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!!!!! BRS YR2 !!!!! > Uro - Sodium + Potassium Balance > Flashcards

Uro - Sodium + Potassium Balance Flashcards

1
Q

What is osmolarity?

A

measure of solute (particle) concentration in a solution

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2
Q

What is 1 osmole equal to?

A

1 mole of dissolved particles per liter

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3
Q

How do we have constant osmolarity in our body?

A

→ water and salt are tightly regulated
→ increased salt = increased water = increased volume
→ decreased salt = decreased water = decreased volume

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4
Q

What is normal plasma osmolarity range?

A

285 - 295 mosmol/L

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5
Q

What is the most prevalent ion in our ECF?

A

sodium = 140 mmol/L

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6
Q

What is the relationship between dietary sodium + body weight?

A

as dietary sodium increases, body weight also increases

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7
Q

How does increased dietary sodium affect blood volume + pressure?

A 
→ increased dietary sodium
→ increased total body sodium
→ increased osmolarity
→ increased water intake + retention
→ increased ECF volume
→ increased blood volume + pressure
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8
Q

How does decreased dietary sodium affect blood volume + pressure?

A 
→ decreased dietary sodium
→ decreased total body sodium
→ decreased osmolarity
→ decreased water intake + retention
→ decreased ECF volume
→ decreased blood volume + pressure
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9
Q

*What are the central mechanisms that regulate sodium intake?

A

region of the brain stem the Lateral Parabrachial nucleus in which there are sets of cells that respond to different aspects of sodium balance

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10
Q

How do central mechanisms regulate sodium in states of sodium deprivation?

A

→ increase appetite for Na+

→ driven by GABA and opiods

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11
Q

How do central mechanisms regulate sodium in states of euvolemia?

A

→ inhibition of sodium uptake

→ driven by serotonin + glutamate

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12
Q

*How do peripheral mechanisms control our sodium intake?

A

→ based on taste
→ enhances taste of salt in food in states of Na+ deprivation
→ makes salt in food taste aversive if in euvolemic state

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13
Q

What is the relationship between sodium excretion + GFR?

A

as GFR goes up, sodium excretion goes up

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14
Q

How much of renal plasma enter the tubular system?

A

20%

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15
Q

*What is the relationship between MAP and RPF + GFR?f

A

→ increases as MAP increases
→ but starts to plateau after a threshold
→ due to regulatory mechanism to conserve sodium

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16
Q

How is GFR regulated as MAP increases?

A

→ DCT and glomerulus are in tight association
→ High tubular sodium = Increased sodium/chloride uptake via triple transporter
→ Adenosine release from Macula Densa cells after a certain threshold
→ Detected by extraglomerular mesangial cells
→ Reduces renin production
→ Promotes afferent smooth muscle cell contraction
→ Reduces perfusion pressure and GFR

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17
Q
  • How is sodium reabsorption + retention increased in the nephron?
A

→ Sympathetic activity cause smooth muscle contraction in the afferent arteriole
→ Sympathetic activity also stimulates sodium uptake in the PCT + stimulates cells of juxtaglomerular apparatus to produce renin, which leads to angiotensin II
→ Angiotensin II stimulates PCT to take up sodium + stimulates adrenal glands to produce aldosterone
→ Aldosterone stimulates uptake of sodium in distal part of DCT + collecting duct
→ Low sodium conc. In tubular fluid stimulates production of renin as well

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18
Q

How does sodium reabsorption affect sodium excretion?

A

→ increased sodium reabsorption = decreased sodium excretion

→ decreased sodium reabsorption = increased sodium excretion

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19
Q
  • How is sodium reabsorption + retention decreased in the nephron?
A

→ Atrial natriuretic peptic acts as a vasodilator in afferent arterioles
→ Reduces sodium uptake in PCT, DCT and collecting ducts
→ Inhibits renin production in the JGA

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20
Q

*What is the affect of low sodium on blood volume + pressure, and how?

