2 Disorders of the Posterior Pituitary Diabetes Insipidus Syndrome of Inappropriate Antidiuretic Hormone (SAIDH). Posterior pituitary hormones are actually produced in the hyopthalamus and only stored in the posterior pituitary Posterior pituitary hormones Antidiuretic hormone (ADH)
Posterior pituitary hormones are actually produced in the hyopthalamus and only stored in the posterior pituitary
Posterior pituitary hormones
Antidiuretic hormone (ADH)
The hormones secreted by the posterior pituitary are
Antidiuretic hormone (ADH) (Also call vasopressin)
ADH contributes to fluid balance by
Controlling renal reabsorption of free water
It also has potent vasoconstrictive properties.
Antidiuretic hormone (ADH) (Also called vasopressin)
Disorders/diseases resulting from dysfunction
Excess: Syndrome of Inappropriate ADH secretion (SIADH)
Deficiency: Diabetes Insipidus
Posterior Pituitary Hypersecretion
SIADH occurs when there is too much vasopression (ADH) with inappropriate water retention and decreased blood Na levels
Results frommany different conditions and drugs
May be produced by certain tumors such as lung cancer or may result from chronic lung diseases. Medicines associated with SIADH include common meds as antidepressants, antianxiety agents, antipsychotic agents, seizure meds, and desmopressin (DDAVP)
Blood & Urine tests
low serum sodium
low plasma osmolality level
Inappropriated concentrated urine (increased urine osmolality level)
These tests indicate
excess of body water relative to the amount of body sodium.
In other words, ADH is inappropriately holding onto too much water.
Important to eliminateother causes of a low sodium level, such as hypothyroidism or adrenal insufficiency, before settling on a dx of SIADH
Rx- removing the offending drug or tumor, & treat the underlying condition.
Decreased plasma osmolality
Urine sodium and urine osmolality elevated
Elevated ADH levels++++++
Normal renal, adrenal, & thyroid functions
Headache,Personality change, Confusion,Irrritability, Dysarthria(difficult, poorly articulated speech), Lethargy,Impaired memory
Restless, weakness, fatigue, gait disturbances
Planning: Pt Goals
The primary goal is that the pt’s fluid balance will be restored
Interventions to treat SIADH (Pt Care Plan) consists of
Restriction water intake
Using diuretics to promote the excretion of water
Administering drugs that interfere with the action of ADH
Replacing lost sodium
Any excessive free water intake will further dilute the serum sodium concentration
Strict I&O, daily weights, guides the determination of the degree of fluid restriction necessary. A wt gain of 2 pounds (or 1 Kg) or more per day or a gradual increase during several days is cause for concern.
A 1 Kg weight increase is equivalent to 1000ml fluid retention (1Kg = 1 L)
Diuretics are sometimes used to treat pt with SIADH, to rid the body of excessive fluid, especially if CHF results from fluid overload
If diuretics are used, be aware of potential effect of electrolyte losses; sodium loss can be potentiated, which further contributes to the clinical picture of SIADH
Hypertonic saline (3% NaCl) may be used to treat SIADH
Helps correct serum sodium level
Raises Na osmolality in the blood
Removes excess intracellular fluid
Cells shrink in hypertonic solution
IV saline is given cautiously because it may contribute to the fluid overload already present & precipitate an episode of CHF.
If the pt needs routine IV fluids, the MD orders a solution in saline (5% dextrose in saline) rather than a solution in water.
High Risk for Injury
Monitor pt neuro status
Subtle Changes, such as muscle twitching before neuro S/S progress to seizures or coma. Check LOC to time, place, & person because disorientation may be present.
Confusion is another neuro sign. Nurse reduces environmental stimuli & explain interventions in simple terms.
Flow sheets contain ongoing info about LOC, motor & sensory neuro assessment, & pertinent lab data helpful in detecting trends.
Decreased LOC and seizures are complications of the low serum sodium level R/T SIADH
Thrist & polyuria 5 - 20L/day
SG < 1005
Urine osmol < 100 mmol/L
Se osmol > 295 mmol/kg
Weakness=> weight loss, hypotension, tachycardia, constipation, shock.
Sleep deprivation-due to interrupted by need to drink fluids & urinate
Urine specific gravity low (1.001-1.005)
Urine osmolality decreased (50-200 mOsm.kg)
Urine less concentrated than plasma
Plasma osmolality elevated (>295 mOsm/kg)
Hypernatremia in blood
Familial or idiopathic
Damage to the hypothalamic areas that produce ADH
Lesion of hypothalmus interferes with ADH synthesis/transport/release
1) Neurogenic -also known as
Causedby a deficiency of the Antidiuretic hormone, vasopressin
2) Nephrogenic-also known as
Vasopressin - resistant
Caused by insensitivity of the kidneys to the effect of the antidiuretic hormone, vasopressin
3) Gestagenic-also known as
Caused by a deficiency of the antidiuretic hormone, vasopressin, that occurs only during pregnancy
4) Dipsogenic, a form of primary polydipsis
Abnormal thirst and the
Excessive intake of water or other liquids
History and examination
Water deprivation test (see next slide)
Vasopressin challenge test (see next slide)
24 hours urine
Highsodium in blood
MRI of pituitary, hypothalmus and skull to see damaged areas
Intravenous fluids Hypertonic saline IV-Extracellular solution to pull fluid from outside the cell to inside the cell
Vasopressin SC/IM/IV, nasal prep
Long term DDAVP (Desmopression) nasal prep. (analog ADH)