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

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
 ...
PMID:Magnesium deficiency and cardiac disorders. 80 29

Fifteen patients were treated in a Phase I study of intracarotid carboplatin (200-400 mg/m2) in 5% dextrose and water infused over 15 to 30 minutes through a transfemoral catheter with a 0.2-micron inline filter. This study was done because intravenous carboplatin has less neurotoxicity than cisplatin and is active against brain tumors. Eleven men and four women ranging in age from 37 to 72 years (median, 59 years) were treated. The Eastern Cooperative Oncology Group performance status was 1 in 3, 2 in 4, and 3-4 in 8 patients. Eight patients had one to three previous chemotherapy regimens; previous radiotherapy had failed in 13 patients. The response of patients in the Phase I study follows: glioblastoma, 6 failed; not evaluated because of early death from pulmonary embolus, 1; recurrent Grade II and III glioma, 1 stable (minor response with neurologic improvement) and 2 failed; malignant oligodendroglioma, 1 failed; brain metastases from nonsmall cell lung cancer, 1 partial remission, 1 stable (minor response), and 1 failed; brain metastases from unknown primary, 1 stable (minor response with neurological improvement). Median survival was 9 weeks. Nausea was mild to moderate. One patient had granulocytopenia, and 2 had thrombocytopenia (mild). At 200 mg/m2 (2 patients), 1 had a focal seizure. At 300 mg/m2 (9 patients), 2 with abnormally small arteries had severe pain early in the treatment and posttreatment ipsilateral conjunctival edema, decreased vision, and cerebral edema (with partially reversible increased hemiparesis); 1 other had mild decrease in ipsilateral vision and 1 had transient aphasia on removal of the catheter (possibly the result of a vascular spasm).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Phase I study of intracarotid administration of carboplatin. 131 64

A combination of metoclopramide, dexamethasone, droperidol, lorazepam, and diphenhydramine was used in prophylaxis of high-dose (greater than or equal to 100 mg/m2) or moderate dose (greater than or equal to 50 mg/m2) cisplatin. Sixty minutes prior to starting cisplatin, 16 mg dexamethasone, 50 mg diphenhydramine, and 0.5 mg lorazepam were given orally (PO). Droperidol 1 mg was given intramuscularly (IM) 15 minutes prior to beginning cisplatin. Repetitive doses of intravenous (IV) metoclopramide, 2 mg/kg in 75 ml 5% dextrose in water over 15 minutes was given 30 minutes prior to, and at 1 1/2, 4 1/2, and 7 1/2 hours after beginning cisplatin chemotherapy. Only patients with nausea and/or vomiting received subsequent doses of 2 mg/kg metoclopramide IV every 3 hours as needed. Patients refractory to metoclopramide were given 1 mg droperidol IM and 50 mg of diphenhydramine PO every 6 hours. There were 19 men and 9 women with a median age of 58 (range 31-75) years. Complete protection from nausea and vomiting in all courses of treatment occurred in 17 (61%) patients. In 63% and 70% of the 57 evaluable courses, there was neither nausea nor vomiting, during the first 24 hours after cisplatin. When present, nausea was mild and the median number of vomiting episodes was 2 (range 1-3). This antiemetic regimen was well tolerated. Toxicities were mild and occurred in 3 patients (angioneurotic edema, transient episode of facial twitching, and heaviness of tongue, respectively). The 5-drug antiemetic combination can prevent cisplatin-induced nausea and vomiting in a majority of patients.
 ...
PMID:Five-drug antiemetic combination for cisplatin chemotherapy. 158 29

