications develop.

144
Q

What are the two types of pancreatitis recognized on imaging?

A

Interstitial and necrotizing pancreatitis

145
Q

When is CT imaging with IV contrast best evaluated for acute pancreatitis?

A

3–5 days into hospitalization if patients are not responding to supportive care

146
Q

What does the Revised Atlanta Criteria outline?

A

Terminology for local complications and fluid collections along with a CT imaging template

147
Q

What is the percentage of admissions for acute pancreatitis that are classified as interstitial pancreatitis?

A

90–95%

148
Q

What are the characteristics of interstitial pancreatitis?

A

Diffuse gland enlargement, homogenous contrast enhancement, mild inflammatory changes or peripancreatic stranding

149
Q

What is the typical resolution time for symptoms in interstitial pancreatitis?

A

Generally resolves within a week of hospitalization

150
Q

What percentage of acute pancreatitis admissions are classified as necrotizing pancreatitis?

A

5–10%

151
Q

What are the imaging characteristics of necrotizing pancreatitis?

A

Lack of pancreatic parenchymal enhancement by IV contrast and/or presence of peripancreatic necrosis

152
Q

What is the natural history of pancreatic and peripancreatic necrosis?

A

Variable; may remain solid or liquefy, remain sterile or become infected, and persist or disappear over time

153
Q

What is the prognosis for patients with only extrapancreatic necrosis compared to those with pancreatic necrosis?

A

More favorable prognosis

154
Q

Why is CT identification of local complications critical in acute pancreatitis?

A

Patients with infected and sterile necrosis are at greatest risk of mortality

155
Q

What is the median prevalence of organ failure in necrotizing pancreatitis?

A

> 50%

156
Q

What is the mortality rate with single-organ system failure in necrotizing pancreatitis?

A

3–10%

157
Q

What is the mortality rate with multiorgan failure in necrotizing pancreatitis?

A

Nearly 50%

158
Q

Fill in the blank: Interstitial pancreatitis is characterized by _______.

A

Diffuse gland enlargement, homogenous contrast enhancement, mild inflammatory changes or peripancreatic stranding

159
Q

True or False: Necrotizing pancreatitis may not evolve until several days of hospitalization.

A

True

160
Q

What is the typical duration for most cases of acute pancreatitis to subside?

A

3–7 days

85–90% of cases are self-limited and resolve spontaneously.

161
Q

What is the first step in managing acute pancreatitis in the emergency ward?

A

Early and aggressive fluid resuscitation

This is critical after diagnosis confirmation.

162
Q

What type of medication is administered to patients with acute pancreatitis for pain management?

A

Intravenous analgesics

Pain management is essential in the management process.

163
Q

What should be assessed after confirming the diagnosis of acute pancreatitis?

A

Severity of the condition

Assessment of severity helps guide further management.

164
Q

What should be done for patients who do not respond to aggressive fluid resuscitation?

A

Consider admission to a step-down or intensive care unit

This allows for further monitoring and management.

165
Q

True or False: Most cases of acute pancreatitis exhibit organ failure or local complications.

A

False

Most cases are self-limited and do not exhibit organ failure.

166
Q

What is the primary goal of the management of acute pancreatitis?

A

To ensure patient stability and prevent complications

Management focuses on supportive care.

167
Q

Fill in the blank: 85–90% of acute pancreatitis cases are _______.

A

self-limited

These cases typically resolve without significant intervention.

168
Q

What is the most important treatment intervention for acute pancreatitis?

A

Early, aggressive intravenous fluid resuscitation to prevent systemic complications from the secondary systemic inflammatory response.

169
Q

What types of intravenous fluids are recommended for initial bolus in acute pancreatitis?

A

Lactated Ringer’s or normal saline.

170
Q

What is the initial bolus amount of intravenous fluids for acute pancreatitis?

A

15–20 mL/kg (1050–1400 mL).

171
Q

What is the recommended maintenance fluid rate after the initial bolus in acute pancreatitis?

A

2–3 mL/kg per hour (200–250 mL/h).

172
Q

What is the target urine output to maintain during fluid resuscitation?

A

Urine output >0.5 mL/kg per hour.

173
Q

How often should serial bedside evaluations be performed to assess fluid resuscitation?

