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Renal 2 > Dyskalemias > Flashcards

Dyskalemias Flashcards

1
Q

Where is concentration of K regulated?

A

Cells and kidneys

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2
Q

How do cells regulate K?

A

Via buffering/short term

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3
Q

How do kidneys regulate K?

A

Long term

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4
Q

What factors that affect K movement into and out of the cells?

A
  1. pH
  2. Insulin
  3. Plasma K level
  4. Catecholamines
  5. Cell production
  6. Cell destruction
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5
Q

What controls cellular K movement?

A

The activity activity of Na/K ATPase (affected by Beta-2 receptors, insulin, pH)
-We take advantage of this knowledge in therapies

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6
Q

What renal regulation of K is present?

A
  1. Plasma K
  2. Aldosterone
  3. Non-resorbable anions
  4. Flow to the distal nephron
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7
Q

What is a normal range of K?

A

3.6-5.1

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8
Q

Is hypokalemia preventable and easy to treat?

A

Yes and yes

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9
Q

What are signs and symptoms of hypokalemia?

A

Muscle weakness, cardiac dysrhymthmia, rhabdomyolysis, chronic kidney disease (long-term effect)

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10
Q

What are some causes of hypokalemia?

A
  1. Poor intake (rare)
  2. Renal conservation of K (15mEq)
  3. Anorexia, alcoholic, elderly, poor
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11
Q

Which is more common to cause hypokalemia, decreased intake or increased loss?

A

INCREASED LOSS

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12
Q

What are the 3 main routes of K loss?

A
  1. Cellular shift
  2. GI losses
  3. Renal loss
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13
Q

What are some renal losses of K?

A
  1. Diuretics
  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
  9. Pseudohyperaldosteronism
  10. Congenital adrenal hyperplasia
  11. Bartter’s and Gitelman’s
  12. Toulene
  13. PCN
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14
Q

What type of diuretics cause hypokalemia?

A

Loop and thiazide

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15
Q

Is K loss due to loop and thiazide diuretics dose related?

A

YES

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16
Q

How do loop and thiazide diuretics cause K loss

A
  1. Increase distal flow

2. Enhanced secretion of aldosterone (underlying disease state and intravascular volume depletion)

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17
Q

What can be given with loop and thiazide diuretics to prevent hypokalemia?

A

K sparing diuretics

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18
Q

What 3 conditions is primary hyperaldosteronism seen in?

A
  1. Adenoma: 65%
  2. Hyperplasia: 30%
  3. Carcinoma: 5%
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19
Q

What 3 features are seen in primary hyperaldosteronism?

A
  1. Hypokalemia
  2. Metabolic alkalosis
  3. Mild hypernatremia
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20
Q

What is the treatment for primary hyperaldosteronism?

A

Surgery, spironolactone, eplerenone

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21
Q

What are the 2 non-renal causes of hypokalemia?

A

Cellular shift and GI losses

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22
Q

What are the 4 topics discussed relating to hypokalemia caused by cellular shift?

A
  1. Insulin
  2. Alkalemia
  3. Catecholamines
  4. Pseudohyperkalemia
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23
Q

What is the effect of insulin on K?

A

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)

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24
Q

What is K in diabetic ketoacidosis?

A

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

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25
Q

How does metabolic or respiratory alkalosis cause hypokalemia?

A

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

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26
Q

How do catecholamines cause hypokalemia?

A

B2 receptor activity causes the Na/K ATPase to drive K into cells

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27
Q

When can you see hypokalemia due to catecholamines?

A

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
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28
Q

What patients can you see a pseudohyperkalemia in?

A

Acute myeloid leukemia

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29
Q

What is seen in pseduohyperkalemia induced by acute myeloid leukemia?

A
  1. Profound leukocytosis
  2. High metabolic activity
  3. Avoided by cooling or quick separation (Patient should be asymptomatic)
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30
Q

Are GI sources a significant cause of K loss?

A

Ehhh.. all GI secretions contain some K, renal losses are more significant

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31
Q

What are some sources of GI loss of K?

A
  1. Diarrhea
  2. Surgical drains
  3. Vipoma
  4. Villous adenoma
  5. Fistulas
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32
Q

How can diarrhea lead to profound hypokalemia?

