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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the present study was to develop a controllable experimental model in the dog that would consistently and predictably produce a malignant hypertensive crisis, and to determine the sequential changes in renal function, salt and water balance, and hormones that are involved in the transition from benign to accelerated hypertension. Norepinephrine (NE) was infused continuously into the renal artery of unilaterally nephrectomized dogs that were maintained on 50 mEq sodium/day. The infusion rate of NE was increased each day according to the following schedule: 0.05, 0.1, 0.2, 0.3, 0.4, and 0.5 microgram/kg/min. During the first 4 to 5 days of intrarenal NE infusion, there was a progressive decrease in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), and increases in plasma renin activity (PRA), mean arterial pressure (MAP), and filtration fraction. At the end of this period of benign hypertension, MAP had risen from a control value of 91 +/- 4 to 132 +/- 8 mm Hg, in association with approximately a 10-fold increase in PRA and a 40% reduction in renal function. Then, suddenly, during the subsequent 24-hour infusion period, the MAP increased abruptly in all animals (MAP = 156 +/- 8 mm Hg), and a hypertensive crisis occurred. This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant hypertensive crisis induced by chronic intrarenal norepinephrine infusion. 637 96

Lethargy, anorexia and vomiting suggest azotemia in cats with FUS. Clinicopathologic findings may include azotemia, hyperphosphatemia, hyperglycemia, hyperkalemia, and signs of urinary tract inflammation on urinalysis. Treatment of FUS depends on the degree of illness but generally includes removal of the urethral obstruction, bladder lavage, fluid and antibiotic therapy, and subsequent feeding of a canned, low-Mg diet with added table salt.
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PMID:Management of acute illness in cats. Feline urologic syndrome. 673 7

The most common cause of hypoadrenocorticism in dogs is idiopathic immune-mediated destruction of the adrenal cortex. Other causes include anterior pituitary insufficiency, pituitary or adrenal neoplasia, acute withdrawal of exogenous corticosteroids, and mitotane toxicity. Females are affected more often than males; only 1 feline case has been documented. Animals 2-5 years old are most commonly affected. Clinical signs include lethargy, weakness, weight loss, anorexia, vomiting, diarrhea and bradycardia. Hematologic and biochemical changes can include eosinophilia, lymphocytosis, anemia, hyperkalemia, hyponatremia and hypercalcemia. Diagnosis is by finding negligible resting levels of plasma cortisol and no response to ACTH administration, and a serum Na:K ratio of 20:1 or less. Treatment involves restoring fluid volume, correcting acidosis, and supplementing salt and glucocorticoids. Daily oral use of prednisone at 0.05 mg/kg can safely maintain most affected dogs. Some dogs only require glucocorticoids in stressful situations. Iatrogenic secondary adrenocortical insufficiency (iatrogenic Cushing's disease) may result from a single injection of long-acting glucocorticoids or from long-term use. Clinical signs are the same as for natural hyperadrenocorticism, but endogenous cortisol release is suppressed. Treatment is gradual withdrawal of the offending glucocorticoid and elimination of the cause that initially prompted glucocorticoid therapy.
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PMID:Diseases of the adrenal cortex of dogs and cats. 674 17

Pseudohypoaldosteronism has been described as a syndrome presenting early in life with profound salt wastage, failure to thrive, and lethargy. The mechanism of sodium loss is renal, not related to aldosterone production. Previous cases have been transient, responding to supplemental salt therapy which was discontinued after one to two years. A child whose pseudohypoaldosteronism was first diagnosed in infancy and whose salt loss persisted to 7 years of age is described.
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PMID:Persistent pseudohypoaldosteronism in a 7-year-old boy. 704 Oct 74

