Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is ample evidence from this retrospective comparison to indicate that emphysematous cholecystitis does merit clinical distinction apart from acute cholecystitis. It is an acute infection of the gallbladder caused by a specific group of bacteria that may be aided by some aspect of local ischemia. Cholelithiasis does not seem to be a major factor in the pathogenesis of emphysematous cholecystitis, and this, in association with some dependence upon ischemia, may account for the predominance of this disease in males rather than females. Gangrene is a common feature of the pathologic process, and thus it is not surprising that the diagnosis of emphysematous cholecystitis implies a risk of gallbladder perforation that is five times that expected from ordinary acute cholecystitis. The key to identifying this disease is the plain abdominal roentgenogram which in most instances will make the diagnosis and provide an impetus for early operative intervention.
 ...
PMID:A comparative appraisal of emphysematous cholecystitis. 17 53

The pathogenesis of acute pancreatitis is based on the following principles: 1. Biliary. In biliary pancreatitis there is a causal relationship between the induction of acute pancreatitis and the migration of gallstones. The basic pathomechanism seems to be a combination of an increase in permeability and pressure in the ductal system. 2. Intraacinar. Caerulein-pancreatitis is a well established experimental model which reflects the intracellular/interstitial type of activation. Basolateral secretion of pancreatic enzymes into the interstitial space represents the initial event. Intracellular activation of trypsin by the fusion of zymogen-granules and lysosomes has been advocated as an alternative mechanism. 3. Alcohol. The acute alcohol pancreatitis comprises a combined pathogenesis. Obstruction and reflux as well as the cytotoxic effect of alcohol seem to be the main principles. 4. Disturbance of pancreatic microcirculation. Ischemia of the pancreas seems to play a key role in the transition from pancreatic edema to necrosis. Improvement of capillary perfusion by isovolemic hemodilution with dextran 60 has been shown to be an efficient therapeutic tool.
 ...
PMID:[Etiology and pathogenesis of acute pancreatitis]. 152 49

Ischemia is one mechanism implicated in the pathogenesis of acute acalculous cholecystitis. Gallbladder specimen arteriography was performed to define the comparative status of cystic artery runoff in the macroscopically normal gallbladder (n = 10), in acute gallstone-associated cholecystitis (n = 10), and in acute acalculous cholecystitis (n = 7). Standardized film exposure and quantity of contrast medium administered permitted objective intergroup comparison. Compared to the macroscopically normal gallbladder, specimens of acute gallstone-associated cholecystitis exhibited arterial dilatation and extensive venous filling. In contrast, multiple arterial occlusions, with absent or minimal venous filling, were consistent features of acute acalculous cholecystitis; the degree of arteriographic abnormality for acute acalculous cholecystitis corresponded to the severity of gallbladder pathologic findings. Small vessel occlusion, on the basis of low splanchnic flow or intravascular coagulation, may be a fundamental element in the pathogenesis of acute acalculous cholecystitis.
 ...
PMID:Small vessel occlusion in acute acalculous cholecystitis. 173 86

A 65 year old woman, who had a giant umbilical hernia since more than 30 years, was admitted for a transitory cerebrovascular ischemia. During her stay, she presented an episode of acute pancreatitis localized in the head of the pancreas. All current causes of acute pancreatitis were ruled out, especially alcoholism and gallstones. Endoscopic retrograde cholangio-pancreatography performed in the patient lying on the left side demonstrated localization of the antrum and the duodenum with the head of the pancreas into the umbilical hernia. It seems clear that the giant umbilical hernia caused a progressive and intermittent passage of the head of the pancreas through chronic traction on the ligament of Treitz and acute pancreatitis by incarceration. At our knowledge, this mechanical cause of acute pancreatitis was not yet described in the literature.
 ...
PMID:[Acute pancreatitis caused by a voluminous umbilical hernia. Case report]. 248 14

