Pancreatic Disease Research Paper

"Cancer of the pancreas is a genetic disease that is the fifth most common cause of death in both men and women. Pancreatic cancer affects approximately 28,000 Americans each year, or five out of 100,000 people" (Mayo Clinic, 1998). According to physicians at Johns Hopkins Medical Institute, "pancreatic cancer is the challenge of the twenty-first century." So, where exactly is the pancreas located in our bodies, and what does it do? The pancreas is a gland found behind the stomach that is shaped somewhat like a fish. The pancreas is about six inches long and less than two inches wide, and it extends across the abdomen. The pancreas consists of two separate glands inside the same organ, the exocrine gland and the

Acute Pancreatitis: Acute inflammation of the pancreas.The most common pathogenic mechanism is autodigestion of the pancreas. The etiological factor injures pancreatic cells or activates the pancreatic enzymes in the pancreas rather than in the intestine which may be due to reflux of bile acids into the pancreatic duct through an open or distended sphincter of Oddi. The result may also be caused by blockage created by a gallstone. Obstruction of pancreatic ducts results in pancreatic ischemia.The pathophysiology involvement of acute pancreatitis is

5. Explain why proteases are secreted in an inactive state and describe the means by which proteases are activated in the stomach and small intestine. – The enzymes protease, amylase and lipase, are potent enzymes that are capable of digesting the pancreatic cells- a process called autodigestion. To protect themselves from autodigestion in case the digestive enzymes accidentally get turned on, pancreatic cells produce enzymes in inactive form called zymogens, which are stored in membrane-bound sacks called zymogen granules. Enteropeptidase (also called enterokinase) is an enzyme produced by cells of the duodenum

“Each year, acute pancreatitis sends more than 200,000 Americans to the hospital. Many of those who suffer from pancreatic problems are also heavy drinkers” (“Beyond Hangovers: Understanding Alcohol's Impact Your Health” 15). The pancreas is an important organ which aids in digestions and energy conversion. The pancreas directs enzymes to the small intestine to digest nutrients and it also secretes insulin and glucagon. The body’s main source of energy is glucose and insulin allows additional glucose to be stored away in the body properly. Too much alcohol damages cells in the pancreas, causing complications with insulin, leaving the organ open to inflammation. Alcohol causes the pancreas to discharge the enzymes intended for the small intestine back into the pancreas which can lead to inflammation and the swelling of tissues and blood vessels. Pancreatitis is the inflammation which causes the organ to malfunction and if one continues to drink, it can magnify into chronic pancreatitis when the inflammation is constant (“Beyond Hangovers: Understanding Alcohol's Impact Your Health” 15-16). Pancreatitis causing severe abdominal pain, persistent diarrhea, and is not curable. Sixty-percent of circumstances result from alcohol; although, some have been linked to gallstones (Freeman).

Incretin based drugs have proven to be effective glucose-lowering agents (Butler et al, 2013). But there have been concerns with respect to the long-term consequences of using such therapies. The issues raised were regarding their causal relationship with acute pancreatitis (AP). There are clearly conflicting evidence that have been presented in preclinical studies and in epidemiologic studies which suggest an association which may or may not be a causal relationship between these drugs and AP. (Butler et al, 2013)

When a cystic duct is continuously obstructed inflammation occurs. Bile stasis triggers release of inflammatory enzymes and can be caused by fasting, obstruction, postsurgical/procedural irritation or ileus (total parenteral nutrition [TPN]), which can lead to bile inspissation that is directly toxic to the gallbladder epithelium. The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which prolong inflammation and can cause a bacterial infection to occur later. The malicious circle of fluid secretion and inflammation leads to necrosis and perforation if it goes unchecked. If acute inflammation resolves then continues to recur, the gallbladder becomes fibrotic and contracted and does not concentrate bile or empty normally which is a feature of chronic cholecystitis. (Huffman, J. et al.,

Dysfunction of the pancreas is treated with an enzyme replacement (provided by the artificial enzyme) and diet to improve absorption of vital

mucus can block the ducts of the pancreas, and that prevents the enzymes from reaching the

In light of question number three A-B, Cystic fibrosis causes variations from the norm in almost all exocrine and numerous endocrine organs. This disturbance of organs extremely thwarts the elements of the Pancreas during absorption bringing about “…an abnormal mucous secretion that causes obstruction of single mucin-producing cells. The pancreas secretes less enzyme (ex: trypsin, lipase and amylase), so malabsorption ensues with its attendant deficiency disorders” (Walsh et al.)

