Unit 7 - Regulation of Plasma Sodium and ECF Volume Flashcards

1
Q

why is maintaining plasma volume so important?

A

blood pressure drives blood flow, and blood pressure is dependent on volume
-so volume –> BP –> flow

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2
Q

what are the sensors, efferent pathways, effectors, and regulated parameters of osmolarity?

A

S: hypothalamic osmoreceptors
EP: ADH and thirst
E: kidney, brain (thirst)
RP: renal free water excretion, water consumption

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3
Q

what are the sensors, efferent pathways, effectors, and regulated parameters of ECF volume?

A

S: carotid sinus, aortic arch, renal afferent arteriole, and atria (actually pressure stretch receptors)
EP: renin-angiotensin-aldosterone, SNS, ADH, ANP (virtually never constant)
E: short term heart and blood vessels, but long term kidney
RP: short term blood pressure (PVR x CO), but long term renal Na excretion

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4
Q

what is the renal response to abrupt increases in dietary Na (to 150 mmol)?

A

if initially in Na+ balance, and Na+ intake is increased, the kidney takes 6 days to catch up (positive balance) by retaining osmolarity by retaining 1 L water (gain 1 kg weight)

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5
Q

what is the renal response to abrupt decreases in dietary Na (by 150 mmol)?

A

if initially in positive Na+ balance, and Na+ intake is decreased, the kidney takes 6 days to recover (negative balance) by retaining osmolarity by losing 1 L water (lose 1 kg weight)

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6
Q

what is hemorrhage an example of and what will it cause?

A

severe ECF volume contraction

-induces decrease in GFR

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7
Q

is kidney’s increase in Na+ excretion in response to an increase in ECF volume, or an increase in Na+ concentration?

A

it’s due to increase in ECF volume

-will increase excretion to retain osmolarity at 300 mmol/L (both 150 mmol Na+ and 150 mmol Cl-)

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8
Q

what is effective circulating volume? what does it do?

A

functional, not anatomical, blood volume reflecting extent of tissue/organ perfusion where blood pressure is sensed

  • induces regulation of Na+ excretion
  • normally paralleles total ECF volume, both intra- and extra-vascular volumes
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9
Q

which induces regulation of Na+ excretion: changes in effective circulating volume, or total ECF volume?

A

changes in effective circulating volume

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10
Q

when is effective circulating volume less than total ECF volume?

A

in disease states that cause edema (like CHF)

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11
Q

what is CHF in regards to edema?

A

increases end diastolic pressure, so increased capillary hydrostatic pressure driving fluid from intravascular to extravascular space

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12
Q

what does pulmonary edema cause volume-wise?

A

if secondary to left ventricular heart failure and pulmonary HTN
-caused by increased capillary hydrostatic pressure in the lung, driving fluid from intravascular to extravascular space, that severely compromises gas exchange in lung

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13
Q

what does liver disease do volume-wise?

A

caused by decrease in synthesis of albumin, so decreased plasma oncotic pressure that upsets normal Starling forces

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14
Q

what does neprhotic syndrome do volume-wise?

A

disease of renal glomerulus allows inappropriate filtration of albumin = albuminuria
-decreases plasma oncotic pressure, disrupting Starling forces

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15
Q

what do diuretic drugs do?

A

decrease plasma volume by “forcing” kidney to increase excretion of Na+ and water in urine
-this decreases hydrostatic pressure, and increases oncotic pressure in capilliaries, which favors absorption of edema in interstitial space back into intravascular space

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16
Q

what are the 3 types of ECF volume baroreceptors?

A
  1. “central” vascular sensors
    - Low pressure (very important): atria and pulmonary vasculature
    - High pressure (less important): carotid sinus, aortic arch, and juxtaglomerular apparatus (renal afferent arteriole)
  2. sensors in CNS (less important)
  3. sensors in liver (less important)
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17
Q

what are 4 parallel effector systems that increase renal Na+ absorption and decrease renal Na+ excretion?

A
  1. renin-angiotensin-aldosterone hormonal system
  2. increased renal sympathetic nerve activity
  3. posterior pituitary (ADH)
  4. ANP
18
Q

what is the RAA hormonal system?

A

renin-angiotensin-aldosterone

  • AII promotes Na+ retention by stimulating Na/H exchange in proximal tubule cells, and decreases renal plasma flow, which promotes increased Na+ resabsorption
  • aldosterone induces increase in Na+ reabsorption by late distal tubule and early collecting duct
19
Q

how does increased renal SNS activity affect blood volume?

A

induces renal vasoconstriction and increased Na+ reabsorption, which reduces renal Na+ excretion

20
Q

how do ADH and ANP affect blood volume?

A

ADH - promotes water reabsorption

ANP - reduces Na+ excretion in response to reduced ECF volume

21
Q

what is angiotensinogen?

A

substrate of renin, and is alpha2-globulin made by liver and released into systemic circulation

22
Q

what is renin? what activates it?

A

made and stored in granular cells of JGA of kidney

-decreased effective circulating volume increases its release, converting angiotensinogen to AI (decapeptide)

23
Q

what is ACE?

A

angiogensin converting enzyme (decapeptide AI to octapeptide AII)
-found on luminal surface of vascular endothelium throughout body, and abundant in vasculature of lung and kidney

24
Q

what is angiotensin II’s half life?

A
2 minutes (rapid degradation by aminopeptidases)
-cleaves AII to heptapeptide AIII with less activity
25
Q

what is the most important factor controlling AII levels in plasma?

