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23 Cards in this Set

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what is the normal brain adaptation in hypernatremia?
initial cell shrinkage --> normal cell volume is maintained due to immediate accumulation of electrolytes (water flows back in) --> organic osmolytes accumulate and extrusion of electrolytes occurs in order to protect cells from having too much water flow back inside brain cells
why would you want to correct hypernatremia slowly?
to protect brain from edema (since dissipation of organic solutes from brain cells during normal correction is slow, giving the pt a lot of water at once will lead to water shift into brain with resultant edema)
which of the following are NOT causes of hypernatremia?

a. decreased access to water
b. defective thirst mechanism
c. abnormally increased ADH release and hyperresonsiveness
d. decreased urinary concentrating ability (CRI)
C. hypernatremia is actually caused by impaired ADH release or responsiveness (CDI or NDI)
diff b/w central diabetes insipidus and nephrogenic diabetes insipidus.

tx of the two?
CDI= brain lacks ability to release/produce ADH (give ddAVP)

NDI= inability of kidney to respond normally to ADH (tx underlying dz)
name some causes of NDI
-mutation in V2 receptor or AQP2
-Li therapy
- hypokalemia/hypercalcemia
-obstruction
-sickle cell anemia
- chronic renal dz
tx of hypernatremia?
replenish water deficit
tx of hypernatremia is via replenishment of water deficit. which would you use:

a. pure water
b. D5W

and why?
a.

hypernatremia is catabolic state, associated with insulin resistance. When you have insulin resistance at the same time you give D5W (to correct hypernatremia), you cannot drive excess glucose (from D5W) into cell and it stays outsdie the cells. Hyperglycemia results.
T or F. Acute hyponatremia is usually acquired in community settings.
F. almost always hospital acquired; resulting from excessive hypotonic fluids (which you should never give to a pt anyways)
symptoms of hyponatremia is mainly ________.
neurological
in the case of hyponatremia + hypovolemia (due to profuse GI bleeding, for example), why does serum ADH remain HIGH in spite of hyponatremia?
the body has given priority to maintaining VOLUME over Na levels. in cases of hypoperfusive shock, for example, the body senses low EABV via baroreceptors in the afferent arterioles of the kidneys and this leads to increased production of ADH to retain more water
T or F. Chronic hyponatremia is usually out of hospital.
true. clinical settings for chronic hyponatremia include use of thiazide diuretics, SIADH, compulsive water drinking
which of the following are NOT non-osmotic pathways for stimulating ADH release?

a. EABV
b. plasma osmolarity
c. nausea
d. pain
e. stress
f. hormones
B
what are some clinical settings for acute hyponatremia?
POST-OP
- TURP
- uterine ablation
- use of hypotonic fluids post-surgery

INAPPROPRIATE PAIN MANAGEMENT (ADH)

OXYTOCIN TX
explain how hypernatremia leads to cerebral shrinkage and is corrected naturally
increase in plasma osmolality and Na conc --> osmotic gradient created that favors water mvmt out of brain cells into ECF (cerebral shrinkage) --> brain cells adapt by increasing # transporters for osmolytes on cell membrane and increasing intracellular solute conc --> restoration of brain cell volume back UP to normal
explain how hyponatremia leads to cerebral edema and is corrected naturally
decrease in plasma osmolality and Na conc --> osmotic gradient created that favors water mvmt from ECF into brain cells (cerebral edema) --> brain cells adapt by losing osmolytes (organic solutes) to the ECF in order to decrease intracellular solute conc --> restoration of brain cell volume back DOWN to normal
T or F. only with acute hyponatremia and hypernatremia will lead to neurological symptoms (lethargy, seizures, comas) due to cerebral edema or cerebral shrinkage, respectively
True
how can you correct for hyponatremia without getting complications of myelinolysis?
by correcting for hyponatremia with sodium and giving <12 mEq per day.anything more than that will lead to abnormal decrease in brain volume
which pt population is most likely to get encephalopathy from hyponatremia?
menstruant (fertile) women who just had a operation who gets hypotonic solution
name the most important osmolytes (organic solutes) found in the brain
taurine (50%)
inositol
glutamine
glutamate
glycine
what happens with too rapid correction (>12 mEq/L per day) in the case of hyponatremia?
as the brain cells naturally adapt to the acute onset of cerebral edema by losing osmolytes to the ECF to try to bring the volume back down, too rapid correction with saline can lead to shrinkage of brain cells and ultimately, pontine myelinolysis (quadriparesis, confusion, coma)
how would you correct asymptomatic vs. symptomatic chronic hyponatremia?
asymptomatic = DEPENDS ON VOLUME STATUS:
-restore volume with normal saline if hypovolemia exists in order to shut off ADH (then re-evaluate)
-fluid restriction if euvolemic or hypervolemic

symptomatic = ALSO BASED ON VOLUME STATUS:
- if hypovolemic, give saline to restore water volume and shut off ADH (then re-evaluate)
- if euvolemic, give 3% NaCl +/- diuretics (so you restore Na concentration without messing with volume)
in what type of pts do you need to be especially cautious of causing myelinolysis when trying to correct for hyponatremia?
hypokalemic
liver dz
malnourished
burns
hypoxemia
female gender
what's the diagnostic approach to hyponatremia?
FIRST look at urine osmolality.
if <100 = person is drinking himself to death (rare, schizophrenic) ==> fluid restriction
if >100 = have to look at urine Na

SECOND, look at urine Na
if <30 = pt doesn't have enough salt in their body ==> give them a hamburger!!
if >30 = pt may be on diuretic use, have adrenal insufficiency, hypothyroidism, or renal failure