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Physiology Unit 7 > Regulation of Plasma Sodium and ECF Volume > Flashcards

Regulation of Plasma Sodium and ECF Volume Flashcards

1
Q

homeostasis of ECF volume and osm

A

sensors:
OSM-hypothalamic osmoreceptors
VOL- carotid sinus, aortic arch, renal afferent arteriole, atria (stretch, deltaP so therefore deltaV)
efferent pathways:
OSM-ADH, thirst
VOL- RAAS, SNS, ADH, ANP
effectors:
OSM- kidney, brain (thirst)
VOL- short term heart and BV, long term kidneys
regulated parameters:
OSM- renal free water excretion, water consumption
VOL-short term BP (PVRxCO), long term renal sodium excretion

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2
Q

renal response to abrupt increase and decrease of Na

A
  • balance, then increases and renal excretion isn’t as high as intake, gain 1 L of weight, 140 meq NaCl, 280 mosm/L)
  • then evens out
  • then decrease intake again, and excretion is greater than intake, water weight drops
  • moles of sodium determines ECF volume
  • more Na means bigger ECF, and retained isosmotically
  • increase/decrease in ECF determined by receptors, expansion of ECF results in increased output of Na and water
  • harder to off load Na as you get older- HTN
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3
Q

increase Na excretion

A
  • in response to an increase in ECF volume, not Na concentration
  • Na concentration stays same, molar amount increases and causes increase in ECF vol that is responded to
  • therefore isosmotic control
  • increase in Na excretion results from a decrease in reabsorption, occurs in a volume of urine necessary to excrete excess isosmotically
  • excretion is urine [Na} x urine flow
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4
Q

effective circulating volume

A
  • changes in effective circulating volume, not total ECF volume, induce regulation of Na excretion
  • effective circulating volume is a functional, not an anatomical blood volume, reflecting the extent of tissue/organ perfusion where BP is sensed
  • normal parallels total ECF volume, both intra and extravascular volumes
  • effective circulating volume may be less than total ECF volume in disease states such as CHF or other pathophysiologies causing edema
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5
Q

edema

A
  • imbalance of hydrostatic and oncotic pressures across the cap wall, fluid shift from intra to extravascular space- isotonic retention of Na and water and decreased effective circulating volume
  • decreased renal perfusion pressure and activates RAA, which further increases Na retention and edema
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6
Q

CHF

A
  • increases end diastolic pressure

- increases cap hydrostatic pressure driving fluid into extravascular space

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7
Q

pulmonary edema

A
  • secondary to left ventricular heart failure and pulmonary hypertension
  • results from increased cap hydrostatic pressure in lung
  • compromise gas exchange
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8
Q

liver disease

A
  • decrease in albumin synthesis

- decreases plasma oncotic pressure

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9
Q

nephrotic syndrome

A
  • disease of renal glomerulus permits inappropriate filtration of plasma proteins and causes albuminuria
  • decreases plasma oncotic pressure
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10
Q

diuretic drugs

A
  • decrease plasma volume by forcing the kidney to increase excretion of Na and water in the urine
  • decreases hydrostatic and increases oncotic pressure
  • fluid back into intravascular space
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11
Q

ECF volume baroreceptors

A

Central vascular sensors:

  • low pressure, very important. in atria and pulmonary vasculature
  • high pressure are less important- carotid sinus, aortic arch, juxtaglomerular apparatus
  • sensors in CNS are less important
  • sensors in liver are less important
  • change in volume results in change in pressure
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12
Q

RAA

A
  • angiotensin II promotes sodium retention by stimulating Na/H exchange in proximal tubule
  • angiotensin II decreases renal plasma flow, which promotes Na reabsorption
  • aldosterone induces an increase in Na reabsorption by the late distal tubule and early collecting duct
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13
Q

increased renal SNS

A

-induces renal vasoconstriction and increased Na reabsorption, which reduces sodium excretion

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14
Q

post pit

A

-releases ADH which promotes water reabsorption

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15
Q

ANP

A

-as volume decreases, ANP decreases so you keep more salt

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16
Q

angiotensinogen

A
  • substrate of enzyme renin (renin cleaves)

- alpha 2 globulin synthesized by the liver and released into systemic circulation

17
Q

renin

A
  • synthesized and stored in granular cells of the juxtaglomerular apparatus of the kidney
  • decreased volume increases renin release
  • protease that converts angiotensinogen to 10 aa peptide angiotensin I
18
Q

angiotensin I

A
  • converted to 8 aa angiotensin II by angiotensin converting enzyme
  • ACE on luminal surface of vascular endo throughout the body
  • abundant in lungs and kidney
  • ANG II has half life of 2 min
19
Q

