Control of Potassium Flashcards

1
Q

What percentage of potasium is found in the ICF as opposed to the ECF?

A

98% of potassium Is found inside the cells at about 120-150mmol/l. The other 2% is found in the ECF.

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2
Q

Which cells of the body contain most of the potassium

A

The majority of potassium in the ICF is found in skeletal muscle cells but also in liver, red blood and bone. If there is a shift of just 1% into the ECF from the ICF the concentration will rise by 50%.

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3
Q

Why can we assume serum potassium is the same as ECF potassium?

A

Because potassium travels freely across capillary walls

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4
Q

Why is maintaining potassium concentrations important?

A

Maintaining [K] is important because of its effects on the resting membrane potential and hence its effects on excitability of cardiac tissues. Changes in [K] risk life threatening arrhythmias with both hyperkalaemia and hypokalaemia.

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5
Q

What would occur if the ECF concentration were to increase/decrease?

A

If ECF [K] increases then this would cause depolarisation of the resting membrane potential of the cell. This is vice versa for if the ECF were to decrease.

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6
Q

How are potassium levels controlled?

A

Immediate control of K+ is done through maintaining the internal balance by moving K+ between ECF and ICF. Longer term control takes place via adjusting K+ renal excretion.

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7
Q

What happens after eating a meal with high amounts of potassium in?

A

4/5ths of this K moves directly into cells within minutes. After a slight delay the kidneys begin to excrete more K+ and this is completed within 6-12 hours, this is stimulated by changes in potassium plasma levels but also by signals from the gut.

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8
Q

What increases the K+ uptake by cells?

A
  • Hormones such as: insulin (directly stimulated by potassium in GI blood), aldosterone (directly stimulated by potassium) and catecholamines (particularly Beta 2 agonists helping to move K into cells during stress and exercise) these all act via the Na-K-ATPase.
  • Increased [K] in the ECF will obviously increase K+ uptake
  • Alkalosis – low ECF [H] causes K+ shift into cells.
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9
Q

What causes K+ movement out of cells?

A
  • Exercise due to Net release of K during action potentials of muscle contraction also damage to muscle cells during exercise. Uptake by non-contracting tissues offsets dangerous rises in K. Also, exercise and trauma causes release of catecholamines which again off sets the loss of K. Cessation of exercise causes dramatic drop in ECF K
  • Cell lysis (such as when giving anti-tumour drugs)
  • Increase in ECF osmolality causes water to leave the cells, dragging potassium with it
  • Low ECF [K] and acidosis – high [H] in the ECF.
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10
Q

What is the link between H+ and K+ ions

A

To maintain electroneutrality. If [H+ ] in ECF is high then some moves into the cells thus K+ moves out of the cells to maintain the charge. And this works both ways leading to hypo/hyperkalaemia. This also works if the primary problem is Potassium being high. It causes the movement of H+ ions to maintain neutrality and leads to acidosis or alkalosis.

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11
Q

What percentage of potassium ingested is excreted by the GI system?

A

5%-10% of potassium ingested is excreted from the GI system.

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12
Q

Where is Potassium excreted/absorbed in the nerphron?

A

K+ is freely excreted in the Glomerulus but the majority is reabsorbed. K+ is secreted in the distal tubule and Cortical collecting duct by the Principle cells. Note the intercalated cells reabsorbs K+ via a H+/K+ ATPase antiporter on the apical side.

K+ secretion in distal tubule and collecting duct is done by Principle cells. Intracellular [K] high and [Na] low. Movement of Na+ into the cells creates an electric gradient and so K+ moves into the lumen down an electrochemical gradient.

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13
Q

What percentages of potassium are absorbed/secreted in the different parts of the Nephron?

A

Proximal tubule = 67% passively by paracellular diffusion.

Thick ascending limb = 20% actively by Na-K-2Cl.

Principle cells of DCT and Cortical collecting system = 15-120% secreted or nothing if low K+ diet.

