Potassium Balance Flashcards

1
Q

Where is potassium typically found?

A

in Leafy vegetables and most fruit and fruit juice and baked or fried potatoes

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2
Q

What does the regulation of potassium imply?

A

Acute regulation- Distribution of K+ through ICF and ECF compartments

Chronic regulation: Achieved by the kidney adjusting K+ excretion & reabsorption

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3
Q

What is the function of Potassium?

A
  1. Determines ICF osmolality - Cell volume
  2. Determines resting membrane potential (RMP) -very important for normal functioning of excitable cells
    - Repolarisation of cell - Myocardial, skeletal muscle & nerve cells
  3. Affectsvascular resistance
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4
Q

How much potassium is found in the ECF?

A

2.5%

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5
Q

How much potassium is found intracellularly?

A

90%

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6
Q

Why is the Na+-K+ pump important?

A

High intracellular [K+] and low [K+]

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7
Q

What should the plasma concentration of K+ not exceed?

A

6.5mmol

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8
Q

Hypokalaemia

A

<3.5 mM

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9
Q

Hyperkalaemia

A

> 5.5 mM

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10
Q

How does changing K affect membrane potential?

A

Normal- [K] = 3.5mM and [K]i = 140mM = Ek = -98.5
Hyperkalemia- [K] = 7mM and [K]i = 140mM =Ek =-80
Hypokalemia -[K]0 = 1.5 mM and [K]i=140 mM= Ek=-121.5

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11
Q

Hypokalaemia and ECG

A

The decrease in Amplitude T-Wave, Polong Q- U interval, prolong P-wave

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12
Q

Hyperkalaemia and ECG

A

Increase QRS complex, increase amplitude T-wave, eventual loss P-wave

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13
Q

Hypokalaemia

A

Caused by renal loss of K+

  • Profuse diarrhea
  • Prolonged vomiting

Results: A decrease release of adrenaline, aldosterone & insulin

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14
Q

Hyperkalaemia

A

Caused by normal prolonged exercise - normal kidneys excrete K+ easily.
Or insufficient renal excretion increased release from the damaged body cells, ADDISON’S disease, and Long term use of K-sparing diuretics.

Results: Plasma [K+] >7mM life-threatining -> asystolic cardiac arrest

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15
Q

What hormones are needed for Hyperkalaemia?

A

Aldosterone, adrenaline stimulates Na+-K+ pump - increase cellular K+ influx

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16
Q

Renal handling Na+/K+

A

Human kidneys designed to conserve Na & excrete K
Na+ & K+ filtered freely at glomeruli
Plasma & GF have same [Na+] & [K+]
In 24 hrs, entire glomerular filtrate (~180 litres) contains: 25 moles Na+ (=1.5 kg NaCl)
0.7 moles K+ (=50g KCl)

17
Q

K+ excretion into Urine in DCT

A

Increased K+ intake
Changes in blood pH
-Alkalosis = increase excretion of K+ = decrease serum [K+]
-Acute acidosis = decrease in excretion of K+ = Increase [K+]

18
Q

Aldosterone & K+ secretion

A

The decrease in the activity of Na+/K+ pump - increase K+ influx - increase [K+] intracellular - cell lumen concentration gradient
Increase ENaC channels - increase Na+ reabsorption - decrease cell negativity and increase lumen negativity - voltage gradient
Redistributes ENaC from intracellular localization to membrane
Increase permeability of the luminal membrane to K+

19
Q

How does plasma [K] increases K secretion?

A

In 3 ways:
-slow exit from basolateral membrane - increase [K+] intracellular - cell lumen concentration gradient
Decrease activity of Na+/K+ ATPase - increase [K+] within the cell
Increase plasma [K] - stimulates aldosterone secretion

20
Q

Secondary adrenal insufficiency

A
  1. A decrease in pituitary ACTH leads to
  2. A decrease in cortisol
  3. Adrenal glands shrink
21
Q

What is Conn’s syndrome?

A

Primary Aldosteronism

  • Due to aldosterone-producing adenoma of ZG adrenal
  • Usually <3cm, unilateral & renin-unresponsive
  • Hyperaldosteronism (excess release of aldosterone) due to various chronic - most common (50-60%) due to Conn’s syndrome, remaining 40-50% due to bilateral adrenal hyperplasia
  • Aldosterone release in absence of stimulation by Angiotensin 2
22
Q

Treatment of Conn’s syndrome

A

Surgical removal of the tumor-containing adrenal gland

-Hypertension &hypokalaemia controlled with K+ - sparing agents e.g. spironolactone