A

sympathetic stimulation:
→ decreases blood pressure
→ decreases fluid volume
→ increases beta-1-sympathetic stimulation
→ increases renin production
→ allows the RAA cascade
→ angiotensin II promotes aldosterone production, vasoconstriction + NaCl/H2O reabsorption
→ aldosterone also promotes NaCl/H2O reabsorption

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21
Q

*What is the affect of high sodium on blood volume + pressure, and how?

A

sympathetic inhibition:
→ increases blood pressure
→ increases fluid volume
→ decreases beta-1-sympathetic stimulation
→ decreases renin production
→ stops the RAA cascade
→ angiotensin II promotes aldosterone production, vasoconstriction + NaCl/H2O reabsorption
→ aldosterone also promotes NaCl/H2O reabsorption

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22
Q

What is aldosterone? Where is it released from?

A

→ steroid hormone

→ synthesised + released from the zone glomerulosa of the adrenal cortex

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23
Q

*What is aldosterone released in response to? Why?

A

→ released in response to angiotensin II as it activates aldosterone synthase
→ also released in response to decrease in blood pressure (via baroreceptors)

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24
Q

What is the function of aldosterone?

A

→ Increased Sodium reabsorption (controls reabsorption of 35g Na/day)
→ this causes increased Potassium secretion
→ Increased hydrogen ion secretion

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25
Q

*Why does Na+ reabsorption in the principal cell cause potassium secretion?

A

→ aldosterone activates sodium reabsorption into the the principal cells
→ this causes Na+ K+ ATPase to pump out more sodium into the blood, causing potassium to come into the principal cells
→ causes potassium to be pumped out of principal cells into lumen

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26
Q

What does aldosterone excess lead to?

A

hypokalaemia alkalosis

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27
Q

How does aldosterone cause its effects?

A

→ crosses cell membrane where it binds to the mineralocorticoid receptor
→ MR then loses its association with HSP90 (where its bound to without aldosterone) and dimerises
→ translocates into the nucleus where it binds to DNA in the promoter region of target genes and stimulates their expression

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28
Q

*What are some of the target genes for aldosterone?

A

→ ENaC (epithelial sodium channel)
→ sodium potassium ATPase and sets of regulatory proteins
→ co-ordinates an increase in the number of sodium transporters and their activity thereby increasing sodium reabsorption

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29
Q

What are the effects of hypoaldosteronism on sodium regulation + urine?

A

→ reduced reabsorption of sodium in the distal nephron
→ increased urinary sodium loss
→ reduces water retention and causes the ECF volume to fall, increasing renin, AII and ADH

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30
Q

What are the symptoms of hypoaldosternism?

A

→ Dizziness
→ Low blood pressure
→ Salt craving
→ palpitations

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31
Q

What are the effects of hyperaldosteronism on sodium regulation + urine?

A 
→ reabsorption of sodium in the distal nephron is increased
→ reduced urinary loss of sodium
→ ECF volume increases (hypertension)
→ reduced renin, Ang II and ADH
→ Increased ANP and BNP
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32
Q

What are the symptoms of hyperaldosternism?

A

→ High blood pressure
→ Muscle weakness
→ Polyuria (as a consequence of thirst + increased drinking)
→ thirst

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33
Q

What can cause hyperaldosternism?

A

adrenal tumours

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34
Q

What is Liddle’s Syndrome?

A

→ inherited disease of high blood pressure
→ mutation in the aldosterone activated sodium channel.
→ channel is always ‘on’
→ results in sodium retention, leading to hypertension

35
Q

What syndrome is often mistaken as hyperaldosteronism? Why?

A

Liddle’s syndrome - same symptoms but has low to normal levels of aldosterone

36
Q

What parts of the cardiovascular system monitor low blood pressure?

A

baroreceptors in the heart, specifically:
→ atria
→ right ventricle
→ pulmonary vasculature

37
Q

What parts of the cardiovascular system monitor high blood pressure?

