11c. Clinical Aspects of Acute and Chronic Pancreatitis Flashcards
serum amylase: why is it relevant?
name several tissues that it comes from?
what does it do?
- cornerstone to diagnosis of pancreatitis! leaks from inflamed pancreas, then is reabsorbed.
- comes from pancreas, salivary glands, fallopian tubes, ovaries, prostate, lung
- acts on starch to split alpha 1-4 glucosidic bonds
serum amylase lab: what is its sensitivity and specificity for pancreatitis? (relative, not numbers)
sensitivity is high, esp early in course
specificity is low, esp at lower elevations
serum lipase: why is it relevant?
how does it change with time?
other conditions that will make it elevated?
- as sensitive for acute pancreatitis as amylase, but more SPECIFIC
- elevated the first day of illness, remains elevated longer than amylase
- other intra-abdominal probs and renal insuff can elevate it (usually only to levels less than 1000 u/L)
Atlanta Criteria for acute pancreatitis?
Two of these three:
- abd pain clinically consistent with acute pancreatitis
- elevated amylase/lipase greater than 3x upper limit of normal
- confirmation via abdominal imaging
clinical diagnosis of acute pancreatitis?
- symptoms and PE
- lab tests
- other conditions ruled out
role of imaging in diagnosing acute pancreatitis?
- not essential
- confirmatory
- stages severity, indicates complications
protective mechanisms in the pancreas that prevent activation of zymogens? (this info is also in another deck, but just for repetition)
- enzymes are synthesized/stored in inactive form
- trypsin inhibitor is packaged in zymogen granule just in case
- enzymes are segregated in membrane-bound compartments
- enterokinase exists only in the small intestine
- acidic pH in granules inhibits trypsin
serum levels of amylase and lipase over time with acute pancreatitis? what levels might be seen in a case with delayed presentation?
both initially rise quickly, then amylase falls more quickly than lipase.
in a delayed presentation, labs may show elevated lipase but normal amylase (since it returned to nl more quickly)
what other conditions may elevate both serum amylase and serum lipase?
- intestinal ulceration, obstruction, ulceration or ischemia. intraluminal pancreatic enzymes are re-absorbed from gut back into bloodstream due to damaged intestinal mucosa.
- elevated amylase and slightly elevated lipase are seen in biliary tract disease and renal failure
two types of acute pancreatitis? what does Benson think about these two types?
mild and severe acute pancreatitis
Bensen thinks they are very distinct from each other (apples/oranges)
what are a few ways to assess the severity of acute pancreatitis?
- BISAP > 2
- BUN > 22
- CRP > 150 at 48h
- SIRS persisting at 48h
what is BISAP?
5 elements, 2+ = severe acute pancreatitis:
- BUN > 25
- Impaired mental status
- SIRS
- Age > 60
- Pleural effusion
what is SIRS?
systematic inflammatory response syndrome. defined by at least 2:
- Tachycardia: pulse > 90
- Pulm: RR > 20 or PCO2 < 32
- Temp: T > 100.4 or < 96.8
- Infection: WBC > 12,000 or < 4,000
what are Ranson’s Criteria of Severity (general overview)?
(not on exam, may still be on boards)
eleven criteria taken both at time of admission and after 48h that predict the severity of outcome (mild v severe) in acute pancreatitis.
what feature of a patient will worsen the prognosis of acute pancreatitis?
OBESITY.
increases both severity and complications
Prognosis of mild (interstitial) v severe (necrotizing) acute pancreatitis?
mild (interstitial): infection and mortality both < 1%
severe (necrotizing): infection 30-50%, mortality 10-30%
Causes of death in acute pancreatitis if death occurs early on (< 1 wk)?
*multiorgan failure
SIRS
Causes of death in acute pancreatitis if death occurs later on (> 1 wk)?
*pancreatic infections, sepsis, infectious complications
multiorgan failure
2 most common causes of acute pancreatitis?
alcohol, gallstones
also idiopathic and ‘other’ causes
mechanisms for gallstone causing acute pancreatitis?
- stone obstructing the common opening of the common bile duct and pancreatic duct, allows reflux of bile into the pancreas
- obstructed pancreatic duct, same reflux problem
what are a few things included in the ‘other’ category of causes of acute pancreatitis?