JGA

A
  • renin release is regulated by 3 mechanisms
    1. local renal baroreceptors in afferent arterioles respond to low pressure and increase secretion of renin by granular cells
    2. decreased systemic arterial BP stimulates baroreceptor reflex, which causes increases SNS drive to JGA, increasing renin
    3. cells of macula densa sense tubular fluid sodium concentration and if low, cause increased release of renin from granular cells into afferent arteriole blood supply
20
Q

actions of angiotensin II

A
  • induces aldosterone release from adrenal cortex
  • acts on hypothal to increase thirst and induce release of ADH
  • vasocontricts renal and other systemic vessels:
  • constricts efferent more than afferent (dec P downstream and allow more time, increases GFR)
  • increases starling forces favoring reabsorption of tubular fluid by peritubular caps
  • enhances Na/H exchange in proximal tubule, which increases reabsorption
  • induces hypertrophy of renal tubule cells
21
Q

aldosterone

A
  • mineralcorticoid secreted into circulation by adrenal cortex
  • primary long term regulator of salt balance and ECF volume, and therefore BP
  • acts on kidney tubules to increase reabsorption of Na as well as water, due to the increase in osm resulting from increased Na reabsorption
  • acts on the distal nephron to increase the secretion and excretion of K
22
Q

actions of aldosterone

A
  • induces increased Na reabsorption by principal cells in late distal tubule and early collecting duct in renal cortex
  • increased Na reabsorption results from induced increase in Na transporter expression:
  • increased basolateral Na/K pumps
  • increased apical membrane Na channels
  • increased mito enzymes to increase ATP
  • solute reabsorption in cortical neprhon segments is rapidly returned to general circulation and does not participate in counter current multiplication of the cortico-medullary solute concentration gradient
23
Q

renal handling of Na

A
  • all reabsorption, no secretion
  • can only get rid of salt by decreasing reabsorption
  • excretion= filtered-reabsorbed
  • 67% out in PT and reabsorbed isosmotically
  • TAL 25 % reabsorbed into 2 anatomically different arterio-venous cap networks
  • in medulla it drives counter current, in cortex it doesn’t
  • in late distal tubule and cortical collecting tubue, 5% of filtered Na reabsorbed- depends on aldosterone
  • in collecting duct, 3% absorbed
  • when in balance, reabsorption of more than 99%
  • 0.4% of filtered load remaining
24
Q

principal cells of cortical collecting tubule

A
  • Na channel for uptake into cell and Na/K ATPase for efflux
  • functionally coupled to K secretion- uptake at basolateral by ATPase, then K goes out into tubule
  • aldosterone therefore regulates K secretion as well
  • increased Na/K pumps and increased K channels
  • lumen negative voltage difference results from net efflux of positive charge
  • pushes Cl paracellular
25
Q

secretogogues for aldosterone

A
  • angiotensin II
  • increased plasma K
  • ACTH
  • angiotensin II induces release of ATCH by anterior pit
26
Q

hypernatremia

A
  • increase in plasma Na above normal 135-145 mEq/L
  • lethargy, weakness, irritability
  • seizures and coma may occur above 158
  • in general, caused by a loss of water in excess of solutes from plasma due to inadequate consumption of water in excess of solute and/or inappropriate renal excretion of water
  • problematic in patients who can’t ask for water
27
Q

hypovolemic hypernatremia causes

A
  • inadequate water consumption
  • extreme sweating
  • severe diarrhea
  • excessive renal excretion of water
  • glucosuria in DM
  • central or nephrogenic diabetes insipidus- not enough ADH
28
Q

hypervolemic hypernatremia causes

A
  • excessive hypertonic fluid consumption (ocean) or infusion of hypertonic saline
  • -compensation doesn’t occur fast enough
  • hyperaldosteronism
  • less ADH released for a given increase in plasma osm, so not enough water is reabsorbed
29
Q

hyponatremia

A
  • decrease below 135-145
  • nausea, vomiting, headache, lethargy, fatigue, loss of appetite, restlessness and irritability, muscle weakness, spasms or cramps.
  • severe symptoms-neuro deficits, brain swelling, seizures, coma may occur at plasma below 125
  • in general caused by a gain of water in excess of solutes in the plasma due to extreme, excess consumption of water or an inappropriate increase in free water reabsorption due to too much ADH
30
Q

hypervolemic hyponatremia

A
  • inappropriate reabsorption of water in excess of solutes from tubular fluid to plasma increases volume and dilutes Na
  • CHF, kidney failure, liver failure, SIADH, polydipsia
31
Q

hypovolemic hyponatremia

A
  • clinical setting where plasma volume reduction is extreme- hemorrhage, prolonged exercise in heat, diuretic drug therapy
  • where consumption of water as well as increased free water reabsorption by kidney is insufficient to to correct volume depletion but is sufficient enough to decrease plasma Na
  • addisons- hypo aldosterone
  • severe vomiting/ diarrhea

Physiology Unit 7 (10 decks)

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