Sodium Flashcards

1
Q

What percentage of an animal’s lean bodyweight is total body water?

A

60%

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2
Q

What is the equation for osmolarity in serum

A

mOsm/kg = 2Na + BG/18 + BUN/2.8

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3
Q

What are the 2 main mechanisms regulating osmolarity in the body?

A

thirst (water intake)
kidney water retention or excretion

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4
Q

how does the body detect osmolality?

A

osmoreceptors in the hypothalamus

detects osmolality of all body compartments as water moves freely between compartments and will equillibrate the osmolality
can sense changes in osmolality as little as 1%

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5
Q

What are the 2 major stimuli for the sensation of thirst?

A
  • hyperosmolality (direct stimulation)
  • decreased effective circulating volume (ECV) (activates RAAS system, which activates angiontensin II, which stimulates ADH release
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6
Q

Where is ADH synthesized and stored?

A

synthesized in the hypothalamus, stored in secretory granules in the posterior pituitary gland

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7
Q

Explain the mechanism of action by which ADH leads to water retention

A

Activates vasopressin 2 (V2) receptors in the luminal membrane of the cortical and medullary collecting tubules
–> insertion of aquaporin 2 (water channels)
–> water will passively move through AQP2 channels down its osmotic gradient

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8
Q

What are the 2 major stimuli for vasopressin release?

A
  • increased osmolality
  • decreased effective circulating volume
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9
Q

where are the baroreceptors located that monitor the effective circulatory volume?

A
  • cardiopulmonary circulation
  • carotid sinus
  • aortic arch
  • afferent glomerular arterioles in the kidney
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10
Q

How does decreased effective circulatory volume lead to ADH release?

A

baroreceptors sense decrease in ECV –> increased sympathetic tone –> RAAS activation –> angiontensin II activation –> ADH release

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11
Q

Explain how a patient may have hypoosmolar plasma but increased water retention

A

decrease in ECV will lead to RAAS and subsequent ADH release despite concurrent hypoosmolality

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12
Q

Explain how a patient in systolic heart failure develops hyponatremia

A

systolic heart failure –> decreased cardiac output –> decreased ECV
* –> RAAS activation (Na and water retention) and ADH release (water retention), thirst –> if water intake+retention exceeds Na retention –> hyponatremia
* decreased tubular flow –> impaired water excretion

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13
Q

What is the expected decrease of serum Na concentration for every 100 mg/dL increase in glucose

A

1.6 to 2.4 mmol/L for every 100 mg/dL

the higher the glucose concentration the greater the reduction in plasma, 2.4 mmol/L likely more reliable as a factor

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14
Q

Why does an increase in BUN not lead to hyponatremia?

A

BUN moves freely in and out of cells –> thus is not an effective osmole –> no water drag into the ECF

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15
Q

Explain how you can use urine Na+ cc to assess a patient’s volume status

A

the urine Na+ cc of a euvolemic patient is expected to be > 30 mmol/L
the urien Na+ cc of a hypovolemic patient is < 30 mmol/L due to decrease in ECV leading to RAAS activation and aldosterone increasing Na retention in the distal nephrone

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16
Q

By which 3 mechanisms can hypovolemia lead to increased TBW and hyponatremia?

A

volume depletion
–> potent nonosmotic stimulus for ADH secretion (through RAAS pathway) –> water retention in kidneys
–> decreased GFR –> increased proximal renal tubular Na+ and water reabsorption –> less fluid delivered to the diluting segments of the tubule –> less free water excreted
–> directly stimulates thirst

17
Q

Explain the theory of cortisol deficiency leading to hyponatremia in Addisonian patients

A

lack of cortisol –> lack of negative feedback from cortisol on CRH –> uninhibited release of ACTH and ADH –> water retention –> hyponatremia

18
Q

What is the expected urine Na+ cc of dogs with hypoadrenocorticism as opposed to dogs with pseudo-addison’s (i.e., hypovolemic hyponatremia with hyperkalemia from other causes)?

A

addisons: > 30 mmol/L, reflecting the absence of aldosterone
other: low urine Na+ (low ECV –> aldosterone –> Na retention)

19
Q

How do diuretics lead to hyponatremia?

A
  • increased thirst and ingestion of water
  • loss of isotonic fluids from diuretics –> ADH release –> dilutional hyponatremia from water retention
  • diminised NaCl reabsorption in the loop of Henle and distal tubule –> less urine dilution
  • severe potassium depletion
20
Q

What artifacts can lead to pseudohyponatremia?

A

*hypoproteinemia
hyperlipidemia

serum Na+ will decreae by ~ 1 mmol/L for every 10 mmol/L increase in total serum lipid cc
high serum protein –> artifactual hyponatremia, low serum protein inverse

21
Q

What is the major organic osmolyte accumulating or decreasing in brain cells in response to Na+ cc changes

A

Myoinositol

22
Q

What condition is caused by too rapid correction of hyponatremia?

A

osmotic demyelination syndrome (ODS)

23
Q

What parts of the brain are most prone to ODS?

A

the midbrain and striatum are the slowest to recover osmolytes and therefore most severely affected by too fact correction of hyponatremia

24
Q

2 mL/kg IV 3% hypertonic saline will raise serum Na+ cc by approximately how much?

A

2 mmol/L

can be used to alleviate neurologic abnormalities from hyponatremia

25
Q

Hyponatremia is considered to be acute if it has a known duration of < ____ hours

A

48 hours

26
Q

How do you calculate the Na deficit?

A

Na deficit = TBW x (normal Na - patient Na)

27
Q

What structure of the brain is most susceptible to osmotic demyelination syndrome?

A

Thalamus

28
Q

How do you calculate the free water deficit?

A

water deficit = (patient Na/normal Na - 1) x BW x 0.6

29
Q

How does congestive heartfailure lead to hyponatremia despite increased total body sodium?

A

RAAS upregulation in heart disease&raquo_space; Na reabsorption increased

decreased perfusion from CHF&raquo_space; ADH release&raquo_space; free water retention

30
Q

What are the 3 phases of compensation to hypo or hypernatremia and what is their time frame?

A

immediately (minutes to hours)
* hyponatremia - increased interstitial pressure will lead to water exiting into the CSF and then venous circulation
* hypernatremia - decreased interstitial hydrostatic pressure&raquo_space; fluid drawn from CSF into brain interstitium

Early:
* hyponatremia - swollen neurons expell solutes (Na, potassium)
* high plasma Na and Cl molecule cc&raquo_space; move from CSF into brain tissue

hours to days
* hyponatremia - swollen neurons also expell organic osmolytes
* hypernatremia - neurons accumulate organic osmolytes, idiogenic osmolytes

31
Q

What is the expected serum Na drop for increases in glucose?

A

for every 100 mg/dL increase 1.6-2.4 mEq/L decrease in Na cc

32
Q

How do you calculate the change in Na+ cc per L of infusate?

A
33
Q

How do you calculate the electrolyte-free water clearance?

A
34
Q

Fill the blanks

A
35
Q

How should severe hyponatremia with neurologic signs be treated?

A

give rapid 1-2 mL/kg 3% HTS solution (20 min)

check serum Na, goal: 4-6 mEq/L increase

36
Q

Fill in the blanks

A