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uro + renal med > 1B sodium and potassium balance > Flashcards

1B sodium and potassium balance Flashcards

1
Q

Define osmolarity

A

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

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

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2
Q

What is osmolarity dictated by?

A

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

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3
Q

How does our osmolarity remain constant?

A
  • By water moving around through semi-permeable cell membranes
  • If there’s increased salt in an area, osmolarity of that area goes up so there will be increased water moving into that area to increase the volume to bring osmolarity back down to normal
  • If there’s decreased salt in an area, osmolarity of that area goes down so there will be water moving out of that area to decrease the volume to bring osmolarity back up to normal
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4
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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5
Q

What is plasma made up of?

A

A sum of all the particles:

  • Na+ 140 mmol/L
  • Cl- 105 mmol/L
  • HCO3- 24 mmol/L
  • K+ 4 mmol/L
  • Glucose 3-8 mmol/L
  • Ca2+ 2 mmol/L
  • Protein 1 mmol/L

Sodium is the most prevalent and important solute in the ECF

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6
Q

What happens if we increase dietary sodium?

A

Increased total body sodium → increased osmolarity (but our body won’t allow this to happen) → increased water intake and retention → increased ECF volume → increased blood volume and pressure and increased body weight

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7
Q

What happens if we decrease dietary sodium?

A

Decreased total body sodium → decreased osmolarity (but our body won’t allow this to happen) → decreased water intake and retention → decreased ECF volume → decreased blood volume and pressure and decreased body weight

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8
Q

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

A

Lateral parabrachial nucleus at the junction of the midbrain and pons

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9
Q

What does the lateral parabrachial nucleus do under normal conditions of euvolemia (normal sodium levels)?

A
  • We are suppressing our desire to intake sodium
  • A set of cells in parabrachial nucleus that respond to serotonin glutamate suppress basal Na+ intake
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10
Q

What do the lateral parabrachial neurones do under conditions of Na+ deprivation?

A
  • There is an increased appetite for Na+
  • This is driven by GABA and opioids
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11
Q

What is the peripheral mechanism for regulating sodium intake?

A
  • Taste- if you have food with no salt it tastes unpleasant
  • When salt is present in low concs in food it makes it appetising so we want to eat it
  • As Na+ conc increases, it becomes more aversive for us so we don’t want to eat it
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12
Q

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

A
  • 67% in PCT (which causes the 67% of water to be absorbed too)
  • 25% in thick ascending limb of loop of Henle
  • 5% in DCT
  • 3% in collecting duct
  • <1% is excreted
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13
Q

Since sodium reabsorption is in % not amounts, what does it mean if we change GFR?

A

This will change sodium excretion- higher GFR means more sodium excreted

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14
Q

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

A
  • RPF rate is proportional to mean arterial pressure
  • Approx 20% of renal plasma enters tubular system so GFR = RPF * 0.2 therefore GFR is also proportional to mean arterial pressure
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15
Q

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

A

RPF and GFR both plateau because at high blood pressures, e.g. when exercising, we don’t want to excrete more sodium than is needed

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16
Q

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

A
  • If there’s high sodium in filtrate, there will be higher than normal amounts of Na+ passing through DCT
  • DCT is in tight association with glomerulus and JGA contains macula densa cells which detect high tubular sodium
  • There is increased Na+ and Cl- uptake in response to this 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 flow of blood into glomerulus, thus reducing perfusion pressure and thus GFR
  • This adenosine release also leads to reduction in renin production (however this is for a short period of time so doesn’t affect overall renin production over long time period)
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17
Q

Describe sympathetic activity in the nephron to increase Na+ reabsorption/retention

A
  • contracts SMC of afferent arteriole
  • stimulates Na+ uptake of PCT cells
  • stimulates JGA cells to produce renin which leads to Ang II production
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18
Q

Describe Ang II system to increase Na+ reabsorption/retention

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

Low tubular Na+ itself will stimulate production of renin from JGA and therefore Ang II

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19
Q

Describe the system in the nephron for decreasing Na+ reabsorption

A

Atrial natriuretic peptide:

  • Acts as vasodilator
  • Reduces Na+ uptake in PCT, DCT and collecting duct
  • Suppresses production of renin by JGA
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20
Q

How does the body react when we have low sodium levels?

