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35 Cards in this Set

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endocrine/exocrine function of pancreas
-Endocrine: produces hormones which regulate digestion (insulin, glucagon, somatostatin, pancreatic polypeptide). 20% of function.
-Exocrine: forms digestive juices rich in enzymes and bicarbonate. Amylase digests carbohydrate. Lipase digests fat. Trypsin digests protein. 80% of function.
pancreatic enzymes
-1 liter of pancreatic juice produced each day, released in a non active state
-trypsin converts proenzymes into active forms in duodenum
acute pancreatitis
-inflamm disease of the pancreas
-discrete episodes of abd pain and elevated serum amylase and lipase levels
-structure and function of pancreas goes back to nml
-usually the pancreas has prior damage from alcohol (5-10yrs of heavy drinking), can also happen from a binge
-alcohol results in spasm of sphincter of oddi, toxicity to tissue and increased secretion of enzymes. It also increases prot content of pancreatic juice forming prot plugs which block pancreatic outflow
-Cholelithiasis and choledocholithiasis can result in stones lodging in the pancreatic duct or ampulla of vater leading to extravasation of enzymes into to the pancreatic parenchyma.
-obstruction may also be cased by sphincter dysfunction, abnormalities of pancreas and pancreatic ca
acute pancreatitis- drugs and toxins
-Drugs: immunosuppressants (azathioprine), valproic acid,DDI, TMP-SMX, diuretics (furosemide), estrogens, tetracycline, corticosteroids
-Toxins: insecticides, methanol, scorpion venom
acute pancreatitis: metabolic
-hypertriglyceridemia: occurs when triglyceride levels are >1000mg/U
acute pancreatitis: other causes
-genetic factors
-instrumentation (ERCP)
-viruses (mumps, EBV, varicella)
-bacteria (mycoplasma, salmonella)
-abd trauma
pathophys acute pancreatitis
-activation of diegestive enzymes results in autodigestion of pancreatic tissue
-digestive enzyme release is stimulated by: toxic metabolites of alcohol, drugs, toxins, infectious agents
-inflamm mediators are released and stick to vessel walls causing injury
acute pancreatitis-SSX
-dull, boring, abd pain which is sudden in onset and intensifies and becomes a constant ache
-pain in epigastric region with radiation to back
-not relieved by vomiting
-N/V, anorexia
-pts lie in fetal position or bend forward
-fever, tachycardia
-dec bowel sounds, local tenderness, generalized rebound, guarding, distension
acute pancreatitis-severe attacks
- hypotension, tachypnea, tachycardia, dyspnea, hemodynamic instability, may occur
-tissue can become necrotic
Greys Turners sign
-in necrotizing pancreatitis
-ecchymosis of flanks from retroperitoneal blood dissecting along tissue planes
Cullen sign
-ecchymosis of periumbilical area
Dx of acute pancreatitis
-H & P: alcohol, meds, trauma, stones
-Serum amylase: rises fast during 1st 2-12 hrs and return to nml over 3-5 days (not specific)
-Serum lipase: increases parallel to amylase; levels remain elevated longer, TEST OF CHOICE
-amylase and lipase levels do not correlate w/severity of disease!
-Labs: WBC, inc Hct, mild hyperglycemia, hypocalcemia, CRP >6 mg/dL
-Abd xrays: dilated loop of small bowel, overlying pancreases (sentinel loop) or dilation of transverse colon with abrupt cut off of gas column at splenic flexure
If CBD obstructed see...
-elevated bilirubin, alkaline phosphatase and aminotransferase levels
-serum triglyceride levels >1000mg?dL
U/S, CXR, CT,MRI, MRCP in acute pancreatitis
-inflammed pancrease may apear hypoechoic due to edema
-uneven outline of gland
CXR: pleural effusion and bibasilar atelectasis
CT: w/IV contrast shows poor perfusion of pancrease suggesting necrosis
MRI: equal to CT
MRCP: shows dilated pancreatic ducts, stones
Endocsopic Ultrasonography
-Endoscopic procedure in which high frequency ultrasound transducer is inserted into GI tract to visualize pancreas and biliary tract.