A

Every 6–8 hours.

174
Q

What two measurements are recommended every 8–12 hours to monitor response to therapy?

A

Hematocrit and BUN (blood urea nitrogen).

175
Q

What is a strong indication that sufficient fluids are being administered during the first 12–24 hours?

A

A decrease in hematocrit and BUN.

176
Q

What should be done if a rise in hematocrit or BUN is observed during serial measurement?

A

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
Q

True or False: A rising BUN during hospitalization is associated with inadequate hydration and higher in-hospital mortality.

A

True.

178
Q

What should be considered if BUN or hematocrit fails to respond to the bolus challenge?

A

Transfer to an intensive care unit for hemodynamic monitoring.

179
Q

What solution has been shown to decrease systemic inflammation in acute pancreatitis?

A

Lactated Ringer’s solution.

180
Q

What should be determined in the emergency ward for acute pancreatitis patients?

A

Severity of acute pancreatitis to assist in patient triage

181
Q

What is the Bedside Index of Severity in Acute Pancreatitis (BISAP)?

A

A scoring system incorporating five clinical and laboratory parameters

182
Q

List the five parameters used in the BISAP score.

A
  • BUN >25 mg/dL
  • Impaired mental status (Glasgow coma scale score <15)
  • SIRS
  • Age >60 years
  • Pleural effusion on radiography
183
Q

What is the significance of having three or more BISAP factors present?

A

Associated with substantially increased risk for in-hospital mortality

184
Q

What hematocrit level is associated with more severe acute pancreatitis?

A

Elevated hematocrit >44%

185
Q

What admission BUN level is associated with more severe acute pancreatitis?

A

Admission BUN >22 mg/dL

186
Q

How can the indices from BISAP and patient response to initial fluid resuscitation be used?

A

To triage patients to the appropriate hospital acute care setting

187
Q

What is the expected response for patients with lower BISAP scores?

A

They tend to respond to initial management and can be safely triaged to a regular hospital ward

188
Q

What does the absence of SIRS at 24 hours indicate?

A

The patient is unlikely to develop organ failure or necrosis

189
Q

What should be considered for patients with persistent SIRS at 24 hours?

A

Consider for a step-down unit setting if available

190
Q

What conditions should lead to consideration for direct admission to an intensive care unit?

A

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
Q

What is recommended in the emergency ward to assess for etiologies that may impact acute management?

A

A careful history, review of medications, selected laboratory studies, and an abdominal ultrasound

Laboratory studies include liver profile, serum triglycerides, and serum calcium. The abdominal ultrasound evaluates the gallbladder, common bile duct, and pancreatic head.

192
Q

What is the initial imaging modality of choice for assessing gallstone pancreatitis?

A

Abdominal ultrasound

193
Q

What should patients with evidence of ascending cholangitis undergo within 24–48 hours of admission?

A

ERCP

194
Q

What procedure should be considered for patients with mild acute pancreatitis during the same admission?

A

Cholecystectomy

195
Q

What is an alternative for patients who are not surgical candidates for gallstone pancreatitis?

A

Endoscopic biliary sphincterotomy

196
Q

What serum triglyceride level is associated with acute pancreatitis?

A

> 1000 mg/dL

197
Q

What is the initial therapy for hypertriglyceridemia in acute pancreatitis?

A

Intravenous insulin

198
Q

What adjunct therapies may be considered for hypertriglyceridemia, despite lacking compelling evidence of improved outcomes?

A

Heparin, plasmapheresis

199
Q

What outpatient therapies are recommended for hypertriglyceridemia?

A

Control of diabetes, lipid-lowering agents, weight loss, avoidance of drugs that elevate lipid levels

200
Q

What other potential etiologies may impact acute hospital care?

A

Hypercalcemia, post-ERCP pancreatitis

201
Q

What methods are effective at decreasing pancreatitis after ERCP?

A

Pancreatic duct stenting, rectal indomethacin administration

202
Q

True or False: There is compelling evidence that heparin or plasmapheresis improve clinical outcomes in hypertriglyceridemia.

A

False

203
Q

What type of diet can be administered to subjects with mild acute pancreatitis once they are able to eat?