Liver biopsy results and clinical records from 13 patients with sickle cell anemia were reviewed to assess the relative importance of local ischemia or of factors unrelated to sickling as a cause of their liver disease. Two of the biopsy specimens were normal and one showed cirrhosis. Nine patients had received multiple blood transfusions and nine had cholelithiasis, of whom two also had choledocholithiasis. Seven had both risk factors. Five had lobular cholestasis and four had acute or chronic hepatitis. One biopsy specimen showed changes of the Budd-Chiari syndrome. Another showed clear portal tract changes of large bile duct obstruction but no mechanical blockage of the biliary system; this suggests the thickened bile as postulated by Muirhead. Otherwise the changes observed were those to be expected in a heavily transfused population with a high prevalence of gallstones.
 ...
PMID:Histopathologic features of liver biopsy specimens in sickle cell disease. 334 26

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.
 ...
PMID:Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. 389

DT, a 63-year-old white male with insulin-dependent diabetes mellitus and severe peripheral vascular disease, was admitted with a five-day history of vague abdominal pain and diarrhea. On the day of admission he vomited three times, was noted to have a bloody stool, and came to the emergency room. DT denied hematemesis, fever, or chills. He had bilateral leg amputations and had sustained three myocardial infarctions, the last one 15 months before this admission. He had never experienced symptoms of abdominal angina. Of significance was his history of congestive heart failure, mitral regurgitation, and atrial fibrillation. His medications on admission included digoxin 0.25mg per day, furosemide 40mg per day, and NPH insulin 15 units per day. On admission to the hospital his oral temperature was 38 degrees C, pulse was 90/min, respiratory rate was 24/min, and blood pressure was 134/80mmHg. Abdominal examination revealed a distended abdomen with hypoactive bowel sounds and mild tenderness. Chest x ray revealed cardiomegaly. The electrocardiogram demonstrated atrial fibrillation. A plain film of the abdomen was positive for gallstones and edema of the bowel wall (thumb-printing). Laboratory results included blood urea nitrogen 48mg%, creatinine 1.2mg%, hemoglobin 18g/dl, and hematocrit 52.9%. White blood cell count was 11,900 cells/cc with 33% polymorphonuclear leukocytes, 47% bands, 8% lymphocytes, 11% monocytes, and 1% atypical lymphocytes. The prime considerations for differential diagnosis were mesenteric ischemia and infectious gastroenteritis. While it was appreciated that mesenteric ischemia, if present, might warrant surgical intervention, the risk of anesthesia itself in this patient was felt by his attending physicians to exceed 30%. Furthermore, the clinical findings were only "suggestive" of mesenteric eschemia. They were certainly not "diagnostic." In view of this dilemma, a consultation with the Division of Clinical Decision Making was requested.
 ...
PMID:Abdominal pain, atherosclerosis, and atrial fibrillation. The case for mesenteric ischemia. 716 38

Although many new antibiotics became available for clinical use, intractable bacterial infections are still major cause of morbidity and mortality in surgical patients. The infections are attributable to multiple factors. Surgical stress such as extensive burns and major surgery results in the depressed host-defense function, which is mediated by cytokine responses. Necrotic tissue, ischemia, hematoma, cholelithiasis, foreign bodies, indwelling catheters, intra-tracheal tubes, and other medical devices are local factors making infection resistant to ordinary chemotherapy. Multi-resistant bacteria such as methicillin resistant Staphylococcus aureus and Pseudomonas, and ampicillin resistant enterococci are the main bacteria causing the infections. 32% of surgical specimens isolated two or more bacteria, making the chemotherapy difficult in clinical setting. Importance of surgical drainage, removal of necrosis and the devices are emphasized.
 ...
PMID:[Intractable bacterial infections in surgical patients]. 812 4

