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Year 2 - BRS > 9.2 - Sodium and potassium balance > Flashcards

9.2 - Sodium and potassium balance Flashcards

1
Q

Define osmolarity.

A

The measure of the solute (particle) concentration in a solution (osmoles/litre)

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2
Q

What is 1 osmole?

A

1 osmole = 1 mole of dissolved particles per litre (1 mole of NaCl = 2 moles of particles in solution = 2 osm/l)

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3
Q

What does osmolarity depend on?

A

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

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4
Q

How does our osmolarity remain constant?

A
  • by water moving around through semi-permeable membranes
  • increased salt = osmolarity increases = increased water moves into that area = increased volume + osmolarity back to normal
  • reduced salt = osmolarity decreases = water moves out = decreased volume + osmolarity back to normal
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5
Q

How does our osmolarity remain constant - put this in terms of ECF mosmoles, concentration and ECF volume?

A
  • mosmoles 2900, conc 290mosm/L, volume 10L
  • mosmoles 3190 (increased by 290), conc 290mosm/L, volume 11L
  • mosmoles 2610 (decreased by 290), conc 290mosm/L, volume 9L
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6
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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7
Q

What is normal plasma osmolarity made up of? (7)

A
  • sodium ~140 mmol/L
  • chloride ~105 mmol/L
  • bicarbonate ~24 mmol/L
  • potassium ~4 mmol/L
  • glucose ~3-8 mmol/L
  • calcium ~2 mmol/L
  • protein ~1 mmol/L
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8
Q

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

A

Sodium

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9
Q

How does dietary sodium affect weight and blood pressure?

A
  • increased dietary sodium –> increased total body sodium –> increased osmolarity (body does not allow) –> increased water intake and retention –> increased ECF volume –> increased blood volume and pressure + increased body weight
  • decreased dietary sodium –> decreased total body sodium –> decreased osmolarity (body does not allow) –> decreased water intake and retention –> decreased ECF volume –> decreased blood volume and pressure + decreased body weight
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10
Q

What part of the brain centrally controls regulation of sodium intake?

A

Lateral parabrachial nucleus (junction of midbrain and pons)

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11
Q

How is sodium intake centrally regulated under normal conditions of euvolemia (normal sodium levels)?

A
  • lateral parabrachial nucleus inhibits Na+ intake - suppresses our desire to intake sodium
  • driven by: serotonin and glutamate (a set of cells in parabrachial nucleus that respond to these)
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12
Q

How is sodium intake centrally regulated under conditions of Na+ deprivation?

A
  • lateral parabrachial nucleus increases appetite for Na+
  • driven by GABA and opioids
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13
Q

What is the peripheral mechanism for regulating sodium intake?

A
  • taste - food with no salt tastes unpleasant
  • salt in low concentrations makes food appetising = we want to eat it
  • as Na+ concentration increases, it becomes more aversive for us so we do not want to eat it
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14
Q

How much (%) sodium is reabsorbed in different parts of the nephron?

A
  • PCT - 67% (therefore 67% of water too)
  • thick ascending LoH - 25%
  • DCT - 5%
  • collecting duct - 3%
  • overall <1% excreted
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15
Q

How does GFR change sodium excretion?

A

Sodium reabsorption values are % not amounts so if we increase GFR, more sodium is excreted

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16
Q

How is GFR linked to renal plasma flow rate and blood pressure?

A
  • RPF proportional to mean arterial pressure
  • approximately 20% of renal plasma enters tubular system
  • GFR = RPF x 0.2
  • therefore GFR is also proportional to MAP
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17
Q

What happens to GFR and RPF at a certain threshold of high blood pressure?

A

RPF and GFR both plateau at high blood pressures e.g. when exercising, as we do not want to excrete more sodium than is needed

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18
Q

Describe the nephron’s system to limit sodium loss through kidney excretion.

