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Pathology > Chemical Pathology - Potassium > Flashcards

Chemical Pathology - Potassium Flashcards

1
Q

what is the normal potassium level?`

A

3.5-5.3mmol/L

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2
Q

how is potassium regulated?

A
  • loss through GI tract
  • renal regulation and secretion (Ang II, aldosterone)
  • movement from intracellular and extracellular
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3
Q

what does renin do?

A

convert angiotensinogen to Ang-1

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4
Q

where is renin released from?

A

Liver

JGA cells

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5
Q

when is renin released?

A
  • low BP in renal artery
  • low Na+ in macula densa by JGA
  • SNS beta-1 receptor activation
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6
Q

what then happens to Ang-1?

A

Ang-1 to Ang-2 in the lungs via ACE

Ang-2 acts on adrenals to release aldosterone

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7
Q

what does aldosterone do?

A

excretes K+ and increases Na+ retention

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8
Q

what are the triggers for aldosterone release?

A
  • Ang 2

- high K

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9
Q

describe the action of aldosterone

A
  • binds to MR steroid receptor
  • aldosterone inc number of open Na channels in luminal membrane
  • inc Na resorption
  • lumen becomes electronegative –> creates electrical gradient
  • causes K to secreted into lumen
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10
Q

what are the causes of hyperkalaemia?

A
  • dec GFR (renal failure)
  • dec renin (T4 RTA e.g. diabetic nephropathy, NSAIDs)
  • ACEi (dec. Ang 1 to Ang 2)
  • ARBs
  • Addison’s disease (adrenal damage = dec aldosterone)
  • aldosterone antagonists
  • K release from cells (rhabdo, acidosis)
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11
Q

how does acidosis cause hyperkalaemia?

A
  • H/K transporter is disrupted with H+ cells taken into cells to stabilise the disturbance
  • K+ is excreted in response (to maintain electronegativity)
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12
Q

what are the main causes of hyperkalaemia?

A
  • renal impairment (reduced renal excretion)
  • drugs (ACEi, ARBs, spironolactone)
  • low aldosterone (Addison’s, T4 RTA)
  • release from cells (rhabdo, acidosis)
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13
Q

what are the ECG changes with hyperkalaemiaq?

A
  • peaked T waves (early)
  • broad QRS
  • flat P wave
  • prolonged PR (and bradycardia)
  • sine wave
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14
Q

what is the management of hyperkalaemia?

A
  • 10mL 10% calcium gluconate (stabilise)
  • 100ml 20% dextrose (drive K into cells)
  • 10U insulin
  • nebulised salbutamol
  • Tx underlying cause
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15
Q

overall what are the causes of hypokalaemia?

A

GRRR

  • GI losses
  • renal losses
  • redistribution into cells
  • Rare causes
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16
Q

how do GI losses cause hypokalaemia?

A
  • diarrhoea
  • vomiting
  • fistulas
17
Q

how does renal losses lead to hypokalaemia?

A
  • MR excess (hyperaldosteronism/Conn’s, Cushing’s)
  • more Na delivery to distal tubule because hasn’t been reabsorbed earlier on
  • in distal nephron, Na in and K out
  • more Na in, more K loss
    = osmotic diuresis
18
Q

which conditions can cause hypokalaemia through redistribution of cells?

A
  • insulin/inulinomas
  • beta-agonists
  • alkalosis
19
Q

how does alkalosis cause hypokalaemia?

A
  • alkalosis = low H+
  • shift of K+ into cells in exchange for H+ in H/K transporter
    = hypokalaemia
20
Q

what are the rare causes of hypokalaemia?

A
  • RTA T1, T2

- hypomagnesaemia

21
Q

which drugs can cause renal potassium loss?

A
  • loop diuretics (furosemide)
  • thiazides (bendroflumethiazide)
    (more Na reaches and is absorbed in DCT, more electronegative, loss of K+ down electrochemical gradient)
22
Q

what are the clinical features of hypokalaemia?

A
  • muscle weakness
  • cardiac arrhythmias
  • polyuria and polydipsia (nephrogenic DI from low K+ or high Ca)
23
Q

ECG changes in hypokalaemia?

A

ST depression
flat T waves
U waves

24
Q

what do you think of with a low K+ and HTN?

A

Conn’s

25
Q

how would you screen for Conn’s?

A

aldosterone: renin ratio

Conn’s = high aldosterone: renin ratio (aldosterone suppresses renin)

26
Q

how do you manage a K level of 3.0-3.5?

A
  • oral KCl (2 SandoK tablets, TDS, 48 hours)
  • recheck K
  • Tx underlying cause (e.g. with spironolactone)
27
Q

how do you manage a K level of <3.0?

A
  • IV KCl
  • Max rate of 10mmol/hour (can irritate peripheral veins)
  • Tx underlying cause (e.g. with spironolactone)
28
Q

what does RTA T1 cause?

A
  • classic distal RTA (normally distal nephron secretes H+)
  • hypokalaemia
  • less H+ excretion
29
Q

what does RTA T2 cause?

A
  • proximal distal RTA (normally proximal tubule resorbs filtered bicarbonate)
  • hypokalaemia
  • less HCO3- reabsorption
30
Q

what does RTA T4 cause?

A
  • hypoaldosteronism (normally aldosterone facilitate excretion of H+ bound to ammonia)
  • hyperkalaemia
  • hypoaldosteronism

Pathology (21 decks)

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