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Systems: Urinary AB > ECF Volume Regulation > Flashcards

ECF Volume Regulation Flashcards

1
Q

What is one of the most important aspects of the ECF regulated by the kidney?

A

Volume

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2
Q

Why is the distribution of TBW between the cells and the ECF determined by the number of active osmotic particles in each compartment?

A

H2O can freely cross all cell membranes so the body fluids are in osmotic equilibrium

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3
Q

What are the major ECF osmoles?

A

Na and Cl

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4
Q

What are the major ICF osmoles?

A

K salts

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5
Q

What is regulation of ECF volume regulated by?

A

Regulation of body Na

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6
Q

How is water distributer within the body?

A

Water= 60% TBW=42l

  • ICF= 2/3= 28l
  • ECF=1/3 =14l
  • Plasma accounts for 3l and interstitial fluid accounts for 11l of the ECF
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7
Q

How do changes in Na content of the ECF affect BP?

A

Changes in Na+ content of the ECF will lead to changes in ECF volume and therefore will affect the volume of blood perfusing the tissues determining effective circulating volume and therefore BP.

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8
Q

What is regulation of Na basically dependent on?

A

High and low pressurebaroreceptors

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9
Q

Hypovolaemia?

A

Low ECF volume

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10
Q

What happens to the body in hypovolaemia?

A
  • Increases in salt and H2O loss
  • Decrease in pulse volume
  • Decrease in venous pressure
  • Decrease in venous return
  • Decrease in atrial pressure
  • Decrease in End diastolic volume
  • Decrease in stroke volume
  • Decrease in cardiac output
  • Decrease in BP
  • Decrease in carotid sinus baroreceptor inhibition of sympathetic discharge
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11
Q

How does the body compensate for hypovolaemia?

A
  • Decreases carotid sinus barocreceptor inhibition of sympathetic discharge leads to increased sympathetic discharge
  • Increase VC
  • Increase TPR
  • Increase BP towards normal
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12
Q

Give examples when there might be increase salt and water loss?

A
  • Vomiting/diarrhoea

- Excess sweating

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13
Q

How does the renal system respond to comepensation for hypovolaemia?

A
  • Increase ADH
  • Increases renal arterial constriction
  • Increases renin
  • Increase angiotensin II
  • Increased NaCl and H2O reabsorption in proximal tubule
  • Increased aldosterone which increases NaCl and H2O reabsorption in the distal tubule
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14
Q

What effect does increased renin have on the proximal tubule of the kidney?

A
  • Increases angiotensin II
  • Decreases peritubular capillary hydrostatic pressure (+ the osmotic pressure)
  • Increased Na reabsorption from the proximal tubule and less Na excreted
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15
Q

What effect does renin have on the distal tubule of the kidney?

A
  • Increased renin
  • Increased angiotensin II
  • Increased aldosterone
  • Increased distal tubule Na reabsorption and less Na excreted
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16
Q

What is the sympathetic discharhe on the kidney determined by?

A

Osmotic pressure

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17
Q

What are changes in proximal tubule Na reabsorption due to?

A

Changes in the rate of uptake by the peritubular capillaries

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18
Q

What are increases in Na reabsorption due to?

A

Greater reabsorptive forces in the peritubular capillaries

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19
Q

What is the reabsorptive range of the proximal tubule?

A
  • 65% in volume excess
  • 75% in volume deficit.
  • Big range of volume just because of changes in Starling’s forces.)
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20
Q

Why is GFR largely unaffected by changes in ECF?

A

Autoregulation maintains GFR and the VC of afferent and efferent means little effect on GFR until volume depletion severe enough to cause considerable decrease in MBP.

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21
Q

What maintains GFR in ECF loss?

A
  • Constriction of afferent due to sympathetic VC

- Constriction of efferent mediated by angiotensin II

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22
Q

What is regulation of distal tubule Na reabsorption under control of?

