Unit 2: Diabetes Insipidus Flashcards
Antidiuretic Hormone (ADH)
“Vasopressin”
- produced in hypothalamus
- stored and secreted in posterior pituitary gland
- regulates amount of water in the body and constricts blood vessels
- regulates the water by telling the renal tubules to retain water
- increased ADH = increased water retention
- decreased ADH = decreased water retention (increased urinary output)
Antidiuresis
no diuresis
-low urinary output
Diabetes Insipidus (DI)
- central or nephrogenic
- decreased ADH
- excretion of water by the kidneys; increased urinary output
- decreased urine specific gravity; urine is like clear water (dilute)
- dehydrated
- receives Vasopressin (need to replace ADH)
Central DI
caused by a decreased secretion of antidiuretic hormone (ADH) from the posterior pituitary gland
Nephrogenic DI
occurs when the kidneys are resistant to ADH and are unable to concentrate urine
-seen in patients w/ chronic renal insufficiency, hypercalcemia, hypokalemia, and interstitial disease of renal tubules
Pathophysiology of DI
- the decrease or absence of ADH results from lack of production in the hypothalamus
- antidiuretic hormone (ADH), stored and released from the posterior pituitary gland, works on the receptor cells in the collecting ducts of the kidney, leading to water reabsorption back into the circulation
- with a lack of ADH, the collecting ducts are less permeable to water, and is excreted in urine
- with DI, lack of ADH leads to excretion of large volumes of very dilute urine
Clinical Manifestations of DI
dependent on the significance of water loss
-polyuria (increased U/O)
-polydipsia (increased thirst)
-nocturia (urinating frequently at night)
>excessive loss of water leads to hemoconcentration that is observed w/ elevations in serum sodium and hematocrit
-may present with hypotension and tachycardia secondary to hypovolemia
-decreased urine specific gravity
-other signs of fluid volume deficit including thirst, skin tenting, and fatigue
What are the primary clinical manifestations seen in DI?
- polyuria (increased U/O)
- polydipsia (increased thirst)
- nocturia (urinating frequently at night)
Causes of DI
DI is a decrease in ADH
- kidney issues
- brain tumor
- develop after intracranial surgery
- head trauma
Diagnosis of Diabetes Insipidus
-serum and urine electrolytes
-serum and urine osmolality
-CT or MRI of the head
-Urine-specific gravity of less than 1.005
-Urine Osmolality less than 200 MOsm/Kg
-while losing free water, increases in serum sodium, serum osmolality, and hematocrit develop secondary to hemoconcentration
-water deprivation test
>Diagnosis of DI is made when serum osmolality continues to increase and there is no resultant increase in urine osmolality
Fluid Management
Management focused on maintaining adequate fluid volume status
- daily weight and I &Os
- if awake and alert, can replace fluid loss by drinking fluids
- in emergency or unconscious patient, IV fluid
- water losses replace w/ a hypotonic fluid (in relation to serum osmolality) such as dextrose in water
- during IV administration, monitor for hyperglycemia, volume overload, and correction of hypernatremia
- avoid food that promotes diuresis (coffee, watermelon, grapes, lemons)
Medication Management: Drug of choice
Desmopressin (DDVAP)
-synthetic analog of ADH
-increases ADH
-subcutaneous, intranasal, and oral preparations
>can also give vasopressin (Pitressin), a less expensive ADH synthetic
>these meds require monitoring of fluid status, serum electrolytes, and urine output
Desmopressin (DDVAP)
drug of choice for DI
-synthetic analog of ADH
-replaces ADH
-subcutaneous, intranasal, and oral preparations
>med requires frequent monitoring of fluid status, serum electrolytes, and urine output
Laboratory Tests
- Hematocrit
- Serum Sodium
- Urine-Specific Gravity
Laboratory Tests: Hematocrit
Male: 43-49%
Female: 38-44%
-volume of red blood cells (RBC) in the body
-hematocrit increased in DI
Laboratory Tests: Serum Sodium
135-145 mEq/L
-increased in DI
Laboratory Tests: Urine-specific gravoty
- 005-1.030
- decreased in DI
Connection Check: The nurse correlates which laboratory value as an indication that desmopressin is effective in the treatment of DI? A. Serum sodium of 140 mEq/L B. Serum osmolality of 305 mOsm/kg C. Urine-specific gravity of 1.004 D. Serum hematocrit 48%
A. Serum sodium of 140 mEq/L
(normal: 135-145)
- sodium will go back to normal because of an increase in ADH from the ADH synthetic medication; ADH would decrease urine output, and allow for more volume of fluid
Complications
- develop dehydration and hypovolemia, which will progress to circulatory collapse w/o adequate fluid administration
- patients w/ permanent DI who require daily administration of hormone replacement are at risk for hypovolemia
- hemoconcentration secondary to DI increases risk for hypernatremia
Clinical Manifestations of Hypernatremia
r/t central nervous system dysfunction secondary to shrinkage of brain cells
-results in confusion, neuromuscular excitability, seizures, or coma
Hemoconcentration
increased concentration of cells and solids in the blood usually resulting from loss of fluid to the tissues
Nursing Management: Assessment and Analysis
DI is directly r/t the lack of ADH; there is a loss of free water
>Assessments include:
-polyuria
-urine specific gravity less than 1.005
-low urine osmolality
-secondary to hemoconcentration, lab analysis revels an increase in serum sodium, osmolality, and hematocrit
-changes in BP and HR r/t volume of fluid loss
-patients who are awake and alert with an intake thirst mechanism are usually able to maintain fluid volume by drinking adequate fluids
Nursing Diagnoses
- Fluid volume deficit r/t loss of free water secondary to lack of ADH
- Risk for ineffective therapeutic regimen management r/t required administration of desmopressin (DDVAP)
- Sensory perceptual alteration (vision) r/t compression of CN II and III secondary to pituitary tumor
Nursing Assessments
- Vital signs
- Intake and Output
- Daily weight
- Visual acuity
- Serum Sodium and Osmolality
- Urine-Specific Gravity
