Term
bicarbonate:
principle ion of physioloci imporantce
neutralizes gastric acid in small intestine
provides appropriate pH for maintaining activity of pancreatic enzymes
digestive enzymes:
secreted as zymogens (inactive enzymes) which are activated in the duodenum
regulation of secretion is complex and depends on hormonal and neuronal mechanism
2 hormones: secretin and cholecystokinin (CCK) important in post-prandial secretion
proteolytic: tryspsinogen, chymotrypsinogen, procarboxypeptidase, protealase
amylotyic: amylase
lipolytic: lipase, phospholipase A, carboxylesterase lipase
nucleolytic: ribonuclease
other: trypsin inhibitor, colipase |
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Definition
| components of the exocrine function of the pancreas |
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Term
both forms of acute pancratitis
interstitial pancreatitis:
milder form
less painful
limited to pancreas and surrounding area
necrotizing pancreatitis:
more painful and severe form
necrosis in and around the pancreas
higher risk of infection, sepsis, organ failure, and death |
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Definition
| intersitial pancreatitis vs. necrotizing pancreatitis |
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Term
causes:
gallstones account for ~90% of causes
2nd most common cause is alcohol
hypertriglyceridemia (>500)
evetnts that initiate injury:
activation of pancreatic zymogens within acinar cells
pancreatic ischemia
pancreatic duct obstruction
secondary events that determine duration and severity:
release of active pancreatic enzymes -> local or distant tissue damage
cytokine generation -> inflammation -> TNF-alpha, IL-1
release of vasoactive substances -> capillary permeability
net effects:
vascular damage: ischemia and edema
tissue damage and cell death
pancreatic infection may result from translocation of colonic bacteria due to increased intestinal permeability |
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Definition
| pathophysiology of acute pancreatitis |
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Term
general:
inflammatory condition that leads to permanent functional and structural damage
progressive and irreversible loss of exocrine and endocrine function leads to maldigestion and diabetes mellitus
increased risk of developing pancreatic cancer
causes:
chronic alcohol use accounts for ~70% of all cases in the US
hypertriglyceridemia
pancreatic duct obstruction
cycstic fibrosis
postnecrotic pancreatitis
pathophysiology:
slow progression from inflammation to cellular necrosis to fibrosis
changes in pancreatic fluid -> environment for formation of intraductal protein plugs -> block small ductules -> progressive structural damage of ducts and acinar cells
calcium complexes with protein plugs -> injury and destruction of tissue
abdominal pain associated with increased intraductal pressure
malabsorption occurs when enzyme secretion decreased by ~90% - lipase secretion decreases before proteolytic enzymes; bicarbonate secretion may or may not fail |
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Definition
| pathophysiology of chronic pancreatitis |
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Term
abdominal pain (~95%):
epigastric - radiates to either upper quadrants or the back
sudden onset and steady with no decrease in pain with repositioning
intensity - "knife-like"
nausea/vomiting (~85%)
epigastric tenderness
abdominal distention
fever - severity depends on severity of pancreatitis |
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Definition
| signs/symptoms of acute pancreatitis |
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Term
increased WBC
serum amylase (< 3 x ULN):
rises within 4-8 hours, peaks at 24 hours, returns to normal within 8-14 days
persistent elevations suggest pancreatic necrosis and complications
serum lipase (> 3 x ULN):
longer half-life than amylase - can be elevated after amylase has returned to normal
more specific than amylase for pancreatic disease
blockage of the common bile duct can lead to liver dysfunction:
increased bilirubin (mild)
increased ALP
increase AST/ALT
decreased albumin |
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Definition
| lab findings of acute pancreatitis |
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Term
abdominal pain - constant or episodic:
less severe than with AP - may be unresponsive to medications
may be painless, even with severe disease
pain radiate to back
deep-seated, positional, and frequently nocturnal
unresponsive to medications
may be aggravated by eating
nausea and vomiting accompany the pain
malabsorption:
steatorrhea
azatorrhea
vitamin B12 deficiency
weight loss
diabetes - late maifestation
jaundice ~ 10% |
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Definition
| signs/symptoms of chronic pancreatitis |
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Term
serum amylase and lipase usually normal
WBC count, fluids, and electrolytes are usually normal
CLASSIC TRIAD: usually confirms the diagnosis
1) calcification
2) steatorrhea
3) diabetes |
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Definition
| lab findings of chronic pancreatitis |
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Term
identify and treat early in the course of attack
therapy is mainly supportive and depends on the severity of the attack:
mild - usually self-limiting and subsides within 2-7 days
severe - more extensive course, treated aggressively, and monitored closely
continuously assess for complications - infection, organ failure |
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Definition
| general treatment approach for acute pancreatitis |
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Term
FLUID RESUSCITATION:
AGGRESSIVE fluid resuscitation is KEY
prognosis depends on rapidity and adequacy of volume resuscitation
intravascular depletion for various reasons: vasodilation from inflammatory response, vomiting and NG suction, 3rd spacing into peritoneal and retroperitoneal cavities
initial fluid resuscitation -> ISOTONIC CRYSTALLOIDS (NS, LR)
IV colloids (albumin) may be needed to aid in restoration of intravascular volume (fluid loss if protein rich)
correct electrolyte deficiencies (Ca, K, Mg)
NUTRITION:
oral nutrition HELD at ONSET OF ATTACK
mild attack - resume oral feeding within several days
severe disease - nutritional deficits develop rapidly
if expect NPO > 1 week or patient malnourished begin parenteral or enteral feedings immediately
parenteral feedings: increased risk of infection, hyperglycemia, and risk of increased TGs (due to lipids)
enteral feedings: safer, less expensive, and may prevent infection by decreasing risk of bacterial translocation across the GI wall; the tip of the OG/NG tube should be in the JEJUNUM (J-tube), distal to the bile duct |
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Definition
| non-pharm treatment for acute pancreatitis |
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Term
abdominal pain control
octreotide?