A

A low-fat solid diet

This diet is appropriate for individuals who have mild acute pancreatitis and can resume eating.

204
Q

When should enteral nutrition be considered for subjects with more severe pancreatitis?

A

2–3 days after admission

This recommendation is made instead of total parenteral nutrition (TPN).

205
Q

What are the advantages of enteral feeding over total parenteral nutrition (TPN)?

A
  • Maintains gut barrier integrity
  • Limits bacterial translocation
  • Less expensive
  • Fewer complications

Enteral feeding is preferred for patients with pancreatitis due to these benefits.

206
Q

Is gastric feeding considered safe for patients with pancreatitis?

A

Yes

Gastric feeding is deemed safe; however, the advantages of nasojejunal enteral feeding over gastric feeding are still being researched.

207
Q

True or False: Total parenteral nutrition (TPN) is preferred over enteral nutrition in severe pancreatitis cases.

A

False

Enteral nutrition is recommended over TPN for patients with severe pancreatitis.

208
Q

What should be assessed in patients exhibiting signs of clinical deterioration despite aggressive fluid resuscitation?

A

Local complications, which may include necrosis, pseudocyst formation, pancreas duct disruption, peripancreatic vascular complications, and extrapancreatic infections.

A multidisciplinary team approach is recommended for assessment.

209
Q

What is the recommended approach for managing necrosis?

A

A multidisciplinary team approach.

This includes specialists from gastroenterology, surgery, interventional radiology, and intensive care.

210
Q

What diagnostic procedure was previously performed to evaluate infected pancreatic necrosis?

A

Percutaneous fine-needle aspiration of necrosis with Gram stain and culture.

This was typically done in patients with sustained leukocytosis, fever, or organ failure.

211
Q

Why has the use of percutaneous fine-needle aspiration decreased in some institutions?

A

To avoid potentially contaminating an otherwise sterile collection.

Culture results may not lead to a clinical decision to de-escalate antimicrobial therapy.

212
Q

Should prophylactic antibiotics be used in necrotizing pancreatitis?

A

No, prophylactic antibiotics do not lead to improved survival and may promote opportunistic fungal infections.

Empiric antibiotics should be considered in those with clinical decompensation.

213
Q

What imaging should be considered with any change in clinical course for patients with necrosis?

A

Repeated CT or MRI imaging.

This is to monitor for complications such as thromboses, hemorrhage, or abdominal compartment syndrome.

214
Q

How is sterile necrosis generally managed?

A

Conservatively, unless complications arise.

Targeted antibiotics should be instituted once infected necrosis is established.

215
Q

What is the step-up approach in managing infected pancreatic necrosis?

A

Percutaneous or endoscopic transgastric/transduodenal drainage followed by surgical necrosectomy if necessary.

This approach has been successful in some pancreatic centers.

216
Q

What is the outcome for one-third of patients treated with the step-up approach?

A

They did not require major abdominal surgery.

This highlights the effectiveness of the conservative management strategy.

217
Q

What did a randomized trial report regarding the initial approach for symptomatic WON?

A

Advantages to an initial endoscopic approach compared to an initial surgical necrosectomy approach.

This is relevant for select patients requiring intervention.

218
Q

For how long should conservative therapy be implemented before considering intervention?

A

4–6 weeks.

This allows pancreatic collections to resolve or develop a more organized boundary.

219
Q

What should be assessed in patients exhibiting signs of clinical deterioration despite aggressive fluid resuscitation?

A

Local complications, which may include necrosis, pseudocyst formation, pancreas duct disruption, peripancreatic vascular complications, and extrapancreatic infections.

A multidisciplinary team approach is recommended for assessment.

220
Q

What diagnostic procedure was previously performed to evaluate infected pancreatic necrosis?

A

Percutaneous fine-needle aspiration of necrosis with Gram stain and culture.

This was typically done in patients with sustained leukocytosis, fever, or organ failure.

221
Q

Should prophylactic antibiotics be used in necrotizing pancreatitis?

A

No, prophylactic antibiotics do not lead to improved survival and may promote opportunistic fungal infections.

Empiric antibiotics should be considered in those with clinical decompensation.

222
Q

What imaging should be considered with any change in clinical course for patients with necrosis?