A
  • high Na+ in filtrate = higher than normal amounts of Na+ passing through DCT
  • DCT in tight association with glomerulus, and JGA contains macula densa cells which detect high tubular Na+
  • increased Na+/Cl- uptake via triple transporter
  • macula densa cells release adenosine which is detected by extraglomerular mesangial cells which interact with smooth muscle cells in afferent arteriole
  • this reduces blood flow into glomerulus, thus reducing perfusion pressure and GFR (reducing Na+ excretion)
  • adenosine release also leads to reduction in renin production (short-term, does not affect renin production over long period)
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19
Q

What various systems in the nephron can increase Na+ reabsorption/retention? (3)

A
  • sympathetic activity
  • angiotensin II (and aldosterone)
  • low tubular Na+ itself will stimulate production of renin from JGA and therefore AT-II
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20
Q

How can sympathetic activity increase Na+ reabsorption/retention in the nephron? (3)

A
  • contracts SMC of afferent arteriole (which reduces blood flow and therefore Na+ loss)
  • stimulates Na+ uptake by PCT cells
  • stimulates JGA cells to produce renin –> angiotensin II
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21
Q

How can angiotensin II increase Na+ reabsorption/retention in the nephron? (3)

A
  • stimulates PCT cells to take up Na+
  • stimulates adrenal glands to produce aldosterone which stimulates Na+ uptake in distal part of DCT and collecting duct
  • vasoconstriction
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22
Q

Describe the system in the nephron for decreasing Na+ reabsorption.

A

Atrial natriuretic peptide:

  • acts as a vasodilator
  • reduces Na+ uptake in PCT, DCT and collecting duct
  • suppresses production of renin by JGA
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23
Q

How does the body react to low sodium levels?

A
  1. low Na+ = lower BP and fluid volume
  2. this increases beta-1 sympathetic activity which stimulates afferent arteriole SMC to contract and reduce glomerular filtration pressure
  3. stimulates renin production = cleaves angiotensinogen into angiotensin I = cleaved by ACE into angiotensin II
  4. angiotensin II stimulates zona glomerulosa of adrenal gland to release aldosterone which increases Na+ reabsorption
  5. angiotensin II also promotes vasoconstriction and Na+ reabsorption
  6. this causes increased Na+ reabsorption and reduces water output
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24
Q

How does the body react to high sodium levels?

A
  1. high Na+ = higher BP and fluid volume
  2. this reduces beta-1 sympathetic activity and causes production of ANP
  3. reduced renin production = reduced angiotensin II
  4. reduced aldosterone which reduces Na+ reabsorption
  5. vasodilation and decreased Na+ reabsorption and increased water output
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25
Q

What is aldosterone and when is it released?

A
  • steroid hormone synthesised and released from adrenal cortex (zona glomerulosa)
  • released in response to angiotensin II
  • also released in response to decrease in blood pressure (via baroreceptors)
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26
Q

How is aldosterone released in response to angiotensin II?

A

Angiotensin II promotes synthesis of aldosterone synthase, which causes the last two enzymatic steps in production of aldosterone from cholesterol

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27
Q

What does aldosterone do in the kidney? (3)

A
  • increased sodium reabsorption (35g per day)
  • increased K+ secretion
  • increased H+ secretion
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28
Q

What can excess aldosterone lead to?

A

Hypokalaemic alkalosis

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29
Q

How does aldosterone work at a cellular level in collecting duct cells?

A
  1. lipid-soluble steroid hormone so passes through cell membrane
  2. binds to a mineralocorticoid receptor sitting in cytoplasm bound to protein called HSP90
  3. once aldosterone is bound, HSP90 is removed and the mineralocorticoid receptor dimerises
  4. translocates into nucleus and binds to DNA and stimulates production of mRNA for genes for epithelial Na+ channel (ENaC) and Na+K+ATPase, which go to their respective membranes
  5. also increases transcription of regulatory proteins that stimulate activity of those two transporters, so both more sodium channels and more active sodium channels
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30
Q

What happens in hypoaldosteronism?

A

Reabsorption of sodium in distal nephron is reduced –> increased urinary loss of sodium –> ECF falls because water moves out with sodium

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31
Q

What does the body do to try and compensate for hypoaldosteronism?

