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Z Year 2 BRS URO > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

What is osmolarity?

A

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

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2
Q

What is 1 osmole equal to?

A

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

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3
Q

What does osmolarity depend on?

A

number of dissolved particles

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4
Q

When is the osmolarity greater?

A

greater the number of dissolved particles, the greater the osmolarity

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5
Q

What determines an constant osmolarity?

A
  • salt
  • water
  • as these contribute to volume
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6
Q

How does volume of ECF change for number of mosmoles in ECF?

A

osmolarity of approximately 290mosmol/L so if your ECF has 2900 mosmols in total you will haven an ECF volume of 10L and for each change on 290 mosmols the volume will change by 1L

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7
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L (sum of all particles)

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8
Q

Where is the major ion in ECF?

A

sodium which is at approximately 140mmol/L

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9
Q

What happens to ECF the more sodium you have?

A

more sodium you have the higher your ECF volume will be

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10
Q

What happens if you increase dietary sodium?

A
  1. Increased total body sodium
  2. Increased osmolarity (but this can’t happen as semipermeable membrane)
  3. Increased water intake and retention
  4. Increased ECF volume
  5. Increased blood volume and pressure
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11
Q

What happens if you decrease dietary sodium?

A
  1. Decreased total body sodium
  2. Decreased osmolarity (but this can’t happen)
  3. Decreased water intake and retention
  4. Decreased ECF volume
  5. Decreased blood volume and pressure
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12
Q

What does the central mechanisms for regulation of sodium intake include?

A

region of the brain stem the Lateral Parabroachial nucleus

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13
Q

What does the lateral parabroacnial nucelus have?

A

sets of cells that respond to different aspects of sodium balance

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14
Q

What happens to the lateral parabroachial nucelus in normal state (euvolaemia)?

A
  • inhibition of Na+ intake through the

- activity of neurotransmitters including serotonin and glutamate

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15
Q

What happens to the lateral parabroachial nucelus in Na+deprived state?

A

appetite for sodium is increased through a separate set of neurotransmitters including GABA and opiods.

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16
Q

What are the peripheral mechanisms controlling intake based on with sodium itnake?

A

taste

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17
Q

How does salt affect the taste?

A
  • lower levels salt enhances the taste of food

- high concentrations it can make things taste bad (aversive)

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18
Q

Where is the bulk of sodium reabsorbed?

A

proximal convoluted tubule (about 67% of filtered sodium) with water

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19
Q

How is sodium reabsorbed in the nephron?

A

use of sodium as a co- or counter transported ion facilitating the reabsorption of other things (e.g. glucose, amino acids, bicarbonate etc)

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20
Q

How is the rest of sodium reabsorbed?

A
  1. 25% of the total filtered sodium is taken up in the thick ascending limb of the loop of Henle as part of the counter-current mechanisms through the activity of the Na+/K+/Cl- triple transporter.
  2. 5% is taken up in the distal convoluted tubule primarily via the Na+/Cl- transporter found in this region of the tubular system
  3. 3% is reabsorbed in the collecting ducts via the Na+ channel ENAC
  4. end less than 1% of the sodium that enters the tubular system is excreted
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21
Q

How much renal plasma enters the tubular system?

A

20% of renal plasma is filtered GFR is affected by the renal plasma flow rate
GFR = RPF * 0.2

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22
Q

What happens as you increase RPF?

A

you increase GFR

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23
Q

What is RPF proportional to?

A

blood pressure (normal range for mean arterial pressure)

24
Q

When is RPF not proportional BP?

A
  1. blood pressure can increase at times of exercise and if this relationship was maintained you would get an inappropriate level of fluid and sodium loss
  2. So once you reach about 100mmHg RPF does not increase with increasing bp preventing this loss
25
Q

What happens as GFR increases?

A
  1. Amount of sodium going through the system increases
  2. So more sodium going through the system in a shorter amount of time
  3. More sodium at dct
26
Q

How is the proximal part of the dct separated from the glomerulus by?

A
  • extraglomerular mesangial cells

- juxta glomerular cells

27
Q

What happens as more Na/Cl is delivered to dct?

A

amount of sodium and chloride transported by the cells of the macula densa increases

28
Q

What happens to the cells above a threshold value?

A
  • start to release adenosine and ATP

- these activate receptors in the extraglomerular mesangial cells

29
Q

What happens if you lose plasma volume?

A

important to retain sodium so that you can retain water

30
Q

What happens when their is low sodium or low water?

A
  1. both reducing sodium and water excretion

2. constricting the vasculature to reduce the volume of the system and increase the pressure in it

31
Q

What is the best way to retain sodium?

A

filter less

32
Q

What happens in the renal system?

