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Y2 Urology & Renal Medicine > Sodium & potassium balance > Flashcards

Sodium & potassium balance Flashcards

1
Q

What is the normal osmolarity of plasma?

A

285-295 mosmol/L

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2
Q

Which part of the brain controls central regulation of sodium intake?
Which neurotransmitters increase appetite for Na+?
Which neurotransmitters decreases appetite for Na+?

A

Lateral parabrachial nucleus
Increase: GABA, opioids
Decrease: serotonin, glutamate

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3
Q

What does the peripheral regulation of sodium intake?

A

Taste buds - salty foods become more appetitive/aversive

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4
Q

Where is the main site of sodium reabsorption in the nephron? What %

A

Proximal convoluted tubule
67%

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5
Q

What is the equation for GFR, incorporating renal plasma flow rate?

A

GFR = RPF x 0.2
~20% of renal plasma enters tubular system

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6
Q

What % of sodium is reabsorbed in:
Thin descending limb
Thick ascending limb
DCT
Collecting duct

A

Desc: 0
Asc: 25%
DCT: 5%
CD: 3%

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7
Q

How does increased tubular sodium affect GFR (tubuloglomerular feedback)? (5 steps)

A
  1. high tubular sodium detected by macula densa cells
  2. Increased sodium/chloride uptake via triple transporter
  3. adenosine released from macula densa cells
  4. adenosine detected by extraglomerular mesangial cells & causes contraction of smooth muscle cells
  5. reduces renin production, renal blood flow and GFR
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8
Q

What 3 methods are used to increase sodium retention?

A
  1. increased sympathetic activity
  2. angiotensin II
  3. aldosterone
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9
Q

How does increased sympathetic activity affect sodium retention?

A

Increases sodium retention
1. constricts SMCs of afferent arteriole
2. stimulates reabsorption of Na+ at PCT
3. stimulates renin production from JGA cells

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10
Q

How does angiotensin II affect sodium retention?

A

Increases sodium retention
1. stimulates Na+ uptake in PCT
2. increases aldosterone production
3. causes SMC contraction

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11
Q

How does aldosterone affect sodium retention? Which parts of the nephron does it act on?

A

Increases sodium retention
1. increases synthesis of epithelial sodium channels (ENaCs)
2. increases synthesis of Na+/K+ ATPase channels

Mineralocorticoid receptors in DCT and collecting duct

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12
Q

How does atrial natriuretic peptide affect sodium retention?

A

Promotes sodium excretion via vasodilation

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13
Q

Where is aldosterone synthesised?

What is it released in response to?

A

Zona glomerulosa of adrenal glands

Angiotensin II and low blood pressure

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14
Q

What are the functions of aldosterone?

What can excess aldosterone lead to?

A
  1. increased Na+ reabsorption
  2. decreased K+ reabsorption
  3. decreased H+ reabsorption

Conn’s - hypokalaemic alkalosis

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15
Q

How does aldosterone act within the cell?

A
  1. steroid hormone; passes through CSM
  2. binds to mineralocorticoid receptor
  3. Hsp90 chaperone protein removed
  4. aldosterone-MR complex moves into nucleus
  5. increases transcription of ENaCs and Na/K+ ATPase
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16
Q

What is Liddle’s syndrome?

A

Genetic condition of high BP due to mutation in ENaCs
Channel always open to Na+ regardless of aldosterone levels
Increased sodium retention, leading to hypertension

17
Q

Where are the baroreceptors found in the body on the low pressure side?

A

Atria
Right ventricle
Pulmonary vasculature

18
Q

Where are the baroreceptors on the high pressure side found in the body?

A

Carotid sinus
Aortic arch
Juxtaglomerular apparatus

19
Q

How do baroreceptors on the low pressure side respond to low pressure?

A

Reduced baroreceptor firing
Signal through afferent fibres to brainstem
Increase sympathetic activity
ADH released, greater H2O retention

20
Q

How do baroreceptors on the low pressure side respond to high pressure?

A

Atrial stretch
ANP and BNP released

21
Q

How do baroreceptors on the high pressure side respond to low pressure?

A

Reduced baroreceptor firing
Signals to afferent fibres to brainstem & JGA cells
Sympathetic activity + ADH
Renin released from JGA

22
Q

Where is atrial natriuretic peptide made?
What is it released in response to?
What are its actions?

A

Atria
Atrial stretch

Actions:
Vasodilation
Inhibition of sodium reabsorption in PCT and CD
Inhibits release of renin and aldosterone
Reduces BP

23
Q

How do osmotic diuretics work?

Where do they act?

A

Substance that does not get reabsorbed, increasing osmolarity of filtrate and reducing water reabsorption out of lumen

PCT, thin descending limb

24
Q

How do carbonic anhydrase inhibitors work?

Where do they act?

A

Blocks carbonic anhydrase
Reduces H+ production
Reduces activity of Na+/H+ antiporter
Less Na+ reabsorbed
Less H2O reabsorbed

PCT

25
Q

How do loop diuretics work? Where do they act?

What is an example?

A

Blocks triple transporter (Na+/K+/2Cl-)
Reduces Na+ reabsorption
Increased Na+ conc in distal nephron
Decreased H2O reabsorption

Thin ascending limb

Furosemide

26
Q

How do thiazides work?

Where do they act?

A

Blocks Na+/Cl- transporter
Stimulates Na+/Ca2+ antiporter on basolateral side
Reduces Na+ reuptake
Increases Ca2+ reabsorption

DCT

27
Q

How do potassium-sparing diuretics work? Where do they act?

What is an example?

A

Aldosterone receptor antagonist
Binds to and blocks ENaCs
Reduces Na+ reabsorption
Increases K+ reabsorption

Late DCT and collecting duct

Spironolactone

28
Q

How does insulin affect plasma K+ levels?

A

Stimulates Na+/H+ antiporter
Increases Na+ uptake into cell
Increases Na+/K+/ATPase activity, bringing more K+ into the cell

29
Q

What are the 4 methods of increasing K+ excretion in the collecting duct?

A
  1. aldosterone
  2. increases tubular flow
  3. increased plasma [K+]
  4. increased plasma pH
30
Q

How does increased tubular flow aid K+ excretion?

A

Increased cilia stimulation of PDK1 on tubular side of cell
Increases intracellular Ca2+
Stimulates opening of K+ channels, more excretion

31
Q

What are some causes of hypokalaemia?

A

Inadequate dietary intake
Diuretics
Vomiting & diarrhoea
Genetics (Gitelman’s syndrome)

Y2 Urology & Renal Medicine (3 decks)

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