A

Increases renin, angiotensin II and ADH (and other sodium-reabsorbing mechanisms) to try and increase reabsorption

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32
Q

What are the symptoms of hypoaldosteronism? (4)

A
  • low blood pressure
  • dizziness (due to low BP)
  • salt craving
  • palpitations (due to change in membrane potential)
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33
Q

What happens in hyperaldosteronism?

A
  • increased reabsorption of sodium in distal nephron –> reduced urinary loss of sodium –> increased total body sodium –> ECF volume increases as lots of water is absorbed (hypertension)
  • this reduces renin, angiotensin II and ADH production, and increases ANP and BNP
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34
Q

What are the symptoms of hyperaldosteronism? (4)

A
  • high blood pressure
  • muscle weakness
  • polyuria (try to get rid of excess water)
  • thirst (since our body thinks there is insufficient water in system)
35
Q

What is Liddle’s syndrome?

A

An inherited disease of high blood pressure

36
Q

What causes Liddle’s syndrome?

A
  • mutation in the aldosterone activated sodium channel means the channel is always on (increased ENaC activity)
  • this leads to increased sodium reabsorption and therefore hypertension
37
Q

What does Liddle’s syndrome look like?

A

Like hyperaldosteronism but with normal/low aldosterone

38
Q

Where do we have low pressure baroreceptors? (3)

A
  • atria (heart)
  • right ventricle (heart)
  • pulmonary vasculature (vascular system)
39
Q

What is the response to low pressure from the low pressure baroreceptors?

A

Low pressure –> reduced baroreceptor firing –> signal through afferent fibres to brainstem –> sympathetic activity and ADH release for water retention

40
Q

What is the response to high pressure from the low pressure baroreceptors?

A

High pressure –> atrial stretch –> ANP and BNP released for greater water loss

41
Q

What is ANP?

A

Atrial natriuretic peptide = small peptide made in the atria (also makes BNP)

42
Q

Describe the mechanism of ANP after release?

A
  1. released in response to atrial stretch
  2. binds to guanylyl cyclase (receptor)
  3. this converts GTP to cyclic GMP (cGMP)
  4. this activates protein kinase G
  5. leads to cellular responses
43
Q

What are the actions of ANP? (4)

A
  • vasodilation of renal (and other systemic) blood vessels
  • inhibition of sodium reabsorption in proximal tubule and collecting ducts
  • inhibits release of renin and aldosterone
  • reduces blood pressure
44
Q

What high pressure baroreceptors do we have? (3)

A
  • carotid sinus (vascular system)
  • aortic arch (vascular system)
  • juxtaglomerular apparatus (vascular system)
45
Q

How do high pressure baroreceptors respond to low pressure?

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

46
Q

How does the body react in response to volume expansion? (4)

A
  • reduction in sympathetic activity leading to reduced Na+ reuptake in PCT
  • reduction in renin production so less angiotensin II and aldosterone production –> more Na+ excretion as less reabsorption
  • more ANP and BNP - affects GFR and promotes Na+ excretion
  • reduction in AVP in brain
47
Q

How does the body react in response to volume contraction?

A
  • increase in sympathetic activity leading to increased Na+ reuptake in PCT
  • increase in renin production so more angiotensin II and aldosterone production –> more Na+ (and therefore water) reabsorption in collecting duct
  • less ANP and BNP
  • more AVP production in brain - promote water reabsorption by inserting aquaporins in collecting duct cells
48
Q

What is the effect of increased sodium levels in the tubular fluid on water secretion in nephron?

A
  • water reabsorbed in nephron because medulla has gradient of osmolarity throughout, which we match with the osmolarity in tubular fluid
  • increased Na+ in tubular fluid reduces gradient from tubular fluid to medulla, so less water moves into medulla = less water reabsorbed
  • more solute arriving in later part of nephron, less water we reabsorb
49
Q

What is the effect of reducing Na+ reabsorption (Na+ excretion) on Na+ levels, ECF volume and BP?

