Diabetes Insipidus Flashcards
What is Diabetes Insipidus ?
A deficiency of production, secretion or ⬇️ renal response of ADH
* ADH is also known as Vasopressin*
results in fluid and electrolyte imbalances caused by:
- ⬆️ UOP
- ⬆️ Plasma osmolality
3 D’s of Diabetes Insipidus
- Diabetes Insipidus
- Decreased ADH
- Diuresis
Central DI (Diabetes Insipidus)
A.K.A Neurogenic
2/2 to intracranial surgery or Head Trauma
- an organic lesion that interferes with ADH synthesis or release
- destruction of the pituitary gland interferes with ADH synthesis, transport, and release*
Nephrogenic DI (Diabetes Insipidus)
Adequate ADH but ⬇️ kidney response to ADH
Caused by: RENAL DAMAGE = inability to conserve water
- Drug Therapy (especially Lithium)
- Hypercalcemia & Hypokalemia
Psychogenic DI (Diabetes Insipidus )
A.K.A Dispogenic
Associated with excessive water intake
Example: excessive water drinking contests or psych patients
What causes Diabetes Insipidus?
- Head Trauma: penetrating injury, GCS 8 or less, cerebral edema
- Brain Tumor
- Surgical ablation or irradiation of pituitary gland
- Infection of the CNS: TB, meningitis, encephalitis
- Tumors: lymphoma of lung or breast, metastatic cancers
- Drugs: LITHIUM, Demeclocycline (impaired kidney water reabsorption)
(Central DI TRIPHASIC PATTERN)
Acute Phase
Abrupt onset of Polyuria
200-1000 cc/hr
(Central DI TRIPHASIC PATTERN)
Interphase
Urine Volume Normalizes
Start to see ⬇️ UOP
(Central DI TRIPHASIC PATTERN)
Third Phase
Central DI becomes permanent
Occurs 10-14 days postoperatively
* Notes* after ⬇️UOP and you see your electrolytes aren’t going back to normal within 10-14 days
* improvement should be seen 24-72 hrs post- op or when head swelling decreases
Clinical manifestations of DI I
- Polyuria: 5-20L/day, very diluted urine w/ Nocturia
- Polydipsia: intense thirst, consumes 2-20 L/day, cold water
- Low ⬇️SG (<1.005 )
- Low ⬇️Urine osmolality (<100 mOsm/kg)
- Elevated ⬆️ serum osmolality (> 295 mOsm/kg)
- Hypernatremia d/t pure water loss
Clinical manifestations of DI II
- Hypovolemia - Hypotension -Tachycardia
- compensatory mechanism*
- Weight loss - constipation
- Shock: 2/2 extreme fluid loss.
- Poor skin turgor
- CNS manifestations: 2/2 ⬆️ serum osmolality, hypernatremia
Water Deprivation Test (Miller- Moses)
Used to differentiate CAUSE of Polyuria
- Central, Nephrogenic, Psychogenic, SIADH
- ADH/ vasopressin administered IV, SQ, nasally
- Central DI: ⬆️ Urine mOsm, ⬇️ UOP
- Psychogenic DI: Normal Urine & Plasma mOsm
- Nephrogenic DI: No response
Preparation for (Miller-Moses) Water Deprivation Test
- Baseline VS, weight, Urine & Serum mOsm, SG
- NPO 8-16 hrs before hand or until 3-5% of body weight lost
- Hourly BP, weight, Urine mOsm
- ADH/ vasopressin given IV, SQ, nasally
- you should see ⬇️ UOP, ⬆️ Serum Na+, ⬇️ weight loss*
Pharmacological management for Central DI
- DDAVP (desmopressin acetate): synthetic ADH/vasopressin
- Pitressin: synthetic ADH/ vasopressin
- Diabinese: CAUSE SIADH to treat DI
- Tegretol: CAUSE SIADH to treat DI
- Hypotonic Saline or Dextrose Solution: 1/2 or 1/4NaCL or D5W (Dry!)
- Titrate to REPLACE UOP
Pharmacological management for Nephrogenic DI
- remember Kidneys DO NOT respond to ADH*
- Diet: ⬇️ Na+ (3g/day) ⬆️solutes ⬇️ water in body
- Diuretics: Thiazides HCTZ ( ⬇️GFR, allows kidneys to reabsorb more water)
- Prostaglandin Inhibitor: Indomethacin (NSAID) ⬆️ response to ADH
