Potassium Disturbances Flashcards

1
Q

What is the normal extracellular potassium level?

A

3.5-4.5 mmol/L

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2
Q

Acute vs Chronic potassium disorder

A

Acute <48hrs
Chronic >48hrs

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3
Q

How does insulin, long-standing alkalemia, hyertonicity, exercise, and cell integrity effect potassium levels?

A

Insulin: Causes a potassium intracellular influx
Alkalemia: hypokalemia
Hypertonicity: Hyperkalemia
Exercise: Transient potassium shift extracellularly
Cell integrity: Ischemia causes hyperkalemia

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4
Q

External factors that effect potassium levels: Kidney elimination, Metabolic Acidosis, Metabolic alkalosis, Aldosterone, Glucocorticoids, Magnesium deficiency

A

Kidney Elimination: Eliminates 90% of dietary K+
Metabolic Acidosis: inhibits K+ secretion, hyperkalemia
Metabolic Alkalosis: stimulates K+ secretion, hypokalemia
Aldosterone: increase in K+ stimulates aldosterone, reduces plasma K+, hypokalemia
Glucocorticoid: enhances renal K+ excretion, hypokalemia alkalosis
Mag deficiency: renal potassium wasting.

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5
Q

Five main causes of hyperkalemia with examples

A
  1. Excessive potassium intake (typically results from IV administration)
  2. Abnormal K+ distribution: Tumor lysis syndrome, rhabdo, burns, hemolytic transfusion reactions, mesenteric ischemia
  3. Pharmaceuticals: Digoxin, Succ
  4. Acute renal failure
  5. Pseudohyperkalemia: hemolyzed blood sample
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6
Q

Definition and causes (3) of acute hypokalemia

A

Hypokalemia developing over hours
DKA: Patients can have a normal K+ level initially, with delivery of insulin K+ shifts back into cells producing hypokalemia
Pharmaceuticals: Albuterol, epinepherine
Therapeutic hypothermia: hypokalemia occurs in cooling phase, careful of replacement due to rebound hyperkalemia.

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7
Q

Cardiovascular, Neuro, and metabolic manifestations of hyperkalemia

A

Cards: Peaked T-wave, loss of p-wave (Sine wave), prolonged PR, and widened QRS, V-fib, asystole, if K >6.5 regardless of EKG treat emergently
Neuro: parathesias, weakness, paralysis, diaphragm spared, decreased reflexes
Metabolic: decrease renal ammoniagenesis, produces hyperchloremic metabolic acidosis. Prevents kidneys ability to excrete

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8
Q

Cardiovascular, Neuromuscular, and metabolic clinical manifestations of hypokalemia

A

Cards: ST depression, decreased T wave amplitude, increased U wave amplitude, increase dig toxicity, ventricular ectopy
Neuro: weakness, myalgias, paralysis, rhabdo
Metabolic: glucose intolerance, increased protein catabolism, polydipsea, polyuria, metabolic alkalosis

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9
Q

What is hyperkalemic Periodic paralysis

A

Rare
Mutation of skeletal muscle Na+ channels
Precipitated by exercise, fasting, cold, and potassium administrations
Prevented with carbs

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10
Q

What is refeeding syndrome?

A

Glucose initiated hyperinsulinemia, causing K to shift hypokalemia

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11
Q

What is hypokalemic periodic paralysis

A

Inherited, sporadic, or thyrotoxic
Muscle weakness following acute hypokalemia
Can cause ventilatory failure or cardiac arrhythmia
Can be caused by ingestion of carbs, salt intake, or exercise
Manage with potassium

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12
Q

What is thyrotoxic periodic paralysis

A

Accompanied by hypophosphatemia
Causes hypokalemia
Manage like hyperthyroidism

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13
Q

What are the labs and questions you want to ask to assess for Hypokalemia or Hyperkalemia

A

EKG
CMP
GFR and Crt
Aldosterone
Medications

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14
Q

Management of Hyperkalemia

A

Treat if K >6.5
Insulin R 10 units with D5 amp
Calcium gluconate 1g/10mls for cardiac protection
Albuterol neb 20mg/4mls for temporary decrease
Bicarb (only useful in severe metabolic acidosis)
Diuretics
K Binder (kayexalate)
HD

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15
Q

Management of Hypokalemia

A

Replete low K+ 10meq corrects by 0.2 mmol K+

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