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GI block > Exocrine Pancreas Path > Flashcards

Exocrine Pancreas Path Flashcards

1
Q

What is the function of acinar cells in the pancreas?

A

Secrete zymogen enzymes

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2
Q

The epithelial cells lining the ducts are susceptible to what genetic mutation?

A

Ductal cells–> secrete mucus and HCO3

***Cystic Fibrosis (CFTR)

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3
Q

What are the pancreatic safety mechanisms?

A
  1. Zymogens
  2. Trypsinogen–> Trypsin requires Duodenal enteropeptidase (enterokinase)
  3. Trypsin inhibitor in cytoplasm
  4. Trypsin cleaves and inactivates itself
  5. Acinar cells are resistant to action of activated enzymes (trypsin + chymotrypsin + phospholipase A2)
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4
Q

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?

A

Pancreas Divisum

Annular= Blocks the 1st part of duodenum

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5
Q

Reversible inflammatory disorder of the pancreas is most often caused by?

A

Acute pancreatitis= ETOH + gallstone

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6
Q

What two infections are know to cause Acute pancreatitis?

A

Mumps + Coxsackievirus

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7
Q

What is the genetic mutation behind Hereditary pancreatitis?

A
  1. AD
  2. Mutation= Hyperactive Trypsin + overactivation of other enzymes
  3. Recurrent bouts of severe pancreatitis
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8
Q

What are the 5 essential alterations in acute pancreatitis?

A
  1. microvascular leakage= edema
  2. Fat Necrosis= Lipases
  3. Acute inflammatory rxn
  4. Proteolytic destruction of parenchyma
  5. BV destruction= hemorrhage
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9
Q

What does Fat necrosis of the pancreas lead to?

A

Calcium deposition = HYPOcalcemia

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10
Q

The cleavage/ activation of what enzyme is a key cause of acute pancreatitis?

A

Trypsin = Activates other enzymes

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11
Q

What are the 3 pathways that can incite the initial enzyme activation that may lead to acute pancreatitis?

A
  1. Gallstone-> backflow-> lipase escapes-> fat necrosis-> inflammation -> vascular damage= ischemia= Acinar cell death
  2. Defective intracellular transport of proenzymes within acinar cells
  3. ETOH= Hyper secretion + constriction of Oddi
    = Directly toxic to acinar cells
    = protein rich secretion leads to PLUGS
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12
Q

Describe the Pathogenesis of Acute pancreatitis caused by Duct obstruction?

A 
Gallstone + ETOH = interstitial edema= ischemia = Acinar cell injury = Activated enzymes causes: 
Inflammation
Proteolysis 
Fat necrosis 
Hemorrhage
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13
Q

Describe the Pathogenesis of Acute pancreatitis caused by Acinar cell injury?

A 
ETOH + Drugs + Ischemia + VIRUSES = Release intracellular proenzymes and hydrolases= Activate enzymes WITHIN pancreas= Acinar cell injury = Activated enzymes causes: 
Inflammation
Proteolysis 
Fat necrosis 
Hemorrhage
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14
Q

Pt with acute abdominal pain, guarding, and ominous absence of bowel sounds?

A

Acute pancreatitis–> Pain radiates to Back because its Retroperitoneal

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15
Q

What are the manifestations of Severe acute pancreatitis attributable to systemic release of enzymes?

A

Leukocytosis (>17,000)
DIC
ARDS
Fat necrosis

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16
Q

What lab findings are seen in acute pancreatitis?

A

Elevated Amylase + Lipase
Hypocalcemia
CT/ MRI showing enlarged pancreas

17
Q

What is the MC sequela of Acute pancreatitis?

A

Pseudocyst= Area of Liquifactive necrosis walled off by fibrous layer (no epithelial lining + filled with enzymes)

18
Q

What is the chief distinction between acute and chronic pancreatitis?

A

Chronic= IRREVERSIBLE impairment in pancreatic function

19
Q

What are MCCs of Chronic pancreatitis?

A

Alcohol abuse
Chronic ductal obstruction
Hereditary pancreatitis
Cystic Fibrosis

20
Q

Pt with repeated bouts of jaundice, indigestion, persistent abdominal pain, recurrent back pain. What is the Most likely cause of his symptoms?

A

Chronic pancreatitis= ETOH

21
Q

70 yo male with Pancreatic cystic neoplasm composed of glycogen rich cuboidal, “straw-colored fluid, von Hippel-Lindau?

A

Serous Cystadenoma

22
Q

Slow growing painless neoplastic mass cystic lesion lined by columnar cells. Most often in women and 1/3 become invasive adenocarcinoma?

A

Mucinous Cystic Neoplasms

23
Q

What are the MOST COMMON precancerous lesions in the pancreas?

A

PanIN (pancreatic intraepithelial neoplasias

24
Q

What are the Most common altered genes in Pancreatic neoplasms?

A

KRAS

p16

25
Q

Strongest environmental risk factor for Pancreatic Cancer?

A

SMOKING

26
Q

Painless Jaundice?

A

Pancreatic Tumor in head of Pancreas

GI block (6 decks)

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