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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The primary pathophysiology of acute pancreatitis is due to a low flow state mediated through the neurohumoral mechanisms. Ischemia of the microcirculation, combined with hormonal and other biochemical factors, produces destruction of cellular elements of the pancreas. These changes can be triggered by one or more stressors, including the psychic factor. Emotional stress may not only be responsible for an initial attack of pancreatitis (idiopathic) but must be considered, like any other stressor, to be responsible for exacerbations, relapses or chronicity of pancreatic disease.
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PMID:Pathogenesis of pancreatitis: a unified concept. 369 76

For experimental analysis of pathogenesis of acute pancreatitis a suitable animal model is necessary. The pancreatic (juice) edema and an alteration of cellular energy metabolism are important pathogenetic factors. A partial intrapancreatic edema was induced by stimulating secretion against permanent or temporary obstruction by ductal ligation. Short-term ischemia was used as tool for alteration of cellular energy metabolism. 24 h postoperatively morphological changes were macro- and microscopically investigated. The data show a correlation between duration of ischemia (10-30 min) and the frequency of acute pancreatitis at preexisting juice edema (44-68 percent). With increasing ischemia the morphological alterations (e.g.: necroses of adipose tissue) were enhanced, too. A hemorrhagic necrotizing pancreatitis was rarely observed. In comparison to other experimental models the presented one is characterized by a mostly moderate and light course of acute pancreatitis offering a good tool for elucidation of the very first stages of the pathogenesis.
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PMID:Contribution of pancreatic edema and short-term ischemia to experimental acute pancreatitis in the rat. I. Procedure and pathomorphological investigations. 382 14

A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.
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PMID:Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. 389

Microcirculatory derangements in the pancreas associated with acute pancreatitis may contribute to a low-flow state and lead to pancreatic necrosis. This study investigated the effects of glucagon, a selective mesenteric arterial dilator, on pancreatic ischemia in canine bile-trypsin-induced pancreatitis (BTP). Measurements of cardiac Index (CI), total pancreatic blood flow (QP), pancreatic oxygen consumption (O2CP), and pancreatic arteriovenous shunt flow (QAVS) were obtained prior to and after inducing BTP. Bile-trypsin-induced pancreatitis was induced in 18 dogs. Nine received lactated Ringer's solution alone (LRPAN) at 6.5 mL/kg/hr, nine received lactated Ringer's solution plus continuous Intravenous (IV) glucagon hydrochloride (GLUPAN) at 1.0 micrograms/kg/min, and nine undergoing periportal dissection without BTP received IV glucagon (GLUCON). Following BTP, CI, QP, and O2CP decreased significantly and QAVS remained unchanged in crystalloid-treated animals (LRPAN). Glucagon administration (GLUPAN) transiently increased CI and QP but failed to improve O2CP and did not change QAVS. The decrease in O2CP observed after BTP in association with a constant QAVS suggests a metabolic block to oxygen uptake at the cellular level. Glucagon in pharmacologic doses does not reverse abnormalities in O2CP and is therefore of questionable physiologic benefit in the treatment of acute pancreatitis.
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PMID:Efficacy of pharmacologic glucagon in acute experimental pancreatitis. 397 Jun 71

Human pancreas tissue was studied electron microscopically during various stages of shock. The subcellular changes of exocrine pancreas affect in particular endoplasmic reticulum (ER), mitochondria, cytoplasm, and nuclei. Alterations correlate with duration and severity of shock, causing cell death in prolonged or severe manifestations of shock. This is obviously due to release of enzymes from zymogen granules; the ensuing damage cannot be distinguished from autodigestive pancreatitis. Lesions of exocrine pancreas cells are of multifactorial origin, arising from general shock-induced hypoxia, but also from local ischemia due to disturbed microcirculation provoking intravasal coagulation. Beyond these main causes, intracellular disorders of metabolism, obstruction of lymph drainage, and nervous factors may be of influence. As the cases surveyed in this paper had no fatal outcome - except for one patient - the changes described can be defined as non-lethal or as reversible.
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PMID:Ultrastructural changes of the human pancreas in acute shock. 402 38

Pylorectomy and end-to-end gastroduodenostomy are surgical procedures that allow excision of abnormal pyloric tissue and provide improved gastric outflow. These techniques were used for the treatment of benign, malignant, and ulcerative conditions that were judged to be not adequately treatable with pyloromyotomies or pyloroplasties. End-to-end gastroduodenostomy was not much more difficult than a standard intestinal anastomosis; however, a thorough knowledge of the pyloric area anatomy was required to avoid serious surgical errors. In addition, gentle tissue manipulation and precise suture placement reduced the chance of iatrogenic pancreatitis, biliary obstruction, tissue ischemia, and/or suture line leakage. The results of surgery depended on the underlying disease process. Dogs with benign lesions such as chronic hypertrophic pyloric gastropathy responded favorably to treatment. Dogs with malignant disease and perforated ulcers had low long-term survival rate. Pyloric adenocarcinoma was not adequately treated with this method alone.
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PMID:Pylorectomy and gastroduodenostomy in the dog: technique and clinical results in 28 cases. 405 13