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

Thirty-six male mink were fed diets that contained 0, 1, 2 or 4% supplemental salt (sodium chloride) and were given drinking water ad libitum for 7 d. Three mink on each diet were then placed on ad libitum, 50% ad libitum or 25% ad libitum drinking water for the next 14 d. Ad libitum water consumption was directly proportional to the salt content of the diets. Feed consumption was inversely related to the level of dietary salt, although water restriction had a greater effect in reducing feed consumption than did the supplemental salt. The clinical signs of salt toxicity-water restriction observed were increased thirst, mild dehydration, decreased feed consumption, decreased body weight, rough coat, crusty nose and eyes, irritability in the early stage, and lethargy in the later stages. In general, serum and urinary sodium and chloride ion concentrations increased with increasing dietary salt concentrations. Expressed as a percent of brain weight, liver, spleen, kidney and heart weights of mink fed supplemental salt were less than the control weights. Adrenal gland weights increased in response to water restriction. Brain sodium concentrations were not affected by salt supplementation when drinking water was provided ad libitum. However, restricting drinking water generally resulted in increased brain sodium concentrations. Mild to moderate micro- or macrovesicular vacuolar changes were observed in the livers of some mink fed each level of dietary salt, but were especially prominent in the mink restricted in drinking water.
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PMID:Effects of supplemental dietary sodium chloride and restricted drinking water on mink. 770 90

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Reproductive toxicity of 2-ethylhexanoic acid (2-EHA) was studied in Wistar rats. The animals (24 animals per sex per group) were given 2-EHA as a sodium salt in drinking water at daily doses of 100, 300, or 600 mg/kg. Control animals received plain water. Male rats were exposed to 2-EHA for 10 weeks and females for 2 weeks prior to mating, both sexes during the mating period and females during the entire gestation and lactation period. 2-EHA caused a slight but dose-dependent decrease in fertility; time to mating increased at 300 and 600 mg/kg and even total infertility ensued. 2-EHA slightly decreased sperm quality in males. The spermatozoa were significantly less motile at 100 and 600 mg/kg and abnormal sperm occurred more frequently at the two highest dose levels. The average litter size was reduced by 16% in the dose group receiving 600 mg/kg. The birth weights of the pups were unaffected but the body weight gain was transiently slower during lactation at 600 mg/kg. Several pups appeared abnormal (kinky tail, lethargic, slightly paralyzed legs) and the physical development assessed by several landmarks (opening of eyes, eruption of teeth, hair growth) and reflexes (grip reflex, cliff avoidance) was delayed at 300 and 600 mg/kg. In another experiment, a single dose of 600 mg/kg 2-EHA was given to pregnant females by gavage on Gestational Day 4, 5, 6, or 7 and the number of implantations were counted on Gestational Day 10. Administration on Day 6 decreased the number of implantations and caused resorptions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 2-ethylhexanoic acid on reproduction and postnatal development in Wistar rats. 840 83

Twenty-three children from 8-60 months (mean age 21.13 months) admitted with neuromuscular manifestations of diarrhea related hypokalemia were studied. Forty four per cent cases were suffering from diarrhea at the time of admission but in majority of cases (56%), the diarrheal episode had already terminated. Mild hypokalemia was seen in 17.4%, moderate in 43.5% and severe in 39.1%. Neck flop was the commonest (100%) neuromuscular manifestations followed by diminished bowel sounds (82.6%), truncal weakness (52.2%), weakness of limbs (52.2%), lethargy (43. 5%), abdominal distension (43.5%), respiratory involvement (4.3%) and phantom hernia (4.3%). Two cases (8.7%) had flaccid paralysis of both the lower limbs. Severe hypokalemia was more frequently observed in children below 24 months of age and those who had received i.v. fluids or salt sugar solution before reporting in the hospital. A significant correlation was noticed between severity of hypokalemia and frequency of stools (p < 0.05), degree of dehydration (p < 0.01), severity of nutrition (p < 0.01) and extent of neuromuscular involvement (p < 0.01). Our results highlights the importance of diarrhea related hypokalemia particularly in young malnourished children who are rehydrated with solutions inadequate in potassium. Early diagnosis and appropriate treatment can promptly reverse these manifestations within 48-72 hours.
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PMID:Neuromuscular manifestations of diarrhea related hypokalemia. 863 3


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