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

A

T

18
Q

TReatment of central DI in older children is BEST accomplished with

A

DDAVP

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

A

T

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
Q

Syndromic causes of hyponat

A

SIADH, CSW

26
Q

Hyponat, inappropriately concentrated urine, normal-to-high urine sodium, low serum uric acid

A

SIADH

27
Q

Initial manifestation of systemic dehydration

A

Hypernatremia and hyperosmolality

28
Q

In patients with normal renal function, kidney can excrete dilute urine with an osm as low as

A

50 mOsm/kg

29
Q

Maximum amount of water a person with normal renal function can consume

A

10L/BSA

30
Q

Maximum amount of water intake to avoid water intoxication for neonates

A

4L/BSA/day

31
Q

Results from hypersecretion of ANP and seen primarily with CNS disorders

A

CSW

32
Q

Hyponatremia, elevated urinary Na excretion , excessive UO, hypovolemia, normal or high uric acid, suppresed vasopressin, elevated ANP

A

CSW

33
Q

Urinary excretion to consider CSW

A

> 150meq/L

34
Q

T/F Pseudohypernatremia can result from hypertriglyceridemia and hyperglycemia

A

F, pseudoHYPOnatremia

35
Q

Serum Na decreases by ___ for every 100mg/dL increase in blood glucose >100mg/dL

A

1.6meq/L

36
Q

Acute hyponat is defined as

A

Onset <12 hrs or a serum Na concentration <120meq/L

37
Q

Emergency treatment for cerebral dysfunction resulting from acute hyponat

A

1) Water restriction 2) HTS

38
Q

Serum Na should be raised no faster than

A

0.5meq/L/hr or 12meq/L/24hr

39
Q

Chronic SIADH is best treated by

A

Oral fluid restriction

40
Q

Treatment of patients with CSW

A

Restoring intravascular volume with NaCl and water