Ch. 558 - DI Flashcards
Principal regulator of plasma tonicity
Vasopressin
Release of vasopressin is largely stimulated by
Increases in plasma tonicity
Volume homeostasis is largely regulated by
RAAS
T/F Vasopressin has both antidiuretic and pressor activity
T
Vasopressin is synthesized in
Paraventricular and supraoptic nuclei of the hypothalamus
T/F Osmotic threshold for thirst is higher than osmotic threshold for vasopressin release
T
Osmotic threshold for thirst is higher than osmotic threshold for vasopressin release, meaning
Vasopressin is released before thirst is initated
Vasopressin exerts its principal effect on the kidney via what receptors
V2 > increase in CAMP > insertion of aquaporin 2 into the apical/luminal membrane > water movement along its gradient > urine concentration
Diagnosis of DI is established if serum osm is ___ and urine osm is ___
> 300 mOsm/kg, <300 mOsm/kg
Test that establishes diagnosis of DI when patient has polyuria and polydipsia but serum osm <300
Water deprivation test
Test that differentiates central from nephrogenic DI
Water deprivation test
DI, DM, optic atrophy, deafness resulting from vasopressin DEFICIENCY
Wolfram syndrome
Triphasic response following CNS surgery
1) Transient DI 12-48h 2) SIADH 10 days 3) DI may be permanent
MC primary brain lesions associated with DI
Germinomas and pinealomas
Common infiltrative disorders causing central DI
1) LCH 2) Lymphocytic hypophysitis
Causes 50% of idiopathic central DI
Hypohysitis
T/F With intact thirst mechanism and free access to oral fluids, a person with complete DI can maintain plasma osm and Na in the high normal range
T
TReatment of central DI in older children is BEST accomplished with
DDAVP
Central DI of acute onset following neurosurgery is best managed with
1) Synthetic aquesous vasopressin (pitressin) 2) Limit TFI to 1L/BSA/day during antidiuresis
T/F Nephrogenic DI may be genetic or acquired
T
Acquired NDI can result from
Hypercalcemia or hypokalemia, drugs (lithium, demeclocycline, foscarnet, clozapine, amphotericin, methicillin, rifampin)
Treatment of acquired DI
Elimination of the underlying disorder
Pharmacologic treatment of NDI
Thiazide diuretics (to DECREASE OVERALL UO by inducing a state of mild volume depletion; Na excretion at the expense of water > decrease in GFR > proximal Na and water reabsorption)
Initial approach to patient with hyponat
Determination of volume status
Syndromic causes of hyponat
SIADH, CSW
Hyponat, inappropriately concentrated urine, normal-to-high urine sodium, low serum uric acid
SIADH
Initial manifestation of systemic dehydration
Hypernatremia and hyperosmolality
In patients with normal renal function, kidney can excrete dilute urine with an osm as low as
50 mOsm/kg
Maximum amount of water a person with normal renal function can consume
10L/BSA
Maximum amount of water intake to avoid water intoxication for neonates
4L/BSA/day
Results from hypersecretion of ANP and seen primarily with CNS disorders
CSW
Hyponatremia, elevated urinary Na excretion , excessive UO, hypovolemia, normal or high uric acid, suppresed vasopressin, elevated ANP
CSW
Urinary excretion to consider CSW
> 150meq/L
T/F Pseudohypernatremia can result from hypertriglyceridemia and hyperglycemia
F, pseudoHYPOnatremia
Serum Na decreases by ___ for every 100mg/dL increase in blood glucose >100mg/dL
1.6meq/L
Acute hyponat is defined as
Onset <12 hrs or a serum Na concentration <120meq/L
Emergency treatment for cerebral dysfunction resulting from acute hyponat
1) Water restriction 2) HTS
Serum Na should be raised no faster than
0.5meq/L/hr or 12meq/L/24hr
Chronic SIADH is best treated by
Oral fluid restriction
Treatment of patients with CSW
Restoring intravascular volume with NaCl and water
