K and electrolytes Flashcards

1
Q

what is the most abundant intracellular cation

A

K

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2
Q

normal serum K

A

3.5-5 mmol/L

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3
Q

what hormones are involved in reg of K in kidney

A
  • Aldosterone
    • Angiotensin II
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4
Q

summarise the renin-angiotensin-aldosterone system

A
  • Angiotensin produced in liver - converted to ang 1 and then ang II by ACE in lung
  • Ang II stim adrenal cortex -> aldosterone
  • -> Na in and K out through urine
  • Happens in principle cells in cortical collecting tubules

If a lot of aldosterone = low K

K also stim aldosterone release = lose K in urine

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5
Q

summarise how Na movement alters K movenment

A
  • More Na comes in = lumen more -ve = loss of K down the electrical gradient
  • Na and K don’t move in same transporter
  • It is the fact that the na makes the lumen -ve which pushes the K out down the electrical gradient
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6
Q

how does aldosterone alter K movement

A

Aldosterone = increase number of open Na channels = reabsorb more Na = more -ve lumen = electrical gradient = more K secreted into lumen

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7
Q

what are the stimuli for aldosterone secretion

A

K
Angiotensin II

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8
Q

causes of hyperkalaemia

A
  • Reduced GFR ie renal failure
  • Low renin - ie diabetic nephropathy, NSAIDs - less Angiotensin to ANg1 = less aldosterone = less K secretion. renin produced in juxtaglomerula apparatus
  • ACEi - less Ang1->ANg2 = less K loss
  • ARB - losartan. Block ang2 receptor = less ang2 action = less loss K
  • Addisons -> low aldosterone
  • Aldosterone antagonist - spirionolactone = less aldosterone action = less K secretion

Release from cells
- rhabdomyolysis
- Acidosis - H ions move into cells - K lost to maintain electroneutrality = high k

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9
Q

ECG with hyperkalaemia

A

peaked T waves

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10
Q

mx of hyperkalaemia - need to know dose

A
  • 10ml 10% ca gluconate - stabalise myocardium
  • 100ml 20% dextrose and 10 units insulin
  • Nebulised salbutamol
  • Treat underlying cause
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11
Q

causes of hypokalaemia

A

GI loss - vomiting

Renal loss
* excess cortisol (bind mineralocorticoid receptor) or excess aldosterone (Conn’s or bilateral hyperplasia)
* Increase na distally
* Osmotic diuresis

Redistribution into cells
* B cell agonist stim K uptake into cells
* Insilin
* Alkalosis - H move out of cell, and K move into the cell.

Rare cayuses - renal tubular acidosis type 1 and 2, hypomagnesia

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12
Q

summarise renal loss of K

A

If block resporption with loop diuretics eg furosemide - more Na will go to DCT - so more K will be lost. Eg with loop diuretics or bartter syndrome

Thiazide diuertics and gitelman syndrome - same thing more distally - more Na reabsorbed more distally -> more -ve lumen -> more k lost

ie deliver more na to distal tubles

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13
Q

sx of hypokalaemia

A
  • Muscle weakness
    • Cardiac arrhythmia
    • Polyuria and polydupsia - hypok gives you nephrogenic DI
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14
Q

Screening test if low K and htn

A

aldosterone:renin ratio

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15
Q

mx of hypokalaemia

A

Serum potassium 3.0-3.5 mmol/L
* Oral potassium chloride (two SandoK tablets tds for 48 hrs)
* Recheck serum potassium

Serum potassium < 3.0 mmol/L
* IV potassium chloride
* Maximum rate 10 mmol per hour
* Rates > 20 mmol per hour are highly irritating to peripheral veins

Treat the underlying cause e.g. spironolactone

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