Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe protein-energy undernutrition is a frequent finding among chronically ill patients. Its causes are anorexia, hypermetabolism, and malabsorption. Adverse consequences include impaired cell-mediated immunity increased susceptibility to infection, poor wound healing, weakness, and death. Spontaneous oral intake is inadequate in patients with this disorder, and therapeutic maintenance or repletion alimentation is needed. Enteral hyperalimentation is the method of choice, if tolerated. A successful treatment program usually requires a small-bore, flexible nasoenteral tube, appropriate feeding solution, and constant flow delivery of nutrient. If only partial dietary requirements are tolerated enterally, peripheral intravenous nutrient solutions can often supply the deficit. Although not suitable for all patients, enteral hyperalimentation is more physiologic, safer, easier, and more economical than central venous hyperalimentation. It would be well tolerated by many patients who now receive nutritional repletion by the latter method.
 ...
PMID:Enteral hyperalimentation: an alternative to central venous hyperalimentation. 10 58

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
 ...
PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

The pathogenesis of the rare hypernatremia, usually described in the literature as "neurogenic" or "essential" hypernatremia, consists of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. As etiology, disturbances of the neoplastic, vascular and degenerative type and malformations in the hypothalamic area are known. In patients with the hypodipsia-hypernatremia syndrome, dysfunction of the anterior pituitary lobe, obesity, abnormal regulation of body temperature, psychomotor retardation and episodic muscular weakness are frequently encountered as additional abnormalities. A 6-year-old patient is described with hypodipsia-hypernatremia syndrome manifest for 3 years. Besides hypernatremia, hypodipsia and the relative insensitivity of the osmoreceptors regulating ADH release, elevated body temperature, polyphagia and obesity, partial hypothalamic-hypophyseal dysfunction, lethargy and psychomotor retardation are the principal findings. An inflammatory lesion or one occupying an intracranial space was not demonstrable until now. Under forced water intake and hypocaloric diet the patient has progressed well with nearly complete normalization of the hypernatremia, body temperature and obesity.
 ...
PMID:Hypodipsia-hypernatremia syndrome. 42 94

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
 ...
PMID:Hypophosphatemia and rhabdomyolysis. 74 77

This paper describes four cats with hyperadrenocorticism. Cat 1 showed polydipsia and polyphagia. Diabetes mellitus was initially diagnosed. As the animal appeared to be insulin resistant, pituitary and adrenocortical function tests were performed and the diagnosis of hyperadrenocorticism was made. Resistance to the high-dose dexamethasone suppression test was noticed in this cat. Pathological examination revealed a pituitary chromophobe adenoma. Cat 2 presented with diabetes mellitus, which was treated with insulin. The animal had a pendulous abdomen and its coat was in a poor condition. The low-dose dexamethasone suppression test demonstrated hyperadrenocorticism. Necropsy findings of pituitary tumour and hyperplasia of the adrenal cortex confirmed the diagnosis. Cat 3 showed clinical abnormalities indicative of hyperadrenocorticism, for instance, muscle weakness, alopecia, multiple abscesses. The diagnosis of hyperadrenocorticism was confirmed by the results of the lowe-dose dexamethasone suppression test. Pathological examination revealed an adrenocortical carcinoma. Cat 4 presented with polydipsia. The cause of this symptom was not found initially. One and a half years later additional symptoms, such as nephritis and polyphagia developed. Hyperadrenocorticism was diagnosed because of a palpable mass cranial to the left kidney. The diagnosis was confirmed by the results of the lowe-dose dexamethasone suppression test and the necropsy findings.
 ...
PMID:Hyperadrenocorticism in four cats. 141 43

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
 ...
PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

Triamcinolone acetonide was administered in excessive dosage to dogs to study the renal mechanism responsible for polyuria which is a clinically undesirable side effect of long term glucocorticoid therapy.Polyuria occurred coincident with a significant increase in urinary solute output. Although continuous administration of triamcinolone acetonide at 0.1 or 0.2 mg/lb/day caused a small but significant increase in creatinine output, the primary mechanism for the polyuria was increased solute excretion. Associated with the polyuria was pronounced hyperphagia and polydipsia. The cause of the hyperphagia was not established. The increase in electrolyte excretion caused by this synthetic steroid was probably compensated for by the hyperphagia. Because all the dogs showed muscle weakness and loss of body condition, it is likely that alteration in protein and amino acid metabolism was responsible for the hyperphagia.
 ...
PMID:Renal effects of long term administration of triamcinolone acetonide in normal dogs. 425 11

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
 ...
PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49

Charts of 28 hyperthyroid patients over 60 years old were retrospectively analyzed and compared with charts of 14 patients under 30 years old. The mean duration of symptoms prior to diagnosis was 16 months in the elderly and five months in the younger group. Heart rate was substantially lower in the older (107 beats/min) vs younger (117 beats/min) study group. The symptom of weakness or fatigue was more prevalent in the elderly group (94 percent) than in the younger group (57 percent). Cardiac palpitation was more prevalent in the elderly patients whereas insomnia, irritability, dysphagia, hyperphagia, and heat intolerance were more prevalent in the younger patients. Fifty percent of the elderly patients complained of chest pain. Cachexia (62 percent), thin, fine hair (50 percent), and weakness (58 percent) were prominent physical findings in the elderly group. Twenty-six percent of the elderly patients had atrial fibrillation. These findings confirm previous studies that show some differences in presentation of hyperthyroidism in elderly patients when compared with younger patients. The authors recommend that thyroid function tests be obtained for broad indications in the elderly.
 ...
PMID:Thyrotoxicosis in the elderly. 664 37

Previous reports have described a syndrome of paresthesias, weakness, seizures and hypophosphatemia in patients and animals receiving intravenous hyperalimentation. In this report we describe a group of five patients who developed this syndrome while on oral caloric intake and three patients who received only modest amounts of hyperalimentation therapy. As an experimental corollary, studies were performed in starved and normal dogs with calories infused via an intragastric catheter. The serum inorganic phosphorus (Pi) fell slightly in normal animals from 4.8-2.5 mg. %. In the starved dogs with diarrhea or vomiting the Pi fell gradually from 4.8-1.6. In starved dogs without gastrointestinal symptoms the Pi fell precipitously from 3.7-1.4 mg % on the first day of infusion and remained at that level. Approximately 50% of the starved animals developed the neurological syndrome; none of the normal animals had neurological symptoms.
 ...
PMID:Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome. 677 12


1 2 3 Next >>