Control of ECF and Osmolality Flashcards
Hyponatremia
Pna<135 typically due to water retention
3 types of hyponatremia
psuedonatremia, isotonic or hypertonic hyponatremia, and Hypotonic hyponatremia
What is psuedonatremia?
Artifactual reading due to a measurement problem, generally due to hyperlipidemia or hyperproteinemia
What is Isotonc or hypertonic hyponatremia?
the presence of unmeasured effective osmoles (mannitol) is causing the shift of H2O from ICF to ECF (hyperglycemia, contrast)
What is Hypotonic hyponatremia?
Effective osmolality of the plasma is LOW, TRUE hyponatremia
Hypotonic hyponatremia has 3 classes
Hypovolemic (volume depletion, low BP), Euvolemic, and Hypervolemic (ECF volume expansion, edema)
Hyponatremia is secondary to
defect in renal water clearance (since low Posm, low ADH, high H2O excretion)
Reasons for defect in renal water clearance?
Excessive water drinking (psychiatric issue) usually due to medications
Psuedohyponatremia
Na levels appear high when measured in total plasma, but normal when measured in plasma water
Isotonic or Hypertonic Hyponatremia causes
presence of effective osmole
Syndrome of Inappropriate ADH (SIADH)
euvolemia; plasma ADH is inappropriately HIGH; presistant ADH and persistant reabsorption of H2O
Tricyclic antidepressants and morphine can cause SIADH
stimulate ADH and can cause hyponatremia
Presentation of patient with SIADH
hyponatremia, (-) free water clearance, despite need to excrete
Treatment for SIADH hyponatremia
H2O restriction, blockade of ADH at the collecting duct
Nephrogenic Syndrome of Inappropriate Antidiuresis
SIADH like symptoms described by a GAIN OF FUNCTION of the ADH receptors (V2)
Exertion and Hyponatremia
prolonged exercise (>4hr) loss of electrolytes through sweat and excessive intake of HYPOTONIC fluids, ALSO during exercise ADH is inappropriately secreted
Hypernatremia
pna >145, often the result of unreplaced water loss
Body’s defense against hypernatremia
ADH and thirst
Diabetes insepidus
excretion of large volumes of HYPOTONIC urine due to a defect in ADH (inability to resorb water properly)
Central diabetes insepidus
decreased production of ADH from pituitary (stroke, tumor, drug-induced, genetic)
Nephrogenic Diabetes insepidus
kidneys inability to respond to ADH (drug-induced [LITHIUM] or defect in V2 receptor)
In a normal patient, water deprivation will result in
ADH secretion, water retention, and concentrated urine
In a patient with Central DI, water deprivation will result it
no ADH, water still lost, Uosm will remain < Posm
Central DI, patient when given endogenous ADH
ADH, will cause water retention, and urine concentration
Nephrogenic DI, patient is given endogenous ADH
urine concentration remains dilute, no response to ADH
under euvolemic conditions, the excretion of Na is
equal to intake of Na
regulation of Na reabsorption occurs at the
proximal tubule and loop of Henle, Fine tuning occurs at distal tubule and collecting duct
Autoregulation of GFR and Na excretion
despite positional changes, changes in BP, etc, GFR is regulated to remain constant and provide a constant filtered load of Na
Tubuloglomerular feedback TGF
Autoregulatory mechanism; macula densa sense NaCl flow and controls afferent arteriole
Glomerular tubular balance
fraction of Na reabsrobed in the proximal tubule is always 67%, even if GFR increases (then absolute reabsorption increases)
What two mechanisms regulate Glomerular tubular balance
Na-solute symport and starling forces in the peritubular capillaries
Na-solute transport increases with an
increase in Filtered load (increased GFR increases the filtration of other solutes (glucose, aa) and the reabsorption increases for these solutes as well as Na
If filtration fraction increases (H2O and electrolytes lost from blood)
then the reabsorptive pressure of the peritubular capillaries will be greater (decreased Pc and increased oncotic P) and Na is more likely to be reabsorbed
Load dependent Na transport in the loop of Henle
if a large amount of Na arrives at ascending limb, a large amount will be transferred, if a small amount arrives a small amount will be transferred; this way a constant amount arrives at distal tubule
Regulators of Na excretion
Aldosterone, ANP, SNS
total Na and ECF volume is controlled by
Aldosterone, ANP, SNS, and ADH
SNS effect on kidney
Increased renin release (beta-1), RAAS, directly increases Na absorption at the proximal tubule
RAAS effects
increased Na reabsorption directly, via AT1 receptors by increasing # of Na/H symporters
Stimulates aldosterone release from adrenal cortex
Increases the FF by increasing GFR (constriction of efferent)
Systemic arterial vasoconstriction (increase BP, TPR, MAP)
ADH release –> water retention (increased ECF, MAP)
Negative feedback to Renin release
ADH stimulation
high plasma osmolality, Ang II, decreased baroreceptor stretch
Atrial Natriuretic Peptide (ANP)
increases Na excretion in response to increased ECF or hypertension
ANP increases Na excretion through
increased GFR, reduced Na reabsorption in proximal tubule, and in the collecting duct
