Monday, April 07, 2025
ADH is stored and released by the posterior pituitary gland. Imbalances can occur and will be treated with pituitary agents along with other drug therapy to manage the associated symptoms and lab abnormalities. For NCLEX, it is important to remember that any insult to the head can result in an imbalance. Surgery on the gland may also be implicated.
Diabetes insipidus (DI) is a deficit of ADH and is a form of hypopituitarism. When there is a deficit, urine output will increase.
SIADH is a surplus of ADH and a form of hyperpituitarism. When there is an excess, urine output will decrease.
“Memory Hints” for the imbalances in ADH include “ADH: Don’t void”; “DI is a Deficit of ADH → ↑ Urine and Dehydration” and “SIADH is a Surplus of ADH → ↓ Urine and Sodium imbalance.”
Diabetes insipidus (DI) is a deficiency of ADH which may be lifelong and includes the neurogenic or nephrogenic (seen infrequently) types. Secondary DI is the most common type and is caused by any insult to the head and is a complication of pituitary surgery.
The surgery is known as a transsphenoidal hypophysectomy and is used to remove a tumor in the brain or the anterior lobe of the pituitary gland. It may be performed via a sublabial (under the lip) or transnasal (through the nose) approach.
DI is a Deficit of ADH leading to a profound increase in urinary output and resultant dehydration. Lab effects include an increase in Na+, urine specific gravity, and serum osmolarity due to the dehydration. K+ will be low due to the high urinary output.
Treatment for DI is the administration of desmopressin (DDAVP) or vasopressin (Pitressin). Weight is monitored to determine the effectiveness of the drugs and there is a risk for water intoxication when the medications are first started, especially if the dose is too high (too much ADH).
Syndrome of inappropriate ADH (SIADH) is a surplus of ADH which may be a rare neurogenic type. If it is secondary, it is primarily caused by brain issues.
SIADH is a Surplus of ADH resulting in fluid retention (water intoxication), cerebral edema, and dilutional hyponatremia. Clinical manifestations are due to the hyponatremia leading to a change in mental status. Lab effects include a decrease in Na+, K+, and serum osmolarity due to the dilution. Serum sodium level around 110 mEq/L can lead to seizures, coma, and death. Urine specific gravity will be high due to the low urinary output.
Treatment for SIADH includes fluid restriction of 800-1,000 mL per day, diuretics such as furosemide (Lasix) as initial therapy, and 3% hypertonic saline cautiously to increase serum sodium level. Long-term drug therapy may also be considered using tolvaptan (Samsca) which is a vasopressin receptor agonists.
• ADH: Don’t void.
• DI is a Deficit of ADH → ↑ Urine and Dehydration → Treated with DDAVP
• SIADH is a Surplus of ADH → ↓ Urine and Sodium imbalance (↓ Na+)
• Any insult to the head can result in DI or SIADH.
In preparing for the NCLEX exam, it is important to remember that ADH balance may be due to any insult to the head or related to a problem with the pituitary, including surgery on the gland. DI is a Deficit in ADH and results in low urine output and hypernatremia. It is primarily treated with DDAVP. SIADH is a Surplus in ADH and results in a low dilutional Sodium level which can be fatal.
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