Banting prepared a lecture to his medical students involving the pancreas. According to Frederick Banting, he thought that possibly others were not able to determine the internal secretion in pancreatic mixtures because it was being demolished by the external secretion. Perhaps if digestive juices could be prevented, then the pancreas would stop creating its secretion and it could be isolated to nurse a diabetic organism.

Diabetes (DM) is a metabolic disorder affecting the endocrine system, the physiognomies consist of either the inability to properly produce and/or use insulin by the body; resulting in unregulated blood sugar (BS) or glucose. This is typically a chronic condition, but there are some outliers that may yield the same results, such as pregnancy, surgery, medication regimen, pancreatic disease and infections. A basic review of the digestive process will help us in understanding this illness; the metabolism of our food by our body forms glucose and used for energy. There’s impairment in diabetic patients with this process and the BS fluctuates, these changes over time have a negative effect on other organs resulting in secondary chronic ailments. For our discussion, we will deal with two types of diabetes; Insulin Dependent Diabetes Mellitus (IDDM) or Type I diabetes and Non-Insulin-Dependent Diabetes Mellitus (NIDDM) or Type II diabetes. In IDDM client 's, the pancreas produces little or no insulin; therefore, they need insulin to help manage their blood glucose levels.

Severe acute pancreatitis is characterised by persistent organ failure. Organ failure that develops during the early phase is set in motion by the activation of cytokine cascades resulting in SIRS. When SIRS is present and persistent, there is an increased risk that the pancreatitis will be complicated by persistent organ failure, and the patient should be treated as if they have severe acute pancreatitis (Banks et al., 2012).

Chronic pancreatitis :- chronic pancreatitis is long lasting inflammation of the pancreas .it is most often happens after an episode of acute pancreatitis . heavy alcohol drinking is another big cause. Damage to the pancreas from heavy alcohol use may not cause symptoms for years , but then a person may suddenly develop severe pancreatitis . symptoms of chronic pancreatitis are patients feels frequently pain in the upper abdomen but in some patient pain may be disabling . weight loss caused by poor absorption of food. This malabsorption happens because the gland is not producing enzyme to break down food. Diabetes may develop if insulin producing cells of the pancreas are damaged . risk factors of chronic pancreatitis include heavy alcohol drinking for a long time , certain hereditary condition such as cystic fibrosis , gallstones, condition such as high in triglyceride and lupus .

This was in the same line with Meier et al., (2005) who reported that in the adult pancreas, exocrine ducts were often surrounded by areas of fibrous tissue, and the extent of this fibrosis is markedly increased in patients with type 1 diabetes. Riccillo et al., (2004) mentioned that in diabetes; there were inter-acinar and inter-lobular fibrosis which suggesting that insulinopenia may cause these injurious effects on exocrine pancreas. Concerning this issue, previous reports localized the pancreatic stellate cell (PSCs,) in the islets(Lee et al., 2011) .Upon activation, it started to proliferate, change their morphology into myofibroblast-like cells and start to secrete extra cellular matrix components (Apte et al.,

Fifty (50) specific pathogen-free adult male Spragure-Dawley (SD) male rats, 250-300gm body weight imported from the specific Pathogen Free Animals department of Dalian medical University (Dalian, China) (SYXK 2013-0006),. Rats were randomly divided into four groups. The animal groups: normal control (Sham); Sever Acute Pancreatitis (SAP); STIM1/Ori1SOCE pathway inhibitor (2-APB) and Qingyi Decoction (QYKL) Each animal in the experimental groups (SAP, 2-APB, QYKL) was injected by 5% sodium taurocholate (1ml/kg body weight) [9] 2% sodium pentobarbital (0.25 mL/100g), (5% sodium taurocholate (1 ml/kg body weight) in the pancreatic duct to induce rats with acute sever pancreatitis (ASP), whereas, the normal control animals were injected with