AM Report 10/20/16 – Diabetes Insipidus

Hypernatremia (>145 mEq/L):

Non-Renal Losses:
1) Excessive sweating/burns
2) Insensible respiratory tract losses
3) Diarrhea, vomiting, NG suctioning

Renal Losses:
1) Diuretics
2) Osmotic diuresis – hyperglycemia, urea, mannitol
3) Post-obstructive diuresis
4) Diuretic phase of ATN

Hypertonic Sodium Gain:
1) Salt intoxication (VERY RARE)
2) Hypertonic IV fluids
3) Primary hyperaldosteronism
4) Central DI
5) Nephrogenic DI

Diabetes Insipidus: passage of large volumes of dilute urine (> 3 L/d); primarily a problem with ADH.
Anterior Pituitary (FLAT PEG): FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH
Posterior Pituitary: Oxytocin, ADH

Mechanism of ADH:
1) Membrane binds ADH
2) Receptor activates cAMP => secondary messenger
3) Insert aquaporin channels
4) Water is absorbed by osmosis

Central DI: problem with ADH production
Etiology – idiopathic, neurosurgery, malignancy, infiltration (sarcoid, wegners, IgG4 disease, etc.), trauma, anorexia nervosa, familial

Nephrogenic DI: problem with ADH response
Etiology – Lithium, other medications (demeclocycine, ampho B, etc.), electrolytes (HyperCa, HypoK), UTI, amyloidosis, Sjogren syndrome, hereditary

Diagnosing DI:
HyperNa (>145) and low urine osm (<200) = DI possible; H20 deprivation test
Normal Na and urine osm > 600 = excludes DI

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