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)

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
 ...
PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.
 ...
PMID:Physiology and pathophysiology of the interstitial cells of Cajal: from bench to bedside. VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias. 1206 86

We report on seven elderly patients with severe hyponatremia (plasma sodium < 125 meq/l). All were symptomatic for central nervous system disturbances, weakness, nausea/vomiting and met clinical and laboratory criteria for the diagnosis of inappropriate secretion of antidiuretic hormone (SIADH). Investigations performed to determine the etiology of the syndrome gave negative results, so that the form was considered to be idiopathic. TC scans or MNR showed brain atrophy and/or chronic ischemic lesions. According to the scant series found in the literature, we believe that aging itself may be a risk factor for SIADH. Lowering of the osmolal threshold and/or reduced receptors sensitivity to osmotic stimula, induced by ischemic changes in the hypothalamic region, can represent the underlying mechanisms.
 ...
PMID:[Severe idiopathic hyponatremia caused by ADH inappropriate secretion in the elderly]. 1208 17

This paper reports that vasopressin is emetogenic in the house musk shrew Suncus murinus. Either intravenous or intracerebroventricular administration of vasopressin caused vomiting within a few minutes. The ED50 of intravenous vasopressin was as high as 4.67 microg/kg, whereas intracerebroventricularly injected vasopressin was effective at a low dose of 20 ng/brain. The emetogenic target of vasopressin may therefore be present in the central nervous system. We propose the Suncus as a useful animal for investigation of vasopressin-mediated emesis, including motion sickness.
 ...
PMID:Vasopressin induces emesis in Suncus murinus. 1218 41

Nausea is an unpleasant sensation usually referred to the stomach and sometimes followed by vomiting. Little is known about the subjective aspects of nausea because like pain and fatigue, it is a private sensation. We conceive of nausea as a complex control mechanism that signals us when not to eat. Our research in the areas of motion sickness and chemotherapy has led us to propose that we each have a dynamic threshold for nausea, which depends on the interaction of inherent factors and more changeable psychological factors, and that this threshold effects the individual's cognitive appraisal of both the nauseogenic stimulus and his/her bodily change in response to the nauseogenic stimulus. Inherent factors that are described are age, gender and race; psychological factors that are included are anxiety, expectation, anticipation and adaptation. The physiological responses that have been found to accompany nausea include an increase in sympathetic nervous system activity, a decrease in parasympathetic activity, an increase of abnormal dysrhythmic gastric activity, and an increase in plasma vasopressin. It is concluded that beneficial selective reduction of nausea will depend on a greater knowledge of the interaction of the psychological and physiological variables.
 ...
PMID:The psychophysiology of nausea. 1250 40

We describe an 18-year-old female who complained of general weakness, nausea, vomiting, headache, and lightheadedness. On physical examination, she was euvolemic without visual or neurological deficits. The striking biochemical abnormality was hyponatremia (125 mmol/l). This hyponatremia met the laboratory diagnostic criteria for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Two litres of normal saline were given per day for 4 days and this did not correct her hyponatremia. A spontaneous diuresis (6.6 l) developed in 1 day, causing a rise in her PNa of 26 mmol and a final PNa of 152 mmol/l. Magnetic resonance imaging revealed a dumbell-shaped intrasellar and suprasellar cyst. During transsphenoidal surgery, a Rathke's cleft cyst (RCC) lined with columnar epithelium containing mucoid material was resected. We speculate that the growing RCC may have produced critical compression over the stalk, thus contributing to the transition from SIADH with hyponatremia to transient central diabetes insipidus with hypernatremia.
 ...
PMID:Rathke's cleft cyst presenting with hyponatremia and transient central diabetes insipidus. 1271 31

