30 Questions
Which portion of the pancreas makes up 90% of the organ and is a major source of enzymes essential for digestion?
Exocrine portion
What do Islets of Langerhans secrete?
Insulin, glucagon, and somatostatin
What is the main clinical manifestation of pancreatitis?
Inflammation of the pancreas
Which disorders are most significant for the endocrine pancreas?
$Diabetes$ $mellitus$ and neoplasms
Which portion of the pancreas secretes enzymes essential for digestion?
$Acinar$ $cells$
What characterizes the severity range of pancreatitis?
$Mild$ $self-limited$ $disease$ to life-threatening idiopathic acute inflammatory process
What is the most common cause of chronic pancreatitis?
Chronic alcohol abuse
Which mutations are associated with potential hereditary factors in idiopathic chronic pancreatitis?
CFTR and PRSS1
What are the clinical features of chronic pancreatitis?
Repeated abdominal pain, jaundice, weight loss, and hypoalbuminemic edema
What are the complications associated with chronic pancreatitis?
Pancreatic insufficiency, diabetes mellitus, and pancreatic pseudocysts
What is the mortality rate over 20 to 25 years for those with chronic pancreatitis?
$50 ext{%}$
What dietary recommendation should be given to patients with chronic pancreatitis?
Consume small, frequent, low-fat meals
Which of the following is a common cause of chronic pancreatitis?
Alcoholism
What are the typical laboratory findings in acute pancreatitis?
Elevated serum amylase and lipase levels, and hypocalcemia
What is the most likely diagnosis for a 60-year-old alcoholic man with recurrent epigastric pain, weight loss, and foul smelling diarrhea, and X-ray revealing multiple areas of calcification in the mid-abdomen?
Chronic pancreatitis
What is the primary triggering event in acute pancreatitis?
Hyperactivation of trypsinogen
What is a possible cause of acute hemorrhagic pancreatitis?
Alcohol abuse and gallstone impaction
Which of the following symptoms is not typically associated with chronic pancreatitis?
Hypoglycemia
Which of the following is a characteristic feature of fat necrosis in acute pancreatitis?
Red-black hemorrhage and yellow-white, chalky foci
What is the result of fat necrosis in acute pancreatitis?
Insoluble calcium salts that form in situ
Where can fat necrosis occur in acute pancreatitis?
Extra-pancreatic collections of fat, including omentum and bowel mesentery
What are the consequences of acute pancreatitis?
Shock, acute renal failure, and multi-organ failure
What laboratory findings are associated with acute pancreatitis?
Markedly elevated serum amylase and lipase, and hypocalcemia
What complications can arise from acute pancreatitis?
Shock, acute respiratory distress syndrome, acute renal failure, sterile or infected pancreatic abscesses, and pancreatic pseudocysts
Which condition is associated with irreversible loss of exocrine pancreatic parenchyma?
Chronic Pancreatitis
What can lead to local fat necrosis in acute pancreatitis?
All of the above
What can cause primary acinar cell injury in acute pancreatitis?
Viral infections
What alterations are seen in acute pancreatitis histology?
All of the above
What can contribute to the development of acute pancreatitis?
All of the above
What is the incidence rate of acute pancreatitis in Western countries?
10 to 20 cases per 100,000 people
Study Notes
- Acute Pancreatitis: Reversible injury to the pancreas associated with inflammation, relatively common with an incidence rate of 10 to 20 cases per 100,000 people in Western countries. Common causes include biliary tract diseases and alcoholism.
- Chronic Pancreatitis: Irreversible loss of exocrine pancreatic parenchyma.
- Acute Pancreatitis Pathology:
- Caused by autodigestion of the pancreas by inappropriately activated pancreatic enzymes.
- Three pathways can incite the initial enzyme activation: pancreatic duct obstruction, primary acinar cell injury, and direct trauma.
- Pancreatic Duct Obstruction:
- Gallstones or biliary sludge impaction, or compression of the ductal system by a mass, resulting in increased intraductal pressure and accumulation of an enzyme-rich interstitial fluid.
- Lipase, secreted in an active form, can lead to local fat necrosis, contributing to local inflammation, interstitial edema, and vascular insufficiency.
- Primary Acinar Cell Injury:
- Impacts acute pancreatitis caused by ischemia, viral infections, drugs, and direct trauma to the pancreas.
- Defective intracellular transport of proenzymes within acinar cells can lead to blockage of ductal flow, increased intraductal pressure, and accumulation of enzyme-rich interstitial fluid.
- Acute Pancreatitis Histology:
- Alterations include microvascular leakage causing edema, fat necrosis by lipolytic enzymes, acute inflammation, proteolytic destruction of pancreatic parenchyma, and destruction of blood vessels resulting in interstitial hemorrhage.
- Acute necrotizing pancreatitis and hemorrhagic pancreatitis can lead to shock and fat necrosis in extra-pancreatic fat, the omentum, pancreatitis bowel mesentery, and even outside the abdominal cavity.
- Etiologic Factors:
- Alcoholism, hyperlipoproteinemia, hypercalcemia, medications (85 drugs), germline mutations in the cationic trypsinogen and trypsin inhibitor genes, mechanical issues (gallstones and obstruction of the pancreatic duct), trauma, iatrogenic injury, perioperative injury, endoscopic procedures with dye injection, vascular issues, and infections.
Overall, acute pancreatitis is a reversible inflammatory condition affecting the pancreas, while chronic pancreatitis is an irreversible condition with exocrine parenchyma loss. Acute pancreatitis is caused by autodigestion of the pancreas by inappropriately activated pancreatic enzymes, and it is associated with microvascular leakage, fat necrosis, acute inflammation, and proteolytic destruction of pancreatic parenchyma. Multiple etiologic factors can contribute to the development of acute pancreatitis, including alcoholism, biliary tract diseases, and medications, among others.
Test your knowledge about the pathology of pancreatic fat necrosis, including the appearance of red-black hemorrhage and foci of yellow-white, chalky fat necrosis, and its occurrence in extra-pancreatic fat collections.
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