(impt because some of these causes are reversible)
- drugs, toxins
- metabolic and structural issues
- autoimmune
- infectious
- neoplastic
- trauma
how does a gallstone look on ultrasound?
white round/oval mass with characteristic acoustic ‘shadow’ – darkened area where US was blocked by stone
how does microlithiasis/biliary sludge look on ultrasound?
dense layer of material in dependent area of gallbladder. does not cause an acoustic shadow like a gallstone will.
what anatomical anomaly puts pts at higher risk for acute pancreatitis?
pancreas divisum
inherited causes of acute pancreatitis?
- altered enzyme activity: trypsinogen mutation
- Cystic Fibrosis (may not be a mutation severe enough to cause CF, but can still cause reduction in CFTR function -> pancreatitis)
- familial hypertriglyceridemia
familial hypertriglyceridemia: what are serum triglyceride levels? mechanism of causing pancreatitis?
- serum TG levels > 1000
- reversible, can also be drug-induced
- mechanism (theoretical): lipase continuously released from pancreas, TG hydrolysis generates short chain FAs that are toxic to the pancreas
mechanism by which trauma can cause acute pancreatitis?
- midline injury, panc compressed against spine
- may sever pancreatic duct
- may cause ductal leak
- may cause a gradual obstructing stenosis of duct at site of trauma
a cause of pancreatitis in south america?
scorpion bite! toxin can cause pancreatitis.
found in central and south america and the caribbean
strategies for altering the severity of acute pancreatitis?
unfortunately there is very little data to show that interventions exist.
in severe gallstone pancreatitis ERCP seems to help (removal of the stone)
supportive care for acute pancreatitis?
aggressive fluid and electrolyte replacement
monitoring
analgesia
systemic complications of acute pancreatitis?
shock/multiorgan failure coagulopathy resp failure renal failure hyperglycemia hypocalcemia
a local complication of acute pancreatitis that may self-resolve?
acute fluid collection, around the pancreas. usually resolve spontaneously but may require drainage (if infected or symptomatic)
what is a pancreatic pseudocyst?
localized pancreatic fluid collection with a well-defined, fibrous wall. not lined by epithelium (hence PSEUDOcyst).
why is someone with acute pancreatitis at incr risk for infection?
in the critically ill pt there is a breakdown in the fut barrier function, allows translocation of gut bacteria
nutrition issues in pancreatitis: what should I do in mild acute pancreatitis? severe acute pancreatitis? TPN vs enteral? composition of diet?
- nutritional support not as impt in mild acute pancreatitis: early recovery is expected
- severe acute pancreatitis: nutritional support will speed recovery, prevent nutritional depletion.
- enteral is beneficial and safe for severe acute panc.
- give low fat elemental diet into the jejunum
cardinal clinical features of chronic pancreatitis?
- pain
- calcification (intraductal)
- panc insufficiency (endo and exocrine)
- eventually: malabsorption, diabetes
western countries; most common cause of chronic pancreatitis? other causes?
alcoholism
other causes include CF, hereditary, hypertriglyceridemia, autoimmune
causes of pain in chronic pancreatitis?
- acute pancreatitis superimposed on chronic (inf, pseudocysts)
- obstruction -> incr pressure
- nerve inflammation
how diminished does a person’s lipase reserve have to get before the pt will show signs of steatorrhea?
- capacity of panc to secrete lipase must decr to 10% of normal level before excess fecal fat excretion (steatorrhea)
- so, we have impressive reserves of lipase
- also, when a pt with chronic pancreatitis presents with steatorrhea, it implies that 90% of their pancreas is destroyed
what’s the best way to detect pancreatic calcifications?
CT: more sensitive than abd Xray, often used if the xray is negative
in patients with fat malabsorption due to severe pancreatic insufficiency, what is a possible treatment?
pancreatic enzyme supplements. decreased fecal fat excretion by greater than 50%
pain management for chronic pancreatitis? what is the role of narcotics, TCAs, anti-inflammatories, decreasing pancreatic stimulation?
- narcotics are first line. AE = addiction, pain from narcotic bowel syndrome
- TCAs help some patients (neuromodulation)
- anti-inf not shown to be helpful
- somatostatin analogs (octreotide) not very helpful
what is a lateral pancreaticojejunostomy?
- aka Puestow procedure.
- reduces pain in chronic pancreatitis
- main pancreatic duct is opened, jejunum anastomosed so that pancreatic duct drains directly into the jejunum.
