Malabsorption diarrhea

Essentiality to Humans Copper deficiency in man is a rare exception, and would not occur if > 2 mg of copper is present in the daily diet. However, secondary copper deficiency can be caused by severe malabsorption, diarrhea accompanied by a copper-deficient diet in infants, or in the genetic disorder of copper transport and utilization that characterized Menkes disease. Except for Menkes disease (for which there is no effective treatment and which is invariably fatal), copper deficiency in man is simply treated by adding 5 mg copper (most conveniently as acetate) to the daily diet. In practical terms it is almost never necessary to supplement any but the most abnormal diets with copper to avoid its deficiency in man (Scheinberg... 

Lactose Milk. May occur in urine during pregnancy. In lactase deficiency, malabsorption leads to diarrhea and flatulence. 

In addition to these two applications, intravenous nutrition and fluid therapy has been given for many years to newborns with chronic diarrhea, malabsorption for various reasons, and other problems associated with disease. 

Noninfectious causes of acute diarrhea include drugs and toxins (Table 18-3), laxative abuse, food intolerance, irritable bowel syndrome (IBS), inflammatory bowel disease, ischemic bowel disease, lactase deficiency, Whipple s disease, pernicious anemia, diabetes mellitus, malabsorption, fecal impaction, diverticulosis, and celiac sprue. 

Chronic diarrhea lasts for longer than 4 weeks. Most cases result from functional or inflammatory bowel disorders, endocrine disorders, malabsorption syndromes and drugs (including laxative abuse). In chronic diarrhea, daily watery stools may not occur. Diarrhea may be either intermittent or persistent. 

Although diarrhea can often be attributed to a specific mechanism, some patients develop diarrhea due to overlapping mechanisms. For example, malabsorption syndromes and traveler s diarrhea are associated with both secretory and osmotic diarrhea. 

Stool may also be analyzed for mucus, fat, osmolality, fecal leukocytes, and pH. The presence of mucus suggests colonic involvement. Fat in the stool may be due to a malabsorption disorder. Fecal leukocytes can be found in inflammatory diarrheas including infections caused by invasive bacteria (e.g., E. coli, Shigella, and Campylobacter species). Stool pH (normally greater than 6) is decreased by bacterial fermentation processes. 

Rati tails often present with chronic fat-containing diarrhea due to dietary lipid malabsorption. 

Trace elements are essential cofactors for numerous biochemical processes. Trace elements that are added routinely to PN include zinc, selenium, copper, manganese, and chromium. There are various commercial parenteral trace element formulations that can be added to PN admixtures (e.g., MTE-5 ). Zinc is important for wound healing, and patients with high-output fistulas, diarrhea, burns, and large open wounds may require additional zinc supplementation. Patients may lose as much as 12 to 17 mg zinc per liter of gastrointestinal (GI) output (e.g., from diarrhea or enterocutaneous fistula losses) however, others have demonstrated that 12 mg/day may be adequate to maintain these patients in positive zinc balance.18 Patients with chronic diarrhea, malabsorption, and short-gut syndrome may have increased selenium losses and may require additional selenium supplementation. Patients with severe cholestasis should have copper and manganese... 

Severe hemodynamic instability Enterocutaneous fistulae Severe diarrhea Severe malabsorption Severe gastrointestinal hemorrhage Intractable vomiting... 

Diarrhea Drug related Antibiotic-induced bacterial overgrowth Hyperosmolar medications administered via feeding tubes Antacids containing magnesium Malabsorption Hypoalbuminemia/gut mucosal atrophy Pancreatic insufficiency Inadequate GIT surface area Rapid GIT transit Radiation enteritis Tube feeding related Rapid formula administration Formula hyperosmolalty Low residue (fiber) content Lactose intolerance Bacterial contamination... 

Small, D. M. Point mutations in the ileal bile salt transporter cause leaks in the enterohepatic circulation leading to severe chronic diarrhea and malabsorption. J. Clin. Invest. 1997,... 

EPEC causes a degeneration of the microvillus brush border, with cupping and pedestal formation of the plasma membrane at the sites of bacterial attachment and reorganization of cytoskeletal proteins [43, 44], Invasion has been observed in some clinical specimens, but the mechanism of how this bacteria produces diarrhea is not fully understood. Some possibilities include an increase in permeability and loss in microvilli leading to malabsorption. 

