Potassium Balance Flashcards

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1
Q

What are the most prevalent cations in body fluids?

A

→ Na+ and K+

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2
Q

Where is potassium found?

A

→ in leafy vegetables
→ Most fruit and juice
→ potatoes

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3
Q

What is the intra and extracellular concentration of potassium?

A

→ I : 150mmol/L

→E : 4.5 mmmol/L

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4
Q

What cell types have the most potassium?

A

→ Muscle cells

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5
Q

What is the internal potassium balance maintained by?

A

→ Insulin
→ Adrenaline
→ pH
→ Aldosterone

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6
Q

What is the external potassium balance maintained by?

A

Input
→Diet

Output
→ urine & stools
→ sweat

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7
Q

What is acute regulation of K+?

A

→The distribution of K+ through ICF and ECF compartments

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8
Q

What is chronic regulation of K+?

A

→ Kidney adjusting K+ excretion + reabsorption

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9
Q

What are the 2 functions of K+?

A
  1. Determines ICF osmolality
  2. Determines resting membrane potential
  3. Affects vascular resistance
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10
Q

What does the sodium/potassium pump do?

A

→ Na+ ions are pumped out of the cell
→ K+ pumped into the cell
→ energy driving the pump is released by ATP hydrolysis

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11
Q

What happens to K+ concentration after a meal?

A

→ Increase in plasma K+

→ shifted into ICF compartment

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12
Q

What hormones is the ICF K+ shift due to?

A

→ insulin
→ adrenaline
→ aldosterone
→ pH changes

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13
Q

What is hyperkalaemia defined as?

A

→ plasma K+ is above 5.5 mM

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14
Q

What is hypokalaemia defined as?

A

→ plasma K+ is below 3.5 mM

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15
Q

What is resting potential formed from?

A

→ ionic gradients

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16
Q

What is the normal distribution between IC and EC K+?

A

→ External - 3.5 mM

→ Internal - 140 mM

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17
Q

What happens to the equilibrium potential when you have hyperkalaemia?

A

→ Less negative

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18
Q

What happens to the equilibrium potential when you have hypokalaemia?

A

→ More negative

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19
Q

What happens during hyperpolarization (less K+) ?

A

→ more negative voltage across the membrane
→ Decreased excitability of neurons
→Longer to reach threshold
→ Longer to reach action potential

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20
Q

What happens during depolarization (more K+)?

A

→ Less negative voltage
→ Threshold is approached quicker
→ Increased excitability

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21
Q

What is hypokalaemia caused by?

A

→ Renal or extra renal loss of K+

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22
Q

What are causes of hypokalaemia?

A

→ Diuretics without KCl
→ Hyperaldosteronism ( Conn’s syndrome)
→ Prolonged vomiting (Increased aldosterone secretion)
→ Profuse diarrhoea

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23
Q

What does hypokalaemia result in?

A

→ Decrease adrenaline, aldosterone and insulin

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24
Q

What is hyperkalaemia caused by?

