Sodium disorders Flashcards
Normal serum Na+?
135-145 Meq/L
Normal plasma/serum osmolality?
285-300 Meq/L
Eqn to estimate plama/serum osmolality?
Na x 2 + BUN/2.8 + Gluc/18
Main contributor to serum osmolality?
Na
Symptoms of hypo/hypernatremia are due to effects on which orhan?
Brain
Sodium abnormalities are usually caused by ____________ NOT ___________.
Water problems
NOT
Salt problems
Extracellular hyp-O-osmolality have what effent on neurons?
swelling
Sx if Na+
nausea
malaise
Sx if Na+ = 115-120:
headache
lethargy
Sx if Na+
obtundation
seizures
coma
More severe sx in fast or slow hyp-O-natremia?
Fast
brain has less time to adapt
Effect of hyp-ER-natremia on neurons?
cells shrink
Sx of hyp-ER-natremia?
lethargy
weakness
irritability
twitching
seizures
coma
death
Decreased brain volume due to hyp-ER-natremia can have what effect on vasculature?
rupture cerebral vessels
Clinically significant water shift occurs with 30-35 mosm/kg osmolar gradient between plasma and brain; what is the corresponding rise in serum Na+?
17 meq/L
Hormone responsible for maintenance of plasma osmolality:
ADH
arginine vasopressin
Where is ADH produced?
supraoptic and paraventricular nuclei of hypothalamus
Where is ADH stored and released?
secretory granules
posterior pituitary
Osmotic stumuli of ADH release:
INCREASED plasma osmolality
Non-osmotic stimuli of ADH release:
hypovolemia –> baroreceptors
pain
esophageal stimuli
medications
What receptor binds ADH to release aquaporin 2 to luminal membrane?
Where does this occur?
V2 (activates protein kinase)
collecting tubule
With high presence of ADH:
Urine osmolality = ?
Plasma osmolality = ?
urine- increased
serum- decreased
**water flows out of tubule back into blood
In low/absent ADH state:
Urine osmolality= ?
Blood osmolality= ?
urine- increased
blood- decreased
**water excreted in urine
Physiologic responses to HIGH plasma osmolality:
thirst
ADH release
water reabsorption
concentration of urine –> high urine osmolality
Physiologic response to LOW plasma osmolality:
No thirst
No ADH release
Loss of free water – collecting tubules impermeable
Low urine osmolality – dilute urine
Plasma osmolality maintained within __%.
1%
Indicator of the presence of ADH?
Urine osmolality
What generally tells you what the kidney THINKS about the body’s volume status?
urine sodium
Range of urine osmolality in a normal kidney?
50-1400 mosm/L
Normal daily osmolar load from dietary protein/salt?
500-750 mosm
excreted in urine
If you have 500 mosm/day to get rid of and your maximum urine osmolarity is 1000 mosm/L, how much urine will be excreted?
0.5 L
If you have 500 mosm/day to get rid of and your minimum urine osmolarity is 50 mosm/L, how much urine will you excrete?
10 L
Hormones responsible for retention of sodium in volume depleted state?
Ang II
Aldosterone
What is the kidney doing of urine sodium is
senses low effective circulating volume, so it’s holding on to sodium
What’s going on in the kidney if urine sodium is > 10 meq/L?
-sensing expanded ECV
OR
-not able to properly retain Na+
OR
-excreting Na as an obligate cation with something else
What is pseudohyp-O-natremia?
What causes this?
low Na with normal or elevated Plasma osmolality.
Caused by:
Hyperlipidemia (normal Posm)
Hyperproteinemia (normal Posm)
Hyperglycemia (elevated Posm)
Hypertonic mannitol (elevated Posm)
How does hyponatremia develop if mechanisms are in place to maintain plasma osmolality within 1%?
Non-osmotic stimuli override osmotic stimuli (or lack of) to secrete ADH at the expense of plasma osmolarity
**perfusion to brain is more important than perfect osmolality in plasma
Four steps in clinical eval of hyponatremia:
- Check Posm: confirm true hypoosmolar hyponatremia
- Check Uosm: is ADH acting?
- 100 – yes, despite hypoosmolar state, either appropriate for volume status or inappropriate - Check UNa+: what is the kidney’s perception of ECV?
- Check the patient: volume status/clinical picture?
Hyponatremia with Uosm
excess water intake (primary polydipsia)
**need to drink 10-15 L/day to overwhelm kidney’s ability to clear free water
Two exceptional causes of hyponatremia with Uosm
beer potomania
tea and toast syndrome
**not ingesting enough(or any) protein/solutes for an extended period (low daily osmolar load)
Treatment for primary polydypsia?
water restriction
UNa+
Reabsorbing Na+ in an effort to reexpand vascular space
UNa+
Recieving the wrong signal.
Edematous states: think CHF/cirrhosis/nephrosis
UNa+ > 10, patient is volume depleted and hyponatremic. What is the kidney doing?
Salt wasting. Receiving the wrong signals. This is rare.
UNa+ > 10, patient is volume expanded and hyponatremic. What is the kidney doing?
Volume is appropriate or expanded
Brain or kidney is confused
Causes of volume depleted hyponatremia with UNa+ of
GI– N/V, diarrhea
Skin– burns
Diuretics– late
Pure cortisol deficiency (Addison’s???)
Causes of hyponatremia with UNa+
Edematous states/poor perfusion–reduced ECV
- CHF
- Cirrhosis/liver failure (low albumin?)
- nephrotic syndrome (proteinuria?)
Causes of salt wasting (hyponatremia with volume depletion and UNa+ > 10):
adrenal insufficiency
salt wasting renal disease
Early diuretics
Hypokalemia with metabolic alkalosis after vomiting (lose sodium and bicarb)
hypothyroid
Causes of hyponatremia with UNa+ > 10 and appropriate or expanded volume:
SIADH– Syndrome of Inappropriate ADH secretion
- oat cell carcinoma (paraneoplastic)
- pulmonary process (TB, PNA, asthma)
- Drugs (chlorpropamide, oxytocin, tegretol, cytoxan)
- esophageal process
- pain
- neuropsychiatric
Reset osmostat
CKD
Fixed ADH secretion without regard to osmotic or volume status:
SIADH
Tx for SIADH:
fluid restriction
increase osmolar load (high protein/Na diet)
Treatment for volume depleted hyponatremia?
NS
**replenish volume, turn off ADH
Tx for volume neutral or expanded hyponatremia:
restrict free water intake
treat state of poor perfusion
Tx for severe hyponatremia not related to pure volume depletion OR with neurologic sx:
hypertonic saline
Pharm tx for volume expanded hyponatremia:
ADH antagonists
Tolvaptan, Conivaptan
Rapid correction of hyponatremia risks?
Central Pontine Myelinolysis (BAD)
Brain’s own mechanism of compensation for slowly developing hyponatremia:
idiogenic osmoles
**more risk in rapid correction
V1a and V1b receptors response to ADH?
vasoconstriction and ACTH release
Hypothalamus/pituitary not releasing ADH?
Central diabetes insipidus
Collecting tublues don’t respond to ADH:
nephrogenic diabetes insipidus
How could you differentiate central vs nephrogenic DI?
give exogenous ADH
if UOsm increases –> central etiology
Dx of diabetes insipidus usually made by patient complaint of?
polyuria (usually not hypernatremia)
Drug to know that causes nephrogenic DI?
lithium
Safe rate for correcting hypernatremia?
slowly
0.5 meq/hour –> 12 meq/24 hr
What to give to replace free water deficit?
Free water ORALLY (NOT IV)
D5W IV
**can give 1/4 NaCl if volume depleted
