Sodium and Potassium Flashcards

(59 cards)

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
Where are the low pressure baroreceptors?
Atria Right ventricle Pulmonary vasculature
26
Where are the high pressure baroreceptors?
Carotid sinus Aortic arch Juxtaglomerular apparatus
27
What is the low pressure side response to low pressure?
Reduced baroreceptor firing Signal through Afferent fibres to the brainstem Sympathetic activity ADH release
28
What is the low pressure side response to high pressure?
Atrial stretch ANP, BNP released
29
What is the high pressure side response to low pressure?
Reduced baroreceptor firing Signal through Afferent fibres to the brainstem Sympathetic activity ADH release JGA cells - renin released
30
What is ANP?
Small peptide made in the atria (also make BNP) | Released in response to atrial stretch (i.e. high blood pressure)
31
What are the actions of ANP?
- 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
What would be the effect on water secretion of increased sodium levels reaching the collecting duct?
Increase osmolarity of tubular fluid by increasing sodium Reduce gradient across membrane Reduce amount of water that can be reabsorbed
33
How are ACE inhibitors diuretics?
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
What are some other diuretics and their site of action
``` Osmotic diuretics -PCT Carbonic anhydrase inhbitors - PCT Loop diuretics - thin limb Thiazide diuretics - DCT Potassium sparing - CD ```
35
How do carbonic anhydrase inhibitors work?
reduced Na+ reuptake in the PCT Increased Na+ in the distal nephron Reduced water reabsorption
36
What does carbonic anhydrase do?
Carbonic anhydrase activity leads to Na+ re-absorption and increased urinary acidity
37
How do loop diuretics work?
``` E.g. Furosemide Triple transporter Inhibitors reduced Na+ reuptake in the LOH Increased Na+ in the distal nephron Reduced water reabsorption ```
38
How do thiazide diuretics work?
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
How do potassium sparing diuretics work?
Inhibitors of aldosterone function (e.g. spironolactone)
40
What does extracellular postassium effect?
Excitable membranes
41
What does high K+ result in?
depolarises membranes - action potentials, heart arrhythmias
42
What does low K+ result in?
heart arrhythmias (asystole)
43
What happens to K+ after a meal?
K+ absorption in gut Increases plasma K+ conc. Tissue uptake stimulated by INSULIN aldosterone and adrenaline
44
How does insulin stimulate uptake of K+ into tissues?
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
What percentage of K+ is reabsorbed in the PCT?
67%
46
What percentage of K+ is reabsorbed in the TAL?
20%
47
What percentage of K+ is reabsorbed in the DCT?
10%-50%
48
What percentage of K+ is reabsorbed in the CCD?
5%-30%
49
Why is there a range of what percentage of K+ is reabsorbed?
Depends on plasma concentration
50
What is hypokalemia?
one of most common electrolyte imbalances (seen in up to 20% of hospitalised patients) low serum potassium
51
What can cause hypokalemia?
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
What is hyperkalemia?
Common electrolyte imbalance present in 1-10% of hospitalised patients high serum potassium
53
What causes hyperkalemia?
Seen in response to K+ sparing diuretics ACE inhibitors Elderly Severe diabetes Kidney disesase
54
what neurotransmitters regulate increased appetite for sodium
GABA and opioids | via lateral parabrachial nucleus
55
what neurotransmitters regulate reduced appetite for sodium intake
serotonin and glutamate | via lateral parabrachial nucleus
56
how is sodium intake/appetite regulated
centrally via lateral parabrachial nucleus | peripherally by taste buds
57
how does angiotensin II cause aldosterone synthesis
upregulates aldosterone synthase enzyme in zona glomerulosa
58
body response to volume expansion
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
body response to volume contraction
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