Intestines malabsorption

Clinical stresses which interfere with vitamin metabohsm, can result in calcium deficiency leading to osteomalacia and osteoporosis (secondary vitamin D deficiency). These stresses include intestinal malabsorption (lack of bile salts) stomach bypass surgery obstmctive jaundice alcoholism Hver or kidney failure decreasing hydroxylation of vitamin to active forms inborn error of metabohsm and use of anticonverdiants that may lead to increased requirement. 

Hypolipoproteinemias Abetaiipoproteinemia No chylomicrons, VLDL, or LDL are formed because of defect in the loading of apo B with lipid. Rare blood acylglycerols low intestine and liver accumulate acylglycerols. Intestinal malabsorption. Early death avoidable by administration of large doses of fat-soluble vitamins, particularly vitamin E. 

A number of genetic diseases that result in defects of tryptophan metabolism are associated with the development of pellagra despite an apparently adequate intake of both tryptophan and niacin. Hartnup disease is a rare genetic condition in which there is a defect of the membrane transport mechanism for tryptophan, resulting in large losses due to intestinal malabsorption and failure of the renal resorption mechanism. In carcinoid syndrome there is metastasis of a primary liver tumor of enterochromaffin cells which synthesize 5-hydroxy-tryptamine. Overproduction of 5-hydroxytryptamine may account for as much as 60% of the body s tryptophan metabolism, causing pellagra because of the diversion away from NAD synthesis. 

Hypocalcemia - To correct plasma calcium levels (eg, neonatal tetany and tetany due to parathyroid deficiency, vitamin D deficiency, alkalosis) prevention of hypocalcemia during exchange transfusions conditions associated with intestinal malabsorption. 

Give orally, except in severe intestinal malabsorption. Although most patients with malabsorption cannot absorb food folates, they are able to absorb folic acid given orally. 

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

Dietary deticiencies of folic acid are most frequently associated wilh anemias imacroeylic, megaloblastic, and pernicious), glossitis, diarrhea, gastrointestinal lesions, intestinal malabsorption, and sprue. 

Factors which tend to decrease the availability of this vitamin include (1) cooking losses, since the vitamin is heat labile (2) cobalt deficiency in ruminants (3) intestinal malabsorption or parasites (4) lack of intrinsic factor (5) intestinal disease (6) aging (7) vegetarian diet (8) excretion... 

Q3 What are the likely signs and symptoms of intestinal malabsorption ... 

Gastrointestinal Incontinence of feces, intestinal malabsorption, fat-soluble vitamins, rectal discharge, rectal bleeding... 

Abetalipoproteinemia is a rare lEM involving lipid dysfunction. Also called Bassen-Komzweig syndrome, it is characterized by extremely low cholesterol due to deficient or absent beta lipoproteins, which are an important component of the cholesterol molecular complex. Symptoms include growth retardation, neurological dysfunction, retinal pigment degeneration, and upper intestinal malabsorption. 

H5 oprothrombinaemia due to intestinal malabsorption syndromes. Menadiol sodium phosphate should be used as it is water-soluble. 

Second the test is repeated with intrinsic factor added to the oral dose. The radioactive vitamin B is now absorbed in pernicious anaemia (but not in intestinal malabsorption) and is detected in plasma and urine. Both stages of the test are needed to maximise reliability of diagnosis of pernicious anaemia. 

Adverse effects include flatulence and liquid, oily stools, leading to faecal urgency, abdominal and rectal pain. Symptoms may be reduced by adhering to a reduced-fat diet. Low plasma concentrations of the fat-soluble vitamins A, D and E have been foimd. OrUstat is contraindicated where there is chronic intestinal malabsorption or cholestasis. 

Zinc deficiency is relatively uncommon in the United States, but may occur in adults with alcoholism or intestinal malabsorption problems. Low plasma zinc has been found in patients with alcoholic cirrhosis, Crohn s disease, and coeliac disease, Zinc deficiency, as well as deficiencies in a variety of other trace minerals, has occurred in hurnans fed for prolonged periods w lth intravenous diets from which the mineral had been inadvertently omitted. Controlled studies with humans have shown that the signs of zinc deficiency present after 2 to 5 weeks of consumption of a zinc-free diet- The signs include a facial rash, diarrhea, and alopecia. The rash occurs on the face, groins, hands, and feet. The symptoms can be reversed by administering zinc. 

Presurgical bowel preparation with oral kanamycin is seldom practiced and can be followed by an intestinal malabsorption syndrome (3). Only negligible amounts of kanamycin are absorbed through an intact intestinal mucosa, but increased systemic availability and potential toxicity can result from the presence of ulcerated or denuded areas. 

Thiamine is a nutritional supplement used during periods of deficiency known as beriberi and its manifestations such as Wernicke-Korsakoff syndrome. Thiamine needs increase during diseases of the small intestine, malabsorption, congenital metabolic dysfunction, liver disease, alcoholism, and during pregnancy and lactation. Supplementation of thiamine for treatment of Alzheimer s disease, congestive heart failure, and cataracts has been investigated however, evidence is unclear as to its benefits at this time. 

