Diabetes insipidus

Refers to the excretion of large volume of hypotonic urine which is usually associated with polyuria and polydipsia.

Arginine vasopressin (AVP) deficiency.

Characterized by large amount of diluted urine, which is not reduced when fluid intake is reduced.

Differential diagnosis includes: inability of the hypothalamus to secrete vasopressin in response to serum osmolality, nephrogenic inability to respond to vasopressin, transient diabetes of pregnancy and primary polydipsia from thirst stimulation.

Differential diagnosis includes pituitary gland and hypothalamus lesions with possibilities including: benign tumors (pituitary adenomas), cancers, inflammatory Disorders and congenital abnormalities.

Hypothalamic diabetes insipidus associated with a low or unmeasurable levels of vasopressin.

Associated with ADH deficiency, with the inability of the kidney to resorb water properly from the urine.

May be related to head trauma, malignancies, and inflammatory disorders and surgery of the hypothalamus and pituitary.

Can arise spontaneously, in the absence of another disorder.

Urination occurs throughout day and night.

In children can lead to impaired food intake, decreased weight gain and slowing of growth.

Adults with untreated disease may be compensated for decades with adequate water intake.

When ADH deficiency is present it s referred to associated central diabetes insipidus.

Nephrogenic diabetes insipidus associated with a high level of plasma vasopressin.

Of pregnancy is caused by elevated levels of cystine aminopeptidase which inactivates vasopressin and makes it unmeasurable.

Generally does not cause hypernatremia as thirst prompts replacement of urinary losses of water.

In DI hypernatremia develops if water is unavailable, or the urge or ability to drink water is impaired.

From polydipsia causes large amounts of ingested water with low levels of vasopressin.

Diagnosis is considered when the urine osmolality is inappropriately low in the presence of an increased serum osmolality from increased serum sodium.

Urinary losses of urine can usually be compensated by drinking water, however patients who are bedridden, or have impaired mentation or otherwise limited may develop severe dehydration.

With urine output less than 4 to 6 liters/day and serum sodium less than 150 mEq/L, mild DI is managed conservatively.

Initial management includes oral fluid replacement.

However, in the event of unresolved DI, therapy is stepped up, ranging from fluid replacement with 5% dextrose to the administration of synthetic ADH analog, desmopressin.

Intranasal desmopressin is the drug of choice for chronic cases of DI.

Treatment uses the synthetic peptide desmopressin, a synthetic analogue of the natural hormone arginine vasopressin.

Desmopressin does not constrict smooth muscle and has a longer antidiuretic affect, then does the natural hormone arginine vasopressin.

Desmopressin lacks vasoconstrictor activity and can be used without precipitating angina, headaches, or abdominal cramps.

Desmopressin can be used during pregnancy, because it is not inactivated by the placenta.

For most patients, intranasal desmopressin is the treatment of choice.

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