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Clin Lab > Potassium > Flashcards

Potassium Flashcards

1
Q

What are measured most commonly in laboratory tests?

A

Plasma electrolytes

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2
Q

What is measured to measure whole body potassium levels

A

Serum potassium

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3
Q

How much potassium is in the ECF?

A

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

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4
Q

What does the ratio of ICF to ECF establish?

A

The resting membrane potential of the cells

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5
Q

What is the maintaince of K balance essential for?

A

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

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6
Q

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

A

Alter the excitability of the tissues

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7
Q

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

A

Na/K pumps

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8
Q

What is responsible for excreting about 90% of K?

A

Kidneys

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9
Q

How is the remaining 10% excreted from the body?

A
  • Stool

- Sweat

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10
Q

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

A
  1. Alkalemia
  2. Insulin Excess/Acute glucose loads
  3. Beta 2 agonists
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11
Q

How does alkalemia effect K?

A
  • 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
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12
Q

How does insulin affect K?

A
  • 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
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13
Q

How do beta 2 agonists affect K?

A
  • AKA epinephrine
  • Stimulates K uptake into cells
  • More K in the cells = the greater excitability
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14
Q

Can inadequate uptake of K cause hypokalemia?

A

Yes it can man

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15
Q

What are 2 examples of renal losses that cause hypokalemia?

A
  1. GI origin

2. Sweating

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16
Q

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

A
  • Vomiting
  • NG suction
  • Diarrhea
  • Laxative abuse
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17
Q

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

A
  1. Loop or thiazide diuretics (Lasix, HCTZ)
  2. Renal tubular acidosis
  3. Hyperaldosteronism
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18
Q

Describe what happens in hyperaldosteronism

A

-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

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19
Q

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

A

24 hours

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20
Q

What are mild affects of hypokalemia?

A
  • Malaise
  • Fatigue
  • Neuromuscular disturbances
  • Weak
  • Hyporeflexive
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21
Q

What are severe affects of hypokalemia?

A
  • GI disorders (constipation, ileus, vomiting)
  • Cardiac arrhythmias
  • Paralysis
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22
Q

What are 2 treatment options for hypokalemia?

A
  • Oral therapy

- IV therapy

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23
Q

Oral K are typically given in the form of _____

A

KCl

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24
Q

When are slow release tablets used?

A

For patients that are unable to tolerate liquid K supplements

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25
Q

Can a patient alter their diet to increase K levels?

A

Yes- usually doesn’t work very well tho

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26
Q

What can result after too much oral K supplements?

A
  • Hyperkalemia

- So monitor K levels throughout therapy

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27
Q

When is IV therapy used?

A
  • For severe hypokalemia

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

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28
Q

Why are large doses of IV K difficult to administer?

A

-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
Q

How is IV K typically given?

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

Should a dextrose solution be used to administer K?

A

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
Q

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

A

The femoral vein

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

32
Q

Can rapid treatments of K be dangerous?

A

YES

33
Q

What is the big picture for hyperkalemia?

A

Redistribution of K from ICF to ECF

34
Q

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

A
  1. Acidosis
  2. Insulin deficiency
  3. Beta 2 receptor blockade
  4. Hyperosmolarity
35
Q

Describe the effects of acidosis

A
  • Inhibits renal tubule K excretion

- Keeps K in ECF

36
Q

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

A

Mineral acids (NH4Cl and HCl)

37
Q

What are examples of organic acids

A

Lactic acid

38
Q

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

A

Low

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

39
Q

What happens if you don’t have enough insulin?

A

K is not driven into the cells

-Ex. Diabetic patient

40
Q

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

A
  • Beta blockers

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

41
Q

Describe what Hyperosmolarity causes

A
  • 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
Q

What are 2 kinds of potassium loads?

A
  1. Exogenous loads

2. Endogenous loads

43
Q

What are examples of exogenous loads?

A

(Outside the body)

  • IV KCl administration
  • Blood transfusions
44
Q

What are examples of endogenous loads?

A

-K from tissue descruction

Rhabdomyolysis, hemolysis, tumor lysis, burns, major surgery, GI bleeding

45
Q

Describe pseudohyperkalemia

A

-RBC hemolysis

caused by a shaken tube

46
Q

What are the 5 examples of decreased renal excretion?

A
  • Acute/Chronic oliguric renal failure
  • Decreased distal nephron sodium delivery
  • Impairment of renin
  • Decreased aldosterone production
  • Impaired response to aldosterone
47
Q

Describe acute or chronic oliguric renal failure

A
  • Not producing urine
  • So K stays high
  • Need to send them to dialysis
  • Very bradycardic
48
Q

Describe decreased distal nephron sodium delivery

A
  • Seen in volume depletion
  • Heart is failing so the kidney is not getting perfused
  • Cant pee out K
  • Seen in CHF
49
Q

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

A
  • Hyporeninemic

- Hypoaldosteronism

50
Q

Describe hyporeninemic

A
  • Associated with diabetic retinopathy

- Low renin, low aldosterone, hold onto K, increase K

51
Q

describe hypoaldosteronism

A
  • Seen with ACE inhibitors
  • Never allows angiotensin 2 to be formed
  • Increases K
52
Q

What does adrenal insufficiency do?

A
  • Decreases aldosterone

- Increases K

53
Q

What causes impaired response to aldosterone?

A

K sparing diuretics

  • Ex. Aldactone, spirolactone
  • aldosterone antagonist
  • Prevents body from holding onto Na- so bye bye Na and hello K
54
Q

What are neuromuscular manifestations of hyperkalemia?

A
  • Weakness
  • Paresthesias
  • Areflexia
55
Q

What are cardiac manifestations of hyperkalemia?

A
  • Bradycardia (less K in cells to excite)
  • Risk for V-fib
  • Cardiac arrest
56
Q

What happens when ECF increases?

A

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

57
Q

What is the goal of hyperkalemia treatment?

A

PROTECT THE HEART

58
Q

When is need for hyperkalemia urgent?

A
  • When serum K is greater than 7 meq/L

- If ECG shows changes consistent with hyperkalemia

59
Q

What are some ways to correct hyperkalemia?

A
  • Shift K from ECF to ICF (stays in the body)

- Reduce total K (leaves the body)

60
Q

What are 3 treatment options for hyperkalemia?

A
  • Calcium administration\
  • Glucose insulin infusions
  • Cation exchange Resins
61
Q

Describe calcium administration

A

-Temporality antagonizes the cardiac and neuromuscular effects of hyperkalemia

62
Q

What medication is used for calcium administration

A 
Calcium gluconate (effects in minutes and lasts about 1 hour)
-Other modalities should be used to actually decrease the K concentration
63
Q

Describe glucose/insulin infusions

A

-Shifts K from outside the cell to inside the cell

give the patient a big meal

64
Q

Describe the role of cation exchange resins

A
  • Binds K in exchange for another cation (Na) in the intestinal tract
  • Results in the removal of K from the body
65
Q

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

A

See if the patient can tolerate Na

66
Q

When is cation exchange resins used ASAP?

A

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

67
Q

Describe hemodiapysis

A
  • Very effective

- Should be used for last

68
Q

What is an example of Cation exchange resins?

A

-Kayexalate

69
Q

What are examples of chronic treatment for hyperkalemia?

A
  • Dietary (restrict K to 40-60 mg/day)

- Pharmalogic (loop diaretics or kayexalate)

Clin Lab (23 decks)

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