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T3: Pancreatitis
| Question | Answer |
|---|---|
| An acute inflammation of the pancreas? | acute pancreatitis |
| What is the most common cause of pancreatitis in the US? | gallbladder disease (gallstones) which is more common in women |
| What is the second most common cause of pancreatitis? | chronic alcohol intake which is more common in men |
| This is a mixture of cholesterol crystals & calcium salts and is found in 20-40 % of patients w/acute pancreatitis. | biliary sludge or microlithiasis; the formation of biliary sludge is seen in pts w/bile stasis |
| Acute pancreatitis attacks are also associated with? | hypertriglyceridemia (serum levels >1000 mg/dL) |
| What are some less common causes of pancreatitis? | certain drugs (corticosteroids, thiazide diuretics, oral contraceptives, sulfonamides, NSAIDs), metabolic disorders (hyperparathyroidism, RF), & vascular diseases; trauma, viral infections, penetrating duodenal ulcer, cysts, abscesses, CF, kaposi sarcoma |
| Pancreatitis may occur after what procedures? | Surgical procedures on the pancreas, stomach, duodenum, or biliary tract; can also occur after endoscopic retrograde cholangioprancreatography (ERCP). |
| What is the most common pathogenic mechanism of pancreatitis? | Autodigestion of the pancreas causes injury to pancreatic cells or activation of the pancreatic enzymes in the pancreas rather than in the intestine. |
| This is an inactive proteolytic enzyme produced by the pancreas that's released into the small intestine via the pancreatic duct and there its activated to tyrpsin by enterokinase. | trypsinogen |
| Normally, trypsin inhibitors in the pancreas & plasma bind & inactivate any trypsin that is inadvertently produced. In pancreatitis activated trypsin is present in the pancreas. This enzyme can digest the pancreas & produce what? | bleeding |
| What are some etiologic factors for acute pancreatitis? | alcoholism, biliary tract disease, trauma, infection, drugs, postop GI surgery |
| Pathophysiology map of acute pancreatitis | Etiologic factors->injury to panc cells & activation of panc enzymes->autodigestion effects of panc enzymes: trypsin: edema, necrosis, hem., elastase: hem.; phoshpolipase A & lipase: fat necrosis, Kalikrein: edema vas. perm. smooth muscle contract & shock |
| Mild pancreatitis is also known as? | edematous or interstitial pancreatitis |
| Severe pancreatitis is also known as? | necrotizing pancreatitis |
| In severe pancreatitis, what occurs in half of affected patients and what are they at high risk for? | Permanent decreases in endocrine & exocrine function & are at risk for developing pancreatic necrosis, organ failure, & septic complications. |
| CM of acute pancreatitis | LUQ pain or midepigastrium can radiate to the back, pain is sudden, severe, deep, piercing, & continuous or steady. Pain is aggravated by eating & starts when pt is recumbent. It isn't relieved by vomiting. |
| Abdominal pain is the predominant manifestation of acute pancreatitis. Why? | Due to distention of the pancreas, peritoneal irritation, & obstruction of the biliary tract. |
| Besides pain what are some other CM of acute pancreatitis? | flushing, cyanosis, dyspnea, N/V, low grade fever, leukocytosis, hypotension, tachycardia, jaundice, abdominal tenderness w/guarding, dec. or absent bowel sounds, crackles, Grey Turner's or Cullen's sign, shock |
| A bluish flank discoloration (ecchymoses) associated with acute pancreatitis. | Grey Turner's spots or sign |
| A bluish periumbilical discoloration (ecchymoses) associated with acute pancreatitis. | Cullen's sign |
| What could cause shock in acute pancreatitis? | Hemorrhage into the pancreas, toxemia from the activated pancreatic enzymes, or hypovolemia as a result of fluid shift into the retroperitoneal space (massive fluid shifts). |
| What are 2 significant local complications of acute pancreatitis? | pseudocyst and abscess |
| An accumulation of fluid, pancreatic enzymes, tissue debris, and inflammatory exudates surrounded by a wall. | pancreatic pseudocyst |
| What are manifestations of pseudocyst? | abdominal pain, palpable epigastric mass, N/V, and anorexia |
