Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
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Proprietary sleep aids and sedatives can cause delirium, coma and occasionally death in children and adults. The constituents in sleep aids that significantly effect central nervous system activity are bromides, methapyrilene, pyrilamine and scopolamine (hyoscine). Constituent proportions and mixtures vary greatly at different times since manufacturers make frequent adjustments. The effects of toxicity resulting from the misuse of ethylenediamines include nausea, vomiting, blurred vision, incoordination, tremors, dry mouth, constipation and an acute poisoning syndrome. Management of adverse reactions produced by either methapyrilene or pyrilamine consists of dosage reduction or discontinuation. The acute poisoning syndrome requires implementation of general symptomatic and supportive principles.
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PMID:Sleep aids and sedatives. 33 Sep 11

Twenty-two patients with refractory intermediate- or high-grade non-Hodgkin's lymphoma were treated with dexamethasone 10 mg every six hours and ifosfamide 1 g/m2, cisplatin 25 mg/m2, etoposide 100 mg/m2 (DICE), and mesna uroprotection daily x4 every 3 to 4 weeks. Pretreatment with prochlorperazine and metoclopramide was given to prevent nausea and vomiting. Eighteen men and four women, aged 21 to 74 years (median age, 65) have received a total of 64 cycles. Seventeen patients had stage IV, one had stage III, and four patients had stage II disease. Seven patients had B symptoms and 11 had marrow involvement. Only two patients had had more than one previous chemotherapy regimen. Median time from last chemotherapy to DICE was 7 months (range 1 to 41). Two patients who suffered early treatment-related deaths (from sepsis) were classified as nonresponders. Six of 22 patients (27%) achieved complete remission (2 to 22+ months), and 11 (50%) had partial remissions (1 to 8+ months) for an overall response rate of 77%. Median survival has not been reached yet, and 12 patients are alive 1 to 22 months from the start of treatment. Nine patients had nadir granulocyte counts less than 0.5 x 10(9)/L; six required RBC transfusions and five, platelet transfusions. The platelet nadir was less than 50 x 10(9)/L in 13 patients. Four patients had microscopic hematuria, two had grade 3 gastrointestinal toxicity, and one had a transient episode of delirium and blurred vision.
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PMID:Dexamethasone/ifosfamide/cisplatin/etoposide (DICE) as therapy for patients with advanced refractory non-Hodgkin's lymphoma: preliminary report of a phase II study. 204 97

Anticholinergic syndrome (AS) due to accidental poisoning is exceptional. Mandragora contains a high concentration of atropine, hiosciamine and scopolamine. We have evaluated 15 patients with AS due to poisoning by Mandragora autumnalis, distributed in two family groups. The latency period since the ingestion was 1-4 hours (Means = 2.7 +/- 0.9). The clinical features corresponded to an AS of variable severity. All patients had blurred vision and dryness of mouth, nine (60%) had difficult micturition, nine dizziness, nine headache, eight (53%) vomit, two difficult swallowing and two abdominal pain. There was no correlation between the latency period and the clinical severity. Blushing, areactive mydriasis and tachycardia were found in all, dry skin and mucosae in 14 (93%), hyperactivity/hallucination in 14 and agitation/delirium in nine (60%). One patient developed a florid psychotic episode. Prostigmine (2-6 mg) was administered to 11 patients and physostigmine (0.5-2 mg) to six. The time until a definite response was observed was variable (3-36 hours). The patients treated with physostigmine had a better reversal of the psychoneurological symptoms. Mandragora was identified intermingled with chard [correction of stalwort] (Beta vulgaris) and spinach (Spinacia oleracea) leaves, and atropine and hiosciamine were identified.
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PMID:[Atropine poisoning by Mandragora autumnalis. A report of 15 cases]. 208 9

