Ch. 558 - DI Flashcards

1
Q

Principal regulator of plasma tonicity

A

Vasopressin

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2
Q

Release of vasopressin is largely stimulated by

A

Increases in plasma tonicity

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3
Q

Volume homeostasis is largely regulated by

A

RAAS

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4
Q

T/F Vasopressin has both antidiuretic and pressor activity

A

T

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5
Q

Vasopressin is synthesized in

A

Paraventricular and supraoptic nuclei of the hypothalamus

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6
Q

T/F Osmotic threshold for thirst is higher than osmotic threshold for vasopressin release

A

T

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7
Q

Osmotic threshold for thirst is higher than osmotic threshold for vasopressin release, meaning

A

Vasopressin is released before thirst is initated

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8
Q

Vasopressin exerts its principal effect on the kidney via what receptors

A

V2 > increase in CAMP > insertion of aquaporin 2 into the apical/luminal membrane > water movement along its gradient > urine concentration

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9
Q

Diagnosis of DI is established if serum osm is ___ and urine osm is ___

A

> 300 mOsm/kg, <300 mOsm/kg

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10
Q

Test that establishes diagnosis of DI when patient has polyuria and polydipsia but serum osm <300

A

Water deprivation test

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11
Q

Test that differentiates central from nephrogenic DI

A

Water deprivation test

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12
Q

DI, DM, optic atrophy, deafness resulting from vasopressin DEFICIENCY

A

Wolfram syndrome

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13
Q

Triphasic response following CNS surgery

A

1) Transient DI 12-48h 2) SIADH 10 days 3) DI may be permanent

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14
Q

MC primary brain lesions associated with DI

A

Germinomas and pinealomas

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15
Q

Common infiltrative disorders causing central DI

A

1) LCH 2) Lymphocytic hypophysitis

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16
Q

Causes 50% of idiopathic central DI

A

Hypohysitis

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17
Q

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

18
Q

TReatment of central DI in older children is BEST accomplished with

19
Q

Central DI of acute onset following neurosurgery is best managed with

A

1) Synthetic aquesous vasopressin (pitressin) 2) Limit TFI to 1L/BSA/day during antidiuresis

20
Q

T/F Nephrogenic DI may be genetic or acquired

21
Q

Acquired NDI can result from

A

Hypercalcemia or hypokalemia, drugs (lithium, demeclocycline, foscarnet, clozapine, amphotericin, methicillin, rifampin)

22
Q

Treatment of acquired DI

A

Elimination of the underlying disorder

23
Q

Pharmacologic treatment of NDI

A

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)

24
Q

Initial approach to patient with hyponat

A

Determination of volume status

25
Syndromic causes of hyponat
SIADH, CSW
26
Hyponat, inappropriately concentrated urine, normal-to-high urine sodium, low serum uric acid
SIADH
27
Initial manifestation of systemic dehydration
Hypernatremia and hyperosmolality
28
In patients with normal renal function, kidney can excrete dilute urine with an osm as low as
50 mOsm/kg
29
Maximum amount of water a person with normal renal function can consume
10L/BSA
30
Maximum amount of water intake to avoid water intoxication for neonates
4L/BSA/day
31
Results from hypersecretion of ANP and seen primarily with CNS disorders
CSW
32
Hyponatremia, elevated urinary Na excretion , excessive UO, hypovolemia, normal or high uric acid, suppresed vasopressin, elevated ANP
CSW
33
Urinary excretion to consider CSW
>150meq/L
34
T/F Pseudohypernatremia can result from hypertriglyceridemia and hyperglycemia
F, pseudoHYPOnatremia
35
Serum Na decreases by ___ for every 100mg/dL increase in blood glucose >100mg/dL
1.6meq/L
36
Acute hyponat is defined as
Onset <12 hrs or a serum Na concentration <120meq/L
37
Emergency treatment for cerebral dysfunction resulting from acute hyponat
1) Water restriction 2) HTS
38
Serum Na should be raised no faster than
0.5meq/L/hr or 12meq/L/24hr
39
Chronic SIADH is best treated by
Oral fluid restriction
40
Treatment of patients with CSW
Restoring intravascular volume with NaCl and water