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Query: UMLS:C0023380 (lethargy)
 5,697 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

Beagle dogs inoculated with the agent of Rocky Mountain spotted fever, Rickettsia rickettsii, developed a clinical syndrome that extended from febrile exanthema to death and appeared to be dose related. Infected dogs were anorectic and lethargic and developed cutaneous lesions characteristic of Rocky Mountain spotted fever, including petechia, ecchymosis, edema, and necrosis. Hematologic changes after inoculation included anemia, leukopenia proceeding to leukocytosis, and thrombocytopenia. Changes in blood chemistry values included increases in serum alkaline phosphatase and cholesterol, and hyponatremia and hypochloremia. The prominent histopathologic change was necrotizing vasculitis. The canine disease is comparable with human Rocky Mountain spotted fever on a clinical, hematologic, biochemical, and pathologic basis, and may provide a model system for this disease in man. The results suggest the dog may be involved in the epidemiology of R rickettsii infections.
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PMID:Studies on the pathogenesis of Rickettsia rickettsii in the dog: clinical and clinicopathologic changes of experimental infection. 87 82

Bilateral renal dysplasia and nephron hypoplasia was diagnosed in a Quarter Horse foal with clinical signs of lethargy, convulsions, and diarrhea. Laboratory evaluation revealed anemia, hypoproteinemia, leukopenia, hyponatremia, hypochloremia, and hyposmolality. The foal also had high concentrations of serum creatinine, BUN, and phosphorus. Evaluation of urinary indices revealed a high ratio of urinary gamma-glutamyl-transferase activity to concentration of creatinine, as well as a high fractional clearance ratio of sodium and potassium. Intravenous treatment with saline solution (0.9% NaCl) and antimicrobials provided only temporary resolution of some of the abnormalities. Diagnosis was partly established by histologic evaluation of renal tissue obtained via an ultrasonographically guided biopsy and was confirmed at necropsy. Pathologic changes in the kidney were unique in that the size of the kidneys, along with the appearance and number of glomeruli, were essentially normal despite marked hypoplasia of nephron tubules in the medulla.
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PMID:Bilateral renal dysplasia with nephron hypoplasia in a foal. 236 27

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

Two male infants with hyperpigmentation, vomiting, lethargy and weight loss were reported. Hypoglycemia, hyponatremia, hypochloremia, hyperkalemia and metabolic acidosis were suggestive diagnosis of salt losing adrenocortical insufficiency. The absence of ambiguous genitalia, low 24 hour urinary 17 KS and pregnanetriol excretion precluded congenital adrenal hyperplasia. Low basal levels of plasma aldosterone and cortisol and low 24 hour urinary 17 OHCS excretion with disability to increase their corticosteroid secretions after ACTH stimulation as well as furosemide and theophylline infusions were supportive for the diagnosis of congenital adrenal hypoplasia. The definitive diagnosis was confirmed by ultrasonogram and computerized tomography. Family histories suggested X-linked recessive inheritance in these reported cases. Evidence of progressive postnatal adrenocortical degeneration was documented by progressive deterioration of adrenocortical functions beginning from mineralocorticoid to total corticosteroid deficiencies. The increased brain serotonin synthesis as the associated pathology of X-linked congenital adrenal hypoplasia was proposed on the basis of elevated basal plasma GH and PRL levels in the reported cases, taken together with an incidence of congenital LH deficiency and persistent ACTH hypersecretion in corticosteroid treated patients reported elsewhere.
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PMID:X-linked congenital adrenal hypoplasia: proposal pathogenesis. 273 38

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

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

Erythema multiforme major and disseminated intravascular coagulation developed in a dog 24 hours after exposure to a d-limonene-based insecticidal dip. Clinical signs included severe lethargy and weakness, ulceration of the oral mucosa, and erythematous serpiginous, annular, and arciform lesions on the head, trunk, and limbs. Clinicopathologic abnormalities included leukocytosis with neutrophilia, normocytic normochromic anemia, thrombocytopenia, prolongation of prothrombin and partial thromboplastin times, increased fibrin degradation products, hypoproteinemia, hyponatremia, hypochloremia, azotemia, high serum alanine aminotransferase and alkaline phosphatase activities, and high serum bilirubin concentration. Despite intensive supportive care, the dog developed severe intrathoracic and abdominal hemorrhage and died. Necropsy revealed severe diffuse epidermal necrosis and widespread hemorrhage within organs. Insecticidal dips containing d-limonene have the potential to induce various toxic effects, including, possibly, erythema multiforme major, and should be used cautiously.
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PMID:Erythema multiforme major and disseminated intravascular coagulation in a dog following application of a d-limonene-based insecticidal dip. 759 26

Two standard poodles were evaluated for painful, episodic muscle cramps affecting their thoracic and pelvic limbs. Both dogs had been diagnosed with hypoadrenocorticism and were being treated with fludrocortisone acetate and prednisone when evaluated for muscle cramps. However, the muscle cramping started approximately 1 month prior to the diagnosis of hypoadrenocorticism. Findings on general physical examination included lethargy and dehydration. Neurological examination was normal between episodes. Serum biochemical abnormalities included hyperalbuminemia, azotemia, hyponatremia, hypochloremia, and hyperkalemia. Altering treatment to desoxycorticosterone pivalate resolved the electrolyte abnormalities and the episodes of muscle cramping in both dogs. The authors conclude that hypoadrenocorticism can be associated with episodes of painful muscle cramping in standard poodles.
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PMID:Muscle cramps in two standard poodles with hypoadrenocorticism. 1222 28


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