Pathophysiology of the Pancreas Flashcards

1
Q

What opioid should be avoided in treating acute pancreatic pain due to its contractile effects on the sphincter of Oddi?

A

Morphine

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2
Q

What are the ionic laboratory findings in acute pancreatitis?

A

Hypocalcemia, hypomagnesemia, hyperkalemia, hyperglycemia

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3
Q

What is the function of cholecystokinin?

A

Simulates release of bile from the gallbladder and digestive enzymes from the pancreas into the duodenum

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4
Q

The endocrine portion of the pancreas contains Islets of Langerhans. What molecules are secreted from these Islets?

A

Insulin, glucagon, somatostatin

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5
Q

What is the gold-standard imaging for diagnosis of acute pancreatitis?

A

CT

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6
Q

How does excessive alcohol use increase the risk of pancreatitis?

A

Increases contraction of the sphincter of Oddi, promotes cholecystokinin secretion, causes calcium dysregulation, oxidative stress

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7
Q

In chronic pancreatitis, there is fibrosis and permanent destruction of the exocrine and endocrine pancreatic functions. Which functions are lost first?

A

Exocrine functions lost first, endocrine function lost in late stages

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8
Q

How are serum amylase and lipase levels affected during acute pancreatitis?

A

Increased at least 3x

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9
Q

What is the clinical presentation of acute pancreatitis?

A

Sudden, severe pain that beings in the epigastrium and radiates to the back, anorexia, nausea, vomiting

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10
Q

Where are most pancreatic digestive enzymes synthesized and stored?

A

Acinar cells

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11
Q

True/False. Decreased calcium levels promote the activation of trypsinogen and acute pancreatitis.

A

False - hypercalcemia promotes trypsinogen activation

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12
Q

Autoimmune pancreatitis is responsible for chronic pancreatitis. What is the difference between Types 1 & 2?

A

Type 1 - IgG4 with plasma cells

Type 2 - neutrophils without IgG4

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13
Q

True/False. The prognosis of pancreatitis is related to the amount of pancreatic necrosis.

A

True. Increased necrosis = poorer prognosis

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14
Q

What transcription factor plays a primary role in the progression of local inflammation to systemic inflammatory response syndrome?

A

NF-kB

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15
Q

Serum amylase and lipase are elevated in acute pancreatitis. What are their levels in chronic pancreatitis?

A

Amylase and lipase may be elevated or low due to the destruction of acinar cells.

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16
Q

What is the clinical presentation of chronic pancreatitis?

A

Episodic abdominal pain triggered by alcohol or overeating, weight loss, steatorrhea, diabetes, jaundice

17
Q

How are inactive pancreatic digestive enzymes activated?

A

Enteropeptidase cleaves trypsinogen to trypsin. Active trypsin cleaves and activates other digestive enzymes

18
Q

What is the most specific and sensitive laboratory marker for acute pancreatitis?

A

Serum lipase - however, it is difficult to measure

19
Q

What cytokines are persistently produced in chronic pancreatitis?

A

TGF-b & platelet-derived growth factor (PDGF)

20
Q

What is the recommended treatment for acute pancreatitis?

A

NPO, IV fluids, opioids for pain management

21
Q

What is the most common cause of chronic pancreatitis?

A

Chronic alcohol use

22
Q

The exocrine portion is responsible for most of the pancreas’s function. What enzymes does it secrete?

A

Digestive enzymes

23
Q

What is the mechanism of colocalization of pancreatic enzymes and lysosome hydrolases?

A

Pancreatic enzymes are trafficked to lysosomes and activated by hydrolases. This causes apoptosis of lysosomes and the release of activated enzymes into acinar cells

24
Q

Acute pancreatitis can have many etiologies. What factors are most responsible for metabolic acute pancreatitis?

A

Alcohol overuse, hypertriglyceridemia

25
Q

In acute hemorrhagic pancreatitis, these signs may be present.

A

Ecchymoses of the flank (Grey Turner’s Sign) and periumbilical region (Cullen’s Sign)

26
Q

Vascular fluid is lost during acute pancreatitis due to inflammation. What effect will this have on hematocrit?

A

Hematocrit is elevated in acute pancreatitis.

27
Q

What is the leading cause of death within the first week for patients with acute pancreatitis?

A

Multi-organ failure. After the first week, sepsis becomes the leading cause of death

28
Q

What factors increase the risk of systemic inflammatory response syndrome due to acute pancreatitis?

A

Obesity, chronic alcohol use

29
Q

True/False. Hereditary factors are responsible for a majority of chronic pancreatitis cases.

A

False - Chronic alcohol use is the leading cause of chronic pancreatitis, but hereditary factors are responsible for 25% of cases

30
Q

What four mechanisms promote premature activation of trypsinogen?

A

Duct obstruction, acinar cell injury, calcium dysregulation, colocalization of pancreatic enzymes and lysosomal hydrolases

31
Q

What is the etiology of cholelithiasis in causing acute pancreatitis?

A

Mechanical obstruction

32
Q

What enzyme is responsible for cleaving trypsinogen to trypsin?

A

Enteropeptidase