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Urinary System > 6. Sodium and Potassium Balance > Flashcards

6. Sodium and Potassium Balance Flashcards

1
Q

What changes ECF volume?

A

Concentration of solute

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2
Q

Which is the most prevalent solute?

A

Na+

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3
Q

How does a high Na+ diet result in weight increasing?

A

Water retention

Thus, weight gain

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4
Q

Describe the effects of increased dietary Na+

A

Increased osmolarity (but body can’t let this happen)
So increases ECF volume
Increased blood volume and BP

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5
Q

Describe the effects of decreased dietary Na+

A

Decreased osmolarity (but body can’t let this happen)
So decreases ECF volume
Decreased blood volume and BP

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6
Q

State the relative amounts of sodium reabsorbed in different parts of the nephron.

A

PCT: 65%
Ascending limb of LOH: 25%
DCT: 8%
CD: Up to 2%

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7
Q

Describe what happens Na+ reabsorption if GFR increases

A

The greater the GFR the greater the Na+ reabsorption:
Putting more Na+ in (as put more fluid in)
Thus when absorbing 65% absolute amount of Na+ will be higher

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8
Q

Describe what happens Na+ reabsorption if GFR decreases

A

Putting less Na+ in (as put less fluid in)

Thus when absorbing 65% absolute amount of Na+ will be lower

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9
Q

How can you preserve Na+ when BP is low?

A

Increase in sympathetic activity:
Reduction in GFR
PCT reabsorbs more Na+ (larger %)
Stimulate cells of JGA (renin secreting cells, also stimulated by low tubular Na+ at JGA)
Release of renin leads to production of Angiotensin II (AII)
AII causes vasoconstriction (increases BP, less blood reaches nephron)
AII stimulates Na+ uptake in PCT
AII causes aldosterone to be released
Aldosterone increases Na+ uptake in DCT and CT

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10
Q

How can you decrease Na+ reabsorption when BP is high?

A

Atrial naturietic peptide (ANP) released:
Increases GFR (by changing relative diameter of AA and EA)
Reduces activity of PCT so less Na+ reabsorbed
Suppresses renin release at JGA
Reduces Na+ reabsorption in CT

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11
Q

What hormone is involved in decreasing sodium reabsorption?

A

Atrial Natriuretic Peptide (ANP)

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12
Q

What are the effects of low Na+ in the distal nephron?

A

Na+/Cl- channel in JGA cells senses amount of Na+:
Low Na+ means less Na+ enters JGA cells
Their osmolarity is lower than their environment, so water leaves, JGA cells shrink
JGA cells produce PGE2 and NO, which stimulate granular cells to secrete renin

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13
Q

What triggers the juxtaglomerular apparatus to produce renin?

A

Low tubular Na+ concentration
Sympathetic nervous system
Local hormones e.g. AII

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14
Q

Describe the Renin-Angiotensin / Aldosterone System

A

Liver produces angiotensinogen
Kidney produces renin
Renin converts angiotensinogen to AI
ACE present in lung (large endothelial surface- major source of ACE) converts AI to AII
Leads to vasoconstritction of arterioles
Stimulation of adrenal gland to secrete aldosterone
Aldosterone is released and acts on the kidney

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15
Q

Describe the effects of a high BP on the Renin-Angiotensin / Aldosterone System

A

Increased fluid volume: decrease sympathetic activity and increase ANP, we get:
Reduction in renin, reduction in AI, reduction in AII and reduction in aldosterone, which will feedback to cause reduction of Na+ and water reabsorption, so fluid volume can reduce

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16
Q

Describe the effects of a low BP on the Renin-Angiotensin / Aldosterone System

A 
Increase release of renin
Increases AI
Increases AII
Increases aldosterone
Increases Na+ and water reabsorption
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17
Q

3 primary effects of Angiotensin II

A

PCT: Increase Na+ uptake
Vascular system: Vasoconstriction
Adrenal gland: Production of Aldosterone

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18
Q

What is Aldosterone and what is it released in response to?

A 
Steroid hormone
Released in response to:
Angiotensin ll
Decrease in BP (via baroreceptors) 
Decreased osmolarity of ultrafiltrate
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19
Q

What does Aldosterone stimulate?

A

Increased Na+ reabsorption
Increased K+ secretion
Increased H+ secretion

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20
Q

What does Aldosterone excess lead to?

A

Hypokalaemic alkalosis

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21
Q

How does aldosterone work?

A

Works on principal cells of CD
Binds to receptor in cytoplasm (bound to an inactivating heat shock protein)
When aldosterone binds, heat shock protein released
Aldosterone receptors dimerise
Enters nucleus
Changes transcription of a set of genes

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22
Q

What is the net effect of Aldosterone changing transcription in the nucleus?

