Na / Water Balance Flashcards
What percentage of water is intra / extracellular
Where is most of the Na?
2/3 water intracellular. 1/3 extracellular
Most Na is extracellular.
Osmolality equation
Normal range for osmolality
2xNa + glucose/18 + BUN/2.8
Normal range is 280-300
Where are osmol receptors?
Hypothalamus
Where are baroreceptors?
Carotid sinus and aortic arch
3 non-osmotic factors that can trigger ADH
Pain, nausea, meds
Causes of hypovolemic hypoosmolar states (5)
- Renal losses (urine Na is inappropriately high [>20 mEq/L]) – kidney disease, diuretics, aldosterone deficiency
- Non-renal losses (urine Na is appropriately low [less than 10 mEq/L]) – GI losses, skin / burns.
3 causes of hypervolemic hypo-osmolarity
CHF, cirrhosis, nephrotic syndrome
9 causes of SIADH
SIADH caused by excess pituitary secretion (tumor, infection trauma), ectopic ADH production (small cell lung cancer), drugs, pulmonary infection, COPD, nausea, or severe pain.
2 hormonal causes of euvolemic hypo-osmolarity that mimic SIADH
- Hypothyroidism – decreased cardiac output → decreased intravascular volume → decreased GFR → increased proximal reabsorption of water / Na → less delivery to diluting segment of nephron. Stimulation of ADH via baroreceptors also occurs.
- Cortisol deficiency – cortisol normally feeds back negatively on ADH production, so deficiency → more ADH than normal. May mimic SIADH.
Beer drinker’s potomania
Poor diet → low solute intake → low solute excretion → limits how much water can be excreted w/ maximally dilute urine
4 causes of hypernatremia
Osmotic diarrhea / diuresis, inadequate replacement of insensible water losses, diabetes insipidus
3 causes of central diabetes insipidus
Caused by CNS abnormalities (pituitary / sellar mass, head trauma, infiltrating disease of hypothalamus)
4 causes of nephrogenic diabetes insipidus
Caused by inherited / congenital receptor dysfunction, meds (lithium, demeclocycline), or hypercalcemia
5 effects of Ang II
Stimulates Epi / Norepi and promotes release of ADH. Constricts efferent arteriole to maintain GFR. Increases proximal tubular Na resorption via Na/H exchange. Triggers thirst
2 things that trigger aldosterone release
Ang II and hyperkalemia
Primary hyperaldosteronism
Presentation (3)
Diagnosis (2)
Treatment (3)
- Presents w/ MILD volume expansion, HTN, and possibly hypokalemia
- Confirmed by salt-loading or administration of normal saline.
- Treat w/ surgery or drugs that block mineralocorticoid receptor: spironolactone, eplerenone
Treating hypoaldosteronism
Fludrocortisone
Syndrome of apparent mineralocorticoid excess
Presentation
Cause
- Presents similarly to primary hyperaldosteronism but renin and aldosterone are both low.
- Cortisol can activate mineralocorticoid receptor, but normally, 11b hydroxysteroid dehydrogenase type 2 in kidney metabolizes cortisol → cortisone to prevent this.
- This enzyme may be inactivated by a mutation or by licorice (glycyrrhiazic acid).
- This is why HTN is common in Cushing’s. Too much cortisol overwhelms 11b hydroxysteroid dehydrogenase
Pheochromocytoma
Sxs (6)
Treatment (4)
- Sxs – HTN (due to vasoconstriction) and paroxysmal headache / palpitations / sweating / pallor / tremor.
- Treat w/ surgery, but BP must be controlled to avoid hypertensive crisis during surgery.
- Alpha blockers are first line, which block α1 mediated vasoconstriction. Subsequent vasodilatation can lead to reflex tachycardia, so volume repletion + beta blockers can be used to control the HR.
- If BB is given first, it will block β2 mediated vasodilatation → “unopposed α1” vasoconstriction → severe hypertension.
What is considered polyuria
Diff Dx for polyuria (5)
- Polyuria is defined as >3L / day
* Diff Dx of polyuria: psychogenic polydipsia, diabetes insipidus, DM, hyperglycemia / calcemia (osmotic diuresis)
