Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14-year-old boy was seen because of irritability, insomnia, lethargy, and profuse sweating, together with hypertension (blood pressure: 160/120 mm Hg), tachycardia, and a diffuse erythematous rash with desquamation of the palms and soles. Initial biochemical investigation suggested a diagnosis of pheochromocytoma, but subsequently a history of exposure to mercury vapor was obtained. This case emphasizes the clinical and biochemical similarities between mercury poisoning (acrodynia) and pheochromocytoma.
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PMID:Acute mercury poisoning (acrodynia) mimicking pheochromocytoma in an adolescent. 841 May 28

Seventy-nine patients admitted in the neurological Intensive care unit because of severe disturbances of consciousness has been evaluated. Protocol based on previous experiences in evaluation of unconsciousness patients was used. Forty-four patients died and thirty-five survived. In 46 patients cause of illness was intracerebral hemorrhage. In 44 of them the cause of hemorrhage was arterial hypertension and in two of them rupture of a-v malformation. The majority of patients actually 41 of them showed hemispheral localization of intracerebral hematoma and five subtentorial. Pontien hemorrhages was found in three and cerebellar in two patients. In majority of 24 patients with hemispheral localization of intracerebral hematoma who showed progressive deterioration of consciousness the signs of descendent transtentorial herniation were found. The symptoms of uncal herniation were rare. In three patients with subtentorial localization of intracerebral hematoma who died signs of upward transtentorial herniation were observed. In 16 patients with ischemic cerebrovascular accident who showed disturbances of the consciousness at the admittance or soon after, nine patients died and seven survived. The cause of their condition were great hemispheral, smaller brain stem ischemic lesion, or deterioration of consciousness was related to the somatic illness. Patients with great ischemic lesions showed similar course of consciousness deterioration as it was observed in patients with hemispherical intracerebral hematomas with difference that biphasic course of illness characterized with temporary stagnation or even slight improvement of patients condition and than secondary progression of deterioration was seen only in patients with intracerebral hematoma, probably because of secondary ischemic complications. Ten patients were admitted because of subarachnoidal and two of them because of intraventricular hemorrhage. Six of them died and four survived. These patients has rupture of great sacular aneurysm with fast development of high intracranial pressure. In two of them the cause of death was rerupture of aneurysm. Stuporous patient with hemispheral neoplasm showed development of descendent transtentorial herniation which was stopped by anti oedematous and corticosteroid therapy. Comatose patient with brisk response on oculocephalic stimulation and normal papillary light reflexes was suspected on intoxication rather than structural brain lesion. He recovered by diuretics and forced rehydratation. After becoming conscious barbiturate intoxication was confirmed. Three patients were admitted in coma because of poisoning with CO, two patients died. Two patients admitted in epileptic status showed late diencephalic state of coma and they survived after anti epileptics and antioedematous treatment.
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PMID:[Disorders of consciousness as a manifestation of neurologic disease]. 864 54

A study was undertaken to provide further information on the ruminal, cardiorespiratory and hypothalamo-pituitary-adrenocortical (HPAC) physiological sequelae of hypocalcaemia in dairy calves. The functional picture observed in standing calves experiencing Na2EDTA-induced progressive hypocalcaemia showed a biphasic pattern. During the first phase (Ca2+ varying between 1.20 +/- 0.09 and 0.64 +/- 0.15 mmol/L, mean +/- SD), the animals became dull and lethargic, shifting their weight from one hind limb to the other, with cool extremities and hypersalivation. Their ventilation was slightly increased but their heart rate, thoracoabdominal pressure, pulmonary mechanics, haemoglobin and temperature remained constant. Conversely, their systemic arterial pressure (SAP) and the amplitude of their ruminal contractions (RCA) were severely decreased. During the second phase (Ca2+ < 0.64 +/- 0.15 mmol/L), there was restlessness, tachycardia, hypertension, polycythaemia and, finally, inability to stay upright. It is suggested that the diminished Ca2+ availability caused smooth-muscle and myocardial dysfunctions which could explain the RCA and SAP changes recorded during the first phase, whereas neural and/or humoral sympathetic discharge probably accounted for the reversal in SAP and heart rate when Ca2+ was decreased further. Serum cortisol increased regularly and remained significantly correlated with Ca2+ in each animal. Moreover, regression of delta cortisol/delta Ca2+ on delta Ca2+/delta Na2EDTA was significant (p < or = 0.001). It was concluded that mild asymptomatic hypocalcaemia severely impairs ruminal function, which will progressively worsen the Ca2+ deficit; that the inability to maintain posture in hypocalcaemia is not due to hypotension; and that the higher the HPAC response to hypocalcaemia, the higher the resistance to its effects. An asymptomatic periparturient cow with barely detectable ruminal activity may merit preventive calcium borogluconate therapy. Also, the physiological role of hypotension in explaining the clinical picture may be less important than other processes, such as neuromuscular failure. Finally, the present results imply a possible HPAC exhaustion in cows with periparturient paretic hypocalcaemia.
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PMID:Ruminal, cardiorespiratory and adrenocortical sequelae of Na2EDTA-induced hypocalcaemia in calves. 869 1