A

Adrenal cortical steroid hormone aldosterone

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23
Q

What hormone is very important in the long-term regulation of Na and ECF volume?

A

Aldosterone

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24
Q

What is aldosterone secretion controlled by?

A

Reflexes involving the kidneys themselves

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25
Q

What cells are present in the smooth muscle media of the afferent arteriole just before it enters the glomerulus?

A

Juxtaglomerular cells (JG): specialized, containing large epithelial cells with plentiful granules

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26
Q

What are the 2 components of the juxtaglomerular apparatus?

A
  • Juxtaglomerular cells

- Macula densa

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27
Q

What are the JG cells closely associated with?

A

A histologically specialized loop of the distal tubule known as the macula densa

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28
Q

What do JG cells produce?

A

Renin

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29
Q

What is renin?

A

A proteolytic enzyme which acts on a large protein in the 2-globulin fraction of the plasma proteins known as angiotensinogen.

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30
Q

What does renin do the angiotensinogen?

A

Renin splits off the decapeptide angiotensin I which is then converted by enzymes in the endothelium to the active octapeptide = angiotensin II

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31
Q

What does ACE stand for?

A

Angiotensin converting enzyme

32
Q

Where is ACE found?

A

It is found throughout the vascular endothelium, but the greatest proportion of the conversion occurs as the blood passes through the pulmonary circuit, but all of the endothelium is important.

33
Q

What does angiotensin II do?

A

Angiotensin II stimulates the aldosterone- secreting cells in the zona glomerulosa of the adrenal cortex

34
Q

What does aldosterone do?

A

The aldosterone passes in the blood to the kidney where it stimulates distal tubular Na+ ion reabsorption

35
Q

What is the rate-limiting step in the renin-angiotensin-aldosterone system?

A

The rate limiting-step is the release of renin since angiotensinogen is always present in plasma.

36
Q

When is renin release increased?

A

When the pressure in afferent arteriole at the level of the JG cells is decreased

37
Q

How do JG cells act as renal baroreceptors?

A

Less distension leads to increased secretion of renin. Intrinsic property occurs if denervated

38
Q

Why does increased sympathetic nerve activity cause increases in renin?

A

Via B1 effect

39
Q

What is rate of renin secretion inversely proportional to?

A

Rate of delivery of NaCl at the macula densa (specialised distal tubule)

40
Q

What inhibits renin?

A
  • Angiotensin II feed back

- ADH r

41
Q

What does the close relationship between the afferent arteriole with JG cells and the macula densa provide a mechanism for?

A

Controlling input and output of tubules and basis of tubuloglomerular balance

42
Q

How are volume deficits restored in hypovolaemia?

A

Increases in proximal AND distal tubule Na+ reabsorption together with osmotic equivalents of H2O, helps restore volume deficits, mediated by CV reflexes

43
Q

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

A
  • It stimulates aldosterone and therefore NaCl and H2O retention
  • It is a very potent biological vasoconstrictor, 4-8x more potent than norepinephrine therefore contributes too increased TPR
  • It acts on the hypothalamus to stimulate ADH secretion which increases H2O reabsorption from CD
  • It stimulates the thirst mechanism and the salt appetite
44
Q

What does tubuloglomerular feedback contribute to?

A

GFR constancy

45
Q

If there is conflicting information received by osmoreceptors and baroreceptors what happens?

A

Volume considerations have primacy if ECV is compromised

46
Q

What is normally the main determinant of [ADH]?

A

Osmolarity

47
Q

When does volume become the primary driver of [ADH]?

A

If there is sufficient volume change to compromise brain perfusion

48
Q

What is the simple rule when it comes to normalising ECF?

A

Simple rule, lose salt and water, replace salt and water.

49
Q

What does aldosterone promote?

A

Na reabsorption

50
Q

What is ANP?

A

Atrial natriuretic peptide

51
Q

What does ANP promote?

A

Na excretion

52
Q

What effect does aldosterone have at the distal tubule?

