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Intestinal dysfunctions

Kubes, P., Hunter, J. and Granger, D.N. (1992). Ischaemia/reperfiision-induced feline intestinal dysfunction importance of granulocyte recruitment. Gastroenterology 103, 807-812. [Pg.166]

Intestinal dysfunction (manifested as increased transit time) and radiologic changes primarily due to chronic infection may take months to resolve. [Pg.1141]

Kirichenko AV, Mason K, Straume M, Teates CD, Rich TA. Nuclear scintigraphic assessment of intestinal dysfunction after combined treatment with 9-amino-20(S)-camptothecin (9-AC) and irradiation. Int JRadiat Oncol Biol Phys 2000 47(4) 1043-1049. [Pg.103]

Since hepatobiliary and intestinal dysfunctions are marked by variation in the concentration and relative proportions of major BAs and by increased levels of their minor forms, individual identification and accurate quantification of these compounds in biological samples are very important prognostic, diagnostic, and therapeutic monitoring indicators of liver and gastrointestinal tract diseases in humans. [Pg.611]

DOT CLASSIFICATION 9 Label None SAFETY PROFILE Deadly poison by ingestion in humans. The seeds contain the deadly poison ricin, a plant lectin (toxalbumin) which inhibits protein synthesis in the intestinal wall. Ingestion of the seeds can cause after a delay period of several hours nausea, vomiting, diarrhea, and intestinal dysfunction. There may be massive fluid and electrolyte loss. Ingestion of as few as 2 seeds could be fatal. A potent allergen. When heated to decomposition it emits toxic fumes of NOx. See also RICIN. [Pg.296]

Fig. 5.13. a A premature infant with intestinal dysfunction, so-called meconium ileus-like syndrome. The supine abdominal film shows dilated intestinal loops because of fecal impaction in ileum, b Cross-table radiograph. Meconium-like ileus with dilated intestinal loops without fluid levels. The whole colonic tract and rectum are airless, c Ultrasound of the right lower quadrant of abdomen demonstrates the impacted and inspissated stool in the ileum... [Pg.176]

The remaining 59 patients, with relatively low serum bile acid concentrations (SGLC = 2.2 0.3,GC = 2.2 0.3, 3a-hydroxy bile acids = 10.3 0.9), included patients with mild liver disease, intestinal dysfunctions such as Crohn s disease, coeliac disease and gastroenteritis, acute lymphatic leukemia treated with methotrexate, contaminated small bowel syndrome and three patients with benign recurrent intrahepatic cholestasis (BRIC). [Pg.226]

Barbara, G., Vallance, B.A. and Collins, S.M. (1997) Persistent intestinal neuromuscular dysfunction after acute nematode infection in mice. Gastroenterology 113,1224-1232. [Pg.396]

OBD comprises a constellation of GI symptoms including OIC, incomplete evacuation, inhibition of gut peristalsis, bloating, pain, nausea/ vomiting, and increased gastric reflux and tone of intestinal sphincters [3]. Approximately 40% of patients taking chronic opioids for nonmalig-nant pain develop bowel dysfunction [25]. [Pg.146]

When the mechanisms restricting bacterial colonization in the upper gut fail, due to disease or dysfunction, bacterial overgrowth develops. The segmental distribution may be gastric, intestinal or both depending on the type of failure. The consequences for the host vary from none to life-threatening complications, caused by severe water and electrolyte deficiencies and septic manifestations. [Pg.2]

Extrinsic Neuropathies. Autonomic dysfunction [141], pandysautonomia [142,143], Shy-Drager syndrome [144] and sympathetic dysfunction are conditions associated with intestinal dysmotility. [Pg.14]

Dean, P., and Kenny, B. (2004). Intestinal barrier dysfunction by enteropathogenic Escherichia coli is mediated by two effector molecules and a bacterial surface protein. Mol. Microbiol. 54, 665-675. [Pg.144]

Renal use Use methotrexate in patients with impaired renal function with extreme caution, and at reduced dosages, because renal dysfunction will prolong elimination. Gl Diarrhea and ulcerative stomatitis require interruption of therapy hemorrhagic enteritis and death from intestinal perforation may occur. [Pg.1969]

Constipation may be caused by slow intestinal transition, pelvic floor dysfunction, bowel dysfunction like irritable Bowel syndrome and tumours, but can also be secondary to other diseases and life conditions. Many medicines cause constipation, for example opiates, calcium channel blockers and drugs with anticholinergic effects, e.g. antidepressants. [Pg.500]