In a 14-day multiple-dose study the pharmacokinetics of paroxetine was investigated in 12 patients with alcoholic cirrhosis and in 6 subjects without liver disease. The dose of 20-30 mg paroxetine daily was adjusted to the reduction in liver function, as assessed by the galactose elimination capacity. Accordingly, all but two of the cirrhotic patients received 20 mg, while all six control subjects received 30 mg. Dose-corrected, trough drug concentration at steady state (CSSmin) and dose-corrected AUC24h were significantly higher in the patients with liver diseases than in the control subjects [3.4 vs 1.5 ng.ml-1 per mg paroxetine and 89 vs 43 h (ng).ml-1 per mg paroxetine]. The elimination t1/2 was prolonged [83 vs 36 h], but the difference was not statistically significant, and the cirrhotic patients were still able to clear almost all the paroxetine by metabolism. All but two patients with cirrhosis experienced nausea during the first two or three days after the first dose, while none of the controls had this symptom. The study showed slower elimination of paroxetine and consequently higher plasma levels in patients with cirrhosis, suggesting that in the latter the dose of paroxetine should be in the lower end of the therapeutic range.
 ...
PMID:Pharmacokinetics of paroxetine in patients with cirrhosis. 183 32

The hypothesis that the lipid emulsion of the emulsion formulation of propofol is responsible for the low frequency of nausea, retching, and vomiting after propofol anesthesia was tested. A randomized, prospective, and comparative study was performed to evaluate the antiemetic effect of 10% lipid solution in 60 women, ASA physical status I and II, scheduled for ambulatory laparoscopic procedures. Two groups of patients were studied. Induction of anesthesia (thiopental) and maintenance of anesthesia (enflurane, nitrous oxide) were similar in both groups. At induction the study group received 10% Intralipid (3 mL/min for 20 min). The control group received 5% dextrose in lactated Ringer's solution at the same rate. Other drugs administered during or after anesthesia were similar among the groups. The groups were similar with respect to duration of anesthesia, characteristics of early and intermediate recovery, as well as pain scores in the postanesthesia care unit. There were no differences in the amount of antiemetic medications administered or postoperative nausea, retching, or vomiting when the patients were evaluated objectively by a blinded observer or subjectively by patient self-evaluation. It is concluded that 10% Intralipid, the lipid in the emulsion formulation of propofol, does not possess significant antiemetic effects.
 ...
PMID:Is the antiemetic effect of the emulsion formulation of propofol due to the lipid emulsion? 222 15

Recently several reports have described the usefulness of meperidine as the sole agent for spinal anesthesia. In this study, meperidine 50mg mixed with 10% dextrose 0.5ml was used for the spinal anesthetic agent for Cesarean section in 182 cases. The subarachnoid injection of meperidine resulted in anesthesia similar to that noted with the intrathecal administration of local anesthetics. Sensory and motor blockades in all patients with meperidine spinal anesthesia were obtained. Prolonged analgesic effect (453.7 +/- 158.1 minutes) and rapid motor recovery (75.9 +/- 17.2 minutes) were obtained. Side effects included nausea (49 patients), hypotension (95 patients) and pruritus (30 patients). Hypotension was easily treated with rapid hydration and ephedrine. Eighteen patients complained of mild pain during the last period of operation. At birth, all newborns cried immediately and the mean Apgar scores were 9.8 +/- 0.4 at one minute and 10 at 5 minutes. It is concluded that meperidine, which has advantages such as rapid motor recovery, prolonged postoperative analgesia, and mild complications which may be easily treated, can serve as a good alternative agent for spinal anesthesia for Cesarean section.
 ...
PMID:Intrathecal meperidine as the sole agent for cesarean section. 263 46

