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BRS YR2 > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

Define osmolarity

A

Osmolarity is a measure of the solute (particle) concentration in a solution (osmoles/liter)

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2
Q

What is the normal range of plasma osmolarity?

A

275-295 mosmoles/L

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3
Q

Why does a high salt diet lead to an increase in blood pressure?

A
  • Increased salt in the diet leads to increased total body sodium so water is taken in to maintain osmolarity and this increases ECF fluid volume.
  • This increases the pressure in the system i.e. increased blood pressure.
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4
Q

Salt is often added to food to improve the flavour. Why does salt improve the flavour, but too much salt make food taste bad, and how do we sense this?

A
  • Salt is one of the 5 basic taste sensations, it is sensed by a specific sense of cells located on the tongue.
  • At low salt concentrations the sensation is positive but as the concentration increases the sensation becomes aversive.
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5
Q

Which part of the brain is central to alter appetite for salt?

A
  • Lateral Parabrachial nucleus.
  • This region takes information from other areas as well as from neurotransmitters including serotonin and glutamate and in euvolemia the main outcome is inhibition of sodium intake
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6
Q

What proportion of filtered sodium load is taken up by Distal convoluted tubule?

A

5%

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7
Q

What proportion of filtered sodium load is taken up by

Thick ascending limb of the loop of Henle?

A

25%

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8
Q

What proportion of filtered sodium load is taken up by Proximal convoluted tubule?

A

65%

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9
Q

What proportion of renal blood flow is filtered into the nephrons?

A

20%

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10
Q

What is the effect of increased tubular sodium concentration on the juxtaglomerular cells of the macular densa?

A

Increased sodium uptake through the Na/K/Cl triple transporter, leading to release of adenosine and ATP

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11
Q

Which cells respond to the adenosine by reducing renin production?

A

Extraglomerular mesangial cells

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12
Q

Why does the release of adenosine lead to a reduction in GFR in the short term?

A

It causes the afferent SMCs to contract reducing renal plasma flow and therefore GFR.

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13
Q

What is the effect of low tubular sodium at the macular densa on the production of Angiotensin II?

A

It increases it because it stimulates the production of renin leading to angiotensinogen conversion to AI and finally to AII

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14
Q

Where in the tubular system does aldosterone work?

A

DCT (distal end of the DCT) and CT

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15
Q

Where is aldosterone released from?

A

adrenal cortex

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16
Q

What is the effect of AII on aldosterone release?

A

increases aldosterone release

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17
Q

How does aldosterone affect potassium balance?

A

It increases potassium secretion by stimulating sodium uptake: increased Na/K+ ATPase expression will increase the rate of K+ uptake and combined with the increase in Na reabsorption from the lumen (and excretion in to the blood) this will lead to increased K+ excretion

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18
Q

What is the effect of hypoaldosteronism on plasma renin?

A

It causes an increase in plasma renin because of the reduction in sodium reabsorption and the consequent loss of water reducing ECF and therefore BP. This leads to low sodium in the nephron and therefore the release of renin

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19
Q

What are the 6 major locations of baroreceptors?

A
  • Atria
  • Right ventricle
  • Pulmonary vasculature
  • Carotid sinus
  • Aortic arch
  • JGA
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20
Q

What are the effects of ANP on sodium reabsorption in the PCT?

A

Reduced Na reabsorption

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21
Q

What proportion of filtered potassium load is reabsorbed by Distal convoluted tubule?

A

Variable depending on potassium status ranges from 3% reabsorbed to secretion of 50%

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22
Q

What proportion of filtered potassium load is reabsorbed by Proximal convoluted tubule?

A

About 67%

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23
Q

What proportion of filtered potassium load is reabsorbed by Thick ascending limb of the loop of Henle?

A

About 20%

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24
Q

What happens to plasma K+ after a meal?

A

It initially increases then it is taken up into cells by the activity of the Na/K ATPase

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25
Q

What is the relationship between osmolarity and the number of dissolved particles?

