Control Of Potassium Flashcards

1
Q

Where is most potassium?

A

Inside cells (98% of K) -mostly in skeletal muscles

[K+] = 120-150mmol/L

ECF = only 2% (3-5mmol/L)

This means that a shift of 1% of ICF K+ to ECF would raise ECF [K+] by 50%.

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2
Q

How is the difference between ECF and ICF maintained?

A

NaKATPase - maintaining it is critical

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3
Q

Why is maintaining ECF [K+] so critical?

A

Because of its effect on the resting membrane potential.

Hence its effect on excitability of cardiac tissue.

Hence the risk of life threatening arrhythmias with hyperkalaemia and hypokalaemia

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4
Q

How is ECF K+ regulated?

A

Immediate control - by internal balance - moves K+ between ECF and ICF

Longer term, overall K+ balance - by external balance (match input with output) adjusting renal secretions.

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5
Q

List some foods that are rich in potassium

A
Raisins 
Honey dew melon 
Banana 
Orange 
Tomato 
Potato chips 
Baked potato 
Milk
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6
Q

How does your body control potassium following a meal?

A

The intestines and colon absorb dietary K+ - This means ECF K+ will increase a little bit.

BUT, 4/5th moves into cells within minutes to stop [K+] increasing my too much.

After a slight delay kidneys begin to excrete K+ -excretion is complete in 6-12 hours.

New research also suggest that the gut has some influence in controlling after meal K+ secretion

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7
Q

How does potassium enter and leave cells?

A

Internal balance is the net result of the movement of K+ into and out of cells.

K+ moves from ECF into cells via NaKATPase

K+ moves out of cells into ECF via K+ channels (channels which determine the K+ permeability of the cell membrane)

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8
Q

What factors increase the K+ uptake by cells?

A

Hormones

  • Insulin (rises anyway with a meal)
  • Aldosterone (secreted from suprarenal gland -stimulated by RAAS)
  • Catecholamines (B2 agonist)

Increased [K+] in ECF

Alkalosis pH - low ECF [H+] - K+ shift into cells.

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9
Q

What factors provost the K+ shift out of cells?

A

Exercise

Cel lysis

Increase in ECF osmolality (e.g. diabetes)

Low ECF [K+]

Acidosis - increase in ECF [H+] camisoles a K+ shift and movement out of the cells.

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10
Q

How does insulin cause an increase in K+ uptake?

A

K+ in splanchnic blood stimulates insulin secretion by pancreas

Insulin increases Na-K-ATPase activity - increases K+ uptake by muscle cells and liver.

I.V insulin + Dextrose is used to treat hyperkalaemia

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11
Q

How does aldosterone cause an increase in K+ uptake?

A

K+ in blood stimulates aldosterone secretion which stimulates the uptake of K+ via NaKATPase.

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12
Q

How do catecholamines stimulate the uptake of K+?

A

Act via B2 adrenoreceptors which stimulate Na-K-ATPase and cellular uptake of K+

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13
Q

What happens to the K+ concentration in exercise?

A

Net release of K+ during recovery phase of action potential, K+ exits the cell.

Also skeletal muscle damage during exercise releases K+.

This means that the increase plasma [K+] is proportional to the intensity of the exercise.

Uptake by non-contracting tissues prevents dangerously high hyperkalaemia.

Exercise and trauma also increases catecholamines, high offset ECF [K+] rise by increasing K+ uptake by other cells.

Cessation of exercise results in a rapid decrease in plasma [K+], often to under 3mmol/L.

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14
Q

How does acidosis lead to hyperkalaemia?

A

In acidosis, H+ shift into cells and there is a reciprocal shift of K+ out of the cells.

The opposite can occur and hyperkalaemia can cause acidosis.

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15
Q

How does alkalosis lead to hypokalaemia?

A

Alkalosis causes a shift of H+ out of the cells.

This means there is a reciprocal shift of K+ Ito the cells.

The opposite can occur and hypokalaemia can cause alkalosis.

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16
Q

Where abouts in the nephron is potassium mainly regulated?

A

Late distal tubule an cortical collecting duct

17
Q

How does the kidney handle potassium?

A

Most of the K+ is reabsorbed.

  • 67% in PCT
  • 20% in Thick ascending limb of LoH
  • Rest in DT and collecting duct

Some K+ is secreted into the distal tubule and cortical collecting duct - this can be varied and controlled so it is this K that will appear in the urine and not that which is reabsorbed.

18
Q

How will K+ reabsorbtion / secretion change if you have a low K+ diet?

A

The reabsorbtion mainly stays the same.

The secretion in the principle cells of DCT and cortical collecting duct will be minimised.

19
Q

How is K+ secreted in the distal tubule and collecting duct?

