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)

The anesthesiologist uses a wide spectrum of drugs, including inhalational general anesthetics, barbiturates, benzodiazepines, narcotics analgesics and their antagonists, and neuromuscular blocking drugs. All of these drugs in sufficient dose impair the ventilatory response to chemical stimuli, and may cause inadequate gas exchange. The effect of depression of ventilatory control depends on the magnitude of depression and the coexistence of functional abnormalities in the respiratory system. The functional abnormalities are the result of preexistent pulmonary disease or other disease processes that impair respiratory function, the anticipated effects of major surgery (e.g., pulmonary resection), and the complications of anesthesia and surgery. From a functional viewpoint, the mechanisms of the effects of these disease processes on ventilatory control are: (1) interference with the neurophysiological control of automatic ventilation; (2) impairment of peripheral or central chemoreceptor function; (3) impairment of respiratory muscle function; (4) increase in the mechanical load to breathing as a result of increased resistance or decreased compliance of the respiratory system; and (5) increase in the ventilatory requirements as a result of ventilation/blood flow maldistribution, metabolic acidosis, or increased metabolic rate. As a result of current trends in the use of multiple drugs and controlled ventilation during anesthesia, the patient is at greatest risk during the early postoperative period in the recovery room. In addition to the functional abnormalities described above, the probability of impaired gas exchange and respiratory failure is increased as a result of impaired metabolism and elimination of drugs as a result of hepatic and renal insufficiency, and acute changes in acidbase status, which alter the ionization and distribution of drugs.
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PMID:The effects of anesthetic drugs and disease on the chemical regulation of ventilation. 1 49

Lithium intoxication was induced in rats by intraperitoneal administration of lithium chloride in a daily dose of 200 mg/kg (0.22 LD50) for 6 days. Polyuria connected with pathological changes in the epithelium of the convoluted tubules and depression of the antidiuretic hormone--acid mucopolysaccharides system in the area of the straight kidney tubules was observed on the 6th day of the experiments. Oligouria and death of some of the animals on the 7th experimental day was caused by severe lesions the kidney structure. Further observation (30 days) demonstrated that, along with the regeneration processes, there developed a marked sclerosing ofthe kidney tissue. A conclusion was drawn that severe lithium intoxication was associated with the development of acute renal insufficiency. Functional reserves of the kidneys after the cessation of lithium chloride administration remained lowered for a long period.
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PMID:[Role of the kidneys in the pathogenesis of lithium poisoning]. 13 80

Nutritional treatment of children with renal insufficiency presents special problems related to undernutrition, i.e., insufficient caloric intake to permit normal growth, vitamin D intake, and protein needs, as well as depressed appetite. With regard to energy, it is suggested that uremia may lead to increased caloric requirements, thus exacerbating growth depression. Protein requirements, which actually may not be as important as caloric needs, have not been determined for uremic children. Another factor in growth failure in such children involves vitamin D metabolism and its role in renal osteodystrophy. Successful dietary management of these various interrelated aspects of childhood renal disease requires sensitive, knowledgeable personnel.
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PMID:Nutritional implications of renal disease. IV. Nutritional aspects of chronic renal insufficiency in childhood. 40 47

Two cases of suicide of patients with renal insufficiency and haemodyalisis commited by liquidation of the shunt are reported. Authors stress the importance of prevention and psychotherapy among haemodyalized patients having depression and neurotic complications.
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PMID:[Suicide of patients with chronic kidney failure by disconnecting their shunt]. 50 95

Serum- or plasma levels of 102 healthy individuals as well as 78 patients with chronic renal insufficiency of various degrees were tested for parathormon (PTH), calcium, magnesium, anorganic phosphate, alkaline phosphatase, kreatinin, total protein as well as magnesium concentrations of the erythrocytes; attempts were made to correlate these parameters with each other. As most important finding in healthy individuals a significant negative correlation could be observed between serum PTH and magnesium of erythrocytes, whereas patients with renal insufficiency had a marked elevation and significant positive correlation between these two parameters. Since all other correlations were not as striking, if compared to these findings, we concluded that a feedback regulation system may exist in the intracellular magnesium concentration and PTH metabolism, so that an increase of the intracellular magnesium stimulates the PTH secretion, whereas elevated PTH activity causes a decrease of the intracellular magnesium together with a depression of the PTH release.
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PMID:[Correlations between metabolisms of magnesium, calcium and parathormon (author's transl)]. 65 59

