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Diabetes insipidus centralis

From WikiLectures

Diabetes insipidus centralis is a disease caused by a deficiency of ADH (vasopressin).

Lack of hormone in the body manifests itself polyurii and large fluid loss leads to polydipsii.

The cause of the disease may be the involvement of the hypothalamic nuclei producing ADH, a disorder neurohypophysis and the transport of ADH into the bloodstream.

Etiology[edit | edit source]

Insufficient ADH production can be caused by various mechanisms

  • Congenital disorders and genetic defects in hormone production.
  • Hypothalamic-pituitary tumors, most commonly craniopharyngeal, pituitary adenoma, meningioma.
  • Autoimmune affects the hypothalamus and destroys the nuclei that produce the hormone.
  • Trauma or other mechanical involvement of the hypothalamus or pituitary gland.
  • Inflammation.
  • Vascular lesions, hemorrhage.
  • Iatrogenic disability.
  • Diabetes insipidus centralis is up to 45% idiopathic.

Clinical symptoms[edit | edit source]

  • Hypotonic urinary polyuria can vary widely, from slightly elevated (3 l / day) to marked (15 l / day).
  • Also, polydipsia is individual in patients. The feeling of thirst may or may not be maintained.
  • When thirst is broken, the patient does not compensate for fluid loss by adequate intake and Dehydration occurs, which can be fatal.

Diagnostics[edit | edit source]

A patient with diuresis greater than 2.5 liters, with a finding of hypotonic urine, hypernatremia and serum hyperosmolality should be examined. . However, if the patient compensates for the loss with higher intakes, serum osmolality and sodium levels may be normal. Then we proceed to the concentration test. The patient thirsts for 36 hours and diuresis, serum and urine osmolality are monitored every hour. The patient must be closely monitored and when the weight is reduced by more than 3%, the test is stopped to avoid dehydration. If the patient is unable to concentrate the urine, serum osmolality increases and polyuria persists, the test is positive. To distinguish the central form of diabetes insipidus from renal, we give at the end of the test [[desmopressin] (synthetic analogue of ADH). Renal diabetes insipidus does not respond to desmopressin administration and the condition does not improve. As an additional examination, MRI of the hypothalamic-pituitary region is performed to clarify the etiology.

Treatment[edit | edit source]

We use desmopressin as a substitute for ADH. Doses should be carefully titrated due to serum osmolality and sodium.




Links[edit | edit source]

Related articles[edit | edit source]

References[edit | edit source]

Diabetes insipidus centralis is a disease caused by a deficiency of ADH (vasopressin).

Lack of hormone in the body manifests itself polyurii and large fluid loss leads to polydipsii.

The cause of the disease may be the involvement of the hypothalamic nuclei producing ADH, a disorder neurohypophysis and the transport of ADH into the bloodstream.

Etiology

Insufficient ADH production can be caused by various mechanisms

  • Congenital disorders and genetic defects in hormone production.

  • Hypothalamic-pituitary tumors, most commonly craniopharyngeal, pituitary adenoma, meningioma.

  • Autoimmune affects the hypothalamus and destroys the nuclei that produce the hormone.

  • Trauma or other mechanical involvement of the hypothalamus or pituitary gland.

  • Inflammation.

  • Vascular lesions, hemorrhage.

  • Iatrogenic disability.

  • Diabetes insipidus centralis is up to 45% idiopathic.

Clinical symptoms

  • Hypotonic urinary polyuria can vary widely, from slightly elevated (3 l / day) to marked (15 l / day).

  • Also, polydipsia is individual in patients. The feeling of thirst may or may not be maintained.

  • When thirst is broken, the patient does not compensate for fluid loss by adequate intake and Dehydration occurs, which can be fatal.

Diagnostics

A patient with diuresis greater than 2.5 liters, with a finding of hypotonic urine, hypernatremia and serum hyperosmolality should be examined. . However, if the patient compensates for the loss with higher intakes, serum osmolality and sodium levels may be normal.↵Then we proceed to the concentration test. The patient thirsts for 36 hours and diuresis, serum and urine osmolality are monitored every hour. The patient must be closely monitored and when the weight is reduced by more than 3%, the test is stopped to avoid dehydration. If the patient is unable to concentrate the urine, serum osmolality increases and polyuria persists, the test is positive.↵To distinguish the central form of diabetes insipidus from renal, we give at the end of the test [[desmopressin] (synthetic analogue of ADH). Renal diabetes insipidus does not respond to desmopressin administration and the condition does not improve.↵As an additional examination, MRI of the hypothalamic-pituitary region is performed to clarify the etiology.

Treatment

We use desmopressin as a substitute for ADH. Doses should be carefully titrated due to serum osmolality and sodium.

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References