A

Repeated CT or MRI imaging.

This is to monitor for complications such as thromboses, hemorrhage, or abdominal compartment syndrome.

223
Q

How is sterile necrosis generally managed?

A

Conservatively, unless complications arise.

Targeted antibiotics should be instituted once infected necrosis is established.

224
Q

What is the step-up approach in managing infected pancreatic necrosis?

A

Percutaneous or endoscopic transgastric/transduodenal drainage followed by surgical necrosectomy if necessary.

This approach has been successful in some pancreatic centers.

225
Q

What is the outcome for one-third of patients treated with the step-up approach?

A

They did not require major abdominal surgery.

This highlights the effectiveness of the conservative management strategy.

226
Q

For how long should conservative therapy be implemented before considering intervention?

A

4–6 weeks.

This allows pancreatic collections to resolve or develop a more organized boundary.

227
Q

What is the incidence of pseudocyst in patients with acute pancreatitis?

A

Low; less than 10% of patients have persistent fluid collections after 4 weeks.

228
Q

What percentage of patients with pseudocyst require intervention?

A

Only symptomatic collections require intervention.

229
Q

What are the two main methods for draining symptomatic pseudocysts?

A

Endoscopic or surgical drainage.

230
Q

What symptoms may indicate pancreatic duct disruption?

A

Increasing abdominal pain or shortness of breath.

231
Q

What diagnostic imaging can confirm pancreatic duct disruption?

A

Magnetic resonance cholangiopancreatography (MRCP) or ERCP.

232
Q

What is the effectiveness of a bridging pancreatic stent in resolving leaks?

A

> 90% effective.

233
Q

What is the effectiveness of nonbridging stents in resolving pancreatic duct leaks?

A

25–50% effective.

234
Q

What complications can arise from perivascular issues in acute pancreatitis?

A

Splenic vein thrombosis, gastric varices, pseudoaneurysms, portal and superior mesenteric vein thromboses.

235
Q

What is a potential life-threatening complication associated with gastric varices?

A

Bleeding.

236
Q

How can a ruptured pseudoaneurysm be diagnosed and treated?

A

Mesenteric angiography and embolization.

237
Q

What percentage of patients with acute pancreatitis develop hospital-acquired infections?

A

Up to 20%.

238
Q

What types of infections should patients with acute pancreatitis be monitored for?

A

Pneumonia, urinary tract infection, and line infection.

239
Q

What is important for the management of patients during hospitalization for acute pancreatitis?

A

Continued culturing of urine, monitoring of chest x-rays, and routine changing of intravenous lines.

240
Q

What can follow-up care for patients with moderately severe and severe acute pancreatitis assess for?

A

Development of diabetes, exocrine pancreatic insufficiency, recurrent cholangitis, or infected fluid collections.

241
Q

When should cholecystectomy be performed for acute gallstone pancreatitis?

A

During the initial hospitalization for mild clinical severity.

242
Q

What needs to be considered for patients with necrotizing gallstone pancreatitis regarding cholecystectomy?

A

The timing of cholecystectomy needs to be individualized.

243
Q

Fill in the blank: The presence of ascitic fluid in pancreatic duct disruption has a high _______ level.

A

amylase

244
Q

What are the two most common etiologic factors for recurrent acute pancreatitis?

A

Alcohol and cholelithiasis

These factors are significant contributors to the recurrence of pancreatitis.

245
Q

In patients with recurrent pancreatitis without an obvious cause, what differential diagnoses should be considered?

A

Occult biliary tract disease, including:
* Microlithiasis
* Hypertriglyceridemia
* Pancreatic cancer
* Hereditary pancreatitis

Identifying the underlying cause is crucial for effective management.

246
Q

What percentage of patients diagnosed with idiopathic or recurrent acute pancreatitis were found to have occult gallstone disease?

A

Approximately two-thirds

This highlights the importance of investigating gallstone disease in recurrent cases.

247
Q

What genetic defects can result in recurrent pancreatitis?

A

Hereditary pancreatitis and cystic fibrosis mutations

Genetic factors play a role in the predisposition to pancreatitis.

248
Q

What are some other diseases of the biliary tree and pancreatic ducts that can cause acute pancreatitis?