The excisional surgical treatment of 50 patients with congenital biliary dilatation (CBD) associated with pancreaticobiliary maljunction (PBMJ) was analyzed. There were two patients who had early complications of lesser bile juice leakage with a maximum duration of 21 days, but no pancreatic juice leakage was noticed. As a late complication, two strictures at the anastomotic portion of the hepaticojejunostomy and one intrahepatic gallstone formation were encountered, but no malignant lesion was evident. Both patients with strictures could be predicted using postoperative cholangiography performed two weeks postoperatively and underwent hepaticojejunostomy. Intrahepatic gallstones were treated with lateral segmentectomy of the liver and electrohydraulic lithotripsy through percutaneous transhepatic cholangioscopy. Accordingly, these results suggest that excisional surgical treatment is the most appropriate method for CBD with PBMJ; however, special care must be taken, such as creating a sufficiently wide anastomotic stoma to enable free drainage of bile into the intestine; also, there should be precautions against ischemia at the anastomotic portion. The importance of the postoperative cholangiography to predict the postoperative outcome should be emphasized. Furthermore, causes of intrahepatic gallstone formation should be studied in such instances.
 ...
PMID:Surgical treatment of congenital biliary dilatation associated with pancreaticobiliary maljunction. 832 33

Four models of acute pancreatitis have been previously developed that use the ex vivo perfused isolated canine pancreas preparation. The four models include the intraarterial infusion of oleic acid (FFA) that mimics hyperlipemic pancreatitis, partial obstruction of the pancreatic duct with secretin stimulation (POSS) that mimics gallstone pancreatitis, a 2-hour period of ischemia before perfusion (ISCH 2) that mimics shock pancreatitis, and the infusion of cerulein at supramaximal stimulatory doses (CER), which lacks an obvious clinical counterpart. In the FFA, POSS, and ISCH 2 pancreatitis, but not in the CER pancreatitis, toxic oxygen metabolites, generated by the enzyme xanthine oxidase (XO), have been shown to be important mediators in the early pathogenesis. Ordinarily XO primarily occurs as xanthine dehydrogenase (XD) but can be converted to XO, which is the form that generates toxic oxygen metabolites. This conversion of XD to XO may take place either reversibly by way of sulfhydryl group oxidation or irreversibly by means of proteolytic cleavage of XD. This study was undertaken to investigate the mechanism of conversion of XD to XO in the FFA-, POSS-, and ISCH 2-induced pancreatitis models. CER pancreatitis was studied for comparison. After 4 hours of perfusion, pancreatitis was manifest by edema, weight gain, and hyperamylasemia in all four models. Dithiothreitol, a sulfhydryl group protector, ameliorated the weight gain in the FFA (40 +/- 14 gm to 18 +/- 13 gm; p < 0.05), POSS (28 +/- 10 gm to 9 +/- 3 gm; p < 0.05), and ISCH 2 pancreatitis (30 +/- 13 gm to 15 +/- 3 gm; p < 0.05), and ameliorated the hyperamylasemia in the POSS pancreatitis (12,062 +/- 4304 units/dl to 5877 +/- 2659 units/dl; p < 0.05). The CER pancreatitis was not ameliorated with dithiothreitol. A serine protease inhibitor of low molecular weight, phenylmethylsulfonyl fluoride, ameliorated only the CER pancreatitis (weight gain from 28 +/- 10 gm to 17 +/- 10 gm, p < 0.05; amylase activity from 38,116 +/- 6491 units/dl to 23,372 +/- 11,654 units/dl, p < 0.05), and not the FFA, POSS, or ISCH 2 pancreatitis. We conclude that in the three models of pancreatitis (FFA, POSS, and ISCH 2) that are mediated by toxic oxygen metabolites, XD is converted to XO reversibly by way of sulfhydryl group oxidation rather than irreversibly by way of proteolysis. In the CER pancreatitis, where XO does not play a role in the pathogenesis, proteolytic enzymes may be important mediators in the injury.
 ...
PMID:The mechanism of conversion of xanthine dehydrogenase to xanthine oxidase in acute pancreatitis in the canine isolated pancreas preparation. 841 95


1 2 3 4 5 Next >>