dysnatremic disorders Flashcards
when is ADH released?
when osmolality in the blood is high
when body is volume depleted
if these are in conflict, volume depletion wins.
What is required to excrete excess water?
- No ADH
- functional DCT
- enough fluid delivered distally
What is required to keep body sufficiently hydrated?
- increase water intake
- working countercurrent mechanism
- ADH
- tubular response to ADH
hyponatremia and relationship with osmolarity
usually hyponatremia is also hypoosmotic
occassionally we see hyponatremia with a hyperosmotic situation:
another factor, like glucose, is in the blood, and this increased osmolarity drives water out of the ICF, thus diluting the Na. treat the diabetes.
2 ways to become hyponatremic
- drink lots of water and don’t pee
2. drink so much water that you overwhelm the kidney’s diluting capacity.
hypovolemic hyponatremia causes
vomiting, diarrhea, NG tube loss, thiazide diuretics, burns or sweats accompanied by lots of water intake
labs for hypovolemic hyponatremia
conc. of na less than 20 meq/l
BUN: cr over 20:1
how do thiazides cause hypovolemic hyponatremia? Why not loops?
thiazides poison the DCT. The DCT is where we normally dilute urine (goes from 200 at end of LOH to 50 at begining of CCT). so, more sodium excretion in comparison to water excretion. But, still, thiazides cause hypovolemia, which induces thirst, which further dilutes the sodium.
Loops don’t do this- they abolish the countercurrent mechanism, so very little water is retained, even in the presence of ADH, because there is not osmotic gradient pushing the water out.
hypervolemic hyponatremia
usually because the extra fluid is in the wrong space. caused by CHF, cirrhosis. this causes decreased renal perfusion because the body reacts as though it is volume depleted: increased thirst and ADH release dilutes sodium.
euvolemic hyponatremia
many causes, including hypothyroidism, adrenal insufficiency, kidney failure, primary polydipsia, syndrome of inappropriate ADH
primary polydypsia
quite rare- must dring 15-20 L in a day. more common among psyche patients. ADH is maximally suppressed and urine diluting ability is retained- the kidney just can’t dilute it enough.
syndrome of inappropriate ADH
normal adrenal, renal, and thyroid studies.
non-physiologic ADH secretion.
inappropriately concentrated urine in the setting of hyponatremia
normal sodium handling
what is SIADH associated with?
bleeds, CNS surgery, lung pathologies, small cell carcinoma, SSRIs, cyclophosphamides, major surgeries
clinical manifestations of hyponatremia
confusion, lethargy, seizure, herniation, death
treatment of hyponatremia
return Na to safe level and treat underlying cause. don’t correct sodium faster than 0.5-1 mEq/hr (central pontine myelolysis)
treatment for hypovolemic hyopnatremia
IV saline to increase BP and directly increase Na. BP correction will also allow for water excretion
hypervolemic hyonatremia treatment
water restriction, loop diurectics to help them loose water. treat underlying cause.
SIADH treatment
don’t give salt: they have normal salt excretion and not enough water secretion, so they will actually take saline and excrete it in a more concentrated form than it was given to them, further worsening their problem. do water restriction and loop diuretics. you can also increase sodium intake and give ADH antagonists (DEMECLOCYLINE)
hyperosmolality
increase in effective osmolality: shift from the ICF to the ECF. causes are hypernatremia and hyperglycemia
causes of hypernatremia
too much salt intake (rare) or not enough water (either not enough in, too much out, or a combo).
causes of not enough water in the body
- not enough water in: rare in alert adults with normal thirst mechanism.
- too much water out/water loss: sweat, burns, renal, GI.
diabetes insipidis
ADH isn’t working. may be central (ADH not secreted: sarcoid, tumor) or nephrogenic (kidney unresponsive to ADH: seen in patients taking LITHIUM. demeclocycline, hypercalcemia, hypokalemia).
treatment for hyponatremia
avoid over rapid correction.
give water if there is no sodium loss; give a saline soln if there is sodium loss.
if hypotensive, give isotonic saline before worrying about water deficit.
treatment of diabetes insipitis
central: ADH replacement
nephrogenic: vol depletion with low salt diet and thiazide diuretic. this will lead to enhanced proximal NaCl and water absorption. Also, excrete dietary protein