| How are pseudocysts detected? | CT, MRI, & endoscopic ultrasonography (EUS); serum amylase levels frequently remain elevated |
| Pseudocysts usually resolve spontanteously within a few weeks but what else can happen to them? | May perforate causing peritonits, or rupture into the stomach or duodenum. |
| What are some treatment options for pseudocysts? | surgical drainage procedure, percutaneous catheter placement and drainage, and endoscopic drainage |
| This is a collection of pus that can occur in acute pancreatitis. | a pancreatic abscess |
| Pancreatic abscess results from this in the pancreas and may become infected or perforate into adjacent organs. | extensive necrosis |
| What are some manifestations of an abscess? | upper abdominal pain, abdominal mass, high fever, and leukocytosis |
| How do you treat pancreatic abscesses? | Need prompt surgical drainage to prevent sepsis. |
| What are the main systemic complications of acute pancreatitis? | pulmonary (pleural effusion, atelectasis, pneumonia, & ARDS) and cardiovascular (hypotension), & tetany caused by hypocalcemia |
| The pulmonary complications in acute pancreatitis are due to what? | the passage of exudate containing pancreatic enzymes from the peritoneal cavity through transdiaphragmatic lymph channels |
| When hypocalcemia occurs in acute pancreatitis, it is a sign of severe disease due to what? | To the combining of calcium & fatty acids during fat necrosis. |
| What are the primary diagnostic tests for acute pancreatitis? | serum amylase and lipase measurements |
| In acute pancreatitis serum amylase levels are usually? | elevated early and remains elevated for 24-72 hours |
| In acute pancreatitis serum lipase levels are? Why is this test important? | elevated; other disorders (mumps, cerebral trauma, renal transplantation) may increase serum amylase levels |
| Besides serum amylase & lipase levels what are some other lab findings? | increase in liver enzymes, triglycerides, glucose, & bilirubin levels and a decrease in calcium level |
| What are some diagnostic studies for acute pancreatitis? | abdominal ultrasonography, xray, contrast CT scan; endoscopic retrograde cholangiopancreatography (ERCP), endoscopic US, MRCP, angiography, chest xray |
| These diagnostic can be used to identify pancreatic problems. | abdominal ultrasonography, xray, contrast enhanced CT scanning |
| This is the best imaging test for pancreatitis and related complications such as cysts and abscesses. | CT scanning |
| In acute pacreatitis, chest xrays may show what? | pulmonary changes, including atelectasis and pleural effusions |
| What are some goals of collaborative care for acute pancreatitis? | relief of pain; prevention or alleviation of shock; reduction of pancreatic secretions; correction of fluid & electrolyte imbalances; prevention or treatment of infections; removal of the precipitating cause, if possible |
| Treatment for acute pancreatitis is focused primarily on supportive care such as? | aggressive hydration; pain mgmt; mgmt of metabolic complications; and minimizing pancreatic stimulation |
| Treatment and control of pain in acute pancreatitis are very important. What pain medications may be used? | IV morphine, antispasmodic agents, meds that relax smooth muscles (spasmolytics) such as nitroglycerin or papaverine |
| What drugs should be avoided with acute pancreatitis and why? | Atropine and other anticholinergic drugs should be avoided when paralytic ileus is present b/c they can decrease GI mobility, thus contributing to the problem. |
| Why is it important to reduce or suppress pancreatic enzymes? | To decrease stimulation of the pancreas and allow it to rest. |
| What are some ways to reduce or suppress pancreatic enzymes? | Pt is NPO; NG suction to reduce vomiting & gastric distention & prevent gastric acidic contents from entering the duodenum; enteral nutrition needed if severe; certain drugs to suppress gastric acid secretion |
| If shock is present in acute pancreatitis how is it treated? | Blood volume replacement: plasma or plasma volume expanders such as dextran or albumin; F&E imbalances are corrected w/LRs or other electrolyte solutions (CVP may be used to assist in determining fluid replacement requirements). |
Created by:
eblanc1
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