Exocrine Pancreas Path Flashcards
What is the function of acinar cells in the pancreas?
Secrete zymogen enzymes
The epithelial cells lining the ducts are susceptible to what genetic mutation?
Ductal cells–> secrete mucus and HCO3
***Cystic Fibrosis (CFTR)
What are the pancreatic safety mechanisms?
- Zymogens
- Trypsinogen–> Trypsin requires Duodenal enteropeptidase (enterokinase)
- Trypsin inhibitor in cytoplasm
- Trypsin cleaves and inactivates itself
- Acinar cells are resistant to action of activated enzymes (trypsin + chymotrypsin + phospholipase A2)
MC congenital anomaly resulting from failure of the fetal pancreatic ductal system to fuse creating high pressure in the pancreas and Increased risk for Chronic Pancreatitis?
Pancreas Divisum
Annular= Blocks the 1st part of duodenum
Reversible inflammatory disorder of the pancreas is most often caused by?
Acute pancreatitis= ETOH + gallstone
What two infections are know to cause Acute pancreatitis?
Mumps + Coxsackievirus
What is the genetic mutation behind Hereditary pancreatitis?
- AD
- Mutation= Hyperactive Trypsin + overactivation of other enzymes
- Recurrent bouts of severe pancreatitis
What are the 5 essential alterations in acute pancreatitis?
- microvascular leakage= edema
- Fat Necrosis= Lipases
- Acute inflammatory rxn
- Proteolytic destruction of parenchyma
- BV destruction= hemorrhage
What does Fat necrosis of the pancreas lead to?
Calcium deposition = HYPOcalcemia
The cleavage/ activation of what enzyme is a key cause of acute pancreatitis?
Trypsin = Activates other enzymes
What are the 3 pathways that can incite the initial enzyme activation that may lead to acute pancreatitis?
- Gallstone-> backflow-> lipase escapes-> fat necrosis-> inflammation -> vascular damage= ischemia= Acinar cell death
- Defective intracellular transport of proenzymes within acinar cells
- ETOH= Hyper secretion + constriction of Oddi
= Directly toxic to acinar cells
= protein rich secretion leads to PLUGS
Describe the Pathogenesis of Acute pancreatitis caused by Duct obstruction?
Gallstone + ETOH = interstitial edema= ischemia = Acinar cell injury = Activated enzymes causes: Inflammation Proteolysis Fat necrosis Hemorrhage
Describe the Pathogenesis of Acute pancreatitis caused by Acinar cell injury?
ETOH + Drugs + Ischemia + VIRUSES = Release intracellular proenzymes and hydrolases= Activate enzymes WITHIN pancreas= Acinar cell injury = Activated enzymes causes: Inflammation Proteolysis Fat necrosis Hemorrhage
Pt with acute abdominal pain, guarding, and ominous absence of bowel sounds?
Acute pancreatitis–> Pain radiates to Back because its Retroperitoneal
What are the manifestations of Severe acute pancreatitis attributable to systemic release of enzymes?
Leukocytosis (>17,000)
DIC
ARDS
Fat necrosis
What lab findings are seen in acute pancreatitis?
Elevated Amylase + Lipase
Hypocalcemia
CT/ MRI showing enlarged pancreas
What is the MC sequela of Acute pancreatitis?
Pseudocyst= Area of Liquifactive necrosis walled off by fibrous layer (no epithelial lining + filled with enzymes)
What is the chief distinction between acute and chronic pancreatitis?
Chronic= IRREVERSIBLE impairment in pancreatic function
What are MCCs of Chronic pancreatitis?
Alcohol abuse
Chronic ductal obstruction
Hereditary pancreatitis
Cystic Fibrosis
Pt with repeated bouts of jaundice, indigestion, persistent abdominal pain, recurrent back pain. What is the Most likely cause of his symptoms?
Chronic pancreatitis= ETOH
70 yo male with Pancreatic cystic neoplasm composed of glycogen rich cuboidal, “straw-colored fluid, von Hippel-Lindau?
Serous Cystadenoma
Slow growing painless neoplastic mass cystic lesion lined by columnar cells. Most often in women and 1/3 become invasive adenocarcinoma?
Mucinous Cystic Neoplasms
What are the MOST COMMON precancerous lesions in the pancreas?
PanIN (pancreatic intraepithelial neoplasias
What are the Most common altered genes in Pancreatic neoplasms?
KRAS
p16
Strongest environmental risk factor for Pancreatic Cancer?
SMOKING
Painless Jaundice?
Pancreatic Tumor in head of Pancreas