A

It is secreted by principle cells.

NaKATPase activity in the basolateral membrane increase [K+] and decrease [Na+].

High intracellular K+ creates a chemical gradient for secretion.

Na+ moves from lumen into cell down its concentration gradient (via apical ENaC) creating an electrical gradient.

Together create a favourable electrochemical gradient for K+ secretion via apical K+ channels.

20
Q

What tubular factors affect K+ secretion by principle cells?

A

ECF [K+]

  • Directly stimulates NaKATPase and increases permeability of apical K+ channels.
  • Also stimulates aldosterone secretion
Aldosterone 
-Increases: 
transcription of relevant proteins 
K+ channels 
ENaC in apical membrane 

Acid base status
-Acidosis - decreases K+ secretion, inhibits NaKATPase and decrease K+ channel permeability. Alkalosis does the opposite.

21
Q

What luminal factors affect K+ secretion by principle cells?

A

Increased distal tubular flow rate - washes away luminal K+ and increases K+ loss.

Increases Na delivery to distal tubule - more Na absorbed which results in more Na absorbed and therefore more K+ loss. (E.g. diuretic - ferosimide bocks Na absorption in thcika spending limb so more available downstream)

22
Q

What cells absorb K+ in the DT and CD?

A

Intercalated cells.

This is an active process that is mediated by the HKATPase in the apical membrane.

23
Q

What are some of the effects of changes in ECF [K+]?

A

Alter cell membrane resting potential

Alter neuro muscular excitability

  • Problems with cardiac conduction and pacemaker automaticity
  • Alter neuronal function
  • Alter skeletal muscle function
  • Alter smooth muscle function

Results in arrhythmias, cardiac arrest, muscle paralysis.

BUT, usually pick it up quite late so need to know situations that this is likely to occur.

24
Q

What could cause hyperkalaemia?

A

Increased intake (unlikely) - only if renal dysfunction is also present. Unless inappropriate dose of IV K+

Decreased renal excretion (more likely)

  • Acute of chronic kidney injury
  • Drugs that block K+ excretion (most frequent) - ACE inhibitors, K+ sparing diuretics
  • Low aldosterone state (addison’s disease).

Also internal shift.

25
Q

What could cause an internal shift in K+ (Start leaving cells)?

A

Diabetic ketoacidosis
-No insulin and plasma hyperosmolarity and metabolic acidosis

Cell lysis
-Muscle crush injury , tumour cell lysis

Metabolic acidosis

Exercise

26
Q

What are the clinical features of hyperkalaemia?

A

Heart - altered excitability (arrhythmias, heart block)

GI - neuromuscular dysfunction, paralytic lieus

Acidosis

27
Q

Describe the ECG of hyperkalaemia

A

7mmol/L - High T wave

8mmol/L - Prolonged PR interval, depressed ST segment, high T wave

9mmol/L - Atrial standstill (no P waves), intraventricular block

10mmol/L - Ventricular fibrillation

28
Q

How do you treat hyperkalaemia (short term)?

A
  1. IV calcium gluconate to prevent arrhythmias (works immediately for half an hour)
  2. IV glucoses and insulin (works in about 30 mins) pushes K+ back into cells.
    Also give nebuliser beta agonist (salbultamol)
    -Lasts 3-4 hours
  3. Dialysis to remove express K+
29
Q

How do you treat hyperkalaemia (long term)?

A
  1. Treat cause - stop meds, treat DKA
  2. Reduce K+ intake
  3. Measures to remove excess K+ -Dialisis or oral K+ biding resins to bind K+ in gut.
30
Q

What could cause hypokalaemia?

A
  1. External balance
    -Excessive loss
    GI - diarrhoea/ vomiting / bulimia
    Renal losses of K+ - Diuretics, osmotic diuresis (diabetes), high aldosterone levels.
  2. Problems with internal balance - shift of K+ into ICF e.g. metabolic alkalosis.
31
Q

What are the clinical features of hypokalaemia?

A
  1. Heart - altered excitability causing arrhythmias.
  2. GI - neuromuscular dysfunction causing paralytic lieus (more likely in low than high K)
  3. Skeletal muscle - neuromuscular dysfunction causing muscle weakness.
  4. Renal - unresponsive to ADH - nephrogenic DI (polyuria and polydipsia).
32
Q

What ECG changes occur in hypokalaemia?

A

3.5 - low T ave

3 - low T wave, high U wave

2.5 - Low T wave, high U wave, Low ST segment.

33
Q

How do you treat hypokalaemia?

A

Treat cause

Potassium replacement - IV / oral

If due to increased mineralcorticoid activity - K sparing diuretics which block the action of aldosterone on principle cells.