Gi - Acute And Chronic Pancreatitis

Front 1

Exocrine acinar cells

Back 1

Manufacture and secrete numerous digestive enzymes including proteases, lipases, and nucleases.

Front 2

Endocrine cells

Back 2

Secrete insulin, glucagon, somatostatin, pancreatic peptide, and vasoactive intestinal peptide.

Front 3

What is the primary event in acute pancreatitis?

Back 3

Altered acinar cell protective mechanism that lead to intracellular activation of digestive enzymes. This initiates a self perpetuating cascade of cellular and glandular inflammation and injury.

Front 4

What are the systemic affects of acute pancreatitis?

Back 4

Respiratory failure, renal failure, disseminated intravascular coagulation, and shock.

Front 5

What causes the respiratory failure?

Back 5

Phospholipase A2 degrades surfactant and alveolar membranes. Subdiaphragmatic inflammation prevents adequate diaphragmatic excursion. Pain causes shallow respiration. Hemorrhage reduces oxygen carrying capacity.

Front 6

What causes renal failure?

Back 6

Hypovolemia (capillary leak, hemorrhage, kallikrein mediated peripheral vasodilation)

Front 7

What causes disseminated intravascular coagulation?

Back 7

Release of cellular mediators leading to diffuse activation of fibrinolytic and coagulation pathways.

Front 8

What causes shock?

Back 8

Activation of kallikrein, bradykinin, hypovolemia, hemorrhage, and SIRS.

Front 9

What are the principle clinical etiologies of acute pancreatitis?

Back 9

Common duct stones, alcohol, idiopathic, other

Front 10

What are the clinical symptoms of acute pancreatitis?

Back 10

Abdominal pain, nausea, vomiting, low grade fever, dehydration, tender abdomen, mild distension, and decreased or absent bowel sounds.

Front 11

What enzymes will be increased in acute pancreatitis?

Back 11

Amylase and lipase. The magnitudes of increase are of no prognostic significance.

Acute injury to the small bowel can also present in this way.

Front 12

Why should contrast not be used for a CT when a patient is first admitted for suspected acute pancreatitis?

Back 12

Patient is often dehydrated, so it is better to wait 72 hours to use contrast.

Front 13

What is the imaging method of choice for acute pancreatitis?

Back 13

CT

Front 14

What is the overall mortality of acute pancreatitis?

Back 14

9%

Front 15

What is the treatment for acute pancreatitis?

Back 15

None. Thats kind of a bummer. Treat the symptoms.

Front 16

What is the supportive care for acute pancreatitis?

Back 16

Aggressive hydration and electrolyte replacement, pain control, anti-emetics, antibiotics (if infection is present), nutritional support, and organ failure support (if needed).

Front 17

What is the pathophysiology of chronic pancreatitis?

Back 17

Acinar and duct cell damage results in increased membrane permeability. Increased intraductal calcium and protein means protein precipitates to form intraductal plugs. Calcium precipitates to form stones. Patient develops partial duct obstruction. Inflammation, fibrosis, atrophy, and disruption of ducts follows suit. A hard fibrotic pancreas is the result, with a reduction in number and size of acini and islets.

Front 18

What is the main etiology of chronic pancreatitis?

Back 18

Dogfishhead 90 minute IPA. Wait, that can't be right.

Front 19

What are the hereditary forms of chronic pancreatitis?

Back 19

Mutations in the trypsinogen gene or trypsin inhibitor gene, cystic fibrosis, or CFTR

Front 20

What percent of chronic pancreatitis develop recurrent acute attacks?

Back 20

50%

Front 21

What is the gold standard test for chronic pancreatitis?

Back 21

MRI with MRCP

Front 22

What are the treatments for chronic pancreatitis?

Back 22

Alcohol abstinence, low fat diets, pancreatic enzymes with or without acid suppression, analgesics, insulin, surgical decompression, and endoscopic decompression.