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Year 2 - Renal > ECF volume regulation > Flashcards

ECF volume regulation Flashcards

1
Q

Name the 2 major osmoles of the ECF (osmoles = osmotically active solutes, i.e. non freely penetrating solutes that require movement of water to equilibrate the osmotic pressure)

A

Na+ and K+

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2
Q

Regulation of ECF volume essentially relies on regulation of what non penetrating solute

A

Na+

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3
Q

Total body water (42L) is distributed into what 2 compartments

A

ECF - 1/3

ICF - 2/4

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4
Q

ECF makes up what fraction of total body water + what is ECF further divided into

A

1/3

Plasma - 3L
ISF - 11L

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5
Q

ICF makes up what fraction of total body water

A

2/3

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6
Q

What’s bigger - ECF or ICF

A

ICF

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7
Q

Hypovolaemia =

A

blood volume loss, i.e. decreased ECF

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8
Q

Hypovolaemia decreases plasma volume which consequently causes what following things to be decreased

A 
↓PV
↓Venous pressure
↓Venous return
↓atrial P
↓EDV
↓SV
↓CO
↓BP
↓carotid sinus baroreceptor discharge as it can sense less stretch of the vessel
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9
Q

Hypovolaemia causes decreased BP which leads to a decrease in carotid sinus baroreceptor discharge (as it senses less stretch from low BP so decreases discharge rate)

What are the different sympathetic responses of the body to this

A

Medullary cardiovascular centre receives this info and stimulates sympathetic nerves
innervating

  • SA node to release NA, acting on the node to depolarise it faster and increase HR to pump more blood around body
  • veins to constrict to squeeze spare capacitance of blood back to heart –> increase VR –> increase EDV –> increase preload –> increase contraction strength –> increase CO –> increase BP
  • arterioles to constrict –> increasing total peripheral resistance –> in order to increase MAP back to normal
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10
Q

Long term control of BP is controlled by what 3 things

A

Renin-angiotensin-aldosterone system

ADH

Atrial natriuretic peptide (ANP)

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11
Q

What is sympathetic response of the kidneys to hypovolaemia (or low BP)

A

Sympathetic nerves innervating it release NA which bind to the a1 receptors of the arterioles and CONSTRICT them –> increasing TPR –> increasing MAP

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12
Q

The sympathetic response of the kidneys to low BP or hypovolaemia is to constrict their afferent arterioles in order to increase TPR and therefore increase MAP

What detects constriction of the renal arterioles and what is subsequently activated from this

A

Juxtaglomerular cells sense decreased distension of the afferent arteriole and causes increased secretion of renin

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13
Q

What cells produce renin

A

juxtaglomerular

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14
Q

What does renin do

A

Convert angiotensinogen to angiotensin I

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15
Q

What does angiotensin converting enzyme (ACE) do

A

convert angiotensin I to II

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16
Q

Functions of angiotensin II towards the kidney (2)

A

Stimulates release of aldosterone –> increases Na+ reabsorption in the distal tubule so reduces diuresis

Increases Na+ and water reabsorption in the proximal tubule so less diuresis

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17
Q

Aldosterone increases sodium and water reabsorption in the proximal or distal tubule

A

distal

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18
Q

Main driving force of reabsorption into the peritubular capillaries

A

oncotic pressure

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19
Q

Reabsorptive range in proximal tubule is 65-75%, how does this differ in times of volume excess or volume deficit (hypovolaemia)

A

if volume excess, nearer 65%

if volume deficit, nearer 75%

20
Q

Reabsorption from proximal tubule to peritubular capillary is largely driven by what

A

starling’s forces, specifically oncotic force as that’s driving the fluid to move into the peritubular capillary

21
Q

Does volume depletion affect GFR

A

Only if volume depletion severe enough to decrease MAP significantly

If not, autoregulation maintains it through constricting its arterioles

22
Q

In hypervolaemia, is the peritubular hydrostatic pressure and oncotic pressure increased or decreased

A

increased

decreased

23
Q

In hypovolaemia, is the peritubular hydrostatic pressure and oncotic pressure increased or decreased

A

decreased

increased - in order to reabsorb as much water back as possible

24
Q

What maintains GFR in times of low BP

A

Constriction of afferent arteriole due to sympathetic activity

Constriction of efferent arteriole due to angiotensin II acting on it

25
Q

Distal tubule na+ reabsorption is controlled by what hormone

A

aldosterone

26
Q

What is the macula densa/function + where is it

A

area of closely packed specialised cells lining the wall of the distal tubule and senses changes in NaCl conc. in the tubul and triggers autoregulatory response to increase/decrease reabsorption of Na+

27
Q

Where are the juxtaglomerular cells that secrete renin

A

in the afferent arteriole

28
Q

Rate limiting step of the renin-angiotensin-aldosterone system

A

release of renin by the juxtaglomerular cells since angiotensinogen is constantly present in plasma

29
Q

Renin release triggered by (3)

A

Decreased distention/pressure of afferent arteriole

Activation of sympathetic nerves innervating the juxtaglomerular cells via NA acting on b1 receptors