Potassium is one of the most abundant ions in the human body and yet it is difficult to assess potassium balance. Potassium chloride is extensively used as a potassium supplement, both by physicians as a therapeutic modality and by the general public, mostly in the form of salt substitute. Therapeutically, both the oral and intravenous forms of potassium are utilised. Overdose of potassium is not as frequently encountered in clinical practice as hyperkalaemia (excess potassium in the body) due to acute or chronic renal disease. Potassium homeostasis is maintained very delicately and is governed by the daily consumption of potassium and the renal excretion mechanisms. Any change in these or related factors can present as hyperkalaemia. However, potassium overdoses leading to serious consequences do occur. Orally, the dose of potassium has to be large enough so that the normal excretory mechanisms for potassium are overcome and clinical toxicity occurs. It takes a much bigger dose of ingested potassium to produce toxicity in a person with normal renal function than in patients with compromised renal function. Potassium toxicity manifests in significant, characteristic, acute cardiovascular changes with ECG abnormalities. Besides cardiovascular effects, neuromuscular manifestations in the form of general muscular weakness and ascending paralysis occur. Gastrointestinal symptoms manifest as nausea, vomiting, paralytic ileus, and local mucosal necrosis which may lead to perforation. It is imperative when treating hyperkalaemia that the whole clinical picture is taken into account rather than the numerical potassium values. Only the extracellular potassium can be measured in the laboratory, yet 98% of the body potassium is intracellular and cannot be measured. In acute overdose situations due to ingestion of potassium salt, the general principles of treatment for overdoses should be followed. Calcium chloride infusion, dextrose and insulin in water, and correction of acidosis with sodium bicarbonate are helpful in controlling the acute, life-threatening cardiac arrhythmias. These modalities do not remove the excess potassium from the body. That is achieved either by utilising ion-exchange resins or by mechanically removing potassium via haemodialysis. To curtail inadvertent or accidental potassium overdoses, physicians should prescribe any potassium supplements very carefully to their patients and monitor the plasma potassium periodically.
 ...
PMID:Clinical features and management of poisoning due to potassium chloride. 268 36

A 37 year old black female presented with congestive cardiac failure, 2 months postpartum. She developed spontaneous hypoglycaemia and symptoms of acute adrenal crisis (hypotension, nausea, abdominal pain and tachycardia with small thready pulse), which responded to i.v. dextrose, sodium chloride and hydrocortisone. Biochemical investigations revealed low serum cortisol and plasma adrenocorticotrophic hormone (ACTH) levels. The patient initially showed an impaired cortisol response to intramuscular aqueous tetracosactrin, but an exuberant response after priming with intramuscular tetracosactrin depot. These findings, together with the normal remaining pituitary function, led us to conclude that this patient had isolated ACTH deficiency associated with congestive cardiac failure and acute adrenal crisis.
 ...
PMID:Isolated adrenocorticotrophic hormone (ACTH) deficiency associated with acute adrenal crisis. 299 71

A 43-year-old alcoholic presented in coma with ketoacidosis, after three days of nausea and feeling generally unwell, which had been preceded by a prolonged three-week period of heavy alcohol consumption with poor dietary intake. The acidosis responded rapidly to intravenous dextrose. This is the first Scottish report of a case of alcoholic ketoacidosis.
 ...
PMID:Alcoholic ketoacidosis: a case report. 344 46

This study evaluated the effectiveness of filtering amphotericin B (ampho B) on the incidence and severity of drug-related complications. Fifteen males receiving ampho B via peripheral vein infusion participated in this randomized, double-blind study. Each patient had his dose of ampho B diluted in 500 ml of dextrose 5% in water, to which hydrocortisone 25 mg was admixed and infused over four to six hours. Eight patients had their ampho B infusions filtered through a 1 micron filter after preparation, while seven patients did not have their ampho B infusions filtered. Patients were evaluated daily for phlebitis and selected adverse effects. The two groups were comparable with regard to diagnosis, concomitant drugs, cannula type and size, vein selection, and frequency of iv site change. Four patients in each group developed phlebitis. Statistical testing using the Mann-Whitney U test revealed no difference between groups with regard to patient age, dose of ampho B, frequency and severity of phlebitis, time to onset of initial phlebitis, and frequency of adverse effects (fever, chills, headache, nausea, vomiting, and anorexia). Filtration of ampho B infusions using a 1 micron filter does not appear to decrease the incidence or severity of phlebitis and associated adverse effects.
 ...
PMID:Effect of filtering amphotericin B infusions on the incidence and severity of phlebitis and selected adverse reactions. 389 Dec 85


1 2 3 4 5 Next >>