Diseases of Potassium Regulation Flashcards Preview

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Flashcards in Diseases of Potassium Regulation Deck (21):
1

What is spurious low serum K?

It is a false low serum K that occurs when there is a very high WBC count (happens in some forms of leukemia) where cells can pull potassium in to the cells. This is rare.

2

What can cause an acute hypokalemia via cell shift?

Catecholamine excess stimulation of beta 2 adrenergic receptors

This can be done by medications (beta 2 adrenergic receptor agonists) or from stress, asthma, alcohol or drug withdrawal, or very rarely insulin overdose.

3

How can you determine if chronic hypokalemia is caused by renal or extrarenal losses?

You need to figure out if the problem is too little K intake or too much K elimination.

If spot urine K is low (less than 20 mEq/L), the problem is extrarenal.

If spot urine K is high (more than 20 mEq/L), the problem is renal.

4

With extra-renal hypokalemia, the urine K is less than 20 mEq/L. There are generally two things that can cause extra-renal hypokalemia. What are they and how can you determine if that is the cause?

First, talk to the patient to see if they have had diarrhea. If for some reason they can't tell you that, you can tell from serum pH.

Diarrhea - If diarrhea is the cause, the patient will have metabolic acidosis along with the hypokalemia since bicarbonate is lost in diarrhea.

Decreased intake - if serum pH is normal, the cause is poor potassium dietary intake.

5

A patient has chronic hypokalemia with a urine K of greater than 40 mEq/L and normal serum pH. What is most likely the problem?

Hypomagnesemia

In the cortical collecting tubule cells, potassium channel efflux is inhibited by magnesium. Thus hypomagnesemia results in an increased excretion of potassium in kidney, resulting in a hypokalaemia. This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the ROMK channels in the apical tubular membrane.

6

How do you treat hypokalemia?

Hypokalemia is a serious issue and patients can die from it even if they are asymptomatic.

It's important that you reverse correctable causes of the hypokalemia such as discontinuing diuretics or correcting hypomagnesemia if present. For symptomatic patients that have arrhythmias and/or digitalis paralysis or weakness, it's very important to give IV K replacement but only up to 40 mEq/h. Potassium is caustic so if you give it too fast in IV it will burn the vessels. Thus, IV K replacement shoudl be limited to 40 mEq/h and the patient's ECG and serum K should be monitored tightly.

If the patient is asymptomatic and the hypokalemia presents with metabolic acidosis, the patient should be given K+ citrate and K+ bicarbonate.

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7

What is spurious high serum K and what causes it?

It is a falsely high serum K that is caused by a high platelet count. Platelets leak potassium when they are in test tubes because they coagulate.

8

True or False: You cant get hyperkalemia from diet alone

True, high K dietary intake is very rarely enough to cause hyperkalemia. You have to have renal dysfunction for diet to result in hyperkalemia.

9

Is hypokalemia or kyperkalemia more likely to occur due to dietary reasons?

hypokalemia.

hyperkalemia almost never happens due to diet alone

10

How can you determine if a pseudohyperkalemia (spurious high serum K) is real hyperkalemia?

Do a repeat serum K and look at the ECG to see if there are any signs of hyperkalemia

11

What is the first test you would order in a patient with hyperkalemia but you're concerned that it's spurious?

A. repeat serum K

B. plasma K

C. urine K

D. ECG

ECG

If the ECG is abnormal, treat first then continue workup

If the ECG is normal, continue the workup

12

What causes acute hyperkalemia?

Cell shift (can be K come out of cells or K not being able to enter into cells)

If you have inadequate insulin (diabetes), you can't push the K into cells.

Some medications, such as non-selective beta blockers (e.g. propanolol), can prevent K from entering into cells.

If you have rhabdomyolysis or ischemia, dead cells leak K into ECF.

13

What causes chronic hyperkalemia?

Major problem is usually K secretion by the cortical collecting tubule.

Urine K is usually (but not always) low (less than 20 mEq/L)

14

If the serum K is high and GFR is greater than 20 ml/min, what should you check?

Aldosterone levels

If aldosterone levels are low, you want to check renin. If the renin is low then the patient has DM. If the renin is high, the patient has adrenal insufficiency.

If aldosterone levels are high, you want to check urine Na. If urine Na is low, that means there is decreased Na delivery. If it is high, there may be drugs that are effecting the potassium excretion.

 

This thinking behind this workup... Remember that potassium secretion is dependent on 2 things: aldosterone and the presence of Na in the lumen of the collecting tubule.

15

What if you have a normal ECG but abnormal K serum? (either hyper or hypokalemia).

