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Med Surg 1 > Electrolyte Disturbances (Online Lecture) > Flashcards

Electrolyte Disturbances (Online Lecture) Flashcards

1
Q

calcium is ECF, ICF or both

A

both

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2
Q

where is majority of calcium located

A

bones and teeth

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3
Q

role of calcium

A

neuromuscular function, heart muscle depolarization, and contraction, coagulation and bone and teeth development

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4
Q

calcium is regulated by

A

PTH and calcitonin

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5
Q

what occurs when low levels of ionized calcium

A

increase PTH
- increase absorption from GI
- Increased released of CA by bones
- Increase reabsorption of CA by kidneys

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6
Q

what occurs when high levels of ionized calcium

A

decrease PTH
Calcitonin secreted
- bones reabsorb more calcium
- more calcium to be excreted via kidney
- less calcium to be absorbed via GI tract

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7
Q

what should we consider Ca levels with

A

albumin
- low ablumin = low ca

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8
Q

symptoms for hypocal are the same as

A

hypomag

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9
Q

causes of hypocal
hypoparathyroidism

A

para thy regulates levels

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10
Q

causes of hypocal
malabsorption (gastric bypass)

A

receive ca from GI

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11
Q

causes of hypocal
massive transfusion of citrated blood

A

citrate is added to packed RBC which binds to Ca and prevents blood from clotting

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12
Q

causes of hypocal
renal failure

A

kidneys regulate

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13
Q

causes of hypocal
medications

A

aluminum antacids
phosphates
loop diuretics
aminoglycosides
steroids
chemo

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14
Q

causes of hypocal
vit d deficiencies

A

necessary for absorption of ca

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15
Q

causes of hypocal

A

hypoparathyroidism, malabsorption, pancreatitis, alkalosis, massive transfusion of citrated blood, renal failure, medications, vit d deficiencies, peritonitis, chronic diarrhea, decreased PTH, alcoholism, radical neck dissection

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16
Q

manifestations of hypocal

A

hyperactive DTRs (deep tendon reflexes, trousseau sign, chvostek, seizures (very severe), abnormal clotting, prolonged QT, anxiety, irritability, pulmonary cardiopulmonary arrest

tetany, circumoral numbness, parestehias, dyspnea, laryngospasms

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17
Q

chvostek

A

twitching of facial nerve

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18
Q

trousseau

A

blood pressure cuff on upper arm and carpal spasm will occur

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19
Q

what other lyte should we check when we suspect hypocal

A

mag (usually hypomag)

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20
Q

hypocal key manifestation

A

increase neuromuscular excitability

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21
Q

medical management of hypocal
IV cal gluconate

A

IV push is life threatening, push slow
piggyback over an hour

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22
Q

medical management of hypocal

A

IV cal gluconate, calcium and vitamin D supplements, diet

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23
Q

why do we need to give vit d supplement as well

A

vit d is neccesary for cal absorption

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24
Q

nursing management hypocal

A

hypocalcemia is life threatening, weight bearing exercises

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25
Q

hypocal level

A

8.6

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26
Q

cal normal level

A

8.6-10.2

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27
Q

hypercal level

A

10.2

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28
Q

hypercal main manifestation

A

decrease neuromuscular excitability

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29
Q

causes of hypercal

A

malignancy (bone cancer), hyperparathyroid, bone loss related to immobility, over use of Ca supplements, acidosis, cortisone therapy, thiazide diuretics, digoxin toxicity, excessive PTH

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30
Q

manifestations of hypercal

A

muscle weakness, incorrdination, constipation, abdominal and bone pain, ECG changes, dysrhythmias, heart block, arrest, bronchospasm, depression, lethargy, coma

anorexia, nausea, vomiting, polyuria, thirst

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31
Q

medical management hypercal

A

treat underlying cause, fluids, furosemide (loops), phosphates, calcitonin (emergency). biphosphonates

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32
Q

nursing management hypercal

A

hypercalcemic crisis has high mortality, fluids 3-4L/d, fiber for constipation, ensure safety

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33
Q

normal mag levels

A

1.3-2.3

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34
Q

hypercal presents the same as

A

hypermag

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35
Q

hypomag level

A

1.3

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36
Q

causes of hypomag

A

alcoholism, GI losses (NG on suction, diarrhea, fistula), enteral or parental feeding deficient in mag, medications (diuretics), rapid administration of citrated blood, diabetic ketoacidosis, sepsis, burns, hypothermia

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37
Q

manifestations of hypomag

A

neuromuscular irritability, ecg changes

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38
Q

medical management of hypomag

A

diet, oral mag, magnesium sulfate IV (severe, piggyback)

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39
Q

nursing management hypomag

A

ensure safety, patient teaching related to diet, alcohol use, IV care

40
Q

hypomag is normally accompanied by

A

hypocal

41
Q

what is common in hypomag patients

A

dysphagia

42
Q

hypermag level

A

2.3

43
Q

hypermag main manifesation

A

decrease neuromuscular excitability

44
Q

causes of hypermag

A

renal failure, DKA, excessive administration of mag, excessive use of antacids

45
Q

manifestations of hypermag

A

lowered BP, muscle weakness, depressed resps, ecg changes

46
Q

medical management of hypermag

A

IV calcium gluconate, loop diuretics, IV NS or RL, hemodyalisis

47
Q

nursing management of hypermag

A

patient teaching regarding mag containing OTC meds

48
Q

normal K level

A

3.5-5

49
Q

K ICF or ECF or both

A

ICF

50
Q

balance of K depends on

A

aldosterone and GFR

and bowel

51
Q

how does diabetic ketoacidosis affect K

A

K pushes put of of cell and treatment will push it back into cell

52
Q

main role of K

A

conduction of myocardial cells

53
Q

hypoK level

A

3.5

54
Q

causes of hypoK

A

GI losses (severe diarrhea, vomiting, NG tube on suction), medications (loop diuretics, steroids, insulin, antibiotics, alterations of acid - base, alkalosis (serum K pushing into cell), hyperaldosterone, poor diet intake, starvation, diuretics, dig tox