The old saying 'red as a beet, dry as a bone, blind as a bat, hot as a hare, mad as a hatter' is often quoted when describing the autonomic effects of drugs that block the muscarinic cholinergic system. These effects may be subtle or dramatic, yet can be overlooked or discounted as a natural consequence of old age. Elderly patients can be particularly sensitive to the anticholinergic action of drugs because of physiological and pathophysiological changes that often accompany the aging process. The use of multiple drugs, a common finding in older patients, may result in pharmacodynamic and pharmacokinetic drug interactions that heighten anticholinergic effects. While the classic anticholinergic problems of decreased secretions, slowed gastrointestinal motility, blurred vision, increased heart rate, heat intolerance, sedation and possibly mild confusion, may be uncomfortable for a younger patient in relatively good health, these effects can be disastrous for older patients. Even the most common peripheral anticholinergic complaint of dry mouth can reduce the ability to communicate, predispose to malnutrition, promote mucosal damage, denture misfit or dental caries, and increase the risk of serious respiratory infection secondary to loss of antimicrobial activity of saliva. Mydriasis and the inability to accommodate will impair near vision and may precipitate narrow angle glaucoma in predisposed patients, but less obviously could lead to an increased risk of accidents, including falls. Somatic complaints of constipation and urinary hesitancy, could, in the presence of anticholinergic challenge, result in faecal impaction or urinary retention. Cardiac effects may be poorly tolerated. Increases in heart rate may precipitate or worsen angina. Finally, thermoregulatory impairment induced by anticholinergics, which block the ability to sweat, may lead to life threatening hyperthermia. Central anticholinergic effects range from sedation, mild confusion and inability to concentration to frank delirium. Even mild effects can reduce function and increase dependency. At any level of care, the loss of independence increases the caregiver burden, costs, and most importantly, can negatively affect quality of life. Many age-related and disease-related conditions may predispose elderly patients to anticholinergic drug toxicity. Careful attention to anticholinergic effects when prescribing drugs, patient education, regular review of the entire drug regimen, and familiarity with the signs and symptoms of anticholinergic toxicity will help to reduce the risk of drug-induced problems.
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PMID:The problems of anticholinergic adverse effects in older patients. 836 93

The causes of Datura intoxication include medication overdose, misuse of edible vegetables, deliberate abuse as a hallucinogen, homicidal or robbery and accidental intoxication from contaminated food. We report an incident of 14 people with Datura intoxication caused by ingesting wild Datura suaveolans for food. The incubation period was 15 to 30 min. The symptoms/signs were dizziness, dry mouth, flushed skin, palpitation, nausea, drowsiness, tachycardia, blurred vision, mydriasis, hyperthermia, disorientation, vomiting, agitation, delirium, urine retention, hypertension and coma. Three patients were hospitalized for 2-3 days. Thirteen persons received supportive fluid therapy. One patient did not receive medical therapy, he induced vomiting and drank a lot of water. Four patients presented with delirium/coma and 3 received physostigmine therapy with good response. One patient was intubated because of coma and respiratory depression. Three persons needed Foley catheterization for urine retention or coma status. One patient had a complication of urinary tract infection and antibiotic management. All patients recovered with no sequelae.
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PMID:Poisoning by Datura leaves used as edible wild vegetables. 1043 80

We reviewed the side effects of antidepressants. Tricyclic antidepressants(TCAs) are associated with a higher frequency of adverse events than those of SSRIs and SNRIs, particularly with respect to anticholinergic-like effects(dry mouth, constipation, and blurred vision), delirium, and cardiovascular adverse events. On the other hand, SSRIs have some special side effects that include nausea, sexual dysfunction, and extrapyramidal symptoms. With regard to milnacipran, a member of the SNRI family, dysuria occurs at a higher frequency than with TCAs or SSRIs. When side effects occur, clinicians give patients symptomatic treatment or substitute the drugs that cause the adverse effects with other antidepressants that have different pharmacological effects.
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PMID:[Side effects and its countermeasures of antidepressant]. 1151 54

