pancrease pathoma Flashcards

1
Q

What is annular pancreas?

A
  • Developmental malformation where pancreas forms ring around duodenum.
  • Risk of duodenal obstruction
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2
Q

Describe acute pancreatitis

A

Acute pancreatitis is reversible enzymatic digestion of pancreas with hemorrhagic damage
(pancreas has lots of blood supply).
-

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3
Q

acute pancreatitis, it’s etiology

A

Etiology
○ EtOH and gallstones cause >75% of cases
EtOh causes contraction of sphincter of oddi which slows drainage of pancreatic
enzymes –> risking premature activation of enzymes in pancreas
○other
 Trauma (ex - automobile accident)
 Hypercalcemia (Ca is activator of enzymes)
 Hyperlipidemia (
Cystic fibrosis (In CF, low bicarb and water drainage to pancreatic ducts; slow flow
and thick enzyme –> enzyme activation)

 Drugs, scorpion venom
 Mumps
 Rupture of duodenal ulcer

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4
Q

acute pancreatitis pathophysiology

A

Activation of trypsinogen is the first step that cause activation of other enzymes

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5
Q

acute pancreatitis presentation.

A

○ Epigastric pain radiating to back (pancreas is secondary retroperitoneal organ)
○ Nausa, vomiting
○ Periumbilical and flank hemorrhage

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6
Q

How do you diagnose acute pancreatitis?

A
  • Elevated lipase (3 times normal) - most commonly used in diagnosis
  • Elevated amylase
  • Hypocalcemia - fat necrosis of peripancreatic fat uses up Ca in blood - poor prognotic indicator
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7
Q

What is complication of acute pancreatitis?

A

Shock - pancreas is very vascular so damage can lead to tons of hemorrhage
Pancreatic pseudocyst -
Pt has abdominal mass with persistent increased in amylase after acute pancreatitis.
Pseudocyst rupture cause release of enzyme and digestion and hemorrhage of gut.
○ Usually due to E.Coli. Pt presents with persistently increased amylase.
- Pancreatic abscess
- DIC - enzymes get on blood, digest coagulation factors
- ARDS - enzymes get to blood, go to lungs and damage alveoli-capillary interface

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8
Q

What causes chronic pancreatitis

A

Chronic pancreatitis is fibrosis of pancreatic parenchyma which occurs after multiple bouts of
acute pancreatitis
-

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9
Q

chronic pancreatitis Etiology

A

EtOH (most common in adults)
○ Cystic fibrosis (most common in kids)
○ Idiopathic
These etiologies cause repeated attack to pancreas. Other etiology of acute pancreatitis (ex -
hypercalcemia, scorpion bite etc happen only once or so.

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10
Q

What are features of chronic pancreatitis?

A
  • Epigastric pain radiating to back
    ○ Leads to malabsorption with steatorrhea
    ○ Fat soluble vitamin deficiency
  • Pancreatic insufficiency (small fibrosed pancreas)
  • Dystrophic calcification of pancreas
  • 20 DM in late phase - due to damage of islet cells
  • High risk of pancreatic carcinoma
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11
Q

Why are serum lipase and amylase not good marker for chronic pancreatitis?

A

Because in chronic pancreatitis, pancreas don’t produce much enzyme so enzymes aren’t
elevated in blood.

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12
Q

Describe pancreatic adenocarcinoma, it’s risk factor and patient population

A

It’s adenocarcinoma arising from pancreatic ducts
- Most commonly seen in elderly
○ Smoking and chronic pancreatitis
- Major risk factor (HY) -

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13
Q

What is presentation of pancreatic adenocarcinoma?

A

f tumor in head of pancreas - obstructive jaundice with pale stool, palpable gallbladder (blocking
of common bile duct)
If tumor in body or tail or pancreas - 20 DM
- Acute pancreatitis - due to obstruction of duct
Migratory thrombophelebitis
Swelling, erythema and tenderness of extremities
- Serum tumor marker is CA 19-9

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14
Q

What is prognosis and treatment of pancreatic adenocarcinoma?

A

Very poor - prognosis (1 year survival <10%)

- Treatment is whipple procedure - take out head & neck of pancreas, duodenum and gall bladder

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