A

→ Prolonged exercise

→ Kidneys excrete K+ easily

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25
What are disease states that cause hyperkalaemia?
→ Insufficient renal excretion → Increased release from damage body cells → Long term use of potassium sparing diuretics → Addisons disease
26
What happens if plasma K+ is above 6.5 mM?
→ Systolic cardiac arrest
27
What is used to drive K+ into the cells?
→ Insulin/glucose infusion
28
What hormones stimulate the Na+-K+ pump?
→ Aldosterone | → Adrenaline
29
What is external balance of K+ regulated by?
→ the kidneys
30
What are human kidneys designed to do?
→ Conserve Na+ and excrete K+
31
What drugs raise serum K+ levels?
→ B blockers | → ACE inhibitoris
32
What drug causes hypokalaemia?
→ loop diuretics
33
Why do the plasma and glomerular fluid have the same concentration?
→ Na+ and K+ are freely filtered at the glomeruli
34
How is K+ maintained at high levels within the kidney cells?
→ Sodium travels from the tubular lumen to the ECF bringing glucose and AA with it →the Na+ and K+ pump maintains this on the basolateral side → Maintains K+ at high levels in the kidney cells
35
How do Na+ and K+ move in the loop of henle?
→Active reabsorption/pumping of Na+ & Cl- out of the fluid into the medulla →done via a Na+/2Cl-/K+ symporter on the luminal membrane →driven by the [Na+] gradient from lumen-cell. →You also have entry of Na+ from Na+-H+ antiporter →On the basolateral side you have a Na+/K+ ATPase pump and co-transport of Cl- & K+ out of the cell (especially in the thick ascending limb).
36
Where is 90% of the potassium reabsorbed?
→ PCT and loop of henle
37
What is excretion of K+ into urine controlled by?
→ secretion in principal cells of late DCT and CD
38
How do you get the K+ to go into the urine in the DCT?
→ eNAC channels are present on the luminal side → activated by aldosterone → as Na+ enters the cell it changes the electrical potential on the luminal side → allow K+ to be secreted out → there are K+/Cl- symporters that pump K+ out
39
What inhibits eNAC channels?
→ diuretics
40
What determines K+ secretion in the DCT?
→ Increased K+ intake | → Changes in blood pH
41
What happens to K+ during alkalosis?
→ Increased excretion of K+ | → Decreased serum K+
42
What happens to K+ during acidosis?
→ Decreased excretion of K+ | → Increased serum K+
43
What causes the switch between secretion and absorption?
→ Activity of Na+ / K+ pump → Electrochemical gradient → Permeability of luminal membrane channel
44
What effect does aldosterone have on the Na+/ K+ pump?
→ Increase K+ influx → Increase intracellular potassium → increase cell-lumen concentration gradient
45
What is the major regulator of K+ balance?
→ aldosterone
46
What effect does aldosterone have on the eNAC channels?
``` → More eNAC channels → Increased Na+ reabsorption → Decreased cell negativity → Increased lumen negativity → Increase voltage gradient ```
47
What does aldosterone do to the luminal membrane?
→ Makes it more permeable to K+
48
How does an increase in plasma K+ increase K+ secretion?
→ Slows exit from basolateral membrane → Increases concentration gradient towards urine → Increases activity of Na+/K+ ATPase → Stimulates aldosterone secretion
49
Flow chart for what happens during increased K+ intake
``` Increased K+ intake ↓ Increased plasma K+ ↓ Increased aldosterone secretion from adrenal cortex ↓ Increased plasma aldosterone ↓ Increased K+ secretion from cortical collecting ducts ↓ Increased K+ secretion ```
50
How is K+ secreted during alkalosis?
→ Increased activity of Na+/K+ pump and increased K+ in the cell → Favours the concentration gradient for K+ secretion → Increase in tubular fluid pH → increases permeability of luminal membrane
51
How is K+ secreted during acute acidosis?
→ increase in H+ of ECF reduces the activity of the Na+/K+ ATPase pump → Decreases intracellular K+ → reduces passive diffusion of K+
52
What does an increase in tubule fluid flow rate result from?
→ increased GFR or inhibition of reabsorption upstream or diuretics
53
What does an increase in tubule fluid flow rate result in?
→ sweeping away of K+ → makes tubular K+ low → more rapid rate of net secretion
54
What does anti diuretic hormone do?
→ Stimulates K+ secretion by increasing the conductance of the luminal membrane
55
Where does reabsorption of K+ occur in severe hypokalaemia?
→ alpha intercalated cells of late DCT | → K+/H+ pump
56
Flow chart for when ECFV decreases
Adrenal cortex increases aldosterone secretion and proximal tubule increases Na+ reabsorption ↓ tubules decrease flow rate ↓ cortical collecting ducts increase K+ secretion (aldosterone) and decrease K+ secretion (flow rate) ↓ K+ unchanged
57
How does the RAAS system regulate sodium and BP?
→ JGA senses a fall in BP → Macula densa detects low Na+ in the DCT → Renin is released from JGA → Angiotensin II → Causes vasoconstriction and stimulates adrenal cortex
58
How does aldosterone restore BP?
→ Acts on DCT to increase Na+ reabsorption → Increases activity and inserts more Na+/K+ ATPase pumps → Na+ ions bring water with them via osmosis
59
How is renin release suppressed?
→ suppressed by -ve feedback with angiotensin II
60
How does aldosterone increase serum pH?
→ Acts on intercalated cells → Increase activity of Na+, H+ antiporter and influences acid- base status → Increases H+ secretion
61
What factors shift K+ into cells?
→ Insulin → Aldosterone → Beta adrenergic stimulation → Alkalosis
62
What factors shift K+ out of cells?
``` → Insulin deficiency → Aldosterone deficiency → Beta adrenergic blockade → Acidosis → Cell lysis → Strenuous exercise → Increased ECF osmolarity ```
63
What does the adrenal cortex produce?
→ Gluco corticoid hormones → Mineralocorticoud hormones →Sex hormones
64
What is primary adrenal insufficiency / Addisons?
→ Damage to cortex → Decreased hormone production → numerous symptoms
65
What is a result of a deficiency in aldosterone?
→ Secretion of large amounts of Na+ → Low serum Na+ levels → Body retains K+
66
What is the treatment of addisons?
→ Treatment usually involves corticosteroid replacement for life
67
What is secondary adrenal insufficiency?
→ pituitary secretes less ACTH → Decrease cortisol → Adrenal glands shrink
68
What is hyperaldersteronism/Conns syndrome?
→ excess release of aldosterone → due to tumor → Aldosterone release without angiotensin II
69
What does an increase in plasma aldosterone mean?
→ Kidneys to stimulate Na+ reabsorption and K+ excretion → increase BP and Na delivery to macula densa → decrease release of renin → Increase fluid volume → Hypokalaemia, hypernatremia and alkalosis
70
What is the treatment for Conns syndrome?
→ surgical removal of tumor containing adrenal gland | → Hypertension and hyperkalaemia