Potassium handling Flashcards

1
Q

What is the serum concentration of potassium?

A

3.5-5.0mmol/l Most abundant intracellular cation

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2
Q

Which hormones are involved in renal regulation of potassium?

A

Angiotensin II and Aldosterone

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3
Q

Describe the renin-angiotensin aldosterone system

A

In response to a drop in blood volume/pressure: Angiotensinogen is released from the liver and converted to angiotensin 1, by renin which is released from Juxta-glomerular cells Angiotensin 1 is then converted to Angiotensin 2 by converting enzyme that is produced by the lungs Angiotensin II then acts on the adrenal glands to increase aldosterone production leading to Na and H20 retention. Angiotensin II also acts on vasculature to cause vasoconstriction. All of which lead to increased blood/volume/pressure

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4
Q

How does the body deal with hyperkalemia?

A

K acts on the adrenal glands to produce more aldosterone to excrete more K from the body

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5
Q

What cells do aldosterone act on to aid potassium secretion?

A

Principal cells of the cortical collecting tubule

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6
Q

How does aldosterone work to secrete potassium from cells for excretion?

A

Aldosterone causes Na reabsorption through epithelium sodium channels which leads to tubular lumen negative electrical potential forming, which drives potassium secretion out of cells into the lumen To excrete potassium, the lumen has to be more negative than inside the cell to allow K to move along an electrical gradient. This is done by reabsorbing Na into cells. This DOES NOT affect the sodium concentration, as water is also removed meaning Na concentration doesn’t change as the ratio of Na to water stays the same

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7
Q

What does aldosterone do to Nedd4?

A

Nedd4 is an enzyme that degrades sodium channels Aldosterone reduces degradation of sodium channels by inhibiting Nedd4 in principal cells

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8
Q

What are the stimuli for aldosterone secretion?

A

Angiotensin II Potassium

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9
Q

What are the main causes of hyperkalaemia?

A

Renal Failure/impairment - reduced renal excretion Drugs - ACE inhibitors, ARBs, sprionolocatone Low aldosterone - Addison’s disease or Type 4 renal tubular acidosis (low renin, low aldosterone) Release from cells - rhabdomyolysis or acidosis

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10
Q

Describe how each of the following cause reduced excretion of K: 1. reduced GFR 2. Reduced renin 3. ACE inhibitors 4. Ag II receptor blocker 5. Addison’s disease 6. Aldosterone antagonists

A
  1. Reduced GFR, reduced K excretion as nephrons no longer as effective 2,3,4. Reduced renin ultimately, ACE inhibitors and Ag II receptor all block the production/action of Ag II one of the main stimuli to aldosterone secretion which is needed to excrete K. 5,6. Addison’s means no aldosterone production and aldosterone antagonists stop the action of aldosterone, so both stop aldosterone being able to reabsorb water and Na and excrete K.
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11
Q

What can cause a reduced renin output?

A

Type 4 renal tubular acidosis (diabetic nephropathy) NSAIDs

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12
Q

What conditions can cause potassium to be released from cells? (no aldosterone involvement)

A

Rhabdomyolysis Acidosis (need to maintain electroneurality, increased H ions pushes K out of cells to maintain electroneutrality)

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13
Q

What is the main ECG change associated with hyperkalaemia?

A

Peaked T waves

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14
Q

How would you manage a patient with hyperkalaemia?

A
  • 10ml 10% calcium gluconate
  • 50ml 50% dextrose +10 units of insulin
  • Nebulized salbutamol
  • Treat the underlying cause

This all drives K into cells

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15
Q

What are the causes of hypokalaemia?

A
  • GI loss e.g. vomiting and diarrhoea
  • Renal loss
    • Hyperaldosteronism
    • Increased sodium delivery to distal nephron e.g. diuretics
    • Osmotic diuresis
  • Redisribution into the cells
    • Insulin
    • Beta-agonists e.g. salbutamol
    • Alkalosis
  • Rare causes:
    • Renal tubular acidosis Type 1 and 2
    • Hypomagnesaemia
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16
Q

How can drugs cause renal potassium loss to occur?

A
  • It takes place in the ascending loop of Henle. If these tubules become blocked, like by loop diuretics or Bartter syndrome, this leads to be more Na being delivered to the distal nephron
  • Thiazide diuretics ans Gitelman syndrome can also increase Na delivery to the distal nephron
  • Here, in the distal nephron, in the principal cells and increase in Na delivery to the area causes the lumen to become negative, and K is excreted from cells as it moves down the electro gradient as is excreted
17
Q

What are the clinical features of hypokalaemia?

A
  • Muscle weakness
  • Cardiac arrhytmias
  • Polyuria and polydipsia (nephrogenic DI)
18
Q

What screening test would you order in a patient with hypokalaemia and hypertension?

A

Aldosterone:Renin ratio

High aldosterone, increases blood pressure which then suppresses renin production from JGA cells by negative feedback

19
Q

How would you treat hypokalaemia:

  1. 3.0-3.5mmol/L
  2. <3.0mmol/L
A
  1. 3.0-3.5mmol/L
  • Oral potassium chloride (two SandoK tablets tds for 48 hours)
  • Recheck serum potassium
  1. <3.0mmol/L
  • IV potassium chloride
  • Maximum rate 10mmol per hour
  • Remember, >20mmol oer hour is highly irritating to peripheral veins

Always treat underlying cause e.g. sprionolactone

20
Q

SBA: Hyperkalaemia is a side effect of which of the following drugs?

A. Furosemide

B. Bendroflumethiazide

C. Salbutamol

D. Ramipril

A

D. Ramipril

21
Q

Hypokalaemia is a side-effect of which of the following drugs?

A. Spironolactone

B. Indomethacine

C. Perindopril

D. Furosemide

A

D. Furosemide