A

A prolonged course… leads to renal conservation (less than 15mEq/day)

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33
Q

What is a rare, potentially fatal complication of hyponatremia?

A

Periodic paralysis

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34
Q

Why is periodic paralysis seen in hypokalemia potentially fatal?

A

When respiratory muscles are involved

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35
Q

What levels are seen hypokalemic periodic paralysis?

A

Super low 1.5 to 2.5

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36
Q

Can there be hyperkalemic forms of periodic paralysis?

A

YES… never assume either way because they have similar symptoms?

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37
Q

What is the familial association with periodic paralysis from hypokalemia?

A

Autosomal Dominant

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38
Q

What is an association of periodic paralysis and what population is this seen in?

A

Thyrotoxicosis… Chinese males

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39
Q

Treating what conditions can cause hypokalemia and why?

A

Anemia and leukopenia –> K is uptook by new, developing cells

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40
Q

When do you see hypokalemia post-treatment of anemia and leukopenia?

A

48 hours after treatment

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41
Q

What can be given for anemia?

A

Folic acid or B12 supplements

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42
Q

What is given for neutropenia?

A

GM-CSF

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43
Q

Do you see hypokaemia in Fe deficient anemia?

A

NO… it is a slower process

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44
Q

What is hyperkalemia?

A

K above 5.1

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45
Q

What can cause hyperkalemia?

A
  1. Increased intake
  2. Shift out of cells
  3. Poor renal function: Acute or chronic
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46
Q

If there is normal kidney function, is it common to OD on oral K?

A

NO… it is very uncommon

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47
Q

What are 4 things associated with excessive intake of K?

A
  1. Kidney disease
  2. IV fluids
  3. Blood
  4. Medications
48
Q

What medications are associated with hyperkameia?

A
  1. Potassium chloride
  2. ACEi/ARB
  3. K sparing diuretics
  4. NSAIDs
  5. Cyclosporine
  6. TMP-SMX
  7. Beta-blockers
  8. Digoxin
  9. Heparin
49
Q

What can cause hyperkalemia caused by K shift or release from cells?

A
  1. Metabolic acidosis (DKA)
  2. Hyperglycemia/lack of insulin
  3. Digoxin
  4. Beta-blockers
  5. Cell death (hypothermia, trauma, chemotherapy)
50
Q

What can cause a spurious elecation of hyerkalemia?

A
  1. Severe leukocytosis: No evidence of tumor lysis
  2. Severe thrombocytosis
  3. Hemolysis
51
Q

What can cause impaired renal K excretion?

A
  1. Renal failure
  2. Volume depletion (lack of distal salt delivery)
  3. Hypoaldosteronism (adrenal insufficiency..hypotension, hyponatremia, hyperkalemia, metabolic acidosis)
52
Q

What are signs and symptoms of hyperkalemia?

A
  1. Muscle weakness
  2. EKG changes
  3. Death
53
Q

What are the EKG changes seen in hyperkalemia?

A
  1. Peaked T waves
  2. Bradycardia
  3. QRS widening
54
Q

What do you give for hyperkalemia is there are EKG findings?

A

IV calcium

55
Q

What are temprozing measures to treat hyperkalemia by shiting K into cells?

A
  1. Insulin + D50
  2. Albuterol nebulizer
  3. Sodium bicarbonate
56
Q

What are temporizing measures to treat hyperkalemia by increasing K excretion?

A
  1. Cation exchange resins
  2. Loop diuretics
  3. Dialysis
57
Q

What else in important in correcting hyperkalemia?

A

LIMIT DIETARY K

58
Q

What are the 3 options for measuring urine K?

A
  1. Spot sample
  2. 24 hour collections
  3. K/cratinine ratio
    * It’s important to have a urine K
59
Q

What is seen on abdominal CT with diarrhea?

A

Colonic air fluid levels with no other pathology

60
Q

What is a big symptoms associated with hypokalemia?

A

Muscle weakness

61
Q

What other electroylte is required for K supplementation to work?

A

Magnesium

62
Q

What is a potential cause of hypokalemia associated with a low urine K?

