Pancreatitis Flashcards
What is acute pancreatitis?
acute inflammation of pancreas and associated adjacent organs without evidence of chronic pancreatitis –> “intraabdominal burn”
- Atlanta criteria 2/3: pain, radiography, amylase/lipase elevated
Severe acute pancreatitis will not occur without _____
retroperitoneal fat around it
Clinical features of acute pancreatitis
severe steady band-like upper abdominal pain, radiating to back –> 10-20 mins onset, lasts several days, 90% vomit/fever, 5-10% painless
What is the nature of most late complications of acute pancreatitis?
infection
Charcot’s triad
fever, jaundice, right upper quadrant pain: cholangitis
Pathophysiology of acute pancreatitis
trypsin activates zymogens in pancreas –> autodigestion of pancreatic cells –> autocascade –> inflammation/polys –> release of neutrophil lactase –> IL1,6 –> leaky capillaries, thrombosis, necrosis –> fluid in lungs –>system response –> hypotension, bowel shutdown, kidney shutdown (all due to blood rushing to pan creas)
How do cardiac arrhythmias occur due to pancreatitis?
fat digestion –> tgs converted to AA –> attract calcium/magnesium –> saponification –> hypocalcemia –> arrhythmia
Most common manifestation of pancreatitis?
mild/interstitial: <1% mortality
Most severe manifestations of pancreatitis?
- infected necrotizing pancreatitis (late): 50% mortality
2. necrotizing/severe pancreatitis (20% of cases): 20 % mortality
2 most common causes of acute pancreatitis
alcohol and gallstones
What kind of effect is pancreatitis?
cholinergic
M or F: Biliary pancreatitis
F
Biliary pancreatitis clinical marker
elevated ALT (not entirely sensitive so can’t rely on this)
Mechanism of alcohol pancreatitis
damages mitochondria, lysosome instability –> ROS, abnormal blood flow and secretion, sensitization to CCK resulting in zymogen activation
M or F alcohol pancreatitis
M
How high to TG have to be to get pancreatitis?
> 1000
How high do amylase/lipase have to be to get pancreatitis?
no threshold…can be normal!
Is pancreatitis a response to high or low glucose?
high glucose –> high TG –> pancreatitis
What is the R122 mutation?
mutation in autodigestion portion of trypsin that leaves it constitutively active
What molecule can activate trypsin?
calcium
What mutation prevents inhibition of trypsin?
loss of both copies of SPINK1
Does this enhance trypsin activation? high pH
no –> low pH does
Does this enhance trypsin activation? bile
yes
Does this enhance trypsin activation? low calcium
no –> high calcium does
Does this enhance trypsin activation? triglycerides
yes
Does this enhance trypsin activation? CCK
yes
Does this enhance trypsin activation? gastric distension
yes
Does this enhance trypsin activation? SPINK1
no –> inhibitor
Does this enhance trypsin activation? somatostatin
no –> inhibitor
Tx of acute pancreatitis
NPO (bowel rest), iv fluids, pain control, ultrasound bladder, CT, surgery, antibiotics
What is chronic pancreatitis?
permanent damage with fibrosis, exocrine/endocrine dysfunction/loss
Features of chronic pancreatitis
calcifications, duct stones, irregular dilated duct without mass, beads on a string dilated side branches, atrophy without mass
Best test for early pancreatitis?
secretin stimulation test/direct test of pancreatic function–> do it b/c damage starts before pain happens so pancreatitis is already underway upon clinical presentation
give secretin and see bicarb production: >80 is normal
T/F cancer risk increases along spectrum of chronic pancreatitis
T
3 theories of pathophysiology of chronic pancreatitis
- ductal obstruction from calcifications/protein precipitates activate trypsin causing upstream damage
- oxidative stress from alcohol/cck/smoking leads to stellate cell activation and fibrosis
- acute inflammatory attacks lead to necrosis and cytokine release that lead to chronic damage and fibrosis
Consequences of chronic pancreatitis
diabetes, steatorrhea, pain, cancer, b12 def, biliary obstruction
Type 3 diabetes
pancreatogenic diabetes: development can indicate cancer, no glucagon/somatostatin so hypoglycemia, usually no ketoacidosis, very insulin sensitive
