Disorders of Potassium Flashcards

1
Q

Where is the majority of potassium stored?

A

intracellularly within muscle (mostly), but also RBCs, liver, and bone.

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2
Q

How is most potassium excreted?

A

in the urine.

*So pts with end stage kidney disease, who cannot form urine as well, have a greater risk for hyperkalemia.

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3
Q
  • What will insulin do to potassium?
A

move it intracellularly. So if a diabetic is in DKA (K+ high extracellularly), you can give them insulin to move the K+ intracellularly. :)

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4
Q
  • What will alpha-agonists (catecholamine) do to K+?
A

move K+ EXTRAcellularly

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5
Q
  • What will beta-agonists (catecholamine) do to K+?
A

keep K+ INTRAcellularly

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6
Q
  • What will nonselective beta-antagonists (propranolol) do to K+?
A

K+ moves EXTRAcellularly

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7
Q
  • What will a non-anion gapped metabolic acidosis do to K+?
A

move it EXTRAcellularly

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8
Q
  • What will a metabolic alkalosis do to K+?
A

move K+ INTRAcellularly

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9
Q
  • What will happen to K+ in a hyperosmolar state such as hemolysis, rhabdomyolysis, or tumor lysis syndrome?
A

K+ efflux in muscle to EXTRAcellular space

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10
Q

Where does most K+ reabsorption occur in the kidney?

A

PCT (mostly) and a little bit in the ascending limb of the loop of henle.

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11
Q

Where is the only place that K+ secretion occurs?

A

in the connecting tubule/collecting duct. This is mediated by ENac activity (Na+) reabsorption occurs and thus K+ is secreted to balance the charge.
*K+ secretion channels= ROMK, Maxi-K, K+/Cl-

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12
Q

What increases ENac activity (Na+ reabsorption)?

A
  • high oral K+ intake
  • hyperaldosteronism
  • high tubular flow rate (more Na+ being delivered distally)
  • alkalosis
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13
Q

What are some causes of HYPERkalemia?

A
  • increased intake= diet, supplements, or blood transfusions.
  • decreased renal excretion= CKD, type 4 RTA, drugs (ACE inhibitors), adrenal insufficiency
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14
Q

** What states can cause an EXTRAcellular shift of K+ (HYPERkalemia)?

A
  • hyperosmolarity
  • low insulin levels
  • non-anion gapped metabolic acidosis
  • drugs (NSAIDS, Cox-2 inhibitors, CNIs, ACE inhibitors, K+ sparing diuretics like amiloride, or blocking any portion of the RAAS).
  • HYPOaldosteronism
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15
Q

What are the consequences of HYPERkalemia?

A
  • decreased myocardial conduction (prolonged PR and QRS, peaked T waves, and flattened P waves).
  • skeletal muscle weakness, fatugue, paralysis
  • decreased kidney ability to secrete NH4+ leading to acidosis.
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16
Q

What is the first thing we want to do with a pt who has high K+?

A
  1. stabilize the myocardium via calcium gluconate or calcium chloride to increase the resting membrane potential of cardiac myocytes.
  2. insulin or albuterol to move K+ into the intracellular space (only TEMPORARY).
  3. eliminate K+ from the body= laxitives (GI tract); new dru Patiromer (less side effects). HEMODIALYSIS is most effective however.
17
Q

** What is important to remember about hemodialysis?

TEST QUESTION

A

It requires a LOT of medical management, and depends on:

  • dialyzer size
  • blood flow rate
  • dialysate flow rate
  • duration of treamtment (4 hrs)
  • amount of K+ in dialysate
18
Q

*** What are the causes of HYPOkalemia?

A
  • pseudohypokalemia
  • leukocytosis in AML (incrased WBC uptake of K+)
  • redistribution= large amount of K+ moved intracellularly when given insulin for DKA (aka you give too much).
  • Grave’s Disease (Low TSH)= hypokalemic periodic paralysis. Hispanic/Asian men.
  • extra-renal loss (urine K+ 15 mmol/day)= antibiotics, diuretics, bicarbonaturia, tubualr damage, megnesium deficiency, Liddle, Bartter, and Gitelman syndromes.
19
Q

** What is Liddle’s syndrome?

A
  • autosomal dominant (chromosome 16q)
  • affects principal cells in the collecting duct causing persistent ENac activation (thus persistent Na+ reabsorption and K+ secretion) and metabolic alkalosis. HTN also.
  • Treat with K+ sparing diuretic (amiloride or triamterene).
20
Q

** What is Bartter’s syndrome?

A
  • autosomal recessive
  • affects thick ascending loop of henle causing loss of function of the Na+/K+/2Cl- channel (thus acting just like a loop diuretic and causing HYPOkalemia). HTN also.
  • Treat with ACE inhibitor or K+ sparing diuretic
21
Q

** What is Gitelman’s syndrome?

A
  • autosomal recessive
  • affects the DCT causing loss of function of the Na+/Cl- co-transporter on the luminal side of the membrane. Thus because you cannot reabsorb Na+ and Cl-, you will lose these (thus acting just like a thiazide diuretic). So this will cause HYPOkalemia since more Na+ will be in the filtrate to be absorbed at the collecting duct in exchange for K+ secretion. You will see HYPOmagnesium as well but will NOT see HTN here.
  • Treat by giving K+ and Mg2+, or K+ sparing diuretic (amiloride).
22
Q

** What will excess aldosterone (i.e. cushings or primary hyperaldosteronism) do to K+?

A

cause HYPOkalemia because excess aldosterone causing increased Na+ reabsorption and thus increased K+ excretion to balance the charge.
*Treat with glucocorticoids to suppress aldosterone.

23
Q

What is syndrome of apparent mineralocorticoid excess?

A
  • autosomal recessive
  • defect in 11B-hydroxysteroid dehydrogenase enzyme or inhibition of this enzyme from eating too much black licorice leading to decreased peripheral conversion of cortisol to inactive cortisone Increased cortisol then binds to mineralocorticoid receptors in the principle cells of the collecting duct (acting just like aldosterone= increased ENac activity and thus Na+ reabsorption and K+ secretion).
  • Treat with Dexamethasone
24
Q

What are the consequences of HYPOkalemia?

A
  • metabolic alkalosis
  • polyuria, polydipsia
  • HTN
  • arrhythmias (U waves)
  • skeletal muscle weakness, paralysis, or myopathy
25
Q
  • How do you treat HYPOkalemia?
A
  • if magnesium is low also, replace this first

- K+ supplementation (avoid D5W prep)

26
Q

What are normal K+ levels?

A

3.5 - 5.0 mEq/L