Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
 ...
PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

Renal failure in itself generates a state of malnutrition, due to three main causes: inadequate ingestion (anorexia, vomiting or diet insufficiencies), the existence of catabolic factors (proteins, acidosis, PTH) and extrarenal depuration (which provokes a lack of amino acids and vitamins). Artificial nutrition constitutes a series of measures that can be adopted to act upon each of the above causes. Adequate ingestion compared to inadequate ingestion can be performed orally (especially in chronic renal failure) by parenteral administration (preferable in acute renal failure) and enteral administration (complementary in both cases). The quantity and quality of adequate nutrients is non-dependent on the method of administration; 500 ml, of water should be administered plus diuresis, plus loss from other tracts; the mineral intake of sodium, potassium and phosphorus should be restricted; in the case of vitamins, these should be administered, especially the B and D complexes; there should be sufficient calories to constitute a hypercaloric diet (from 30-50 kg/day), at least 50% in the form of carbohydrates (hypertonic glucose, if administered intravenously, and dextrinolmaltose or starch if administered through the digestive tract) and at least 40% in the form of lipids (preferably of vegetable origin, rich in non-saturated fatty acids); proteins are the mainstay of nutrition in renal failure; thus, with a normal renal function or in dialysis, a dose of 1 g/kg/day is recommended; in chronic renal failure, 0.5 g/kg/day; in cases of renal failure not on dialysis, 0.3 g/kg/day, supplemented by essential amino acids or cetoacids (the effectiveness of the latter is still in dispute).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Artificial nutrition in kidney failure]. 176 Apr 78

Patient L.A. (f., 20 yrs), affected by bulimia and self-induced vomiting, was hospitalized because of severe malnutrition (BMI 13.1), hypopotassemia (2.8 mEq/l) and prolonged QTc interval (0.469"). Intensive care treatment aimed to normalize mineral balance mainly serum potassium, consisted of administering e.v. potassium (mg 2346/day), magnesium (mg 72/day), calcium (mg 80/day), phosphorus (mg 769/day), chloride (mg 710/day), iron (mg 40/day). Dietary treatment was deliberately chosen to be slightly above minimum energy requirements in order to avoid possible side effects of forced hyperalimentation. The patient, immediately after hospitalization, interrupted vomiting and 2 wks later weight increased by 5 kg (from 34.9 kg to 40.0 kg). On the other hand normalization of serum potassium levels was slow and QTc interval reached normal range only after the 10th day of treatment (0.447"). This case supports the hypothesis that major ECG abnormalities may be present in severe malnutrition due to anorexia nervosa or bulimia with self-induced vomiting. The dangers of these complications were substantiated by the fact that intensive care treatment allowed prompt body weight recovery but normalization of electrolytic balance and cardiac function was very slow. For such patients, electrocardiographic monitoring should be routine.
 ...
PMID:[Hypopotassemia and prolongation of the Q-T interval in a patient with severe malnutrition caused by bulimia and post-prandial vomiting]. 237 4

Radiation is an effective modality for palliation of osseous metastases. In patients with a limited number of lesions, local external beam irradiation is the most expedient method of delivering radiation therapy. Complete or partial relief of pain will occur in 80-90% of patients. When metastases are widespread or when new sites continue to appear, localized external irradiation becomes logistically difficult. In such cases, hemibody irradiation has been effective with an overall response rate of 85%. However, nausea, vomiting, diarrhea, and bone marrow and pulmonary toxicity may complicate therapy. In these cases, an effective alternative is systemic phosphorus-32 (32P) or strontium-89 (89Sr). Relief of pain in the range of 60-90% has been reported. Toxicity of 32P is largely that of bone marrow suppression, while 89Sr appears to be relatively marrow-sparing. In this review, we consider systemic 32P or 89Sr as viable options to external beam or hemibody irradiation in the presence of numerous bone metastases.
 ...
PMID:The palliation of osseous metastasis with 32P or 89Sr compared with external beam and hemibody irradiation: a historical perspective. 247 19

