ASPEN ch 28 pancreatitis Flashcards
__ released in acinar cytoplasm activates ____
trypsin; TNFa, IL1+6, pro-inflam cytokines
cascade of inflam peaks ___ h after inciting event, can lead to ___
24-36; organ failure
poorer outcomes associated with:
alcoholism, starvation, undernutrition, chronic inflammation (obesity)
risk of severe acute pancreatitis is ___x higher in obese
2-3
why alcohol abuse common associated with pancreatitis?
ethanol sensitize pancreas to injury
pancreatitis with alcohol/gene etiology commonly associated with:
ductal stones, strictures, outflow obstruction
90% of AP caused by:
alcohol abuse, gallstones, idiopathic
other causes AP?
drugs, autoimmune/tropical disease ,infection, hypertriglyceridemia, herediatry, malignancy
what is the sentinel acute pancreatitis event (SAPE) hypothesis?
virtually any etiology of AP if severe enough may lead to scarring and end organ damage
autoimmune induced pancreatitis usually associated with:
less severe acute attacks, small duct disease, silent disease–> chronic pancreatitis with malabsorption
ppl with hereditary pancreatitis , particularly ___ mutations, have increased risk of ____
PRSS1; pancreatic cancer
__ lvls ^ in first hours of AP, then ___
amylase; serum lipase
why amylase/lipase presence not specific?
cleared by kidneys so could be ^ if secretion impaired, many organs produce these
^ liver enzymes, or if liver enzymes wax and wane with bouts of ab pain, suggest ___etiology
biliary
nonbiliary causes of AP associated with:
pain steadily ^ then constant
to optimally manage pt and prevent complications, clinicians need to determine:
severity of acute event ASAP
how to determine disease severity?
CT scans assess necrosis, Ranson, Imrie, Apache 2 scores, SIRS criteria, blood tests for CRP
among scoring methods , ____ is more predictive of both severity and clinical outcomes
APACHE 2
early recognition of SIRS can prompt adequate management with __
intravascular volume replacement (prevent ischemic end organ damage)
why end organ damage
hypoperfusion, changes in microvascular blood flow induced by inflamm cascade
most beneficial management strategies for SAP:
ICU, delay CT, early EN, avoid prophylactic antibiotics, treat local complications
___ scans are used therapeutically as well as for dianosis
EUS and ERCP
why stones in common bile duct and pancreatic cysts often misssed?
artifacts from overlying gas and fluid filled bowel
__ scans used to grade AP:
CT
what is grade B pancreatitis?
focal/diffuse enlargement of pancreas
what is grade C pancreatitis?
pancreatic gland abnormalities accompanied by mild parapancreatic inflamm changes
what is grade D pancreatitis?
fluid collection in single location, usually in anterior pararenal space
what is Grade E pancreatitis?
2+ fluid collections near pancreas or gas either within pancreas or within parapancreatic inflam
grade A-E score is coupled with score for degree of ___ to see if ^ mortality risk
necrosis
endoscopic procedure providing ultrasound exam of pancreas thru gastric wall
EUS (after AP attack)
___ provides direct cannulation of pancraes and biliary ducts
ERCP
ERCP beneficial to treat pt with ____
ascending cholangitis or retained common duct stones
ERCP with ____ highly beneficial for manage pancreatic ascites and pleural effusions
stenting of pancreatic duct disruptions
ERCP with measurement of presssure at ___ useful determine cause of idiopathic
sphincter of Oddi
major indication for endoscopic therapy?
need for long term relief of bile duct strictures that occur as complication of fibrosis from chronic pancreatitis
are prophylactic antibiotics useful?
nope
mild vs severe nutr concerns?
wt loss from muscle catabolism minimal vs. hypermetabolic similar to sepsis (ox stress, catabolism SIRS)
nutr decline in AP can result from reduced oral intake due to:
ab pain, nausea, vomiting, ileus, pancreatic rest
why malabsorb and maldigest?
v enzyme output
why excess pro loss?
steatorrhea, pancreatic fistulas, inflamm of peritoneal/retroperitoneal surface
hyperglycemia risk relate to:
degree of pancreatic inflam, necrosis, obesity, prediabetes
damage to inflam islet cells leads to decreased ___ production and impaired __ metabolism, resulting in hypertriglyceridemia from inadequate glucose control and v of lipoprotein lipase
insulin; lipid
why v calcium?
v PTH, ^ calcitonin, v magnesium
why EN?
maintain fut integrity, stim bloood flow to gut, stim secretory IGA and bile salts (prevent bacteria adherece), maintain gut-associated lympohid tissue, support commensal bacteria, lessen disease severity, v ox stress, faster resolution, reduce complications
in SAP, pt on EN have increases in ___ capacity, faster decreases in ___ levels, and faster resolution of ____ when compared with PN pt
antioxidant; CRP; SIRS
3 bad possibilities of early use of EN?
1) clinically silent ^ in pancreatic enzyme output 2) uncomplicated exacerbation of symptoms 3) significant exacerbation of symptoms and ^ in SIRS
when EN indicated , ___ access easier than ___
gastric; jejunal
pt who will not tolerate EN:
severe ileus or gastroparesis
polymeric formulas infused distal to ___ inhibited pancreatic secretions better than PN
ligament of Treitz
most common causes of diarrhea
sorbitol containing meds and C difficile
if quantity of lipids in PN limited to less than ____and ____ control maintained, hypertriglyceridemia during PN diminished
1g/kg; glucose
how to assess for readiness resume oral?
reduction in pain, absence of vomiting, CT, biochem markers
in CP, gland has ____ changes including irreversible loss of _____ and ___ mass with replacement of stroma by ___ tissue, with or without lymp inflam cell infiltrate
ultrastructural; exocrine; endocrine; fibrous
___ quadruples pt risk of AP progressing to CP
tobacco smoking
why smoking cause CP?
vasoconstrictive nicotine, ox stress, toxic effects
ppl at risk for hypertriglyceridemia induced pancreatitis:
hyperlipoproteinemia, DM, alcohol abuse, obesity, pregnancy
fear of pain w/ eating
sitophobia
complications of CP
diabetes, malabsorption, bile duct stricture, portal hypertension, duodenal stricture, pseudocysts, fistulas and ascites
exocrine insufficiency occurs ____ yrs after onset of CP
10-12 (asini destruction)
exocrine insufficiency manifests as:
diarrhea, steatorrhea, malassimilation
what is steatorrhea?
quantitative appearance of >7 g fat/day after consuming 100g diet fat
reliable, pt friendly, relatively inexpensive way to find out if ppl have steatorrhea
fecal elastase 1 test
vitamin deficiencies common in CP?
fat sol, vit B12
alcohol abuse contributes to ____ deficiencies
thiamin, folate, Mg, Zn
major late sequelae of CP and independent risk factor for mortality
diabetes
hallmark clinical symptom of CP
pain
categories of pain:
nocioceptive (normal), neuropathic, psychogenic
long term EN through ___
PEG
enteric coated preparations of pancreatic enzymes resist degradation by gastric acid and require luminal pH greater than ___
5
if use uncoated enzymes, prevent inactivation with ____
gastric acid suppression
