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BRS 12 Urology and renal > 1b Sodium and Potassium Balance > Flashcards

1b Sodium and Potassium Balance Flashcards

1
Q

What is the osmolarity?

A

measure of the amount of solute dissolved in a solution (osmoles/Litre)

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2
Q

What is meant by osmole?

A

1 mole of dissolved solute per litre

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3
Q

Describe how there is a constant osmolarity?

A

water and salt are inter-related

When there is increased salt, there will be increased water as water follows salt, resulting in an increased volume

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4
Q
  • During water deprivation, how does the change in urine osmolarity compare to that of plasma osmolarity?
A

Urine concentrates = as the osmolality increases
Plasma = remains at the homeostatic set point

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5
Q

What allows the homeostatic set point of plasma osmolarity?

A

The semi permeable cell membrane allows the movement of water across the cell

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6
Q

What is the normal plasma osmolarity?

A

285-295 mosm/L

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7
Q

What is the most important and prevalent solute in the ECF?

A

Sodium - 140 mmol/L

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8
Q

What effect does increasing dietary sodium have on blood volume and pressure and how does it do this?

A

Increased dietary sodium → Increased total body sodium → Increased osmolarity (but this can’t happen - because of the semi permeable membrane, water will always follow) → Increased water intake and retention → Increased ECF volume → Increased blood volume and pressure

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9
Q

At euvolemia, what effect is had on Na+ intake and through what nucleus does this occur in?

A

Inhibition of sodium intake

Lateral parabrachial nucleus

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10
Q

Which neurotransmitters are working to inhibit sodium intake?

A

Seretonin and glutamate

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11
Q

Which neurotransmitters are working to increase a persons appetite for sodium?

A

GABA, Opiods

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12
Q

What is the peripheral control of sodium intake?

A

Taste, small amounts of Na+ is desirable, but as this increases it becomes aversive

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13
Q

How much sodium is absorbed into each part of the nephron?

A

Proximal - 67%
Thick ascending limb - 25%
Distal convoluted tubule - 5%
Collecting duct - 3%

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14
Q

What is GFR proportional to?

A

Renal Plasma Flow

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15
Q

Why do GFR and RPF eventually plateau?

A

We don’t want to excrete more sodium than is needed

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16
Q

What percent of renal plasma enters the tubular system and therefore how do you calculate GFR from renal plasma flow?

A

20%

GFR = RPF * 20

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17
Q

How is increased tubular sodium levels reacted to by the macula densa and how does this affect perfusion pressure and GFR?

A
  1. High tubular sodium
  2. Increased uptake of sodium from the macula dense (via the triple transporter)
  3. This triggers ADENOSINE release
  4. This is detected by the extraglomerular mesangial cells
  5. Renin production is reduced, which promotes smooth muscle cell contraction
  6. This reduced perfusion pressure so GFR decreases
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18
Q

What is the best way to retain sodium?

A

Filter less sodium

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19
Q

How can you filter less sodium?

A

Reducing efferent arteriole pressure to increase pressure gradient and so more blood flow from afferent arteriole rather than being filtered out

So more retention of both sodium and water

-

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20
Q

What are 3 main physiological mechanisms that increase Na+ reabsorption and retention?

A
  1. Increased sympathetic activity
  2. Angiotensin II
  3. Aldosterone
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21
Q

How does increased sympathetic activity lead to more sodium retention?

A
  • Causes SMC of afferent arteriole to contract so less is filtered
  • Stimulates sodium uptake in the proximal convoluted tubule
  • Stimulates juxtaglomerular apparatus to release Renin which forms angiotensin II (This further stimulates sodium reabsorption in the proximal convoluted tubule)
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22
Q

How does angiotensin effect sodium retention?

A

Stimulates sodium uptake from cells of PCT

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23
Q

how does aldosterone affect sodium reabsorption?

A

Stimulates sodium reabsorption in the DCT and collecting duct

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24
Q

How does the juxtaglomerular apparatus respond to low tubular sodium?

A

Causes the stimulation of renin production which makes angiotensin and aldosterone

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25
Q

What is the main protein involved in decreasing sodium reabsorption?

