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Urinary System > ECF Volume Regulation 1 > Flashcards

ECF Volume Regulation 1 Flashcards

1
Q

What organ regulates ECF volume?

A

Kidneys

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2
Q

What is the distribution of of water between cells and ECF determined by?

A

Number of osmotically active particles in each compartment

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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 osmokes?

A

K salts

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5
Q

How is water distributed in the body?

A
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6
Q

What volume of water is found in ICF, what is this volume?

A

66% (28L)

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7
Q

What volume of water is found in ECF, what is this volume?

A

33% (14L)

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8
Q

What percentage of total body weight is water?

A

60%

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9
Q

What is the volume of water in the entire body?

A

42L

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10
Q

What is ECF water split into?

A

Plasma

Interstitial fluid

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11
Q

What volume of water is found in plasma?

A

3L

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12
Q

What volume of water is found in interstitial fluid?

A

11L

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13
Q

What is the volume of blood perfusing tissues known as?

A

Effective circulating volume

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14
Q

How does changes in Na content of the ECF impact blood volume and blood pressure?

A

Changes in Na of the ECF causes changes in ECF volume so affects volume of blood perfusing tissues and blood volume

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15
Q

What is regulation of Na dependent on?

A

High and lower pressure baroreceptors

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16
Q

What is the medical term for low blood volume?

A

Hypovolaemia

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17
Q

What can hypovolaemia be caused by?

A

Salt and water loss (such as in vomiting, diarrhoea or excess sweating)

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18
Q

Explain the renal response to hypovolaemia?

A

Decrease in perfusing volume -> decrease in venous pressure -> decrease in venous return -> decrease in atrial pressure -> decrease in EDV -> decrease in stroke volume -> decrease in cardiac output -> decrease in blood pressure -> decrease in carotid sinus baroreceptor inhibition of sympathetic discharge

Causes increase in sympathetic discharge -> increase vasoconstriction -> increased total peripheral resistance -> increased blood pressure towards normal

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19
Q

What is the best way to deal with low volume?

A

Vasoconstriction

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20
Q

What does VC stand for?

A

Vasoconstriction

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21
Q

What impact does hypovolaemia have on the kidney?

A

Increased sympathetic discharge -> increase renal VC nerve activity -> increase renal arteriolar constriction and increase in renin

Increase in renin -> increases angiotensin II -> decrease in peritubular capillary hydrostatic pressure (and increase in oncotic pressure) -> increased Na reabsorption from proximal tubule and therefore less Na excreted

Increased angiotensin II also increases aldosterone -> increased distal tubule Na reabsorption and therefore less sodium excreted

22
Q

How is Na absorption changes if you have lost NaCl and water, such as in vomiting?

A

Increase in Na reabsorption, therefore more of the “wet stuff” then increase in oncotic pressure even more so can reabsorb up to 75% of filtrate at the proximal tubule

23
Q

What are the 2 ranges of Na reabsorption in proximal tubule at the 2 extremes of volume excess and volume deficit?

A

Volume excess - 65%

Volume deficit - 75%

24
Q

How does GFR change with changes in sodium reabsorption due to for example vomiting?

A

GFR remains largely unaffected:

  • Autoregulation maintains GFR and the VC of afferent and efferent means little effect on GFR until volume depletion severe enough to cause considerable ¯ MBP
25
Q

How is GFR maintained even in decreased renal blood flow?

A

Increased resistance in efferent arteriole due to angiotensin II

26
Q

What is regulation of distal tubule sodium reabsorption under the control of?

A

Aldosterone

27
Q

What is aldosterone very important for?

A

Long term regulation of Na and ECF volume

28
Q

What forms the juxtaglomerular apparatus?

A

Juxtaglomerula cells and macula densa

29
Q

What is renin secreted from?

A

Juxtaglomerular cells

30
Q

What is renin?

A

A proteolytic enzyme which acts on a large protein in the a2-globulin fraction of the plasma proteins = angiotensinogen

31
Q

How does renin result in the creation of angiotenin II?

A

Renin converts angiotensinogen in angiotensin 1, which is converted into angiotensin II by ACE (enzyme)

32
Q

What enzyme is responsible for the conversion of angiotenin I to angiotenin II?

A

Angiontenin converting enzyme (ACE)

33
Q

Where is angiotenin converting enzyme found?

A
  • Found throughout the vascular endothelium, but greatest proportion of conversion occurs as blood passes through the pulmonary circuit
34
Q

What effects does angiotensin II have?

A
  • Angiotensin II stimulates the aldosterone-secreting cells in the zona glomerulosa of the adrenal cortex
  • 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 RAAS?

A

Release of renin since angiotensinogen is always present in plasma

36
Q

What effects does angiotenin II have?

A
37
Q

When is renin release?

A

JG cells act as “renal baroreceptors”, less distension ® ­ secretion of renin. Intrinsic property, occurs if denervated.

Increase in sympathetic innervation increases renin release via B1 effect

38
Q

How does tubuloglomerular feedback contribute to GFR consistancy?

A

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

39
Q

What is the relationship between rate of renin secretion and rate of delivery of NaCl at the macula densa?

A

Inversely proportional

(decreased NaCl delivery causes increases renin secretion)

40
Q

What inhibits renin release?

A

Angiotensin II feeds back to inhibit

ADH (osmolarity control)

41
Q

Why is angiotenin II fundamentally important in the bodoies response to hypovolaemia?

A
  • It stimulates aldosterone and therefore NaCl and water retention
  • Is a very potent vasoconstrictor, 4-8x more potent than NE, therefore contributing to TPR
  • Acts on hypothalamus to stimulate ADH secretion, which increases water reabsorption from CD
  • Stimulates the thirst mechanism and the salt appetite (in the hypothalamus)
42
Q

In some scenarios there are opposing inputes to ADH secreting cells. Such as a person suffering from severe diarrhoea, who has lost 3l of salt and water (from ECF) and drinks 2L of pure water (decrease in ECF osmolarity inhibits ADH secretion whilst decrease in volume increases ADH secretion). Which takes priority?

A

Volume considerations have primacy if ECF is compromised so that ADH will be increased, this is an emergency mechanism to save perfusion for the brain

Normally, osmolarity is the main determinant of [ADH] but if sufficient volume change to compromise brain perfusion occurs then volume becomes the primary drive, so to conserve volume, tolerate disturbed osmolarity:

  • Once volume is restored in hypovolaemia then osmolarity will be normalised and again becomes the main determinant of ADH
43
Q

Is volume or osmolarity normally the main determinant of ADH secretion?

A

Osmolarity, however when volume is so low than brain perfusion is compromised this changes to volume

44
Q

What effect does angiontenin II have on arterioles?

A

Vasoconstriction to increase blood pressure

45
Q

What effect does angiotenin II have on CV centre in medulla oblongata?

A

Increases cardiovascular response to increase blood pressure

46
Q

What effect does angiotenin II have on the hypothalamus?

A

Increases vasopressin secretion and thirst to increase volume and maintain osmolarity which will increase blood pressure

47
Q

What effect does angiotensin II have on the adrenal cortex?

A

Increases aldosterone, which increases Na reabsorption, increasing volume and maintaining osmolarity which will increase blood pressure

48
Q

Where is angiotensinogen found?

A

Constantly found in plasma

49
Q

What organ produces angiotensinogen?

A

Liver

50
Q

Where is ACE enzyme found?

A

Blood vessel endothelium

Urinary System (29 decks)

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