A

baroreceptors in:
→ carotid sinus
→ aortic arch
→ juxtaglomerular apparatus

38
Q

What happens when low BP is detected on the low pressure side of the CVD system?

A

→ low blood pressure = reduced baroreceptors firing
→ sends signal through afferent fibres to the brainstem
→ stimulates sympathetic activity + ADH release

39
Q

What happens when high BP is detected on the low pressure side of the CVD system?

A

→ high blood pressure = atrial stretch + increased baroreceptor firing
→ causes ANP and BNP to be released

40
Q

What happens when low BP is detected on the high pressure side of the CVD system?

A

→ low pressure = reduced baroreceptor firing
→ this sends signals through afferent fibres to brain stem, stimulating sympathetic activity + ADH release
→ also stimulates JGA cells to release renin

41
Q

What happens when low BP is detected on the high pressure side of the CVD system?

A

→ low pressure = reduced baroreceptor firing
→ this sends signals through afferent fibres to brain stem, stimulating sympathetic activity + ADH release
→ also stimulates JGA cells to release renin

42
Q

What is ANP?

A

→ atrial natriuretic peptide

→ small peptide made in the atria

43
Q

When is ANP is released?

A

in response to atrial stretch (i.e. high BP)

44
Q

*What is the mechanism of action of ANP?

A

when it binds to its receptor, it stimulates the production of cyclic GMP and activates protein kinase G

45
Q

What are the actions of ANP?

A

→ Vasodilatation of renal (and other systemic) blood vessels
→ Inhibition of Sodium reabsorption in proximal tubule and in the collecting ducts
→ Inhibits release of renin and aldosterone
→ Reduces blood pressure

46
Q

*What happens when there is an expansion in blood volume?

A

→ you need to increase sodium and water excretion → leads to reduced sympathetic activity, afferent arteriolar dilation and increased GFR (throwing away more water and sodium).
→ also reduce sodium uptake in the PCT and reduce renin- angiotensin and aldosterone levels to reducing sodium reuptake in the PCT, DCT and CT
→ reduced sodium reabsorption = reduced water reabsorption so increased excretion of both. → ANP release compliments these effects; suppressing renin, increasing GFR and inhibiting sodium reuptake in the CT
→ also suppresses the release of ADH
→ the combination of these responses cause a reduction in volume

47
Q

*What happens when there is an contraction in blood volume?

A

→ increased sympathetic activity
→ more renin, more angiotensin I + II, more aldosterone
→ more sodium + water retention in PCT, DCT + CT
→ decrease in BNP + ADP , and increase in ANP (arginine vasopressin) expression

48
Q

*What is required for water reabsorption in the nephron?

A

osmotic gradient between the interstitium and tubules

49
Q

How do sodium levels impact ECF volume + BP?

A

→ increased sodium excretion = increased water excretion, which reduces ECF volume + BP
→ decreased sodium excretion = decreased water excretion, which increases ECF volume + BP

50
Q

What is the mechanism of action for ACE inhibitors?

A

inhibits ACE from converting angiotensin I to angiotensin II

51
Q

What are the vascular effects of ACE inhibitors?

A

→ increases vascular volume
→ decreases blood pressure
→ decreased water reabsorption

52
Q

What are the direct renal effects of ACE inhibitors?

A

→ decreased Na+ reuptake in the PCT

→ increased Na+ in the distal nephron

53
Q

What are the adrenal effects of ACE inhibitors?

A

→ reduced aldosterone due to reduced angiotensin II
→ decreases Na+ uptake in the CCT
→ increases Na+ in the distal nephron

54
Q

Where do osmotic diuretics act on the nephron?

A

PCT + thin descending loop of Henle

55
Q

Where do carbonic anhydrase inhibitors act on the nephron?

A

PCT

56
Q

Where do loop diuretics act on the nephron?