Lactoferrin, a protein found in secondary granules of polymorphonuclear cells, was observed to be mildly to moderately elevated in the stools of children with endemic cryptosporidiosis [91] and healthy adult volunteers with experimental infection [92], Indeed, in another study of malnourished children in Haiti, cryptosporidiosis was noted to stimulate an inflammatory response, as evidenced by elevated IL-8, TNF-a, lactoferrin, IL-13 and IL-10 [93]. Further studies are needed to elucidate the role of inflammatory mediators in the development of prolonged diarrhea, malabsorption and malnutrition in immunocompromised hosts and children in endemic areas. 

Chronic diarrhea is likely to result in a disturbance of water and salt balance. This has been shown to be so in the malabsorption syndrome (C9, F5). These changes, especially potassium deficiency, may cause some aggravation of the intestinal situation and increase of abdominal distension. Some improvement in absorption may consequently occur on appropriate rehabilitation. However, a residual defect of absorption will remain until more specific therapy is instituted. 

Nausea, vomiting, diarrhea (most common) malabsorption syndrome characterized by increased fecal fat, decreased serum carotene, and fall in xylose absorption. Clostridium difficile-assoaated colitis (following neomycin therapy) nephrotoxicity and ototoxicity (following prolonged and high-dosage therapy in hepatic coma). 

A major symptom of fat malabsorption is steatorrhea, production of bulky, foul-smelling feces that float due to high fat content, which may be accompanied by diarrhea and abdominal pain, and if sustained for a period of days or weeks, lead to deficiencies of the fat-soluble vitamins. 

The answer is B. This patient s greasy, foul-smelling stools indicate steatorrhea. Her vision problems may be a manifestation of vitamin A deficiency due to fat malabsorption. The most likely explanation is biliary insufficiency, ie, decreased bile salt production leading to poor emulsification of dietary fats. Active ileal disease is a possibility, but the WBC count would likely be elevated unless her condition was in remission. Infection with Giardia is less likely due to the absence of pathogenic organisms in her stool. Lactose intolerance can produce diarrhea but not steatorrhea. 

Patients having a delayed response to treatment should have treatment prolonged to 9 months (or 4-6 months after culture conversion is documented). Malabsorption of the antituberculosis should be considered as a possible cause of treatment failure or the acquisition of drug resistance, particularly if gastrointestinal symptoms or chronic diarrhea is present. 

Diarrhea is the frequent passage of watery, unformed stools. Its many causes include IBS, infectious disorders, thyrotoxicosis, malabsorption, medication side effect, and laxative abuse. Attempts to treat diarrhea should first focus on the patient s list of medications followed by a search for an underlying systemic disorder. Opioids and 5-HT3 receptor antagonists, such as alosetron, slow motility and can therefore decrease or eliminate diarrhea. 

Prolonged use or overdose may result in electrolyte or metabolic disturbances (such as hypokalemia, hypocalcemia, and metabolic acidosis or alkalosis), as well as persistent diarrhea, vomiting, muscle weakness, malabsorption, and weight loss. 

Many i rsons from non-Eastern European-derived cultures are unable to tolerate large quantities of the milk sugar lactose because of the absence of enough of the active digestive enzyme, lactase. In these persons, consumption of lactose results in effects similar to those described for oligosaccharide consumption. Severe intolerance can result in malabsorption of all nutrients from the diet due to diarrhea. 

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

Acarbose and miglitol have been reviewed (17,32,33). Their major adverse effects are flatulence, abdominal discomfort, diarrhea, and bloating, particularly at the start of therapy, which sometimes prevent further use. They should not be given to patients with intestinal obstruction, malabsorption, inflammatory bowel disease, or hepatic impairment. 

Abdominal pain and diarrhea with malabsorption have been described in patients taking acarbose, which can also cause carbohydrate malabsorption (39). 

Zinc deficiency is clinically characterized by the development of a moist eczematous dermatitis most apparent in the nasolabial folds and around orifices. Other presenting signs and symptoms may include hypogeusia (blunted sense of taste), alopecia, diarrhea, rash (which may vary from papular, scaly lesions to weeping, open erosions), apathy, and depression. Clinical zinc deficiency occurs most frequently in the setting of abnormal losses, such as in Crohn s disease, malabsorption states, and fistula losses, or from prolonged inadequate intake, such as with zinc-free parenteral nutrition. 

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