To evaluate the ability to provide short hemodialysis (less than 9 hr per week) without the requirement for costly ultra-high efficiency dialyzers and ultrafiltration control delivery systems, 69 patients maintained on chronic hemodialysis were studied. Standard dialysis was delivered with bicarbonate dialysate, Baxter CF 1211 dialyzers, QB = 300 ml/min, mean time 215 min. The mean KT/V was 1.16. Hemodialysis prescription was changed to maintain the KT/V unchanged. Time was decreased by increasing urea clearance by increasing the QB (400 ml/min in 65 patients, 350 ml/min in 4 patients) and employing the Baxter CF 2308 dialyzer. This produced an increase in urea clearance from 192 ml/min to 256 ml/min, and a decrease in duration of dialysis to 164 min. The CF 2308 dialyzer has an ultrafiltration coefficient of 4 ml/mmHg/hr, which is easily managed without ultrafiltration control equipment. Patients were in the study group for a mean of 176.5 days. The short period of time caused no significant change in blood urea nitrogen, creatinine, potassium, bicarbonate, calcium, phosphorus, hematocrit, or symptomatic hypotension and vomiting. Patient acceptance of the change in hemodialysis time was excellent. Hemodialysis times similar to those reported by others with large experience in shortening hemodialysis time can be achieved in many instances with standard hemodialysis equipment.
 ...
PMID:Reasonably short hemodialysis time can be achieved without ultra-high efficiency dialyzers and without ultrafiltration-controlled delivery systems. 259 58

Animals with renal failure have a number of fairly predictable metabolic abnormalities. They are commonly presented to the veterinarian in a state of negative water balance, although prior fluid therapy in an oliguric patient may result in overhydration. Animals with oliguric ARF have sodium retention; those with polyuric ARF have increased urinary sodium loss. Chronic renal failure does not necessarily affect the ability of the renal tubule to conserve or excrete sodium, although the response to changes in sodium load is much slower than in the normal animal. Potassium retention occurs in oliguric ARF and potassium wasting in polyuric ARF; potassium balance is approximately normal in animals with CRF. Both ARF and CRF cause metabolic acidosis, although the acid-base status in a given animal will be affected by respiratory compensation, as well as other problems such as vomiting. Calcium levels are usually normal to slightly decreased in renal failure, whereas phosphorus levels are generally increased. The basic principles of fluid therapy should be used when constructing a plan for such therapy in an animal with renal failure. Intravenous administration of fluids is almost always necessary. The choice of the type of fluid, solutes, and electrolytes to be administered is based on the predicted abnormalities associated with renal failure as well as the laboratory abnormalities in the animal. Careful monitoring of the patient and periodic assessment of various laboratory parameters are necessary in order to make appropriate adjustments in fluid therapy.
 ...
PMID:Fluid therapy for acute and chronic renal failure. 264 69

A series of 3-phenyl-2-piperazinyl-5H-1-benzazepines and related compounds were synthesized and evaluated for potential neuroleptic activity. The preparation of these compounds was carried out by 2,3-dichlorination of 3-phenyl-2,3,4,5-tetrahydro-1H-1-benzazepin-2-ones with phosphorus pentachloride followed by amination and concurrent dehydrochlorination. Compounds having the 4-chloro or 4-fluoro substituent in the 3-phenyl group were found to possess the neuroleptic-like activity. Among them, 2-(4-methyl-1-piperazinyl)-3-(4-fluorophenyl)-5H-1-benzazepine dihydrochloride (23) was comparable to chlorpromazine in inhibiting exploratory activity, conditioned avoidance response, and self-stimulation response and more potent than chlorpromazine in antagonizing apomorphine-induced emesis. These neuroleptic effects may be based on an antidopaminergic property of the compound. In causing catalepsy or ptosis, however, 23 was weaker than chlorpromazine. Therefore, this ring system is of interest as a novel class of neuroleptics. Some compounds having the 7-chloro or 7-bromo substituent showed potent anticonvulsant effects against maximal seizures induced by electroshock or pentylenetetrazole.
 ...
PMID:A novel class of potential central nervous system agents. 3-Phenyl-2-(1-piperazinyl)-5H-1-benzazepines. 289 53

