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diabetes insipidis patho
posterior pituitary disorder
water loss is caused by either
anti-diuretic hormone deficiency
inability of kidneys to respond to ADH
results in excretion of large volumes of dilute urine
polyuria
dehydration
fluid and electrolyte imbalance
increased plasma osmolarity
increased serum sodium—hypernatremia
increased thirst sensation
DI neruogenic
primary
caused by defect in hypothalamus or pituitary gland
resulting in lack of ADH production or release
secondary
result fo tumors in or near hypthalamus or pituitary gland, head trauma, infectious processes, or brain injury
DI nephrogenic
problems with kidney response to ADH
renal tubules do not respond to ADH
DI drug related
most often caused by lithium carbonate and demeclocycline
interere with response to kindeys
DI history
ask about recent surgery, head trauma, drug use
DI physical assessment
hypotension, tachycardia, weak peripheral pulses, hemoconentration
increased urine output (polyuria) greater than 4L ingested, dilute and low specific gravity
poor turgor, dry mucous membranes
constipation
decreased cognition, irritability, fatigue
increased thirst
ataxia
DI urine testing
as urine volume increases, urine osmolarity decreases
decreased urine specific gravity (less than 1.005)
decreased urine osmolarity (less than 200mOsm/L)
decreased urine pH, sodium, and potassium
DI blood testing: think concentrated
as blood volume decreases, blood osmolarity increases
increased blood osmolality greater than 300 mOsm/L
increased serum sodium and potassium
DI drug therapy with desmopressin (DDAVP)
synthetic form of vasopressin (ADH)
replaces ADH and decreases urination
increased water absoption from kidneys
induces water retention
routes of administration
mild: oral, sublingual, intranasal via metered dose spray
severe: IV, IM
neruogenic: chlorpropamide and thiazide diuretics facilitate vasopressin action
nephrogenic: prostaglasulin inhibitors, thiazide diuretics, and mild salt depletion are prescribed
DI drug alert
the parenteral form of desmopressin is 10x stronger than the oral form, and the dosage must be reduced
dose is adjusted based on urine output
give cautiously to those with coronary artery disease due to vasoconstriction
monitor for signs of water toxicity
DI nursing management
early detection of dehydration and maintaining adequate hydration
accurately measure I&O
check urine specific gravity
record daily withg
urge to drink fluids in amount equal to output
ensure patency of IV
nerogenic DI nuring management
lifelong drug therapy
chech ability
assess symptoms
adjust soages as prescribed for changes in condition and urine output
teach
polyuria and polydipsia indicate need for dose of DDAVP
monitor for indication of dehydration
weigh daily and observe to sins of lfuds overload due to medication
monitor for signs of water toxicity and report immediately to ED
headache, confusion, nausea, vomiting
wear medical bracelet to identify disorder
syndrome of inappropriate anti diuretic hormone patho
ADH (vasopressin) is secreted even when plasma osmolarity is low or normal
ADH is released when it is not needed
excess ADH leads to renal reabsortion of water
result in water retention and fluid overload
water retention causes dilutional hyponatremia
also known as Scwarts-Bartter syndrome
malignancies cause SIADH
small cell lung cancer
pancreatic, duodenal, and GU carcinomas
thymoma
hydgkin lymphoma
non-hodgkin lymphoma
pulmonary disorders causes SIADH
viral and bacterial pneumonia
lung abcesse
activity tuberculosis
pneumothorax
chronic lung disease
myocoses
positive pressure ventilation
CNS disorders cause SIADH
trauma
infection
tumors
strokes
prophyreia
systemic lupus erthematouse
drugs causeing SIADH
exogenous ADH
chlorprpamide
vincristine
cyclophophamide
carbamazepine
opioid
tryicylic antidepressents
general anesthetics
fluoroquinolone antibiotics
SIADH assessment
early symptoms: related to water retention causing dilutional hyponatremia, GI disturbances may occur first (loss of appetite, nausea, vomiting)
Dependent edema is not present due to free water being retaining, not salt
letharhy, headaches, hostility, disorentation, change in LOC
can progress to decreased responsiveness, seizures, and coma
decreased deep tendon reflexed
full, bounding pulse
hyponatremia
SIADH urine testing: think concentrated
as urine volume decreases, urine osmolatiy increases
increased urine specific gravity to greater than 1,030
increased urine osmolatity
increased urine sodium
SIDAH blood testing: think dilute
as blood volume increases, blood osmolatily decreases.
decreased blood dodium (dilutinal hyponatremia)
decreased blood osmolatily (less than 270)
decreased in BUN, Hgb, creatinine clearance
SIADH drug therapy
tolvaptan (oral), conivaptan (IV)
vaopressin receptor antagonist (vaptans)
promote water excretion without causing sodium loss
only administered in hospital settings
serum sodium monitoring for hypernatremia complications
Diuretics are used on limited basis when dosium levels are near normal and heart failure is present
hypertonic saline, 3% NaCl
used when sodium levels is very low
give cautiously due to risk of fluid overflow and promotion of heart failure
SIADH focus interventions
restricting fluid intake
romoting excretion of water
Replacing lost sodium
interfere with action of ADH
SIADH interventions
Monitor response to therapy and prevent complication
fluid overload and pulmoary edema
monitor neruogic status due to fluid shifts in the brain
teach about fluid restrictions and drug therapy
prevent injury
needed when serum sodium falls below 120
risk for neurologic changes and seizures
prevent overstimulation