Potassium Balance Flashcards

1
Q

What proportion of potassium is intracellular?

A

95%

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2
Q

What is the internal [K+]?

A

150 mmol/L

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3
Q

What is the external [K+]?

A

4.5 mmol/L

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4
Q

What is internal potassium balance under the influence of?

A

Insulin, adrenaline, pH and aldosterone

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5
Q

How do we get potassium into our bodies?

A

Diet

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6
Q

How do we remove potassium from our diet?

A

Urine, stools, sweat

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7
Q

What is the external potassium balance influenced by?

A

Intake and output

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8
Q

What are the two types of potassium regulation?

A

Acute and chronic

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9
Q

What does acute potassium regulation deal with?

A

Distribution of potassium between intra and extracellular fluid compartments (internal balance)

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10
Q

How is chronic potassium regulation achieved?

A

By the kidney adjusting potassium excretion and reabsorption (external balance)

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11
Q

What are the functions of potassium in the body?

A

Determines intracellular fluid osmolality, resting membrane potential and affects vascular resistance

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12
Q

What does the sodium potassium ATPase do in terms of ion concentrations?

A

High intracellular [K+] and low intracellular [Na+]

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13
Q

What is the threshold for hyperkalaemia?

A

Plasma [K+]> 5.5mm

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14
Q

What is the threshold for hypokalaemia?

A

Plasma [K+]<3.5mm

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15
Q

What is the definition of a resting membrane potential?

A

Membrane potential formed by creation of ionic gradients (combination of electrical and chemical gradients)

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16
Q

What changes to an ECG do you see in hypokalaemia?

A

Decreased T wave amplitude, long Q-U interval and prolonged P wave

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17
Q

What changes to an ECG do you see in hyperkalaemia?

A

Increased QRS complex, increased T wave amplitude and eventual loss of P-wave

18
Q

What happens to the resting potential at low [K+]o?

A

Hyperpolarisation- less excitable as further from threshold point

19
Q

What happens to the resting potential at high [K+]o?

A

Depolarisation (closer to threshold) - more excitable

20
Q

What is hypokalaemia caused by?

A
  • extensive diuretic use
  • hyperaldosteronism
  • prolonged vomiting
  • profuse diarrhoea
21
Q

How does prolonged vomiting -> hypokalaemia?

A

Sodium loss -> inc aldosterone secretion -> potassium excretion in kidneys

22
Q

What does hypokalaemia result in?

A

Decreased resting membrane potential and a decreased release of adrenaline, aldosterone and insulin

23
Q

When is acute hyperkalaemia normal?

A

Prolonged exercise

24
Q

What can cause hyperkalaemia?

A
  • insufficient renal excretion
  • increased release from damaged body cells
  • long term use of potassium sparing diuretics
  • Addison’s disease
25
Q

What types of damaged cells release potassium?

A

Chemo, long lasting hunger, prolonged exercise or severe burns

26
Q

What happens if plasma [K+] >7mm?

A

Life threatening as leads to systolic cardiac arrest

27
Q

What mechanisms are used to drive potassium back into cells?

A

Insulin/ glucose infusion and aldosterone and adrenaline stimulate the sodium potassium pump

28
Q

How can CVD treatments lead to hyperkalaemia?

A

Beta blockers and ACE inhibitors increase serum potassium levels

Loop diuretics result in net potassium loss

29
Q

How does potassium concentration change in the proximal convoluted tubule?

A

Potassium ions are reabsorbed passively between cells

30
Q

How is potassium reabsorbed in the loop of henle?

A

SGLT2 transporters transport sodium, chloride and potassium

31
Q

What determines potassium secretion in the distal convoluted tubule?

A

Increased potassium intake, changes in blood pH

32
Q

How does increased plasma [K+] increase potassium secretion?

A
  • Slows exit from basolateral membrane
  • Increased activity of sodium potassium ATPase
  • stimulates aldosterone secretion
33
Q

What is the major regulator of potassium balance in the body?

A

Aldosterone

34
Q

How does aldosterone affect potassium concentration?

A

Increased plasma aldosterone -> cortical collecting ducts increasing potassium excretion

35
Q

What does aldosterone act to do?

A

Increase Na+/K+ ATPase pump
Increase ENaC channels
Redistribute ENaC from intracellular localisation to membrane
Increased permeability of luminal membrane

36
Q

What happens to potassium conc in alkalosis?

A

Sodium potassium ATPase Increased so cellular K+ conc is increased -> more K+ secretion and more sodium is taken into epithelial cells

37
Q

What happens to potassium conc in acidosis?

A

Inhibition of sodium potassium ATPase so less potassium in and so less it secreted

38
Q

What is an increased flow rate in the nephron caused by?

A

Increased GFR, inhibition of reabsorption or potassium wasting diuretics

39
Q

What happens to potassium concentration when ADH increases?

A

Increased potassium channel activity so increased secretion and therefore decreased cellular potassium concentration

40
Q

Where is potassium reabsorbed in severe hypokalaemia?

A

Alpha intercalated cells or the late distal convoluted tubule is active

41
Q

What effect does increased aldosterone have on potassium concentration?

A

Increased potassium secretion

42
Q

What effect does increased sodium reabsorption have on potassium concentration?

A

Decreased flow rate in the tubules so less potassium secretion so increased potassium concentration