Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Salt wasting syndrome is caused by a congenital or acquired synthesis disorder or by the aldosterone function disorder. It manifests itself by ionic disorders where the sodium and chlorine level decrease with the simultaneous potassium retention. Synthesised aldosterone is in the glomerular zone of the adrenal cortex. Symptoms of dyselectrolitemia are not distinctive, they develop within a few first days of life. The suction aversion, apathy, lack of growth or progressing, body mass loss is being noticed. The most often cause of salt wasting syndrome is the congenital cortical adrenal hyperplasia (CAH) caused by 21-hydroxylase enzyme deficit. The classic form with and without salt wasting (SW), as well as non-classic form is distinguished. The therapy of SW form depends on Hydrocortisone and Cortineff administering. The other forms of salt wasting syndrome occur not so often and these are: aldosterone synthesis deficit, dehydrogenase 3beta-hydroxysteroid deficit, lipoid cortical hyperplasia, adrenal hypoplasia congenital (AHC), adrenoleukodystrophy and pseudohypoaldosteronism. The knowledge of the symptoms and causes of salt wasting syndrome allows for the proper therapeutic management and contributes to the regular psychophysical infantile development of the children.
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PMID:[Salt wasting syndrome caused by congenital, insufficient synthesis or aldosterone function--etiology, diagnosis and management]. 1599 40

Frontal-subcortical dementias are a heterogeneous group of disorders that share primary pathology in subcortical structure and a characteristic pattern of neuropsychologic impairment. Their clinical presentation is characterized by memory disorders, an impaired ability to manipulate acquired knowledge, important changes of personality (apathy, inertia, or depression), and slowed thought processes (or bradyphrenia). It also has marked frontal dysfunction. Classic frontal-subcortical dementias include Huntington chorea, Parkinson disease dementia, progressive supranuclear palsy, thalamic degeneration, subcortical vascular dementia, multiple sclerosis, the acquired immunodeficiency syndrome dementia complex, depressive pseudodementia, and some other rare dementias like spinocerebellar degenerative syndromes, Hallervorden-Spatz disease, choreoacanthocytosis, idiopathic basal ganglia calcification, Guamanian parkinsonism-dementia complex, corticobasal degeneration multiple system atrophy, Wilson disease, metachromatic leukodystrophy, adrenoleukodystrophy, hypoparathyroidism, sarcoidosis, and other CNS inflammatory disorders. Anatomic data suggest that the frontal signs result from a disconnection of the frontal cortex from the basal ganglia. However, most frontal-subcortical dementias show cortical atrophy in later stages, and cortical dementias have subcortical pathology at some point. In fact, the concept might be seen as a continuum, and only the 2 extremes would be represented by pure cortical or subcortical pathology. Anyway, subcortical disorders may still be more similar to one another than they are to AD. Possibly, frontal-subcortical and cortical dementias are the description of the prior main target of the disease process, ending up in both cases in a global dementia. Although the dichotomy cortical versus frontal-subcortical dementia is not strict, the 2 concepts still seem to have advantages.
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PMID:Frontal-subcortical dementias. 1833 39