Deficiency conditions Pernicious anemia, deficiency caused by inadequate diet or intestinal malabsorption, hemolytic anemia, hyperthyroidism, bowel and pancreatic malignancies, gastrectomy, GI lesions, neurologic damage, malabsorption syndrome, metabolic disorders, renal disease... 

Intestinal malabsorption of vitamin B12 may be caused by gastrectomy or ileal resection, with an inverse relationship between the length of ileum resected and the absorption of vitamin B12. Other causes of malabsorption are tropical sprue, inflammatory disease of the small intestine, intestinal stasis with overgrowth of colonic bacteria, which consume the vitamin 6,2 ingested by the host, and HIV infection. Another cause of vitamin B malabsorption is failure to extract cobalamin from food. Some patients fail to absorb cobalamin bound to food, whereas absorption of nonfood-bound cobalamin in the Schilling test is unimpaired. This is particularly a problem in patients with compromised gastric status or early in the course of development of pernicious anemia. 

The Schilling test is primarily a test of vitamin B12 absorption and not of status, but it permits differentiation of causes of vitamin B12 deficiency (pernicious anemia or intestinal malabsorption). The proportion absorbed from orally administered Co- or Co-labeled vitamin 6,2 is measured by determining the radioactivity in feces, urine, or serum or by externally scanning the liver. The usual procedure is to measure radioactivity in a 24-hour urine sample, which is collected after oral administration of 0.5 Xg of radioactive Co-labeled vitamin B12 after an overnight fast. In normal individuals, 8% or more of the dose administered is excreted in the urine, whereas in people with pernicious anemia, less than 7% (often 0% to 3%) is excreted. A confirmatory test for lack of IF requires mgestion of vitamin B,2 and IF. ... 

Combinations of poor dietary supply, intestinal malabsorption because of the antagonistic effects of other trace elements, or blockage of uptake by substances Uke phytate — together with increased excretory losses as a result of disease, injury, and infection—can result in overt, symptomatic trace element deficiency disease. Liver disease, inflammatory bowel disease, and renal disease will affect trace element absorption and excretion to a variable extent and may cause an acquired deficiency disease. 

Carroccio A, Verghi F, Santini B, Lucidi V, lacono G, Cavataio F, et al. Diagnostic accuracy of fecal elastase 1 assay in patients with pancreatic maldigestion or intestinal malabsorption. Dig Dis Sci 2001 46 1335-42. 

Lo CW, Paris PW, Clemens TL, Nolan J, Holick ME Vitamin D absorption in healthy subjects and in patients with intestinal malabsorption syndromes. 

The answer is c. (Murray, pp 627-661. Scriver, pp 3897—3964. Sack, pp 121-138. Wilson, pp 287-320.) Hemorrhagic disease of the newborn is caused by poor transfer of maternal vitamin K through the placenta and by lack of intestinal bacteria in the infant for synthesis of vitamin K. The intestine is sterile at birth and becomes colonized over the first few weeks. Because of these factors, vitamin K is routinely administered to newborns. Deficiencies of the fat-soluble vitamins A, E, D, and K can occur with intestinal malabsorption, but avid fetal uptake during pregnancy usually prevents infantile symptoms. Hypervltaminosis A can cause liver toxicity but not bleeding, and deficiencies of E (neonatal anemia) or C (extremely rare in neonates) have other symptoms besides bleeding. 

Treatment of osteomalacia from vitamin D deficiency is vitamin D therapy, with dose depending on severity. Supplements of 800 to 4000 units/day or 50,000 units weekly for 8 weeks may be necessary. For sprue, a gluten-free diet is necessary. With intestinal malabsorption, high oral doses (50,000 to 100,000 units/day) or daily intramuscular injections of 10,000 units of vitamin D may be initially required. With disordered vitamin D metabohsm caused by anticonvulsants or rifampin, supplemental vitamin D (4000 units/day) can be effective. Sun exposure can also be useful. Serum calcium and 25(OH) vitamin D monitoring is necessary with high vitamin D doses. 

Diarrhea and steatorrhea are common in patients with hepatic cholestasis because of intestinal malabsorption (due in part to mucosal edema from hypoalbuminemia), inadequate bile acid delivery to the duodenum, and pancreatic dysfunction with decreased secretion of hpase. Micelle formation is impeded, and thus the long-chain fatty acids pass through the colon, resulting in a foul-smelling, soapy diarrhea. 

Intestinal malabsorption due to parasites (fish tapeworm, a.k.a. Dinhvllabothrium latum), bacteria (blind-loop syndrome), or Crohn s disease of ileum... 

The most important adverse effects resulting from the oral administration of neomycin are intestinal malabsorption and superinfection. Individuals treated with 4 to 6 g/day of the drug by mouth sometimes develop a spruelike syndrome with diarrhea, steatorrhea, and azotorrhea. Overgrowth of yeasts in the intestine also may occur this is not associated with diarrhea or other symptoms in most cases. 

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