Hypo and hypernatremia - Basok Flashcards
What is the equation for plasma osmolarity
Posm (mOsm/kg) = 2*[Na+] + [BUN]/2.8 + [Glucose]/18
Usually [Na+] ~ 140 (120 is hyponatremia)
[BUN] ~10 so [BUN]/2.8 is about 3 (=[urea]/6)
[glucose] ~100 so [glucose]/18 ~5
So Na+ is the only effector while other values
Causes of hypernatremia
Not generally in healthy people or not bedridden
Water loss (water deficit \>sodium deficit):
- Diarrhea, vomiting, fistulas, significant burns, insensible loss (hyperventilation)
Renal losses:
-CDI, NDI, Osmotic diuretics, postobstructive diuresis,
Hypothalamic disorders:
-Adipsic hypernatremia due to decreased thirst, secondary to damage to the hypothalamic thirst centers, reset osmostat.
Sodium retention (sodium gains >water gains)
- Hypertonic saline, sodium bicarbonate administration (iatrogenic, often in rhabdomyolysis)
- Accidental salt ingestion (eg, infant formula error)
Etiology of Central DI
Idiopathic-familial (not found in CT
Neurosurgery-Craniopharyngeoma (requires head surgery), transfenoidal surgery
Head trauma
Hypoxic or ischemic encephalopathy-shock, Sheehan’s syndrome (pituitary damage after childbirth)
Neoplastic- cranyopharyngeoma, cyst, MTS;breast, lung
Miscellaneous-Histiocytosis X, Sarcoidosis, Anorexia nervosa, encephalitis, meningitis (diseases of brain)
Majority of the patients maintain normal Na+ concentration because of intact thirst mechanism (live well unless lose access to water)
Patients complain of polyuria and polydipsia
Nephrogenic DI
Etiology, causes
Normal AVP, no response from kidney (nor to DDAVP)
X-linked or autosomal in V2R (90%) or AQP2 (10%) genes (or downregulation from hypercalcemia, hypokalemia, polycystic kidney disease, urinary tract obstruction or low protein diet and low urea)
Treatment with hydrochlorothiazide palliative (increases proximal reabsorption over time, chlorpropamide and carbamazepine)
Causes:
Advanced renal disease (interstitial disease-kidney stone)
Electrolyte disturbances - Chronic Hypokalemia, hypercalcemia (like in Mult My- treat with saline)
Systemic/immune diseases - Sickle cell disease, Sjögren syndrome, amyloidosis, Fanconi syndrome, sarcoidosis, renal tubular acidosis, light chain nephropathy
Dietary disturbances - Excessive water intake, decreased salt intake, decreased protein intake (low urea in vegetarians)
Drugs - Lithium (20-70% of Li pts, lasts 8 years beyond Li cessation), demeclocycline, colchicine, vinblastine, amphotericin B (fungal infection), gentamicin, furosemide, angiographic dyes, osmotic diuretics
Miscellaneous - Postobstructive diuresis, diuretic phase of acute renal failure, osmotic diuresis.
Graph of results of water deprivation test
Stimuli for ADH release
NaCl, mannitol 3-fold increase AVP release
Nonosmotic stimuli- pain, stress, decrease of BP or blood volume (bleeding) are potent stimuli for ADH secretion
Not urea and glucose
Causes of hypovolemic hyponatremia
What is the treatment?
Vomiting, diarrhea, burns, 3rd space (surgery)
(Urinary sodium less than 10 mmol/l)
Renal losses-diuretics, Addison, osmotic diuresis
(Urinary sodium more than 20 mmol/l)
Treatment: restore volume with normal saline
Causes of normovolemic Hyponatremia
SIADH
Addison, hypothyroidism, pain, psychosis
(Urinary Na more than 20 mmol/l)
No edema
Causes of hypervolemic hyponatremia
CHF, Nephrotic Syndrome, Cirrhosis
- Edema, ascites-low effective blood volume
- High renin and high AngII
-Indicates decompensation
(Urinary Na less than 20 mmol/l)
Algorithm for evaluation of hyponatremia
Plasma osmolarity
-low - true hyponatremia
-high - pseudohyponatremia (probably extreme hyperglycemia)
Urine osmolarity
-low-primary polydipsia,
-high-SIADH
Urine Sodium -less than 25-low effective blood volume (CHF, cirrhosis, Nephrotic Syndrome)
-more than 40 meq/l-SIADH, RF,diuretics,vomiting