A
  • Increased Na reabsorption

- Increased K secretion

53
Q

What does administering aldosterone lead to?

A
  • Increased weight because of retention of H2O with increased Na
  • Volume expansion
  • Stimulation of release of ANP from atrial cells
  • Loss of Na and H20
  • Continued K loss due to increased K secretion
54
Q

What is aldosterone escape?

A

ANP overrides aldosterone effects on Na+ reabsorption because of volume expansion

55
Q

When is ANP secreted?

A

ANP is secreted by atrial cells in response to expansion of ECF volume and causes natriuresis, loss of Na+ and H2O in urine

56
Q

When is osmotic diuresis particularly important to consider?

A

In uncontrolled diabetes (hyperglycaemic coma)

57
Q

What happen in uncontrolled DM where [BG] is not kept within strict control?

A

The high plasma glucose level exceeds the maximum reabsorptive capacity in the proximal tubule

58
Q

What happens when glucose levels exceed the maximum reabsorptive capacity?

A

Glucose remains in the tubule and exerts an osmotic effect to retain H2O in the tubule.

59
Q

Why is there a decreased ability to reabsorb glucose in uncontrolled diabetes?

A
  • [Na+] in the lumen is decreased because the Na+ is present in a larger volume.
  • Since Na+ gains access to the proximal tubule cells by passive diffusion down a concentration gradient created by the active transport out of the basolateral surfaces, Na+ reabsorption will be decreased
  • This decreases the ability to reabsorbe glucose since it shares a symport with Na
60
Q

In uncontrolled diabetes, why is the movement of H2O out of the tubule into the interstitium reduced in the descending loop of Henle?

A

The glucose and excess Na exert an osmotic effect to retain H2O therefore fluid in the descending limb is not so concentrated

61
Q

If the fluid in the descending loop of Henle is less concentrated in uncontrolled diabetes, what does that mean for the ascending limb?

A

The fluid delivered to the ascending limb is less concentrated

62
Q

Why is there a large volume of NaCl and H2O delivered to the distal tubule and the interstitial gradient is gradually abolished in uncontrolled diabetes?

A
  • Since the NaCl pumps in the ascending limb are gradient limited, medullary interstitial gradient is much less
  • Therefore there is a considerable reduction in the volume of NaCl and H2O reabsorbed fro the loops of Henle
63
Q

Under normal conditions what does a large volume of NaCl and H2O delivered to the distal tubule mean?

A

There is excess ECF volume and therefore the need to get rid of NaCl and H2O

64
Q

What detects high rates of delivery of NaCl to the distal tubule?

A

The macula densa

65
Q

How does the macula densa respond to high rates of NaCl delivery to the distal tubule?

A
  • Renin secretion is supressed

- Na reabsorption at the distal tubule is decreased

66
Q

What type of urine do uncontrolled diabetics produce?

A

Large volumes of nearly isotonic urine which decreases the PV

67
Q

What will decreased PV stimulate in uncontrolled diabetes?

A

ADH release via baroreceptors but they cannot be effective because the interstitial gradient has run down

68
Q

How much urine can a patient with uncontrolled diabetes produce?

A

Up to 6-8l per day causing slat and water depletion

69
Q

What is one of the first signs of DM?

A

Raging thirst

70
Q

Why does hyperglycaemic comas occur?

A

Hypotension may become so severe

71
Q

What is a hyperglycaemic coma due to?

A

Inadequate blood flow to the brain

72
Q

What is a hypoglycaemic coma due to?

A

Inadequate glucose to the brain

73
Q

What can cause an osmotic diuresis in uncontrolled diabetes?

A

Any solute which remains in the tubule can cause an osmotic diuresis eg NaCl or urea but this helps to eliminate their excess.

74
Q

Why is osmotic diuresis not self-limiting in uncontrolled diabetes?

A

The liver keeps producing glucose

75
Q

What affect can loop diuretics have on K?

A

Can cause K wasting

Systems: Urinary AB (26 decks)

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