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

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
 ...
PMID:Human physiology under cold exposure. 181 74

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
 ...
PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47