A

Atrial naturietic peptide

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26
Q

Describe the mechanism of action of ANP in order to decreased sodium reabsorption?

A

Vasodilator - reduces afferent arteriolar pressure so more is filtered to be excreted

ANP

Decreases uptake of Na+ from PCT, DCT, CT

Reduces renin secretion from Juxtaglomerular apparatus

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27
Q

What happens to blood pressure and volume when there is low sodium?

A

Decreases blood pressure and blood volume
This increases beta sympathetic activity

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28
Q

What does decreased Beta1 sympathetic activity due to high sodium induce?

A

Atrial-Naturietic Protein production

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29
Q

Where is aldosterone synthesized and released?

A

The adrenal cortex - zona glomerulosa

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30
Q

When is aldosterone released?

A

released in response to angiotensin II
or a decrease in blood pressure which is detected by the baroreceptors

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31
Q

What effect does aldosterone have on blood pressure?

A

increases blood pressure

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32
Q

How is aldosterone release triggered by increased sympathetic activity?

A

Increased sympathetic activity stimulates the cells of the juxtaglomerular apparatus to release renin

Renin activity cleaves angiotensinogen to angiotensin I

Angiotensin I is cleaved by angiotensin converting enzyme to produce angiotensin II

Angiotensin II stimulates the synthesis of aldosterone synthase in the zona glomerulosa to increase the synthesis of aldosterone.

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33
Q

What effect does aldosterone have in the distal convoluted tubule and the collecting duct?

A

Increases sodium reabsorption
Increases potassium secretion
Increases H+ secretion

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34
Q

What does aldosterone excess lead to?

A

Hypokalaemic alkalosis

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35
Q

Can aldosterone pass through the lipid membrane?

A

Yes - it is lipid soluble

36
Q

Describe the mechanism by which aldosterone works?

A

Passes through cell membrane - steroid hormone

Binds mineralocorticoid receptor

Binds another and becomes a dimer

Translocates into the nucleus

Binds and enables transcription of genes and mRNA of proteins which help it carry out its function

37
Q

Transcription of what proteins are increased by Aldosterone?

A

ENaC
Na+ K+ ATPase
regulatory proteins needed for the channels

Resulting in more sodium and more active sodium channels

38
Q

What are the symptoms of hypoaldosteronism?

A

Dizziness, low blood pressure, salt craving and palpitations

39
Q

Describe the pathophysiology of hypoaldosteronism?

A
  • Less aldosterone
  • Less reabsorption of sodium in the distal convoluted tubule
  • More sodium is lost in the urine, and more loss of water
  • ECF falls

Increases Renin, Angiotensin II and ADH to try and compensate

40
Q

Describe the pathophysiology of hyperaldosteronism?

A
  • Too much Aldosterone
  • Reabsorption of sodium in the distal nephron is increased
  • Less urinary loss of sodium, more water retention, ECF increases

reduced renin, Ang II and ADH

41
Q

In states of hyperaldosteronism which two proteins are raised?

A

ANP and BNP

ANP - tries to decreases sodium reabsorption to compensate for the increase which the hyperaldosterone is causing

42
Q

what are the symptoms of hyperaldosteronism?

A

high blood pressure
Muscle weakness
Polyuria
Thirst

43
Q

What is Liddle’s syndrome?

A

An inherited disease of high blood pressure = where there is a mutation in the aldosterone activated sodium channel meaning it is always on, resulting in constant sodium retention = hypertension

44
Q

Describe the pathway involving the kidney though which increased sympathetic stimulation increases aldosterone levels

A

Increased sympathetic activity stimulates the cells of the juxtaglomerular apparatus (0.5 mark) to release renin (0.5 mark). Renin activity cleaves angiotensinogen to angiotensin I (0.5 mark). Angiotensin I is cleaved by angiotensin converting enzyme (0.5 mark) to produce angiotensin II (0.5 mark). Angiotensin II stimulates the synthesis of aldosterone synthase (0.5 mark) in the zona glomerulosa (0.5 mark) to increase the synthesis (0.5 mark) of aldosterone.

