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
Nephrogenic DI, patient is given endogenous ADH
urine concentration remains dilute, no response to ADH
26
under euvolemic conditions, the excretion of Na is
equal to intake of Na
27
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
29
Tubuloglomerular feedback TGF
Autoregulatory mechanism; macula densa sense NaCl flow and controls afferent arteriole
30
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
33
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
35
Regulators of Na excretion
Aldosterone, ANP, SNS
36
total Na and ECF volume is controlled by
Aldosterone, ANP, SNS, and ADH
37
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
41
ANP increases Na excretion through
increased GFR, reduced Na reabsorption in proximal tubule, and in the collecting duct