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BRS Y2 > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

Define osmolarity and give its units

A

Measure of the solute concentration in a solution (osmoles/liter)

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2
Q

What does osmolarity depend on?

A

The number of dissolved particles

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3
Q

As the number of dissolved particles increases what happens to osmolarity?

A

It also increases

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4
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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5
Q

What is the most prevalent solute in the ECF?

A

Sodium

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6
Q

What is the osmolarity of sodium in the ECF?

A

140 mmol/L

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7
Q

When sodium levels are normal what happens to desire to intake sodium?

A

Its supressed

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8
Q

What structure suppresses or stimulates sodium intake?

A

Lateral parabrachial nucleus

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9
Q

What receptors are involved in suppressing sodium intake?

A

Serotonin and glutamate

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10
Q

What receptors are involved in stimulating sodium intake?

A

GABA and opioids

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11
Q

What are the 2 mechanisms involved in sodium intake? Briefly describe them

A

Central mechanism- involves lateral parabrachial nucleus

Peripheral mechanism- involves taste

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12
Q

How does the peripheral mechanism for sodium intake work?

A

When we have low levels of salt in our body foods with salt will taste more appetising

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13
Q

Where does most sodium reabsorption occur?

A

PCT (67%)

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14
Q

What happens to GFR and renal blood flow as MAP increases

A

GFR and renal blood flow will increase proportionally to MAP until a certain point but then they will plateau

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15
Q

As the BP and amount of sodium entering the nephron increases, what happens in the DCT to reduce perfusion pressure and GFR?

A

High sodium levels are detected by specialised macula densa cells in the juxtoglomerular apparatus
There is increased sodium/chloride uptake via triple transporter
Adenosine is released from macula densa cells
Detected by extraglomerular mesangial cells
Adenosine also reduces renin production
Promotes afferent SMC contraction
Reduces perfusion pressure and so GFR

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16
Q

In the DCT what specialised cells detect high sodium levels?

A

Macula densa cells in the juxtoglomerular apparatus

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17
Q

Where is adenosine released from in the DCT?

A

From macula densa cells

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18
Q

What affect does increased sympathetic activity have on the nephron

A

Increased contraction of the afferent arteriole
Stimulates sodium uptake by PCT cells
Stimulates cells of the juxtaglomerular apparatus to produce renin, renin leads to angiotensin II production, this stimulates cells of the PCT to take up sodium
Stimulates adrenal glands to produce aldosterone, aldosterone stimulates sodium uptake in the distal DCT and collecting duct

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19
Q

What hormone does renin increase production of?

A

Angiotensin II

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20
Q

What effect does angiotensin II have on the PCT?

A

Stimulates cells to take up sodium

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21
Q

What hormone stimulates production of aldosterone?

A

Angiotensin II

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22
Q

How does anti naturietic peptide affect sodium levels?

A

Reduces sodium movement into the nephron and reduces reabsorption in the PCT, DCT and CD

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23
Q

How is sympathetic activity affected when blood pressure falls?

A

As blood pressure falls, fluid vol falls, which increases beta 1 sympathetic activity

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24
Q

How does sympathetic activity affect renin production?

A

Increases it

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25
Q

How does blood pressure falling affect ANP?

A

Increases ANP

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26
Q

How is sympathetic activity affected when blood pressure rises?

A

As blood pressure rises, fluid vol rises, which decreases beta 1 sympathetic activity

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27
Q

What type of hormone is aldosterone?

A

Steroid

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28
Q

Where is aldosterone synthesised and released?

A

From the adrenal cortex (zona glomerulosa)

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29
Q

What is aldosterone released in response to?

A

Angiotensin ll

Decrease in blood pressure (via baroreceptors)

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30
Q

How does angiotensin II specifically increase aldosterone synthesis?

A

Promotes synthesis of aldosterone synthase which carries out the final 2 steps in aldosterone synthesis

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31
Q

What does aldosterone stimulate?

