potassium Flashcards

1
Q

typical intake of potassium

A

100

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2
Q

after a meal, potassium is rapidly taken up into cells by

A

Na/K ATPase

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3
Q

extracellular K+

A

4

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4
Q

principal cells contain what for potassium to flow into tubular fluid

A

K+ channel

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5
Q

increased Na delivery to principal cells

A

lumenal membrane becomes less lumenal positive which causes an increase in K+ secretion

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6
Q

furosemide

A

loop diuretic and inhibits the Na/K/Cl co-transporter and increases Na delivery to the CT

  • K+ wasting
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7
Q

thiazide diuretic

A

inhibits the Na/Cl in DT which again causes increase in Na delivery to principal cells

  • K+ wasting
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8
Q

gitelmans syndrome

A

characterized by hypotension (increased excretion of NaCl) and hypokalemia

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9
Q

amiloride

A

INHIBITS Na channels leading to a positive lumen and this K+ secretion decreases

  • K+ sparing
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10
Q

defect in luminal Na/Cl co transporter

A

Gitelmans

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11
Q

potassium shifting into ICF

A
  • insulin
  • B-agonists
  • catecholamines
  • alkalemia
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12
Q

potassium shift our of ICF

A
  1. hyperosmolarity
  2. exercise
  3. cell lysis
  4. acedemia
  5. glucagon
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13
Q

transcellular shifts:

  1. sensitive to
  2. common in
  3. paralysis
  4. alkalemia or acidosis
  5. associated drugs
A
  1. sensitive to catecholamines
  2. hypokalemic periodic paralysis
  3. acute alkalemia
  4. associated with albuterol and insulin
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14
Q

clinical manifestations of hypokalemia

A
  1. muscle weakness and paralysis
  2. impaired urinary concentration
  3. arrhythmias- increased U wave
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15
Q

treatment of hypokalemia

A
  1. underlying cause
  2. cautious replacement by oral rout– not overshoot
  3. IV replacement with slower administration and not exceed 20 mEq/hr
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16
Q

etiologies of hyperkalemia

A
  1. pseudohyperkalemia
  2. increased intake
  3. decreased urinary excretion
  4. transcellular shift/cell lysis
17
Q

pseudohyperkalemia

A
  • hemolysis (think about blood draws)
  • leukocytosis
  • thrombocytosis
18
Q

decreased excretory capacity of potassium can be from

A
  1. reduced GFR
  2. tubular secretory defect with preserved GFR
  3. drugs
19
Q

what drugs are associated with hyperkalemia

A

ACEi, ARBs, K+ sparing, Heparin, NSAIDS

20
Q

reduced GFR and hyperkalemia can be from

A
  1. Acute kidney injury

2. chronic kidney disease

21
Q

tubular secretory defect with preserved GFR that leads to hyperkalemia (3)

A
  1. hyporeninemic hypoaldosteronism
  2. addison’s disease
  3. tubular dysfunction associated with lupus, sickle cell
22
Q

what type of drug can cause a transcellular shift of K out of cells

A

Beta blockers

23
Q

clinical manifestations of hyperkalemia

A
  1. muscle weakness and paralysis
  2. renal tubular acidosis due to impaired ammoniagenesis
  3. EKG abnormality- T wake is peaked
24
Q

treatment of hyperkalemia

A
  1. stabilization of cardiac membranes- giving calcium
  2. transfer of potassium into cells
  3. removal of potassium from the body