Pathology - Diabetes Insipidus
Diabetes Insipidus Central diabetes insipidus is characterized by a lack of ADH secretion from the posterior pituitary. It can be either idiopathic or result from damage to the hypothalamus, such as from neoplastic or traumatic causes, or histiocytosis. Nephrogenic diabetes insipidus is characterized by faulty ADH receptors in the kidney. It can be caused by hereditary deficiency, certain medicines (such as lithium and demeclocycline), hypercalcemia, or tubulointerstitial renal disease. Insufficient ADH or the kidney's inability to detect ADH leads to the inability to retain water, causing excessive urine production. Insufficient water retention causes a rise in serum osmolality, triggering the activation of thirst receptors in the brain and the posterior pituitary gland to secrete additional ADH. Clinical Symptoms and Signs Symptoms include excessive thirst and urination, seizures, headaches, and indications of dehydration. Laboratory results: Elevated serum osmolality, high levels of sodium in the blood, and reduced urine specific gravity. Desmopressin treatment for central diabetic insipidus. Low-sodium diet and thiazide diuretic prescribed for nephrogenic diabetic insipidus.
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