Hyponatremia Flashcards
tonicity
the volume behavior of cells in a solution
hypotonic, isotonic, and hypertonic
effective mOsms/total body H2O
effective vs. ineffective mOsms
effective means that the mOsms affect transmembrane water flow across an impermeable membrane, while ineffective mOsms do not
osmolarity
(effective + ineffective osms)/total body H2O
organum vasculosum of the lamina terminalis (OVLT)
circumventricular oran organ in the brain that lacks a blood-brain barrier
may be a site of principal brain osmoreceptors affecting thirst and release of ADH from the posterior pituitary
areas of adjacent hypothalamus near the anterior wall of the third cerebral ventrical may also serve a similar purpose
What is the true determinant of osmoreceptor activity?
the degree of stretch of the osmoreceptor cell membrane in the face of changing tonicity that engages stretch-activated or stretch-inactivated channels
Where is ADH synthesized and release from?
synthesized in the supraoptic and paraventricular nuclei of the hypothalamus
released from the posterior pituitary
What are some of the signals that trigger ADH release?
osmoreceptors in the OVLT responding to plasma tonicity
other neural paths to the brain from non-osmotic stimuli related to volume depletion, nausea, pain, sedation, and slected drugs
What components make up urine volume?
electrolyte clearance (Ce) + electrolyte-free H2O clearance (CefH2O)
What are the three types of hyponatremia?
isotonic hyponatremia - artifactual
hypotonic hyponatremia - decreased CefH2O
hypertonic hyponatremia - translocational
causes of isotonic hyponatremia
hypergammaglobulinemia
hypertriglyceridemia
hyperchylomicronemia
cause of hypertonic hyponatremia
the addition of effective mOsms in the ECF such as glucose, mannitol, and sucrose
symptoms of hypotonic hyponatremia
most early symptoms occur as the SNa drops below 125 mEqv/L
nausea
fatigue
headache
lethargy
somnolence
coma
seizures
brain response to hypotonic hyponatremia
rapid adaptation through loss of sodium, potassium, and chloride
slow adaptation through loss of organic osmolytes
What is the only way to get hypotonic?
take in H2O and fail to excrete it
water intake needs to exceed the CefH2O
never caused by the kidney excreting more Na than H2O
What are the three outcomes of hypotonic hyponatremia?
volume depletion
near euvolemia
edema
hypotonic hyponatremia with volume depletion
high H2O and low TB Na
caused by vomiting/diarrhea, sweating, exercise, diuretics, Addisons, etc.
reduction of EABV -> increased baroreceptor/sympathetic effect on renal afferent arterioles reducing GFR and activation of RAAS
antiotensin II increases Na/H, Na/K/Cl2, and Na/Cl transporters
persistent aldosterone effect on the collecting duct associated with ADH release ensures recapture of both Na and H2O, resulting in oliguria
patient takes hypotonic fluids increasing TB H2O relative to TB effective mOsms
hypotonic hyponatremia with edema
increased H2O and increased TB Na
caused by cirrhosis, nephrosis, heart failure, and renal failure
perception of a reduced EABV stimulates retention of Na and H2O through RAAS and ADH
patient then takes in hypotonic fluids increasing TB H2O relative to TB effective mOsms
near euvolemia
increased H2O and normal TB Na
common causes are:
psychogenic polydipsia
potomania
thiazide induced SIADH
reset osmostat
What is the maximum rate at which two normal kidneys can two normal kidneys excrete absent ADH?
28L of H2O/day
or
1.2 L/hr
psychogenic polydipsia
near euvolemia hypertonic hyponatremia
seen in the setting of psychosis, particularly schizophrenia with OCD
patient drinks a lot of water, 3-4L/hr, retain 2-3L/hr, seizure, excrete H2O, and then repeat the cycle
potomania
near euvolemia hypertonic hyponatremia
alcohol inhibits ADH and thus increases urine volume
if a patient takes in a steady diet or drinks water beyond thirst while on a crash diet, they will develop potomania
thiazide-induced hyponatremia
near euvolemia hypertonic hyponatremia
usually occurs within a couple weeks of starting the drug
more common in those with lower GFRs
no obvious volume deplesion
increased water reabsorption in the intermedullary collecting duct
syndrom of inappropriate ADH secretion (SIADH)
leads to near euvolemia hypertonic hyponatremia
no evidence of heart disease, liver disease, edema, or orthostasis
Uosm is inappropriate for the Posm
if the Posm is lower than normal range (275-290 mOsm/L), the Uosm should be below 100 mOsm/L
urine Na should reflect dietary Na intake
BUN and uric acid levels are low
cannot secrete a H2O load
reset osmostat
leads to near euvolemia hypertonic hyponatremia
the set point for the osmoreceptors is lower
looks like SIADH except the patient with a reset osmostat can excrete a H2O load, ex. pregnancy
treatment of hypotonic hyponatremia
safest approach is water restriction to allow for evaporation
if volume depleted, administer normal saline (0.9%) intravenously until euvolemic
if there is edema, treat primary disease to try and increase CeH2O
oral V2-receptor antagonists can be used to raise tonicity in SIADH and in heart failure, ubt are contraindicated in liver disease
3% Na administration in acute intoxication with symptoms of cerebral edema
SNa should not rise faster than 8 mEq/L/day to avoid osmotic dmyelination
should avoid normal saline in SIADH unless coupled with loop diuretics because the kidney will dumpy the Na asnd keep the H2O
formula for calculating serum Na
(infusate Na - serum Na)/(total body water + 1)
or
[(infusate Na + infusate K) - serum Na]/(total body water + 1)
guidelines for using the spot urine electrolytes
if (UNa + UK)/SNa is greater or equal to 1.0 don’t give any H2O
if between 0.5-1.0, restrict to 500 mL/day
if less than or equal to 0.5 restrict to 1000 mL/day
