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67 Cards in this Set
- Front
- Back
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what is acute pancreatitis
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acute inflammatory response to pancreatic injury
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what is chronic pancreatitis
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progressive inflammatory changes resulting in permanent structural and functional damage
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what are the functions of the pancreas
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endocrine
exocrine |
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what does the pancreas produce via endocrine secretion
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insulin
glucagon somatostatin |
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what cells in the pancreas produce the hormones
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islets of langerhans
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what does the pancreas produce via exocrine function
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digestive enzymes and alkaline fluid
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what is in the pancreatic juice
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digestive enzymes and alkaline fluid
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why is the fluid secreted into the small intestine by the pancreas alkaline
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this is to protect the digestive enzymes from the gastric acid that is also present in the small intestine therefore the alkaline fluids increase the pH otherwise the digestive enzymes would denature
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what are the pancreas' self preservation mechanisms
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required extrapancreatic triggers for proteolytic enzyme activation
secretion of a low concentration of digestive enzyme inactivators in pancreatic juice |
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what are the enzyme inactivators secreted along with pancreatic juice
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trypsin inhibitor
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what are the most common causes of acute pancreatitis
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gall stones
alcohol abuse |
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what are all the possible causes of acute pancreatitis
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gall stones
alcohol abuse hypertriglyeridemia (>1000) Post ERCP medication induced |
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gall stones of what size increase the increase the risk of pancreatitis
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<5mm
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since alcohol abuse is a cause of pancreatitis would you expect pancreatitis to be higher or lower in alcoholics
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even though this is the 2nd most common cause of pancreatitis, the occurrence is low in alcoholics meaning there is another risk factor
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what are drugs that can cause acute pancreatitis
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estrogens
furosemide mercaptopurine (CI w/ allopurinol and febuxostat use due to being xanthine oxidase substrate) azathioprine (CI w/ allopurinol and febuxostat use due to being xanthine oxidase substrate) metronidazole sulfonamides tetracycline thiazides valproic acid |
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what are the possible pathogenesis of acute pancreatitis
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alcohol induced
biliary pancreatitis |
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how does alcohol induced pancreatitis occur
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pancreas is responsible for NONOXIDATIVE METABOLISM of alcohol
this metabolism results in FATTY ACID ETHANOL ESTERS (FAEE) accumulation of these esters damages the pancreas and leads to ALCOHOLIC ACUTE PANCREATITIS |
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how does biliary pancreatitis occur
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gall stone goes into the bile duct resulting in:
-reflux of bile to pancreatic duct or gall stone blocks duct resulting in outflow obstruction and the accumulation of pancreatic juice in the pancreas leading to damage |
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what is the sequence of events that lead to inflammation and digestion of pancreatic tissue
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premature activation of intrapancreatic digestive enzymes
activation and sequestration of neutrophils and macrophages inside pancrease activation of proteolytic enzymes intrapancreatic inflammation and digestion of pancreatic tissue this can be alcohol induced or due to biliary pancreatitis |
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what are the Signs and symptoms of Acute pancreatitis
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abdominal pain - most common symptom (radiates to back)
N/V abdominal distention decrease bowel sounds |
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what are signs and symptoms of acute pancreatitis becomes systemic
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fever
tachycardia tachypnea |
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what are the signs and symptoms of acute pancreatitis if it is allowed to progress
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organ dysfunction (respiratory distress, acute renal failure)
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what are the lab findings of acute pancreatitis
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increase serum amylase and lipase (3xULN)
leukocytosis dehydration hyperglycemia hypocalcemia hyperbilirubinemia decrease albumin |
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what do the lab finding tell us about acute pancreatitis
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let us know there is damage to pancreas
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why must you be careful when looking at amylase and lipase levels
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both can be elevated due to other disease states
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is the increase in amylase/lipase correlated with the severity of acute pancreatitis
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no
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when pt with acute pancreatitis is dehydrated what can be the cause
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hemoconcentration
increase BUN:Scr |
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why would you see hyperglycemia in acute pancreatitis
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pancreas no longer carrying out endocrine production of insulin
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what kind of pancreatitis will you see hyperbilirubinemia
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gall stone pancreatitis (biliary pancreatitis)
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why would you see a decrease in albumin
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this is seen in very severe cases of acute pancreatitis
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what is the purpose of image studies
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very important in diagnosing and looking at the severity of pancreatitis
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what are the imaging studies for acute pancreatitis
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abdominal ultrasound
contrast enhanced CT scan MRI |
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what imaging would be more prefered if gall stone pancreatitis (biliary pancreatitis) was suspected
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abdominal ultrasound
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what does contrast enhanced CT tell us about acute pancreatitis
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whether it is interstitial or necrotizing
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what are the local complication of acute pancreatitis
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pancreatic- infections