Intercalated cells of DCT and cortical collecting duct and medullary collecting duct = 10-12% reabsorbed

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14
Q

What effects the secretion of K+

A
  1. ECF [K] which directly simulates Na-K-ATPase and increases permeability of apical K+ channels.
  2. High ECF potassium stimulates aldosterone secretion which increases transcription of all three proteins (ENaC is the third).
  3. Acidosis decreases K+ secretion inhibiting Na-K-ATPase and decreasing K+ channel permeability. Alkalosis does the opposite.
  4. Increased tubular flow rate washes away luminal K+ which increases K+ loss and increases Na delivery to distal tubule will mean more Na absorbed which results in more K+ secretion.
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15
Q

How is K+ absorbed in the intercalated cells of the DCT and Cortical collecting duct?

A

This is done using a Potassium hydrogen pump which required ATP. A hydrogen channels moves hydrogen ions back into the lumen.

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16
Q

What problems occurs when the ECF [K+] changes?

A

If we change the ECF [K+] then this will alter the resting membrane potential. This alters neuromuscular excitability causing problems with cardiac conduction and pacemaker automaticity, neuronal function skeletal muscle function and smooth muscle function. This results in arrhythmias, cardiac arrest and muscle paralysis.

17
Q

What causes are there for hyperkalaemia?

A
  • Due to increased intake (very unlikely) usually only if renal dysfunction is also present. Unless you have given inappropriate doses of IV K+.
  • Decreased renal excretion due to acute or chronic kidney injury, drugs which block potassium excretion such as ACE Inhibitors (reduces aldosterone) and K+ sparing diuretics.
  • Low aldosterone states such as Addison’s disease.
18
Q

What other abstract causes are there for hyperkalaemia?

A
  • Diabetic ketoacidosis (no insulin action leading to plasma hyper Osmolarity and metabolic acidosis).
  • Cell lysis such as muscle crush injuries and tumour lysis.
  • Metabolic acidosis
  • Exercise.
19
Q

What effect does hyperkalaemia have on cardiac myocytes and the Gi system?

A

Hyperkalaemia depolarises cardiac tissue and so more fast Na channels remain in an inactive form so heart becomes less excitable. Causes gastro intestinal issues due to neuromuscular dysfunction - paralytic ileus (blockage due to neuromuscular failure). May cause acidosis.

20
Q

What emergency treatment is there for hyperkalaemia?

A
  • Reduce K+ effect on heart by giving IV calcium gluconate (immediate effect)
  • Shift K+ into ICF by giving IV glucose and insulin and nebulised beta agonists (salbutamol).
21
Q

What long term treatments are available for hyperkalaemia?

A
  • Treat cause by stopping medication, treat DKA etc.
  • Reduce intake
  • Measures to remove excess K+ - dialysis (in acute or chronic kidney injury or oral K+ binding resins to bind K+ in gut (CKI)
22
Q

What causes hypokalaemia?

A
  • Excessive loss in the GI (diarrhoea, bulimia/vomiting).
  • Renal loss of potassium due to diuretic drugs, osmotic diuresis (diabetes) and high aldosterone levels.
  • Shifts of potassium into ICF such as metabolic alkalosis
23
Q

What clinical features present with Hypokalaemia?

A

Heart – hypokalaemia hyperpolarises RMP causing a greater number of fast Na channels to be available in an active form so heart is much more excitable. Causes gastro intestinal issues due to neuromuscular dysfunction - paralytic ileus (blockage due to neuromuscular failure). Neuromuscular dysfunction leading to muscle weakness. May make the kidneys unresponsive to ADH causing nephrogenic DI. May cause alkalosis.

24
Q

How do you treat hypokalaemia?

A

Treat cause, potassium replacement – IV/oral
If due to increased mineralocorticoid activity give potassium sparing diuretics which block action of aldosterone on principle cells.

25
Q

What are some of the main roles of intracellular potassium?

A

Cell volume maintenance
pH regulation
Cell enzyme function e.g. K+ dependent ATPases
DNA/Proteins synthesis - lack of K+ causes reduction in protein synthesis and stunted growth.

26
Q

How does the plasma Potassium levels effect Neuromuscular activity?

A

Low - muscle weakness, muscle paralysis, intestinal distension, peripheral vasodilation and respiratory failure

High - increased muscle excitability, and eventually muscle weakness

27
Q

How does the plasma Potassium levels effect cardiac activity?

A

Low - slowed conduction of pacemaker activity and arryhthmias

High - arrhythmias, fibrillation and conduction disturbances

28
Q

How does the plasma Potassium levels effect vascular resistance?

A

Low - Vasoconstriction

High - Vasodilation