Acute toxicity of cefodizime sodium (THR-221) was examined in mice of both sexes, rats of both sexes (including 5-day-old young), and male dogs. The LD50 values of THR-221 (mg/kg) were as follows: (1) mice: intravenous, 7200 for males and 5000 for females; intraperitoneal, 10500 for males and 11000 for females; subcutaneous, 17500 for males and 16500 for females; and oral, 28000 for males and 29000 for females. (2) rats (adult): intravenous, 7000 for males and 8200 for females; intraperitoneal, 9500 for males and 8800 for females; subcutaneous, 17000 for males and 15500 for females; oral, more than 20000 for both sexes; and intramuscular, more than 3200 for both sexes. (3) 5-day-old rats: subcutaneous, 5278 for males and 5314 for females. (4) male dogs: intravenous, more than 5000. Major changes in general conditions observed in mice and rats were decreased spontaneous activity, lying prone, respiratory changes, staggering gait, clonic or clonic-tonic convulsions, and cyanosis, and in the animals dosed orally, diarrhea or salivation was also noted. The changes in 5-day-old rats were respiratory changes, agony, loss of reflex to an external stimulus, and congestion at the injection site, and those in dogs were vomiting, dryness of the nose, and soft or mucous stools. Autopsies on the mice and rats which died revealed hemorrhage on the brain surface. In addition, the following were seen: intraperitoneal retention of fluid and dark red spots on the abdominal wall (i.p.), subcutaneous retention of fluid or jellylike material and hemorrhage at the injection site (s.c.), and retention of fluid and dark red spots on the mucosa in the digestive tract (mice p.o.). In 5-day-old rats which died, the subcutaneous tissue at the injection site showed hemorrhage macroscopically and inflammatory changes microscopically. Hematological and blood chemical tests performed in dogs showed an increase in white blood cells and changes suggesting anemia, increases in GOT, LDH and ALP activities, and slight changes in urea nitrogen and inorganic phosphorus. In one animal given a low dose of 2500 mg/kg, an increase in GPT activity was also seen. However, these changes were all transient. Microscopic findings in dogs were slight inflammatory changes in the subcutaneous tissue around the injection site.
 ...
PMID:[Acute toxicity study of cefodizime sodium]. 317 86

The main purpose of this study was to evaluate the effectiveness of an oral fluid therapy alone or combined with parenteral administration of a 5% dextrose solution to attenuate the clinical signs and the pathophysiological consequences of transmissible gastroenteritis in neonatal piglets. Eighteen two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as controls (Group 1). At the onset of diarrhea, infected piglets were divided into three groups of six (Groups 2, 3 and 4). Piglets in group 2 were not treated and were fed a milk replacer ad libitum. Piglets in group 3 were removed from the milk replacer and placed on an oral glucose-glycine-electrolyte solution ad libitum. Those in group 4 were placed on oral fluid therapy and received a 5% dextrose solution intraperitoneally at the rate of 25 mL/kg of body weight once a day. Blood samples were collected in heparin within minutes after the infected piglets became comatose and from the controls at four or five days of age. The following variables were measured: packed red cell volume, blood pH, total plasma protein and bicarbonate, blood urea nitrogen, and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets. There was a sudden and rapid progression into a comatose and moribund state one or two days later whether the infected piglets were treated or not.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Fluid therapy trials in neonatal piglets infected with transmissible gastroenteritis virus. 407 36

One hundred cases of hypophosphataemia (</= 2.0 mg/100 ml) and 84 cases of hyperphosphataemia (>/= 5.0 mg/100 ml) occurring in a hospital population were studied in order to determine the cause of the abnormality. Examples of hyperphosphataemia due to renal failure were excluded from the study.A low serum phosphorus concentration was most frequently due to intravenous administration of carbohydrate, usually glucose, which accounted for 40% of cases. The next commonest cause was vomiting (12%). No obvious explanation could be found in 26% of cases, but in most of these factors were present which are known to affect phosphorus metabolism.No one cause of hyperphosphataemia was outstanding in frequency and in over 50% of cases no definite explanation for the abnormality could be found.
 ...
PMID:Hypophosphataemia and hyperphosphataemia in a hospital population. 500 77


1 2 3 4 5 6 7 Next >>