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SilversteinHopper > 50: Sodium Disorders > Flashcards

50: Sodium Disorders Flashcards

1
Q

What is the normal plasma Na concentration?

A

147-156 mEq/L

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2
Q

what is the unit of osmolality?

A

mOsm/kg

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3
Q

what is the unit of osmolarity?

A

mOsm/L

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4
Q

what is the calculation for serum osmolality?

A

2Na +BUN/2.8 + glucose/18

2.8 and 18 to convert BUN and glucose from mg/dL to mmol/L

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5
Q

What are the main effective osmoles?

A

Na and K

effective because do not cross cell membrane freely

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6
Q

What regulates the plasma osmolality?

A

hypothalamic osmoreceptors

induces compensation from changes in osmolality as low as 2-3 mOsm/kg

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7
Q

What are the 2 main compensatory systems counteracting changes in osmolality

A
  • ADH system
  • thirst
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8
Q

Where is ADH secreted?

A

by the posterior pituitary gland

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9
Q

What stimuli lead to ADH secretion?

A
  • elevated plasma osmolality
  • decreased effective circulating volume
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10
Q

Where are the osmoreceptors located?

A

Hypothalamus

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11
Q

What receptors sense decreased circulating volume and where are they located?

A

baroreceptors located in the aortic arch and carotid bodies

==> send neuronal impulses to the pituitary gland ==> ADH release

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12
Q

Explain how ADH regulates water balance

A

low circulating volume/high osmolality ==> ADH release by pituitary gland
* ADH activates V2 receptors on renal collecting tubular cells
* inserts aquaporin-2 molecules into luminal cell membrane
* aquaporin = channels allowing water to move across renal tubular cell membrane
* water will follow its osmotic gradient, kidneys must generate hyperosmolar medulla to achieve this

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13
Q

What may impair effective water reabsorption by ADH secretion

A
  • water will follow its osmotic gradient through aquaporin channels
  • kidneys must generate hyperosmolar medulla to achieve this
  • impaired in disease or administration of diuretics ==> loss of osmotic gradient
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14
Q

What is prioritized, maintenance of effective circulating volume or osmolality?

A

circulating volume is always prioritized
if low effective circulating volume ==> ADH will be released regardless of osmolality ==> hyponatremia/hypoosmolality

e.g., congestive heart failure

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15
Q

What are the effects of Aldosterone?

A
  • water resorption
  • Na resorption
  • K excretion
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16
Q

What are the effects of ADH?

A
  • water resorption
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17
Q

What is considered severe hypernatremia?

A

serum Na cc > 180 mEq/L

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18
Q

List clinical signs of hypernatremia

A
  • obtundation
  • head pressing
  • seizures
  • coma
  • death
19
Q

What happens to cells during hypernatremia?

A

shink
water moves down osmotic gradient

20
Q

How may hypernatremia affect the heart?

A

associated with decreased myocardial activity

21
Q

Explain the early (minutes) neuronal adaption to hypernatremia

A
  • neuronal water is lost to the hypernatremic circulation ==> decreased interstitial hydrostatic pressure ==> fluid drawn from CSF to interstitium of the brain
  • Na and Cl move from CSF into cerebral tissue ==> increases neuronal osmolality ==> draws back water into the IC space
22
Q

Explain the delayed (24h+) neuronal adaption to hypernatremia

A

neurons accumulate organic solutes to increase IC osmolality and retain water

23
Q

how long does accumulation of idiogenic osmoles in neurons take?

A

begins within few hours
full compensation within 2-7 days

24
Q

name 3 idiogenic osmoles

A
  • inositol
  • glutamin
  • glutamate
25
Q

What are the recommended Na correciton rates in animals with serum Na < 180 and > 180 mEq/L?

A
  • < 180 mEq/L ==> no faster than 1 mEq/L/hr
  • > 180 mEq/L ==> no faster than 0.5-1 mEq/L/hr
26
Q

What is the calculation for free water deficit?

A
27
Q

What is the treatment for cerebral edema from too fast correction of hypernatremia?

A
  • mannitol 0.5-1 g/kg IV over 20-30 min
  • 7.2% NaCl 3-5 mL/kg over 20 min
28
Q

What is more common, hyper- or hyponatremia?

A

Hypernatremia

29
Q

List causes for Hyponatremia

A
  • decreased effective circulating volume, e.g., CHF, GI losses, urinary losses, body cavity effusions, edematous state
  • hypoadrenocorticism
  • diuretics
  • SIADH
  • GI parasititism, infectious/inflammatory diseases
  • psychogenic polydipsia
  • pregnancy
  • feeding low-Na home-prepared diet
30
Q

Explain how CHF leads to hyponatremia

A

leads to decreased perfusion/effective circulating volume ==>
* activation of RAAS ==> increased total body Na/overhydration
* ADH release increased ==> increased free water retention

31
Q

How can atypical addison’s lead to hyponatremia?

A

have normal aldosterone but low circulating cortisol leads to increased ADH secretion ==> water retention

normal/typical addisons ==> decreased aldosterone ==> less Na retention

32
Q

Which diuretics can cause hyponatremia and how?

A
  • Thiazide and loop diuretics (i.e., not K sparing)
    ==> hypokalemia ==> IC shift of Na for K ==> hyponatremia
  • inability to cause medullary hyperosmolality ==> aquaporin channels don’t work
33
Q

What is severe hyponatremia?

A

serum Na < 120 mEq/L

34
Q

What are clinical signs of severe or acute hyponatremia?

A
  • obtundation
  • head pressing
  • seizures
  • coma
  • death
35
Q

How can hyponatremia affect the heart?

A

increaes cardiac contractility

36
Q

How does the CNS adjust to hyponatremia

A
  • hyponatremia == neuronal cell swelling + interstitial CNS edema ==> increase in intracranial hydrostatic pressure ==> enhances fluid movement from intracranial to CSF ==> to venous circulation
  • neurons expel solutes, e.g., Na, K (rapid), organic osmoltyes (slow, hours to days)
37
Q

How do you treat sympomatic hyponatremic patient?

A

free water excretion with mannitol (0.5-1 g/kg IV over 20 min) + furosemide (0.5-1 mg/kg IV)

38
Q

What is maximum rate for treating the hyponatremic patient?

A
  • no more than 10 mEq/L over first 24 hours
  • no more than 18 mEq/L over first 48 hours
  • never exceed 147 mEq/L (low end reference range)
39
Q

How do you calculate the Na deficit?

A
use target Na cc of no more than 10-15% higher than patient's current Na cc
40
Q

What is the maximum per hour rate for raising the plasma Na cc?

A

no more than 2 mEq/L/hr

41
Q

What is the complication of too fast correction of hyponatremia?
Where is it most commonly located in dogs compared to humans?

A

myelinolysis
more common in thalamus in dogs, pons in people

42
Q

What are clinical signs of myelinolysis?

A
  • paresis
  • dysphagia
  • ataxia
  • obtundation
  • other neurologic signs
43
Q

How much does the plasma Na cc drop with every 100 mg/dL increase in blood glucose?

A

by ~ 1.6 mEq/L

nonlinear, lower changes cause less Na decrease

SilversteinHopper (11 decks)

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