A

Diarrhea (patient might also be mildly acidotic)

63
Q

WHat is anuria?

A

Under 100mL of urine a day or less (can’t give a lot K with out frequently checking levels in this circumstance)

64
Q

What is oliguria?

A

400-500mL of urine a day or less

65
Q

What is non-oliguria?

A

Above 500mL of urine

66
Q

When does hypokalemia need a cardiac monitor and why?

A

Any thing 2 or below (even low 3) to check for dysrhythmias

67
Q

If giving K IV, how it is normally dosed?

A

In short fills of 10mEq

68
Q

WHat are the oral forms of K that can be given?

A

KCl or KBicarb

69
Q

What is a problem with giving K IV?

A

It can burn going in (maybe need a central line with a triple lumen catheter)

70
Q

How often should K levels be assessed?

A

Every 4 hours

71
Q

What medications do you need to check for and stop in hypokalemia?

A

K-wasting diuretics (loop and thiazide)

72
Q

What things need to be considered in treatment of hypokalemia?

A
  1. How it patient’s renal function
  2. Are the non-oliguric
  3. Do they need a cardiac monitor
  4. Type
  5. Amount
  6. Route
  7. Rate
  8. Recheck
  9. Medications that should be stopped
  10. Magnesium level
73
Q

What is seen on EKG sometimes in hypokalemia?

A

A U WAVE (V3)

74
Q

What are 8 special populations that we worry about with hypokalemia and want to quickly correct it and monitor with a cardiac monitor?

A
  1. Digoxin/antiarrhythmic drugs
  2. Ventricular arrhytmias (history of Vtach)
  3. Organic heart disease (coronary blockage)
  4. Rhabdomyolysis: Muscle breakdown (low K can get spontaneous rhabdo)
  5. Paralysis
  6. Cirrhosis: Sensitive to K levels… low K can cause production of ammonia leading to acute hepatic encephalopathy)
  7. Hypokalemic periodic paralysis: K redistribution
  8. Diabetic Ketoacidosis: K might appear normal to high, but they are severely hypokalemia…keep their K over 4
75
Q

If someone is hypokalemic and their urine K is normal, is this appropriate?

A

NO… even through urine K is normal, it’s inappropriate for someone who is hypokalemic

76
Q

Situation of mild hypernatremia, hypokalemia, and a presumed metabolic acidosis… what are you thinking?

A

Possibly primary hyperaldosteronism (Conn’s syndrome)

-Especially if prior labs show history of a mild hypokalemia

77
Q

What patients will you think primary hyperaldosteronism in?

A

New onset HTN and hypokalemia

78
Q

Does normal K rule out Conn’s syndrome?

A

NOPE… even with people who have normal K and new onset HTN, it would be Conn’s syndrome

79
Q

What can help diagnose Conn’s Syndrome?

A

A plasma renin/aldosterone ratio

80
Q

What can be done next if the plasma renin is low and the plasma aldosterone is high?

A

Looking at doing a CT to look for mass on adrenal glands causing Conn’s syndrome

81
Q

What is the treatment for primary hyperaldosteronism?

A

If it’s unilateral, can have it removed

Bilateral or patient doesn’t want surgery…drugs

82
Q

What drugs can be given for primary hyperaldosteronism

A

Spironolactone (want to control aldosterone levels)

83
Q

What are some bad SE of spironolactone that might convince patients to get their mass removed?

A

Gynecomastia and sore boobs

84
Q

If you have a patient that some kind of accident, fell, ect., with a pretty normal exam, bradycardia, little edema and realllllly high K, what are you thinking?

A

RHABDOMYOLYSIS

85
Q

What is seen lab wise with rhabdomyolysis?

A

High Na, REALLY high K, low CO2, Acute renal failure (high creatinine), increased AST and ALT

86
Q

Which is more specific for liver, AST or ALT

A

ALT (this one has a L in it for LIVER)

87
Q

Besides blood work, what other test is useful for diagnosing rhabdomyolysis and what is seen on it?

A

Urine… you would see blood on urinamysis but no RBCs (Heme + urine without RBCs)

88
Q

What other blood test is important for rhabdomyolysis?

A

CPK

89
Q

What a drug that can cause hyperkalemia?

