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UROLOGY AND RENAL MEDICINE 2 > SODIUM AND POTASSIUM BALANCE > Flashcards

SODIUM AND POTASSIUM BALANCE Flashcards

1
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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2
Q

How does increased dietary sodium lead to high BP/volume?

A 
Increased dietary sodium
Increased total body sodium
Increased ECF osmolarity - doesn't acc happen due to semipermeable membranes
Increased water intake and retention
Increased ECF volume
Increased BP/volume

Vice versa

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3
Q

How do we regulate sodium intake?

A

Euvolemia and normal sodium levels:
Lateral parabrachial nucleus inhibits Na+ intake via serotonin/glutamate

Na+ deprivation:
Lateral parabrachial nucleus increases appetite for Na+ via GABA/opioids

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4
Q

How does taste of salt change depending on concentrations in food?

A

Appetitive at low conc.

Aversive at high conc.

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5
Q

In which parts of the nephron is sodium reabsorbed and their percentages?

A

PCT (67%)
Thick ascending limb (25%)
DCT (5%)
Collecting duct (3%)

Excretion (<1%)

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6
Q

How does mean arterial pressure affect sodium excretion?

A

As arterial BP increases so does renal plasma flow (RPF) and thus (GFR). A greater GFR means greater amount of sodium excreted (and reabsorbed)

However, ~ 100 mmHg BP, RPF and GFR plateau despite increasing BP. Thus, sodium excretion also plateaus

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7
Q

What is the relationship between GFR and renal plasma flow (RPF)?

A

GFR = RPF * 0.2

20% of RPF enters tubular system

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8
Q

Why do you want RPF and GFR to plateau at a certain BP?

A

Over a certain BP you don’t want to excrete more sodium than you need to. The BP may be that high due to exercise

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9
Q

How is the short term plateau effect of RPF and GFR carried out?

A

As RPF increase so does GFR. This means you get more sodium going through the system in a shorter period of time.

At the DCT, this high tubular sodium is sensed by the macula densa causing them to increase sodium/chloride uptake via a triple transporter. This then causes them to release adenosine which is detected by extraglomerular mesangial cells. These cells:

  • Promote afferent arteriole smooth muscle cells to
    contract which reduces blood flow, perfusion pressure
    and thus GFR
  • Reduce renin production (minimal affect)
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10
Q

What happens when the human body needs to retain more sodium?

A

Increased sympathetic activity

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11
Q

How does sympathetic activity decrease sodium excretion?

A

Afferent arteriole contraction +
Sodium uptake in PCT +
Juxtaglomerular apparatus activity/renin production +

Renin production + means angiotensin II +
Sodium uptake in PCT +
Aldosterone production + means:
Sodium uptake in DCT +
Sodium uptake in collecting duct +
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12
Q

What happens when the human body needs to excrete more sodium?

A

Atrial naturietic peptide (ANP) production

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13
Q

How does ANP increase sodium excretion?

A

Afferent arteriole vasodilation +
Sodium uptake in PCT -
Juxtaglomerular apparatus activity/renin production -

Renin production - means angiotensin II -
Aldosterone production -
Sodium uptake in DCT -
Sodium uptake in collecting duct -

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14
Q

How does angiotensin II increase aldosterone?

A

Angiotensin II promotes synthesis of aldosterone synthase which catalyses the last 2 steps steps of aldosterone synthesis from cholesterol

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15
Q

What does aldosterone do?

A

Increased sodium reabsorption
Increased potassium secretion
Increased hydrogen ion secretion

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16
Q

What does an excess of aldosterone lead to?

A

Hypokalaemic alkolosis

Hypertension

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17
Q

Describe the process by which aldosterone works

A

Aldosterone passes through cell membrane (lipid soluble)
Binds to mineralocorticoid receptor - HSP90 complex
HSP90 is removed
MCR-aldosterone complex is dimerised
Dimer moves into nucleus and binds to DNA
Transcription and translation making:

  • ENaC (apical sodium channel)
  • Na+K+ATPase (basolateral)
  • Regulatory proteins which stimulate both transporters to
    be more active
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18
Q

What does hypoaldosteronism cause?

A

Reduced reabsorption of sodium in distal nephron
Increased urinary loss of sodium

ECF volume falls
Increased renin, angiotensin II and ADH to counter and retain water but not enough

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19
Q

What are the symptoms of hypoaldosteronism?

A

Dizziness
Low BP
Salt cravings
Palpitations (changes in mem. potential)

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20
Q

What is Liddle’s syndrome?

A

Inherited disease causing hypertension
Mutation in aldosterone activated sodium channel
Channel is always on resulting in excess sodium retention

21
Q

List all the locations where baroreceptors are found and whether they are low/high pressure side of the cardiovascular system

A 
Atria (low)
Right ventricle (low)
Pulmonary vasculature (low)
Carotid sinus (high)
Aortic arch (high)
Juxtaglomerular apparatus (high)
22
Q

In the low pressure side of the CV system, how is blood pressure detected and managed?

A

Low pressure:

  • reduced baroreceptor firing
  • signal via afferent fibres to brainstem
  • SNS activity, ADH release

High pressure:

  • atrial stretch
  • ANP, BNP released
23
Q

In the high pressure side of the CV system, how is blood pressure detected and managed?

A

Low pressure:
- reduced baroreceptor firing causing…

  • signal via afferent fibres to brainstem
  • SNS activity, ADH releasedand
  • JGA cells stimulated
  • Renin release
24
Q

What is atrial natriuretic peptide (ANP) and what does it do?