A

1) Low sodium means lower blood pressure and low fluid volume

  • This increases beta1-sympathetic activity which stimulates afferent arteriole SMC to contract and reduce glomerular filtration pressure

2) Stimulates renin production which cleaves angiotensinogen into Ang I which is cleaved by ACE into Ang II

  • Ang II stimulates zona glomerulosa of adrenal gland to release aldosterone which increases Na+ reabsorption
  • Ang II also promotes vasoconstriction

This all reabsorbs more Na+ and reduces water output

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21
Q

How does the body react when we have high sodium levels?

A

High sodium means higher fluid volume meaning higher blood pressure which

1) suppresses beta1-sympathetic activity and
2) Causes production of ANP

  • This reduces renin which reduces Ang I which reduces Ang II which reduces aldosterone
  • This promotes vasodilation and decreases Na+ and water reabsorption
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22
Q

What is aldosterone and when is it released?

A

A steroid hormone synthesised and released from adrenal cortex (zona glomerulosa)

  • Released in response to Ang II
  • Also released when there’s a decrease in blood pressure via baroreceptors
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23
Q

How is aldosterone released in response to Ang II?

A

Ang II promotes synthesis of aldosterone synthase which causes last 2 enzymatic steps in production of aldosterone from cholesterol

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24
Q

What does aldosterone do in the kidney?

A
  • Stimulates Na+ reabsorption (35g per day)
  • Increased K+ secretion
  • Increased H+ secretion
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25
Q

What can happen if there’s an aldosterone excess?

A

Hypokalaemic alkalosis

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26
Q

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

A

1) It’s a steroid hormone which are lipid soluble so passes through cell membrane

2) It binds to a mineralocorticoid receptor sitting in cytoplasm bound to a protein called HSP90

3) Once aldosterone is bound, HSP90 gets removed and the mineralocorticoid receptor dimerises

4) It now translocates into nucleus where it binds to DNA and stimulates production of mRNA for genes for epithelial Na+ channel and Na+ K+ ATPase which go to their respective membranes

5) It also increases transcription of regulatory proteins that stimulate activity of those 2 transporters- so you get both more sodium channels and more active sodium channels

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27
Q

What happens in hypoaldosteronism?

A

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

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28
Q

What does the body do to try and compensate hypoaldosteronism?

A

Increases renin, Ang II and ADH (other sodium absorbing mechanisms) to try to increase reabsorption

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29
Q

What symptoms does hypoaldosteronism cause?

A
  • Low blood pressure
  • Dizziness- caused by low bp
  • Salt craving
  • Palpitations- due to change in membrane potential
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30
Q

What happens in hyperaldosteronism?

A
  • Increased reabsorption of sodium in distal nephron is increased → reduced urinary loss of sodium → increase in total body sodium → ECF volume increases as we’re absorbing lots of water (hypertension)
  • This reduces renin, Ang II and ADH production and increases ANP and BNP
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31
Q

What symptoms does hyperaldosteronism cause?

A
  • High bp
  • Muscle weakness
  • Polyuria- since we have more water we try to get rid of more
  • Thirst- since our body thinks there’s insufficient water in system
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32
Q

What is Liddle’s syndrome?

A

An inherited disease of high blood pressure

33
Q

What causes Liddle’s syndrome?

A
  • A mutation in the aldosterone activated sodium channel so it’s always on
  • This leads to increased sodium reabsorption and therefore hypertension
34
Q

What other disease does Liddle’s syndrome look like?

A

Like hyperaldosteronism but with normal or low aldosterone levels

35
Q

Where do we have low pressure baroreceptors?

A
  • Atria- heart
  • Right ventricle- heart
  • Pulmonary vasculature- vascular system
36
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

37
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

38
Q

What is ANP?

A

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

39
Q

Describe the mechanism of ANP working after it’s released

A

1) released in response to atrial stretch

2) binds to a receptor which is guanylyl cyclase

3) this converts GTP to cyclic GMP (cGMP)

4) this activates protein kinase G

5) this leads to cellular responses

40
Q

What are these cellular responses (actions of ANP)?

A
  • Vasodilation of renal (and other systemic) blood vessels
  • Inhibition of Na+ reabsorption in proximal tubule and in collecting duct
  • Inhibits release of renin and aldosterone
  • Reduces blood pressure
41
Q

What high pressure baroreceptors do we have?

