Acute Pancreatitis Case Summary
History of current condition: Patient J.A. is a 39-year-old female that originally reported to the ED two days ago with complaints of epigastric pain, nausea, vomiting, weakness, and fatigue. Along with assessment findings, laboratory results indicated the diagnosis of acute pancreatitis. Additionally, upon admission she presented with signs and symptoms of alcohol intoxication, alcohol dependence with withdrawal, and a blood alcohol concentration of 0.40. She’s currently being administered Serax every 4 hours to relieve alcohol withdrawal symptoms. Also, Dr. Wells just ordered her to be switched from a full liquid diet to a regular diet. She also currently is being infused Lactated Ringers at 125 ml/hour in the right antecubital fossa.
Past …show more content…
Medical History: Anxiety, Hepatitis, Seizures, Cholecystitis
Pathophysiology:
Acute pancreatitis is usually a mild disease that causes the pancreas to become edematous, and usually resolves spontaneously.
The inflammation of the pancreas results from an obstruction of the bile and pancreatic duct, which then impedes the outflow of pancreatic digestive enzymes (Huether & McCance, 2012). Thereafter, the occluded ducts cause the accumulation of pancreatic secretions along with the activation of specific enzymes within the pancreas, which further activate other enzymes (Huether & McCance, 2012). For example, activated trypsin then activates chymotrypsin, amylase, lipase, and elastase. This further explains why patient J.A.’s blood findings reported elevated serum amylase and lipase. Although, elevated serum amylase concentration is characteristic of pancreatitis, it is not used to confirm diagnosis; however, an elevated serum amylase is the primary diagnostic marker for acute pancreatitis (Huether & McCance, 2012). Furthermore, the activation of these enzymes causes the self-digestion of both pancreatic cells and tissues, causing the pancreas to become inflamed. If this self-digestion of the pancreas progresses, it can cause vascular damage, coagulation, and fat necrosis (Huether & McCance,
2012).
Furthermore, in cases of alcohol abuse, such as presented in patient J.A., “the pancreatic acinar cell metabolizes ethanol with the generation of toxic metabolites that injure pancreatic acinar cells, causing the release of the activated enzymes” (Huether & McCance, 2012). These series of events then cause auto-digestion of the pancreas, resulting in inflammation. The inflammation of the pancreas then can result in mid-abdominal or epigastric pain, as experienced by client J.A. Also, J.A. originally presented to the ED with nausea and vomiting, which was caused by paralytic ileus, secondary to the inflamed pancreas (Huether & McCance, 2012).
Past …show more content…
Medical History: Anxiety, Hepatitis, Seizures, Cholecystitis
Pathophysiology:
Acute pancreatitis is usually a mild disease that causes the pancreas to become edematous, and usually resolves spontaneously.
The inflammation of the pancreas results from an obstruction of the bile and pancreatic duct, which then impedes the outflow of pancreatic digestive enzymes (Huether & McCance, 2012). Thereafter, the occluded ducts cause the accumulation of pancreatic secretions along with the activation of specific enzymes within the pancreas, which further activate other enzymes (Huether & McCance, 2012). For example, activated trypsin then activates chymotrypsin, amylase, lipase, and elastase. This further explains why patient J.A.’s blood findings reported elevated serum amylase and lipase. Although, elevated serum amylase concentration is characteristic of pancreatitis, it is not used to confirm diagnosis; however, an elevated serum amylase is the primary diagnostic marker for acute pancreatitis (Huether & McCance, 2012). Furthermore, the activation of these enzymes causes the self-digestion of both pancreatic cells and tissues, causing the pancreas to become inflamed. If this self-digestion of the pancreas progresses, it can cause vascular damage, coagulation, and fat necrosis (Huether & McCance,
2012).
Furthermore, in cases of alcohol abuse, such as presented in patient J.A., “the pancreatic acinar cell metabolizes ethanol with the generation of toxic metabolites that injure pancreatic acinar cells, causing the release of the activated enzymes” (Huether & McCance, 2012). These series of events then cause auto-digestion of the pancreas, resulting in inflammation. The inflammation of the pancreas then can result in mid-abdominal or epigastric pain, as experienced by client J.A. Also, J.A. originally presented to the ED with nausea and vomiting, which was caused by paralytic ileus, secondary to the inflamed pancreas (Huether & McCance, 2012).