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Year 2 Uro > Sodium and Potassium > Flashcards

Sodium and Potassium Flashcards

1
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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2
Q

What is the most prevalent solute in the plasma?

A

Sodium

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3
Q

What happens when you increase sodium dietary intake?

A 
Increase total body sodium
Increased osmolarity (but this can't happen)
Increased water intake and retention
Increased ECF volume
Increased blood volume and pressure
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4
Q

What happens during euvolemia?

A

Inhibition of Na+ intake via serotonin and glutamate in lateral parabrachial nucleus

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5
Q

What percentage of water is reabsorbed in the PCT?

A

60-70%

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6
Q

What percentage of sodium is reabsorbed in the PCT?

A

67%

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7
Q

What percentage of sodium is reabsorbed in the thick ascending limb?

A

25%

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8
Q

What percentage of sodium is reabsorbed in the DCT?

A

5%

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9
Q

How would you increase the amount of sodium excreted into urine?

A

Increase GFR

Increase sodium excretion

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10
Q

What impacts renal plasma flow and GFR

A

mean arterial pressure

proportional up to a plateau

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11
Q

how does the macula densa sense high GFR and return it to normal?

remember macula densa is in the DCT

(tubular glomerular feedback)

A

High tubular sodium in DCT

Macula densa cells increase sodium/chloride uptake via triple transporter

Adenosine release from Macula Densa cells

Reduces renin production (short term) from juxtaglomerular cells

adenosine detected by extraglomerular mesangial cells

Promotes afferent SMC contraction of afferent arteriole, reducing blood flow to glomerulus

Reduces renal plasma flow and so GFR

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12
Q

Why is the macula densa production of renin in response to high tubular sodium less important?

A

short period of inhibition

So does not affect overall renin production long term

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13
Q

What is the best way to retain sodium and water?

A

Filter less - reduce GFR

Reduction of pressure gradient at Bowman’s capsule

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14
Q

what factor reduces GFR/lowers filtration and therefore causes sodium retainment

A

increased sympathetic activity

Contracts SMC of afferent arteriole (lowers GFR)

Stimulates sodium uptake of cells of PCT

Stimulates JGA to produce renin

Renin –> Angiotensin II - promotes reabsorption of sodium in PCT

Angiotensin II –> Aldosterone - promotes reabsorption in collecting duct and distal DCT

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15
Q

What factors allow for increased GFR/filtration so sodium excretion

A

Atrial naturetic peptide - vasodilator +inhibits renin (therefore angiotensin)
Reduces reabsorption of Sodium throughout nephron

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16
Q

What is the role of aldosterone in the kidney?

A

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

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17
Q

What can aldosterone excess lead to?

A

hypokalaemic alkalosis

hypertension

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18
Q

How does aldosterone work?

A

Steroid hormone

Passes through cell membrane

Binds to mineralocorticoid receptor inside cytoplasm bound to protein

protein is removed and the receptor is dimerised

Moves into nucleus binds to DNA stimulates transcription of mRNA genes for epithelial sodium channels and NaKATPase proteins

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19
Q

What proteins are produced in response to aldosterone?

A

Na/K ATPase

Epithelial sodium channel

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20
Q

What is hypoaldosteronism?

A

Reabsorption of sodium in the distal nephron is reduced - increased Na+ loss in urine
ECF volume falls
Increased renin, Ang II and ADH

aka low blood pressure

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21
Q

What are symptoms of hypoaldosteronism?

A

Dizziness
Low blood pressure
Salt craving
palpitations

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22
Q

physiological effects of hyperaldosteronism

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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23
Q

What are symptoms of hyperaldosteronism?

A

High blood pressure
Muscle weakness
Polyuria
thirst

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24
Q

What is Liddle’s syndrome?

A

inherited genetic mutation in aldosterone activated sodium channel.
-channel is always ‘on’
-Results in sodium retention, leading to hypertension
no actual high levels of aldosterone in blood

25
Q

Where are the low pressure baroreceptors?

A

Atria
Right ventricle
Pulmonary vasculature

26
Q

Where are the high pressure baroreceptors?

A

Carotid sinus
Aortic arch
Juxtaglomerular apparatus

27
Q

What is the low pressure side response to low pressure?

A

Reduced baroreceptor firing

Signal through Afferent fibres to the brainstem

Sympathetic activity

ADH release

28
Q

What is the low pressure side response to high pressure?

A

Atrial stretch

ANP, BNP released

29
Q

What is the high pressure side response to low pressure?

A

Reduced baroreceptor firing

Signal through Afferent fibres to the brainstem

Sympathetic activity

ADH release

JGA cells - renin released

30
Q

What is ANP?