A
  • Carotid sinus- vascular system
  • Aortic arch- vascular system
  • JGA- vascular system
42
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 released

reduced baroreceptor firing also → JGA cells → renin released

43
Q

How does the body react in response to volume expansion?

A
  • Reduction in sympathetic activity leading to reduced Na+ reuptake in PCT
  • Reduction in renin production so less Ang II and aldosterone production leading to more Na+ excretion because we’re reabsorbing less
  • More ANP and BNP which affects GFR and Na+ reabsorption to promote Na+ excretion
44
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 Ang II and aldosterone production stimulating Na+ and therefore water reabsorption in collecting duct
  • Less ANP and BNP
  • More AVP production in brain to promote water reabsorption by inserting aquaporins in collecting duct cells
45
Q

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

A
  • Water is reabsorbed in nephron because medulla has gradient of osmolarity throughout it which we match with the osmolarity in the tubular fluid
  • If there’s increased Na+ in tubular fluid, there’s a reduced gradient from tubular fluid to medulla because tubular fluid osmolarity is higher now so water won’t move into medulla so won’t be reabsorbed
  • So the more solute arriving in later part of nephron, the less water we can absorb
46
Q

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

A
  • Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP
  • This is because Na+ levels determine ECF volume and reducing ECF volume reduces BP
47
Q

What do ACE inhibitors primarily do?

A

Reduced Ang II production

  • What vascular effects does this have?
    • Vasodilation since less Ang II which contracts blood vessels
    • This increases vascular volume which decreases blood pressure
48
Q

What direct renal effects do ACEi have?

A
  • Reduced Na+ reuptake in PCT
  • Increased Na+ in the distal nephron which reduces gradients from tubular fluid into interstitium meaning reduction in water reabsorption
  • Less water reabsorption means lower blood pressure
49
Q

What adrenal effects does reduced Ang II production have?

A
  • Reduced aldosterone
  • This leads to reduced Na+ uptake in cortical collecting duct
  • This also increases Na+ in distal nephron (the region of nephron with the highest osmolarity) which reduces water reabsorption because of reduction in osmotic gradient across tubular wall
  • Less water reabsorption means lower blood pressure
50
Q

What diuretics other than ACEi are there?

A
  • Osmotic diuretics (PT)
  • Carbonic anhydrase inhibitors (PT)
  • Loop diuretics (TAL)
  • Thiazide diuretics (DT)
  • K+ sparing diuretics (CD)
51
Q

What do osmotic diuretics do?

A
  • Put something un-reabsorbable into PCT
  • Since it can’t be reabsorbed it stays in PCT and increases osmolarity there
  • This means less water will get reabsorbed from PCT (which is usually where most water is reabsorbed so we will see the greatest effect here)
52
Q

Where do carbonic anhydrase inhibitors work?

A

These enzymes are most active in PCT which is where these inhibitors work

53
Q

What do carbonic anhydrase inhibitors do?

A

1) Block carbonic anhydrase which can’t convert bicarbonate into H2CO3 then H2O and CO2

2) so CO2 can’t go into cell to then be added to H2O to make H2CO3 using another carbonic anhydrase (which wouldn’t work either)

3) so no H2CO3 is split into H+ and HCO3- so H+ can’t be used to move Na+ into cell using Na+/H+ exchanger so net sodium uptake goes down and reduction in urinary acidity

so overall carbonic anhydrase inhibitors reduce Na+ reuptake in PCT, increase Na+ in distal nephron and reduce water reabsorption

54
Q

Where do loop diuretics work?

A

Thick ascending limb of loop of Henle

55
Q

Give an example of a loop diuretic

A

Furosemide

56
Q

What do loop diuretics do?

A
  • Block the Na+/2Cl-/K+ triple transporter
  • This reduces Na+ reuptake in LOH
  • Increased Na+ in distal nephron
  • This decreases osmotic gradient across tubular wall into interstitium so reduced water reabsorption
57
Q

Where do thiazide diuretics work?

A

DCT

58
Q

What do thiazide diuretics do?

A
  • Block NaCl transporter in DCT
  • This increases Na+ in DCT
  • Leads to increased Na+ in distal nephron
  • So there’s reduced water reabsorption due to reduced osmotic gradient across tubular wall
59
Q

What affect other than diuretic do thiazide diuretics have?

