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Flashcards in Dyskalemias Deck (117)
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1

Where is concentration of K regulated?

Cells and kidneys

2

How do cells regulate K?

Via buffering/short term

3

How do kidneys regulate K?

Long term

4

What factors that affect K movement into and out of the cells?

1. pH
2. Insulin
3. Plasma K level
4. Catecholamines
5. Cell production
6. Cell destruction

5

What controls cellular K movement?

The activity activity of Na/K ATPase (affected by Beta-2 receptors, insulin, pH)
-We take advantage of this knowledge in therapies

6

What renal regulation of K is present?

1. Plasma K
2. Aldosterone
3. Non-resorbable anions
4. Flow to the distal nephron

7

What is a normal range of K?

3.6-5.1

8

Is hypokalemia preventable and easy to treat?

Yes and yes

9

What are signs and symptoms of hypokalemia?

Muscle weakness, cardiac dysrhymthmia, rhabdomyolysis, chronic kidney disease (long-term effect)

10

What are some causes of hypokalemia?

1. Poor intake (rare)
2. Renal conservation of K (15mEq)
3. Anorexia, alcoholic, elderly, poor

11

Which is more common to cause hypokalemia, decreased intake or increased loss?

INCREASED LOSS

12

What are the 3 main routes of K loss?

1. Cellular shift
2. GI losses
3. Renal loss

13

What are some renal losses of K?

1. Diuretics
2. Vomiting or NG suction
3. Diabetic ketoacidosis
4. Primary hyperaldosteronism
5. Renal tubular acidosis
6. Renovascular HTN
7. Excessive IV fluids
8. Cushing's Syndrome
9. Pseudohyperaldosteronism
10. Congenital adrenal hyperplasia
11. Bartter's and Gitelman's
12. Toulene
13. PCN

14

What type of diuretics cause hypokalemia?

Loop and thiazide

15

Is K loss due to loop and thiazide diuretics dose related?

YES

16

How do loop and thiazide diuretics cause K loss

1. Increase distal flow
2. Enhanced secretion of aldosterone (underlying disease state and intravascular volume depletion)

17

What can be given with loop and thiazide diuretics to prevent hypokalemia?

K sparing diuretics

18

What 3 conditions is primary hyperaldosteronism seen in?

1. Adenoma: 65%
2. Hyperplasia: 30%
3. Carcinoma: 5%

19

What 3 features are seen in primary hyperaldosteronism?

1. Hypokalemia
2. Metabolic alkalosis
3. Mild hypernatremia

20

What is the treatment for primary hyperaldosteronism?

Surgery, spironolactone, eplerenone

21

What are the 2 non-renal causes of hypokalemia?

Cellular shift and GI losses

22

What are the 4 topics discussed relating to hypokalemia caused by cellular shift?

1. Insulin
2. Alkalemia
3. Catecholamines
4. Pseudohyperkalemia

23

What is the effect of insulin on K?

Insulin causes K to be driven into cells by the Na/K ATPase (insulin and D50 can actually be used as a temporary treatment for hyperkalemia)

24

What is K in diabetic ketoacidosis?

K is normal to high in serum (no insulin, K not going into cells) --> Total body depletion of K
-Can lower K levels with insulin therapy

25

How does metabolic or respiratory alkalosis cause hypokalemia?

To maintain electorneurtality, there is an exchange of H for K (K is going into cells)
-Again, can give bicarb (inducing a "alkalosis" to treat hyperkalemia by driving K into cells

26

How do catecholamines cause hypokalemia?

B2 receptor activity causes the Na/K ATPase to drive K into cells

27

When can you see hypokalemia due to catecholamines?

Times of physiological stress:
1. Coronary ischemia
2. Delirium tremens
3. Acute head trauma
4. After CPR
*Catecholamine induced hypokalemia can be used as a temporizing measure for hyperkalemia

28

What patients can you see a pseudohyperkalemia in?

Acute myeloid leukemia

29

What is seen in pseduohyperkalemia induced by acute myeloid leukemia?

1. Profound leukocytosis
2. High metabolic activity
3. Avoided by cooling or quick separation (Patient should be asymptomatic)

30

Are GI sources a significant cause of K loss?

Ehhh.. all GI secretions contain some K, renal losses are more significant