45
Q

What would be the expected effect of spironolactone treatment on the blood pressure of a person with Liddle’s Syndrome?

A

No effect (1 mark). The mutation in Liddle’s syndrome is in the aldosterone sensitive ENaC sodium channel. This mutation means that the channel is always on so that there will be minimal effect on sodium reuptake (1 mark).

46
Q

When hypertension is resistant to diuretics, what is then used?

A

Diuretics = spironolactone

47
Q

In the heart where are the baroreceptors that respond to low pressure?

A

Atria
Right ventricle

48
Q

In the heart, where are the baroreceptors which respond to high pressure?

A

Carotid sinus
Aortic Arch

49
Q

In the low pressure side, how is low pressure dealt with?

A

Low pressure → Reduced baroreceptor firing → Signal through Afferent fibres to brainstem → Sympathetic activity & ADH Release which promotes Water retention to try and increase pressure again

50
Q

In the low pressure side, how is high pressure dealt with?

A

High pressure → Atrial stretch → ANP, BNP released

Stop sodium retention, therefore more sodium excreted

51
Q

On the high pressure side, how is low pressure dealt with? (2 ways)

A

Low pressure → Reduced baroreceptor firing → Signal through Afferent fibres to brainstem → Sympathetic activity and ADH Release

Low pressure → Reduced baroreceptor firing → JGA cells → Renin released

52
Q

When is ANP released?

A

In response to atrial stretch

53
Q

What are the four actions of ANP?

A
  1. Vasodilation of renal blood vessels
  2. Inhibition of sodium reabsorption in th PCT and CD
  3. Inhibits renin and aldosterone
  4. Reduces blood pressure
54
Q

Which protein kinase does ANP stimulate?

A

Protein Kinase G

55
Q

Describe the physiology which occurs in response to volume expansion?

A

Volume expansion = decreased sympathetic activity ===

  1. Reduces renin → reduced Angiotensin I → reduced angiotensin II → reduced aldosterone
  2. Increases ANP & BNP → Reduces GFR and Na+ uptake in the DCT and CT and also DECREASES AVP from the brain, reduces renin, Reduces aldosterone production from adrenal gland, Reduces AVP → Decreased aquaporins into the epithelial wall in the CT
56
Q

Describe the physiology which occurs in response to volume contraction?

A

Volume contraction = increased sympathetic activity

  1. Increases renin -> increases angiotensin 1 -> increases angiotensin II -> increases aldosterone so increased sodium reabsorption
  2. Decreases ANP and BNP
  3. Increased AVP from brain = increased sodium reabsorption in collecting duct
57
Q

Where does angiotensin II cause increased sodium reabsorption?

A

Distal convoluted tubule

58
Q

What would be the effect on water reabsorption of increased sodium levels reaching the collecting duct and why?

A

Increased Na+ in the collecting duct means there is increased osmolarity and so it is more difficult to reabsorb water since water will migrate via osmosis into the collecting duct since there is a higher osmolarity here

59
Q

How does sodium excretion relate to ECF volume?

A

reducing sodium reabsorption reduces total Na+ levels, ECF volume and therefore blood pressure

60
Q

What are the vascular effects of ACE Inhibitors?

A

Vasodilation -> Increased vascular volume -> Lower blood pressure

61
Q

What are the renal effects of ACEi?

A

decreased sodium reuptake in the proximal PCT-> increased Na+ in distal nephron → decreased water reabsorption → decreased blood pressure

62
Q

What are the adrenal effects of ACEi?

A

Reduced aldosterone resulting in the following indirect renal effects:

  • Lower Na+ reabsorption in the collecting duct
  • Therefore more sodium in the distal nephron, therefore more water retention, so blood volume is higher, blood pressure higher
63
Q

Which part of the nephron do osmotic diuretics and carbonic anhydrase inhibitors work on?

A

PCT

64
Q

Which part of the nephron do Loop Diuretics work on?

A

Thick Ascending Limb

65
Q

Which part of the nephron do Thiazides work on?

A

Distal CT

66
Q

Which part of the nephron do K+ sparring diuretics work on?

A

CCD

67
Q

How do carbonic anhydrase inhibitors work?

