11b. Pancreatitis: Acute and Chronic Flashcards

1
Q

acute pancreatitis as seen clinically and on path?

A

clinically: abdominal pain, high amylase and/or lipase
path: acute inflammation of panc, often with necrosis

Below: mild acute

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2
Q

mild pancreatitis: appearance on histo?

A

lobules separated due to edema, some inflammatory cells scattered throughout interstitial area

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3
Q

difference between mild and severe acute pancreatitis?

A

bottom line: difference is NECROSIS/HEMOR mild: edema with inflammatory infiltrate. NO necrosis severe: extensive necrosis of parenchyma and fat, hemorrhage due to leaky blood vessels

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4
Q

besides necrosis of the pancreatic parenchyma and fat, what else might severe acute pancreatitis cause?

A

fat necrosis extensively spread throughout abdomen. due to release of pancreatic lipase

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5
Q

what structures of the pancreas succumb to necrosis and inflammation earliest in severe acute pancreatitis?

A

acinar tissue first, then ducts, then islets fat will also necrose.

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6
Q

what is the course of severe acute pancreatitis?

A

focal (causes focal scarring) then multifocal (patchy scarring) then extensive (SIRS, death, or pseudocysts and abscesses)

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7
Q

define a pseudocyst in the context of acute pancreatitis

A

walled-off collection of fluid or liquefied tissue. progressively fibrotic. can be small or large, and can involved tissue adjacent to the pancreas

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8
Q

define an abscess in the context of acute pancreatitis. how to diagnose?

A

necrotic tissue or pseudocyst that has become infected. dx: identify microbe in aspirated liquid

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9
Q

very briefly, what characterizes chronic pancreatitis?

A

-fibrosis and atrophy, resulting from bouts of inflammation -can be focal, multifocal or diffuse -may see dilated main duct, stones in duct

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10
Q

general causes of chronic pancreatitis?

A

-alcoholism (repeated acute -> chronic) -cystic fibrosis (due to duct obstruction) -autoimmune -hereditary (repeated acute -> chronic) -progression from acute to chronic via repeated episodes

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11
Q

histologically, what is the biggest difference between acute and chronic pancreatitis?

A

chronic specimens have replaced the areas of necrosis with fibrosis. still may be some inflammation and edema, but definitely will see fibrosis.

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12
Q

what are complications of chronic pancreatitis?

A

-dietary malabsorption -diabetes -incr risk of pancreatic carcinoma

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13
Q

Two biggest causes of pancreatitis in US?

A

alcohol, gallstones

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14
Q

Besides alcohol and gallstones, causes of pancreatitis?

A

drug toxicity, viral infection (mumps, CMV), trauma (steering wheel to the gut), genetic, autoimmune dz

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15
Q

Pathogenesis of pancreatitis? two pathways

A

-injury to acinar cells. inappropriate release of panc enzymes leading to autodigestion and inflammation -ductal obstruction. increased pressure, interstitial leakage, activation of pancreatic enzymes

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16
Q

Typically enterokinase in the duodenal brush border activates trypsin and thus triggers the activation cascade for pancreatic enzymes. What else can activate trypsin? (comes from leukocytes)

A

Cathepsin B can trigger a huge cascade which ends in autodigestion of the pancreas, fat necrosis, and systemic shock

17
Q

gallstones: cause acute or chronic pancreatitis or both?

A

acute. NOT a major cause of chronic pancreatitis

18
Q

hereditary cause of pancreatitis: due to mutation in what gene?

A

mutant trypsinogen gene. normally has a site to prevent its own activation (has ability to auto-digest if needed). the mutation turns off this ability -> trypsin resists inactivation, persists longer, causes damage, pt is predisposed to pancreatitis.

19
Q

pts with hereditary familial pancreatitis: what is the incidence of pancreatic carcinoma in pts with this mutation?

A

40% have pancreatic carcinoma by 70y

20
Q

how does cystic fibrosis cause chronic pancreatitis?

A

the CFTR gene causes a defect in epithelial cell electrolyte transport. cannot adequately hydrate mucus. viscous material collects in ducts. leads to ductal obstruction -> chronic pancreatitis

21
Q

CF patients with pancreatitis: characteristic change seen on histo?

A

diffuse fibrosis, dilated ducts, there is mucous inside the ducts

22
Q

autoimmune pancreatitis (AIP): how will the pancreas appear grossly? what has it historically been mistaken for?

A

the pancreas has a mass on the head of the pancreas, visible with imaging. historically this has been mistaken for cancer and the pancreas removed.

23
Q

how will a patient with AIP present? what treatment should work for them?

A

presents with jaundice (maybe other things; ppt was sparse on this) tx = steroids

24
Q

how does AIP look on histology?

A

path diagnosis is chronic and acute pancreatitis, with fibrosis and atrophy. periductal inflammation, lumens are being squeezed closed. fibrosis and inflammation are focused on ducts.

25
Q

what immune components are involved in AIP? Labs?

A

AIP Type 1 is associated with IgG4-related diseases and involvement of other nearby organs. labs will have elevated serum IgG4 or autoantibodies. Note that there is also AIP Type 2: associated with IBD.

26
Q

how does alcoholism cause acute pancreatitis?

A

thought that it’s a direct toxic effect of alcohol or one of its metabolites -> altered lipid metabolism -> oxidative stress -> free radicals