11b. Pancreatitis: Acute and Chronic Flashcards
acute pancreatitis as seen clinically and on path?
clinically: abdominal pain, high amylase and/or lipase
path: acute inflammation of panc, often with necrosis
Below: mild acute
mild pancreatitis: appearance on histo?
lobules separated due to edema, some inflammatory cells scattered throughout interstitial area
difference between mild and severe acute pancreatitis?
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
besides necrosis of the pancreatic parenchyma and fat, what else might severe acute pancreatitis cause?
fat necrosis extensively spread throughout abdomen. due to release of pancreatic lipase
what structures of the pancreas succumb to necrosis and inflammation earliest in severe acute pancreatitis?
acinar tissue first, then ducts, then islets fat will also necrose.
what is the course of severe acute pancreatitis?
focal (causes focal scarring) then multifocal (patchy scarring) then extensive (SIRS, death, or pseudocysts and abscesses)
define a pseudocyst in the context of acute pancreatitis
walled-off collection of fluid or liquefied tissue. progressively fibrotic. can be small or large, and can involved tissue adjacent to the pancreas
define an abscess in the context of acute pancreatitis. how to diagnose?
necrotic tissue or pseudocyst that has become infected. dx: identify microbe in aspirated liquid
very briefly, what characterizes chronic pancreatitis?
-fibrosis and atrophy, resulting from bouts of inflammation -can be focal, multifocal or diffuse -may see dilated main duct, stones in duct
general causes of chronic pancreatitis?
-alcoholism (repeated acute -> chronic) -cystic fibrosis (due to duct obstruction) -autoimmune -hereditary (repeated acute -> chronic) -progression from acute to chronic via repeated episodes
histologically, what is the biggest difference between acute and chronic pancreatitis?
chronic specimens have replaced the areas of necrosis with fibrosis. still may be some inflammation and edema, but definitely will see fibrosis.
what are complications of chronic pancreatitis?
-dietary malabsorption -diabetes -incr risk of pancreatic carcinoma
Two biggest causes of pancreatitis in US?
alcohol, gallstones
Besides alcohol and gallstones, causes of pancreatitis?
drug toxicity, viral infection (mumps, CMV), trauma (steering wheel to the gut), genetic, autoimmune dz
Pathogenesis of pancreatitis? two pathways
-injury to acinar cells. inappropriate release of panc enzymes leading to autodigestion and inflammation -ductal obstruction. increased pressure, interstitial leakage, activation of pancreatic enzymes
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)
Cathepsin B can trigger a huge cascade which ends in autodigestion of the pancreas, fat necrosis, and systemic shock
gallstones: cause acute or chronic pancreatitis or both?
acute. NOT a major cause of chronic pancreatitis
hereditary cause of pancreatitis: due to mutation in what gene?
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.
pts with hereditary familial pancreatitis: what is the incidence of pancreatic carcinoma in pts with this mutation?
40% have pancreatic carcinoma by 70y
how does cystic fibrosis cause chronic pancreatitis?
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
CF patients with pancreatitis: characteristic change seen on histo?
diffuse fibrosis, dilated ducts, there is mucous inside the ducts
autoimmune pancreatitis (AIP): how will the pancreas appear grossly? what has it historically been mistaken for?
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.
how will a patient with AIP present? what treatment should work for them?
presents with jaundice (maybe other things; ppt was sparse on this) tx = steroids
how does AIP look on histology?
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.
what immune components are involved in AIP? Labs?
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.
how does alcoholism cause acute pancreatitis?
thought that it’s a direct toxic effect of alcohol or one of its metabolites -> altered lipid metabolism -> oxidative stress -> free radicals
