Potassium Flashcards

1
Q

What is a normal intracellular potassium cc?

A

140 mEq/L

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2
Q

What are the body’s protective mechanisms to prevent hyperkalemia?

A

increased ECF K+ –> aldosterone secretion –> increased basolateral collecting duct principal cell NaKATPase acitvitiy –> more K excretion

kaliuretic feeforward control
* K-sensing cells in stomach and hepatic portal circulation
* high K intake –> signals to kidneys to increase K secretion independent of aldosterone

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3
Q

List differentials for disorders of internal balance leading to hypokalemia

A
  • alkalosis
  • insulin administration
  • increased catecholamine levels
  • beta-adrenergic agonist therapy or intoxication
  • refeeding syndrome
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4
Q

List differentials for external balance disorders leading to hypokalemia

A
  • pyloric outflow obstruction
  • severe diarrhea
  • prolonged inadequate intake
  • Renal tubular acidosis
  • renal loss (e.g., CKD)
  • hyperaldosteronism
  • glucocorticoid administration
  • diuretic therapy
  • osmotic or postobstructive diuresis
  • inadequate fluid supplementation in hospital
  • DKA
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5
Q

What are the consequences of hypokalemia?

A
  • decreased glucose tolerance - hypokalemia causes decrease pancreatic beta-cell insulin release
  • hyperpolarization of myocytes from lowered resting membrane potential
  • rhabdomyolysis -> pigmenturia can damage kidneys
  • hyperpolarization of cardiac myocytes -> arrhythmias
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6
Q

What are expected ECG changes from hypokalemia?

A
  • ventricular tachycardias, Vtach or Vfib
  • atrioventricular dissociation
  • ST segment depression
  • QT and PR prolongation
  • Increased P wave
  • widened QRS
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7
Q

Why can hypokalemia-induced ventricular tachycardias be more difficult to treat?

A

hypokalemia causes myocardium to become refractory to effects of class I antiarrhythmics

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8
Q

What is the recommended treatment for the apneic hypokalemic patient?

A

rapid infusion of 0.01 mL/kg KCl (2 mEq/mL)

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9
Q

What is a “safe” potassium serum cc to reach before starting Nabicarbonate or insulin administration?

A

3.5 mEq/L

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10
Q

What coexisitng conditions may worsen hypokalemic neuromuscular dysfunction and make patients more refractory to supplementation?

A
  • hypomagnesemia
  • hypocalcemia
  • alkalosis
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11
Q

List differentials for hyperkalemia

A
  • oliguric/anuric AKI
  • Urinary obstruction
  • uroabdomen
  • reperfusion injuries (PCA, extremity reperfusion after ATE
  • tumor lysis syndrome
  • insulin deficiency (DKA, DM)
  • mineral acidosis
  • hypoadrenocorticism
  • GI disease
  • Chylothorax, pleural or peritoneal effusion managed with intermittent or continual drainage
  • expired RBC transfusion
  • oversupplementation
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12
Q

Why does only mineral acidosis but not organic acidosis lead to hyperkalemia?

A

organic acids (e.g., lactate, ketoacids) can maintain electroneutrality

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13
Q

What are causes for pseudohyperkalemia?

A
  • high WBC (>100k) or PLT (>1million) counts
  • Akitas - increased RBC IC K+ cc
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14
Q
A
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