Cyclophosphamide (CY) is an alkylating agent used to treat a variety of autoimmune disorders. Water intoxication is a well-known complication of high-dose intravenous (i.v.) CY, but is rare in patients treated with low dose i.v. CY. We describe two patients with lupus nephritis and water intoxication following low dose i.v. CY. The first patient was treated with oral prednisolone and azathioprine for eight weeks with inadequate response and persistent renal inflammatory activity. Eight hours after the first i.v. CY pulse she had a grand mal seizure. The second patient had WHO class III lupus nephritis, and after a single i.v. CY pulse developed vomiting, diarrhoea and grand mal seizures. They were both fluid-restricted and their serum sodium levels returned to normal. In conclusion, even at low doses i.v. CY may induce hyponatremia related to inappropriate antidiuretic hormone secretion. This potentially life-threatening complication of i.v. CY could be minimized by avoidance of overhydration following pulse i.v. CY.
 ...
PMID:Water intoxication induced by low-dose cyclophosphamide in two patients with systemic lupus erythematosus. 1294 25

A 52-year-old man presented with vomiting, general fatigue and hyponatremia. His symptoms and signs were consistent with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Endocrine studies revealed hypopituitarism and administration of hydrocortisone resulted in a marked polyuria. The patient was diagnosed as masked diabetes insipidus. The lymphocytic hypophysitis was also diagnosed on the basis of MRI findings and anti-pituitary antibody. Six months later, these abnormalities disappeared. Diabetes insipidus may exist in a case of hyponatremia due to contrastive SIADH. Such patients may recover spontaneously and careful follow-up is required, avoiding a long-term treatment by monotonous continuation of hormonal replacement.
 ...
PMID:Transient lymphocytic panhypophysitis associated with SIADH leading to diabetes insipidus after glucocorticoid replacement. 1460

Hyponatremia caused by an inappropriately high level of antidiuretic hormone secretion after spinal surgery is an uncommon and self-limiting phenomenon that resolves within 2 or 3 weeks. During the early postoperative period, the patient's urine output and serum level of sodium should be monitored closely to prevent possible serious complications of the syndrome of inappropriate secretion of antidiuretic hormone. Symptoms vary depending on the severity of the hyponatremia and can range from mild headache, muscle cramps, nausea, and vomiting to convulsions, coma, and death. Treatment options include fluid restriction, oral intake of salt, and hypertonic saline. It is important that spine surgeons recognize this phenomenon early and treat it appropriately and conservatively to prevent possible serious complications.
 ...
PMID:Syndrome of inappropriate secretion of antidiuretic hormone and hyponatremia after spinal surgery. 1519 39

The aim of this study was to investigate the effect of intestinal electrical stimulation on small intestinal dysrhythmia and motion sickness-like symptoms induced by vasopressin. Female dogs chronically implanted with two pairs of electrodes on jejunum serosa were used in a four-session study. Saline and vasopressin were infused in sessions 1 and 2, respectively. Sessions 3 and 4 were the same as session 2, except a long- or short-pulse intestinal electrical stimulation was applied on the proximal pair of electrodes. Intestinal slow waves and motion sickness-like symptoms were recorded in each session. Results were as follows. (1) Vasopressin induced intestinal dysrhythmia, uncoupling of slow waves, and vomiting and motion sickness-like symptoms (P < 0.05, ANOVA). (2) Intestinal electrical stimulation with long pulses, but not short pulses, was capable of preventing vasopressin-induced intestinal dysrhythmia. (3) Intestinal electrical stimulation with short pulses, but not long pulses, prevented vomiting and the motion sickness-like symptoms. It is concluded that vasopressin induces intestinal dysrhythmia. Long-pulse intestinal stimulation normalizes vasopressin-induced intestinal slow-wave abnormalities with no improvement in symptoms. Short-pulse stimulation prevents emetic symptoms induced by vasopressin but has no effect on slow waves. These data suggest different mechanisms involved with different methods of intestinal stimulation.
 ...
PMID:Effects of intestinal electrical stimulation on intestinal dysrhythmia and symptoms in dogs. 1525 90


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>