Diabetes Insipidus Flashcards
what does ADH do
it is the thirst hormone
it causes water reabsorption and allows for high urine osmolality since aquaporins in distal convoluted tubule will reabsorb water back in
DI or diabetes insipidus will cause
High volume urine output can be measured in a 24 hr urine ouput
see low ADH from some reason either nephrogenic or central. _Cannot reabsorb water in kidne_y
low urine osmolality because all the water is leaving with urine see high urine output
two types of diabetes insipidus?
central DI - no ADH so no water is reabsorbed in convoluted tubule and see low urine osmolality nephrogenic DI - ADH resistance or renal disease
what causes central diabetes insipidus
ADH deficiency or CNS pathology
idiopathic
trauma - SAH
pituitary surgery
ischemic encephalopathy
what causes nephrogenic diabetes insipidus?
ADH resistance (renal dx)
chronic lithium use
hypercalcemia
hereditary AVPR2 and
aquaporin 2 mutations AVPR2 (vasopressor)
what is primary polydipsia?
ADH independent (excessive water intake) see excessive water intake causing high urine output
what causes primary polydipsia?
antipsychotics (causes dry mouth) psychiatric conditions
what happens in water deprivation in all three cases
primary polydipsia: see high urine osmolality (retains ability to concentrate urine with ADH and normal renal function)
Central DI: _low urine osmolalit_y (see weight loss and increasing serum osmolality) . adding DDAVP will increase urine osmolality as body is now able to concentrate urine with ADH.
Nephrogenic DI: low urine osmolality. See low urine osmolality because there’s no change in urine osmolality. Due to defect in kidney
what happens in response to desmopressin in all three cases?
desmopressin = synthetic ADH
Primary Polydipsia: no change
Central DI: increased urine osmolality
Nephrogenic DI: no change
central DI = missing DDAVP so adding it will increase urine osmolality as ADH now allows the body to concentrate urine. Other conditions were not because of a body deficit of ADH
if pt has increased thirst and normal Na and urine osmolality that is
primary polydipsia
primary polydipsia if pts with intact thirst mechanism will have adequate water intake to compensate for water loss and can have normal sodium levels
if Na>145 and urine osmolality
DI
what happens in central DI with water deprivation test.
weight loss after water deprivation test as they continue to pee (i_ncreasing plasma osmolality and due to renal loss) and urine osmolality being <300_
water deprivation test protocol
Causes of polyuria and dilute urine chart
how does lithium caused nephrogenic DI
it causes nephrogenic DI by creating ADH resistance by imparing water channel functio nand water reabsorption.
see acute onset nocturia and polyuria.
Diagnosed via the water deprivation test to rule out primary polydipsia. If no change in water deprivation or administration of DDAVP (ADH) by 50% or higher then it’s ADH resistance of nephrogenic DI.
lithium side effects on kidney are
chronic interstitial nephritis, type 1 RTA, hyperparathyroidism wiht hypercalcemia and nephrogenic DI.
what happens in a water deprivation test?
there’s a component of no water drinking 2-3 hrs before. baseline urine osmolality is checked prior to test then checked after 2-3 hrs of no water.
If urine osmolality is >600 after no water intake means that low urine osmolality (b/c pt can still concentrate urine) was because pt was drinking a lot of water (primary polydipsia)
If urine osmolality remains low (<295) then give (DDAVP) ADH to distinguish if it’s central or nephrogenic.
Central DI - lacks ADH so see increase in urine osmolality by >50%
If nephrogenic DI- resistant to ADH so giving DDAVP won’t have an effect on urine osmolality or won’t increase >50%.
diagnosis of nephrogenic DI by lithium
Diagnosed via the water deprivation test to rule out primary polydipsia.
If no change in water deprivation** or **administration of DDAVP (ADH) by 50% or higher then it’s ADH resistance of nephrogenic DI.
how to treat lithium induced nephrogenic DI:
can be permanent or partially reversible and so will need to discontinue lithium.
In pts who cannot discontinue lithium, need salt restriction, and use of amiloride or thiazide
amiloride - blocks Na channels in collecting duct ot prevent lithium’s entry
Thiazide diuretics with sodium restriction casues mild hypovolumia and causes increased proximal tubule sodium and water reabsorption.
characteristics of primary polydipsia is
low normal serum sodium or hyponatremia
low urine osmolality
rapid increase of urine osmolality with water restriction or water deprivation test (by >50%)
who is disqualified from getting a water depirvation test? what labs rules out DI?
urine osmolality >600 (shows that you can have urine concentration) see ADH action present.
