Potassium disorders Flashcards

(27 cards)

1
Q

Functions of Potassium

A
  • Regulation of neuromuscular excitability and muscle contraction
  • Regulation of insulin secretion (low K inhibits secretion; high K stimulates insulin secretion)
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1
Q

Functions of Potassium

A
  • Regulation of neuromuscular excitability and muscle contraction
  • Regulation of insulin secretion (low K inhibits secretion; high K stimulates insulin secretion)
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2
Q

Alkalosis and K levels

A

Alkalosis causes H to move out and K into the cell –> potential hypokalemia

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2
Q

Alkalosis and K levels

A

Alkalosis causes H to move out and K into the cell –> potential hypokalemia

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3
Q

Acidosis and K levels

A

Acidosis causes H to move into the cell and K out

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3
Q

Acidosis and K levels

A

Acidosis causes H to move into the cell and K out

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4
Q

Diarrhea and K levels

A

There is a loss of K and HCO3 in the stool –> hypokalemia and metabolic acidosis

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4
Q

Diarrhea and K levels

A

There is a loss of K and HCO3 in the stool –> hypokalemia and metabolic acidosis

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5
Q

Drugs that commonly cause low K

A

MCC: Loop and thiazide diuretics

Also, Insulin and beta-2 agonists may shift K into the cell

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5
Q

Drugs that commonly cause low K

A

MCC: Loop and thiazide diuretics

Also, Insulin and beta-2 agonists may shift K into the cell

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6
Q

Clinical findings in hypokalemia

A
  • Muscle weakness (due to changes in membrane potential)
  • U waves on ECG
  • Collecting tubules become refractory to ADH –> nephrogenic DI –> polyuria
  • Tubule cells become distended with fluid (vacuolar nephropathy)
  • Rhabdomyolysis (low K inhibits insulin –> decreased muscle glycogenesis)
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6
Q

Clinical findings in hypokalemia

A
  • Muscle weakness (due to changes in membrane potential)
  • U waves on ECG
  • Collecting tubules become refractory to ADH –> nephrogenic DI –> polyuria
  • Tubule cells become distended with fluid (vacuolar nephropathy)
  • Rhabdomyolysis (low K inhibits insulin –> decreased muscle glycogenesis)
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7
Q

MCC of hyperkalemia

A

Renal failure

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7
Q

MCC of hyperkalemia

A

Renal failure

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8
Q

Pseudohyperkalemia

A

RBC hemolysis from difficult venipuncture

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8
Q

Pseudohyperkalemia

A

RBC hemolysis from difficult venipuncture

9
Q

Clinical findings of hyperkalemia

A
  • Ventricular arrhythmias
  • Peaked T waves on ECG (due to accelerated depolarization of cardiac muscle)
  • Muscle weakness (high K interferes with membrane excitability by partially depolarizing it)
9
Q

Clinical findings of hyperkalemia

A
  • Ventricular arrhythmias
  • Peaked T waves on ECG (due to accelerated depolarization of cardiac muscle)
  • Muscle weakness (high K interferes with membrane excitability by partially depolarizing it)
10
Q

Functions of Potassium

A
  • Regulation of neuromuscular excitability and muscle contraction
  • Regulation of insulin secretion (low K inhibits secretion; high K stimulates insulin secretion)
11
Q

Alkalosis and K levels

A

Alkalosis causes H to move out and K into the cell –> potential hypokalemia

12
Q

Acidosis and K levels

A

Acidosis causes H to move into the cell and K out

13
Q

Diarrhea and K levels

A

There is a loss of K and HCO3 in the stool –> hypokalemia and metabolic acidosis

14
Q

Drugs that commonly cause low K

A

MCC: Loop and thiazide diuretics

Also, Insulin and beta-2 agonists may shift K into the cell

15
Q

Clinical findings in hypokalemia

A
  • Muscle weakness (due to changes in membrane potential)
  • U waves on ECG
  • Collecting tubules become refractory to ADH –> nephrogenic DI –> polyuria
  • Tubule cells become distended with fluid (vacuolar nephropathy)
  • Rhabdomyolysis (low K inhibits insulin –> decreased muscle glycogenesis)
16
MCC of hyperkalemia
Renal failure
17
Pseudohyperkalemia
RBC hemolysis from difficult venipuncture
18
Clinical findings of hyperkalemia
- Ventricular arrhythmias - Peaked T waves on ECG (due to accelerated depolarization of cardiac muscle) - Muscle weakness (high K interferes with membrane excitability by partially depolarizing it)