Administrative deficiencies

One component of the age-ielated decline in immune function is decreased production of the lymphokine that promotes the growth of T-ceUs, interleukin 2 (IL-2). Administration of recombinant-derived IL-2, both in vitro and in vivo, appears to restore certain immune functions in aged mice. Recovery of T-regulatory effects on B-ceU differentiation has been reported in human cells from elderly patients treated with IL-1 and/or IL-2 (42). Similar effects have been observed in the presence of the pentapeptide thymopentin [69558-55-0] (Arg Lys Asp Val Tyr), a weU-known IL-2 inducer. Recombinant IL-2 adrninistered to aged mice for three weeks has been shown to correct the T-ceU functional deficiency associated with antigen-specific immunoglobulin production by certain lymphoid tissue (43). 

Iodized Salt. Iodized table salt has been used to provide supplemental iodine to the U.S. population since 1924, when producers, in cooperation with the Michigan State Medical Society (24), began a voluntary program of salt iodization in Michigan that ultimately led to the elimination of iodine deficiency in the United States. More than 50% of the table salt sold in the United States is iodized. Potassium iodide in table salt at levels of 0.006% to 0.01% KI is one of two sources of iodine for food-grade salt approved by the U.S. Food and Dmg Administration. The other, cuprous iodide, is not used by U.S. salt producers. Iodine may be added to a food so that the daily intake does not exceed 225 p.g for adults and children over four years of age. Potassium iodide is unstable under conditions of extreme moisture and temperature, particularly in an acid environment. Sodium carbonate or sodium bicarbonate is added to increase alkalinity, and sodium thiosulfate or dextrose is added to stabilize potassium iodide. Without a stabilizer, potassium iodide is oxidized to iodine and lost by volatilization from the product. Potassium iodate, far more stable than potassium iodide, is widely used in other parts of the world, but is not approved for use in the United States. 

Although both estrone and estradiol are available for replacement therapy, they suffer the disadvantage of poor activity on oral administration and short duration of action even when administered parenterally, because of ready metabolic disposition. In order to overcome these deficiencies, there was developed a series of esters of estradiol with long-chain fatty acids. These esters are oil-soluble and correspondingly water-insoluble compounds. 

Wernicke s syndrome is a serious consequence of alcoholism and thiamine (vitamin Bx) deficiency. Certain characteristic signs of this disease, notably ophtalmoplegia, nystagmus, and ataxia, respond rapidly to the administration of thiamine but to no other-vitamin. Wernicke s syndrome may be accompanied by an acute global confusional state that may also respond to thiamine. Left untreated, Wernicke s syndrome frequently leads to a chronic disorder in which learning and memory are strongly impaired. This so-called Korsakoff s psychosis is characterized by confabulation, and is less likely to be reversible once established. 

Deficient knowledge is die absence or deficiency of cognitive information to a specific subject. In the case of self-administration of dm die patient lacks sufficient knowledge to administer the drug regimen correctiy. It may also relate to a lack of interest in learning, cognitive limitation, or the inability to remember. 

Risk for Deficient Fluid Volume related to administration of a diuretic as an antihypertensive drug (when appropriate)... 

A common problem associated with the administration of the bile acid sequestrants is constipation. Constipation may be severe and may occasionally result in fecal impaction. Hemorrhoids may be aggravated. Additional adverse reactions include vitamin A and D deficiencies, bleeding tendencies (including gastrointestinal bleeding) caused by a depletion of vitamin K, nausea, abdominal pain, and distention. 

Iron dextran is a parenteral iron that is also used for die treatment of iron deficiency anemia It is primarily used when the patient cannot take oral drugs or when the patient experiences gastrointestinal intolerance to oral iron administration. Other iron preparations, both oral and parenteral, used in the treatment of iron deficiency anemia can be found in the Summary Drug Table Dragp Used in the Treatment of Anemia... 

M ale and female hormones play a vital role because they aid in development and maintenance of secondary sex characteristics and are necessary for human reproduction. Although hormones are naturally produced by die body, administration of a male or female hormone may be indicated in the treatment of certain disorders, such as inoperable breast cancer, male hypogonadism, and male or female hormone deficiency. Hormones also are used as contraceptives and for treating the symptoms of menopause... 

