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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.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

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

Description of 23 patients (21 women, 2 men) with an average age of 36.6 (19--68) years, who were hypokalemic during 6.5 years on the average (range 1/2--16 years). The cause of the potassium depletion was malnutrition (anorexia nervosa, vomiting) and/or abuse of laxatives and/or diuretics. With increasing duration of potassium depletion renal function deteriorated; in two cases terminal renal failure developed. Histology of the kidneys (9 cases) showed the picture of chronic abacterial interstitial nephritis. Urinalysis was negative or non-specific. The blood pressure levels were normal or low, hypertensive values being exceptional. Aside of hypokalemia a tendency to hyponatriemia, hypochloremia and metabolic alcalosis was observed, the latter turning into hypokalemic normochloremic acidosis with advancing renal insufficiency. Plasma renin activity and aldosterone concentration or excretion frequently were elevated, but no close correlation was found between these parameters or with the blood pressure. Bacterial infection of the urinary tract occured, if at all, in the late phase and seems to be complication rather than the cause of the kidney disease. The discussion of other possible pathogenetic factors leads to the conclusion that the term "chronic kaliopenic nephropathy" is justified. Some diagnostic and therapeutic consequences are mentioned.
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PMID:Chronic hypokalemic nephropathy: a clinical study. 73 56

Twenty-seven patients of hypertrophic pyloric stenosis operated on at our hospital between 1977 and 1991 were reviewed. The patients consisted of 22 boys and 5 girls, with males accounting for 81%. Seventeen of the 27 patients were the first children of their mothers. Vomiting was first noted between 10 and 58 days after birth with a mean of 26.5 days, and neonatal onset was observed in 67% of all patients. The body weight decreased after the onset in 17 patients, including 1 in which it decreased below the birth weight. Hypochloremia was the most frequent preoperative electrolyte imbalance, being observed in 41% of all patients. Alkalosis was noted in 17 of the 22 patients in which arterial blood gas analysis could be performed. The olive was palpated preoperatively in 24 (89%) of the 27 patients. The body weight increased in all patients after operation, and the mean daily increase was 26.7 g. The mean period of hospitalization after operation was relatively short at 8.3 days. Postoperative vomiting was observed in 16 patients (59%), with its mean duration being 26 days. All patients showed normal growth after operation, and no postoperative complications were noted.
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PMID:[Study on 27 surgical cases of hypertrophic pyloric stenosis at Kyoto City Hospital]. 147 21

A 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
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PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

1. Bulimia involves more serious problems than previously thought. Bulimia nervosa is a psychiatric disorder characterized by binge eating followed by some form of combination of purging, including laxative or diuretic use, strenuous exercise, and self-induced vomiting to eliminate unwanted calories. 2. Physical problems of bulimia include oral and neck problems, metabolic acid-base imbalances, volume depletion, hypochloremia, hypokalemia, hyponatremia, hypomagnesia, hypocalcemia, hyperuricemia, gastrointestinal problems, and edema. 3. The physical problems of bulimia are less well known than those of anorexia. Nurses must be alert for clues, act on suspicions, use a nonjudgmental approach, and be knowledgeable of all assessment factors, including psychological parameters.
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PMID:Bulimia nervosa. Associated physical problems. 157 14

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

Sometimes it is difficult to compare data coming from different drug monitoring studies because of differences in methods, training of the monitors and other reasons. Many algorithms have been designed for permitting the objective and reproducible assessment of the causality of ADRs, but there is a lack of this kind of assessment for the severity of ADRs. This work was developed in order to show how important the standardized assessment of the severity of ADRs could be. For that purpose the same drug surveillance data were used for obtaining the frequency, characteristics and predisposing factors of ADRs, first considering all definite and probable ADRs--independently of their severity (study I)--and excluding after those considered as mild (study II). By means of an intensive prospective drug surveillance program, 2,559 patients hospitalized at the Medicine Service of the Clinical Hospital of the University of Chile were surveyed. The found frequencies of ARDs were 34.2% and 20.6% for study I and II, respectively. In both studies gastrointestinal and metabolic systems were the most ADRs-affected systems but some differences on adverse signs and/or symptoms were observed. For example, in study I the three most frequent reactions were hyponatremia, hypochloremia and hypokalemia while in study II the three commonest reactions were hypokalemia, vomiting and hypochloremia. In both studies similar characteristics of beginning and probability of ADRs were found, and the highest part of the reactions was dose-dependent. But when mild reactions were excluded (study II) an increase on the proportion of dose-independent ADRs was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of the assessment of the severity on the frequency of adverse drug reactions (ADRs). 362 38

The frequencies of various forms of eating-related behaviour (such as vomiting and laxative abuse) are reported for a series of non-anorectic bulimia patients seen for evaluation in an eating disorders clinic. The results of serum electrolyte, glucose and other screening tests in these patients are presented. Electrolyte abnormalities were found in 82 of the 168 patients (48.8%) who were diagnosed as having either bulimia or atypical eating disorder. The most common abnormality was metabolic alkalosis (27.4%); hypochloremia (23.8%) and hypokalemia (13.7%) were also commonly seen. No significant blood sugar abnormalities were encountered. An elevated serum amylase level was found to be associated with frequent binge-eating and vomiting behaviour. The pathophysiology of electrolyte abnormalities in this patient group is briefly reviewed.
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PMID:Electrolyte and other physiological abnormalities in patients with bulimia. 619 59


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