A

Diseases include:
* Choledochocele
* Ampullary tumors
* Pancreas divisum
* Pancreatic duct stones, stricture, and tumor

These conditions can complicate the clinical picture of acute pancreatitis.

249
Q

What two reasons theoretically increase the incidence of acute pancreatitis in patients with AIDS?

A
  1. High incidence of infections involving the pancreas
  2. Frequent use of certain medications

These factors can contribute to the development of pancreatitis in this population.

250
Q

Name some infections that can affect the pancreas in patients with AIDS.

A

Infections include:
* Cytomegalovirus
* Cryptosporidium
* Mycobacterium avium complex

These infections are significant in the context of AIDS-related pancreatitis.

251
Q

Which medications commonly used by patients with AIDS have been associated with an increased risk of acute pancreatitis?

A

Pentamidine, trimethoprim-sulfamethoxazole, and protease inhibitors

Awareness of these medications is important for managing potential side effects.

252
Q

Has the incidence of acute pancreatitis in patients with AIDS changed, and if so, why?

A

Yes, it has been markedly reduced due to advances in therapy

The disuse of didanosine has contributed to this reduction.

253
Q

What characterizes chronic pancreatitis?

A

Irreversible damage to the pancreas

In contrast to reversible changes seen in acute pancreatitis.

254
Q

What leads to the inflammatory process in chronic pancreatitis?

A

Stellate cell activation leading to cytokine expression and extracellular matrix protein production

This contributes to acute and chronic inflammation and collagen deposition.

255
Q

What histologic abnormalities are present in chronic pancreatitis?

A

Chronic inflammation, fibrosis, progressive destruction of exocrine and endocrine tissue

This includes atrophy of both tissue types.

256
Q

What are the cardinal manifestations of chronic pancreatitis?

A
  • Abdominal pain
  • Steatorrhea
  • Weight loss
  • Diabetes mellitus
  • Pancreatic cancer (less common)

These manifestations result from the underlying disease process.

257
Q

What role does alcohol play in chronic pancreatitis?

A

Believed to be a primary cause, but other factors are likely required for disease development

This explains why not all heavy alcohol consumers develop pancreatic disease.

258
Q

What is the association between smoking and chronic pancreatitis?

A

Increased susceptibility to pancreatic autodigestion and dysregulation of duct cell CFTR function

Smoking is an independent, dose-dependent risk factor.

259
Q

Which proinflammatory cytokines are involved in chronic pancreatitis?

A
  • Tumor necrosis factor α (TNF-α)
  • Interleukin 1 (IL-1)
  • Interleukin 6 (IL-6)

These can induce PSC activity and subsequent new collagen synthesis.

260
Q

What is the role of transforming growth factor β (TGF-β) in chronic pancreatitis?

A

Stimulates self-activating autocrine pathways in PSCs

This may explain disease progression even after removal of noxious stimuli.

261
Q

What is the most common cause of clinically apparent chronic pancreatitis among adults in the United States?

A

Alcoholism

Alcoholism is identified as the leading cause of chronic pancreatitis in adults, while cystic fibrosis is more common in children.

262
Q

What is the prototypical genetic defect associated with chronic pancreatitis?

A

Cationic trypsinogen gene (PRSS1)

Mutations in this gene are linked to the pathogenesis of chronic pancreatitis.

263
Q

What is the consequence of the PRSS1 gene defect?

A

Prevents destruction of prematurely activated trypsin

This leads to continual activation of digestive enzymes, resulting in acute injury and chronic pancreatitis.

264
Q

What does the CFTR gene function as?

A

A cyclic AMP–regulated chloride channel

CFTR mutations can block pancreatic ducts and are associated with cystic fibrosis.

265
Q

What is the risk of pancreatitis for patients with two CFTR mutations (compound heterozygotes)?

A

Fortyfold increased risk

This highlights the genetic risk factors associated with chronic pancreatitis.

266
Q

What additional genetic mutation increases the risk of pancreatitis twentyfold?

A

N34S SPINK1 mutation

This mutation, in combination with CFTR mutations, significantly heightens the risk.

267
Q

What is the combined risk of pancreatitis for patients with two CFTR mutations and an N34S SPINK1 mutation?