antibiotics? |
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Definition
| pharmacologic treatments for acute pancreatitis |
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Term
| most important consideration in selection = efficacy and safety
meperidine - OLD drug of choice:
little effect on sphincter of Oddi
not as effective as other narcotics - requires high doses
metabolite accumulates in renal failure - increasing risk of adverse CNS events (SEIZURES, psychosis)
morphine:
good pain relief
increases serum amylase
rarely may be etiology of pancreatitis
hydromorphone:
similar effects of morphine
may be better tolerated by patient ( |
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Definition
| abdominal pain control for acute pancreatitis |
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Term
efficacy controversial
potent inhibitor of pnacreatic enzyme secretion
BUT also increases sphincter of Oddi pressure and decreases splanchic blood flow
limited to patients with severe disease due to lack of data to support use |
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Definition
| use of actreotide in acute pancreatitis |
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Term
therapy should be driven by cultures
EMPIRIC THERAPY NOT INDICATED FOR ALL PATIENTS
high risk patients may benefit:
necrotizing pancreatitis with signs of infection
pancreatic abscess or infected pseudocyst
regimen should cover enteric GNRs and anaerobes
commonly used agents:
imipenem/cilastatin
fluoroquinolone PLUS metronidazole (PCN-allergy)
gram positive and fungal infections increasing in patients receiving antibiotic prophylaxis: empiric fungal prophylaxis commonly added |
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Definition
| use of antibiotics in acute pancreatitis |
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Term
alcohol abstinence!!!
smoking cessation
small, frequent meals (6 meals per day)
fat restricted diet
increased dietary fiber
surgical prcedures |
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Definition
| non-pharm treatment of chronic pancreatitis |
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Term
| chronic pain management and pancreatic enzymes |
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Definition
| pharmacologic treatment of chronic pancreatitis |
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Term
general:
begin with non-narcotic analgesics at lowest effective dose
scheduled not PRN
step-wise therapy: non-narcotics -> (+) tramadol or low-dose narcotic -> PO narcotics -> IV narcotics
consider addition of non-narcotic modulators of chronic pain in difficult-to-manage patients: SSRIs or TCAs
consider referral to pain clinic/specialist
APAP:
caution in patients with history or current use of alcohol
limit to 2 g/day in alcohol induced pancreatitis
NSAIDs:
increased risk of GI bleed
COX2 for patients at high risk of GI bleed
caution in renal failure
tramadol:
narcotic-like effect
contraindicated in alcohol intoxication
caution in elderly and renal failure (CNS effects)
narcotics:
abuse potential - concern in alcoholic patients
be aware of total APAP dose in combo products
numerous combinations, doses, and potencies
celiac nerve block:
corticosteroid injected into celiac nerve
effects last ~1 month
last line option |
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Definition
| chronic pain management of chronic pancreatitis |
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Term
general:
indicated with STEATORRHEA and weight loss present
combo of pancreatic enzymes and reduction in dietary fat
lipase, amylase, protease
enteric coating and increasing gastric pH increases BA of enzymes
pancreatic enzymes - many formulations
dosed in numberous tablets/capsules that need to be taken with each meal and with each snack -> compliance issues
non-enteric coated pancreatic enzymes:
addition of antisecretory agent may increase efficacy
ADRs - nausea, cramping, hyperuricemia
contraindications - hypersensitivity to pork protein
enteric coated pancreatic enzymes:
requires fewer capsules/tablets per meal
does not require additional antisecretory therapy
ADRs - nausea, cramping, hyperuricemia
contraindications - hypersensitivity to pork proteins |
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Definition
| use of pancreatic enzymes in chronic pancreatitis |
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