A

the greater the number of dissolved particles, the greater the osmolarity

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26
Q

How can the concentration of water be described as?

A
  • the proportion of a solution that is water

- concentration of water is inversely proportional to the number of dissolved solutes

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27
Q

What does decreased salt levels lead to?

A
  • a reduction in water levels

- reduction in volume

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28
Q

What does increased salt levels lead to?

A
  • an increase in water levels

- an increase in volume

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29
Q

What is the most important solute in determining ECF volume?

A

sodium (at 140mmol/L)

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30
Q

What is the impact of increased sodium in the diet?

A
  • increased total body sodium, increasing osmolarity
  • increased water retention
  • increased body weight
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31
Q

How does increased dietary sodium cause hypertension?

A
  • increases total body sodium and therefore osmolarity
  • water retention increases extracellular fluid volume
  • the fixed volume causes an increase in the pressure
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32
Q

Where is sodium reabsorbed in the nephron?

A
  • PCT: 67%
  • Thick ascending limb of the Loop of Henle: 25%
  • DCT: 5%
  • Collecting duct: 3%
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33
Q

How is sodium reabsorbed in the proximal convoluted tubule?

A
  • the use of sodium as a co- or counter transported ion facilitating the reabsorption of other things (glucose, amino acids, bicarbonates)
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34
Q

How is sodium reabsorbed in the Thick ascending limb of the Loop of Henle?

A

Na+/K+/Cl- triple transporter

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35
Q

How is sodium reabsorbed in the distal convoluted tubule?

A

Na+/Cl- transporter

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36
Q

How is sodium reabsorbed in the collecting duct?

A

collecting ducts via the Na+ channel ENAC

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37
Q

What is the impact of GFR on sodium excretion?

A
  • if GFR goes up, total amount of sodium excreted would go up
  • increasing water loss and reduced blood volume
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38
Q

What part of the brain is responsible for regulating sodium intake?

A

Lateral Parabroachial nucleus

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39
Q

What is the normal state (euvolaemia) of the Lateral Parabroachial nucleus?

A

the inhibition of Na+ intake through the activity of neurotransmitters (sodium, glutamate)

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40
Q

What is the action of the Lateral Parabroachial nucleus in a sodium deprived state?

A

increases the appetite for sodium using a seperate set of neurotransmitters (GABA and opioids)

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41
Q

What are the peripheral mechanisms used to regulate sodium intake?

A

based on taste

- taste for salt is bimodal, meaning that at low levels salt enhances taste, but at high levels can be aversive

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42
Q

Where are the baroreceptors that detect low blood pressure?

A
  • atria
  • right ventricle
  • pulmonary vasculature
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43
Q

Where are the baroreceptors that detect high blood pressure?

A
  • carotid sinus
  • aortic arch
  • juxtaglomerular apparatus
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44
Q

What happens when low blood pressure is detected by both the low and high blood pressure mechanisms?

A
  • signals are sent from baroreceptors to the brainstem via afferent fibres
  • this is due to a reduction in the firing of the receptors, which tonically suppress sympathetic activity
  • renal baroreceptors suppress renin release normally, so low blood pressure increases renin release
  • ADH is also released
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45
Q

What happens when high blood pressure is detected by both the low and high blood pressure mechanisms?

A
  • high pressure mechanisms do not react
  • low pressure detects atrial synthesis
  • which promotes the release of ANP and BNP
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46
Q

What is Arial Natriuretic Peptide (ANP)

A
  • small peptides that are made in the atria (also make BNP)

- released in response to atrial stretch

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47
Q

What are the actions of ANP and BNP?

A
  • Vasodilatation of renal (and other systemic) blood vessels
    (produced cGMP and protein kinase G)
  • Inhibition of Sodium reabsorption in proximal tubule and in the collecting ducts
  • Inhibits the release of renin and aldosterone
  • Reduces blood pressure
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48
Q

What happens when there is an unrelated increase in blood volume?

