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Biomedical subjects

C A Osborne

Publications and source records attributed to C A Osborne.

At least 127 records · Page 7Linked to original sources
PubMed1986

Etiopathogenesis of uric acid and ammonium urate uroliths in non-Dalmatian dogs.

The etiopathogenesis of uric acid, sodium acid urate, and ammonium acid urate uroliths in non-Dalmatian dogs appears to be a complex phenomenon. It may involve one or more pathologic and/or physiologic processes acting independently or in concert to increase urinary concentration of lithogenic substances that result in initiation, growth, and retention of urate uroliths. Increased urine uric acid concentration and/or urinary excretion of uric acid appear to be primary predisposing factors in urate lithogenesis. Specific disorders resulting in hyperuricuria may involve abnormalities of increased synthesis, diminished biodegradation, and/or enhance excretion of uric acid. In addition, ammonium ion, hydrogen ion, and other organic and inorganic urine constituents appear to have major influences on urate urolith formation. Unfortunately, many specific disorders of uric acid metabolism and other factors promoting or inhibiting urate urolith formation remain poorly characterized in the majority of non-Dalmatian dogs with urate urolithiasis. Growing awareness of the significance of urate uroliths in non-Dalmatian dogs should encourage further investigation into the identification, characterization, and quantitation of parameters influencing urate lithogenesis. Results of such studies are required for development of practical and effective strategies for treatment and prevention of canine urate urolithiasis.

Animals↗
PubMed1986

Etiopathogenesis, clinical manifestations, and management of canine calcium oxalate urolithiasis.

Calcium oxalate uroliths are commonly called metabolic uroliths because they are sequelae of a variety of metabolic abnormalities that alter the composition of body fluids and urine. Factors incriminated in the etiopathogenesis of calcium oxalate urolithiasis include hypercalciuria, hyperoxaluria, and hyperuricosuria. The predominant type of calcium oxalate urolith encountered in dogs is the monohydrate form; however, the dihydrate form may also occur. Male dogs have been more frequently affected than female dogs. Medical therapy should be formulated with the goal of reducing urine concentration of calculogenic substances.

Allopurinol↗
PubMed1986

Canine calcium phosphate uroliths.

Uroliths composed primarily of calcium phosphate are identified in approximately 3 per cent of canine stone patients. Predisposing factors to the formation of calcium phosphate uroliths include elevated urine pH, hypercalciuria, and the presence of crystallization inhibitors and promoters. Medical therapy of patients forming calcium phosphate uroliths should initially be directed at removing factors contributing to urine supersaturation with calcium phosphate.

Acidosis, Renal Tubular↗
PubMed1986

Canine primary hyperparathyroidism and its association with urolithiasis.

Primary hyperparathyroidism results from autonomous secretion of parathyroid hormone by a single or multiple parathyroid glands. Clinical signs result from various combinations of hypercalcemia, hypercalcemic nephropathy, urolithiasis, or mobilization of calcium and phosphorus from bone. Following parathyroidectomy, the prognosis for dogs with primary hyperparathyroidism is good if the disorder is diagnosed before renal disease is advanced.

Animals↗
PubMed1986

Canine distal renal tubular acidosis and urolithiasis.

Distal RTA is characterized by decreased distal renal tubular hydrogen ion secretion, decreased ability to acidify urine, hypercalciuria, hyperphosphaturia, hypocitraturia, and metabolic acidosis. Because of the resulting alterations in urine composition and pH, patients with distal RTA are predisposed to urolithiasis and renal calcification. Diagnosis of distal RTA is important because it is a potentially reversible disorder that, left untreated, may cause nephrocalcinosis, recurrent urolith formation, moderate to severe metabolic acidosis, and renal failure.

Acidosis, Renal Tubular↗
PubMed1986

Biologic behavior of canine uroliths.

Canine uroliths may form rapidly or slowly, progressively increase or decrease in size, or become inactive. Associated clinical signs are usually dependent on their locations but may also be influenced by underlying causes. Recurrence of uroliths is unpredictable, being influenced by several variables. Recurrent uroliths are usually, but not invariably, similar in mineral composition to those present during the initial episode.

Animals↗
PubMed1986

Comparison of qualitative and quantitative analyses of canine uroliths.

A study was performed to compare qualitative test results of canine uroliths with quantitative test results. Qualitative test results were in agreement with quantitative test results in only 96 of 223 specimens (43 per cent). Lack of agreement was caused by false-negative qualitative test results (85 of 223), false-positive qualitative test results (15 of 233), and a combination of false-negative and false-positive qualitative test results (27 of 233). This study indicates that the veterinary profession should abandon exclusive use of qualitative chemical test kits for uroliths.

Animals↗
PubMed1986

Nonsurgical management of canine obstructive urolithopathy.

Obstruction to urine outflow is a common complication of urolithiasis. However, varying degrees of recovery of renal function may occur following examination of the cause of obstruction. Therefore, in the absence of conclusive evidence of irreversible dysfunction, one should consider efforts to decompress the urinary tract and to eliminate the cause of obstruction. Nonsurgical methods that may be used for management of obstructive urolithiasis include cystocentesis, palpation, urohydropropulsion, and catheterization.

Animals↗
PubMed1986

Medical dissolution of canine struvite uroliths.

Medical therapy is an effective method of canine struvite urolith dissolution. Recommendations include (1) eradication or control of urinary tract infection (if present), (2) use of calculolytic diets, and (3) administration of urease inhibitors to patients with persistent urinary tract infection caused by urease-producing microbes.

