Regulation of ECF Volume - Pt 1 Flashcards

1
Q

What are the major ECF and ICF osmoles?

A

ECF - Na+ and Cl-
ICF - K+

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2
Q

What is regulation of ECF volume equal to?

A

Regulation of body Na+

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3
Q

What is the distribution of total body water?

A

ECF - 14l (1/3) with 3l in plasma and interstitial fluid is 11l
ICF - 28l (2/3)
Total 42l

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4
Q

What does changes in Na content of the ECF lead to?

A

Changes in ECF volume and will affect volume of blood perfusing the tissues - effecting circulating volume and BP

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5
Q

What is regulation of Na basically dependant on?

A

High and low pressure baroreceptors

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6
Q

Describe the renal response to decreased ECF volume (hypovolaemia)

A

Increase salt and H2O loss (vomiting, diarrhoea or excess sweating) - Decreases PV, venous pressure, VR, atrial P, EDV, SV, CO then BP which decreases carotid sinus baroreceptor inhibition of sympathetic discharge

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7
Q

What does increase sympathetic discharge lead to?

A

Increase vasoconstriction, total peripheral resistance and increase BP towards normal
By increased renin and renal constriction

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8
Q

What does decreased atrial pressure and carotid sinus baroreceptor discharge lead to?

A

Increase ADH release - may cause hypo-osmolarity

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9
Q

What does increased renin lead to?

A

Increased angiotensin II - increased proximal tubule NaCl and H2O reabsorption
Increased aldosterone - increased distal tubule NaCl and H2O reabsorption

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10
Q

What is the effect of sympathetic discharge specifically on the kidneys?

A

Increased renal VC nerve activity then increased renal arteriolar constriction and an increase in renin

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11
Q

What is the effect of increased renin specifically on the kidneys?

A

Increased angiotensin II - decreased peritubular capillary hydrostatic pressure (increased oncotic pressure) and increased Na reabsorption from proximal tubule so less Na excreted

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12
Q

What are changes in proximal tubule Na reabsorption due to?

A

Changes in rate of uptake by peritubular capillaries determined by oncotic pressure
greater absorptive forces in peritubular capillaries

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13
Q

What happens to oncotic pressure when NaCl and H2O is lost?

A

Oncotic pressure forces increase even more than normal so can reabsorb 75% of the filtrate in the proximal tubule

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14
Q

How does GFR remain largely unaffected?

A

Autoregulation maintains GFR and VC of afferent and efferent means little effect on GFR until volume depletion causes decrease MBP

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15
Q

What 2 things mainly maintain GFR?

A

Construction of afferent due to to sympathetic VC coupled with angiotensin II mediated constriction of efferent arterioles

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16
Q

What controls the regulation of distal tubule Na reabsorption?

A

Aldosterone - adrenal cortical steroid hormone

17
Q

What is aldosterone secretion controlled by?

A

Reflexes involving the kidneys themselves
Juxtaglomerular cells (JG) at macular densa

18
Q

What are juxtaglomerular cells?

A

Epithelial cells with plentiful granules which are on smooth muscle of afferent arteriole before entering the glomerulus where they become specialised

19
Q

What is the macula densa?

A

Histologically specialised loop of distal tubule

20
Q

What do JG cells produce?

A

Renin which acts on large protein in alpha2 globulin fraction of plasma proteins - angiotensinogen

21
Q

Where is angiotensin produced?

A

Liver constantly produces angiotensinogen in the plasma

22
Q

What contains ACE enzyme?

A

Blood vessel endothelium - converts ANGI to ANGII in plasma
Greatest conversion occurs as blood passes through pulmonary circuit

23
Q

What does angiotensin II stimulate?

A

Aldosterone - secreting cells in zona glomerulosa of adrenal cortex

24
Q

What is the rate limiting step of aldosterone?

A

Release of renin as angiotensinogen is always in the plasma

25
Q

What controls the increase of renin release?

A

Pressure in afferent arteriole at level of JG cells decrease - renal baroreceptors so less distention, more secretion
Sympathetic nerve activity via B1 effect
Decreased NaCl at macula densa delivery increases renin

26
Q

What controls the inhibition of renin release?

A

Angiotensin II feeds back
ADH inhibits renin release by osmolarity control

27
Q

What provides the basis of tubuloglomerular balance?

A

Close relationship between afferent arteriole with JG cells and macula densa

28
Q

What happens in hypovolaemia?

A

Increased proximal and distal tubule Na reabsorption together with osmotic equivalents of H2O - helps restore volume deficits mediated by CV reflexes

29
Q

Why is angiotensin II important in body’s response to hypovolaemia?

A

Stimulates aldosterone - NaCl and H2O retention
Vasoconstriction - increases TPR
Acts on hypothalamus to stimulate ADH secretion - increase H2O reabsorption from CD
Stimulates thirst mechanism and salt appetite

30
Q

What does aldosterone directly effect?

A

Increase Na reabsorption which increases volume and maintain osmolarity

31
Q

What does GFR increase lead to?

A

Flow through tubule increases so flow past macular densa increases - paracrine from macular densa to afferent arteriole - afferent constricts - resistance increases - hydrostatic pressure in glomerulus decreases so GFR decreases

32
Q

What contributes to GFR constancy?

A

Tubuloglomerular feedback

33
Q

What happens if a patient has lost 3l of salt and water from ECF and drinks 2l of pure water?

A

Opposing inputs to ADH secreting cells
Decreased ECF osmolarity means inhibition of ADH via osmoreceptors
Decreased ECF volume means increase ADH via baroreceptors

34
Q

What has primary effect is ECF osmolarity and volume is decreased?

A

Volume considerations
ADH will be increased as baroreceptors

35
Q

What happens when volume in restored in hypovolaemia?

A

Osmolarity will be normalised then again be the main determinant of ADH
So if loss salt and water - replace with salt and water