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Clin Med 3 > Fluids, Electrolytes, and Imbalances - Exam 2 > Flashcards

Fluids, Electrolytes, and Imbalances - Exam 2 Flashcards

1
Q

Na is the major what?

A

major cation in extracellular fluid (ECF)

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2
Q

what does Na regulate?

A

regulates transmission of impulses in nerve and muscle fibers

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3
Q

Na is the main factor in determining what?

A

main factor in determining volume of extracellular space

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4
Q

who is a risk with hyponatremia?

A

elderly

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5
Q

what does Na help maintain?

A

helps maintain acid-base balance

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6
Q

what is dysnatremias?

A

disruptions of Na concentration

has more to do with hydration (fluid status) than circulating sodium

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7
Q

what is the most common type of hyponatremia?

A

hypo-osmolality with hypervolemia

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8
Q

hyponaturemia and impaired water excretion?

A

pt is fluid overloaded, so Na is diluted -> have impaired water excretion

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9
Q

causes of impaired water excretion and hyponatremia

A

HF, cirrhosis, renal failure, aggressive IV fluid admin (give too much fluid)

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10
Q

how does hyperglycemia cause hyponatremia

A

high serum sugar causes the cells to release water diluting sodium while not overloading the body with water

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11
Q

how does hypertonic mannitol admin cause hyponatremia?

A

water movement out of brain cells

-given for cerebral edema to try to decrease ICP -> try to move water out of brain cells, but also moves water out of other cellist the body, so can dilute Na in the entire body

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12
Q

how does SIADH occur? what does SIADH cause?

A
  • hyponatremia as a result of excess water
  • result of increase in circulating ADH
  • caused by hypersecretion or ectopic source (secreting too much ADH)
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13
Q

chronic alcoholics and hyponatremia

A

beer potomania syndrome - binge drinkers

-get chronic suppression of ADH with alcoholics

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14
Q

hyponatremia caused by water into occurs in who?

A

marathon athletes (need to check their Na first b/c don’t want to dilute them too much), drugs (ecstasy)

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15
Q

what is acute hyponatremia? chronic hyponatremia?

A

acute: < 48 hrs
chronic: >48 hrs or duration, unclear how long they’ve had it

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16
Q

the more acute the hyponatremia, the great there what?

A

the greater the complications

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17
Q

what are the most important determinants of onset of symptoms for hyponatremia?

A

the degree of hyponatremia and rapidity that it develops

-the more acute it is, the more severe it is

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18
Q

what are the first presentations of hyponatremia and at what levels of Na do you get them?

A

nausea and malaise

-Na falls below 125-130

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19
Q

hyponatremia sx’s at levels below 115-120

A

HA, lethargy, obtunded, seizures, coma, resp arrest, pulmonary edema

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20
Q

goals of tx for hyponatremia

A
  • prevent further decline in serum Na concentration (#1)
  • decr ICPin pts at risk for developing brain herniation
  • relieve sx of hyponatremia
  • avoid excessive overcorrection in pts at risk for osmotic demyelination syndrome
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21
Q

what is the first thing to do when treating hyponatremia?

A

prevent further decline in serum sodium concentation

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22
Q

what people are at risk for developing brain herniation from hyponatremia/are at risk of hyponatremia?

A
  • competitive exercise, ecstasy, psychosis
  • women and children post-op
  • recent brain injury, surgery, neoplasm
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23
Q

what happens if you overcorrect Na too quickly?

A

get neurologic sx’s -> osmotic demyelination syndrome

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24
Q

how do you treat hyponatremia?

A

bolus 3% saline

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25
Q

what is the most common cause of hypernatremia? causes?

A

volume depletion/hypovolemia (fluid volume is low, so salt goes high)

-fever, sweating, vomiting, diarrhea, primary hypodipsia (ex: condition where you don’t drink)

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26
Q

what diabetes causes hypernatremia?

A

diabetes insipidus

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27
Q

how does diabetes insidious cause hypernatremia?

