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Flashcards in Potassium Deck (69):
1

What are measured most commonly in laboratory tests?

Plasma electrolytes

2

What is measured to measure whole body potassium levels

Serum potassium

3

How much potassium is in the ECF?

Only 1-2% (the majority of K is in the ICF

4

What does the ratio of ICF to ECF establish?

The resting membrane potential of the cells

5

What is the maintaince of K balance essential for?

The normal function of excitable tissues (nerves, skeletal muscles, cardiac muscle)

6

Changes in ICF or ECF will alter the membrane potential and do what to the excitability of the tissues?

Alter the excitability of the tissues

7

What controls the movement of K in and out of the cell

Na/K pumps

8

What is responsible for excreting about 90% of K?

Kidneys

9

How is the remaining 10% excreted from the body?

-Stool
-Sweat

10

What are 3 causes of K movement into the cells? (Transcellular shifts)

1. Alkalemia
2. Insulin Excess/Acute glucose loads
3. Beta 2 agonists

11

How does alkalemia effect K?

-High pH causes H+ to come out of the cell to lower the pH
-To balance this shift, K needs to go into the cells
-Uses the H/K pump
-Hypokalemia

12

How does insulin affect K?

-Excess glucose in the body causes insulin levels to increase
-Insulin attaches to K and pulls it inside the cell
-Decreased K in the ECF= hypokalemia

13

How do beta 2 agonists affect K?

-AKA epinephrine
-Stimulates K uptake into cells
-More K in the cells = the greater excitability

14

Can inadequate uptake of K cause hypokalemia?

Yes it can man

15

What are 2 examples of renal losses that cause hypokalemia?

1. GI origin
2. Sweating

16

What are examples of extra renal losses caused by the GI system?

-Vomiting
-NG suction
-Diarrhea
-Laxative abuse

17

What are 3 examples of Renal losses that result in hypokalemia?

1. Loop or thiazide diuretics (Lasix, HCTZ)
2. Renal tubular acidosis
3. Hyperaldosteronism

18

Describe what happens in hyperaldosteronism

-Aldosterone stimulates the Na/K pump to hold onto Na- since Na and K are inversely related, you hold onto Na and then you get rid of K

19

How many hours should you measure K to obtain the correct etiology of hypokalemia?

24 hours

20

What are mild affects of hypokalemia?

-Malaise
-Fatigue
-Neuromuscular disturbances
-Weak
-Hyporeflexive

21

What are severe affects of hypokalemia?

-GI disorders (constipation, ileus, vomiting)
-Cardiac arrhythmias
-Paralysis

22

What are 2 treatment options for hypokalemia?

-Oral therapy
-IV therapy

23

Oral K are typically given in the form of _____

KCl

24

When are slow release tablets used?

For patients that are unable to tolerate liquid K supplements

25

Can a patient alter their diet to increase K levels?

Yes- usually doesn't work very well tho

26

What can result after too much oral K supplements?

-Hyperkalemia
-So monitor K levels throughout therapy

27

When is IV therapy used?

-For severe hypokalemia
-If people are unable to take oral supplements (like people with an NG tube)

28

Why are large doses of IV K difficult to administer?

-Because IVs have a large volume of fluid so to give people lots of K you would need to give them a large amount of fluid as well

29

How is IV K typically given?

-In runs of 10 meq/hr
-Up to 30-40 total
-START LOW GO SLOW

30

Should a dextrose solution be used to administer K?

No because dextrose=sugar and that will cause insulin to be made and that will take K into the cells and decrease K levels even further

31

Last is the last resort location that K can be added into?

The femoral vein
-Avoid using central venous lines because that is too close to the heart and can cause severe arrhythmias and problems

32

Can rapid treatments of K be dangerous?

YES

33

What is the big picture for hyperkalemia?

Redistribution of K from ICF to ECF

34

What are the 4 things that cause K to move from ICF to ECF?

1. Acidosis
2. Insulin deficiency
3. Beta 2 receptor blockade
4. Hyperosmolarity

35

Describe the effects of acidosis

-Inhibits renal tubule K excretion
-Keeps K in ECF

36

What type of acids is acidosis most likely to happen with?

