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Query: UMLS:C0085584 (encephalopathy)
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The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.
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PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.
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PMID:Antacid therapy--changes in mineral metabolism. 629 43

Electrolyte and acid-base disturbances are common occurrences in daily clinical practice. Although these abnormalities can be readily ascertained from routine laboratory findings, only specific clinical correlates may attest as to their significance. Among a wide phenotypic spectrum, acute electrolyte and acid-base disturbances may affect the peripheral nervous system as arreflexic weakness (hypermagnesemia, hyperkalemia, and hypophosphatemia), the central nervous system as epileptic encephalopathies (hypomagnesemia, dysnatremias, and hypocalcemia), or both as a mixture of encephalopathy and weakness or paresthesias (hypocalcemia, alkalosis). Disabling complications may develop not only when these derangements are overlooked and left untreated (e.g., visual loss from intracranial hypertension in respiratory or metabolic acidosis; quadriplegia with respiratory insufficiency in hypermagnesemia) but also when they are inappropriately managed (e.g., central pontine myelinolisis when rapidly correcting hyponatremia; cardiac arrhythmias when aggressively correcting hypo- or hyperkalemia). Therefore prompt identification of the specific neurometabolic syndromes is critical to correct the causative electrolyte or acid-base disturbances and prevent permanent central or peripheral nervous system injury. This chapter reviews the pathophysiology, clinical investigations, clinical phenotypes, and current management strategies in disorders resulting from alterations in the plasma concentration of sodium, potassium, calcium, magnesium, and phosphorus as well as from acidemia and alkalemia.
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PMID:Neurologic complications of electrolyte disturbances and acid-base balance. 2436 6