A

-passage of large volume of dilute urine

cause hypovolemic hypernatremia thru 2 mechanisms

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28
Q

2 mechanisms that diabetes insipidus causes hypernatremia?

A
  1. decreased secretion of ADH from posterior pituitary

2. increased renal resistance to ADH - can’t concentrate urine (passing lots of dilute urine)

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29
Q

most common cause of diabetes insipidus causing hypernatremia?

A

damage after trauma or surgery to the region of the pituitary and hypothalamus

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30
Q

primary hyperaldosteronism causing hypernatremia

A
  • problem with the adrenal (usually a benign tumor)

- have excess production of aldosterone -> increased Na and water and decreased K

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31
Q

increased what and decreased what in primary hyperaldosteronism?

A

increased sodium and water and decreased K

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32
Q

altered thirst mechanism causing hypernatremia - common in who?

A

psych pts and elderly institutionalized pts

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33
Q

signs and sx’s of hypernatremia

A

AMS, ataxia, seizures, hyperreflexia, spasticity/twitching, irritability, lethargy

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34
Q

management of hypernatremia?

A

D5W IV

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35
Q

caution in what when treating hypernatremia?

A

hyperglycemia

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36
Q

treatment of diabetes insipidus?

A

desmopressen - ADH analog

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37
Q

K+ is the most abundant what?

A

cation

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38
Q

what is K+ vital to?

A

cell metabolism and neurologic and cardiac electrical transmission

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39
Q

what are the main regulators of K+?

A

kidneys

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40
Q

98% of K+ is ___?

A

intracellular, chiefly in muscle

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41
Q

K+ is secreted and reabsorbed where?

A

within the nephrons of the kidneys

42
Q

most common causes of hypokalemia?

A

diuretic therapy, diarrhea, vomiting

43
Q

what meds cause large shifts of K+ from extracellular to intracellular?

A

diuretics (esp Loops and Thiazides)

insulin

beta-adrenergic agonists (albuterol, terbutaline)

44
Q

hypo___ can cause hypoK?

A

hypomagnesemia (b/c K and Mg are very intimately related)

45
Q

hyperaldosteronism does what to K?

A

increases K excretion from kidneys

46
Q

sx’s of hypokalemia?

A

muscle weakness/cramping

respiratory muscle weakness

palpitations

ileus, constipation, fatigue

47
Q

get mostly what type of sx’s when hypokalemic?

A

muscle sx’s b/c most K is stored in the muscles (and also in muscles of the gut)

48
Q

what is seen on an EKG if pt is hypokalemic?

A

flat T waves, ST segment depression, U waves

49
Q

what can mild hypokalemia be treated with?

A

oral KCl

50
Q

what does severe and symptomatic hypokalemia need to be treated with?

A

IV replacement w/K and continuous telemetry

51
Q

if hypokalemic and also hypomagnesemia, what do you replete first?

A

must replete Mg first before K + replacement (b/c both are related)

52
Q

Mg+ plays a big role in regulation of what?

A

the Na+K+ATPase pump

53
Q

if see K+ above 7 or 8, what do you want to do?

A

redraw
-sometimes when draw blood cells, they smack against tube and break open and release K (hemolysis), so K will be falsely elevated -> redraw to confirm actually hyperkalemia

54
Q

hyperkalemia can be due to what?

A

impaired urinary K+ excretion

common complication in renal disease/insufficiency

medications (ACEIs, ARBs, Aldosterone antagonists - spironolactone)

55
Q

hyperkalemia is a common complication in what?

A

renal disease/insufficiency

56
Q

meds that cause hyperkalemia?

A

ACEIs - Lisinopril

ARBs - Losartan

Aldosterone antagonist - spironolactone

57
Q

what are the sx’s of hyperkalemia?

A

muscle weakness/paralysis, paresthesias, arrhythmias

58
Q

what is seen on an EKG when hyperkalemic?

A

tall or peaked T waves, widened/bizarre QRS, flat P wave

TWiFP

59
Q

what is the first thing given when treating hyperkalemia? why?