A

Increase amount of Na+/K+ ATPase on basolateral side
Increase number of Na+ channels on tubulular side (apical)
Increase expression of regulatory proteins that cause opening of channels
Allows us to pump more Na+ out basolateral side, so more Na+ is reabsorbed from the tubule

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23
Q

What are the consequences of hypoaldosteronism?

A

Reabsorption of Na+ in the distal nephron is reduced
Increased urinary loss of Na+
ECF volume falls
Increased renin, AII and ADH secretion
Low BP, dizziness, palpitations, salt craving

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24
Q

What are the consequences of hyperaldosteronism?

A 
Increased Na+ reabsorption in the distal nephron 
Reduced urinary loss of Na+
ECF volume increases (HYPERTENSION) 
Reduced renin, AII and ADH secretion 
Increased ANP and BNP
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25
Q

What are the symptoms of hyperaldosteronism?

A

High BP
Muscle weakness
Polyuria
Thirst

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26
Q

Why are polyurea and thirst seen in hyperaldosteronism if reabsorbing Na+?

A

Thirst: as higher osmolarity (so want to take in more to reduce osmolarity)
Polyurea: drinking more water, have to get rid of more water

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27
Q

What is Liddle’s Syndrome?

A

Inherited disease of high BP
Mutation in the aldosterone dependent Na+ channel - the channel is permanently switched on
Results in Na+ retention
Leads to hypertension

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28
Q

What is the effect of increased/decreased ECF volume on blood pressure?

A

Increased ECF volume results in increased BP

Decreased ECF volume results in decreased BP

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29
Q

Where are the low pressure baroreceptors?

A

Atria
Right ventricle
Pulmonary vasculature

30
Q

Where are the high pressure baroreceptors?

A

Carotid sinus
Aortic arch
Juxtaglomerular apparatus

31
Q

Describe the difference in responses to baroreceptor activity between the low pressure side and high pressure side

A

LPS: can respond to both high and low pressure
HPS: can only respond to low pressure

32
Q

How does the low pressure side respond to low pressure?

A

Signal through afferent fibres to brainstem

Increases sympathetic activity leads to ADH release

33
Q

How does the low pressure side respond to high pressure?

A

Atrial stretch stimulates release of ANP and BNP

34
Q

How does the high pressure side respond to low pressure?

A

Signal through afferent fibres to brainstem
Increases sympathetic activity leads to ADH release
JGA cells cause renin release

35
Q

Where are ANP and BNP made?

A

In the Atria

36
Q

What are the actions of Atrial Natriuretic Peptide (ANP)?

A

Vasodilatation of renal (and other systemic) blood vessels
Inhibition of Na+ reabsorption in PCT and CD
Inhibits release of renin and aldosterone
Reduces BP (as excreting more water)

37
Q

How does the body respond to increase in ECF volume?

A

Increases GFR
Increases ANP and BNP: Signals to reduce ADH production
Results in increasing water and Na+ excretion
Also signals through reduction in sympathetic activity to reduce renin: decreased AII: decreased Aldosterone
results in increased Na+ and water excretion

38
Q

How does the body respond to decrease in ECF volume?

A

Increases sympathetic activity
Reduction in GFR (don’t want to excrete Na+, as will lead to water excretion)
Increase in ADH: stimulates cells to be permeable to water in CD
Increased production of AII and aldosterone
Na+ and water reabsorption increased
Reduction of excretion of water and Na+
Start to restore ECF volume

39
Q

Describe the effects of ACE inhibitors on sodium reabsorption.

A

Reduce the amount of Na+ reabsorption in the PCT (that would’ve been caused by Angiotensin II)
Reduce the amount of Na+ reabsorption in the DCT and CD (due to indirect inhibition of aldosterone production)
Reduces BP

40
Q

State five types of diuretics and where they act in the nephron.

A 
Osmotic diureticsL (glucose in diabetes and mannitol) 
Carbonic Anhydrase Inhibitors 
Loop Diuretics
Thiazides
Potassium Sparing Diuretics
41
Q

How does glucose act as a diuretic in diabetes?

A

Increases osmolarity of tubular fluid
Glucose can’t be reabsorbed in distal part
Higher osmolarity means theres a smaller osmotic gradient so less water is reabsorbed

42
Q

What is the basis behind diuretics with regards to tubular osmolarity?

A

Increase the tubular osmolarity so there is less of a gradient between the collecting duct and the interstitial compartment so less water is reabsorbed.

43
Q

How do Carbonic anhydrase inhibitors act as diuretics?