A

900-fold increased risk

This demonstrates the compounded risk associated with multiple genetic defects.

268
Q

True or False: CFTR mutations are uncommon in the general population.

A

False

CFTR mutations are common, making it unclear if they alone can cause pancreatitis as an autosomal recessive disease.

269
Q

Fill in the blank: The presence of CFTR mutations may reduce the frequency of _______ in heterozygous carriers.

A

acute pancreatitis

This suggests a potential protective effect of CFTR modulators.

270
Q

What does autoimmune pancreatitis (AIP) refer to?

A

A form of chronic pancreatitis with distinct histopathology and unique clinical phenotype.

271
Q

What are the two recognized subtypes of autoimmune pancreatitis?

A

Type 1 AIP and idiopathic duct-centric chronic pancreatitis (IDCP, type 2 AIP).

272
Q

What is type 1 AIP associated with?

A

Pancreatic manifestation of IgG4-related disease.

273
Q

What are the characteristic histopathologic findings of type 1 AIP?

A
  • Lymphoplasmacytic infiltrate
  • Storiform fibrosis
  • Abundant IgG4 cells
274
Q

How is IDCP histologically defined?

A

Presence of granulocytic infiltration of the duct wall without IgG4-positive cells.

275
Q

What is a common association of type 1 AIP?

A

Involvement of other organs including bilateral submandibular gland enlargement and retroperitoneal fibrosis.

276
Q

What is the association of IDCP with inflammatory bowel disease?

A

IDCP is associated with inflammatory bowel disease in ~10% of patients.

277
Q

What are the most common presenting symptoms of AIP?

A
  • Jaundice
  • Weight loss
  • New-onset diabetes
278
Q

What laboratory finding supports the diagnosis of type 1 AIP?

A

Elevated serum IgG4 levels.

279
Q

What imaging findings are typical in AIP?

A

Diffuse or focal enlargement of the pancreas.

280
Q

What is the capsule sign in AIP?

A

Presence of an inflammatory rim that is highly specific for AIP.

281
Q

What do ERCP or MRCP reveal in patients with AIP?

A

Strictures in the bile duct.

282
Q

What mnemonic can help remember the key diagnostic features of AIP?

A

HISORt: Histology, Imaging, Serology, Other organ involvement, Response to glucocorticoid therapy.

283
Q

What is the typical glucocorticoid treatment for AIP?

A

Prednisone at an initial dose of 40 mg/d for 4 weeks, followed by tapering.

284
Q

What is the expected response time to glucocorticoid therapy in AIP patients?

A

Typically within a 2- to 4-week period.

285
Q

What percentage of type 1 AIP patients achieve clinical remission with steroids?

A

99%.

286
Q

What percentage of type 2 AIP patients achieve clinical remission with steroids?

A

92%.

287
Q

What percentage of patients experience disease relapse after treatment for type 1 AIP?

A

31%.

288
Q

What should a poor response to glucocorticoids raise suspicion for?

A

An alternate diagnosis, such as pancreatic cancer.

289
Q

What are potential treatments for patients with multiple relapses of AIP?

A
  • Immunomodulators (e.g., azathioprine)
  • B-cell depletion therapy (e.g., rituximab)
290
Q

True or False: The appearance of interval cancers following a diagnosis of AIP is common.

A

False.

291
Q

What does autoimmune pancreatitis (AIP) refer to?

A

A form of chronic pancreatitis with distinct histopathology and unique clinical phenotype.

292
Q

What are the two recognized subtypes of autoimmune pancreatitis?

A

Type 1 AIP and idiopathic duct-centric chronic pancreatitis (IDCP, type 2 AIP).

293
Q

What is type 1 AIP associated with?

A

Pancreatic manifestation of IgG4-related disease.

294
Q

What are the characteristic histopathologic findings of type 1 AIP?

A
  • Lymphoplasmacytic infiltrate
  • Storiform fibrosis
  • Abundant IgG4 cells
295
Q

How is IDCP histologically defined?

A

Presence of granulocytic infiltration of the duct wall without IgG4-positive cells.

296
Q

What is a common association of type 1 AIP?

