Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

Twenty consecutive patients with chronic renal failure (CRF) and 20 control patients received subarachnoid anaesthesia with 3 ml of 0.75% bupivacaine plain for surgery in the lower abdomen. Sensory analgesia (onset) developed significantly more rapidly in the CRF patients: maximum segmental level of pin-prick analgesia was reached in an average of 21 min in the CRF patients and in 35 min in the control patients. An observed tendency to acidosis and a possible reduced intrathecal space in the uraemic patients may account for the more rapid blockade. The mean spread of the sensory block in CRF patients (T4) was two segments higher than that in the control patients, but because of marked inter-individual variation this difference cannot be considered clinically important. Three CRF patients and two control patients had insufficient analgesia for surgery. In the CRF patients, both sensory and motor blockades were of shorter duration than in the control patients. The incidence of complaints of nausea and backache was similar in the groups. One control patient had a headache.
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PMID:Subarachnoid anaesthesia with 0.75% bupivacaine in patients with chronic renal failure. 370 97

Previous intravital staining techniques for parathyroid localisation have met with variable success and complications. Modification of these techniques, employing a more consistent dose, combined with a prolonged infusion time has provided more uniform staining of normal and abnormal parathyroid tissue, other tissues showing little or no colour change. Locally induced oedema, not previously described, was found to be a great asset in the dissection of glands. In 38 of 40 patients (95%), 4 glands were demonstrated and in the remaining 2 cases, only 3 glands appeared to be present. One case alone has required reoperation, due to the presence of a fifth gland. Intra-thyroid and intra-thymic tumours were found easily, as was glandular tissue split accidentally. Apart from slight nausea in one patient, there were no complications attributable to the dye, in the series which included 12 patients with chronic renal failure. Uniformly normal postoperative serum calcium levels indicated the accuracy of the method. The technique is safe, inexpensive and easily reproducible, and would seem to have many advantages over other methods of tumour localisation.
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PMID:Intravital methylene blue staining of parathyroid glands and tumours. 621 12

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

The converting-enzyme inhibitor, captopril, was given to ten patients with refractory severe hypertension of renal origin: 6 patients had chronic renal failure, 3 patients had hypertension following renal transplantation, and one patient had hypertension and congestive cardiac failure. Control of blood pressure was achieved with doses from 78 to 400 mg/day. Severe hyperkalaemia occurred in one patients, ageusia (dose dependent) in another, and one patients withdrew from treatment because of nausea.
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PMID:Captopril for refractory hypertension in patients with chronic renal failure and renal transplantation. 701 37

The effects of sequential prostacyclin infusions at 2, 4, and 8 ng/kg/min for 1 hr were determined in six patients with chronic renal failure. Diastolic blood pressure decreased in a dose-dependent fashion from 74 +/- 4 mm Hg (mean +/- SEM) to 70 +/- 4, 66 +/- 5, and 55 +/- 5 during the 2, 4, and 8 ng/kg/min infusions, respectively; systolic blood pressure was not affected by prostacyclin. The fall in diastolic blood pressure was associated with a progressive rise in heart rate from 77 +/- 3 to 91 +/- 4 bpm and lowering of body temperature from 36.7 +/- 0.1 to 36 +/- 0.2 degrees. The threshold concentration of adenosine diphosphate that evoked reversible and irreversible platelet aggregation increased progressively from 1.2 to 2.8 and from 2.8 to 6 microM, respectively, during the prostacyclin infusions. Prostacyclin infusions had no effect on prothrombin time, activated partial thromboplastin time, or platelet count, but template bleeding time increased (not statistically significantly) from 5.8 to 12.3 min. In three of six patients, the 8 ng/kg/min infusion was terminated prematurely due to nausea, vomiting, and/or hypotension. We conclude that platelet aggregability can be inhibited in patients with chronic uremia by infusing 4 ng/kg/min prostacyclin without causing untoward side effects. When infused at hemodynamically tolerable doses, prostacyclin might serve as an in vivo inhibitor of platelet aggregation during hemodialysis or cardiopulmonary bypass.
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PMID:Effects of prostacyclin infusion in uremic patients: hematologic and hemodynamic responses. 701 91

