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Y2 Urology > Sodium and potassium balance (Regulation of Sodium) > Flashcards

Sodium and potassium balance (Regulation of Sodium) Flashcards

1
Q

How do we calculate vol. (ECF) from:
- no. of mosmoles (ECF)
- conc

A

no. of mosmoles(ECF) / conc = vol (ECF)

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2
Q

What is a normal plasma osmolarity?

A

275-295 mosmol/L

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3
Q

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

A

sodium

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4
Q

What are the 2 most prevalent solutes in the plasma?

A

sodium
chloride

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5
Q

What is the counter ion for Na

A

Cl

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6
Q

Describe how dietary sodium can affect blood volume and BP

A
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7
Q

What part of the brain is responsible for regulation of sodium intake

A

lateral parabrachial nucleus

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8
Q

How does the body regulate sodium intake in the body?

A

central mechanism:
lateral parabrachial nucleus detects Na+ deprivation and euvolemia.
- when euvolemia, inhibition of Na+ intake is driven by cells that respond to serotonin glutamate
- when Na+ deprived, increase for appetite for Na+ is driven by GABA and opioids

peripheral mechanism:
taste
- salt is appetitive when present in low conc in food
- salt in high conc is unpleasant to taste

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9
Q

When the body is euvolemic, where is this detected in the body and what drives the inhibition of Na+ intake?

A

lateral parabrachial nucleus

driven by serotonin glutamate

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10
Q

When the body is deprived of Na+, where is this detected in the body and what drives the increase in appetite for Na+

A

lateral parabrachial nucleus

driven by GABA, opioids

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11
Q

label the % of sodium absorbed in each part of the nephron

A

re

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12
Q

Explain this graph

A

@ lower rates of mean arterial pressure,
renal plasma flow and GFR are proportional to MAP
therefore, GFR is also proportional to RPF

@ higher MAP, the graph plateaus (ie w/ exercise)
therefore, GFR doesn’t continue to increase and not as much sodium is lost)

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13
Q

label

A
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14
Q

How does the macula densa respond to a high tubular sodium?

A
  1. macula densa sense the high sodium levels in the tubular fluid
  2. increase the Na/Cl uptake via the triple transporter
  3. this increased uptake of Na/Cl caused the cells to release adenosine
  4. release of adenosine causes the extraglomerular mesangial cells to interact with the smooth muscle cells on the afferent arteriole
  5. smooth muscle cells contract
  6. therefore reduced flow into glomerulus
  7. release of adenosine also leads to reduction of renin production (this is short term)

overall, there is a reduction in perfusion pressure and there is a reduction in GFR

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15
Q

The the best way to retain sodium is to filter less. How can we do this?

A

lower pressure gradient

lower pressure in efferent arteriole so that less is filtered into the glomerulus

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16
Q

What kind of activity acts on the proximal end of the nephron when there is increased need for Na reabsorption and retention?

How does this activity achieve this?

A

increase b1 sympathetic activity

  • contracts AA
  • stimulates Na uptake in PCT
  • stimulated cells of JGA to produce renin
17
Q

After there is b1 sympathetic activity to increase Na reabsorption/retention, what is produced to continue this process of Na reabsorption/retention?

How does this work?

A

renin

  • renin leads to production of angiotensin 2
  • stimulate Na reabsorption at PCT
  • stimulates adrenal glands to produce aldosterone, which stimulate Na reuptake in PCT and CD
18
Q

What 2 things stimulate the production of renin and therefore angiotensin 2?

What suppresses renin production?

A
  • b1 sympathetic activity
  • low tubular Na
    …
  • atrial naturietic peptude
19
Q

How does angiotensin 2 work?

A
  • stimulate Na reabsorption at PCT
  • stimulates adrenal glands to produce aldosterone, which stimulate Na reuptake in PCT and CD
20
Q

What molecule is involved when we need decreased Na reabsorption?

How does it act?

A

atrial naturietic peptide

  • vasodialator, so more blood is filtered
  • reduces uptake of Na+ at PCT, DCT and CD
  • suppresses renin production
21
Q

just to revise

A
22
Q

Where is aldosterone synthesised?
What stimulates its synthesis?

A

Synthesised and released from the adrenal cortex (zona glomerulosa)

  • Released in response to Angiotensin ll
  • Decrease in blood pressure (via baroreceptors)
23
Q

What are aldosterone’s functions?

A

St imulates: Increased Sodium reabsorption
(controls reabsorption of 35g Na/day) Increased Potassium secretion Increased hydrogen ion secretion
Aldosterone excess:
leads to hypokalaemic alkalosis

24
Q

How does aldosterone influence the reabsorption and excretion of particular ions in the kidneys? Name the particular ions and the effect of aldosterone on them.

A

Stimulates:
- Increased Sodium reabsorption
- Increased Potassium secretion
- Increased hydrogen ion secretion

25
Q

What exactly does angiotensin 2 promote the synthesis of to stimulate aldosterone synthesis?

A

aldosterone synthase

26
Q

What acid-base disturbance does excess Aldosterone lead to?

A

hypokalaemic alkalosis

26
Q

What acid base disturbance does Aldosterone excess lead to?

A

hypokalaemic alkalosis

27
Q

How does aldosterone work?

A

it is a steroid hormone, thus it will pass through the cell membrane

once inside the cell, aldosterone binds to the mineralocorticoid receptor, which is bound to a protein called HSP-90

HSP-90 is removed and the mineralocorticoid receptor dimerises

it translocates to the nucleus and binds to DNA where it stimulates the production of mRNAs

28
Q

Once aldosterone does it’s stuff and the mRNAs are produced, what proteins are made?

A

the sodium channel (epithelial sodium channels -0- ENaC) and the NaKATPase

regulatory proteins are also produced and they stimulate the activity of the above 2 transporters

29
Q

What is the result of hypoaldosteronism?

A
29
Q

Name some symptoms of hypoaldosteronism

A
30
Q

What is the result of hyperaldosteronism? What physiological symptoms may you get?

A

-

31
Q

Name some symptoms of hyperaldosteronism

A
32
Q

Describe the permeability of the nephron to sodium

A
33
Q

What is Liddle’s Syndrome?

A

an inherited disease of high blood pressure

it looks like hyperaldosteronism but with a normal or low aldosterone

34
Q

What is the mutation is Liddle Syndrome that causes hypertension?

A

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

Y2 Urology (7 decks)

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