A

thick ascending loop

57
Q

Where do thiazides act on the nephron?

A

DCT

58
Q

Where do K+ sparing diuretics act on the nephron?

A

distal part of DCT and CCD

59
Q

Where do aquaretics act on the nephron?

A

distal collecting duct

60
Q

How does mannitol work as a diuretic?

A

A diuretic that can’t be reabsorped
As water is reabsorbed from the tubular fluid, the osmolality of the tubular fluid increases, more than it normally would.
So along the nephron, water reabsorption reduces, resulting in more water excretion.
Usually given as an infusion.

61
Q

How does a carbonic anhydrase inhibitor work? Where?

A

Carbonic anhydrase activity leads to Na+ re-absorption in the PCT
Increases Na+ levels in the distal nephron
Leads to reduced water re-absorption

62
Q

How do loop diuretics work? Where?

A 
Thick ascending limb of loop of henle
Triple transporter inhibitors
Reduced Na+ reuptake in the LoH
Increases Na+ levels in the distal nephron
Reduced water re absorption
63
Q

How do thiazides work? Where?

A

Reduced Na+ re uptake in the early DCT
Increases Na+ in the distal nephron
Reduces water reabsorption

64
Q

What are the side effects of thiazides? Why?

A

Increased calcium reabsorption

65
Q

How do potassium sparing diuretics work? Where?

A

Work in the late DCT
Inhibits aldosterone function
Reduces Na+ reabsorption
Reduces K+ excretion

66
Q

What is the main intracellular ion?

A

Potassium

67
Q

What is the purpose of extracellular K+?

A

Has effects on excitable membranes of nerve + muscle

68
Q

What is the effect having high extracellular K+?

A

Depolarises membranes - action potentials, heart arrhythmias

69
Q

What is the effect of having low K+ ?

A

Heart arrhytmias (asystole)

70
Q

Where is potassium most present?

A

In most foods or all foods (especially processed foods) due to it being a major intra-cellular ion.

71
Q

What does eating a meal (containing potassium) result in?

A
72
Q

What hormones regulate potassium uptake into cells?

A

Insulin (mainly), also aldosterone and adrenaline

73
Q

How does insulin stimulate K+ uptake into cells?

A

1) Insulin stimulates Na+ H+ exchanger, so Na+ enters the cell, H+ leaves the cell
2) Intracellular Na+ needs to be decreased as a result, so Na+ K+ ATPase is stimulated - Na+ leaves the cell, K+ enters.

74
Q

What proportions of K+ is reansorped in the kidney when the body is in potassium depletion?

A
75
Q

How much K+ is reabsorped or excreted in the nephron when there is normal or increased potassium intake?

A
76
Q

What causes increased potassium secretion in principal cells?

A
77
Q

What effect does tubular flow have on potassium excretion? How?

A

Increased tubular flow = increased primary cilia movement + PDK1 stimulation
This increase Ca+ conc in the cell
Activated the K+ channels and causes K+ excretion out of the cells

78
Q

How common is hypokalaemia?

A

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

79
Q

What are the main causes of hypokalaemia?

A

Inadequate dietary intake (too much processed food)
Diuretics (due to increased tubular flow rates)
Surreptitious vomiting
Diarrheoa
Genetics (Gitelman’s syndrome, mutation in the NaCl transporter in the distal nephron)

80
Q

How common is hyperkalaemia?

A

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

81
Q

What can cause hyperkalaemia?

A

ACE inhibitors
In resonse to K+ sparing diuretics
Elderly
Severe diabetes (diminished capacity to excrete potassium)
Kidney disease (diminished capacity to excrete potassium)

82
Q

What is an example of a loop diuretic?

A

Furosemide

83
Q

What is an example of a K+ sparing diuretic?

A

Spironolactone

84
Q

What is effect of most diuretics on sodium levels in the kidney?

A

They increase sodium excretion

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