Antidiuretic hormone (ADH) inhibition

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  1. Released by posterior pituitary with direct neural contact from fibers originating in the hypothalamus (mainly supraoptic nuclei)
  2. Main stimulus of ADH = increased osmotic pressure of body water sensed by osmoreceptors in the hypothalamus, also volume depletion sensed by baroreceptors in the left atrium, pulmonary veins, carotid sinus, and aortic arch mediated through CN 9 and 10; ADH also released by pain, stress, vomiting, exercise, hypoglycemia, cholinergic agonists, beta-adrenergic agonists, angiotensin, prostaglandins
  3. Main inhibitors of ADH = alcohol, alpha-adrenergic agonists, glucocorticoids
  4. Affects permeability of the collecting duct in the kidney increasing permeability which results in more water being absorbed which conserves water and concentrates urine
    1. Failure to release ADH = Central DI: causes – head trauma, CNS infections, metastatic lung , breast, pancreatic cancer, surgical trauma
    2. Failure to respond to ADH = Nephrogenic DI: causes – acute tubular necrosis, multiple myeloma, amphotericin B, lithium
    3. Diagnosis: serum osmo > 300; urine osmo < 300
    4. Triphasic course of DI: Initial diuresis in first 1-2 days; second phase due to release of ADH from injured axons lasts 2-4 days; third phase return of diuresis and overt diabetes insipidus
    5. Treatment DDAVP with ½ life of 8-12 hours given intranasally with adequate free water replacement
  5. SIADH – commonly associated with breast, lung and pancreas carcinoma, Guillain Barre, acute intermittent porphyria, meningitis, MS, medication -induced, but also post-op and after head trauma
    1. other causes: opiates, barbiturates,
    2. diagnosis: inappropriately hypertonic urine with respect to serum – Urine osmolality less than serum osmolality but is > 130 mOsm/kg in the presence of hyponatremia
      1. urine Na > 20 mEq/L
    3. treatment: 3% saline if Na < 120 mEq/L and the patient has symptomatic hyponatremia: mental ststus change, seizures; water restriction, demeclocycline (interferes with ADH action at renal collecting duct,inducing a nephrogenic diabetes insipidus); conivaptan (V1A, V2 ADH receptors inhibitor, inducing aquaresis) -indicated for euvolemic/hypervolemic hyponatremia
    4. Don’t correct more than 12 mEq/L in 24 hours- risk of central pontine and extrapontine myelinolysis
  6. Cerebral Salt Wasting – usually accompanies intracranial disease
    1. differences between CSW and SIADH – in CSW have decreased plasma volume, decreased CVP, decreased weight, increased hematocrit – SIADH has the opposite
  7. symptoms of hyponatremia
    1. initially: anorexia, headache, irritability, muscle weakness; severe hyponatremia may cause neuromuscular excitability, cerebral edema, muscle twitching and cramps, nausea and vomiting, confusion, seizures
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