A

Small peptide made in atria released in response to atrial stretch (high bp)

Causes:
- vasodilation
- inhibition of sodium reabsorption in PCT and collecting
ducts
- inhibits release of renin and aldosterone
- reduces bp

25
Q

What does volume expansion of ECF cause?

A

Decreased SNS
Decreased renin
Increased ANP/BNP production in heart
Indirect decreased AVP

26
Q

What does volume contraction of ECF cause?

A

Increased SNS
Increased renin
Decreased ANP/BNP from heart
Increased AVP

27
Q

What does reducing salt reabsorption do to ECF volume and thus BP?

A

Reduces

28
Q

What are the effects of ACE inhibitors?

A

Vasodilation:

  • Decreased BP
  • Decreased water reabsorption

Decreased sodium uptake in PCT
Increased sodium in distal nephron

Reduced aldosterone:

  • Decreased sodium uptake in collecting duct
  • Increased sodium in distal nephron
29
Q

Name all the different types diuretics

A 
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazides
K+ sparing diuretics
Aquaretics
30
Q

How do carbonic anhydrase inhibitors work?

A

Inhibits carbonic anhydrase which is necessary for the reversible reaction of H2CO3 –> H20 + CO2 in the tubular fluid. Without H20 + CO2 the reverse reaction can’t happen in the cell so less H2CO3 in the cell

This means H2CO3 –> H+ + HCO3- can’t occur and thus reduced less Na+ H+ apical antiporter action.

31
Q

What is the effect of carbonic anhydrase inhibitors

A

Reduced Na+ reuptake in PCT
Increased NA+ in distal nephron
Reduced water reabsorption
Decreased urine acidity

32
Q

How do loop diuretics work and what do they cause?

A

Na+ 2Cl- K+ triple transporter inhibitor

Reduced Na+ reuptake in the LOH
Increased Na+ in the distal nephron
Reduced water reabsorption

33
Q

How do thiazides work and what do they cause?

A

Na+ Cl- transporter inhibited at DCT

Reduced Na+ reuptake
Increased Na+ in distal nephron
Reduced water reabsorption

Increased calcium reabsorption

34
Q

Why do thiazides cause increased calcium reabsorption?

A

Less Na+ in cell since Na+ K+ basolateral antiporter isn’t blocked. This increases gradient of Na+ between the cell and blood. Thus more Na+ crosses back via the basolateral Na+ Ca+ antiporter.

Calcium is therefore pumped out of the cell causing decreased calcium conc. in cell. More calcium moves in from the lumen via ion channel due to the gradient.

35
Q

How do potassium sparing diuretics work and what do they cause?

A

Bind to mineralocorticoid receptor preventing aldosterone function

Thus less Na+ is reabsorbed from tubular fluid –> less Na+ reabsorbed into blood via 3Na+ 2K+ basolateral antiporter and less K+ pumped into cell from blood

Less K+ loss into urine via apical K+ ion channel

36
Q

Give an example of a potassium sparing diuretic

A

Spironolactone

37
Q

Give an example of a loop diuretic

A

Furosemide

38
Q

What is the main intracellular ion?

A

Potassium

39
Q

What does irregular levels of potassium cause?

A

Heart arrhythmias

40
Q

What substances stimulate the uptake of plasma K+?

A

Insulin (indirect)
Aldosterone
Adrenaline

41
Q

How does insulin stimulate uptake of plasma K+?

A

Insulin stimulates the H+ Na+ basolateral antiporter. This increases intracellular sodium conc. which needs to be reduced via the Na/K ATPase bringing more K+ into cell

42
Q

Where is potassium exchanged in the nephron and at what percentages for a patient with normal/increased intake?

A

PCT (67% reabsorbed)
Thick ascending limb (20% reabsorbed)
DCT (10-50% secretion)
Collecting duct (5-30% secretion)

15-80% excreted

43
Q

Where is potassium exchanged in the nephron and at what percentages for a patient with decreased intake?

A

PCT (67% reabsorbed)
Thick ascending limb (20% reabsorbed)
DCT (3% reabsorbed)
Collecting duct (9% reabsorbed)

1% excreted

44
Q

What is K+ secretion stimulated by?

A

Increased plasma [K+]
Increased aldosterone
Increased tubular flow rate
Increased plasma pH

45
Q

Which cells secrete potassium?

A

Principle cells

46
Q

During periods of hyperkalaemia, how do the kidneys secrete potassium?

A

Potassium flows into principle cells via the basolateral Na/K ATPase increasing intracellular potassium conc. They then diffuse out into the tubular lumen via K+ ion channels.

Membrane potential of the principle cell is also affected which helps potassium secretion

47
Q

How does increased tubular flow increase K+ secretion and therefore excretion?

A

During an increase in tubular flow, the apical primary cilium of distal cells senses and stimulates PDK1 to increase calcium conc. in the cell. This stimulates activity of potassium channels

48
Q

List the causes of hypokalaemia

A 
Inadequate dietary intake
Diuretics (increase tubular flow rates)
Surreptitious vomiting
Diarrhoea
Genetics
49
Q

List the causes of hyperkalaemia

A 
K+ sparing diuretics
ACE inhibitors
Elderly
Severe diabetes
Kidney disease

UROLOGY AND RENAL MEDICINE 2 (5 decks)

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