A

we throw away 20% of everything and then get back as much of what we wanted as we can so that we don’t lose it

33
Q

How do you reduce loss of sodium and water by reducing glomerular filtration?

A
  1. reducing the filtration pressure across the bowmans capsule
  2. constricting the afferent arteriole more than the efferent arteriole
  3. or relaxing the efferent arteriole more than the afferent arteriole
34
Q

What does a sympathetic stimulation lead to to retain sodium?

A
  1. Contracts muscle cell in afferent arteriole
  2. Stimulates sodium uptake by cells in pct
  3. Stimulates cells in juxtaglomerular apparatus to produce renin
  4. That renin leads to production of angiotensin II which also stimulates cells in pct to take up sodium
  5. Angiotensin II also stimulates adrenal glands to produce aldosterone which causes reabsoprtion of sdium in dct and ct
  6. If low tubular Na causes stimulation of production of renin and so angio II
35
Q

What happens if you increase GFR?

A

Increase amount of sodium excreted at end (as percentages not numbers)

36
Q

What do macula densa cells do when high tubular fluid?

A
  1. Increased sodium/chloride uptake via triple transporter
  2. Adenosine release from Macula Densa cells
  3. Detected by extraglomerular mesangial cells
  4. Reduces renin production
  5. Promotes afferent SMC contraction
  6. Reduces perfusion pressure and so GFR
37
Q

How do you decrease sodium reabsoprtion?

A
  1. Atrial naturietic peptide acts as a vasodilator and reduces sodium uptake in pct, dct, ct
  2. also suppresses production of renin by JGA
38
Q

What happens when low sodium levels?

A
  1. Decreased BP
  2. Decreased fluid volume
  3. Increase beta 1 sympathetic activity
39
Q

What happens when high sodium levels?

A
  1. Increased BP
  2. Increased fluid volume
  3. Decrease beta 1 sympathetic activity and produce ANP
40
Q

What is aldosterone?

A

steroid hormone

41
Q

Where is aldosterone produced?

A

synthesised and released from adrenal cortex (zona glomerulosa)

42
Q

When is aldosterone released?

A
  • in response to angiotensin II

- decrease in BP via baroreceptors

43
Q

What does angiotensin II do?

A

promote synthesis of aldosterone synthase (enzyme in last two steps in production of aldosterone from cholesterol)

44
Q

What does aldosterone stimulate?

A
  1. Increased sodium reabsorption (controls reabsorption of 35g Na/day)
  2. Increased potassium secretion
  3. Increased hydrogen ion. secretion
45
Q

What does an excess of aldosterone cause?

A

leads to hypokalameic alkalosis

46
Q

How does aldosterone work?

A
  1. Steroid hormones are lipid soluble
  2. Once inside the cell will bind to mineralocorticoid receptor (in cytoplasm) normally bound to a protein HSP90
  3. Once aldosterone bind the HSP90 gets removed
  4. Now instead of being a monomer, the mineralocorticoid receptor with dimerise
  5. That allows it to translocate to the nucleus, bind to DNA where t stimulates production of mRNAs for genes that are under its control
47
Q

What are some of these important target genes?

A
  1. ENaC (epithelial sodium channel)
  2. sodium potassium ATPase
  3. sets of regulatory proteins
    - increase in the number of sodium transporters and their increasing activity thereby increasing sodium reabsorption
48
Q

What is hypoaldosteronism?

A
  • Reabsorption of sodium in distal nephron is reduced

- Increased urinary loss of sodium

49
Q

What is the result of this increase urinary loss of sodium in hypoaldosteronism?

A
  • ECF volume falls

- Increased renin, Ang II, and ADH

50
Q

What are symptoms in hypoaldosteornism?

A
  1. Dizziness
  2. Low BP
  3. Salt craving
  4. Palpatations
51
Q

What is hyperaldosteronism?

A
  • Reabsorption of sodium in the distal nephron is increased

- Reduced urinary loss of sodium

52
Q

What is a result of the reduced urinary loss of sodium?

A
  1. ECF volume increases (hypertension)
  2. Reduced renin, Ang II and ADH
  3. Increased ANP and BNP
53
Q

What are the symptoms of hyperaldosteronism?

A
  1. High BP
  2. Muscle weakness
  3. Polyuria
  4. Thirst
54
Q

What is Liddle’s syndrome?

A
  • normal or low aldosterone levels and looks like hyperaldosterone
  • An inherited disease of high blood pressure
55
Q

What causes Liddle’s syndrome?

A
  • mutation in the aldosterone activated sodium channel.
  • channel is always ‘on’
  • Results in sodium retention, leading to hypertension

Z Year 2 BRS URO (5 decks)

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