A

Involvement of other organs including bilateral submandibular gland enlargement and retroperitoneal fibrosis.

297
Q

What is the association of IDCP with inflammatory bowel disease?

A

IDCP is associated with inflammatory bowel disease in ~10% of patients.

298
Q

What are the most common presenting symptoms of AIP?

A
  • Jaundice
  • Weight loss
  • New-onset diabetes
299
Q

What laboratory finding supports the diagnosis of type 1 AIP?

A

Elevated serum IgG4 levels.

300
Q

What imaging findings are typical in AIP?

A

Diffuse or focal enlargement of the pancreas.

301
Q

What is the capsule sign in AIP?

A

Presence of an inflammatory rim that is highly specific for AIP.

302
Q

What do ERCP or MRCP reveal in patients with AIP?

A

Strictures in the bile duct.

303
Q

What mnemonic can help remember the key diagnostic features of AIP?

A

HISORt: Histology, Imaging, Serology, Other organ involvement, Response to glucocorticoid therapy.

304
Q

What is the typical glucocorticoid treatment for AIP?

A

Prednisone at an initial dose of 40 mg/d for 4 weeks, followed by tapering.

305
Q

What is the expected response time to glucocorticoid therapy in AIP patients?

A

Typically within a 2- to 4-week period.

306
Q

What percentage of type 1 AIP patients achieve clinical remission with steroids?

A

99%.

307
Q

What percentage of type 2 AIP patients achieve clinical remission with steroids?

A

92%.

308
Q

What percentage of patients experience disease relapse after treatment for type 1 AIP?

A

31%.

309
Q

What should a poor response to glucocorticoids raise suspicion for?

A

An alternate diagnosis, such as pancreatic cancer.

310
Q

What are potential treatments for patients with multiple relapses of AIP?

A
  • Immunomodulators (e.g., azathioprine)
  • B-cell depletion therapy (e.g., rituximab)
311
Q

True or False: The appearance of interval cancers following a diagnosis of AIP is common.

A

False.

312
Q

What is the primary reason patients with chronic pancreatitis seek medical attention?

A

Abdominal pain or symptoms of maldigestion

Symptoms of maldigestion include chronic diarrhea, steatorrhea, and weight loss.

313
Q

What is a common consequence of severe abdominal pain in chronic pancreatitis patients?

A

Narcotic dependence

There is often a disparity between reported pain severity and physical findings.

314
Q

What are some symptoms of maldigestion associated with chronic pancreatitis?

A

Chronic diarrhea, steatorrhea, weight loss

Fat-soluble vitamin deficiencies are also increasingly recognized.

315
Q

What percentage of patients with chronic pancreatitis have metabolic bone disease?

A

~65%

This includes conditions like osteopenia or osteoporosis.

316
Q

What serum enzyme levels are moderately specific but poorly sensitive for chronic pancreatitis?

A

Low serum pancreatic enzyme levels

Elevated serum bilirubin and alkaline phosphatase may indicate cholestasis.

317
Q

What cumulative prevalence is associated with exocrine pancreatic insufficiency in chronic pancreatitis?

A

> 80%

Overt steatorrhea is highly suggestive of this complication.

318
Q

What test may be needed to confirm exocrine pancreatic insufficiency in milder cases?

A

Random fecal elastase-1 level

This test is conducted on a formed stool specimen.

319
Q

What is the initial imaging modality of choice for suspected chronic pancreatitis?

A

Abdominal CT imaging

This is followed by MRI, endoscopic ultrasound, and pancreas function testing.

320
Q

What features may be seen on CT imaging in chronic pancreatitis?

A

Calcifications, dilated pancreatic or biliary ducts, atrophic pancreas

CT also helps exclude pseudocyst and pancreatic cancer.

321
Q

What diagnostic test has the best sensitivity for pancreatic disease?

A

Hormone stimulation test using secretin

The secretin test becomes abnormal when ≥60% of pancreatic exocrine function is lost.

322
Q

True or False: EUS alone is specific enough for detecting early chronic pancreatitis.

A

False

EUS may show positive features in patients with diabetes or normal aging.

323
Q

What does diffuse calcifications on plain film of the abdomen indicate?

A

Significant damage to the pancreas

This is pathognomic for chronic pancreatitis.

