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Occlusion, intestinal

Crmlraindicalions Inflammation or occlusion of the bile duct intestinal occlusion. [Pg.16]

No oral MRLs were derived for metallic (elemental) mercury due to the lack of data. Oral exposure to liquid metallic mercury would be expected to present little health risk, since it is so poorly absorbed (<0.01%) through the healthy intestine. Sufficiently large quantities could, however, present a risk of intestinal blockage, and some could enter the systemic circulation (blood or lymphatic) through open lesions, presenting a risk of occlusion of smaller arteries, especially within the pulmonary circulation. [Pg.259]

Gastrointestinal effects were not seen in animals dermally exposed to 1,1,1-trichloroethane. Rats exposed to 280 mg/kg/day of 1,1,1-trichloroethane under an occlusive dressing for 3 weeks showed no evidence of pancreatic damage, as determined by histopathological examination and serum lipase and amylase levels (Viola et al. 1981). Rabbits exposed to 500 mg/kg/day without occlusion for 90 days had no gross or microscopic lesions in the stomach or intestines (Torkelson et al. 1958). [Pg.77]

Table 112-1 summarizes many of the potential causes of bacterial peritonitis. These include inflammatory processes of the GI tract or abdominal organs, bowel obstruction, vascular occlusions that may lead to gangrene of the intestines, and neoplasia that may cause intestinal perforation or obstruction. Other possible causes include those resulting from traumatic injuries or postoperative infections. [Pg.2056]

Palmer, T. N., Caride, V. J., Fernandez, L. A., and Twickler, J. (1981) Liposome accumulation in ischaemic intestine following experimental mesenteric occlusion. Biosci. Rep. 1, 337-344. [Pg.188]

Plasma levels of both nifedipine and diltiazem are increased by concurrent use and blood pressure is reduced accordingly. Verapamil is predicted to interact similarly. There are isolated reports of intestinal occlusion attributed to the concurrent use of nifedipine and diltiazem. Note that if nimodipine is used with another calcium-channel blocker, monitoring, with possible dose reduction or discontinuation of the other calcium-channel blocker is recommended. [Pg.865]

X-ray suggested paralytic ileus, which resolved but then recurred when the drugs were restarted. The excessive relaxation of the intestine was attributed to elevated nifedipine plasma levels, which were said to be caused by diltiazem.Another report describes complete or partial intestinal occlusion in a patient taking diltiazem on three occasions, each time when nifedipine was added. ... [Pg.865]

A reduction in the metabolism of both the nifedipine and diltiazem in the liver seems to be the explanation for the increase in drug levels. An increased relaxant effect on smooth muscle is suggested for the cases of intestinal occlusion. ... [Pg.865]

Bile acids have two major functions in man (a) they form a catabolic pathway of cholesterol metabolism, and (b) they play an essential role in intestinal absorption of fat, cholesterol, and fat-soluble vitamins. These functions may be so vital that a genetic mutant with absence of bile acids, if at all developed, is obviously incapable of life, and therefore this type of inborn error of metabolism is not yet known clinically. A slightly decreased bile acid production, i.e., reduced cholesterol catabolism, as a primary phenomenon can lead to hypercholesterolemia without fat malabsorption, as has been suggested to be the case in familial hypercholesterolemia. A relative defect in bile salt production may lead to gallstone formation. A more severe defect in bile acid synthesis and biliary excretion found secondarily in liver disease causes fat malabsorption. This may be associated with hypercholesterolemia according to whether the bile salt deficiency is due to decreased function of parenchymal cells, as in liver cirrhosis, or whether the biliary excretory function is predominantly disturbed, as in biliary cirrhosis or extrahepatic biliary occlusion. Finally, an augmented cholesterol production in obesity is partially balanced by increased cholesterol catabolism via bile acids, while interruption of the enterohepatic circulation by ileal dysfunction or cholestyramine leads to intestinal bile salt deficiency despite an up to twentyfold increase in bile salt synthesis, to fat malabsorption, and to a fall in serum cholesterol. [Pg.192]

