Potassium control Flashcards

1
Q

Describe the distribution of potassium in the body. (2)

A

98% ICF, 2% ECF. Mainly stored in skeletal muscle cells, but also liver RBC bone.

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2
Q

Explain how and why the body maintains [K+]e. (2)

A

Through the Na+/K+ ATPase.
Maintained because hypo- or hyperkalaemia can have drastic effects on the resting membrane potential, and the excitability of cardiac tissue.

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3
Q

Describe the internal balance of potassium. (2)

A

Normally there’s a balance between the electrical gradient for positive potassium to enter the negative cell, and the chemical gradient of low [K+]e for K+ to leave the cell.

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4
Q

Describe how [K+]e is regulated. (2)

A

Short term - internal balance changes - moves K+ from ECF to ICF.
Long term - external balance changes - changes in renal excretion.

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5
Q

Explain 5 things that increase [K+]i. (10)

A

Insulin - K+ in splanchnic blood stimulates insulin secretion, which increases Na+/K+ activity, increases K+ uptake into cells, increases [K+]i. (This is why insulin + dextrose is a treatment for hyperkalaemia).
Aldosterone - K+ in blood stimulates aldosterone secretion, increases Na+/K+ activity, increases K+ uptake into cells, increases [K+]i.
Catecholamines - stimulates B2 adrenoceptors, which increases Na+/K+ activity, increases K+ uptake into cells, increases [K+]i.
High [K+]e - increased concentration gradient leading to more diffusion, which increases K+ uptake into cells, increases [K+]i.
Alkalosis - low [H+] drives K+ into cells.

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6
Q

Explain 4 things that decrease [K+]i. (8)

A

Exercise and cell lysis - net release of [K+] from within the cell during recovery phase of action potential. Cell lysis from muscle damage also releases all of the [K+]i. (Catelochamines are also released in exercise to offset this change).
Increase in ECF osmolarity eg in diabetes - water moves out of cells, lowers concentration of [K+]e, so K+ moves out of cell.
Low [K+] in the ECF.
Acidosis - high [H+] in ECF drives K+ out of cells.

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7
Q

Explain the relationship between acid base disturbances and internal balance of potassium. (8)

A

Acidosis - too much H+ in ECF - H+ moves into cells - reciprocal K+ shift out of cells - hyperkalaemia.
Alkalosis - too little H+ in ECF - H+ moves out of cells - recirpocal K+ shift into cells - hypokalaemia.
Hyperkalaemia - shift of K+ into cells - reciprocal H+ shift out of cells - acidosis.
Hypokalaemia - shift of K+ out of cells - reciprocal H+ shift into cells - alkalosis.

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8
Q

Describe external K+ balance. (3)

A

Control of the total body potassium over the long term. Regulates K+ secretion into the late DT and collecting duct. Slower - 6-12 hours. Secreted K+ can be 15-120% of filtered amount.

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9
Q

Describe 5 factors affecting K+ secretion into the lumen. (5)

A

Tubular features
High [K+]e - directly stimulates Na+/K+ ATPase and stimulates aldosterone. Increases loss.
Aldosterone - increased translation of proteins like Na+/K+ ATPase, ENaC, and K+ channels. Increases loss.
Acid base status - acidosis decreases K+ secretion, alkalosis increases K+ secretion.

Luminal factors
Increased flow rate - increases loss because K+ is washed away.
Increased Na+ delivery - more Na+ reabsorbed = more K+ lost.

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10
Q

Describe the clinical causes of hyperkalaemia (5)

A

Inappropriate IV K+.
Drugs that increase K+ retention (ACE inhibitors and K+ sparing diuretics)
Diabetic ketoacidosis - acidosis and reduced insulin.
Cell lysis due to trauma.
Metabolic acidosis
Exercise.

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11
Q

Describe the clinical features of hyperkalaemia. (4)

A

Reduced excitability of cardiac muscle leading to arrhythmia sand heart block.
Paralytic ileus
Acidosis
ECG changes - high T wave, depressed ST segement - ventricular fibrillation.

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12
Q

Describe the emergent treatment of hyperkalaemia. (3)

A

Calcium gluconate - Reduce K+ effect on the heart.
IV glucose and insulin to shift K+ into cells.
Dialise excess K+.

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13
Q

Describe the long term treatment of hyperkalaemia. (3)

A

Treat cause - stop medication, treat DKA.
Reduce intake.
Measures to remove excess K+ - dialysis, oral binding drugs.

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14
Q

Describe the causes of hypokalaemia. (2)

A

Excessive loss - GI (D+V) or renal (diuretics, osmotic diuresis).
Things that shift K+ into cells (metabolic alkalosis).

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15
Q

Describe the clinical features of hypokalaemia. (6)

A

Heart - raised excitability leading to arrhythmias because more Na+ channels remain open.
Paralytic ileus.
Muscle weakness
Nephrogenic diabetes insipidus due to unresponsive ness to ADH.
ECG - low T wave, high U wave, low ST segment.

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16
Q

Describe the treatment of hypokalaemia. (3)

A

Treat the cause.
Potassium replacement.
K+ sparing diuretics.