324
Q

What is the most common cause of pancreatic calcification?

A

Alcohol

Other causes include hereditary pancreatitis, posttraumatic pancreatitis, idiopathic chronic pancreatitis, and tropical pancreatitis.

325
Q

What is the lifetime prevalence of chronic pancreatitis–related diabetes?

A

Exceeds 80%

This indicates that a significant majority of patients with chronic pancreatitis will develop diabetes over their lifetime.

326
Q

What causes hyperglycemia in chronic pancreatitis patients?

A

Insulin deficiency due to loss of islet cells

The loss of islet cells impairs insulin production, leading to elevated blood sugar levels.

327
Q

Are diabetic ketoacidosis and diabetic coma common in chronic pancreatitis?

A

Uncommon

Despite the prevalence of diabetes, severe complications like ketoacidosis are rare.

328
Q

What type of retinopathy may occur in chronic pancreatitis?

A

Nondiabetic retinopathy

This may be associated with deficiencies in vitamin A and/or zinc.

329
Q

What bone conditions are increasingly recognized in chronic pancreatitis?

A

Osteoporosis and osteopenia

These conditions may be linked to factors like alcohol use, cigarette smoking, and vitamin D deficiency.

330
Q

What are potential causes of gastrointestinal bleeding in chronic pancreatitis?

A
  • Peptic ulceration
  • Gastritis
  • Pseudocyst eroding into the duodenum
  • Arterial bleeding into the pancreatic duct (hemosuccus pancreaticus)
  • Ruptured varices secondary to splenic vein thrombosis

These complications arise from various pathophysiological processes associated with chronic pancreatitis.

331
Q

What complications can arise from chronic inflammation around the intrapancreatic portion of the common bile duct?

A
  • Jaundice
  • Cholestasis
  • Biliary cirrhosis

These complications result from the obstruction and damage associated with chronic pancreatitis.

332
Q

Which genetic conditions increase the risk of pancreatic cancer in chronic pancreatitis?

A
  • Hereditary PRSS1
  • Tropical pancreatitis

These conditions are associated with a higher incidence of pancreatic cancer compared to other forms of chronic pancreatitis.

333
Q

What is the cornerstone of therapy for steatorrhea in chronic pancreatitis?

A

Pancreatic enzyme replacement therapy

Complete correction of steatorrhea is uncommon, but enzyme therapy helps control diarrhea and restore fat absorption.

334
Q

What dosage of lipase is generally recommended for adult patients with exocrine pancreatic insufficiency?

A

25,000–50,000 units of lipase taken during each meal

The dose may need to be increased up to 100,000 units based on symptoms and pancreatic function test results.

335
Q

What additional therapy may some patients require to optimize the response to pancreatic enzymes?

A

Acid suppression with proton pump inhibitors

This helps improve the effectiveness of pancreatic enzyme replacement therapy.

336
Q

What effect did pregabalin have in a short-term randomized trial for chronic pancreatitis?

A

Decreased pain and lowered pain medication requirement

This suggests a potential option for managing pain in these patients.

337
Q

What endoscopic treatments may be employed for pain management in chronic pancreatitis?

A

Sphincterotomy, pancreatic duct stenting, stone extraction, drainage of a pancreatic pseudocyst

These interventions are most appropriate in the setting of a dominant stricture.

338
Q

What are some complications that can occur from endoscopic stenting?

A

Stent migration, stent occlusion, stent-induced pancreatic duct strictures

These complications raise concerns about the use of endoscopic stenting.

339
Q

What is the therapy of choice for patients with pancreatic duct dilation?

A

Ductal decompression with surgical therapy

80% of such patients obtain immediate relief, but pain recurrence occurs in half by 3 years.

340
Q

What did randomized trials compare regarding endoscopic and surgical therapy for chronic pancreatitis?

A

Surgical therapy was superior to endoscopy at decreasing pain and improving quality of life

This applies particularly to selected patients with dilated ducts and abdominal pain.

341
Q

What is total pancreatectomy used for in chronic pancreatitis patients?

A

In highly selected patients with abdominal pain refractory to conventional therapy

Some patients may continue to experience pain postoperatively.

Gastroenterology (14 decks)

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