A
  • reducing Na+ reabsorption reduces total Na+ levels, ECF volume and blood pressure
  • this is because Na+ levels determine ECF volume, and reducing ECF volume reduces BP
50
Q

What do ACE inhibitors primarily do?

A

Reduce angiotensin II production

51
Q

What are the vascular effects of ACE inhibitors?

A
  • vasodilation (less angiotensin II which contracts blood vessels)
  • this increases vascular volume, which decreases blood pressure
52
Q

What direct renal effects do ACE inhibitors have? (3)

A
  • reduced Na+ reuptake in PCT
  • increased Na+ in distal nephron (reduces gradients from tubular fluid into interstitium, reducing water reabsorption)
  • less water reabsorption = lower blood pressure
53
Q

What adrenal effects does reduced angiotensin II from ACE inhibitors have?

A
  • reduced aldosterone
  • leads to reduced Na+ reuptake in cortical collecting duct
  • also increases Na+ in distal nephron (region of nephron with the highest osmolarity) - reduces water reabsorption due to reduction in osmotic gradient across tubular wall
  • reduced water reabsorption = lower blood pressure
54
Q

What type of drug are ACE inhibitors?

A

Diuretics - reduce water reabsorption

55
Q

What are some types of diuretics other than ACE inhibitors? (5)

A
  • osmotic diuretics (PCT)
  • carbonic anhydrase inhibitors (PCT)
  • loop diuretics (thick asc LoH)
  • thiazide diuretics (DCT)
  • K+ sparing diuretics (CD)
56
Q

What do osmotic diuretics do?

A
  • put something un-reabsorbable into PCT
  • since it cannot be reabsorbed, it stays in PCT and increases osmolarity
  • this means less water will be reabsorbed from PCT (usually where most water is reabsorbed so will see greatest effect here)
57
Q

Where do carbonic anhydrase inhibitors work?

A

Carbonic anhydrase enzymes are most active in PCT where these inhibitors work

58
Q

How do carbonic anhydrase inhibitors work?

A
  1. block carbonic anhydrase, so cannot convert HCO3- into H2CO3 then H2O + CO2
  2. CO2 cannot go into cell and react with H2O to make H2CO3 using another carbonic anhydrase
  3. no H2CO3 is split into H+ + HCO3- = H+ cannot be used to move Na+ into cell using Na+/H+ exchanger so net sodium uptake decreases and reduction in urinary acidity
59
Q

What are the effects of carbonic anhydrase inhibitors? (3)

A
  • reduced Na+ reuptake in PCT
  • increased Na+ in distal nephron
  • reduced water reabsorption
60
Q

Where do loop diuretics work?

A

Thick ascending loop of Henle

61
Q

What is an example of a loop diuretic?

A

Furosemide

62
Q

What do loop diuretics do?

A
  • block Na+/2Cl-/K+ triple transporter
  • reduces Na+ reuptake in LoH
  • increased Na+ in distal nephron
  • decreases osmotic gradient across tubular wall into interstitium so reduced water reabsorption
63
Q

Where do thiazide diuretics work?

A

DCT

64
Q

What do thiazide diuretics do?

A
  • block NaCl transporter in DCT
  • reduced Na+ reuptake in DCT, increasing Na+ in DCT
  • leads to increased Na+ in distal nephron
  • reduced water reabsorption due to reduced osmotic gradient across tubular wall
65
Q

What other effects do thiazide diuretics have?

A
  • increase Ca2+ reabsorption - because Na+K+ATPase is not affected so pumps Na+ into blood from cell
  • but NaCl transporter in DCT is blocked so Na+ cannot move into cell from tubular fluid
  • therefore decrease in Na+ in cell, so Na+ moves from blood into cell via Na+/Ca2+ antiporter, so Ca2+ builds up in blood

Increased Ca2+ reabsorption = symptoms of hypercalcaemia!!!

66
Q

Where do K+ sparing diuretics work?

A

Collecting duct

67
Q

What is an example of a K+ sparing diuretic?

A

Spironolactone

68
Q

What do K+ sparing diuretics do?