A

renin release from granular cells of JGA

26
Q

what are the three renal mechanisms regulating renin release?

A
  1. local renal baroreceptors in afferent arterioles respond to low pressure and increase secretion of renin by granular cells
  2. decreased systemic arterial blood pressure stimulates baroreceptor reflex, that causes increased sympathetic drive to JGA, increasing renin secretion
  3. cells of macula densa sense tubular fluid Na+ concentration and, if low, cause increased release of renin from granular/JG cells into afferent arteriole blood supply
27
Q

what are actions of AII?

A
  • induces aldosterone release from adrenal cortex
  • acts on hypothalamus to increase thirst and induce release of ADH from posterior pituitary
  • vasoconstricts renal and other systemic vessels:
  • -in kidney: constricts efferent more than afferent arterioles to increase GFR
  • -increases Starling forces favoring reabsorption of tubular fluid by peritubular capillaries
  • enhances Na/H exchange in proximal tubule, which increases Na+ reabsorption
  • induces hypertrophy of renal tubule cells
28
Q

what does aldosterone do?

A

mineralcorticoid secreted by adrenal cortex

  • is primary long term regulator of salt balance and ECF volume, thus blood pressure
  • acts on kidney tubules to increase reabsorption of Na+ and water due to increase in osmolarity from increased Na+ reabsorption
  • -acts on “principal” cells in late distal tubule and early collecting duct in renal cortex
  • acts on distal nephron to increase secretion and excretion of K+
29
Q

how does aldosterone increase Na+ reabsorption?

A

induced increase in Na+ transporter expression

  • increased basolateral membrane Na+/K+ pumps
  • increased apical membrane Na+ channels
  • increased mitochondrial enzymes (ATP)

doesn’t work immediately

30
Q

why doesn’t solute reabsorption in cortical nephron participate in counter current exchange?

A

due to separate venous circulations in cortex and vasa recta of medulla; the cortical circulation is rapidly returned to renal vein

31
Q

Na+ filtration through the nephron?

A

glomerular head: 100%

  • 67% reabsorbed in proximal tubule –> 33% left
  • 25% reabsorbed in thick ascending LoH –> 8% left at macula densa
  • 5% reabsorbed in convoluted tubule –> 3% left in collecting duct
  • 3% reabsorbed in collecting duct –> 0.4% left to be excreted
32
Q

how does reabsorbion of NaCl in principal cells of cortical collecting tubule work?

A
tubular lumen (luminal side) has passive Na+ reaborbtion and K+ excretion
blood (basolateral side) has active Na/K pump (3 Na+ into blood, 2 K+ into cell) and passive K+ channel into blood

Cl- travels paracellularly, from tubular lumen to blood

33
Q

what is the transcellular/transepithelial voltage difference in the cortical collecting tubule? why is it important?

A

lumen negative; due to net efflux of positive charge from tubular fluid across epithelia

  • uncoupled exchange is not stoichiometric, so it’s not electroneutral
  • important b/c it’s the driving force pushing transepithelial transport of Cl- between cells (paracellularly) instead of transcellularly
34
Q

what regulates sodium reabsorption in late distal tubule and collecting duct?

A

circulating levels of aldosterone

35
Q

what are secretogogues for aldosterone?

A
  • angiotensin II
  • increased plasma [K+]
  • ACTH (release induced by anterior pituitary)
36
Q

what is hypernatremia?

A

increase in plasma [Na+] to a level above normal range of 135-145 mEq/L

  • symptoms: lethargy, weakness, and irritability
  • -severe symptoms (seizure/coma) at >158 mEq/L
  • caused by loss of water in excess of solutes from plasma due to inadequate water consumption in excess of solute, and/or inappropriate renal excretion of water in excess of solute
  • problematic in patients who cannot ask for water or when water consumption is limited
37
Q

what are the 2 causes of hypernatremia?

A

hypovolemic - inadequate water consumption

  • extreme sweating
  • severe diarrhea
  • polyuria
  • caused by diabetes mellitus (glucosuria) or insipidus (central and/or nephrogenic)

hypervolemic - excessive hypertonic fluid consumption (seawater) or IV infusion of hypertonic saline
-hyperaldosteronism

38
Q

central VS nephrogenic diabetes insipidus

A

central: inadequate release of ADH from posterior pituitary in response to increased osmolarity
- collecting duct not sufficiently permeable to water, causing polyuria

nephrogenic: inability of collecting tubule and collecting duct to respond to ADH, even though ADH is readily available, causing polyuria

39
Q

what is hyponatremia?

A

decrease in plasma [Na+] below 135-145 mEq/L

  • symptoms: nausea, vomiting, headache, lethargy, fatigue, loss of appetite, restlessness, irritability, muscle weakness, spasms, or cramps
  • -severe: neurological deficits, brain swelling, seizures, coma if reabsorption by kidney
40
Q

hypervolemic VS hypovolemic hyponatremia

A

hyper: inappropriate reabsorption of water in excess of solutes from tubular fluid to plasma effectively increases plasma volume and dilutes plasma [Na+]
- occurs: CHF, kidney failure, liver failure, SIADH, psychogenic polydipsia

hypo: in clinical setting where plasma volume reduction is extreme (hemorrhage, prolonged exercise in heat, diuretic drug therapy) where consumption of water and increased “water in excess of solute” reabsorption by kidney is insufficient to correct volume depletion, but is sufficient to decrease plasma [Na]
- Addison’s disease (adrenal insufficiency - hypoaldosteronism)
- severe vomiting or diarrhea