Seventy-five non-dialized patients with chronic renal failure (CRF) and severe renal anemia were enrolled in a study, receiving r-HuEPO subcutaneously thrice weekly for 6 months. In 64 patients (85%) 7 weeks of treatment with a weekly dose of 158 U/kg were required to achieve Hb concentrations within the target range of 10 to 12 g/dl. Of the 11 patients (15%) who failed to achieve the target Hb range, none were considered to be non-responders as they were excluded for unrelated reasons prior to week 16 (8 cases), or were iron deficient (2 cases), or had bleeding complications (1 patient). Maintaining the Hb concentration at a level of 10.5 g/dl required a mean r-HuEPO dose of 92 U/kg per week. Adverse events were generally mild or moderate. The most commonly reported were hypertension (8%), viral infection/including flu-like syndrome (7%), nausea (7%), and dizziness (5%). Statistically significant increases in mean creatinine concentrations observed after 12 and 24 weeks were most likely due to the progression of renal disease. These results confirm that 50 U/kg of r-HuEPO given 3 times per week subcutaneous provide a safe and effective therapy for anemic predialysis patients.
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PMID:Effectiveness and safety of recombinant human erythropoietin (r-HuEPO) in the treatment of anemia of chronic renal failure in non dialysis patients. European Multicentre Study Group. 807 Sep 41

Diet and nutrition are integral to the management of individuals with renal disease. Uremia engenders anorexia, nausea, meat aversion, and emesis, disturbances that ultimately reduce appetite and cause weight loss and malnutrition. Protein restriction can alleviate these uremic symptoms and improve patient health and vigor, but overly zealous protein restriction may, itself, produce malnutrition. This is particularly likely when energy intake is restricted by either design or anorexia. End-stage renal disease patients require renal replacement therapy for survival, and although dialysis is life sustaining, it neither replaces normal kidney function nor obviates the need for dietary management. In this setting of controlled, persistent uremia, undernutrition can develop surreptitiously. Dialysis physicians have long regarded malnutrition as a sign of uncontrolled uremia and failing health. This supposition has now been validated by epidemiologic studies demonstrating that serum albumin and protein catabolic rate (PCR) discriminate between dialysis patients at high and low risk of death or illness. This correlation of undernutrition with health and survival persists across wide ranges of age, medical diagnoses, and dialysis prescriptions. Because PCR is readily measured using urea kinetic analyses, it has been promoted as a patient monitoring tool and under steady-state conditions it is a reliable method of determining protein intake. Although a single PCR measurement does not integrate day-to-day dietary and metabolic fluctuations and contains an inherent uncertainty of +/- 20%, sequential measurements can be used to assess changes in an individual's dietary protein intake. PCR defines nitrogen losses and, when normalized to a realistic index of metabolic activity (metabolically active body size), it can disclose subtle individual variances in nitrogen utilization. These normalized protein catabolic rates (NPCR) do not, however, measure or describe overall nutrition. The normalization schemes employed are based on population averages and only approximate an individual's true metabolic activity. Thus, using NPCR to define nutritional needs can result in overfeeding obese and underfeeding wasted subjects. Instead, nutritional adequacy should be defined by clinical inspection and comparison with defined standards. Once that state is defined, and desirable protein and calorie intakes are determined, NPCR can be used to monitor the patient's ability to maintain homeostasis.
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PMID:The significance of protein intake and catabolism. 859 Nov 24

A 25-year-old man developed nausea, vomiting, severe headache, and confusion. He had a past history of hyperuricemia and mild renal dysfunction. On admission he had somatic growth retardation, hypertrichosis, and bilateral auditory impairment. A cranial CT scan showed a small area of low density in the left temporal lobe and cerebellar atrophy. Five days later, he developed right homonymous hemianopia, sensory aphasia, and sensory inattention, and a new, large area of low density in the left occipital lobe on a cranial CT scan. On laboratory examination, lactate, pyruvate, and the lactate-to-pyruvate ratio were elevated in both the serum and cerebrospinal fluid. The biopsied muscle showed ragged red fibers and strongly SDH-reactive blood vessels. Gene analysis revealed the presence of the A 3243 G point mutation of the mitochondrial tRNA(Leu) gene in his blood leucocytes and muscle. Serum concentrations of BUN and creatinine were elevated to 46 mg/dl and 2.2 mg/dl, respectively. Creatinine clearance was 14.1 ml/min. An abdominal CT scan disclosed atrophy of his left kidney with subcapsular calcification and the findings of his abdominal ultrasonography were compatible with chronic renal failure. His mother, who suffered from renal failure and became dialysis dependent in her late forties also bore the A 3243 G mutation of the mitochondrial tRNA(Leu) gene in her circulating leucocytes. Though the association between MELAS and renal dysfunction still remains obscure, we speculate that renal failure can be a manifestation of MELAS.
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PMID:[Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with chronic renal failure: report of mother-child cases]. 897 30


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