Malabsorption

Many antibiotics are unsuitable for therapeutic use, frequently because of their general toxicity or as a result of other drawbacks such as instability, inadequate solubility or malabsorption. 

Malabsorption syndrome Steatorrhea Tropical sprue Idiopathic hypercalcemia... 

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. 

The energy substrates are contraindicated in patients with hypersensitivity to any component of the solution. Dextrose solutions are contraindicated in patients with diabetic coma with excessively high blood sugar. Concentrated dextrose solutions are contraindicated in patients with increased intracranial pressure, delirium tremens (if patient is dehydrated), hepatic coma, or glucose-galactose malabsorption syndrome Alcohol dextrose solutions are contraindicated in patients with epilepsy, urinary tract infections, alcoholism, and diabetic coma... 

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

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. 

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. 

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. 

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. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Several factors contribute to development of bone disease in CF (1) malabsorption of vitamins D and K and calcium (2) poor... 

Anemia may be present in some patients due to impaired erythropoietin regulation, nutritional factors (vitamin E and iron malabsorption), or chronic inflammation. With chronic pulmonary disease, increased cytokine production can lead to shortened red blood cell survival, reduced erythropoietin response, and impaired mobilization of iron stores. 

Additionally, with chronic hypoxia, normal hemoglobin and hematocrit values may represent relative anemia.12 Increased red blood cell production is a physiologic response to hypoxia however, this response may be blunted in CF and may result in symptoms of anemia despite normal lab values. Abnormal bleeding may also be observed as a result of vitamin K malabsorption or antibiotic-associated depletion of gastrointestinal flora and vitamin K synthesis. 

Fat-soluble vitamin supplementation is usually required in pancreatic insufficiency. Specially-formulated products for CF patients (ADEKs and Vitamax ) are usually sufficient to attain normal serum vitamin levels at a dose of 1 tablet daily for younger children and 2 tablets daily for teenagers and adults. Additional supplementation may be needed in uncontrolled malabsorption or for replacement of severe vitamin deficiency.5,15 Appetite stimulants such as cyproheptadine may be an option for promoting nutrition and weight gain, but efficacy has not been established. 

Formation of strictures, abscesses, fistulae, and obstructions in patients with CD is possible. Patients with CD may develop significant weight loss or nutritional deficiencies secondary to malabsorption of nutrients in the small intestine, or as a consequence of multiple small- or large-bowel resections. Common nutritional deficiencies encountered in IBD include vitamin B12, fat-soluble vitamins, zinc, folate, and iron. Malabsorption in children with CD may contribute to significant reductions in growth and development. 

Patients with IBD, particularly those with CD, are also at risk for bone loss. This may be a function of malabsorption or an effect of repeated courses of corticosteroids. Patients with IBD should receive a baseline bone density measurement prior to receiving corticosteroids. Vitamin D and calcium supplementation should be used in all patients receiving long-term corticosteroids. Oral bisphosphonate therapy may also be considered in patients receiving prolonged courses of corticosteroids or in those with osteopenia or osteoporosis. 

Surgical intervention is a potential treatment option in patients with complications such as fistulae or abscesses, or in patients with medically refractory disease. Ulcerative colitis is curable with performance of a total colectomy. Patients with UC may opt to have a colectomy to reduce the chance of developing colorectal cancer. Patients with CD may have affected areas of intestine resected. Unfortunately, CD may recur following surgical resection. Repeated surgeries may lead to significant malabsorption of nutrients and drugs consistent with development of short-bowel syndrome. 

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. 

Long -term sequelae of chronic pancreatitis include dietary malabsorption, impaired glucose tolerance, cholangitis, and potential addiction to opioid analgesics. 

As patients lose exocrine function of the pancreas, they have decreased ability to absorb lipids and protein ingested with normal dietary intake. Weight loss from nutritional malabsorption is a common symptom of chronic pancreatitis not often seen in acute pancreatitis. Fatty- or protein-containing stools are also common carbohydrate absorption is usually unaffected. Even though patients with chronic pancreatitis have decreased ability to absorb lipid from the gastrointestinal tract, there does not appear to be an increased incidence of fat-soluble vitamin deficiency in these patients.34... 

Weight loss can result from chronic fat and protein malabsorption. 

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

The goals of pharmacotherapy for chronic pancreatitis are (1) prevention and resolution of chronic abdominal pain and (2) correction of dietary malabsorption with exogenous pancreatic enzymes. 

When dietary malabsorption exists, monitor patients for weight gain or loss, activity level, and ability to perform activities of daily living. 

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