Animals↗
PubMed1986

Dissolution of canine ammonium urate uroliths.

Medical therapy that may be effective in promoting dissolution of canine ammonium urate uroliths includes the following: reduction of dietary purines, reduction in in vivo production of uric acid, and alkalinization of urine.

Animals↗
PubMed1986

Surgical removal of canine uroliths.

Surgery is indicated for patients with obstructive uropathy; calcium oxalate, calcium phosphate, silica, and perhaps cystine uroliths; uroliths refractory to medical dissolution; nephrolithiasis and progressive renal dysfunction; anatomic defects predisposing to urinary tract infection; and problems precluding medical management. The goals of surgical management include removal of all uroliths while preserving organ function, eliminating partial or complete obstruction to urine outflow, and correction of anatomic abnormalities that predispose the patient to infection and or urolithiasis.

Animals↗
PubMed1986

Immune responses in rats supplemented with selenium.

It is generally accepted that Selenium (Se) is necessary for optimum performance of the immune system. Selenium deficiency results in immune suppression but little is known concerning the effect of excess Se on immune function. Recent evidence suggests that oral Se supplementation may impede oncogenesis, but the mechanism of this action is currently unknown. Conversely, under certain conditions, Se is suspected of promoting neoplasia. The studies described herein delineate the effects of excess Se (0.5, 2.0 or 5.0 p.p.m.) on specific immune functions of Se-adequate rats, namely, antibody synthesis, delayed-type hypersensitivity (DTH), natural killer (NK) cell activity, prostaglandin E2 (PGE2) synthesis, and interleukin 1 (IL-1) activity. Selenium administered to female Sprague-Dawley rats for 10 weeks at 0.5 and 2.0 p.p.m. resulted in significant (P less than or equal to 0.01) enhancement of splenic NK activity while the NK response in the 5.0 p.p.m. Se-treated rats was equivalent to the non-Se-treated controls. Conversely, the DTH response was significantly (P less than or equal to 0.01) suppressed at all three dosages while antibody synthesis and prostaglandin E2 activity were significantly (P less than or equal to 0.05) reduced compared to the controls at the highest dosage of Se. IL-1 activity was unaffected by Se exposure. These data could partially explain the contradictory oncogenic characteristics of Se. For instance, tumours that are NK sensitive could be prevented and/or responsive to Se therapy, while NK insensitive neoplasms could be enhanced by Se supplementation due to the impaired function of both humoral and cell-mediated immunity.

Animals↗
PubMed1986

Teratogenic effect of acetohydroxamic acid in clinically normal beagles.

Acetohydroxamic acid (AHA), a potent urease inhibitor used for treatment of infection-induced struvite urolithiasis, was teratogenic after administration of 25 mg of AHA/kg of body weight/day orally to 5 clinically normal Beagles from the onset of proestrus until parturition. Thirty pups exposed to AHA in utero developed anomalies of the skeletal system, heart, and ventral midline. Cardiac anomalies included atrial septal defects (20%), ventricular septal defects (3%), and atrial and ventricular septal defects (3%). Skeletal anomalies included coccygeal hemivertebrae and fused coccygeal vertebrae (50%), supernumerary vertebrae (67%), supernumerary ribs (50%), duplicated sternebrae (3%), and lumbar hemivertebrae (3%). Defects of the ventral midline of the abdominal wall occurred in 20% of AHA-exposed pups. Other abnormalities included retarded growth, high neonatal mortality, and a decreased number of circulating RBC, compared with those in 30 control pups born to 5 Beagles given a placebo. Adverse effects of AHA in pregnant Beagles were limited to morphologic alterations (Howell-Jolly bodies, spherocytes, and target cells) in a small number of circulating RBC. Slight neutrophilic leukocytosis and monocytosis occurred between 0 and 30 days of pregnancy in dogs given AHA, compared with those in controls. Seemingly, AHA did not influence fertility, conception rate, or length of gestation.

Abnormalities, Drug-Induced↗
PubMed1986

Effects of urinary bladder distention on location of the urinary bladder and urethra of healthy dogs and cats.

Evaluation of the anatomic location of the distended and empty urinary bladders and urethras of healthy adult male and female dogs and cats by retrograde urethrocystography revealed substantial variations. In 15 dogs in lateral recumbency with empty bladder lumens, the caudal portion of the urinary bladder was within the pelvic canal in 5 of 7 male and 5 of 8 female dogs. In female dogs examined in ventrodorsal recumbency, only 4 of 8 had the empty urinary bladders in part within the pelvic canal. After luminal distention, 3 of 7 male and 3 of 8 female dogs, while in lateral recumbency, had the urinary bladders in part intrapelvically. However, when female dogs were placed in ventrodorsal recumbency, only 1 of 7 urinary bladders was in part within the pelvis. The urinary bladders of 14 cats were consistently within the abdominal cavity, irrespective of whether the bladder lumen was distended or empty. Urethral flexures occurred in dogs with intrapelvic bladders that were distended or empty. Urethral flexures were not found in cats. The urethras of dogs and cats in lateral recumbency were generally closer to the floor of the pelvis after urinary bladder distention than when the bladder was empty. The urethra of the dogs and cats in ventrodorsal recumbency was to the left or right of or on the midsagittal plane, whether the urinary bladder was empty or distended. A greater degree of lateral displacement was encountered in ventrodorsal recumbency after urinary bladder distention.

Animals↗