Clin Lab > Potassium > Flashcards

Potassium Flashcards

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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
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)
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