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BRS YR2 > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

Define osmolarity

A

The 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

285-295 mosmoles/L

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3
Q

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

A
  • sodium
  • dictates the volume of the ECF
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4
Q

What is the relationship between dietary sodium and bodyweight?

A
  • increased sodium intake will increase the total body sodium over time
  • leads to increased water intake and increased water retention in order to maintain osmolarity
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5
Q

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

A
  • increased water intake and retention leads to increased ECF volume
  • increased blood volume and pressure
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6
Q

What is the peripheral mechanism for controlling sodium intake and how does it work?

A
  • taste
  • salt is one of the major taste sensations
  • appetitive when present at lower concetrations in food
  • aversive at higher concentrations
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7
Q

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

A

Lateral Parabrachial nucleus.

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8
Q

How is sodium intake affected by euvolemia?

A
  • serotonin and glutamate receptor cells suppress the desire for salt
  • sodium intake is inhibited
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9
Q

How is sodium intake affected by sodium deprivation?

A
  • GABA and opiod receptor cells increase the appetite for sodium
  • sodium intake is increased
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10
Q

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

A

5%

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11
Q

What proportion of filtered sodium load is taken up by the Thick ascending limb of the loop of Henle?

A

25%

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12
Q

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

A

67%

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13
Q

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

A

20%

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14
Q

How much sodium which enters the kidney tubule is excreted?

A

< 1%

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15
Q

What is the juxtoglomerular apparatus?

A
  • anatomical unit at the hilus of the glomerulus
  • 3 components: extraglomerular mesangial cells, juxtoglomerular cells and macula densa
  • macula densa is the region where the DCT comes into contact with the glomerulus
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16
Q

What is the function of the juxtoglomerular apparatus?

A

Feedback control of renal blood flow and glomerular filtration rate

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17
Q

What is the effect of increased tubular sodium concentration on the macula densa?

A
  • increased sodium uptake through the Na/K/Cl triple transporter
  • leads to release of adenosine
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18
Q

What is the effect of adenosine release by macula densa cells?

A
  • adenosine detected by extraglomerular mesangial cells
  • detection causes smooth muscle cells on the arteriole wall to contract
  • also reduces renin production by the juxtoglomerular cells
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19
Q

What is the effect of the contraction of smooth muscle cells on the arteriole wall?

A
  • reduced renal blood flow into the glomerulus
  • reduces the GFR
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20
Q

What is the effect of sympathetic activity on sodium excretion?

A
  • contraction of smooth muscle cells on afferent arteriole which decreases GFR
  • stimulates sodium uptake by proximal convoluted tubule
  • stimulates release of renin by the JGA which in turn stimulates angiotensin II production
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21
Q

What else can increase renin release from the JGA?

A

Low tubular sodium

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22
Q

What is the action of renin?

A

Cleaves angiotensinogen into angiotensin I

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23
Q

What is angiotensin I converted to and how?

A

Cleaved by angiotensin converting enzyme to produce angiotensin II

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24
Q

What is the effect of angiotensin II?

A
  • stimulates synthesis of aldosterone synthase in the zona glomerulosa
  • aldosterone synthase increases aldosterone synthesis
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25
Q

What else stimulates aldosterone release?

A

Decreased blood pressure detected by baroreceptors

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26
Q

What are the functions of aldosterone?

A
  • increased sodium reabsorption
  • increased potassium secretion
  • increased H+ secretion
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27
Q

What is the effect of excess aldosterone?

A

Hypokalaemic alkalosis

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28
Q

Where in the tubular system does aldosterone work?

A

Distal end of the DCT and CD

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29
Q

What acts to decrease sodium reabsorption?

A

Atrial natureitic peptide (ANP)

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30
Q

What are the actions of ANP?

A
  • vasodilation of the afferent arteriole to increase GFR
  • decreased sodium reabsorption at the PCT, DCT and CD
  • suppresses renin production by the JGA which reduces angiotensis II and aldosterone
  • reduces blood pressure
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31
Q

How does aldosterone work?

