Flashcards in Dyskalemias Deck (117)
Where is concentration of K regulated?
Cells and kidneys
How do cells regulate K?
Via buffering/short term
How do kidneys regulate K?
What factors that affect K movement into and out of the cells?
3. Plasma K level
5. Cell production
6. Cell destruction
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
What renal regulation of K is present?
1. Plasma K
3. Non-resorbable anions
4. Flow to the distal nephron
What is a normal range of K?
Is hypokalemia preventable and easy to treat?
Yes and yes
What are signs and symptoms of hypokalemia?
Muscle weakness, cardiac dysrhymthmia, rhabdomyolysis, chronic kidney disease (long-term effect)
What are some causes of hypokalemia?
1. Poor intake (rare)
2. Renal conservation of K (15mEq)
3. Anorexia, alcoholic, elderly, poor
Which is more common to cause hypokalemia, decreased intake or increased loss?
What are the 3 main routes of K loss?
1. Cellular shift
2. GI losses
3. Renal loss
What are some renal losses of K?
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
10. Congenital adrenal hyperplasia
11. Bartter's and Gitelman's
What type of diuretics cause hypokalemia?
Loop and thiazide
Is K loss due to loop and thiazide diuretics dose related?
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)
What can be given with loop and thiazide diuretics to prevent hypokalemia?
K sparing diuretics
What 3 conditions is primary hyperaldosteronism seen in?
1. Adenoma: 65%
2. Hyperplasia: 30%
3. Carcinoma: 5%
What 3 features are seen in primary hyperaldosteronism?
2. Metabolic alkalosis
3. Mild hypernatremia
What is the treatment for primary hyperaldosteronism?
Surgery, spironolactone, eplerenone
What are the 2 non-renal causes of hypokalemia?
Cellular shift and GI losses
What are the 4 topics discussed relating to hypokalemia caused by cellular shift?
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)
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
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
How do catecholamines cause hypokalemia?
B2 receptor activity causes the Na/K ATPase to drive K into cells
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
What patients can you see a pseudohyperkalemia in?
Acute myeloid leukemia
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)