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RENAL PHYSIOLOGY > ECF Regulation 1 > Flashcards

ECF Regulation 1 Flashcards

1
Q

What are the major ECF osmoles?

A

Na+

Cl-

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2
Q

What are the major ICF osmoles?

A

K+ salts

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3
Q

What proportion of the body water is in ICF?

A

2/3 (28L)

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4
Q

What proportion of the water is in the ECF?

A

1/3 (14L)

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5
Q

What compartments make up the extracellular fluid?

A

Plasma

Interstitial fluid

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6
Q

What is the renal response to decreased ECF volume due to vomiting/diarrhoea/sweating?

A 
↓ Plasma volume
↓ venous pressure
↓ Venous return
↓ Atrial pressure
↓ End diastolic volume
↓ systolic volume
↓ cardiac output
↓ blood pressure
= DECREASED SINUS BARORECEPTOR INHIBITION OF SYMPATHETIC DISCHARGE
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7
Q

What is the effect of increased sympathetic discharge?

A

Increased total peripheral resistance

Increased BP towards normal

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8
Q

Both decreased carotid sinus baroreceptor discharge and atrial pressure do what?

A

Increased ADH

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9
Q

What is the effect of decreased carotid sinus baroreceptor discharge on the kidneys?

A

Increased sympathetic vasoconstriction, which includes renal arterial constriction, this increasing renin secretion

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10
Q

Increased renin increases what?

A

Angiotensin II

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11
Q

What are the effects of increased angiotensin II?

A
  1. Increased proximal tubule NaCl + H2O reabsorption

2. Increased aldosterone secretion

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12
Q

What are the effects of increased aldosterone secretion?

A

Increased distal tubule NaCl + H2O reabsorption

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13
Q

Proximal tubule

NaCl & H2O reabsorption is affected by what?

A

Angiotensin II levels

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14
Q

Distal tubule

NaCl & H2O reabsorption is affected by what?

A

Aldosterone levels

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15
Q

How does increased renin effect Na+ reabsorption?

A 
↑Renin = ↑Angiotensin II
↑AGTII = ↓ peritubular capillary hydrostatic Pressure and ↑oncotic pressure = ↑Na+ reabsorption
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16
Q

Angiotensin II is a what?

A

VASOCONSTRICTOR

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17
Q

Why is oncotic pressure the driving force of reabsorption?

A

Capillaries have lost a lot of salt + water

Plasma proteins remain, oncotic pressure drives reabsorption

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18
Q

What is the reabsorptive range of the proximal tubule?

A

65-75%

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19
Q

How does GFR rate vary throughout volume/pressure changes?

A

Very little unless volume depletion is severe to cause ↓MBP

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20
Q

What, in normovolaemia, is the pressure in the peritubular capillaries?

A

Below normal due to efferent arteriole constriction by angiotensin II

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21
Q

What, in normovolaemia, is the oncotic pressure in the peritubular capillaries?

A

Greater than normal due to lost NaCl and H2O, causing a relative ↑ in plasma [protein]

22
Q

How much salt is reabsorbed in the proximal tubule in hypovolaemia?

A

75%

23
Q

What, in hypervolaemia, is the oncotic pressure in the peritubular capillaries?

A

Decreased due to increased water levels diluting the proteins

24
Q

What, in hypervolaemia, is the pressure pressure in the peritubular capillaries?

A

Increased because the efferent arteriole is less constricted

25
Q

What regulates constriction of the afferent arteriole?

A

Sympathetic VC

26
Q

What regulates constriction of the efferent arteriole?

A

Angiotensin II

27
Q

Aldosterone regulates what?

A

Regulation of distal tubule Na+ reabsorption

28
Q

Where is aldosterone produced?

A

Adrenal cortex

Zona glomerulosa

29
Q

What are Juxtaglomerular cells?

A

Specialised, granular epithelial cells on the smooth muscle of the afferent arteriole

30
Q

What is the macula densa?

A

Specialised loop of the distal tubule

31
Q

What is the Juxtaglomerular apparatus?

A

Juxtaglomerular cells and the macula densa

32
Q

Where is Renin produced?

A

Juxtaglomerular cells

33
Q

What is renin?

A

Proteolytic enzyme which acts on angiotensinogen

34
Q

ANGI –> ANGII is regulated by what?

A

ACE

35
Q

Where is ACE produced?

A

Blood vessel epithelium

36
Q

What fraction of the plasma proteins is acted on by renin?

A

alpha2-globulin

37
Q

What is the rate limiting step of the RAAS system?

A

Renin concentration

38
Q

What is the effect of increased ANGII on arterioles?

A

Vasoconstriction

39
Q

What is the effect of increased ANGII on the cardiovascular control centre of the medulla oblongata??

A

Increased cardiovascular response to increase blood pressure?

40
Q

What is the effect of increased ANGII on the hypothalamus?

A

↑ Vasopressin

↑ Thirst

41
Q

What is the effect of increased ANGII on the adrenal cortex?

A

↑ Aldosterone = ↑ Na+ reabsorption

42
Q

What is the effect of increased ANGII on the adrenal cortex?

A

↑ Aldosterone = ↑ Na+ reabsorption

43
Q

What are the controls of renin release?

A
  1. ↑ when Pressure at JG cells ↓
  2. ↑ via ↑sympathetic nerve activity via beta1
  3. ↑ when NaCl to macula densa ↓
  4. Inhibited by Angiotensin II
  5. Inhibited release by ADH
44
Q

What is the effect of Angiotensin II on renin?

A

Angiotensin II feeds back to inhibit renin

45
Q

What is the effect of ADH on renin?

A

Feeds back to inhibit renin

46
Q

What is the effect of increased NaCl at the macula densa on renin?

A

Decreased renin secretion

47
Q

What are the roles of Angiotensin II?

A

Stimulate aldosterone
Vasoconstriction (↑ TPR)
Stimulates ADH secretion
Stimulates thirst/salt appetite

48
Q

What is the vasoconstrictive potency of norepinephrine compared to angiotensin II?

A

Angiotensin 4-8x more potent than norepinephrine

49
Q

How does the macula densa communicate with the arteriole?

A

Paracrine

50
Q

Increased salt flow through the macula densa has what effect?

A

Constriction of the afferent arteriole, reducing GFR

51
Q

What is the most important factor deciding the action of ADH?

A

Osmolarity in normal volume

Volume in emergency

RENAL PHYSIOLOGY (10 decks)

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