A
  • binds to mineralocorticoid receptor inside cell bound to HSP90
  • HSP90 is removed and to MR receptors bind to form a dimer
  • MR dimer translocates to nucleus and binds to DNA
  • transcribes genes for epithelial sodium channels and Na+/K+ ATPase as well as the regulatory proteins which activate them
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32
Q

What is the effect of hypoaldosteronism?

A
  • reduced reabsorption of sodium in the distal nephron
  • increased sodium excretion
  • ECF volume falls
  • renin, angiotensin II and ADH increase
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33
Q

What are the symptoms of hypoaldosteronism?

A
  • dizziness
  • low blood pressure
  • salt cravings
  • palpitations
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34
Q

What are the effects of hyperaldosteronism?

A
  • increased sodium reabsorption in the distal nephon
  • reduced sodium excretion
  • increased ECF volume
  • reduced renin, angiotensin II and ADH
  • increased ANP and BNP
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35
Q

What are the symptoms of hyperaldosteronism?

A
  • high blood pressure
  • muscle weakness
  • polyuria
  • thirst
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36
Q

What happens to the filtered potassium load at the distal convoluted tubule?

A
  • 3% is reabsorbed when potassium is depleted
  • 10-50% is excreted potassium is normal or increased
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37
Q

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

A

About 67%

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38
Q

What happens to the filtered potassium load at the collecting duct?

A
  • 9% is reabsorbed when potassium is depleted
  • 5-30% is excreted when potassium is normal or increased
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39
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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40
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

41
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

42
Q

How is sodium reabsorbed in the collecting duct?

A

collecting ducts via the Na+ channel ENAC

43
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
44
Q

Where are the baroreceptors that detect low blood pressure?

A
  • atria
  • right ventricle
  • pulmonary vasculature
45
Q

Where are the baroreceptors that detect high blood pressure?

A
  • carotid sinus
  • aortic arch
  • juxtaglomerular apparatus
46
Q

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

A
  • reduced baroreceptor firing
  • afferent signals sent to the brainstem
  • sympathetic activity is increased
  • ADH released
  • high pressure mechanism suppresses renin release from JGA
47
Q

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

A
  • atrial stretch
  • ANP and BNP is released
48
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
49
Q

What happens when there is an expansion in blood volume?

A
  • reduced sympathetic activity
  • decreased renin, angiotensin II and aldosterone
  • afferent arteriolar dilation
  • ANP release
  • increased GFR (increased water and Na+ excretion)
  • reduce Na+ uptake in the PCT, DCT and CT
  • suppressed release of ADH
50
Q

What happens when there is a contraction 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.
51
Q

How do you ensure water movement in a nephron?

A

generate a gradient of interstitial osmolarity through the renal medulla

52
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

53
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

54
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

55
Q

What is the major method used to reduce blood pressure?

A

diuretics by increasing sodium excretion

56
Q

What is the mechanism of ACE inhibitors?

A

reduce the production of angiotensin II from angiotensin I

57
Q

How do ACEi cause vasodilation?

A
  • increases the vascular volume
  • reduces blood pressure
  • diuretic effects (reduced sodium reuptake 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
58
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
59
Q

What is the basis of osmotic diuretics?

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
60
Q

Where do carbonic anhydrase inhibitors act?

A

PCT

61
Q

What is an example of an osmotic diuretic?

A

Mannitol

62
Q

What is the action of carbonic anhydrase inhibitors?

A
  • inhibits sodium uptake in the PCT
  • increases levels of sodium in the distal nephron
  • reduced difference between the tubular and interstitial osmolarity to reduce water reabsorption
63
Q

What is the action of carbonic anhydrase?

A
  • increase Na+ reabsorption
  • increases proton excretion (increases urinary acidity)
64
Q

Where do loop diuretics work?

A

Thick ascending loop of Henle

65
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
66
Q

What is an example of a Loop diuretic?

A

Furosemide

67
Q

Where fo Thiazides act?

A

DCT

68
Q

What is the mechanism of Thiazides?