A

Sodium reabsorption

Potassium secretion

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32
Q

What does aldosterone excess lead to?

A

Hypokalaemic alkalosis

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33
Q

How does aldosterone work?

A

Binds to mineralocorticoid receptor
Aldosterone then binds to HSP90, which causes HSP90 to be removed
The mineralocorticoid receptor now dimerises so it can translocate into the nucleus
It binds to DNA and stimulates production of mRNAs for genes under its control

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34
Q

What genes does aldosterone help upregulate?

A

The gene for the sodium channel in the collecting duct

The sodium potassium ATPase

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35
Q

What occurs physiologically in hypoaldosteronism?

A

Reabsorption of sodium in the distal nephron is reduced
Increased urinary loss of sodium
ECF volume falls
Increased renin, Ang II and ADH

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36
Q

What are some symptoms of hypoaldosteronism?

A

Dizziness, low BP, salt craving, palpitation

37
Q

What occurs physiologically in hyperaldosteronism?

A

Reabsorption of sodium in the distal nephron is increased
Reduced urinary loss of sodium
ECF volume increases (hypertension)
Reduced renin, ang II and ADH

38
Q

What are some symptoms of hyperaldosteronism?

A

High blood pressure, muscle weakness, polyuria, thirst

39
Q

What is Liddle’s syndrome?

A

Looks like hyperaldosteronism

An inherited disease of high blood pressure.

40
Q

What occurs physiologically in Liddle’s syndrome?

A

Mutation in the aldosterone activated sodium channel.
Channel is always ‘on’
Results in sodium retention, leading to hypertension

41
Q

Where are baroreceptors that detect low BP located?

A

Atria
Right ventricle
Pulmonary vasculature

42
Q

Where are baroreceptors that detect high BP located?

A

Carotid sinus
Aortic arch
Juxtaglomerular apparatus

43
Q

What is the response of the low pressure side baroreceptors to high pressure?

A

Atrial strech

ANP and BNP are released

44
Q

What is the response of the low pressure side baroreceptors to low pressure?

A

Reduced firing
Signals sent via afferent fibres to brainstem
Sympathetic activity increased and ADH released

45
Q

What is the response of the high pressure side baroreceptors to low pressure?

A

Reduced firing
Signals sent via afferent fibres to brainstem
Sympathetic activity increased and ADH released
Reduced firing also detected by JGA cells so renin is released

46
Q

How do ANP and BNP affect water loss?

A

They increase it

47
Q

Where is ANP made?

A

Atria

48
Q

What stimulates ANP release?

A

Atrial strech

49
Q

What are the actions ANP?

A

Vasodilatation of renal (and other systemic) blood vessels
Inhibition of sodium reabsorption in proximal tubule and in the collecting ducts
Inhibits release of renin and aldosterone
Reduces blood pressure

50
Q

What is the mechanism of action of ACE inhibitors?

A

Block the angiotensin converting enzyme which inhibits the conversion of angiotensin I to angiotensin II

51
Q

Do ACE inhibitors cause vasodilation or vasocnstriction?

A

Vasodilation

52
Q

What effect do ACE inhibitors have in the kidney?

A

Reduced Na+ reuptake in the PCT

Increased Na+ in the distal nephron

53
Q

What effect do ACE inhibitors have in the adrenals?

A

Reduced aldosterone (this results in reduced Na+ uptake in the CCT and increased Na+ in the distal nephron)

54
Q

Where in the nephron do osmotic diuretics work?

A

PCT and descending limb of LOH

55
Q

Where in the nephron do carbonic anhydrase inhibitors work?

A

PCT

56
Q

Where in the nephron do loop diuretics work?

A

Thick ascending limb of the LOH

57
Q

Where in the nephron do thiazides work?

A

DCT

58
Q

Where in the nephron do K+ sparing diuretics work?

A

Collecting duct

59
Q

Where in the nephron do aquaretics work?

A

Distal collecting duct

60
Q

How does carbonic anhydrase activity affect Na+ levels?