A
  • reduced sympathetic activity
  • afferent arterioar dilation
  • ANP release
  • increased GFR (increased water and Na+ excretion)
  • reduce Na+ uptake in the PCT, DCT and CT
  • suppressed release of ADH
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49
Q

What happens when there is an unrelated decrease in blood volume?

A
  • increased sympathetic activity
  • increased renin/angiotensin/aldosterone production
  • increased AVP expression which increase sodium reuptake, water retention and prevent further loss of volume.
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50
Q

How do you ensure water movement in a nephron?

A

generate a gradient of interstitial osmolarity through the renal medulla

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51
Q

What happens if the osmolarity of the fluid in the tubule is the same as the fluid in the interstitium?

A

no net water movement into the interstitium

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52
Q

What happens if the osmolarity of the fluid in the tubule is the higher than the fluid in the interstitium?

A

reduce water reabsorption

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53
Q

What happens if the osmolarity of the fluid in the tubule is the lower than the fluid in the interstitium?

A

increased water reabsorption

54
Q

What is the major method used to reduce blood pressure?

A

diuretics by increasing sodium excretion

55
Q

What is the mechanism of ACEi?

A

reduce the production of angiotensin II from angiotensin I

56
Q

How do ACEi cause vasodilation?

A
  • increases the vascular volume
  • reducing blood pressure
  • diuretic effects (reduced sodium in the PCT)
  • reduced aldosterone reduces sodium intake in the CCT
  • increased sodium in the distal nephron, reducing the osmotic difference between the tubular fluid and the interstitium to reduce water reabsorption and reduce blood pressure
57
Q

What are the effects of reduced angiotensin II?

A
  • vasodilation
  • reduced Na reuptake in the PCT
  • increased Na+ in the distal nephron
  • reduced aldosterone
  • reduced Na+ uptake in the CCT
58
Q

What is the basis of diuretics that do not directly increase sodium in the distal nephron?

A
  • adding something that can’t be reabsorbed as the water moves from the tubular fluid
  • concentration of the non-reabsorbed substance increases
  • osmolarity increases, reducing water reuptake
59
Q

Where do carbonic anhydrase inhibitors act?

A

PCT

60
Q

What is an example of diuretics that do not directly increase sodium in the distal nephron?

A

Mannitol

61
Q

What is the action of carbonic anhydrase inhibitors?

A
  • inhibits sodium uptake
  • high levels of sodium in the distal nephron
  • reduced difference between the tubular and interstitial osmolarity to reduce water reabsorption
62
Q

What is the action of carbonic anhydrase?

A
  • increased Na+ reabsorption

- increased proton export (increases urinary acidity)

63
Q

What is the mechanism of loop diuretics?

A
  • target the triple transporter in the ascending loop of Henle
  • inhibit sodium reuptake
  • higher levels of sodium in the distal nephron
  • reduced osmolarity of the interstitial fluid
  • reduced difference between the tubular and interstitial osmolarity to reduce water reabsorption
64
Q

What is an example of a Loop diuretic?

A

Furosemide

65
Q

Where fo Thiazides act?

A

DCT

66
Q

What is the mechanism of Thiazides?

A
  • target the sodium chloride transporters
  • reduces Na+ uptake
  • increases tubular Na+ concentration
67
Q

What is a side effect of Thiazides?

A
  • increased calcium reabsorption
68
Q

What causes the unwanted increased calcium reabsorption in Thiazides?

A
  • Blocking the entry of sodium into the cell through the Na+/Ca+ exchanger whilst the Na+/K+ exchanger still functions means that the return of Na+ into the cell via the Na+/Ca+ exchanger is increased.
  • This reduces the Ca+ concentration in the cell and therefore increases the potential for calcium to be removed from the tubular fluid.
69
Q

What is the mechanism of potassium sparing diuretics?