You have to treat the patient. Even though ECG looks normal at the moment, things could get bad quickly. "Don't feel good"

16

What is initial therapy for hyperkalemia with ECG changes present? (5)

  1. Give calcium (calcium gluconate). Calcium protects the heart from hyperkalemia (the lecturer says he doesn't know why). It buys you about 10-15 minutes.
  2. Give sodium bicarbonate. The idea is that acidosis causes K to come out of cells while alkalosis causes K to move into cells. This is only mildly effective.
  3. Give IV insulin (and glucose if needed). Insulin will move glucose and K into cells.
  4. Give albuterol
  5. Give K exchange resin (binds potassium in the gut and makes you poop it out. not effective acutely but effective for chronic treatment)

17

Would insulin predispose hypo or hyperkalemia?

What about hydrochlorothiazide?

What about ACE inhibitors?

Insulin - can cause hypokalemia. Insulin brings K into cells.

Hydrochlorothiazide - can cause hypokalemia. This is done by 3 mechanisms. 1) Thiazide diuretics block the Na-Cl symporter in the distal convoluted tubules. This causes more Na to reach the collecting ducts where they enter the ENaCs and interact more heavily with the Na/K-ATPase exchanger which causes more K to be secreted into the lumen through the apical channels. 2) HCTZ can also cause hypovolemia which will trigger the renin-angiotensin-aldosterone system which also upregulates the Na/K exchanger at the collecting ducts resulting in more K wasting in exchange for sodium. 3) nephron flow rate is increased during diuresis which reduces potassium concentration in the lumen. This increases the potassium gradient so potassium is lost faster through passive diffusion through ROMK channels in the principal cells.

ACE inhibitors - can cause hyperkalemia. Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors can cause retention of potassium

18

55 yr old woman with DM1

Meds: Insulin, HCTZ, ACE-i, Statin

Acute substernal chest pain

Ventricular tachycardia

Na 140

K 2.5

Cl 105

HCO3- 24

Glu 110

1. Why did she develop VT?

2. Why was the K low?

3. How do you treat the low K?

She developed VT because of hypokalemia.

What caused the hypokalemia? It's an acute event so we should think of cell shift. She presented with acute substernal chest pain so she most likely has hypokalemia from the catecholamines.

You treat the low K by giving more K to relieve the heart issues. Since her total body K is normal and it's just cell shift, this is easy to treat.

19

26 year old man with HIV/AIDS

On HIV regimen with medications known to be associated with renal K wasting.

New onset diarrhea

Na 140

K 2.5

Cl 115

Bicarbonate 15

ECG is fine.

Chronic onset

What do you do first?

First, you get a urine K. Urine K was less than 10 mEq/L. This means that the cause of hypokalemia is extrarenal (GI/diarrhea). If the urine K had been 60 mEq/L, the cause would have been renal.

The bicarbonate is low (only 15) so there is metabolic acidosis. This means that the problem was diarrhea because bicarbonate is lost in diarrhea too. This way, you know it wasn't from a lack of K in diet.

20

62 year old man with a long history of HTN.

New onset of severe SOB diagnosed as CHF

Na 140

K 5.8

Cl 111

Bicarbonate 17

BUN 56

Creatinine 1.3 (0.8 6 months later)

1. What would you predict for urine K?

2. Renin? Aldosterone?

3. What is the cause of hyperkalemia?

 

Is it a cell-shift or chronic? Chronic... so next test to do is a urine potassium. Do we think it will be low or high?

Urine K should be low. Renin and aldosterone should be high because the body is trying to increase EABV.

Patients with CHF have low effective arterial blood pressure which causes the kidneys to try to keep more Na. Keeping more Na causes less Na to make it to the collecting duct so there is no Na to exchange with the K in the principal cells (even though aldosterone is high). This causes hyperkalemia.

21

62 year old man with a long history of HTN.

New onset of severe SOB diagnosed as CHF

Na 140

K 5.8

Cl 111

Bicarbonate 17

BUN 56

Creatinine 1.3 (0.8 6 months later)

Treated with oxygen, diuretics, and an ACEI. After 48 hours

Na 135, K 2.8, Cl 90, Bicarbonate 35.

Why did he become hypokalemic and (presumably) alkalotic?

What medication should you consider adding at this time?

The diuretic given (probably furosemide or a thiazide) blocks Na reabsorption upstream to the collecting duct so more Na arrives at the collecting duct. Since aldosterone is high in this patient (CHF causing low EABV), the high Na concentration at the collecting duct causes a large amount of exchange of Na for K causing the patient to secrete more K resulting in hypokalemia.

A good medication to add at this time would be Spironolactone.