PHYS - Osmotic and Volume Regulation Flashcards

1
Q

EFFECT OF VOLUME ON ADH RELEASE

A
  • Decrease in plasma volume
    • Decrease P in circulation
      • Decrease baroreceptor activity
        • Stimulate ADH release
          • Increase tubular permeability to H2O
            • Increase H2O reabsorption
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2
Q

VOLUME STIMULUS VS OSMOTIC STIMULUS

A
  • Osmotic stimulus → drink water → decrease Posm → decrease ADH → excrete H2O
  • Volume stimulus → IV saline → increase EFV → decrease ADH → excrete H2O → increase Posm → increase ADH
  • Regulate volume by regulating sodium reabsorption
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3
Q

CONTROL OF EFV BY SODIUM

A
  • Volume (stretch) receptors:
    • Intrarenal – JG cells of afferent arteriole
    • Venous stretch receptors
    • Baroreceptors
  • Regulate extracellular volume by regulating sodium reabsorption which then regulates water reabsorption
    • The following mechanisms that act on Na+ retention in the kidney
      • GFR
      • Aldosterone
      • Natriuretic hormone
      • Peritubular pressure
  • Glomerulotubular Balance (GTB) – ensures a constant percent of the filtered load of sodium gets reabsorbed
    • Always about 67%, while the amount in the 67% will change based on sodium intake
  • Increased Na+ intake → increased Posm
    • First → shift of fluid from IFC compartment to EFC → increased water reabsorption → increased EFV
    • → ADH release → increased EFV
    • → thirst → consume water → increased EFV
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4
Q

ALDOSTERONE

A
  • Intercellular receptors in principle cells of the collecting duct
  • Release stimulated by:
    • Blood pressure/volume → Angiotensin II
    • Hyperkalemia
  • Affects protein synthesis
    • Increases Na+ channels on apical (tubular) membrane
      • Allows Na+ to rush in and depolarize membrane so that K is stimulated to diffuse into tubule
    • Increases Na+/K+ ATPases on basal membrane (blood side)
    • Enhances ATP synthesis
  • Functions:
    • Na+ reabsorption
    • K+ excretion
    • H+ excretion
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5
Q

CS: CHANGES IN ALDOSTERONE LEVEL

A
  • Hypoaldosteronemia (adrenal insufficiency; Addison’s disease)
    • Hyperkalemia
    • Acidosis (K+ put into cells)
    • Hypotension (salt wasting)
  • Hyperaldosteronemia
    • Hypokalemia
    • Alkalosis (K+ withdrawn from cells for pump function)
    • Hypertension (without overt volume expansion)
    • Primary – overstimulation of adrenal gland by a tumor
    • Secondary – caused by RAS
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6
Q

HORMONES AFFECTING SODIUM/H2O REABSORPTION

A
  • Natriuresis – excretion of excess sodium in water
  • Aldosterone - Na+ reabsorption in CD
  • ADH - H2O reabsorption in CD
  • Angiotensin II
    • Secreted in response to low GFR
    • Stimulates adrenal gland to secrete aldosterone
    • Direct increase in proximal Na+ reabsorption
  • ANP (Atrial natriuretic hormone)
    • Binds membrane receptors in CD that GC*
    • Prevents Na+ reabsorption
    • Increases GFR in glomerulus (decreased Na+ reabsorption)
    • Diminishes effects of renin, angiotensin II, and aldosterone
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7
Q

CONGESTIVE HEART FAILURE

A
  • CHF patients exhibit positive and increasing sodium balance
  • Arterial baroreceptors function to maintain ECV (effective circulating volume)
  • CHF → decreased CO → shift in blood volume to venous side → decreased P/V on arterial baroreceptors → renin/angiotensin II/aldosterone release → Na+ retention → increases Posm → increase ADH → H2O reabsorption
  • With volume trapped in venous circulation → increased edema
  • Treatment: diuretics to try to prevent edema
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8
Q

CHRONIC KIDNEY DISEASE

A
  • Progressive decline in GFR due to loss of nephrons
  • However, sodium balance and plasma osmolarity are still maintained!
  • Sodium – overall filtered load decreases because of the decreased number of nephrons working to filtered the blood
    • So, less plasma filtered per cycle through kidneys, and more sodium drawn out per cycle to maintain constant excretion rate
    • Decreased filtered load
    • Increased fractional excretion
    • No change in excretion rate
  • Creatinine – since less plasma is being filtered, creatinine concentration builds up more quickly in plasma creating a steeper gradient for filtration
    • More concentrated filtered load
    • No change in excretion rate
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9
Q

ERYTHROPOIETIN

A
  • Kidneys function in regulation of RBC production
  • Release erythropoietin in response to reduced tissue oxygenation
    • 90% from kidney
    • 10% from liver
  • Erythropoietin stimulates HSCs in the bone marrow to produce proerythroblasts→ RBCs → increased tissue O2 → decreased erythropoietin release
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