A

Lisinopril

90
Q

How does simvastatin affect K levels?

A

It can contribute to rhabdo-associated hyperkalemia, but alone it doesn’t cause hyperkalemia (only in setting of rhabdo)

91
Q

What acid-base disorder can cause hyperkalemia?

A

Metabolic acidosis

92
Q

Does acute renal failure atribute to hyperkalemia?

A

YES

93
Q

If your hyperkalemic patient has an EKG showing bradycardia and a wide QRS with peaked T waves, is this okay?

A

NO…serious trouble, potential death

94
Q

Which drug can cause high K and make HR worse in a hyperkalemic patient?

A

Metoprolol

95
Q

What is the first thing done with an acute hyperkalemia?

A

Give Calcium gluconate IV (stat dose of 1g over an hour initally)

96
Q

What is the second step in an acute hyperkalemia treatment?

A

IV dextrose followed by IV regular insulin (give the dextrose to make sure blood sugar doesn’t drop too much with the insulin, which is forcing K into the cells to lower serum K levels)

97
Q

What other thing can be given in an acute hyperkalemia setting?

A

Nebulized albuterol

98
Q

What isn’t a good type of fluid for someone with hyperkalemia?

A

A lactate ringer because this has K in it

99
Q

If your patient is in acute renal failure, can you give them an ACEi or ARB?

A

NOPE… at this point the kidneys are dependent on angiotensin for perfusion… if you block this, you ruin their kidneys

100
Q

If someone has hyperkalmeia, what kind of diet do they need?>

A

A LOW K DIET

101
Q

What does a salt substitute increase?

A

Just K (no effect on creatinine

102
Q

Does ibuprofen increase K and creatinine?

A

YESSS… someone with chronic kidney disease, NO NSAIDS

103
Q

Is acetaminophen safe for patients with chronic kidney disease (ie it won’t affect K and creatinine)

A

YES

104
Q

Will glucosamine and chondroitin affect K and creatinine?

A

Nooooo

105
Q

What are some foods that are high in K and should be avoided in patients with hyperkalemia

A

Tomatoes, potatoes, bananas, honeydew (but apples don’t have high K)

106
Q

What medications can cause high K?

A

i) ACE inhibitors
ii) Amiloride
iii) Angiotensin receptor blockers
iv) Beta Blockers
v) Cyclosporine
vi) Digoxin
vii) Eplereone
viii) Heparin
ix) NSAIDs
x) Pentamidine
xi) Spironolactone
xii) Succinylcholine
xiii) Tacrolimus
xiv) Transfusions of blood
xv) Triamterene
xvi) Trimethoprim
xvii) Yasmin

107
Q

What is a sign that causes you to worry and get STAT dialysis treatment in a patient presenting with super high K and creatining and a low CO2 (in metabolic acidosis?

A

Respiratory decline (crackles, edema, ect.)

108
Q

What is a mainstay for quick correction or a quick dose for someone with mildly elevated K levels?

A

Sodium polystyrene sulfonate

109
Q

What can sodium polystyrene sulfonate cause in someone who is post-op or has bowel issues?

A

Bowel necrosis (can lead to death)

110
Q

How does sodium polystyrene sulfonate work?

A

This drug is a binder for K that works in the colon to exchange K for Na (so it is given orally usually, sometimes as an enema)

111
Q

Does sodium polystyrene sulfonate work in someone with an ileostomy?

A

No… it requires contact with the colon to work

112
Q

What is a SE of sodium polystyrene sulfonate?

A

Diarrhea (it can get pretty ugly)

113
Q

What is the first symptom of hyperkalemia?

A

DEATH

114
Q

If your patient presents with weak arms and legs, feeling heavy, what are you gonna check?

A

K

115
Q

What monitoring should patients with hyper or hypokalemia have?

A

Cardiac monitoring… check for QRS, bradycardia ect.

116
Q

How often should K levels be assessed?

A

3-4 hours after dosing to make sure it improves

117
Q

What do you need to assess with hyperkalemia in your patients history?

A

See if they are taking supplements, diet high in K, and medications that might cause hyperkalemia (AND STOP THEM)

Renal 2 (10 decks)

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