Pancreatic Disorders Flashcards

1
Q

Pancreas fxns as an endocrine gland producing what hormones? What else does it fxn as?

A
  • insulin
  • glucagon
  • somatostatin
  • fxns as an exocrine gland secreting digestive enzymes via a duct - it secretes approx 1.5 L of enzyme rich fluid everyday for digestion of fats, starch and protein
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2
Q

Hormonal mechanisms that control pancreatic secretion? These stimulate the release of what?

A
  • secretin: released from duodenal mucosa in response to presence of acid in the duodenum, it stimulates the release of bicarb and water
  • CCK: released from SI endocrine cells in response to the entry of fats and proteins into the proximal intestin - acts directly and through vagal afferents to stimulate pancreatic acinar cells to release digestive proenzymes
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3
Q

What is acute pancreatitis? Etiologies? Most common cause in women and in men?

A
  • acute pancreatitis is acute inflammatory process of the pancreas
  • etiologies:
    mechanical:gallstones
    toxic: alcohol
    trauma: surgical, blunt
    metabolic: high TGs
    infection: HBV, HIV, CMV
    Misc: preg, renal failure
  • MC in men: alcohol
  • MC in women: gallstones
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4
Q

Most common causes of acute pancreatitis? Other less common causes?

A
  • gallstones and ETOH abuse cause 60-75%
  • idiopathic 30% - 1st attack
  • if 2nd attack and not one of main 2 causes then look for less common causes such as:
    hypercalcemia
    hyperlipidemias
    biliary sludge
    drugs
    cancer
    missed stone in duct
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5
Q

Classification of acute pancreatitis? (mild, moderately severe, and severe)

A
  • mild acute: absence of organ failure and local or systemic complications
  • moderately severe acute pancreatitis: transient organ failure (resolves within 48 hrs) and/or local or systemic complications w/o persistent organ failure ( longer than 48 hrs)
  • severe: persistent organ failure that may involve one or multiple organs
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6
Q

Clinical manifestations of acute onset pancreatitis?

A
  • persistent, severe epigastric pain
  • or RUQ pain may be steady or colicky
  • N&V
  • 50% experience band like radiation of pain to back, some may get relief with bending forward or sitting up
  • dyspnea: pancreas inflamed - may affect diapghram, pleural effusion
  • shock/coma
  • 5-10% of pts may have painless disease and have unexplained hypotension (losing a lot of fluid in retroperitoneal space, abdomen - tx with IV fluids)
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7
Q

Physical exam findings of pt with acute pancreatitis?

A
  • fever, tachycardia (hypotension if severe)
  • epigastric/RUQ tenderness
  • shallow respirations - pain with deep breaths
  • possible dyspnea if pleural effusion
  • epigstric mass if pseudocyst or tumor
  • in 3% of pts, ecchymotic discoloration may be observed in periumbilical region (cullen’s sign) or along flank (grey-turner’s sign)
  • could also have hypoactive bowel sounds: can cause ileus
  • jaundice
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8
Q

Lab tests results in acute pancreatitis?

A
  • serum amylase:
    rise quickly (6-12 hrs)
    elevated 3-5 days
  • serum lipase:
    sensitivity 82-100%, more specific than amylase
    elev. occur earlier and last longer, if 3-4x normal think pancreatitis
  • CRP: levels above 150 mg/dL at 48 hrs after pt presents can predict more severe course. Used to diff severe from mild disease
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9
Q

Imaging in acute pancreatitis?

A
  • abdominal plain film: help to exclude other causes of abd. pain, may have localized ileus 2ndry to iflammation
  • CXR: 1/3 of pts with pancreatitis have abnormal findings:
    elevation of hemidiaphragm, pleural effusions, pulmonary infiltrates
  • US: diffusely enlarged, hypoechoic pancreas and gallstones if present
  • CT: most impt test for dx acute pancreatitis and intraabdominal complications and assessment of severity (with oral and IV contrast)
  • MRI: higher sensitivity for dx of early pancreatitis than CT scan, lack of nephrotoxicity, ability of MRI to better detect fluid collections, necrosis, hemorrhage and pseudocyst, MRCP better shows pancreatic and bile ducts
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10
Q

Tx of pancreatitis?

A
  • admit to hosp with acute pancreatitis
  • NPO
  • IV hydration with crystalloids to keep UO above 30ml/hr (LRs except in hypercalcemia)
  • pain control (morphine, fentanyl, ketorolac)
  • zofran or phenergan prn nausea
  • +/- abx, +/- surgery (cholecystectomy, necrosectomy - severe dz)
  • labs: CBC, lipase, amylase, CMP, bilirubin, CRP in 48 hrs
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11
Q

What is severe pancreatitis? Complications and tx?

