POSTERIOR PITUITARY GLAND DISORDERS

By: Pn Zanida Zainon

Posterior pituitary hormone.

Pituitary Gland
Learning Objective
1. Define diabetes insipidus
2. State the etiology of diabetes insipidus
3. State the pathophysiology of diabetes
insipidus
4. State the manifestations of diabetes
insipidus
5. State the management of diabetes
insipidus
6. Explain nursing intervention for patient
diabetes insipidus using nursing proces.
Introduction
Diabetes insipidus results when the
pituitary gland does not produce
enough ADH, or from an acquired
insensitivity of the kidney to ADH.
Water is inadequately reabsorbed
from the collecting ducts, so a large
quantity of urine is produced.
Antidireutic Hormon
a hormone produced in a region of
the brain called the hypothalamus.
It is then stored and released from
the pituitary gland, a small gland at
the base of the brain.
Responsible for re absoption of
water by the distal tubules &
collecting duct at the kidney.
If ADH ; adequate absorption is
prevented = diuresis
Type of Diabetes Inssipidu
1.1.Neurologic diabetes insipidus
result from disruption of hypothalamus &
pituitary gland (due to trauma, irridiation
or cranial surgery, or idiopathic)

2. Nephrogenic diabetes insipidus.

due to renal tubules are not
sensitive to ADH. Can be hereditary or
result from renal failure.
Etiology
tumors or infections
cerebral Vascular Accidents
pituitary surgery or hypothalamic
damage
certain drugs that can interfere with
ADH secretions or actions (e.g.,
phenytoin, alcohol, lithium carbonate),
complication of closed head trauma
with increase intracranial pressure.
Pathophysiology
Occurs when injury to the posterior
pituitary gland causes
decrease in vasopressin secretion or

an inability of the kidney tubules to

respond to ADH.
This leads to increase serum

osmolarity & dehydration.

Clinical Manifestations
increase output (5 to 20 liter/ day) of
dilute urine.
Nocturia
extreme thirst (polydipsia)
Weight loss
Possible tachycardia

hypotension,

weakness
If water loss is not replaced; client
become hydrated &
hypernatremic.

If disorder caused by cerebral

injury = symptom may appear 3 to
6 days after the initial injury & last
for 7 to 10days.
Laboratory & diagnostic study
findings.

plasma osmolarity & serum sodium

levels
water (fluid deprivation test
demonstrate inability of kidneys to
concentrate urine despite increase
plasma osmolarity and low plasma
vesopressin level.
vasopressin test shows; kidney can
Therapeutic Interventions for
Diabetes Insipidus.

Hypotonic intravenous (I/V) fluids

such as 0.45% saline may be
ordered to replace intravascular
volume without adding excessive
sodium.
 Medical treatment of DI involves
replacement of ADH.

In acute cases; vasopressin (synthetic form

of ADH is given I/V or subcutaneous route)
together with I/V fluid replacement.

For long term therapy; synthetic ADH

(Desmopressin, or DDAVP) nasal spray is
used BD.
Chlorpropamide (Diabinese) help kidney
respond better to ADH.

Tiazide diuretics may increase urine flow in

the absence of ADH (increase urine output)
Assessment/Data collection.

Give special attention on fluid balance.

daily weights = most reliable method
for monitoring amount fluid lost.

accurate I/O chart

monitor skin integrity = dehydration

causing skin breakdown easily

monitor vital sign for sign of shock

check specific gravity using
urimeter/dipstick

monitor serum electrolyte

watch for client level of

consciousness.

assess client level of

understanding about the disease
& treatment.
Deficient fluid volume related
failure of regulatory mechanisms.

Expected outcome: Fluid balance will

be maintained as evidence by urine
specific gravity between 1.010 and
1.025, skin turgor within normal limits
and stable daily weight.
 Provide free access to oral fluids if
the DI is not psychogenic. If the
patients thirst mechanism is not
intact, give the patient fluids every
hour.
Oral fluids are essential to replace
the excess lost in diereses. If the
patient is alert with an intact thirst
mechanism, the patient can usually
manage this independently.
Encourage the patient to participate
in maintaining intake and output
records, monitoring weight and
checking urine specific gravity, if able.
This involves the patient and helps
prepare him or her for self-monitoring
at home.

Report a significant drop in blood

pressure and a rising pulse to the
registered nurse or physician
because these may be signs of
hypovolemic shock.
Risk for ineffective health
maintenance related to deficient
knowledge.

Expected outcome: Patient will

verbalize and demonstrate
understanding of medication
administration and self-monitoring of
disease.
 Assess patients understanding of
his or her disease process and
treatment. Teaching should build on
baseline knowledge.
Teach the patient about DI. The
patient will have to self-meditate
and monitor his or her disease at
home.
Include:
How to administer medications
and monitor their effectiveness.
How to measure urine specific
gravity and the significance of
results.
Sign and symptoms of
dehydration and fluid overload.
monitoring daily weight: losses or
gains of greater than 2 pounds in a
day should be reported to the
physician.
Weight loss or gain can indicate
fluid imbalance and need for a
change in medication regimen.

Advise the patient to wear

identification, such as a medical
alert bracelet, that identifies the
disorder.
Faster treatment can be initiated
if emergency personnel are aware
Evaluation:

If treatment has been effective,

signs of dehydration will be
absent and weight and vital signs
will be stable. The patient should
be able to explain what is
happening in the disease,
symptoms to report and
demonstrate how to manage self-
care.
Specific nursing care for diabetes
Insipidus.

administer prescribed medications; which

may include ADH replacements.
Replace fluid as indicated; assess & report
if any problem that can prevent adequate
fluid intake.
Encourage the client to drink fluid in
respond to thirst.
REFERENCES;
LEMODE MEDICAL SURGICAL NURSING.
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WILLIAMS HOPPER MEDICAL SURGICAL

NURSING
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