-Can be used to guide needle aspiration
Endoscopic Retrograde Cholangiopancreatography- ERCP
-take tube stick it into mouth through duodenum and finds the point of the blockage
-not helpful in Dx of pancreatitis Detects bile duct stones. Pancreatitis may occur after ERCP
Ranson's Criteria on admission
-evaluates inflamm repsonse and complications
-Age > 55yrs
-AST >250 U/L
-WBC >16,000
-LDH > 350
-glucose >200
-3 + on admission predicts severe course and pancreatic necrosis
Ransons criteria 48 hrs after admission
Hct drop of > 10%
Arterial PO2 of < 60 mm Hg
Serum Ca < 8 mg/dL
BUN increase of > 5 mg/dL
Base deficit of > 4 meq/L
Fluid sequestration of > 6 L
-Development of above in 48 hours indicates worsening prognosis.
-7-8 = 100% mortality rate
Tx of acute pancreatitis
-no therapy directly affects inflamm
-fluid resuscitation, maintaining fluid balance, monitor of complications
-may require ICU
-if abd pain and dec BS, no food or fluid PO
-NG suction is vomiting and ileus present (replace fluids)
-total parenteral nutrition (TPN) needed to maintain caloric needs
-gallstones --> surgically correction during mild episode, with severe --> ERCP, spinchterotomy, stone extraction
Pain control
-acetaminophen for mild pain
-Tranadol (Ultram): centrally acting analgesic for moderately severe pain
-Meperidine (Demerol)
-Hydromophone (Dilaudid) IV
Pancreatic necrosis
-in infected pancreatic necrosis see worsening of sx, fever, leukocytosis
-may require emergency CT, aspiration of fluid for Gm stain and Cx
-abx: imipenem/cilastin or fluoroquinolones or metronidazole
Pancreatic pseudocyst
-complication from AP
-leakage of pancreatic juices from ducts
-Dx w/Us or CT
Pancreatic ascites
-complication from AP
-results when pancreatic fluids drain into peritoneal cavity
complications of AP
-Renal and respiratory failure
-Renal failure form hypovolemia and decreased perfusion, Tx by fluid correction
-resp failure may progress to ARDS (occurs when enzymes are absorbed into circulation injuring epithelium of pulmonary capillaries.)
Chronic pancreatitis
-inflamm disease of the pancreas characterized by changes in structure and function of pancreas which persist after correction of precipitating cause
-highest in alcoholics
-calcifying chronic pancreatitis with fibrosis
-obstructive chronic pancreatitis: dilation fo ductal system, atrphy of parenchyma, and fibrosis
Etiology of chronic pancreatitis
-malnutrition, injury, diet
-cystic fibrosis resulting in plugging of ducts
-Tropical pancreatitis” from casava in diet or malnutrition
clinical manifestations of chronic pancreatitis: ssx
-abd pain, epigastric, dull, constant
-pain attacks can last for several days with pain free intervals or constant. Aggravated by eating
-may improve as pancreatitis worsens
-causes: inflammation, increased intrapancreatic pressure, stenosis of CBD
-N/V, anorexia, wt. loss
clinical manifestations of chronic pancreatitis
-malabsorption from pancreatic insufficiency: when pancreatic lipase is reduced, diarrhea and steatorrhea occur. Amylase deficiency results in decreased carbohydrate digestion resulting in osmotic diarrhea. Maldigestion of fat soluble vitamins: A,D,E,K.
-DM: occurs late in disease
Dx of chronic pancreatitis
-H&P, imaging, labs
-Pancreatic exocrine function eval with 72hr fecal fat. If >7g/d exocrinse secretion dec by >90%
-amylase/lipase may be eleva, nml or low
-Structural studies ie; calcifications on plain film diagnostic of chronic pancreatitis
U/S, CT, in chronic pancreatitis
US: see irregular contour of gland, dec echogenicity, dilation of duct, calcification and dilation of main pancreatic duct
CT: shows ductal dilation, calcifications, cystic lesions
ERCP MRCP and in chronic pancreatitis
-ERCP: most sensitive and specific. Ducts become more stenotic, tortuous and dilated as disease increases in severity.
-MRCP: shows pancreatic parenchyma and ductal system
Tx of chronic pancreatitis
-pain control: stop alcohol, analgesics, dec triglycerides, D/C drugs
-acetaminophen or NSAIDS, opiates
-oral pancreatic enzymes may reduce pain by inhibiting their secretion (25,000-30,000 units of lipase per meal)
-surgery last resort
complications of chronic pancreatitis
1. Pancreatic cancer
2. Portal HTN/gastric varices from obstructed splenic vein
3. Pseudocysts (may rupture or become infected)
4. Pancreatic ascites (from duct leakage or pseudocyst rupture)