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Query: UMLS:C0003123 (anorexia)
 13,794 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of jejunum in conduit urinary diversion may lead to electrolyte disturbances, characterized by hyponatremia, hypochloremia, hyperkalemia, acidosis, and azotemia, and a clinical picture of nausea, vomiting, dehydration, anorexia, and lethargy. Four out of six patients deviated with a jejunal loop developed this syndrome, the cause of which is discussed. It is concluded that the use of jejunum in urinary diversion should be avoided.
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PMID:Electrolyte distrubances after jejunal conduit urinary diversion. 63 83

1. Bulimia involves more serious problems than previously thought. Bulimia nervosa is a psychiatric disorder characterized by binge eating followed by some form of combination of purging, including laxative or diuretic use, strenuous exercise, and self-induced vomiting to eliminate unwanted calories. 2. Physical problems of bulimia include oral and neck problems, metabolic acid-base imbalances, volume depletion, hypochloremia, hypokalemia, hyponatremia, hypomagnesia, hypocalcemia, hyperuricemia, gastrointestinal problems, and edema. 3. The physical problems of bulimia are less well known than those of anorexia. Nurses must be alert for clues, act on suspicions, use a nonjudgmental approach, and be knowledgeable of all assessment factors, including psychological parameters.
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PMID:Bulimia nervosa. Associated physical problems. 157 14

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

Although used as a condiment and essential supplement since pre-Biblical times, chlorine as a part of the molecule salt has received little research effort by large animal nutritionists. Its low cost and the continued popularity of salt as a condiment and sodium supplement has precluded the appearance of chloride deficiencies. There is great variation in the chloride and sodium content of feedstuffs fed to lactating cows so that some formulations require no supplemental chloride or sodium. Chloride is highly available from feedstuffs, and when dietary chloride is low, the cow can reduce sharply her losses of chloride in urine, feces, skin secretions, and to some degree in milk. Clinical symptoms of chloride deficiency in the lactating cow include pica, lethargy, anorexia, lowered milk yield, constipation, and cardiovascular depression. Metabolic changes are expressed as a severe primary hypochloremia, secondary hypokalemia, and metabolic alkalosis. Requirement for chloride by the lactating cow is about .20%; a working allowance of .25% seems reasonable for cows in positive energy balance. With gradual resolution of the requirements for chloride and more data on chloride in feedstuffs, use of supplemental salt for either sodium or chloride can be reduced greatly.
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PMID:Mineral utilization by the lactating cow--chlorine. 370 Jul 98

Rupture of the urinary bladder at the time of parturition occurred in a 2 year old Angus cow. Anamnesis included a dystocia followed by a gradual (16 days) onset of anorexia and abdominal distension. Prominent findings on the physical examination were marked dehydration, symmetrical distension of the lower abdomen with ascitic fluid, pneumoperitoneum, absence of rumen contractions, and constipation. Significant laboratory findings were elevations of plasma protein, serum urea nitrogen (SUN) and creatinine, hypochloremia, hyponatremia, hyperkalemia, and metabolic acidosis. The ascitic fluid was present in large quantities (50 liters) and had a markedly elevated urea nitrogen and creatinine concentration when compared to serum values for these substances. Parotid salivary secretion had a reversal of the normal sodium: potassium ratio which was attributed to an increase in aldosterone levels brought about by the hyponatremia. A ventral tear in the urinary bladder was successfully repaired by laparotomy.
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PMID:Ruptured urinary bladder in a post-parturient cow. 682 50

Effects of total nephrectomy were studied in six sheep. There was no marked deterioration in the clinical condition of the animals except anorexia and reduced water intake. Three sheep survived the period of observation of 120 hours when they were euthanized. One animal suddenly died at each of 76, 80 and 100 hours. Progressive increase of blood urea nitrogen concentration was accompanied by severe metabolic acidosis in the later stages. Plasma creatinine rose significantly but the change was not marked. Plasma inorganic phosphorous and calcium decreased significantly. Unaffected plasma sodium levels were accompanied by hyperkalemia and hypochloremia. Plasma total proteins and albumin decreased significantly in the later stages. Results showed markedly different responses to total nephrectomy in sheep as compared to changes reported in cattle and nonruminants.
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PMID:Studies on the effects of total nephrectomy in sheep. 688 88