Extrahepatic manifestations due to an immunologic response to a surface antigen of hepatitis B virus have been identified. These include a serum sicknesslike syndrome and a necrotizing vasculitis. The latter is far more important and in indistinguishable histologically from nonhepatitis related polyarteritis. At least 90 cases have been reported in the decade since 1970, and five are added here. The necrotizing vasculitis syndrome results from fibrinoid necrosis and inflammation of small and medium-sized arterial walls recognizable angiographically by arterial microaneurysms and often by visceral infarction and hemorrhage. Renal failure is common and often associated with pulmonary edema. Gastrointestinal symptoms are a prominent feature due to bowel ischemia. Infarction and perforation are significant causes of morbidity and mortality. Necrotizing vasculitis is also one cause of pancreatitis and of cholecystitis. Plain films, contrast studies, computed tomography, and sonography have been shown to be useful in the recognition of these complications.
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PMID:Radiologic recognition of extrahepatic manifestations of hepatitis B antigenemia. 611 55

The incidence of unexplained pancreatitis in patients dying after cardiac operations has been recorded as 16%, with evidence to implicate ischemia in the pathogenesis of the pancreatitis. Increased amylase--to--creatinine clearance ratios (ACCR), suggesting pancreatic dysfunction, have been reported in patients following nonpulsatile cardiopulmonary bypass (CPB). Pulsatile CPB is increasingly recognized to be a more physiological form of perfusion, particularly with respect to capillary blood flow. In this study the ACCR has been determined before, during, and after cardiac operations performed with both nonpulsatile and pulsatile CPB. Twenty patients undergoing elective cardiac operations were studied. Ten patients had nonpulsatile CPB (nonpulsatile group) and 10 had pulsatile CPB (pulsatile group). The two groups were comparable as regards perioperative variables and perfusion parameters. In both groups the ACCR was estimated preoperatively, on three occasions during the operation, and daily on the first 5 postoperative days. A significant elevation in ACCR was observed in nine of 10 patients in the nonpulsatile group but in only one of 10 patients in the pulsatile group (p less than 0.001). The significant improvement of ACCR stability following pulsatile CPB may indicate that this form of perfusion will reduce the risk of pancreatitis following cardiac operations performed with CPB.
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PMID:The amylase-creatinine clearance ratio following cardiopulmonary bypass. 616 15

Acute pancreatitis may be initiated in the ex vivo, perfused canine pancreas preparation by a variety of stimuli. These include oleic acid infusion (FFA), partial duct obstruction with secretin stimulation (POSS), and a 2-hour period of ischemia (ISCH). In each model, pancreatitis is characterized by weight gain, edema, and hyperamylasemia. Oxygen-derived free radicals such as superoxide, hydrogen peroxide, and the hydroxyl radical are highly reactive toxic substances that are normally produced in small amounts during oxidative metabolism. Ordinarily, these substances are detoxified by endogenous intracellular enzymes called free radical scavengers (FRS), such as superoxide dismutase (SOD) and catalase (CAT). These studies were undertaken to evaluate the possible role of oxygen-derived free radicals in the initiation of acute pancreatitis in the isolated canine model. All preparations were perfused for 4 hours with autologous blood. Controls (N = 6): these glands remained normal in appearance, gained minimal weight (6 +/- 1 g), and serum amylase remained normal (less than 1000 u/dl). FFA pancreatitis, FFA alone (N = 6): these glands became edematous, gained weight (113.5 +/- 27.0 g), and developed hyperamylasemia (2087 +/- 387 u/dl). FFA + FRS (N = 6), SOD (50 mg) and CAT (50 mg) were added to the perfusate at time zero: these glands became only minimally edematous, gained less weight (31.8 +/- 10.1 g, p less than 0.05), and amylase remained normal (p less than 0.05). POSS pancreatitis, POSS alone (N = 8): these glands became edematous, gained weight (38.6 +/- 4.6 g), and developed marked hyperamylasemia (9522 +/- 3226 u/dl). POSS + FRS (N = 6): these glands did not develop edema, gained less weight (15.1 +/- 2.6 g, p less than 0.05), and serum amylase only increased to 1815 +/- 343 u/dl, (p less than 0.05). ISCH pancreatitis, ISCH alone (N = 6): these glands became edematous, gained weight (75.8 +/- 25 g), and developed hyperamylasemia (1679 +/- 439 u/dl). ISCH + FRS (N = 6): these glands did not develop edema, gained only 18.3 +/- 9.0 g (p less than 0.005), and serum amylase remained normal (p less than 0.05). These studies demonstrate that, in this canine preparation, acute pancreatitis is significantly ameliorated by oxygen-free radical scavengers. Since this was true whether the pancreatitis was produced by FFA infusion, POSS, or ischemia, it suggests that oxygen-derived free radicals may mediate a common essential step in the pathogenesis of all forms of pancreatitis.
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PMID:The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis. 620 83

The influence of a short-term ischemia of the pancreas for the pathogenesis of a hemorrhagic necrotising pancreatitis was investigated in 28 mongrel dogs. Ischemia of the pancreas in 20 minute intervals repeated three times did not leave any macroscopic, histologic or electron microscopic changes and no alterations of the level of the alpha-amylase, the lipase, and the glucose in the serum. An ischemia of 20 minutes' duration by starvation of the celiac artery and the superior mesenteric artery produces a hemorrhagic necrotising pancreatitis under the precondition of a following pancreatic edema by ligature of the pancreatic duct and secretomotoring with secretin and pancreozymin. The necrosis starts histologically in the perilobular adipose and affects the parenchyma later. Whether the lipase is the starting enzyme for the acute pancreatitis or only conditions the early adipose necrosis should be discussed after these findings. Already a fugitive pancreatic edema produces a hemorrhagic necrotising pancreatitis after previous ischemic damage.
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PMID:[Animal experiment studies on the role of ischemia in the pathogenesis of acute pancreatitis]. 633 88


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