Decreased delivery of Na+ and Cl- through the tubule

30
Q

Renin release inhibited by (2)

A

Angiotensin II feeding back on it

ADH

31
Q

Summary of renal responses to hypovolaemia (2)

A

Increased renin –> increased angiotensin II

  • decreases peritubular capillary hydrostatic pressure –> increasing Na+ reabsorption in proximal tubule
  • stimulates aldosterone production –> increases distal tubule Na+ reabsorption
32
Q

Effects of angiotensin II (4)

A

Stimulates aldosterone release

Potent vasoconstrictor –> increases TPR –> increases MAP

Stimulates ADH release

Stimulates thirst mechanism and salt appetite

33
Q

If GFR increases, what is the intrinsic response of the kidney to counteract this

A

constrict afferent arteriole to decrease hydrostatic pressure

34
Q

What effect does the following have on ADH release:

  • decreased ECF osmolarity
  • decreased ECF volume
A

decreased via OSMORECEPTORS

increased via BARORECEPTORS

35
Q

Main determinant of ADH conc. at any given time?

But if there’s a big volume change that would compromise brain perfusion, then what becomes the primary determinant of ADH conc.

(i.e. these are triggers of ADH release/inhibition of release)

A

ECF osmolarity

ECF volume - as brain perfusion more important than disturbed osmolarity

36
Q

Function of ANP

A

Increase excretion of Na+ (natriuresis) and therefore diuresis

37
Q
  • Renin-angiotensin-aldosterone system
  • ADH
  • Atrial natriuretic peptide (ANP)

are long term controls of BP, what is different about ANP from the other 2

A

ANP stimulates diuresis (i.e. excretion of sodium and water) while the other 2 do the opposite

38
Q

What triggers ANP release from myocardial cells in the atria

A

Distension of the atria (i.e. higher BP)

39
Q

Aldosterone causes secretion of what into the distal tubule

A

K+

40
Q

Hyperaldosteronism would cause hypo or hyperkalaemia

A

Hypo because aldosterone stimulates K+ secretion into distal tubule to be secreted out

41
Q

Why does hyperaldosteronism (e.g. conn’s syndrome) not cause hypernatraemia if aldosterone stimulates Na+ reabsorption

A

Because the increased blood volume caused by the Na+ reabsorption stretches the atria which triggers ANP release from atrial myocardial cells to cause increased natriuresis (excretion of sodium in urine)

42
Q

In uncontrolled DM, BG conc. exceeds the maximum reabsorptive capacity in the proximal tubule so remains in the tubule which has what effect on water

Since it has this effect on water, the conc. of what cation decreases in the lumen

A

causes water to stay in tubule as well

Na+ because it’s diluted in a large volume of water

43
Q

In hyperglycaemia, excess glucose is retained in tubule as maximum capacity is already reabsorbed which creates an osmotic effect and causes water to be retained as well

This causes Na+ conc. to decrease in the tubule as it’s diluted in more water so what effect does this have on Na+ reabsorption and glucose reabsorption

A

both decrease as Na+ conc. inside the lumen is decreased so the conc. gradient that it passively diffuses down from the lumen to the proximal tubule cell is reduced

glucose shares a symporter with Na+ therefore its reabsorption will be reduced too

44
Q

Summarise the process of how hyperglycaemia in diabetes mellitus causes osmotic diuresis (4)

A

Glucose remains in tubule so exerts osmotic effect to retain water in tubule

Retaining water therefore decreases Na+ conc. in tubule so less passive sodium reabsorption in the proximal tubule as well

In the descending limb, water movement out into the interstitium reduced because of the osmotic effect that glucose and excess Na+ exert to retain water –> so diluted fluid is sent to the ascending limb and since NaCl pumps in the ascending limb are gradient limited, the medullary interstitial gradient is REDUCED so much less reabsorption of NaCl into the interstitium
-so altogether decreased loop of henle reabsorption

Therefore large volume of isotonic urine produced a day

45
Q

If there’s increased delivery of NaCl and water to the distal tubule, the macula densa cells detect this and subsequently do what to help this

A

inhibit renin secretion in order to decrease Na+ reabsorption at the distal tubule and excrete the excess Na+

46
Q

In hyperglycaemia in uncontrolled DM, the medullary interstitial gradient is abolished which causes osmotic diuresis (i.e. excrete large volumes of urine a day)

This therefore decreases plasma volume which would be detected by baroreceptors and they would stimulate ADH to reabsorb water in the CD but why won’t ADH work in these uncontrolled diabetics

A

because the medullary interstitial gradient doesn’t exist, fluid in the collecting duct is isotonic with the fluid around it so increased ADH won’t have much affect as there needs to be a gradient for water to be reabsorbed

47
Q

How does a hyperglycaemic coma work - usually you hear more about hypoglycaemic comas because of reduced glucose to brain but why can high glucose cause a coma

A

because high glucose causes osmotic diuresis so lose a lot of water in urine which decreases plasma volume so in very severe circumstances, may reduce blood flow to brain

Year 2 - Renal (21 decks)

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