Sodium and Potassium Balance Flashcards

(38 cards)

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
What are causes of hypokalemia?
Diuretics due to increase in tubular flow rate Surreptitious vomiting Diarrhoea Genetics (gitelman's syndrome; mutation in Na/Cl transporter in distal nephron)
26
What is gitelman's syndrome?
mutation in Na/Cl transporter in distal nephron | cause hypokalemia
27
Where is sodium reabsorbed?
65% in proximal convoluted tubule 25% in ascending loop of Henle 8% in distal convoluted tubule 2% in collecting duct
28
How to decrease Na+ reabsorption
``` 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
What is the JXA
Juxtaglomerular apparatus | Which has granular cells that produce renin
30
What do loop diuretics do? (furosemide)
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
Where in the nephron is K+ absorbed?
``` 30% in PCT 10% in thin ascending loop of loH 10% in DCT 1-80% in CD amount released as urine really varies ```
32
What affect does aldosterone have on potassium?
Stimulates uptake of K+ in principle cells (apical K+ transporter stimulated) Apical Na+ transporter also stimulated Basolateral sodium/potassium ATPase
33
How does tubular flow stimulate K+ release/excretion
``` Cells in collecting tubules have cilia. Flow increases Cilia stimulate PDK1 Cascade system Increase intracellular Ca2+ Activate apical potassium channels Release more potassium ```
34
How is potassium secreted? (mediated by? coupled with?)
Secretion mediated by Na+/K+ ATPase and is coupled with Na+ absorption in the blood
35
What can cause hyperkalemia?
In response to K+ sparing diuretics, which prevents K+ secretion when it's needed ACE inhibitors Elderly
36
Where are baroreceptors found?
``` 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
How much potassium is filtered and excreted daily?
Filtered 10mEq/Kg/day | 15% excreted by kidneys
38
What mediates K+ uptake into cells after a meal?
Insulin | Sodium/potassium ATPase uptake into cells