A
  • most pts with acute pancreatitis have mild disease and recover in 3-5 days
  • 20% have severe disease with local or systemic complications or organ failure
  • complications with pulm, renal, circulatory and hepatobiliary dysfxn can occur
  • ICU monitoring and supp O2
  • prevent infection w/ broad spectrum abx
  • nutrition preferably enteral - tube feeding
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12
Q

RF for pancreatitis severity?

A
  • older than 55
  • obesity BMI: greater than 30 kg/m2
  • organ failure at admission
  • pleural effusion or pulmonary infiltrate
  • elevated CRP
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13
Q

What is chronic pancreatitis? Etiologies?

A
  • progressive inflammatory changes result in permanent structural damages to pancreas, leading to impairment of exocrine and endocrine fxn

etiologies:

  • alcohol abuse (75%)
  • genetic: CF, hereditary pancreatitis
  • ductual obstruction: trauma, pseudocysts, stones, tumors
  • systemic: SLE, hypertriglyceridemia
  • idiopathic
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14
Q

Main differences b/t acute and chronic pancreatitis??

A
  • acute is usually nonprogressive
  • recurrent episodes of acute lead to chronic over time
  • features: chronic may be asx over long periods of time
    serum amylase and lipase concentrations tend to be normal in chronic
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15
Q

Clinical manifestations in chronic pancreatitis?

A
  • chronic abdominal pain: cardinal feature although 20% may have little to no pain
  • pancreatic insufficiency: exocrine dysfxn can’t digest complex foods or absorb digestive breakdown products, wt loss: 90% of pancreatic fxn has to be lost for this to occur
  • fat malabsorption: steatorrhea - lipolytic activity decreases faster than proteolysis: malabsorption of fat soluble vitamins (A, D, E, K)
  • pancreatic diabetes: DM late in course of disease - seen in pts with calcifying disease (calcifications are pathognomonic for pancreatitis)
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16
Q

Dx chronic pancreatitis - labs?

A
  • labs: amylase, lipase usually normal b/c pancreatic fibrotic resulting in decreased abundance of these enzymes within the pancreas
  • steatorrhea: 72 hr quantative fecal fat determination is the gold std, excretion more than 7 g fat/day, pts with steatorrhea usually more than 10 g q day
  • direct pancreatic fxn tests are performed via specialized centers
17
Q

Dx chronic pancreatitis - imaging?

A
  • calcificaitons on plain films
  • CT/MRI/US: may show ductul dilatation, enlargement of pancreas, pseudocysts
  • ERCP: can reveal changes in the ducts
18
Q

Tx of chronic pancreatitis?

A
  • est dx: differential: PUD, biliary obstruction, pancreatic cancer, pancreatic duct strictures or stones
  • pain management & control N/V: approp meds, placebo alone effective in 30% pts in most studies, NSAIDs, low dose amitriptyline, opiates
  • diet: cessation of ETOH and smoking, small low fat meals with pancreatic enzyme supplements and acid suppression (H2 blockers or PPIs) to reduce inactivation of enzymes from gastric acid
  • surgery: for those who fail medical therapy, for pain relief - decompression of main pancreatic duct/pseudocyst, resection of part of the pancreas, denervation procedures
19
Q

Why does pancreatic cancer have such a poor prognosis? Rfs? Most common type?

A
  • because of late presentation
  • 4th leading cause of cancer death in US
  • RFs:
    chronic pancreatitis
    smoking
    obesity
    male gender
  • ductal adenocarcinoma: 85% of all pancreatic cancers
20
Q

Clinical features of pancreatic cancer? PE findings?

A
  • +/- wt loss, jaundice, (***painless jaundice with wt loss)
  • tumors in body or tail present with pain and wt loss
  • tumors of the head present with wt loss, steatorrhea and jaundice
  • PE: abdominal mass/ascites 20% of pts, L supraclavicular node (virchow’s node) and palpabe periumbilical mass (sister mary joseph’s node)
21
Q

Workup for pancreatic cancer?

A
  • imaging: US/CT shows pancreatic mass, dilated bile ducts, liver mets (usually incidental findings)
  • labs: LFTs show elevated bili, alk phos, aminotransferases normal or slightly elevated
  • serum tumor marker:
    CA 19-9 closely related to tumor size
    can be elevated in pts with benign pancreatobiliary disorders
    serial monitoring can assess the response to tx
  • bx: FNA, via ERCP or duing surgery
22
Q

Tx of pancreatic cancer?

A
  • surgical resection is preferred tx
  • +/- radiation therapy or chemo
  • usually unresectable if involves vascular structures
  • endoscopic stent insertion or palliative surgery
  • pain control and pancreatic enzyme replacement
23
Q

Prognosis of pancreatic cancer?

A
  • resectable disease (stage I, II): 15-20% of pts have resectable disease at time of dx, median survival rate is 15-20 mos, 5 year survival rate is 20%
  • unresectable locally advanced (stage III): 30% present in stage IIII, chemo with or w/o radiation gives modest improvement in survival and palliation
  • mets (stage IV): 50% have limited survival of 3-6 months