Sodium and Potassium Balance Flashcards

1
Q

What are the 3 effects of angiotensin II

A

Stimulate vasoconstriction of the vascular system to raise BP
Act on proximal convoluted tubule to increase Na+ reabsorption to increase BP
Stimulate adrenal cortex make aldosterone

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2
Q

What is aldosterone? Where is it made and released?

A

Steroid hormone

Synthesised and released from adrenal cortex

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3
Q

What is aldosterone synthesised in response to?

A

AG II
Decrease in BP via baro receptors
Decrease in osmolarity of ultrafiltrate

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4
Q

What does aldosterone stimulate?

A

Increased Na reabsorption
Increase K secretion
Increase H+ secretion

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5
Q

What does excess aldosterone do?

A

Lead to hypokalaemic alkalosis

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6
Q

What are the 3 main effects of aldosterone inside the cell?

A

Upregulate production of apical sodium transporters
Upregulate production of basolateral Na+/K+ ATPase
Upregulate regulatory proteins

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7
Q

What is hypoaldosteronism?

A

Less Na+ reabsorption in distal tubule
More Na+ lost in urine.
ECF volume falls
increased renin, angII and ADH

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8
Q

What are symptoms of hypoaldosteronism?

A

Dizziness
Low blood pressure
Salt cravings
Palpitations

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9
Q

What is hyperaldosteronism

A
Sodium reabsorption in distal nephron increased
Less Na lost in urine
ECF vol increase - hypertension
Less renin, ang II and ADH
more ANP and BNP
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10
Q

What are symptoms of hyperaldosteronism?

A

High blood pressure
Muscle weakness
Polyuria
Thirst

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11
Q

What is Liddle’s syndrome?

A

Inherited disease of high blood pressure due to a mutation meaning the aldosterone activated sodium channel always on
Leading to Na retention leading to hypertension

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12
Q

How to low pressure side of baroreceptors respond?

A

Responds to lower and higher pressures involving SNS (afferent brainstem fibres - sympathetic activity) and ADH in low pressures and ANP and BNP in high pressures

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13
Q

How do the high pressure side of baroreceptors respond?

A

Only to low pressures using SNS, ADH and renin release - renin only released from responses to low pressure in high pressure side

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14
Q

What is ANP?

A

Atrial natriuretic peptide ATP

Small peptide made in the atria, which also makes BNP

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15
Q

When is ANP released?

A

In response to atrial stretch

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16
Q

What are the actions of ANP?

A
  • Vasodilation of renal blood vessels - and other systemic
  • Inhibition of sodium reabsorption in PCT and CD
  • Inhibits release of renin (therefore aldosterone)
  • > to reduce blood pressure
17
Q

Give examples of diuretic drugs

A
  • Osmotic diuretics (glucose and mannitol)
  • Carbonic anhydrase inhibitors
  • Loop diuretics (furosemide)
  • Thiazides
  • K+ sparing diuretics (amiloride and spironalactone that prevent K+ loss in distal)
18
Q

What do amiloride and spironalatone do? (K+ sparing diuretics)

A

Amiloride - block Na channels

Spironolactone - aldosterone antagonist, inhibit activity of Na+ channel and Na/K ATPase

19
Q

What do thiazides do?

A

Block Na/Cl co transport

In distal convoluted tubule

20
Q

What do carbonic anhydrase inhibitors do?

A

Lead to Na+ reabsorption and increased urinary activity

Inhibit production of H+ in the PC tubular cells. Less H+ out, so less Na+ in, more sodium excreted

21
Q

What is the concentration of potassium intracellularly? Extracellularly?

A

Intracellular: 150 mmol/l
Extracellular: 3-5 mmol/l

22
Q

What does extracellular K+ have an effect on?

A

Excitable membranes of nerves and muscles
High K+: depolarises membranes - action potentials and heard arrhythmias
Low K+: heart arrhythmias (asystole)

23
Q

What happens to in regards to K+ after a meal?

A

K+ absorption
Plasma K+ conc increase
Insulin, aldosterone, adrenaline released - regulate tissue uptake

24
Q

What is K+ secretion stimulated by?

A
Increase in:
Plasma [K+]
Aldosterone
Tubular flow rate
Plasma pH
25
Q

What are causes of hypokalemia?

A

Diuretics due to increase in tubular flow rate
Surreptitious vomiting
Diarrhoea
Genetics (gitelman’s syndrome; mutation in Na/Cl transporter in distal nephron)

26
Q

What is gitelman’s syndrome?

A

mutation in Na/Cl transporter in distal nephron

cause hypokalemia

27
Q

Where is sodium reabsorbed?

A

65% in proximal convoluted tubule
25% in ascending loop of Henle
8% in distal convoluted tubule
2% in collecting duct

28
Q

How to decrease Na+ reabsorption

A
Atrial naturietic peptide
Changes diameter of afferent and efferent tubules
Reduces activity of PCT
Suppresses renin release in the JXA 
Reduces sodium reabsorption in CT
29
Q

What is the JXA

A

Juxtaglomerular apparatus

Which has granular cells that produce renin

30
Q

What do loop diuretics do? (furosemide)

A

Block the triple transporter in ascending limb of loop of henle -
Stop Na+ reabsorption in tubular fluid
Prevent Na+ entering interstitial space
MOST POTENT affect up to 25% of filtered load

31
Q

Where in the nephron is K+ absorbed?

A
30% in PCT
10% in thin ascending loop of loH
10% in DCT
1-80% in CD
amount released as urine really varies
32
Q

What affect does aldosterone have on potassium?

A

Stimulates uptake of K+ in principle cells (apical K+ transporter stimulated)
Apical Na+ transporter also stimulated
Basolateral sodium/potassium ATPase

33
Q

How does tubular flow stimulate K+ release/excretion

A
Cells in collecting tubules have cilia. Flow increases
Cilia stimulate PDK1
Cascade system
Increase intracellular Ca2+ 
Activate apical potassium channels 
Release more potassium
34
Q

How is potassium secreted? (mediated by? coupled with?)

A

Secretion mediated by Na+/K+ ATPase and is coupled with Na+ absorption in the blood

35
Q

What can cause hyperkalemia?

A

In response to K+ sparing diuretics, which prevents K+ secretion when it’s needed
ACE inhibitors
Elderly

36
Q

Where are baroreceptors found?

A
Heart
- atria low pressure
- right ventricle low pressure
Vascular system
- pulmonary vasc low pressure
- carotid sinus high pressure
- aortic arch high pressure
- JGA high pressure
37
Q

How much potassium is filtered and excreted daily?

A

Filtered 10mEq/Kg/day

15% excreted by kidneys

38
Q

What mediates K+ uptake into cells after a meal?

A

Insulin

Sodium/potassium ATPase uptake into cells