Control of ECF and Osmolality Flashcards Preview

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Flashcards in Control of ECF and Osmolality Deck (41):
1

Hyponatremia

Pna<135 typically due to water retention

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3 types of hyponatremia

psuedonatremia, isotonic or hypertonic hyponatremia, and Hypotonic hyponatremia

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What is psuedonatremia?

Artifactual reading due to a measurement problem, generally due to hyperlipidemia or hyperproteinemia

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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)

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What is Hypotonic hyponatremia?

Effective osmolality of the plasma is LOW, TRUE hyponatremia

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Hypotonic hyponatremia has 3 classes

Hypovolemic (volume depletion, low BP), Euvolemic, and Hypervolemic (ECF volume expansion, edema)

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Hyponatremia is secondary to

defect in renal water clearance (since low Posm, low ADH, high H2O excretion)

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Reasons for defect in renal water clearance?

Excessive water drinking (psychiatric issue) usually due to medications

9

Psuedohyponatremia

Na levels appear high when measured in total plasma, but normal when measured in plasma water

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Isotonic or Hypertonic Hyponatremia causes

presence of effective osmole

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Syndrome of Inappropriate ADH (SIADH)

euvolemia; plasma ADH is inappropriately HIGH; presistant ADH and persistant reabsorption of H2O

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Tricyclic antidepressants and morphine can cause SIADH

stimulate ADH and can cause hyponatremia

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Presentation of patient with SIADH

hyponatremia, (-) free water clearance, despite need to excrete

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Treatment for SIADH hyponatremia

H2O restriction, blockade of ADH at the collecting duct

15

Nephrogenic Syndrome of Inappropriate Antidiuresis

SIADH like symptoms described by a GAIN OF FUNCTION of the ADH receptors (V2)

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Exertion and Hyponatremia

prolonged exercise (>4hr) loss of electrolytes through sweat and excessive intake of HYPOTONIC fluids, ALSO during exercise ADH is inappropriately secreted

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Hypernatremia

pna >145, often the result of unreplaced water loss

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Body's defense against hypernatremia

ADH and thirst

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Diabetes insepidus

excretion of large volumes of HYPOTONIC urine due to a defect in ADH (inability to resorb water properly)

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Central diabetes insepidus

decreased production of ADH from pituitary (stroke, tumor, drug-induced, genetic)

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Nephrogenic Diabetes insepidus

kidneys inability to respond to ADH (drug-induced [LITHIUM] or defect in V2 receptor)

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In a normal patient, water deprivation will result in

ADH secretion, water retention, and concentrated urine

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In a patient with Central DI, water deprivation will result it

no ADH, water still lost, Uosm will remain < Posm

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Central DI, patient when given endogenous ADH

ADH, will cause water retention, and urine concentration

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Nephrogenic DI, patient is given endogenous ADH

urine concentration remains dilute, no response to ADH

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under euvolemic conditions, the excretion of Na is

equal to intake of Na

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regulation of Na reabsorption occurs at the

proximal tubule and loop of Henle, Fine tuning occurs at distal tubule and collecting duct

28

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

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Tubuloglomerular feedback TGF

Autoregulatory mechanism; macula densa sense NaCl flow and controls afferent arteriole

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Glomerular tubular balance

fraction of Na reabsrobed in the proximal tubule is always 67%, even if GFR increases (then absolute reabsorption increases)

31

What two mechanisms regulate Glomerular tubular balance

Na-solute symport and starling forces in the peritubular capillaries

32

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

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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

34

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

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Regulators of Na excretion

Aldosterone, ANP, SNS

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total Na and ECF volume is controlled by

Aldosterone, ANP, SNS, and ADH

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SNS effect on kidney

Increased renin release (beta-1), RAAS, directly increases Na absorption at the proximal tubule

38

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

39

ADH stimulation

high plasma osmolality, Ang II, decreased baroreceptor stretch

40

Atrial Natriuretic Peptide (ANP)

increases Na excretion in response to increased ECF or hypertension

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ANP increases Na excretion through

increased GFR, reduced Na reabsorption in proximal tubule, and in the collecting duct