A
  • inhibitors of aldosterone function e.g. spironolactone
  • bind MR and block its function
  • aldosterone usually increases production of Na+ channel and Na+/K+ATPase to increase Na+ reuptake and K+ secretion and H+ excretion, so an excess of aldosterone can lead to hypokalaemic alkalosis
  • if this is blocked, activity of this uptake system reduces, so Na+ reuptake in distal nephron reduces, reducing water reabsorption
69
Q

How are K+ sparing diuretics K+ sparing?

A

Since Na+K+ATPase pumps K+ out of blood into cell and then K+ moves into lumen, if we block it then K+ remains in blood (spared)

K+ sparing diuretics block aldosterone, which is involved in K+ excretion (so blocking = reduced excretion)

70
Q

How important is K+ extracellularly vs intracellularly?

A
  • main intracellular ion (150 mmol/L)
  • extracellular K+ much lower at 3-5 mmol/L
71
Q

What are the effects of extracellular K+?

A
  • has effects on excitable membranes (of nerve and muscle)
  • high K+ depolarises membranes –> action potentials and heart arrhythmias
  • low K+ makes depolarisation more difficult –> arrhythmias and asystole (flatline with no ventricular depolarisation)
72
Q

What happens to potassium when we eat a meal?

A
  • potassium is present in most/all foods
  • eating a meal leads to K+ absorption - especially unprocessed foods with a lot of K+
  • this increases plasma K+ concentration
  • this needs to be reduced which happens via tissue uptake
73
Q

What stimulates tissue uptake of potassium? (3)

A
  • insulin
  • aldosterone
  • adrenaline
74
Q

How does insulin stimulate tissue uptake of potassium?

A
  • indirect - stimulates Na+/H+ exchanger which increases Na+ coming into tissue cells
  • this increases intracellular Na+ which needs to be reduced
  • achieved via Na+K+ATPase which moves Na+ back into blood and K+ into cell
75
Q

Under normal conditions, how is K+ excreted and reabsorbed through the nephron?

A
  • 67% of K+ is reabsorbed in PCT
  • 20% is reabsorbed in thick ascending limb of LoH through Na+2Cl-K+ triple transporter
  • 10-50% of K+ is secreted in DCT and up to 30% secreted in collecting duct
  • leads to 15-80% of K+ from glomerular filtrate being excreted
76
Q

What stimulates K+ secretion? (4)

A
  • high plasma K+
  • increased aldosterone
  • increased tubular flow rate
  • increased plasma pH
77
Q

How does high plasma K+ cause K+ secretion by principal cells?

A
  • increased activity of Na+/K+ exchanger means more K+ moves into cell
  • more K+ in the cell means more K+ leaves cell in tubular fluid
  • also an effect on membrane potential which helps stimulate K+ secretion
78
Q

How does increased tubular flow rate cause K+ secretion?

A
  • distal cells have primary cilia
  • increased tubular flow = cilia stimulate PDK1 which increases Ca2+ in cell
  • this stimulates openness of K+ channels, allowing K+ to move out of cell into tubular fluid after being pumped into cell from blood via Na+K+ATPase
79
Q

How much K+ is excreted when there is low K+ (instead of normal K+)?

A
  • instead of secretion and DCT and collecting duct, K+ is reabsorbed as well similar to earlier parts of the nephron
  • 3% reabsorbed in DCT and 9% reabsorbed in collecting duct
80
Q

How common is hypokalaemia?

A

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

81
Q

What causes hypokalaemia? (4)

A
  • inadequate dietary intake (too much processed food)
  • diuretics (increased tubular flow rates –> K+ secretion via PDK1 mechanism)
  • surreptitious vomiting (reduced K+ intake)
  • diarrhoea (reduced K+ intake)
82
Q

What genetic conditions can lead to hypokalaemia?

A

Gitelman’s syndrome (mutation in NaCl transporter in distal nephron) leads to increased K+ loss

83
Q

How common is hyperkalaemia?

A

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

84
Q

What causes hyperkalaemia? (5)

A
  • K+ sparing diuretics
  • ACE inhibitors
  • elderly
  • severe diabetes
  • kidney disease

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