#32 - Potassium Flashcards

1
Q

Which 5 things can change the INTERNAL regulation of potassium?

A
  • insulin
  • catecholamines
  • acid/base balance
  • plasma tonicity
  • cell lysis/proliferation
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2
Q

T/F: EKG is an important part of the workup in potassium disorders.

A

TRUE - Cardiac death can occur due to altered potassium, and urgent intervention may be needed. You can track changes via serial EKG monitoring.

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3
Q

Goals of therapy for hyperkalemia - 3

A
  • stabilize the cardiac membrane
  • shift potassium intracellularly
  • remove excess K+
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4
Q

T/F: Hyperkalemia, but not hypokalemia, can lead to cardiac dysrhythmias.

A

False. They both lead to cardiac dysrhythmias.

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5
Q

T/F 2/3 of patients die if their hyperkalemia is not treated.

A

True.

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6
Q

Normal range for potassium

A

3.5-5.0 mEq/L

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7
Q

T/F The Potassium gradient is largely maintained by the Na/K ATPase pump, which pumps K out of the cell.

A

False. The pump pumps K+ INTO the cell (98% of K+ in the body is inside cells)

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8
Q

What does “internal balance” of K+ refer to?

A

the distribution of K+ between intracellular fluid and extracellular fluid

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9
Q

What does “external balance” of K+ refer to?

A

regulation of potassium through K+ intake and excretion (mainly kidney)

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10
Q

Which cell is most responsible for K+ excretion in the kidney?

A

Principle cell, in the collecting duct.

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11
Q

K+ excretion in the kidney is dependent on 2 things:

A
  • distal sodium delivery

- aldosterone

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12
Q

Describe excretion of K+ in the kidney, including role of Na and aldosterone

A

sodium arrives in collecting duct. Sodium comes into the principal cell through ENaC,–>
charge in urine becomes negative—> negative charge attracts which pulls potassium out of the principal cell into the lumen.

Aldosterone activates ENaC (Na channel), and K channel, helping both steps of the process.

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13
Q

Insulin effect on K+

A

Insulin lowers K+

Insulin activates the Na/K ATPase pump, pushing K inside the cells of the liver/ muscle.

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14
Q

Catecholamines effect on K+

A

Catecholamines lower K+

Norepinephrine and epinephrine activate the Na/K ATPase through B2 adrenergic receptors.

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15
Q

How does being acidotic affect your K+?

A

Raises K+

If your bloodstream is acidotic, it will send H+ ions inside the cell to reduce acidity, in exchange for K+ ions, which leak out of the cell, raising your K+.

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16
Q

How does plasma tonicity affect K+?

A

Increased plasma tonicity (eg, increased sugar in blood) = increased K+, since it follows water out of the cells. (solvent drag)

17
Q

How does diabetes cause hyperkalemia (2 ways)

A
  • increased sugar in the bloodstream causes efflux of water to balance tonicity, dragging K+ with it.
  • low insulin does not allow for as much K+ absorption into the muscle and liver with meals, raising K+.
18
Q

How does cell lysis/cell proliferation affect potassium?

A
  • Cell lysis releases intracellular K+ (tumor lysis)
  • Cell proliferation eats up K+

Therefore, cancer can cause hypokalemia or hyperkalemia

19
Q

Why does volume depletion decrease distal sodium delivery?

A

through ADH and aldosterone - increased Na uptake IN THE PROXIMAL tubules, before it gets to the collecting duct.

20
Q

4 ways hyperkalemia can happen through disorders of EXTERNAL balance

A
  • kidney disease (acute or chronic)
  • decreased distal sodium delivery to the collecting duct (volume depletion)
  • mineralocortidoid (aldosterone) deficiency (ACEi’s, ARBs)
  • distal tubular dysfunction (interstitial nephritis)
21
Q

What drugs can cause hyperkalemia through messing with aldosterone?

A
  • ACE inhibitors
  • ARBs.
  • Spironolactone (aldosterone antagonist.)
22
Q

2 main symptoms that hyperkalemia can cause

A
  • mm weakness (ascending)

- cardiac toxicity

23
Q

Treatment for hyperkalemia

A

1 - Calcium gluconate to protect heart (membrane stabilization)
2-EKG monitor
3-Glucose+insulin to push K+ inside cells

24
Q

How should Calcium gluconate be dosed?

A

it acts in 1-3 minutes. Repeat the dose if EKG changes don’t go away instantly.

25
T/F MI can cause hypokalemia
True. Excessive sympathetic stimulation pushes K+ inside cell.
26
Hypokalemia due to renal loss of K+ is divided into 2 categories:
Hypertensive and Non-hypertensive
27
Hypertensive renal loss of K+ - what is the main cause?
Primary hyperaldosteronism
28
In hypokalemia, How can you tell if it is GI loss of potassium or renal loss of potassium?
low serum potassium + low urine potassium = GI loss low serum potassium + high urine K = renal loss of potassium
29
Normotensive disorders which cause renal loss of K+ --> hypocalcemia
diuretics | osmotic diuresis
30
clinical picture of hyperaldo
- low K+ - hypertension - alkalosis
31
Why does hyperaldosteronism make you alkalotic?
When aldo increases Na reabsorption in the kidneys, not only increases efflux of K, but also increases efflux of H+ ions, causing alkalosis, increased Na, decreased K, and hypertension (volume overload).
32
Labs in Primary hyperaldosteronism (tumor secreting aldosterone)
High Aldosterone | -low renin
33
Labs in secondary hyperaldosteronism
high aldosterone, high renin
34
Which condition causes secondary hyperaldosteronism (High aldosterone, high renin)
renal artery stenosis.
35
Why does renal artery stenosis cause hyperaldosteronism?
kidney senses low volume state, upregulates renin/ aldosterone. High volume state but the kidney can never recognize it.
36
Symptoms of hypokalemia
weakness cardiac arrhythmias/EKG changes (very similar to hyperkalemia)
37
Treatment for hypokalemia
Oral potassium chloride, unless symptoms are present (muscle weakness/paralysis) - if symptoms - IV potassium chloride