Cholesterol and fat-soluble vitamins require bile acid induced micellar solubilization for absorption, which takes place in the upper small intestine (c/. 32,116-118). Accordingly, in bile salt deficiency states, cholesterol absorption should be markedly impaired and fecal neutral sterol excretion increased. The fact that fecal neutral steroid excretion on a low-cholesterol diet is actually normal, as after ileal resection, ileal bypass, and cholestyramine treatment, or even decreased, as in cirrhosis of the liver or biliary occlusion (11), is due to a markedly reduced biliary secretion of cholesterol. In gluten enteropathy, in which no excessive bile salt loss usually exists, fecal neutral sterol excretion is markedly augmented (119). However, in occasional cases in which fecal bile salt elimination is markedly enhanced, the fecal neutral steroid excretion is quite normal, probably owing to decreased biliary cholesterol secretion as a consequence of low biliary bile salt secretion. Detailed information on the role of bile salts in both intraluminal and mucosal phases of fat and sterol absorption is presented in many recent reviews (6,10,113,114,117). [Pg.206]

Antral contractions (3 per min) are responsible for mixing and grinding of a solid meal into smaller particles (<5 mm) that can pass onto the duodenum. These antral contractions can easily be seen at ultrasonography. The contractions can be occlusive or non lumen-occlusive. An antral contraction is defined as an indentation of the gastric wall greater than one antral wall thickness, which is not due to respiration, pulsation transmitted from the aorta or heart, or to movements of adjacent intestine. [Pg.192]

Gay G, Delvaux M, Laurent V et al (2005) Temporary intestinal occlusion induced by a patency capsule in a patient with Crohn s disease. Endoscopy 37 174-177 Gonvers J, Burnand B (1996) Appropriateness and diagnostic yield of upper gastrointestinal endoscopy in an open-access endoscopy unit. Endoscopy 28 661-666 Gore RM, Balthazar EJ, Ghahremani GG et al (1996) CT features of ulcerative colitis and Crohn s disease. AJR Am J Roentgenol 169 3-15... [Pg.237]

Intestinal occlusion has been observed in the fetus causing meconium plugs before birth, at birth, or sometimes in older infants, but the typical injury occurs at birth. A plug of thick greyish mucus with the consistency of putty blocks the terminal ileus. The part of the intestine proximal to the block is distended and may contain fecal material. [Pg.321]

If the child has been fed, the part of the intestine distal to the plug is atrophic. Often the ileal occlusion is associated with volvulus. [Pg.321]

Intestinal transplantation represents an alternative in patients with irreversible, chronic intestinal failure in order to restore enteral absorption of ingested food and fluid. In adults the most common cause of chronic intestinal failure results from extensive resection of the small bowel due to occlusion of the superior mesenteric vessels, inflammatory bowel disease, or abdominal trauma. In children the causes of short-... [Pg.226]

The most serious vascular complication is arterial and venous graft thrombosis and can result in intestinal graft necrosis necessitating graft enterectomy. Typically, contrast-enhanced CT displays either an intraluminal filling defect or complete occlusion of the involved artery with non-enhancement of the intestinal wall indicating graft necrosis (Fig. 7.44d). Sometimes an intraluminal membrane can be ob-... [Pg.239]

Fig.7.47a,b. 67-year-old man after multivisceral transplantation necessitated by liver cirrhosis with intrahepatic hepatocellular carcinoma and chronic thrombotic occlusion of portomesenteric venous system with clinical evidence of infection. a Contrast-enhanced helical CT obtained 2 weeks after operation shows enlargement of pancreatic head with reduced contrast enhancement (white arrow) consistent with edematous pancreatitis. Annotation ascites (black asterisk), gastric tube (white arrowhead), periportal lymphedema (black arrow), stomach (white asterisk), b Contrast-enhanced helical CT obtained 4 weeks after operation displays unspecific enlargement of mesenteric lymph nodes (arrow) of intestinal graft. Annotations ascites (asterisk), calcification of iliac artery (arrowhead)... [Pg.242]


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See also in sourсe #XX -- [ Pg.66 ]




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