In general, ethanol in low to moderate amounts, is relatively benign to most body systems. A moderate amount of ethanol causes peripheral vasodilation, especially of cutaneous vessels, and stimulates the secretion of salivary and gastric fluids the latter action may aid digestion. On the other hand, ethanol consumption in high concentrations, as found in undiluted spirits, can induce hemorrhagic lesions in the duodenum, inhibit intestinal brush border enzymes, inhibit the uptake of amino acids, and limit the absorption of vitamins and minerals. In addition, ethanol can reduce blood testosterone levels, resulting in sexual dysfunction. [Pg.414]

Nitrofurantoin is administered orally and is rapidly and almost completely absorbed from the small intestine only low levels of activity are achieved in serum because the drug is rapidly metabolized. Relatively high protein binding (about 70%) also affects serum levels, reducing potential for systemic toxicity and alteration of intestinal flora. Relative tissue penetration is much lower than other antimicrobials for UTIs, and therefore, nitrofurantoin is not indicated in the therapy of infections such as pyelonephritis and renal cortical or perinephric abscesses. Nitrofurantoin is rapidly excreted by glomerular filtration and tubular secretion to yield effective urinary levels. In moderate to severe renal dysfunction, toxic blood levels may occur while urinary levels may be inadequate. The drug is inactivated in the liver. [Pg.521]

Contraindications Chronic intestinal diseases associated with marked disorders of digestion or absorption, cirrhosis, colonic ulceration, conditions that may deteriorate as a result of increased gas formation in the intestine, diabetic ketoacidosis, hypersensitivity to acarbose, inflammatory bowel disease, partial intestinal obstruction or predisposition to intestinal obstruction, significant renal dysfunction (serum creatinine level greater than 2 mg/dl)... [Pg.5]

Contraindications Hypersensitivitytocarbonicanhydraseinhibitors, local anesthetics, salicylates, sulfonamides, sulfonylureas, sunscreens containing PABA, or thiazide or loop diuretics intestinal or urinary tract obstruction porphyria severe hepatic or renal dysfunction... [Pg.1159]

Ezetimibe Blocks sterol transporter NPC1L1 in intestine brush border Inhibits reabsorption of cholesterol excreted in bile decreases LDL and phytosterols Elevated LDL, phytosterolemia Oral duration 24 h Toxicity Low incidence of hepatic dysfunction, myositis... [Pg.793]

Oral bioavailability of adefovir dipivoxil is about 59% and is unaffected by meals it is rapidly and completely hydrolyzed to the parent compound by intestinal and blood esterases. Protein binding is low (< 5%). The intracellular half-life of the diphosphate is prolonged, ranging from 5 to 18 hours in various cells this makes once-daily dosing feasible. Adefovir is excreted by a combination of glomerular filtration and active tubular secretion and reguires dose adjustment for renal dysfunction however, it may be administered to patients with decompensated liver disease. [Pg.1085]

While affected neonates are often small for gestational age [37], postnatal growth failure may occur at any age, after apparently normal development. Severe anorexia, recurrent vomiting, chronic diarrhea with villous atrophy, and/or exocrine pancreatic dysfunction occasionally occur [ 38]. In adulthood, chronic intestinal pseudoobstruction has been occasionally ascribed to MRC deficiency [21]. [Pg.267]

If more cholesterol enters the bile than can be solubilized by the available bile salts and phosphatidylcholine, cholesterol gallstone disease (cholelithiasis) can occur. This is generally caused by gross malabsorption of bile acids from the intestine, obstruction of the biliary tract, or severe hepatic dysfunction, leading to abnormalities in bile or bile salt production. [Pg.489]


See other pages where Intestinal dysfunctions is mentioned: [Pg.299]    [Pg.2072]    [Pg.226]    [Pg.228]    [Pg.254]    [Pg.299]    [Pg.2072]    [Pg.226]    [Pg.228]    [Pg.254]    [Pg.1149]    [Pg.1149]    [Pg.6]    [Pg.72]    [Pg.205]    [Pg.102]    [Pg.48]    [Pg.392]    [Pg.158]    [Pg.11]    [Pg.269]    [Pg.159]    [Pg.516]    [Pg.459]    [Pg.127]    [Pg.35]    [Pg.224]    [Pg.1156]    [Pg.653]    [Pg.346]    [Pg.18]   
See also in sourсe #XX -- [ Pg.226 ]




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