Diabetes Insipidus Flashcards

1
Q

what does ADH do

A

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

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2
Q

DI or diabetes insipidus will cause

A

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

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3
Q

two types of diabetes insipidus?

A

central DI - no ADH so no water is reabsorbed in convoluted tubule and see low urine osmolality nephrogenic DI - ADH resistance or renal disease

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4
Q

what causes central diabetes insipidus

A

ADH deficiency or CNS pathology

idiopathic

trauma - SAH

pituitary surgery

ischemic encephalopathy

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5
Q

what causes nephrogenic diabetes insipidus?

A

ADH resistance (renal dx)

chronic lithium use

hypercalcemia

hereditary AVPR2 and

aquaporin 2 mutations AVPR2 (vasopressor)

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6
Q

what is primary polydipsia?

A

ADH independent (excessive water intake) see excessive water intake causing high urine output

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7
Q

what causes primary polydipsia?

A

antipsychotics (causes dry mouth) psychiatric conditions

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8
Q

what happens in water deprivation in all three cases

A

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

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9
Q

what happens in response to desmopressin in all three cases?

A

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

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10
Q

if pt has increased thirst and normal Na and urine osmolality that is

A

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

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11
Q

if Na>145 and urine osmolality

A

DI

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12
Q

what happens in central DI with water deprivation test.

A

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_

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13
Q

water deprivation test protocol

A
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14
Q

Causes of polyuria and dilute urine chart

A
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15
Q

how does lithium caused nephrogenic DI

A

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.

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16
Q

lithium side effects on kidney are

A

chronic interstitial nephritis, type 1 RTA, hyperparathyroidism wiht hypercalcemia and nephrogenic DI.

17
Q

what happens in a water deprivation test?

A

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%.

18
Q

diagnosis of nephrogenic DI by lithium

A

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.

19
Q

how to treat lithium induced nephrogenic DI:

A

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.

20
Q

characteristics of primary polydipsia is

A

low normal serum sodium or hyponatremia

low urine osmolality

rapid increase of urine osmolality with water restriction or water deprivation test (by >50%)

21
Q

who is disqualified from getting a water depirvation test? what labs rules out DI?

A

urine osmolality >600 (shows that you can have urine concentration) see ADH action present.