A

Carbonic anhydrase is part of exporting H+ at the expense of Na+
If we inhibit Carbonic anhydrase, we inhibit production of H+
If there is less H+ to be exported, less Na+ can come into cell
If less Na+ comes into cell, more Na+ will be excreted
More Na+ reaches distal part of nephron

44
Q

Inhibition of carbonic anhydrase can lead to… of filtered load of Na+ reaching distal part of nephron

A

5-10%

45
Q

What do loop diuretics do? Name a loop diuretic.

A

Block the Na+/K+/Cl- triple transporter
Stop reabsorption of Na+ in ascending LOH (so more in tubular fluid)
e.g. Furosemide

46
Q

Loop diuretics can lead to… of filtered load of Na+ reaching distal part of nephron

A

25%

47
Q

What do thiazide diuretics do?

A

Block Na+/Cl- symporter in DCT

48
Q

Thiazide diuretics can lead to… of filtered load of Na+ reaching distal part of nephron

A

5-10%

49
Q

What do K+ sparing diuretics do?

A

In Distal tubule/ cortical collecting duct
Direct inhibitor of Na+ channel
By reducing amount of Na+ that can come in, we reduce the amount of Na+ that can be pumped out.
By reducing the amount of Na+ that can be pumped out, we reduce the amount of K+ that can enter cells, thus reducing the amount of K+ that can be excreted

50
Q

Name 2 K+ sparing diuretics

A

Amiloride: Na+ channel blocker, prevents entry of Na+ from the tubule lumen
Spironolactone : aldosterone antagonist

51
Q

K+ sparing diuretics can lead to… of filtered load of Na+ reaching distal part of nephron

A

3-5%

52
Q

Why is Spironolactone required to be an effective K+ sparing diuretic?

A 
Aldosterone stimulates:
Increased expression of Na+/K+ ATPase
Increased expression of Na+ channel
Increased expression of K+ channel
So we need to inhibit aldosterone
53
Q

K+ concentrations intracellularly and extracellularly

A

Intracellular: 150 mmol/l
Extracellular: 3-5 mmol/l

54
Q

Describe the effects of extracellular K+ on excitable membranes

A

High K+: depolarises membranes= APs, heart arrhythmias.

Low K+: heart arrhythmias (asystole).

55
Q

Why do you get a smaller natriuresis with K+ sparing diuretics?

A

Because they act on the CD, which is only responsible for 2% of the reabsorption of Na+

56
Q

Why are they called K+ sparing diuretics?

A

They don’t cause increased excretion of K+

57
Q

What stimulates the uptake of K+ into tissues?

A

Insulin
Aldosterone
Adrenaline

58
Q

What channel present in all cells helps regulate high levels of K+?

A

Na+/K+ ATPase

Maintains membrane potential

59
Q

State the relative amounts of K+ reabsorbed in different parts of the nephron.

A

PCT: 70%
DCT: 20%
CD: Variable (1-80%) excreted

60
Q

What stimulates K+ secretion?

A

High plasma K+ concentration
Increase in Aldosterone
Increase in tubular flow rate
Increase in plasma pH

61
Q

Which cells secrete K+?

A

Principal cells of the CD

62
Q

Describe the movement of K+ in and out of principal cells

A

Na+/K+ ATPase pumps K+ into the cell (basolateral side)

K+ leaks out through the transporter into the tubular fluid

63
Q

How is K+ secretion regulated by membrane potential?

A

If outside the cell is more negative, more K+ will exit cell into tubular fluid
If outside the cell is more positive, less K+ will exit into the tubular fluid

64
Q

How does aldosterone affect K+ uptake of principal cells?

A

Stimulates uptake of K+ into principal cells
Increases amount in cell
More K+ leaks out into tubular fluid
Also stimulates activity of K+ channels on tubular side

65
Q

How does tubular flow affect K+ secretion?

A

Principal cells have cilia
As flow increases, movement of the cilium stimulates PDK1 (enzyme), which stimulates an increase in intracellular Ca2+ concentration
This stimulates the activity of the K+ channels

66
Q

What is a problem with non-potassium sparing diuretics?

A

Flow is increased by diuretics
Thus, they cause an increase in K+ secretion
(As increase in tubular flow stimulates the cilia)

67
Q

State 4 causes of hypokalaemia.

A

Diuretics (increased tubular flow)
Diarrhoea (losing K+ in faeces)
Surreptitious Vomiting (Not taking in enough)
Genetics (Gitelmans syndrome)

68
Q

How does Gitelmans syndrome cause hypokalaemia?

A

Mutation in Na+/Cl- transporter in distal nephron
Leads to reduced Na+ reabsorption
Causes increased flow rate and thus increase in K+ excretion

69
Q

State 3 causes of hyperkalaemia.

A

Ageing
Response to Potassium-sparing diuretics
Response to ACE inhibitors

70
Q

Which K+ imbalance is more common?

A

Hypokalaemia

Urinary System (8 decks)

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