Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

Ranitidine was first marketed in 1981; since then many patients have been treated such that much experience has been accumulated on the safety of this histamine H2-receptor antagonist in the treatment of gastroduodenal disease. A wide array of ranitidine-associated side effects has been described, but infrequently. As so much information is now available, the aim of this review is to assess the weight of evidence for a causal link between ranitidine and the reported side effects. Overall, ranitidine is well tolerated. The incidence of general side effects at less than 2% is very similar to placebo. Headaches, tiredness, dizziness and mild gastrointestinal disturbance (e.g. diarrhoea, constipation and nausea) are among the most frequent complaints, but have very seldom resulted in stopping treatment. Cardiovascular side effects are extremely rare and unpredictable with the usual doses of oral ranitidine (at most 1 in 1 million patients). They mostly comprise sinusal bradycardia and atrioventricular blockade, especially after rapid intravenous administration, receding after cessation of the drug. Clinical studies, however, have not shown a significant pharmacological effect of ranitidine on the cardiovascular system via H2-receptors, even though individual sensitivities cannot be ruled out in a few isolated reports. Ranitidine is unlikely to be directly hepatotoxic: a transient change in liver function tests has been noted in only 1 in 100 to 1 in 1000 patients. Several cases of mixed hepatitis have been reported, but very few were fully documented. The incidence of ranitidine-associated acute hepatitis has been estimated to be less than 1 in 100,000 patients. Neuropsychiatric complications may be less common and clinically quite similar to those reported with cimetidine, i.e. confusion, disorientation, hallucinations, delirium. These side effects have occurred especially in critically ill and multiple-therapy patients, or patients with chronic renal or hepatic failure, so that the direct causal link with ranitidine treatment was often difficult to ascertain. Even though an H2-receptor-mediated effect is an attractive hypothesis (since similar complications were noted with other H2-receptor antagonists), other mechanisms have been suggested to play a role, e.g. cholinergic or histaminic effects. The overall incidence of neuropsychiatric complications is probably markedly less than 1%. White cell injury (i.e. agranulocytosis) appears to be the most frequent haematological complication, even though case reports are very few and poorly documented.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Side effects of ranitidine. 204 87

Alterations of consciousness with impaired perception and drive persisting over hours to days can be due to a nonconvulsive status epilepticus. This possibility has to be considered not only in patients with already known epilepsy, but also in those with a negative history for seizure disorders. The immediately recorded electroencephalogram (EEG) provides decisive clues. In the case of petit mal status most frequently appear tiredness, reduced vigilance and lack of drive. The EEG shows a generalized spike-wave activity. In status psychomotoricus, the clinical symptomatology varies from case to case. It can be characterized by anxiety, dreamy states or productive-psychotic states with agitation, automatisms and hallucinations. In the EEG a temporal or temporally-accentuated epileptic activity will be recorded. Transitional and mixed forms of petit mal status and status psychomotoricus can also be found. I.v. injections of benzodiazepines (clonazepam, diazepam) are an appropriate therapy for any type of nonconvulsive status epilepticus. Phenytoin is indicated in status psychomotoricus, but contra-indicated in the case of petit mal status.
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PMID:[Epileptic impaired consciousness in adults]. 250 9

beta-Adrenoreceptor antagonists are liable to produce behavioural side-effects such as drowsiness, fatigue, lethargy, sleep disorders, nightmares, depressive moods, and hallucinations. These undesirable actions indicate that beta-blockers affect not only peripheral autonomic activity but also some central nervous mechanisms. In experimental animals beta-blockers have been found to reduce spontaneous motor activity, to counteract isolation-, lesion-, stimulation- and amphetamine-induced hyperactivity, and to produce slow-wave and paradoxical sleep disturbances. Furthermore, central effects such as tranquilizing influences are used for the treatment of conditions such as anxiety. Several different mechanisms of action could be responsible for these CNS effects: Centrally mediated specific actions on centrally located beta-adrenergic receptors, known to exist downstream from, and at the terminals of, 'vigilance-enhancing' central noradrenergic pathways. Centrally mediated specific actions on centrally located receptors of the non-adrenergic type; an affinity of some beta-blockers towards 5-HT-receptors is well documented. Centrally mediated non-specific actions on centrally located neurones, owing to the membrane-stabilizing effects of beta-blockers. Peripherally mediated actions whereby beta-blockers induce changes in the autonomic activity in the periphery, which are relayed to the CNS to induce changes in activity of a variety of central systems. It can be assumed that with any one of the beta-blockers all these mechanisms come into play, yet with varying degrees depending on characteristics of the drugs such as lipophilicity and hydrophilicity, the ratio of antagonist versus (partial) agonist properties, affinity to 'alien' receptor sites, strength of membrane-stabilizing activity, stereospecific affinity, and potency.
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PMID:CNS-related (side-)effects of beta-blockers with special reference to mechanisms of action. 286 51

The overall effect of zotepine was a "slightly improved" or better response in 20 patients (64.5%), "unchanged" in 10 (32.3%) and "worsened" in 1 (3.2%). Zotepine exhibited some degree of improvement in 54.5% of patients unresponsive to prior drugs. The onset of effect of zotepine was within one month in 19 patients. The improvement rate in the hebephrenic type (66.7%) was almost the same as in the paranoid type. The improvement rate classified by psychopathology was highest for hypobulia, followed by restlessness-excitement and hallucination, depressive mood, hypochondria and delusion. The side-effects were subjective complaints, such as general fatigue, dryness of mouth, sleepiness or fainting in a small number of cases. There was a slight increase in S-GPT in one patient and a slightly increased blood platelet count, also in one patient. Serial EEG changes associated with zotepine studied in another 17 chronic schizophrenics could be classified into three groups: those with increased slow waves, those with enhanced alpha waves and those with unchanged EEGs. There was a positive correlation between the incidence of slow waves and higher plasma levels of zotepine.
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PMID:Clinical and EEG studies of zotepine, a thiepine neuroleptic, on schizophrenic patients. 288 87