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43

Black henbane (BH) or Hyoscyamus niger, has been used as a medicine since last centuries and has been described in all traditional medicines. It applies as a herbal medicine, but may induce intoxication accidentally or intentionally. All part of BH including leaves, seeds and roots contain some alkaloids such as Hyoscyamine, Atropine, Tropane and Scopolamine. BH has pharmacological effects like bronchodilating, antisecretory, urinary bladder relaxant, spasmolytic, hypnotic, hallucinogenic, pupil dilating, sedative and anti-diarrheal properties. Clinical manifestations of acute BH poisoning are very wide which include mydriasis, tachycardia, arrhythmia, agitation, convulsion and coma, dry mouth, thirst, slurred speech, difficulty speaking, dysphagia, warm flushed skin, pyrexia, nausea, vomiting, headache, blurred vision and photophobia, urinary retention, distension of the bladder, drowsiness, hyper reflexia, auditory, visual or tactile hallucinations, confusion, disorientation, delirium, aggressiveness, and combative behavior. The main treatment of BH intoxicated patients is supportive therapies including gastric emptying (not by Ipecac), administration of activated charcoal and benzodiazepines. Health care providers and physicians particularly emergency physicians and clinical toxicologists should know the nature, medical uses, clinical features, diagnosis and management of BH poisoning.
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PMID:Black henbane and its toxicity - a descriptive review. 2538 92

The use of medication with anticholinergic properties is widespread among older subjects. Many drugs of common use such as antispasmodics, bronchodilators, antiarrhythmics, antihistamines, anti-hypertensive drugs, antiparkinson agents, skeletal muscle relaxants, and psychotropic drugs have been demonstrated to have an anticholinergic activity. The most frequent adverse effects are dry mouth, nausea, vomiting, constipation, abdominal pain, urinary retention, blurred vision, tachycardia and neurologic impairment such as confusion, agitation and coma. A growing evidence from experimental studies and clinical observations suggests that drugs with anticholinergic properties can cause physical and mental impairment in the elderly population. However, the morbidity and management issues associated with unwanted anticholinergic activity are underestimated and frequently overlooked. Moreover, their possible relation with specific negative outcome in the elderly population is still not firmly established. The aim of the present review was to evaluate the relationship between the use of drugs with anticholinergic activity and negative outcomes in older persons. We searched PubMed and Cochrane combining the search terms "anticholinergic", "delirium", "cognitive impairment", "falls", "mortality" and "discontinuation". Medicines with anticholinergic properties may increase the risks of functional and cognitive decline, morbidity, institutionalization and mortality in older people. However, such evidences are still not conclusive probably due to possible confounding factors. In particular, more studies are needed to investigate the effects of discontinuation of drug with anticholinergic properties. Overall, minimizing anticholinergic burden should always be encouraged in clinical practice to improve short-term memory, confusion and delirium, quality of life and daily functioning.
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PMID:Anticholinergic drugs and negative outcomes in the older population: from biological plausibility to clinical evidence. 2593 85

Use of medications with anticholinergic activity is widespread in older adults. Several studies have highlighted that anticholinergic use may be associated with an increased risk of dementia. The objective of this narrative review is to describe and evaluate studies of anticholinergic medication use and dementia and provide practical suggestions for avoiding use of these medications in older adults. A comprehensive review of the literature, citations from recent reviews and the author's personal files was conducted. Four studies were found that evaluated anticholinergic use and dementia as the primary outcome. Three studies focused on overall anticholinergic medication use and reported a statistically significantly increased risk of Alzheimer's disease or dementia. In one study, dementia risk was primarily found with higher cumulative doses; people using anticholinergic medications at the minimum effective dose recommended for older adults for at least 3 years were at highest risk. In contrast, a study conducted in nursing-home residents with depression did not find that paroxetine [a highly anticholinergic selective serotonin reuptake inhibitor antidepressant, (SSRI)] increased risk for dementia compared with other SSRIs (without anticholinergic activity). Further study is needed to understand the mechanism by which anticholinergic medications may increase risk. In conclusion, there is evidence from three observational studies suggesting that anticholinergic medications may increase dementia risk. Given this potential risk and the myriad of other well-known adverse effects (i.e. constipation, blurred vision, urinary retention, and delirium) associated with anticholinergic medications, it is prudent for prescribers and older adults to minimize use of these medications and consider alternatives when possible.
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PMID:Anticholinergic medication use and dementia: latest evidence and clinical implications. 2769 23


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