55
Q

what other lab value do we look at for hypoK

A

BUN and creatine (kidney function is crucial for excretion of K)

56
Q

manifestations of hypoK

A

dysrhythmias, Flat T waves or U wave, muscle weakness, decreased responsiveness, tornadoes, vfib, hypotension

fatigue, N/V, paresthesias, decreased muscle strength, DTR

57
Q

medical management HypoK

A

increase diet potassium (orange juice, melon, banana, citrus fruit, meat, milk) K replacement, IV for severe deficit

58
Q

nursing management hypok

A

monitor ECG and ABG (alkalosis may cause), diet potassium, IV care

59
Q

IV potassium

A

must be given slowly through IV (60 mins)
NEVER GIVE IV PUSH

60
Q

hyperK level

A

5

61
Q

causes of hyperK
usually treatment related

A

too aggressive with hypoK treatment

62
Q

causes of hyperK
impaired renal function

A

kidneys are the main way of removing K
- elderly
- hemodialysis

63
Q

causes of hyperK
tissue trauma / crush/ burns

A

cells release potassium into blood

64
Q

causes of hyperK
metabolic acidosis

A

K leaves cells to allow hydrogen to go in

65
Q

causes of hyperK
stored PRBC

A

pt recieving blood transfusion if that blood has been stored for longer, when blood sits increase in K as compared to fresh blood

66
Q

causes of hyperK

A

treatment, renal function, hyperaldosterone, tissue trauma, crush injury, burns, metabolic acidosis, stored PRBC, ace and NSAIDs

67
Q

manifestations of hyperK

A

cardiac changes and dysrhythmias
(tachy to Brady to asystole) peaked T waves, wide QRS

muscle weakness, parenthesis, GI mainifestaions

68
Q

medical management

A

monitor ECG, cation exchange resin (Kayexalate or Lokelma), B 2 agonists, dialysis, cocktail

69
Q

Cocktail/shifter reason

A

used to temporarily shift K into cell, buys time for kayexalate and lokelam to work

70
Q

cocktail/shifter ingredients

A

IV AMP push sodium bicarb (shift)
AMP calcium gluconate (neutralizer)
10 units regular insulin IV push (shift)
AMP D50/hypertonic dextrose (shift)

follow with kayexalate, lokelma and dialysis (remover)

71
Q

katexalate vs lokelma

A

Kay: exchange potassium in bowel and cause severe diarrhea
Lok: does not cause diarrhea

72
Q

nursing management

A

frequent electrolyte monitoring
assess VS, CV, and near closely
accurate I and O
- foley
maintain safety
patient/family teaching

73
Q

CBIGKID

A

calcium gluconate IV push
Bicarb
Glucose/Amp D50
Katexalate
insulin 10 unit Iv push
dialysis

Lokelam

74
Q

sodium normal

A

135-145

75
Q

sodium role

A

neuromuscular function, water balance, cellular depolarization, acid base

76
Q

sodium ICF, ECF, both

A

ECF

77
Q

a gain or loss in sodium normally results in

A

gain or loss of water

78
Q

sodium imbalances main manifestation

A

neuro issues

79
Q

what systems help regulate sodium

A

kidneys, ADH, thirst, RAAS

80
Q

hyponat level

A

135

81
Q

what other labs to look at for hyponat

A

serum osmo: less than 280= dilute
urine specific gravity: less than 1.010

82
Q

what occurs because of hyponat

A

ecf becomes diluted, intracellular swelling because there is less ECF osmolality

83
Q

what do symptoms of hyponat depend on

A

how rapid sodium change is

84
Q

clinical effects of hyponat

A

neurological changes
mild: N/V, irratibility, disorientation
severe: stupor, comatose, seizures

poor skin turgor, dry mucosa, rapid pulse, decrease BP

85
Q

medical management of hyponat

A

water restriction
sodium replacement
mild: salt tabs, isotonic solution, high sodium foods
less than 120: ICU, hypertonic saline

86
Q

nursing management of hyponat

A

neuro status, I and O, patient safety, medications, lab studies

87
Q

hypernat level

A

145

88
Q

what occurs during hypernat

A

ECF becomes concentrated and fluid moves out of cell causing cell shrinkage

89
Q

symptoms of hypernat are very similar to

A

fluid volume def
- which commonalty causes hypernat

90
Q

we see hypernat in patients who cannot regulate thirst / respond and communicate to thirst, examples of this patient

A

comatose
unconscious
dementia
elderly

91
Q

clinical effects of hypernat

A

neurologic symptoms
weakness, lethargy, confusion
as it gets worse: stupor, seizures, coma, twitching, tremor

thirst, elevated temp, dry swollen tongue, restlessness, weakness

92
Q

medical management hypernat

A

hypotonic electrolyte, D5W

93
Q

some causes of hypernat

A

tube feeding with no free water, heat stroke, drowning in salt water

94
Q

nursing management for hypernat

A

neuro status

OTC sources of sodium, fluids, VS, HR, I and O

95
Q
A

Med Surg 1 (47 decks)

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