In some patients who are calcium deficient, the uterus may not respond to ergonovine. The nurse immediately reports a ladk of response to ergonovine. Administration of calcium by tV injection usually restores response to the drug. 

The immune globulins are contraindicated in patients with a history of allergic reactions after administration of human immunoglobulin preparations and individuals with isolated immunoglobulin A (IgA) deficiency (individuals could have an anaphylactic reaction to subsequent administration of blood products that contain IgA). 

The effects of protein deficiency on endosulfan toxicity were studied in Wistar rats (Boyd and Dobos 1969 Boyd et al. 1970). Rats fed a diet totally deficient in protein for 28 days prior to administration of a single oral dose of endosulfan had an LDjq of 5.1 mg/kg of endosulfan. Rats fed a low-protein diet (3.5% protein) for 28 days had an LDjq of 24 mg/kg of endosulfan. Rats fed standard laboratory chow (26% protein) had an LDjq of 102-121 mg/kg. The immediate cause of death in all animals was respiratory failure following tonic-clonic convulsions. This study demonstrated that, while a protein-deficient diet does not affect the nature of the toxic reaction, it may affect the sensitivity of rats to the lethal effects of endosulfan. 

History. This includes the severity grading of the clinical reaction, the time of administration and onset of symptoms, the concomitant use of other drugs, foods or compounds (latex), previous history of drug allergy, atopy in the personal or family history, other underlying conditions such as mastocytosis or Cl esterase inhibitor deficiency. The actual preparation in its galenic identity should be stored or at least listed. 

Lung surfactant is composed mainly of lipid with some proteins and carbohydrate and prevents the alveoli from collapsing. Surfactant activity is largely attributed to dipalmitoylphosphatidylcholine, which is synthesized shortly before parturition in full-term infants. Deficiency of lung surfactant in the lungs of many preterm newborns gives rise to respiratory distress syndrome. Administration of either natural or artificial surfactant has been of therapeutic benefit. 

Another condition involving ceruloplasmin is aceru-loplasminemia. in this genetic disorder, levels of ceruloplasmin are very low and consequently its ferroxidase activity is markedly deficient. This leads to failure of release of iron from cells, and iron accumulates in certain brain cells, hepatocytes, and pancreatic islet cells. Affected individuals show severe neurologic signs and have diabetes mellitus. Use of a chelating agent or administration of plasma or ceruloplasmin concentrate may be beneficial. 

No specific dietary restrictions are recommended for patients with IBD, but avoidance of high-residue foods in patients with strictures may help to prevent obstruction. Nutritional strategies in patients with long-standing IBD may include use of vitamin and mineral supplementation. Administration of vitamin B12, folic acid, fat-soluble vitamins, and iron may be needed to prevent or treat deficiencies. In severe cases, enteral or parenteral nutrition maybe needed to achieve adequate caloric intake. 

For acute symptomatic hypocalcemia, 200 to 300 mg of elemental calcium is administered IV and repeated until symptoms are fully controlled. This is achieved by infusing 1 g of calcium chloride or 2 to 3 grams of calcium at a rate no faster than 30 to 60 mg of elemental calcium per minute. More rapid administration is associated with hypotension, bradycardia, or cardiac asystole. Total calcium concentration is commonly monitored in critically ill patients. Under normal circumstances, about half of calcium is loosely bound to serum proteins while the other half is free. Total calcium concentration measures bound and free calcium. Ionized calcium measures free calcium only. Under usual circumstances, a normal calcium level implies a normal free ionized calcium level. Ionized calcium should be obtained in patients with comorbid conditions that would lead to inconsistency between total calcium and free serum calcium (abnormal albumin, protein, or immunoglobulin concentrations). For chronic asymptomatic hypocalcemia, oral calcium supplements are given at doses of 2 to 4 g/day of elemental calcium. Many patients with calcium deficiency have concurrent vitamin D deficiency that must also be corrected in order to restore calcium homeostasis.2,37,38... 

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