Hydrogen, Potassium, Calcium and Magnesium Flashcards

1
Q

What are symptoms of hyperkalaemia

A
  • High serum potassium leads to smaller potassium gradient
  • Decreases membrane excitability as some Na channels already closed
  • Risk of cardiac arrhythmias
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2
Q

What are symptoms of hypokalaemia

A
  • Low serum potassium leads to bigger potassium gradient between intracellular and extracellular compartment
    • Depolarization leads to increased excitability - risk of arrhythmias
    • U wave present on ECG
  • Weakness
  • Polyuria - low potassium causes ADH resistance
  • Constipation - smooth muscle dysfunction
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3
Q

Explain how vomiting leads to metabolic alkalosis

A
  • Vomiting results in loss of HCl with the stomach contents
    • Loss of H+
  • Severe vomiting also leads to loss of K and Na
  • Kidney compensates by retaining sodium in the collecting ducts at the expense of H ions, leading to metabolic alkalosis
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4
Q

State some causes of hypokalaemia

A
  • Reduced dietary intake
  • Increased entry into cells
    • Metabolic alkalosis
    • Increased ß-adrenergic activity - noradrenaline with stress
  • Increased GI loss
    • Vomiting/diarrhoea
  • Increased urine loss
    • Hyperaldosteronism
    • Increased urine flow
    • Diuretics
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5
Q

Describe potassium movement in the proximal convoluted tubule

A
  • 65-70% absorbed
  • Early in the proximal tubule, potassium reabsorption mainly through solvent drag (transported with water)
  • Later on in the proximal tubule, positive charge within lumen due to loss of Na causes paracellular diffusion
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6
Q

Describe movement of potassium in the thick ascending limb

A
  • 20% absorbed
  • ROMK helps potassium secretion which is then reabsorbed through NaKCC
  • Net movement of potassium reabsorption in interstitium
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7
Q

Describe movement of potassium in the DCT

A
  • Secretion of potassium dependent on amount of reabsorption of sodium
  • Potassium secreted through ROMK
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8
Q

Describe potassium movement in collecting duct

A
  • Secretion
    • ENaC cause sodium to be reabsorbed, causing potassium to be secreted
      • BK channel are flow channels - good flow = more potassium lost
  • Reabsorption
    - Hydrogen exits the cell, causing potassium to be reabsorbed in the opposite direction
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9
Q

Describe the factors that affect potassium entry into cells

A
  • Na/K ATPase activation moves potassium into cells

- Activity influenced by K concentration in plasma, insulin and noradrenaline effect on ß2 adrenoceptors

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10
Q

Describe the factors that affect potassium exit from cells

A
  • Potassium channels move potassium out of cells
  • Decrease in ICF potassium through high osmolality, acidosis, cell damage
  • Increase in ICF potassium during alkalosis
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11
Q

What factors increase potassium secretion

A
  1. High intracellular potassium
  2. High electronegative lumen (increased sodium reabsorption)
  3. Increase permeability of luminal membrane
  4. Decrease in luminal potassium
    - Aldosterone upregulates the first 3 points
    - High flow increases potassium secretion due to 2,4
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12
Q

Explain the aldosterone paradox

A
  • The ability of the kidney to stimulate NaCl retention with minimal K secretion under conditions of volume depletion and maximize K secretion without Na retention in hyperkalaemia
  • In volume depletion, RAAS activated
    • Angiotensin increases NaCl reabsorption in DCT and also inhibit ROMK channel (facilitates Na reabsorption and decreases K secretion)
  • After eating a lot of potassium, blood volume normal so only aldosterone effect occurs without RAAS
    - Allows K secretion without having to hanging on to Na
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13
Q

What is the risk of high calcium concentrations

A
  • Problem with calcium is that it is difficult to keep in solution
  • Crystallization would occur without inhibitors (eg. Magnesium)
  • High calcium in urine increases risk of kidney stones
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14
Q

In what form is calcium present as in the blood and which are filtered

A
  • Only unbound calcium can be filtered by kidney - 55%
  • Rest is bound to proteins such as albumin
  • Only ionized form filtered
  • 2% is excreted in urine
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15
Q

Describe how calcium is reabsorbed in the kidney

A
  • Calcium is dependent on sodium through paracellular reabsorption in PCT and thick ascending limb
  • Transcellular reabsorption in DCT - immediately buffered when it enters cell (calmodulin)
  • Collecting duct - calcium not normally absorbed in collecting duct
    • Will upregulate aquaporin and H-ATPase
      • Increase in acid formation reduces chance of stones formation
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16
Q

What are symptoms of hypocalcaemia

A
  • Pins and needles at finger tips/lips
  • Tetany
  • Reduced myocardial contractility
17
Q

What is the role of PTH in the kidney

A
  • PTH increased in hypocalcaemia to cause more mobilisation from bone and decreased renal excretion of Ca
    • PTH also stimulates formation of calcitriol, which is then released into the circulation
  • Calcitriol synthesis increases to help increase mobilisation of calcium, increased gut absorption and increased reabsorption from kidney
18
Q

What is the effect of PTH on phosphate

A
  • PTH inhibits the reabsorption of phosphate, therefore decreasing plasma phosphate concentrations
  • However PTH also stimulates production of calcitriol, which increases phosphate release from bones and increases reabsorption of phosphate in the gut
  • Overall is slight decrease in serum phosphate levels