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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
What are the recommended Na correciton rates in animals with serum Na < 180 and > 180 mEq/L?
* < 180 mEq/L ==> no faster than 1 mEq/L/hr * > 180 mEq/L ==> no faster than 0.5-1 mEq/L/hr
26
What is the calculation for free water deficit?
27
What is the treatment for cerebral edema from too fast correction of hypernatremia?
* mannitol 0.5-1 g/kg IV over 20-30 min * 7.2% NaCl 3-5 mL/kg over 20 min
28
What is more common, hyper- or hyponatremia?
Hypernatremia
29
List causes for Hyponatremia
* 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
Explain how CHF leads to hyponatremia
leads to decreased perfusion/effective circulating volume ==> * activation of RAAS ==> increased total body Na/overhydration * ADH release increased ==> increased free water retention
31
How can atypical addison's lead to hyponatremia?
have normal aldosterone but low circulating cortisol leads to increased ADH secretion ==> water retention | normal/typical addisons ==> decreased aldosterone ==> less Na retention
32
Which diuretics can cause hyponatremia and how?
* 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
What is severe hyponatremia?
serum Na < 120 mEq/L
34
What are clinical signs of severe or acute hyponatremia?
* obtundation * head pressing * seizures * coma * death
35
How can hyponatremia affect the heart?
increaes cardiac contractility
36
How does the CNS adjust to hyponatremia
* 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
How do you treat sympomatic hyponatremic patient?
free water excretion with mannitol (0.5-1 g/kg IV over 20 min) + furosemide (0.5-1 mg/kg IV)
38
What is maximum rate for treating the hyponatremic patient?
* 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
How do you calculate the Na deficit?
40
What is the maximum per hour rate for raising the plasma Na cc?
no more than 2 mEq/L/hr
41
What is the complication of too fast correction of hyponatremia? Where is it most commonly located in dogs compared to humans?
myelinolysis more common in thalamus in dogs, pons in people
42
What are clinical signs of myelinolysis?
* paresis * dysphagia * ataxia * obtundation * other neurologic signs
43
How much does the plasma Na cc drop with every 100 mg/dL increase in blood glucose?
by ~ 1.6 mEq/L | nonlinear, lower changes cause less Na decrease

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