Cyclobenzaprine (CBP) has a cyclic structure similar to amitriptyline. In overdose, CBP has been suggested to produce the cardiovascular and neurologic toxicity found with the cyclic antidepressants. To examine this possibility, a retrospective chart review of all cases of CBP exposure reported to five regional poison centers was performed for the years 1989-93. There were a total of 750 charts identified for CBP exposure, of which 523 had data sufficient for evaluation. There were 121 polydrug ingestions leaving 402 pure CBP ingestions. Ages ranged from 7 mo to 77 yrs, with a mean of 20 yrs; 26% were 6 yrs or less. Females comprised 63% of the patient group. No deaths occurred. Dysrhythmias beyond sinus tachycardia were infrequent, and none were life-threatening. No seizures occurred. Common effects were lethargy, sinus tachycardia, and agitation, and both hypertension and hypotension were seen. All symptomatic cases with a known time of ingestion were symptomatic within 4 h of ingestion. Doses ingested ranged from 5-1000 mg, with a mean of 133 mg. Asymptomatic and symptomatic patients had a mean dose ingested of 45 mg and 183 mg, respectively. Treatment was primarily gastrointestinal (GI) decontamination and supportive care. Other therapies required were mechanical ventilation, dopamine, fluid bolus, sedation, and foley catheter. Symptoms requiring treatment beyond GI decontamination did not occur with ingestions less than 100 mg. In conclusion, cyclobenzaprine does not appear to produce the life-threatening cardiovascular or neurologic effects of the cyclic antidepressants in doses less than 1 g. Lethargy and anticholinergic effects are prominent, though serious toxicity is infrequent.
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PMID:Five-year multicenter retrospective review of cyclobenzaprine toxicity. 874 27

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99

A boy presented with hypertension, seizures, lethargy, headache, and occipital blindness. He improved with antihypertensive therapy. Other reported children with a similar distinctive clinical condition are compared with adults with a syndrome termed reversible posterior leukoencephalopathy. Because both gray and white matter are involved, we suggest that the name be changed to occipital-parietal encephalopathy syndrome.
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PMID:Occipital-parietal encephalopathy: a new name for an old syndrome. 930 87

5 cases with obesity-hypoventilaion syndrome were reported. The clinical manifestations were obesity, palpitation, dyspnea, lethargy, cyanosis, distention of cervical vein, edema, enlargement of liver and hypertension. All of them were initially diagnosed as chronic bronchitis or heart diseases. Pulmonary function test showed restrictive ventilative defect and hypercapnia with hypoxemia. Mouth oclusion pressure at 0.1 second was higher than the normal value. The response to CO2 was decreased. Hypertrophy of right heart was shown in ECG and X-ray film improvement in symptoms and blood gases analyses were found to be associated with body weight decrease in a follow up period of one year.
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PMID:[Obesity-hypoventilation syndrome]. 927 46

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

Children with hypertension, seizures, lethargy, encephalopathy, headache, and occipital blindness are reviewed. After undergoing antihypertensive therapy, most children improve. Some patients have a similar syndrome associated with chemotherapy, transplantation, transfusion, or human immunodeficiency virus-1 (HIV-1) infection. These latter children can develop symptoms with only minimal or no discernible elevations in blood pressure and improve, in the case of cancer-associated encephalopathy, after discontinuing chemotherapy. The reported children with this distinctive clinical condition are compared to adults with reversible posterior leukoencephalopathy syndrome. Since both gray and white matter are involved, we had suggested previously that the name be changed to (reversible) occipitoparietal encephalopathy syndrome. However, reversible posterior leukoencephalopathy has been used in the adult population and probably should be employed in children for the sake of uniformity, since both children and adults have the same clinical presentation and presumably a similar pathophysiology for the encephalopathy syndrome. The diagnosis is confirmed by reversible posterior abnormalities seen on T2-weighted brain magnetic resonance imaging, and by the presence of either headache, altered mental status, seizures, or visual disturbances.
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PMID:Hypertensive encephalopathy, reversible occipitoparietal encephalopathy, or reversible posterior leukoencephalopathy: three names for an old syndrome. 1034 93

Chronic severe subclinical systemic hypertension was diagnosed in a 28-yr-old male western lowland gorilla (Gorilla gorilla gorilla). Thoracic radiography, electrocardiography, and echocardiography revealed an enlarged heart with a hypertrophied left ventricle, mitral regurgitation, and a persistent left bundle branch block. Enalapril, later combined with nifedipine, was of some value in reducing the hypertension, with partial reversal of cardiac enlargement and resolution of the bundle branch block. Two years after initiation of treatment, the gorilla developed lethargy and dyspnea. The diagnosis of heart failure was confirmed under anesthesia; the gorilla did not recover and was euthanized. Postmortem examination confirmed congestive heart failure with chronic, fibrosing cardiomyopathy similar to that in other gorillas.
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PMID:Chronic hypertension with subsequent congestive heart failure in a western lowland gorilla (Gorilla gorilla gorilla). 1048 43


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