A
  • Inhibitors of aldosterone function
  • reduces sodium reabsorption
  • reduced potassium excretion
70
Q

What are the effects of aldosterone?

A
  • increase sodium reabsorption

- increase potassium excretion

71
Q

What can be caused by excess aldosterone?

A

hypokalaemic alkalosis

72
Q

What affects the GFR?

A

Renal plasma flow rate

73
Q

What is the relationship between GFR and Renal Plasma Flow Rate?

A

proportional

74
Q

What is Renal Plasma Flow Rate proportional to?

A

blood pressure over a significant range of blood pressures (including MAP)

75
Q

Describe the relationship between Renal Plasma Flow Rate and blood pressure?

A
  • proportional

- However, at 100mmHg, RPF does not increase with increasing BP to prevent fluid and sodium loss

76
Q

What causes this relationship between GFR, RPF and blood pressure?

A
  • increased GFR
  • flow rate in the PCT and LOH increases
  • increased amount of Na+ reabsorbed
  • maximum rate is dependent on transporters and flow
77
Q

What is the main intracellular ion?

A

potassium (150mmol/L)

78
Q

What is the intracellular concentration of potassium?

A

150mmol/L

79
Q

What is the extracellular concentration of potassium?

A

3-5mmol/L

80
Q

What maintains the strict intracellular potassium concentration?

A

sodium potassium ATPase

81
Q

What does extracellular potassium have an affect on?

A

excitable membranes (of nerves and muscles)

82
Q

What is the impact of high extracellular potassium?

A
  • membrane depolarisation
  • action potentials
  • heart arrhythmias
83
Q

What is the impact of low extracellular potassium?

A
  • arrhythmias (asystole)
84
Q

What is the impact of dietary potassium?

A
  • in most foods
  • plasma protein needs to be brought down after eating
  • increases plasma insulin
85
Q

What is the impact of insulin on potassium uptake?

A

increases plasma uptake of potassium - indirectly

86
Q

How does insulin indirectly increase the uptake of potassium?

A
  • Insulin stimulates the activity of the sodium proton exchanger, increases intracellular sodium.
  • increased intracellular sodium activates the Na+/K+ ATPase increasing potassium uptake.
87
Q

Which parts of the nephron responsible for potassium absorption are effected by varying factors?

A
  • DT

- CCD

88
Q

What is the impact of potassium depletion on potassium reabsorption?

A

further potassium reabsorption occurs

  • DCT (3%)
  • CCD (9%)
89
Q

What is the impact of normal/high potassium levels on potassium reabsorption?

A
  • potassium is secreted
90
Q

What stimulates K+ secretion?

A
  • high plasma K+
  • high aldosterone
  • high tubular flow rate
  • high plasma pH
91
Q

What is the impact of high plasma K+?

A
  • increased Na+/K+ ATPase activity
  • reduced K+ plasma return
  • increased K+ excretion
92
Q

How does tubular flow regulate potassium excretion?

A
  • activates cilia that activate PDK1
  • increases Ca+ in the cell
  • stimulates the opening of potassium channels on the apical membrane
93
Q

What can cause hypokalaemia?

A
  • inadequate dietary intake
  • increased tubular flow rate (due to diuretics)
  • non-renal excretion (vomiting, diarrhoea)
  • genetics
94
Q

What genetic mutations can cause hypokalaemia?

A

Gitelman’s syndrome

- mutation in the Na+/Cl- transporter in the distal nephron

95
Q

How common is hypokalaemia?

A

Common electrolyte imbalance present in 20% of hospitalised patients

96
Q

How common is hyperkalaemia?

A

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

97
Q

What can cause hyperkalaemia?

A
  • K+ sparing diuretics
  • ACEi
  • Elderly
  • Severe diabetes
  • kidney disease
98
Q

What is Liddle’s syndrome?