Parathormone (PTH) excess limits renal bicarbonate reabsorption. This may aggravate the acidosis in patients with renal insufficiency and secondary hyperparathyroidism. Why parathormone, the primary action of which is thought to be stabilization of the inonized fraction of calcium, affects acid-base balance remains uncertain. Parathormone not only promotes the release of calcium from bone but also mobilizes salts, including bicarbonate and phosphate. Accumulation of these anions in the extracellular fluid would limit the ionization of calcium. Teleologically it is not unexpected to find that, coincident with evolution of a mechanism which permits rapid mobilization of calcium from bone, a system had to develop which removed the byproducts of bone dissolution. If this concept is valid, parathormone-induced depression of renal bicarbonate reabsorption in uremia represents an undesired side effect of an adaptive mechanism. This would extend Bricker's "trade-off" hypothesis which ascribes metabolic bone disease due to PTH-induced phosphate loss to include metabolic acidosis resulting from diminished renal bicarbonate regeneration. Parathyroidectomy or phosphate restriction have been proposed for correction of the side effects of secondary hyperparathyroidism. These therapeutic manipulations cannot be recommended for general use. A more rational apprach for prevention of secondary hyperparathyroidism is the combined use of phosphate restriction with a short-acting vitamin D derivative.
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PMID:Parathyroid hormone and the regulation of acid-base balance. 110 50

Cardiac arrest developed in two patients after the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal.
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PMID:Cardiac arrest due to oral potassium administration. 111 63

Lymphocyte blastogenic transformation in response to plant lectins and allogenic cells was studied in patients with nonuremic, far-advanced, chronic renal failure and in healthy controls. Cell cultures were studied in the presence of normal sera, patient's sera, and with media of different buffering capacities. Minimal blastogenic depression was observed when patient's lymphocytes were cultured in indifferent plasma with effective bicarbonate buffering compared with the use of pooled patient's plasma or HEPES buffer. Fresh plasma in culture depressed concanavalin A (Con A) blastogenesis. The data suggest that, under optimal conditions, lymphocytes from patients with chronic severe renal insufficiency are more responsive to stimuli than previously reported and as a group are near normal control values. Further, the defect observed may be a result of intracellular acidosis.
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PMID:Lymphocyte blastogenesis in patients receiving hemodialysis. 127 24

Glomerular permselectivity and dynamics were evaluated serially in 14 nephrotic patients with membranous glomerulopathy (MG). Analysis of transglomerular dextran sieving, before and again after proteinuria remitted, revealed persistent depression by 60-80% of glomerular pore density and the two-kidney ultrafiltration coefficient, Kf. The glomerular filtration rate was lowered by half on each occasion. Morphometric examination of glomeruli in a second group of 16 nephrotic patients with MG revealed a low prevalence of glomerulosclerosis (5 +/- 3%) and a twofold increase in filtration surface due to marked glomerular hypertrophy. Presumably, widening by threefold of the basement membrane and/or epithelial podocytes accounted for the computed reduction in ultrafiltration capacity. There was no correlation between glomerular structure and the subsequent course of MG over the ensuing 24-96 mo. Rather, a twofold expansion of the interstitial compartment predicted those who went on to exhibit progressive renal insufficiency. We conclude that increasing resistance to water flow by walls of patent and perfused glomerular capillaries is the proximate cause of progressive renal insufficiency in MG.
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PMID:Extent and course of glomerular injury in human membranous glomerulopathy. 128 82

This study was designed to determine the incidence, etiology and consequences of severe hypermagnesemia. We retrospectively reviewed all hospital admissions over a 5-year period from 1984 to 1989 and identified 8 cases of severe hypermagnesemia (serum Mg > or = 6.0 mg/dl) due to magnesium ingestion. All but 1 patient were elderly (mean age 70 +/- 6 years). The etiology when identified was due to magnesium-containing cathartics (n = 3) or antacids (n = 3). The total amount of magnesium ingested was not excessive, but bowel disorders that may have enhanced absorption (such as active ulcer disease, gastritis, colitis, perforated viscus, massive gastric dilatation) were present in 7 of the 8 patients. Unexpectedly, only 1 had preexisting renal failure. Renal function was found to be normal in 1, only mildly to moderately impaired in 5 (creatinine < 3.6 mg/dl) and severely impaired in 2 (creatinine 7.6, 15.7 mg/dl). Clinical sequelae of hypermagnesemia were hypotension (n = 7), bradycardia (n = 2), respiratory depression (n = 3), EKG abnormalities (n = 6), depressed mental status (n = 5). Hypocalcemia (range 5.7-7.4 mg/dl) more severe than could be attributed to either hypoalbuminemia or acute renal failure was present in 7. A low anion gap (range-2 to 9) was present in 5. Most striking was the fact that despite clinical sequelae, the hypermagnesemia was unsuspected in 6 of the 8 cases. Hypermagnesemia can occur without severe renal insufficiency in association with bowel disease, particularly in elderly individuals, and may be a clinically unrecognized cause of cardiovascular dysfunction, hypocalcemia and neurologic or respiratory depression.
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PMID:Unsuspected morbid hypermagnesemia in elderly patients. 148 3


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