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Glucocorticoid deficiency absence of cortisol insufficient carbohydrate is formed from protein hypoglycemia and diminished liver glycogen result weakness follows. Resistance to infection, trauma, and other stress is diminished, myocardial weakness and dehydration can occur.
Glucocorticoid deficiency absence of cortisol insufficient carbohydrate is formed from protein hypoglycemia and diminished liver glycogen result weakness follows. Resistance to infection, trauma, and other stress is diminished, myocardial weakness and dehydration can occur.
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Glucocorticoid deficiency absence of cortisol insufficient carbohydrate is formed from protein hypoglycemia and diminished liver glycogen result weakness follows. Resistance to infection, trauma, and other stress is diminished, myocardial weakness and dehydration can occur.
Copyright:
Attribution Non-Commercial (BY-NC)
Formati disponibili
Scarica in formato PPTX, PDF, TXT o leggi online su Scribd
cortical hormones V utoimmune V Idiopathic atrophy V Removal of both adrenal organs V Infection of the adrenal organs V ddisonǯs disease V Tuberculosis and histoplasmosis Risk factors: autoimmune, idiopathic atrophy, removal of both adrenal glands, infection of the adrenal organ Glucocorticoid deficiency absence of cortisol insufficient carbohydrate is formed from protein hypoglycemia and diminished liver glycogen result Weakness follows; Resistance to infection, trauma, and other stress is diminished, myocardial weakness and dehydration, and circulatory failure can occur Risk factors Glucocorticoid deficiency Decreased blood cortisol results in increased pituitary TH production and increased blood Ⱦ-lipotropin Melanocyte- stimulating activity produces the hyperpigmentation of skin and mucous Risk factors Mineralocorticoid deficiency deficiency results in increased excretion of Na and decreased excretion of K low serum concentration of Na and a high concentration of K resullt Inability to concentrate the urine, combined with changes in electrolyte balance produce severe dehydration, plasma hypertonicity, acidosis, decreased circulatory volume, hypotension, and, eventually, circulatory collapse V Muscle weakness V norexia V Gastrointestinal symptoms (vomiting, diarrhea) V Fatigue V Emaciation V Dark pigmentation of the mucous membrane and the skin (especially of the knuckles, knees and elbows) V Hypotension V Low blood sugar V Low serum sodium V High serum potassium levels V Mental Status (depression, emotional ability, apathy and confusion) V hronic dehydration V ddisonian crisis develops (condition characterized by cyanosis and the classic signs of circulatory shock: pallor, apprehension, rapid and weak pulse, rapid respirations and low blood pressure) V Low Serum cortisol level- less than 165 nmol/L V Increased Plasma TH level- more than 22.0 pmol/L V Hypoglycemia V Hyponatremia V Hyperkalemia V Leukocytosis V Restoring blood circulation V dministering fluids and corticosteroids V Monitoring vital signs V Placing the patient in a recumbent position with the legs elevated V Hydrocortisone is administered intravenously, followed by 5%dextrose in normal saline. V ntibiotics may administered if infection has precipitated V If the adrenal gland does not regain function, the patient needs lifelong replacement of corticosteroids and mineralcorticoids to prevent recurrence of adrenal insuffiency. V Supplement dietary intake with added salt during gastrointestinal losses of fluids ssessing the patient V 1. Monitor blood pressure and pulse rate V 2. sses skin color, turgor and mucous membrane V 3. heck for weight changes, muscle weakness and fatigue Monitoring and Managing ddisonian risis V 1. void exposure to cold, overexertion, infection and emotional distress V 2. Requires immediate treatment with IV administration fluid, glucose and electrolytes, especially sodium V 3. Replacement of missing steroids and vasopressors Marilyn B. Monzon Susette G. Napoles A316