Acute Pancreatitis

Acute Pancreatitis

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Acute Pancereatita is an acute inflammation of the pancreas often encountered over 40 years, more common in men, but also diagnosed at younger ages, even children. The pancreas is a gland responsible for insulin production and secretion of digestive enzymes necessary for synthesis and metabolism of fats, proteins and carbohydrates. Approximately 80% of the exocrine pancreas, 20% are endocrine. Acute pancreatitis is a disease of the exocrine pancreas-producer of digestive enzymes. The most frequent causes of acute pancreatitis are: -Gallstones, pancreatic trauma -Pancreas divisum -Alcohol, drugs Coxachie-virus, bacteria -Coronary bypass -CF -Duodenal ulcer. Symptoms vary greatly in intensity, the total lack of symptoms until the grand drama of the pancreas. Abdominal pain is the most frequent symptom, and is described by the patient as a sensation of crushing or torn. The pain is so intense the patient may induce syncope episode. Is accompanied by hypotension, hypertension sudden shortness of breath. Nausea and vomiting, relieves pain is not constantly present. Paralytic ileus always accompanies pain. Confusion, shock or coma in severe forms are present. They describe three types of therapy in this disease: medical and surgical endoscopy. Goals of therapy are pain relief, restoration and maintenance of electrolyte balance and volume expansion, decreased pancreatic secretion, limiting mortality and preventing inflammatory femonelor. The mortality rate in patients with acute pancreatitis is 10-15%. Those with biliary pancreatitis tend to present a higher rate than those with alcoholic pancreatitis. In patients with chronic severe mortality is 30% organic. Patients with necrosis without organ failure mortality rate is 0. During the first week after onset, most deaths result from organ failure. In weeks following the infection plays an important role, but remains the leading cause organ failure or death.
Pathogenesis
Acute pancreatitis may occur when the factors involved in maintaining cellular homeostasis is altered. Triggers can be any damaging acinar cells and blocks the secretion granules zimogene, eg alcohol abuse, gallstones and been called or toxic drugs. It is still unclear mechanism that triggers the events of acute pancreatitis. It is assumed that extracellular factors are involved: the nervous response, arterial, as well as intracellular: activation of intracellular enzymes, growth as the intracellular activation of shock proteins. In addition, acute pancreatitis may develop when damage leads to absence of bile duct cells secrete enzymes such as CFTR gene mutation. Once it has been initiated cascade of pathological events after pancreatic acinar cell injury, cell membrane traffic becomes chaotic with disastrous consequences: Granule-lysosomal compartments and fuse zimogene tripsinogenul Activating the active trypsin Cause intracellular trypsin activation-zimogenelor -Secretory vesicles are released into the interstitium, where they will be chemoatractante for inflammatory cells. Superoxide and activated neutrophils release proteolytic enzymes (cathepsin B, D, G, collagenase and elastase). Macrophages release cytokines that will mean local or systemic inflammatory response in severe cases. Mediators are released TNF-alpha, IL-6, IL-8. These mediators of inflammation increases permeability of pancreatic vasculature, leading to hemorrhage, edema and pancreatic necrosis. As these mediators are released into general circulation complications, such as bacteremia, the translocation of intestinal flora, acute respiratory distress syndrome, pleural effusion, gastrointestinal bleeding and renal failure. Systemic inflammatory response syndrome leading to shock and death cardiocirculator.