Pathogenesis/ Pathophysiology
Human beings are at risk of being affected by various health conditions. These conditions can be caused by various factors such as genetic or lifestyle. Some of these diseases require immediate treatment so that they can be healed. In case these diseases are not treated early, they may become severe and pose a danger to the life of various people. An example of a condition that can attack any person is pancreatitis. Pancreatitis refers to the unexpected inflammation of the pancreases and is characterized by severe epigastric pain, vomiting, nausea, fever, and loss of appetite. This condition can be further defined using pathology, which includes pathogenesis as well as pathophysiology.
Pathogenesis of Pancreatitis
Severe pancreatitis tends to occur when the body started to experience abnormal activation of digestive enzymes in the pancreases. This situation happens when there is inappropriate activation of zymogens within the pancreas. Zymogens can also be called inactive enzyme precursors. During this activity, trypsinogen is transformed into an active form that is called trypsin, and this occurs in the duodenum, which is the starting point of the small intestine whereby enzymes are used in the digestion of proteins. In the case of acute pancreatitis, the trypsinogen and lysosomal enzymes get into contact, and this activates the conversion of trypsinogen to become trypsin. The article, “Pathogenesis and management of postprandial hyperglycemia: role of incretin-based therapies,” explains that the trypsin becomes active, and this result in the activation of other trypsinogen molecules (Gerich, 2013). As the digestive enzymes continue to be activated, so does the inflammation begins to occur, vascular injury, edema, and cellular death. There are two ways that the death of the pancreatic cells occurs. One of the mechanisms is necrosis, which is more damaging and less organized. The second method that the death of the pancreatic cells occurs is Apoptosis. The apoptosis method is more controlled compared to necrosis. The article, “Pancreatic exocrine insufficiency: diagnosis and treatment, “A balance can occur between these mechanisms, which results in the death of the pancreatic cells, but it can be mediated using caspases (Domínguez‐Muñoz, 2011). Caspases are used to regulate Apoptosis, and it has essential anti-necrosis functions that can be used during pancreatitis. Therefore, these actions prevent the action of trypsinogen and depletion of ATP by constraining the inhibitors of Apoptosis. However, the caspases can be accomplished as a result of exposure to chronic ethanol or severe insult which may provide room for necrosis to predominate
Pathophysiology of Pancreatitis
Pathophysiology can be used to define pancreatitis, and this starts by explaining that are two types of pancreatitis, and that is severe and mild. According to the article, “Pathogenesis of chronic pancreatitis: A comprehensive update and a look into the future,” a severe or mild pancreatitis is explained on the basis that the predominant response to any injury of the cell is necrosis (severe) or inflammation (mild) (Andersson, Tingstedt & Xia, 2009). In cases of mild pancreatitis, inflammation, as well as edema of the pancreases, is noted. On the other hand, in severe pancreatitis, the pancreases experience necrosis, and the organism surrounding the pancreases can be injured. During the initial injury, extensive inflammation response occurs due to the synthesizing of the pan, creating cells as well as the secreting of the inflammatory mediators. The primary inflammatory mediators include IL-1 and TNF- alpha. The presence of acute pancreatitis is an indication of the inflammatory response that is happening in the body, and this can be referred to as the recruiting neutrophils into the pancreases. Furthermore, t the inflammatory response results in the secondary occurrence of pancreatitis, and this may be characterized by acute respiratory syndrome, renal failure, cardiovascular failure, disseminated intravascular coagulation, and gastrointestinal hemorrhage.
References
Andersson, R., Tingstedt, B., & Xia, J. (2009). Pathogenesis of chronic pancreatitis: a comprehensive update and a look into the future. Scandinavian journal of gastroenterology, 44(6), 661-663. Retrieved from https://www.tandfonline.com/doi/abs/10.1080/00365520902718739
Gerich, J. (2013). Pathogenesis and management of postprandial hyperglycemia: role of incretin-based therapies. International journal of general medicine, 6, 877. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884108/
Domínguez‐Muñoz, J. E. (2011). Pancreatic exocrine insufficiency: diagnosis and treatment. Journal of gastroenterology and hepatology, 26, 12-16. Retrieved from https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1440-1746.2010.06600.x