Running head: PATHOPHYSIOLOGY OF ACUTE PANCREATITIS1Pathophysiology Of Acute PancreatitisStudent’s nameInstitution
PATHOPHYSIOLOGY OF ACUTE PANCREATITIS2Pathophysiology of Acute Pancreatitis1)Describe the pathophysiology of acute pancreatitis leading to acute lung injury andrespiratory failure, sepsis and septic shock and relate the pathophysiology of Betty’shealth problems to her deterioration in the Emergency Department. Acute pancreatitis is a condition characterized by the acute inflammation of the pancreaticgland leading to oedema/necrosis. The clinical indications of acute pancreatitis can rangefrom mild stomach pain to serious organ failure manifestations. In severe cases of acutepancreatitis, necrosis, abscess or organ damage is established. Acute pancreatitis can be theoutcome of gallstones, alcohol abuse, recent abdominal surgery, invasive endoscopicprocedures, abdominal trauma or drug use (Pezzill, 2008). A family history ofhypertriglyceridemia is another pathophysiology of the disorder. Another major cause ofacute pancreatitis is biliary colic and binge alcohol consumption. In severe cases of acutepancreatitis, fever, tachycardia and hypotension are common manifestations. Some patientssuffer from abdominal tenderness, distention and in rare cases from jaundice. The generalcondition of the patient will be paleness, diaphoresis, hemodynamic instability etc. amongothers. In rare cases, patients show hypocalcemia followed by muscular spasms.Acute pancreatitis is often associated with Cullen sign which is a blue discoloration of theumbilicus as a result of hemoperitoneum. Another condition is the reddish discoloration ofthe flanks as a result of retroperitoneal blood dissecting tissue which is known as Grey-Turner sign. Erythematous skin nodules on the exterior skin surface is another uncommonphysical finding in acute pancreatitis (“Acute Pancreatitis,” 2017). Patients suffering withacute pancreatitis are susceptible to acute lung damage which causes 20% death in thepatients. Acute lung damage is manifested as initial exudative phase that lasts for three daysresulting in alveolar damage (Akbarshahi, 2012). Secondary pancreatic infection and sepsishas claimed the lives of 80% patients suffering from acute pancreatitis. Secondary infections
PATHOPHYSIOLOGY OF ACUTE PANCREATITIS3and sepsis develops due to bacterial contamination. To prevent the infection systemicadministration of antibiotics is the only available step (Mifkovic, 2006).Betty Turner showed clinical symptoms such as nausea, vomiting and lethargy which arecharacteristic of acute pancreatitis. In ED, Betty continued to deteriorate and her consciouslevel decreased and she was intubated for airway management and ventilation support.Respiratory failure and ventilation damage is a characteristic of severe case of pancreatitis.2)Drawing upon the pathophysiology of acute pancreatitis and acute lung injury,describe and rationalise what physical assessment findings you would expect tosee in a patient with acute lung injury and sepsis. In your description, you shouldconsider: a) expected system-based findings; b) haemodynamic parameters,including right and left-sided heart pressures; and c) acid-base balance results,serum biochemistry and haematology markers.The assessment of a patient suffering from acute pancreatitis can exhibit clinical impressionssuch as disturbances in the level of serum amylase and lipase, these are digestive enzymesthat are found in higher levels during pancreatic damage. Blood urea nitrogen, creatinine andelectrolyte levels are altered due to damage in liver, blood glucose levels vary and so doesserum cholesterol and triglyceride levels. The complete blood count and haematocrit due toauto-digestion. Arterial blood gas, serum lactic dehydrogenase and bicarbonate values alterdue to these disorders. Diagnostic imaging is not essential in most conditions, it is onlyrequired when the pancreatitis is severe or to confirm a doubt. Methods employed includevarious radiographic methods. Acute pancreatitis occurs due to imbalance in cellular homeostasis, leading to an injury of theacinar cell and impaired secretion of zymogen granules. Pathologic events that trigger theonset of acute pancreatitis is not discovered yet. Extracellular factors and intracellular factors
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