A
  • target the sodium chloride transporters
  • reduces Na+ uptake in the DCT
  • increases tubular Na+ in the distal nephron
69
Q

What is a side effect of Thiazides?

A

Increased calcium reabsorption

70
Q

What causes the unwanted increased calcium reabsorption in Thiazides?

A
  • Blocks the Na+/Cl- transporter on apical membrane whilst the Na+/K+ ATPase on basolateral membrane still functions
  • intracellular sodium is reduced
  • Na+ into the cell via the Na+/Ca+ antiporter on basolateral membrane is increased
  • this reduces the Ca+ concentration in the cell and therefore increases the potential for calcium to be removed from the tubular fluid.
71
Q

Where do potassium sparing diuretics work?

A

Collecting duct

72
Q

What is the mechanism of potassium sparing diuretics?

A
  • Inhibitors of aldosterone function by binding to mineralocorticoid receptor
  • reduces sodium reabsorption
  • reduced potassium excretion
73
Q

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

A

proportional

74
Q

What is the main intracellular ion?

A

potassium (150mmol/L)

75
Q

What is the extracellular concentration of potassium?

A

3-5mmol/L

76
Q

What maintains the strict intracellular potassium concentration?

A

sodium potassium ATPase

77
Q

What does extracellular potassium have an affect on?

A

excitable membranes (of nerves and muscles)

78
Q

What is the impact of high extracellular potassium?

A
  • membrane depolarisation
  • action potentials
  • heart arrhythmias
79
Q

What is the impact of low extracellular potassium?

A

Heart arrhythmias (asystole)

80
Q

What is the impact of dietary potassium?

A
  • in most foods, especially unprocessed foods
  • plasma potassium will increase after a meal
  • needs to be taken up into tissues
  • uptake of potassium is mainly stimulated by insulin but also aldosterone and adrenaline
81
Q

How does insulin cause potassium uptake?

A
  • indirectly
  • stimulates Na+/H+ exchanger
  • increases intracellular Na+ which needs to be reduced
  • therefore Na+/K+ ATPase activity is increased and more K+ is absorbed into the cells
82
Q

Where in the nephron can potassium be both reabsorbed and excreted?

A

Distal convoluted tubule and collecting duct

83
Q

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

A

Potassium is secreted

84
Q

What stimulates K+ excretion?

A
  • high plasma K+
  • high aldosterone
  • high tubular flow rate
  • high plasma pH
85
Q

What is the impact of high plasma K+?

A
  • increased Na+/K+ ATPase activity in principal cells
  • reduced K+ plasma reabsorption
  • increased K+ excretion
86
Q

How does tubular flow regulate potassium excretion?

A
  • activates primary cilia that activate PDK1
  • increases Ca+ in the cell
  • stimulates the opening of potassium channels on the apical membrane
  • increases K+ excretion
87
Q

What can cause hypokalaemia?

A
  • inadequate dietary intake (too much processed food)
  • increased tubular flow rate (due to diuretics)
  • non-renal excretion (vomiting, diarrhoea)
  • genetics (Gitelman’s syndrome)
88
Q

What is Gitelman’s syndrome?

A
  • mutation in the Na+/Cl- transporter in the distal nephron
89
Q

How common is hypokalaemia?

A

Common electrolyte imbalance present in 20% of hospitalised patients

90
Q

How common is hyperkalaemia?

A

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

91
Q

What can cause hyperkalaemia?

A
  • K+ sparing diuretics
  • ACEi
  • Elderly
  • Severe diabetes
  • kidney disease
92
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
  • looks like hyperaldosteronism but aldosterone levels are normal
93
Q

What part of the nephron is impermeable to Na?

A

the descending LOH

94
Q

What part of the nephron is permeable to Na?

A

the ascending LOH

95
Q

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

A

Collecting Duct

96
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.
97
Q

What is the best way to retain sodium?

A

reduce glomerular filtration

98
Q

When is spironolactone used in hypertension?

A

used in hypertension which is resistant to other diuretic

BRS YR2 (67 decks)

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