Sodium Flashcards
What percentage of an animal’s lean bodyweight is total body water?
60%
What is the equation for osmolarity in serum
mOsm/kg = 2Na + BG/18 + BUN/2.8
What are the 2 main mechanisms regulating osmolarity in the body?
thirst (water intake)
kidney water retention or excretion
how does the body detect osmolality?
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%
What are the 2 major stimuli for the sensation of thirst?
- hyperosmolality (direct stimulation)
- decreased effective circulating volume (ECV) (activates RAAS system, which activates angiontensin II, which stimulates ADH release
Where is ADH synthesized and stored?
synthesized in the hypothalamus, stored in secretory granules in the posterior pituitary gland
Explain the mechanism of action by which ADH leads to water retention
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
What are the 2 major stimuli for vasopressin release?
- increased osmolality
- decreased effective circulating volume
where are the baroreceptors located that monitor the effective circulatory volume?
- cardiopulmonary circulation
- carotid sinus
- aortic arch
- afferent glomerular arterioles in the kidney
How does decreased effective circulatory volume lead to ADH release?
baroreceptors sense decrease in ECV –> increased sympathetic tone –> RAAS activation –> angiontensin II activation –> ADH release
Explain how a patient may have hypoosmolar plasma but increased water retention
decrease in ECV will lead to RAAS and subsequent ADH release despite concurrent hypoosmolality
Explain how a patient in systolic heart failure develops hyponatremia
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
What is the expected decrease of serum Na concentration for every 100 mg/dL increase in glucose
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
Why does an increase in BUN not lead to hyponatremia?
BUN moves freely in and out of cells –> thus is not an effective osmole –> no water drag into the ECF
Explain how you can use urine Na+ cc to assess a patient’s volume status
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
By which 3 mechanisms can hypovolemia lead to increased TBW and hyponatremia?
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
Explain the theory of cortisol deficiency leading to hyponatremia in Addisonian patients
lack of cortisol –> lack of negative feedback from cortisol on CRH –> uninhibited release of ACTH and ADH –> water retention –> hyponatremia
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)?
addisons: > 30 mmol/L, reflecting the absence of aldosterone
other: low urine Na+ (low ECV –> aldosterone –> Na retention)
How do diuretics lead to hyponatremia?
- 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
What artifacts can lead to pseudohyponatremia?
*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
What is the major organic osmolyte accumulating or decreasing in brain cells in response to Na+ cc changes
Myoinositol
What condition is caused by too rapid correction of hyponatremia?
osmotic demyelination syndrome (ODS)
What parts of the brain are most prone to ODS?
the midbrain and striatum are the slowest to recover osmolytes and therefore most severely affected by too fact correction of hyponatremia
2 mL/kg IV 3% hypertonic saline will raise serum Na+ cc by approximately how much?
2 mmol/L
can be used to alleviate neurologic abnormalities from hyponatremia
Hyponatremia is considered to be acute if it has a known duration of < ____ hours
48 hours
How do you calculate the Na deficit?
Na deficit = TBW x (normal Na - patient Na)
What structure of the brain is most susceptible to osmotic demyelination syndrome?
Thalamus
How do you calculate the free water deficit?
water deficit = (patient Na/normal Na - 1) x BW x 0.6
How does congestive heartfailure lead to hyponatremia despite increased total body sodium?
RAAS upregulation in heart disease»_space; Na reabsorption increased
decreased perfusion from CHF»_space; ADH release»_space; free water retention
What are the 3 phases of compensation to hypo or hypernatremia and what is their time frame?
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»_space; fluid drawn from CSF into brain interstitium
Early:
* hyponatremia - swollen neurons expell solutes (Na, potassium)
* high plasma Na and Cl molecule cc»_space; move from CSF into brain tissue
hours to days
* hyponatremia - swollen neurons also expell organic osmolytes
* hypernatremia - neurons accumulate organic osmolytes, idiogenic osmolytes
What is the expected serum Na drop for increases in glucose?
for every 100 mg/dL increase 1.6-2.4 mEq/L decrease in Na cc
How do you calculate the change in Na+ cc per L of infusate?
How do you calculate the electrolyte-free water clearance?
Fill the blanks
How should severe hyponatremia with neurologic signs be treated?
give rapid 1-2 mL/kg 3% HTS solution (20 min)
check serum Na, goal: 4-6 mEq/L increase
Fill in the blanks