Thirteen infants, 2 to 10 months of age, developed hypochloremic alkalosis (serum chloride 59 to 92 mEq/l) while taking Neo-Mull-Soy (Syntex), a soy-based formula low in chloride (measured to be 0 to 2 mEq/l) but with considerable potassium citrate. Range of symptoms included lethargy, anorexia, mild spitting up, diarrhea, hematuria, and growth failure. Urine chloride excretion was less than 3 mEq/l. Plasma renin activity or aldosterone, measured in six infants, was elevated. All responded promptly to supplemental salt. One infant receiving Neo-Mull-Soy redeveloped alkalosis when supplemental salt was discontinued. Two of nine apparently normal infants receiving Neo-Mull-Soy also had hypochloremia (85, 86 mEq/l). Three of four receiving Prosobee (Mead Johnson; Cl content 7 mEq/l) had urine chloride concentration less than 20 mEq/l. The chloride content of some infant formulas is insufficient to offset salt losses following mild stress.
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PMID:Hypochloremic alkalosis in infants associated with soy protein formula. 718 58

Chloride deficiency signs were produced in young Holstein calves by a low chloride diet (.063% chlorine) and daily removal of chloride in abomasal contents. General clinical signs included anorexia, weights loss, lethargy, mild polydipsia, and mild polyuria. In latter stages of the deficiency, severe eye defects (scleral injection, sunken eyes, scaliness around eyes) and reduced respiration rate became evident. Feces contained varying amounts of blood and mucus. The chloride imbalance resulted in severe alkalosis and hypochloremia leading to secondary hypokalemia, hyponatremia, and azotemia. All deficient calves died after 24, 28, 38, and 46 days of treatment. Chloride concentrations of plasma in each of the calves just prior to death were similar at 31 to 35 meq/liter, which compares with normal 96 meq/liter. One additional calf made chloride deficient was recovered to normal health in 9 days following a single treatment with salt water and feeding of control diet containing .48% chlorine. Control calves fed a diet with .48% chlorine and which also had their abomasal contents removed daily grew normally and exhibited no deficiency signs. When dietary chloride was adequate, removal of abomasal contents (and chlorine) had no adverse effects on the animals.
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PMID:Chloride deficiency in Holstein calves from a low chloride diet and removal of abomasal contents. 719 42

Nine adult female sheep were each surgically fitted with an Ivan and Johnston reentrant cannula in the cranial part of the duodenum just distal to the pylorus. By diversion (loss) of abomasal outflow, this model has been shown to consistently induce hypochloremic, hypokalemic metabolic alkalosis, accompanied by hyponatremia and dehydration. Each sheep was subjected to 3 treatment trials, each preceded by a 24-hour prediversion period, and a diversion period during which a syndrome of hypochloremia (68 +/- 2 mEq/L), hypokalemia, hyponatremia, and metabolic alkalosis was induced. Development of this syndrome was attributable to losses of large amounts of acid and electrolytes in the abomasal effluent. Mean total electrolyte contents of the effluent were: Cl-, 650 +/- 27 mEq; Na+, 388 +/- 23 mEq; and K+, 123 +/- 12 mEq, with total volume loss ranging from 3.6 to 10.0 L of gastric contents and pH ranging from 3 to 5. Decreases in plasma electrolyte concentrations also can be attributed to decreased intake, because anorexia developed shortly after the onset of diversion. Electrolyte losses in urine during diversion were minimal for Cl- (mean +/- SEM, 12.0 +/- 5.1 mEq), but were greater for Na+ (124.2 +/- 14.5 mEq) and K+ (185.1 +/- 31.2 mEq). Treatments consisted of 0.9% NaCl (300 mosm/L), 3.6% NaCl (1,200 mosm/L), and 7.2% NaCl (2,400 mosm/L) administered over a 2-hour period, with the administered volume determined by the estimated total extracellular fluid Cl- deficit. Significant difference was not found among treatments, with all solutions resulting in return of clinicopathologic and physical variables to prediversion values within 12 hours of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of 0.9, 3.6, and 7.2% NaCl for correction of experimentally induced hypochloremic, hypokalemic metabolic alkalosis in sheep. 836 15

Values of blood gas, serum chloride, and potassium were tabulated for 21 dairy cows with coliform mastitis. Severe cases showed marked clinical signs such as loss of appetite and depression of digestive tract motility, and metabolic alkalosis such as an increase in blood pH, hypochloremia and hypokalemia compared with normal and mild cases (p < 0.01). The results showed that metabolic alkalosis can be detected more easily than acidosis in cases of severe coliform mastitis.
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PMID:Metabolic alkalosis in coliform mastitis. 923 24


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