Consequent to rapidly declining mortality and birth rates, developing countries, including Malaysia, can expect a rapid increase in the population aged 60 years and above. The health of the elderly is intimately tied up with both biophysical as well as psychosocial factors which include status loss, loneliness, fear of illness and death, poverty, harmful life-styles and deterioration of the quality of life. The effects of these psychosocial factors can manifest as sleep difficulties, worry and anxiety, depression, loss of interest, and a feeling of tiredness. In extreme cases, there may be auditory or visual hallucinations or paranoia. In the present paper, which is based upon a WHO sponsored study of 1001 elderly Malaysians, it is noted that 36% of the elderly have sleep difficulties, 47% "feel tired", 31% have a "loss of interest" and 22% are "worried tense". However 71% of the elderly are able to correctly perform at least 12 of 15 cognitive tests. 20% of elderly men smoke 15 or more cigarettes a day while 44% smoke at least one cigarette a day. 40% of elderly men indicate that their families complain about the amount of alcohol they drink. Undoubtedly primary health care programmes need to be re-oriented to the problems and needs of the elderly in countries such as Malaysia.
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PMID:Psychosocial factors and the health of the elderly Malaysian. 359 76

Since the introduction of ophthalmic timolol solution in 1978 there have been numerous reports of systemic toxicity associated with its use. The majority of the systemic side effects reported are the same as those associated with oral timolol. Several cases of respiratory distress have been described generally in patients with underlying restrictive airway disease. Cardiovascular effects range from effects on resting pulse rate to the development of overt bradycardia and heart failure. Central nervous system effects reported include fatigue, confusion, depression, and hallucinations. A variety of other systemic effects have also been described. Caution should be used when ophthalmic timolol is administered to elderly patients or those patients with contraindications to systemic beta-blockers.
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PMID:Systemic side effects associated with the ophthalmic administration of timolol. 388 77

Epidemics of epilepsy, a form of mass hysteria, were known in Eastern and Western cultures in the 17th and 18th centuries. A unique situation in the United States during the 19th centurey was the frontier religious movement, the setting in which the "jerks" occurred. The "falling exercise," "dancing exercise," "barking exercise," "laughing exercise," and the "running exercise" centered around the excitement involved in the religious revival. During some exercises, people saw "visions," and exhibited bizarre behavior and sudden jerking motions. During the summers of 1801-1803 on the Kentucky frontier, some pioneers who attended the religious revival camp meetings had convulsions, hallucinations, tremors, jerks, compulsive dancing and "epileptic trances." Although these have been assumed to be psychological in origin, the epidemiology of the symptoms may correlate with the diagnosis of ergotism. Those affected were usually children and young adults. Symptoms of ergotism include giddiness, fatigue, depression, formications, muscle twitching, tonic spasms, convulsions, delirium, and loss of speech.
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PMID:Ergot, the "jerks," and revivals. 636 76

A wide range of neuropsychiatric side effects are attributed to propranolol including visual hallucinations, somnulence, memory impairment, decrease in response time, dizziness, confusional states, insomnia, nightmares, fatigue, sedation and depression. Benson et al., in a summary review of several clinical studies of 5,846 patients being treated with a variety of beta adrenergic blocking agents, listed depression as a rare side effect of propranolol that was usually reported only after long term treatment at high doses. Despite the widely circulated attribution that depression is a side effect of propranolol, there is a paucity of evidence to directly link this drug with clinically significant mood disturbance. For example, the most widely quoted reference attributing propranolol as a depressogenic agent was a "letter to the editor" which was a retrospective, uncontrolled, unblinded study that did not use a standardized depression rating scale. Most of the evidence linking propranolol to depressive symptoms have derived from scattered case reports in which the onset of depressive symptoms were attributed to this agent. Given the well known cyclic onset and remissions of affective disorders, and the prevalence of depression in the general medical population as a whole, the role of propranolol in these cases is debatable.
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PMID:Propranolol and depression: a reevaluation based on a pilot clinical trial. 640 May 97

In summary, procainamide is a useful agent for suppressing premature depolarization frequency. Its short half-life of elimination requires a dosing frequency of every 3 hours with regular dosage forms or every 6-8 hours with a sustained action dosage. Because of the extreme unpredictability of plasma concentration, the dosage must be titrated in each patient with electrocardiographic monitoring serving as the most useful method of evaluating efficacy. Maximum and minimum plasma concentrations are helpful in monitoring the achievement of therapeutic plasma levels and adjusting the frequency of dosing, especially in the presence of impaired renal function or low cardiac output. Adverse effects of procainamide include anorexia, nausea, vomiting, fatigue, insomnia, visual hallucinations, and disorientation; these are minor and cease with discontinuation of the drug. Agranulocytosis has rarely been reported. Long-term treatment has resulted in the occurrence of a lupus-like syndrome that is reversible when the drug is stopped. Procainamide is excreted in breast milk and infants of mothers receiving procainamide should not be nursed.
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PMID:Pharmacokinetics of a sustained release procainamide preparation. 703 27


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