Control of ECF and Osmolality Flashcards

1
Q

Hyponatremia

A

Pna<135 typically due to water retention

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2
Q

3 types of hyponatremia

A

psuedonatremia, isotonic or hypertonic hyponatremia, and Hypotonic hyponatremia

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3
Q

What is psuedonatremia?

A

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

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4
Q

What is Isotonc or hypertonic hyponatremia?

A

the presence of unmeasured effective osmoles (mannitol) is causing the shift of H2O from ICF to ECF (hyperglycemia, contrast)

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5
Q

What is Hypotonic hyponatremia?

A

Effective osmolality of the plasma is LOW, TRUE hyponatremia

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6
Q

Hypotonic hyponatremia has 3 classes

A

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

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7
Q

Hyponatremia is secondary to

A

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

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8
Q

Reasons for defect in renal water clearance?

A

Excessive water drinking (psychiatric issue) usually due to medications

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9
Q

Psuedohyponatremia

A

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

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10
Q

Isotonic or Hypertonic Hyponatremia causes

A

presence of effective osmole

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11
Q

Syndrome of Inappropriate ADH (SIADH)

A

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

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12
Q

Tricyclic antidepressants and morphine can cause SIADH

A

stimulate ADH and can cause hyponatremia

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13
Q

Presentation of patient with SIADH

A

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

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14
Q

Treatment for SIADH hyponatremia

A

H2O restriction, blockade of ADH at the collecting duct

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15
Q

Nephrogenic Syndrome of Inappropriate Antidiuresis

A

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

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16
Q

Exertion and Hyponatremia

A

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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17
Q

Hypernatremia

A

pna >145, often the result of unreplaced water loss

18
Q

Body’s defense against hypernatremia

A

ADH and thirst

19
Q

Diabetes insepidus

A

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

20
Q

Central diabetes insepidus

A

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

21
Q

Nephrogenic Diabetes insepidus

A

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

22
Q

In a normal patient, water deprivation will result in

A

ADH secretion, water retention, and concentrated urine

23
Q

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

A

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

24
Q

Central DI, patient when given endogenous ADH

A

ADH, will cause water retention, and urine concentration

25
Q

Nephrogenic DI, patient is given endogenous ADH

A

urine concentration remains dilute, no response to ADH

26
Q

under euvolemic conditions, the excretion of Na is

A

equal to intake of Na

27
Q

regulation of Na reabsorption occurs at the

A

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

28
Q

Autoregulation of GFR and Na excretion

A

despite positional changes, changes in BP, etc, GFR is regulated to remain constant and provide a constant filtered load of Na

29
Q

Tubuloglomerular feedback TGF

A

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

30
Q

Glomerular tubular balance

A

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

31
Q

What two mechanisms regulate Glomerular tubular balance

A

Na-solute symport and starling forces in the peritubular capillaries

32
Q

Na-solute transport increases with an

A

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

33
Q

If filtration fraction increases (H2O and electrolytes lost from blood)

A

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
Q

Load dependent Na transport in the loop of Henle

A

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

35
Q

Regulators of Na excretion

A

Aldosterone, ANP, SNS

36
Q

total Na and ECF volume is controlled by

A

Aldosterone, ANP, SNS, and ADH

37
Q

SNS effect on kidney

A

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

38
Q

RAAS effects

A

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
Q

ADH stimulation

A

high plasma osmolality, Ang II, decreased baroreceptor stretch

40
Q

Atrial Natriuretic Peptide (ANP)

A

increases Na excretion in response to increased ECF or hypertension

41
Q

ANP increases Na excretion through

A

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