A

inherited genetic high blood pressure

  • mutations in the aldosterone activated sodium channel
  • increases ENaC activity causing increased sodium retention and hypertension
99
Q

What is the impact of the mutation that causes Liddle’s syndrome?

A
  • alters re-internalisation and degradation of the channel - - others change the opening time of the channel increasing the likelihood of it being open.
100
Q

How do you differentiate between Liddle’s syndrome and hyperaldosteronism?

A
  • same phenotype

- normal/low aldosterone levels

101
Q

What is the impact of hyperaldosteronism?

A
  • increased sodium reabsorption in the distal nephron
  • ECF volume increases (hypertension)
  • reduced renin, angiotensin II and ADH
  • increase ANP, BNP
102
Q

What are the symptoms seen due to the effects of hyperaldosteronism?

A
  • high blood pressure
  • muscle weakness
  • polyuria
  • thirst
103
Q

What part of the nephron is impermeable to Na?

A

the descending LOH

104
Q

What part of the nephron is permeable to Na?

A

the ascending LOH

105
Q

What part of the nephron is permeable to Na in the presence of aldosterone?

A

Collecting Duct

106
Q

What is the impact of hypoaldosteronism?

A
  • reduced reabsorption of Na+ in the distal nephron
  • reduced water retention
  • reduced ECF volume
  • increased renin, angiotensin II and ADH
107
Q

What are the symptoms seen due to the effects of hypoaldosteronism?

A
  • dizziness
  • low blood pressure
  • salt craving
  • palpitations
108
Q

What is the impact of aldosterone acting on the Cortical Collecting Duct?

A

targets the genes that produce:

  • ENaC
  • Na+/K+ ATPase
  • regulatory proteins
  • increase the number of sodium transporters and increased stimulation
  • increasing sodium reabsorption
109
Q

How does aldosterone impact the number of sodium transporters on the CCD?

A
  • binds to a mineralocorticoid receptor
  • MR loses associated with HSP90 and dimerises
  • translocates to the nucleus to bind to DNA in the promoter region of target genes to stimulate their expression
110
Q

What happens the mineralocorticoid receptor in the absence of aldosterone?

A
  • monomer bound to HSP90

- kept in the cytoplasm

111
Q

What does aldosterone stimulate?

A
  • Increased Sodium reabsorption
    (controls reabsorption of 35g Na/day)
  • Increased Potassium secretion
  • Increased hydrogen ion secretion
112
Q

How does aldosterone increase hydrogen ion secretion?

A
  • The change in voltage promotes an indirect stimulation of proton secretion
  • direct effects of aldosterone on the secretion of protons via alterations in the expression of anion exchanges as H+-ATPases
113
Q

Where is aldosterone synthesised?

A

Synthesised and released from the adrenal cortex (zona glomerulosa)

114
Q

What triggers aldosterone release?

A
  • Angiotensin ll

- Decrease in blood pressure (via baroreceptors)

115
Q

How does angiotensin II trigger aldosterone release?

A

due to an increase in the activity of aldosterone synthetase which is required for the last 2 steps of aldosterone synthesis

116
Q

What happens when blood volume falls or sodium levels are low?

A
  • Increased sympathetic activity leads to a reduced GFR, reduced delivery of sodium and water to the nephron
  • Increased renin production (converts angiotensinogen into angiotensin I which is then converted into angiotensin II in circulation)
  • Angiotensin II promotes NaCl reabsorption and water reabsorption to reduce volume loss and causes vasoconstriction to increase blood pressure.
  • causes the release of aldosterone, causing Na+ reabsorption and water reabsorption.
117
Q

What happens when blood volume rises or sodium levels are high?

A
  • Reduction in sympathetic activity, increasing GFR, increased RPF
  • It causes ANP release, which reduces sodium and water retention and reduces blood pressure by causing relaxation of the renal arteriolar SMCs and some in the periphery, especially those in skeletal muscle.
118
Q

What is the best way to retain sodium?