A

Leads to more Na+ reabsorption

61
Q

How does carbonic anhydrase activity affect urine pH?

A

Make it more acidic

62
Q

How do carbonic anhydrase inhibitors lead to less Na+ reabsoption?

A

Blocking carbonic anhydrase means less h2co3 is produced
Less dissociation into H+ and Hco3-
Less H+ produced, less co transport of H+ out of the cell and less Na+ in

63
Q

How do loop diuretics lead to reduced water reabsorption?

A

They are triple transporter Inhibitors
Reduced Na+ reuptake in the LOH
Increased Na+ in the distal nephron

64
Q

How do thiazide diuretics lead to reduced water reabsorption?

A

They block sodium chloride uptake transporter
Reduced Na+ reuptake in the DCT
Increased Na+ in the distal nephron

65
Q

What other marked effect do thiazide diuretics have?

A

They increase calcium reabsorption

66
Q

How do potassium sparing diuretics lead to reduced water reabsorption?

A

They are inhibitors of aldosterone function (e.g. spironolactone)
They bind to the mineralocorticoid receptor and block its function
This will reduce sodium reuptake in the distal nephron

67
Q

What is the main intracellular ion?

A

K+

68
Q

What does extracellular K+ affect?

A

Excitable membranes of nerve and muscle

69
Q

What does high K+ cause?

A

Membrane depolarisation, can lead to heart arrhythmias

70
Q

What does low K+ cause?

A

Heart arrhythmias (asystole)

71
Q

What are potassium levels in the ECF?

A

Low

72
Q

Why does the body usually have to reduce potassium levels?

A

There is potassium in almost all food so levels are usually high

73
Q

How are potassium levels reduced?

A

Potassium is taken into tissues, this is promoted by insulin (and a bit by aldosterone and adrenaline)

74
Q

What hormone promotes uptake of K+ into tissues?

A

Insulin mainly, aldosterone and adrenaline a bit

75
Q

What is the mechanism of potassium uptake into tissues?

A

Insulin stimulates the sodium proton exchanger
This leads to more sodium in the tissue cells
Sodium conc is reduced via sodium potassium ATPase bringing more potassium into the cell

76
Q

Where is potassium reabsorbed in the nephron?

A

Mainly the DCT and a bit in the TAL of the LOH

77
Q

What happens to potassium in the DCT and CD when levels are normal and when they are depleted?

A

When levels are normal it is secreted into the tubular fluid

When levels are low it is reabsorbed

78
Q

How much potassium is usually excreted in the urine?

A

15-80% of what entered the filtrate

79
Q

What stimulates potassium secretion in the DCT and CD?

A

Increased plasma [K+]
Increased aldosterone
Increased tubular flow rate
Increased plasma pH

80
Q

How is potassium secreted in principal cells?

A

Via Na+/K+ ATPase

81
Q

How does tubular flow affect K+ secretion?

A

As tubular flow increases, cilia are more stimulated
Cilia stimulate PDK1
PDK1 increases calcium conc in the cell via uptake
This opens potassium channels and allows more secretion

82
Q

How common is hypokalaemia?

A

One of the most common electrolyte imbalances (seen in up to 20% of hospitalised patients)

83
Q

What are some causes of hypokalaemia?

A

Inadequate dietary intake (too much processed food)
Diuretics (due to increase tubular flow rates)
Surreptitious vomiting
Diarrhoea
Genetics (Gitelman’s syndrome)

84
Q

What is Gitelman’s syndrome?

A

Mutation in the Na/Cl transporter in the distal nephron

85
Q

How common is hyperkalaemia?

A

Common electrolyte imbalance present in 1-10% of hospitalised patients

86
Q

What response can commonly cause hyperkalaemia?

A

K+ sparing diuretics

87
Q

What can cause hyperkalaemia?

A

ACE inhibitors

88
Q

Who is hyperkalaemia often seen in?

A

Elderly
Severe diabetics
Those with kidney disease

BRS Y2 (85 decks)

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