A

Small peptide made in the atria (also make BNP)

Released in response to atrial stretch (i.e. high blood pressure)

31
Q

What are the actions of ANP?

A
  • Vasodilation of renal (and other systemic) blood vessels
  • Inhibition of Sodium reabsorption in PCT and collecting ducts
  • Inhibits release of renin and aldosterone
  • Reduces blood pressure
32
Q

What would be the effect on water secretion of increased sodium levels reaching the collecting duct?

A

Increase osmolarity of tubular fluid by increasing sodium

Reduce gradient across membrane

Reduce amount of water that can be reabsorbed

33
Q

How are ACE inhibitors diuretics?

A

Reduced Na+ reuptake in the PCT
Reduced Na+ in the distal nephron
Reduced aldosterone indirect effects: decreased reuptake in collecting duct and increased Na in distal nephron
Increases vascular volume - decreases BP

34
Q

What are some other diuretics and their site of action

A 
Osmotic diuretics -PCT
Carbonic anhydrase inhbitors - PCT
Loop diuretics - thin limb
Thiazide diuretics - DCT
Potassium sparing - CD
35
Q

How do carbonic anhydrase inhibitors work?

A

reduced Na+ reuptake in the PCT
Increased Na+ in the distal nephron
Reduced water reabsorption

36
Q

What does carbonic anhydrase do?

A

Carbonic anhydrase activity leads to Na+ re-absorption and increased urinary acidity

37
Q

How do loop diuretics work?

A 
E.g. Furosemide
Triple transporter Inhibitors 
reduced Na+ reuptake in the LOH
Increased Na+ in the distal nephron
Reduced water reabsorption
38
Q

How do thiazide diuretics work?

A

reduced Na+ reuptake in the DCT
Increased Na+ in the distal nephron
Reduced water reabsorption

Increased Calcium reabsorption (sodium calcium antiporters) Pump Ca out reducing intracellular Ca conc
Increases gradient

39
Q

How do potassium sparing diuretics work?

A

Inhibitors of aldosterone function (e.g. spironolactone)

40
Q

What does extracellular postassium effect?

A

Excitable membranes

41
Q

What does high K+ result in?

A

depolarises membranes - action potentials, heart arrhythmias

42
Q

What does low K+ result in?

A

heart arrhythmias (asystole)

43
Q

What happens to K+ after a meal?

A

K+ absorption in gut
Increases plasma K+ conc.
Tissue uptake stimulated by INSULIN aldosterone and adrenaline

44
Q

How does insulin stimulate uptake of K+ into tissues?

A

Stimulate Na+/H+ exchanger
Increases sodium entering cells, increased intracellular sodium
To reduce intracellular sodium Na+/K+ ATPase used
Bring K+ in to cells

45
Q

What percentage of K+ is reabsorbed in the PCT?

A

67%

46
Q

What percentage of K+ is reabsorbed in the TAL?

A

20%

47
Q

What percentage of K+ is reabsorbed in the DCT?

A

10%-50%

48
Q

What percentage of K+ is reabsorbed in the CCD?

A

5%-30%

49
Q

Why is there a range of what percentage of K+ is reabsorbed?

A

Depends on plasma concentration

50
Q

What is hypokalemia?

A

one of most common electrolyte imbalances (seen in up to 20% of hospitalised patients)
low serum potassium

51
Q

What can cause hypokalemia?

A

Inadequate dietary intake (too much processed food)

Diuretics (due to increase tubular flow rates)

vomiting/diarrhoea

Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)

52
Q

What is hyperkalemia?

A

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

53
Q

What causes hyperkalemia?

A

Seen in response to K+ sparing diuretics

ACE inhibitors

Elderly

Severe diabetes

Kidney disesase

54
Q

what neurotransmitters regulate increased appetite for sodium

A

GABA and opioids

via lateral parabrachial nucleus

55
Q

what neurotransmitters regulate reduced appetite for sodium intake

A

serotonin and glutamate

via lateral parabrachial nucleus

56
Q

how is sodium intake/appetite regulated

A

centrally via lateral parabrachial nucleus

peripherally by taste buds

57
Q

how does angiotensin II cause aldosterone synthesis

A

upregulates aldosterone synthase enzyme in zona glomerulosa

58
Q

body response to volume expansion

A

increased Na excretion :
reduced sympathetic activity, reduced Na+ reuptake in PCT
reduced renin, so reduced angiotensin and aldosterone
increased ANP and BNP - GFR increased promoting excretion

59
Q

body response to volume contraction

A

increased Na+ reabsorption:
increased sympathetic activity - increased Na+ reuptake in PCT
increased renin so increased angiotensin and aldosterone
reduced ANP and BNP

brain also released ADH - more aquaporins in collecting duct for water reabsorption

Year 2 Uro (5 decks)

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