Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cantharidin toxicosis in horses has become an increasing problem in certain regions of the United States. Toxicosis occurs when horses ingest alfalfa hay or products that are contaminated with "blister" beetles. Clinical signs may vary from depression to severe shock and death, depending upon the amount of toxin ingested. The most frequently observed signs include varying degrees of abdominal pain, anorexia, depression, and signs suggestive of oral irritation. Many horses make frequent attempts to void urine. Less commonly observed signs include synchronous diaphragmatic flutter and erosions of the oral mucosal surfaces. Clinical laboratory abnormalities suggestive of cantharidin toxicosis include persistent hypocalcemia and hypomagnesemia, development of hypoproteinemia, microscopic hematuria, and mild azotemia with inappropriate urine specific gravity. Chemical analysis for cantharidin is accomplished by evaluation of urine or stomach contents. Treatment of cantharidin toxicosis is symptomatic, but must include removal of toxin source. Gastrointestinal protectants, laxative, intravenous fluids, analgesics, diuretics, calcium gluconate, and magnesium are all included in the treatment regimen. Early and vigorous therapy is imperative if it is to be successful. In horses that remain alive for several days, persistence of elevated heart and respiratory rates and increasing serum creatine kinase concentration are associated with a deteriorating condition. Prevention is aimed at timely harvesting of alfalfa hay. Hay fields should be inspected for the presence of beetle clusters before harvesting. Involved areas of the field should not be harvested.
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PMID:Cantharidin toxicosis in horses. 268 72

Two horses were admitted separately for evaluation and treatment of profound hyperchloremic metabolic acidosis without azotemia. One, an 11-year-old Quarter Horse mare, had been depressed and ataxic for 2 days. The other, a 2-year-old Quarter Horse colt, had a 6-week history of depression, anorexia, and weight loss. Both horses responded to fluid and electrolyte therapy, but required daily oral administration of sodium bicarbonate for maintenance. In each case, the diagnosis was renal tubular acidosis.
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PMID:Clinical features and treatment of renal tubular acidosis in two horses. 303 Sep 84

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

Ingestion of ethylene glycol was responsible for severe azotemia, acidosis, and abnormal anionic gap value in a pygmy goat. Clinical signs consisted of ataxia, polydipsia, decreased rumen motility, and constipation. Nervous signs included depression, absence of menace response, vertical nystagmus, and terminal convulsions. Four days after onset of clinical signs, antidotal treatment was ineffective. Lesions and oxalate crystals in the kidney were typical of ethylene glycol or plant oxalate toxicosis in other species. Toxicologic analysis revealed ethylene glycol in the rumen content and glycolic acid in urine and ocular fluid.
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PMID:Ethylene glycol toxicosis in a pygmy goat. 319 47

Bilateral ureteral defects were diagnosed as the cause of depression and azotemia in an 8-day-old Thoroughbred filly. The azotemia resulted from accumulation of urine in the retroperitoneal area. A ventral midline laparotomy was performed, and defects found in both the left and right ureter were repaired. Uroperitoneum and abdominal distention, presumably from urine leakage at the left ureteral surgery site, were detected on the fourth postoperative day and necessitated abdominal drainage. Thirty-six hours later, the leakage stopped spontaneously, and the foal recovered normally. This report should help to differentiate ureteral defects in foals from the more common syndrome of ruptured bladder.
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PMID:Correction of bilateral ureteral defects in a foal. 335 81

Experiments were designed to test the hypothesis that growth depression and azotemia in chronic renal failure can be minimized by providing a nutritional formula that is adequate is essential nutrients but minimizes urinary excretion of all solutes. Unrestrained rats were fed exclusively by continuous intragastric infusion with a mixture containing sucrose, essential amino acids, N-free analogues thereof, minerals, corn oil, and vitamins, designed to minimize urinary solute excretion while permitting growth. After 5 days, renal excretory function was reduced to 1/10 by reinfusing 90% of each day's urinary output intragastrically for the next 3 wk. Weight gain (3.6 +/- 0.1 g/day), linear growth and carcass N accretion were the same as in nonreinfused rats receiving substantially the same formula by intragastric catheter. Except for sight acidosis (CO2 18.5 mM) accumulation of electrolytes did not occur. Average final serum urea N was only 42.5 +/- 7.1 mg/dl. The results are considered as supporting the hypothesis.
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PMID:Growth of rats with severe renal insufficiency fed a formula designed to minimize urinary solutes. 640 12

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

Maintenance hemodialysis patients are known to be lymphopenic, and it was previously felt that T and B cells were equally and moderately depressed. With modification of the B cell technique, however, we have shown that MHD patients have a relatively more pronounced depression of B cells, with decreased proportions and markedly reduced total numbers. B cells bearing specific immunoglobulin types are all proportionally reduced. This marked B cell deficiency could be responsible for the increased rate of some infections in MHD subjects. Its relationship to azotemia, malnutrition, toxic or deficiency states, or dialysis itself is unknown, and the stages of cellular maturation or interaction which are affected have not been identified.
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PMID:Lymphocyte populations in maintenance hemodialysis patients - reassessment and analysis of B cell subtypes. 733 42

A state of 131-albumin metabolism has been investigated in 70 patients with some diffuse renal disease. In patients with chronic renal insufficiency an intravascular albumin mass was in the normal limits, while an albumin concentration was decreased because of an anemia. A depression of albumin catabolism has been noticed in azotemia as well as in albuminuria. A conclusion has been made that serum albumin concentration cannot be a reliable index of the state of protein metabolism in patients with chronic renal failure.
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PMID:[Albumin metabolism in chronic renal insufficiency]. 734 14


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