A
  • reduce glomerular filtration
119
Q

How can you reduce glomerular filtration?

A

Reducing the filtration pressure across the bowmans capsule:

  • constricting the afferent arteriole more than the efferent arteriole
  • relaxing the efferent arteriole more than the afferent arteriole
120
Q

What is the action of Atrial Naturietic Peptide?

A
  • promotes dilation of the afferent arteriole
  • inhibits renin release
  • reduces the uptake of sodium in the PCT, DCT and CT
121
Q

What happens as sodium is concentrated in the distal nephron?

A
  • the amount of sodium and chloride transported by the cells of the macula densa increases (above the threshold)
  • The cells start to release adenosine and ATP and these activate receptors in the extraglomerular mesangial cells
122
Q

What happens when the receptors in the extraglomerular mesangial cells are activated?

A
  • reduced renin production (LT response)
  • directly stimulating the contraction of the smooth muscle cells of the afferent arteriole
  • This reduced the RPF and a reduction in the perfusion pressure.
  • Tubular flow rate responds to ST changes in blood pressure preventing sodium and fluid loss due to increased activity
123
Q

What happens when tubular sodium is high?

A
  • High tubular sodium
  • Increased sodium/chloride uptake via triple transporter
  • Adenosine release from Macula Densa cells
  • Detected by extraglomerular mesangial cells
  • Reduces renin production
  • Promotes afferent SMC contraction
  • Reduces perfusion pressure and so GFR
124
Q

What causes the contraction of smooth muscle in the afferent arteriole?

A

sympathetic stimulation

125
Q

What is the primary mechanism in which the sympathetic stimulation impacts salt excretion?

A
  • reduces GFR
  • increases sodium uptake by the cells in the proximal convoluted tubule
  • increasing the activity of the sodium proton exchanger in a mechanism that may rely on an intra-renal renin-angiotensin system
  • activates the production of renin by the juxtaglomerular cells which results in increase Na+ rebsorption
126
Q

What is the secondary mechanism in which the sympathetic stimulation impacts salt excretion?

A
  • reduction in sodium reaching the distal tubule (measured at the JGA)
  • This reduces the production of adenosine
  • reduces the inhibition of renin production by the juxtaglomerular cells.
  • the sympathetic activity overrides any effect of the extraglomerular cells on the smooth muscle of the afferent arteriole
  • overall contraction of the smooth muscle and reduced GFR.
  • Renin production increases angiotensin II
  • Angiotensin II increases vascular resistance and stimulates sodium uptake by the PCT
  • stimulates aldosterone production of stimulates sodium uptake in the distal convoluted tubule and collecting duct.
127
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 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.
128
Q

What would be the expected effect of spironolactone treatment on the blood pressure of a person with essential hypertension?

A

a reduction in blood pressure by inhibiting the increased sodium excretion leading to reduced water retention.

129
Q

When is spironolactone used in hypertension?

A

used in hypertension which is resistant to other diuretic

130
Q

What would be the expected effect of spironolactone treatment on the blood pressure of a person with normal blood pressure?

A
  • A reduction in blood pressure because of the increased sodium excretion leading to reduced water retention.
  • Even with normal blood pressure, reducing sodium content would cause a reduction in water and therefore a reduction in blood pressure.
131
Q

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

A
  • No effect, as the mutation in Liddle’s syndrome is in the aldosterone sensitive ENaC sodium channel. This means that the channel is always on so that there will be minimal effect on sodium reuptake.
  • aldosterone levels are already low (so inhibiting them will have only a minor effect if any on ENaC expression),
  • the channel is on and will not respond to the regulatory proteins stimulated by aldosterone.
  • any change in the expression of these regulatory proteins (which would be minimal) would have no effect.
132
Q

A drug that inhibits the release of renin impacts which part of the nephron?

A

the Juxta-Glomerular Apparatus

BRS YR2 (70 decks)

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