-necrosis (necrotizing pancreatitis) -abscesses -pseudocysts |
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what are the systemic complications of acute pancreatitis
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sepsis
hypotension hemorrhagic complications multiple organ dysfunction |
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what is the course of treatment for Mild acute pancreatitis
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bowel rest (start PO when proper)
IV hydration analgesia following recovery in gallstone pancreatitis > cholecystectomy (removal of gallbladder) |
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what is the course of treatment for Severe acute pancreatitis with <30 percent necrosis
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aggressive fluid resusitation
enteral nutrition (TPN if EN not telerated) analgesia |
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what is the course of treatment for Severe acute pancreatitis with >30 percent necrosis
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aggressive fluid resusitation
enteral nutrition (TPN if EN not telerated) analgesia AND ANTIBIOTICS |
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what drug can you give to pt with severe acute pancreatitis that may reduce mortality
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octreotide 0.1 mg SQ q8h
(this drug is also used to manage esophageal variceal bleeding) |
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what opioids can you used to control pain in acute pancreatitis
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morphine
hydromorphone fentanyl |
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why is meperidine no longer used to control pain
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the metabolite is toxic and its accumulation can lead to seizures
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why was it believed that morphine shouldn't be used to tx pain in pts with pancreatitis
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it increased the pressure at the sphincter of oddi and it was believed that this worsened acute pancreatitis BUT THIS WAS UNTRUE
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what does the sphincter of oddi do
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control flow of digestic juices (pancreatic and bile) into duodenum
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what are the dose equivalents for the morphine, hydromorphone, fentanyl
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hydromorphone 1.5 mg = morphine 10mg = fentanyl 0.2 mg
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what is the role in nutrition with acute pancreatitis
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NPO initially
mild pancreatitis: oral intake resumed when feasible, low fat diet severe pancreatitis: jejunal feeding, parenteral nutrition, or enteral (prefered) |
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what is the purpose of jejunal feeding in severe acute pancreatitis
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bypasses pancrease so its not stimulated to secrete juices
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why is enteral feeding preferred over parenteral in severe acute pancreatitis
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prevents bacterial translocation
eliminates catheter related infections due to parenteral |
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when would you tx a pt with acute pancreatitis with antibiotics
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when pt has >30% pancreatic necrosis
1/3 of these pts die b/c of infection |
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what antibiotics adequately penetrate the pancreas
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imipenem
3rd gen cephalosporins piperacillin fluoroquinolone metronidazole |
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what 3rd gen cephalosporins can be used to tx acute pancreatitis when >30% risk of necrotizing pancretitis
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cefdinir
cefotaxime (also used to tx SBP) ceftriaxone (also used to tx SBP) |
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what are risk factors for chronic pancreatitis
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alcohol
tropical disease ductal obstruction genetic factors |
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what is the #1 cause of chronic pancreatitis
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alcohol
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what is the pathogenesis of chronic pancreatitis
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progressive inflammation that results in structural damage:
-pancreatic ducts become dilated, irregular, and strictured -pancreatic tissue becomes irregular and fibrotic |
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what are signs and symptoms of chronic pancreatitis
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abdominal pain
weight loss (in advanced disease) exocrine and endocrine deficiency diabetes steatorrhea |
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why would someone with chronic pancreatitis experience abdominal pain post prandial
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this is due to the pancreas being stimulated after a meal but due to it not being able to secrete its juices it damages itself and causes you pain
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why would someone with chronic pancreatitis experience weight loss
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this is due to the pt no longer absorbing all their nutrition due to lack of pancreatic digestive enzymes
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why would someone with chronic pancreatitis develop diabetes
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due to the pancreas no longer carrying out its endocrine function one of which is the secretion of insulin
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what is steatorrhea
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this is due to malabsorption of fat
results in greasy, stinky stools |
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what are the labs of a pt with chronic pancreatitis
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amylase and lipase normal to low levels in advanced disease (high early in acute episodes)
fecal pancreatic elastase 1 |
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what is fecal pancreatic elastase a marker of and when could it indicate chronic pancreatitis
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marker of exocrine function of the pancreas
<100 mcg/g of stool indicates chronic pancreatitis |
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what are the imaging studies for chronic pancreatitis
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contrast enhanced CT
MRI magnetic resonance cholangiopancreatography (MRCP) - less invasive endoscopic ultrasound |
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what is the treatment for chronic pancreatitis
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life style modifications
pain control (start with nonopioids first) pancreatic enzymes H2 blockers/PPI Insulin |
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what life style modifications can you do to tx chronic pancreatitis
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alcohol cessation
low fat meals quit smoking |
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when would you supplement a pt with pancreatic enzymes and when would you titrate the dose
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if low fat meals aren't helping the steatorrhea then the pt isn't absorbing nutrition which can lead to weight loss and malnurishment therefore IMPORTANT TO SUPPLEMENT THOSE ENZYMES
STEATORRHEA is used to gauge how well the pt is doing and you titrate up based on it |
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why would you give a pt with chronic pancreatitis PPI/H2
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to reduce stomach acid production
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when you give a pt with chronic pancreatitis insulin
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when they has diabetes however there is a risk of hypoglycemia
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