A
  • Less bicarbonate produced
  • Therefore less H+, so less H+ Na+ exchange, so less Na+ to exchange with K+ into the blood, therefore less sodium reuptake

Therefore LESS Na+ reabsorption in the PCT and reduced water reabsorption

68
Q

what is an example of a loop diuretic?

A

Furosemide

69
Q

How do loop diuretics work?

A

They are triple transporter inhibitors

Therefore less Na+ Reuptake in the LOH
Increased Na+ in the distal nephron

70
Q

How do thiazides work?

A

Inhibit the Na+ Cl- transporter on the apical side of the distal collecting duct

  • Therefore reduced reuptake of Na+ in the DCT, and reduced water reabsorption
71
Q

Why does calcium reabsorption increase when on thiazides?

A

The basolateral Na+ K+ ATPase is unaffected
Therefore since more sodium is entering into the cell, the gradient is going to increase

Therefore the 3Na+ Ca2+ transporter is going to becomes more active so more Ca2+ pumped back into the blood

72
Q

How do potassium sparing diuretics work?

A

They bind to the MR receptor and cause an inhibition of aldosterone function

73
Q

What is the main intracellular ion?

A

Potassium

74
Q

How does high extracellular potassium effect the membrane?

A

Depolarises the membrane = action potentials leading to heart arrhythmias

75
Q

What condition does low potassium lead to?

A

Heart arrhythmias (Asystole)

76
Q

Describe how dietary potassium is absorbed?

A

Meal = increased potassium absorption = increased plasma K+ = increased tissue uptake

77
Q

What stimulates an increased tissue uptake of potassium?

A

Insulin, aldosterone and adrenaline

78
Q

How does insulin stimulate K+ uptake after dietary intake?

A

Indirectly

Insulin stimulates basolateral sodium proton exchanger

This increases intracellular Na+ so to decrease this, the Na+K+ ATPase is stimulated to increase uptake of K+

79
Q

Where is most of the K+ reabsorbed from in the nephron?

A

PCT

80
Q

What 4 factors stimulate K+ secretion from CCD and DCT?

A

Increased Plasma [K+]

Increased aldosterone

Increased tubular flow rate

Increased plasma pH

81
Q

Which cells in the kidney are involved in potassium secretion?

A

Potassium

82
Q

In K+ depletion, how does the reabsorption of K+ change?

A

Instead of being secreted, in the DCT and CCD, it is reabsorbed from the tubular fluid

This leads to less K+ being excreted

83
Q

How does potassium secretion (back into urine) by principal cells in the DCT and CCD occur, in response to increased plasma [K+]?

A

Activity of basolateral Na+/K+ATPase increases intracellular K+ which is then removed into the tubular fluid by K+ channels on the apical side

Therefore more K+ excreted in the urine to counteract the increased K+ the blood

84
Q

How does potassium secretion occur in the DCT and CCD as a result of increased tubular flow?

A

Increased tubular flow stimulates the primary cilium present on the distal cells in the nephron

This activates PDK1 which increases calcium concentrations in the cell

This stimulates the ‘openness’ of the K+ channels on the apical side of the cell so K+ can leave the cell & enter tubule since there is a higher K+ intracellularly due to the Na+/K+ATPase

85
Q

What are some causes of hypokalemia?

A

Inadequate dietary intake

Diuretics - increased tubular flow rate

Surreptitious vomiting - reduced intake

Diarrhoea - reduced intake

Genetics

Gitelman’s syndrome - Mutation in the Na+/Cl- transporter in the distal nephron

86
Q

What are some causes of hyperkalaemia?

A

Seen in resonse to K+ sparing diuretics - Blocks aldosterone

ACE inhibitors

Seen in elderly

Severe diabetes

Kidney disease

87
Q

Describe how Potassium Sparing Diuretics are potassium Sparing?

A

They are inhibitors of Aldosterone

This means, there is less Sodium reabsorption in the DCT, so the basolateral 3 Na+ 2 K+ Channels are not needing to work as much, therefore less potassium is taken from the blood into the principal cells and therefore the lumen

BRS 12 Urology and renal (11 decks)

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