A
  • They also increase Ca2+ reabsorption because the Na+/K+ ATPase isn’t affected so pumps Na+ into blood from cell
  • But the NaCl transporter into the DCT is blocked so Na+ can’t move into cell from tubular fluid
  • There’s a decrease of Na+ therefore in the cell so Na+ moves from blood into cell via Na+/Ca2+ antiporter so Ca2+ builds up in blood
60
Q

Where do K+ sparing diuretics work?

A

Collecting duct

61
Q

What do K+ sparing diuretics do?

A
  • Inhibitors of aldosterone function e.g. spironolactone
  • They bind to mineralocorticoid receptor and block its function
  • Aldosterone usually increases production of Na+ channel and Na+/K+ ATPase to increase Na+ reuptake and also increases K+ secretion and H+ excretion so an excess of aldosterone can lead to hypokalaemic alkalosis
  • So if this is blocked, activity of this uptake system reduces so Na+ reuptake in distal nephron reduces
62
Q

How are K+ sparing diuretics K+ sparing?

A

Since the Na+/K+ ATPase pumps K+ out of blood into cell then K+ moves into lumen, if we block it then K+ will remain in blood (be spared)

63
Q

How important is K+ extracellularly vs intracellularly?

A
  • It’s the main intracellular ion (150 mmol/L)
  • Extracellular K+ is much lower at 3-5 mmol/L
64
Q

What main effect does extracellular K+ have?

A

On excitable membranes of nerve and muscle

65
Q

What does high K+ do?

A

Depolarises membranes to form action potentials and heart arrythmias

66
Q

What does low K+ do?

A

Makes depolarisation more difficult- also leading to heart arrhythmias and asystole (flatline with no ventricular depolarisation)

67
Q

What happens K+ wise when we eat a meal?

A
  • Eating a meal leads to K+ absorption- especially unprocessed foods which have a lot of K+
  • This increases plasma K+ conc
  • This needs to be reduced which happens via tissue uptake
68
Q

What stimulates tissue uptake of K+?

A
  • Insulin
  • Aldosterone
  • Adrenaline
69
Q

How does insulin stimulate tissue uptake of K+?

A
  • It’s indirect- insulin stimulates Na+/H+ exchanger which increases Na+ coming into tissue cells
  • This increases intracellular Na+ conc which needs to be reduced
  • This is done through Na+/K+ ATPase which moves Na+ back into blood out of cell and K+ into cell
70
Q

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

A
  • 67% of K+ is reabsorbed in PCT
  • 20% is reabsorbed in thick ascending limb of LOH through Na+/K+/Cl- triple transporter
  • 10-50% of K+ is secreted in DCT and up to 30% in collecting duct
  • Leads to 15-80% of K+ from glomerular filtrate being excreted
71
Q

What stimulates K+ secretion in the nephron?

A
  • Higher plasma K+
  • Increased aldosterone
  • Increased tubular flow rate
  • Increased plasma pH
72
Q

How does the stimulation of K+ secretion in the nephron mechanism work?

A
  • Increased activity of Na+/K+ exchanger meaning more K+ moves into cell
  • More K+ in the cell then means more K+ leaving the cell in tubular fluid
  • There is also an effect on membrane potential which helps
73
Q

How does increased tubular flow rate mechanism work at a cellular level?

A
  • Distal cells have primary cilia
  • When there’s increased tubular flow, these 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
74
Q

How does K+ secretion compare with how K+ is excreted when K+ is depleted?

A
  • Same as above but instead of secretion at DCT and collecting duct, K+ is reabsorbed as well instead similar to the earlier parts of nephron
  • 3% reabsorbed in DCT and 9% reabsorbed in collecting duct
75
Q

How common is hypokalaemia?

A

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

76
Q

What causes hypokalaemia?

A
  • Inadequate dietary intake (too much processed food)
  • Diuretics which increases tubular flow rates
  • Surreptitious vomiting- reduced K+ intake
  • Diarrhoea- reduced K+ intake
77
Q

What genetic conditions can lead to hypokalaemia?

A

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

78
Q

How common is hyperkalaemia?

A

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

79
Q

What causes hyperkalaemia?

A
  • K+ sparing diuretics
  • ACE inhibitors
  • Being old
  • Severe diabetes
  • Kidney disease

uro + renal med (6 decks)

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