Mineral acids (NH4Cl and HCl)

37

What are examples of organic acids

Lactic acid

38

Is cellular permeability to anions low or high in mineral acids?

Low
-This means that H moves unaccompanied into the cells and increases the K gradient favoring K efflux (out of the cell)

39

What happens if you don't have enough insulin?

K is not driven into the cells
-Ex. Diabetic patient

40

Describe what happens when you use a beta 2 receptor blockade?

-Beta blockers
-Stimulate K to come out of cells to slow the HR

41

Describe what Hyperosmolarity causes

-Hypertonic ECF causes water to move out of the cell
-This causes high K inside the cell
-This creates a K gradient that moves from high to low (inside to outside)

42

What are 2 kinds of potassium loads?

1. Exogenous loads
2. Endogenous loads

43

What are examples of exogenous loads?

(Outside the body)
-IV KCl administration
-Blood transfusions

44

What are examples of endogenous loads?

-K from tissue descruction
(Rhabdomyolysis, hemolysis, tumor lysis, burns, major surgery, GI bleeding)

45

Describe pseudohyperkalemia

-RBC hemolysis
(caused by a shaken tube)

46

What are the 5 examples of decreased renal excretion?

-Acute/Chronic oliguric renal failure
-Decreased distal nephron sodium delivery
-Impairment of renin
-Decreased aldosterone production
-Impaired response to aldosterone

47

Describe acute or chronic oliguric renal failure

-Not producing urine
-So K stays high
-Need to send them to dialysis
-Very bradycardic

48

Describe decreased distal nephron sodium delivery

-Seen in volume depletion
-Heart is failing so the kidney is not getting perfused
-Cant pee out K
-Seen in CHF

49

What are the 2 types of impairment of the RAA system?

-Hyporeninemic
-Hypoaldosteronism

50

Describe hyporeninemic

-Associated with diabetic retinopathy
-Low renin, low aldosterone, hold onto K, increase K

51

describe hypoaldosteronism

-Seen with ACE inhibitors
-Never allows angiotensin 2 to be formed
-Increases K

52

What does adrenal insufficiency do?

-Decreases aldosterone
-Increases K

53

What causes impaired response to aldosterone?

K sparing diuretics
-Ex. Aldactone, spirolactone
-aldosterone antagonist
-Prevents body from holding onto Na- so bye bye Na and hello K

54

What are neuromuscular manifestations of hyperkalemia?

-Weakness
-Paresthesias
-Areflexia

55

What are cardiac manifestations of hyperkalemia?

-Bradycardia (less K in cells to excite)
-Risk for V-fib
-Cardiac arrest

56

What happens when ECF increases?

-The membrane is partially depolarized and Na permeability is diminished and the ability to generate action potentials is decreased

57

What is the goal of hyperkalemia treatment?

PROTECT THE HEART

58

When is need for hyperkalemia urgent?

-When serum K is greater than 7 meq/L
-If ECG shows changes consistent with hyperkalemia

59

What are some ways to correct hyperkalemia?

-Shift K from ECF to ICF (stays in the body)
-Reduce total K (leaves the body)

60

What are 3 treatment options for hyperkalemia?

-Calcium administration\
-Glucose insulin infusions
-Cation exchange Resins

61

Describe calcium administration

-Temporality antagonizes the cardiac and neuromuscular effects of hyperkalemia

62

What medication is used for calcium administration

Calcium gluconate (effects in minutes and lasts about 1 hour)
-Other modalities should be used to actually decrease the K concentration

63

Describe glucose/insulin infusions

-Shifts K from outside the cell to inside the cell
(give the patient a big meal)

64

Describe the role of cation exchange resins

-Binds K in exchange for another cation (Na) in the intestinal tract
-Results in the removal of K from the body

65

What has to be checked before you give your patients Na in exchange for K?

See if the patient can tolerate Na

66

When is cation exchange resins used ASAP?

If hyperkalemia results from decreased K excretion or from increased K load

67

Describe hemodiapysis

-Very effective
-Should be used for last

68

What is an example of Cation exchange resins?

-Kayexalate

69

What are examples of chronic treatment for hyperkalemia?

-Dietary (restrict K to 40-60 mg/day)
-Pharmalogic (loop diaretics or kayexalate)