ECF Volume Regulation 1 Flashcards

1
Q

What solutes account for the “major osmoles” (oncotic pressure) in the ICF and ECF?

A

ICF: K ions are the major osmoles

ECF: Na & Cl ions

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2
Q

How is water distributed between the ICF and ECF? What about between the components of the ECF?

A

Water - 1/3 ECF, 2/3 ICF

ICF:

  • 3L plasma
  • 11L ISF
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3
Q

When there is salt and water loss (vomiting / diarrhoea) what effects does this have on kidney function?

A
  • Causes lower atrial pressure & BP, which results in increased ADH secretion and therefore water reabsorption at the kidneys
  • Sympathetic response to low BP causes renal artery constriction and an increase in renin
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4
Q

What are the functions of Angiotensin II?

A
  • Vasoconstriction
  • CVS responses to increase BP (inc. HR / CF)
  • Stimulate ADH release at hypothalamus
  • Stimulate thirst & salt craving at hypothalamus
  • Stimulate the release of aldosterone
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5
Q

What causes the increased reabsorption at the proximal tubule during times of hypovolaemia (dehydration)?

A
  • Angiotensin II causes peritubular capillary constriction, lowers the pressure and hydrostatic force
  • The loss of salt & water that leads to hypovolaemia results in a greater oncotic pressure at the proximal tubule, as [protein] is higher than usual
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6
Q

Does GFR change in times where plasma volume is reduced?

A

No, unless the volume decrease is extremely significant

  • Sympathetic nerves and Angiotensin II keep the afferent arterioles constricted so the GFR remains constant (might actually be the efferent arterioles constricted, afferent dilated to keep GFR up? - check that)
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7
Q

Which hormone controls Na reabsorption at the distal tubule? What is the rate limiting step in the release of this hormone?

A

Aldosterone

  • Production and release of renin is the rate limiting step, as this causes activation of the RAAS
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8
Q

What are the components of the juxtaglomerular apparatus? Where is the apparatus located?

A

Macula densa cells + juxtaglomerular cells

  • Located at the articulation of the glomerulus and the distal convoluted tubule
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9
Q

What cells are responsible for the secretion of renin?

A

Juxtaglomerular cells

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10
Q

Describe the production of angiotensin II

A
  • Angiotensinogen produced by the liver and secreted to the blood
  • Renin produced by the juxtaglomerular cells of the kidney
  • Renin cuts angiotensinogen to angiotensin I
  • Blood vessel endothelium secretes ACE, ACE cuts angiotensin I to active angiotensin II
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11
Q

How does the vasoconstriction produced by angiotensin II lead to increased absorption at the distal tubule?

A
  • Via constriction of the peritubular capillaries which lowers the hydrostatic pressure

This along with the increased osmolarity of blood during dehydration (increased oncotic pressure) causes salt and water reabsorption at the proximal tubule

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12
Q

What stimulates the release of renin?

A
  1. A decrease in pressure at the afferent arteriole
  2. Sympathetic nerve activity (Beta 1 effect)
  3. Reduced NaCl delivery (presence) at the macula densa of the distal tubule
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13
Q

How is the decrease in pressure at the afferent arteriole that triggers the release of renin detected?

A
  • The juxtaglomerular cells act as baroreceptors, when they experience less distension (swelling) they release renin

(intrinsic property that occurs even if denervated)

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14
Q

Where does NaCl reabsorption in the distal tubule occur?

A

The macula densa

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15
Q

What inhibits the release of renin?

A
  • Angiotensin II feeds back to inhibit renin

- ADH inhibits renin release

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16
Q

In which vasculature of the body does angiotensin II stimulate vasoconstriction? How effective is it?

A
  • In all arteries / arterioles. Increases TPR and therefore MAP
  • Is 4-8x more effective than norepinephrine
17
Q

In a patient with diarrhoea who has lost 3L of salt & water, and attempted to replace it by drinking 2L of pure water, what will happen to ADH secretion?

A
  • ADH secretion stimulated bc ECF volume concerns take precedent over osmolarity

patient would have hypo-osmolarity: inhibits ADH
patient has lost plasma volume: stimulates ADH
Volume wins

18
Q

What is the main determinant of [ADH]? Is this always the case? Why?

A
  • Osmolarity is usually the main determinant of [ADH]
  • No, when blood volume becomes significantly low, ADH secretion will be stimulated regardless of osmolarity
  • Represents a safeguard to ensure there is enough blood volume to perfuse the brain