A

IV calcium-gluconate or chloride

-CARDIOPROTECTIVE - DOESN’T DECREASE K+

60
Q

what meds actually treat hyperkalemia?

A

IV hypertonic glucose with regular insulin (moves excess K+ into the cells)

IV loop or thiazide diuretics (rapid removal of K+ from body)

61
Q

treat what causes for hyperkalemia?

A

treat reversible causes - hypovolemia

62
Q

PO treatment of hyperkalemia?

A

have to give resins that bind K+ and excreted in stool

-Kayexalate-sodium polysterene (not used much)

63
Q

what else, besides meds, treats hyperkalemia?

A

hemodialysis

64
Q

where is Ca primary stored?

A

bones and teeth

65
Q

what processes require Ca+?

A
  • blood coagulation
  • nerve excitability
  • development of action potentials for muscle contraction (skeletal, cardiac, smooth)
66
Q

what factors influence serum Ca+ concentration?

A

PTH, vitamin D, calcium ion, phosphate

67
Q

what is crucial for osteoclastic activity in bone? and ability of the intestines to store Ca?

A

Ca, phosphorous, and Vitamin d

68
Q

what is the most common form of Ca found in the body and that is also usually measured?

A

ionized Calcium

69
Q

most common causes of hypocalcemia?

A
  • parathyroid disease
  • thyroid disease
  • thyroid or parathyroid-ectomy
  • CKD
  • vitamin d deficiency
70
Q

Ca+ is bound to what in the serum? means what?

A

albumin

-means need to check Ca and also albumin

71
Q

what is albumin and what is it produced what?

A

it’s a protein produced by the liver

72
Q

what is the function of albumin/

A

the distribution of body fluids

carrier protein in the blood for steroids, fatty acids, and thyroid hormone

73
Q

hypoalbuminemia can cause?

A

pseudohypocalcemia

74
Q

to determine true Ca levels, what is required?

A

correction for albumin

75
Q

sx’s of hypocalcemia?

A
  • parasthesias
  • hyperreflexia
  • TETANY
  • MUSCLE SPASM
  • muscle cramps
  • seizures
76
Q

classic physical findings of hypocalcemia?

A

Chvostek sign - facial spasm following the percussion of the facial nerve

Trousseau’s sign - spasm of the hand elicited by inflation of a BP cuff

77
Q

what does an EKG look like when hypocalcemia?

A

prolonged QT interval

78
Q

treatment of severe symptomatic hypocalcemia?

A

IV supplements - calcium gluconate

79
Q

if have low Mg and also low Ca, what must you correct first?

A

must correct a Mg deficit first

80
Q

tx for asymptomatic or mild hypocalcemia?

A
  • PO Ca+ replacement with asymptomatic hypocalcemia

- PO calcium carbonate, calcium citrate, calcium carbonate

81
Q

what are the most common causes of hypercalcemia?

A

hyperparathyroidism and bone malignancy (multiple myeloma)

82
Q

signs and sx’s of hypercalcemia?

A

MOANS, GROANS, STONES, AND PSYCHIATRIC UNDERTONES

-bone pain, muscle weakness, confusion, lethargy, constipation, nephrolithiasis

83
Q

common sx’s seen in multiple myeloma and bone mets from cancers?

A

MOANS, GROANS, STONES, AND PSYCHIATRIC UNDERTONES

84
Q

hypercalcemia tx

A
  • volume expansion with isotonic saline
  • salmon calcitonin with a bisphosphenate
  • zoledronic acid (bisphosphenate)
85
Q

how does calcitonin work to decrease Ca levels?

A

it decreases bone reabsorption and increases renal excretion of Ca

86
Q

Mg+ is responsible for what?

A
  • ATP processing
  • macronutrient and energy metabolism
  • neuromuscular transmission
  • can block Ca+ and K+ channels
87
Q

what is the principle reservoir of Mg+?

A

bone

88
Q

Mg+ levels regulated by what?

A

intestinal absorption and renal excretion

if these are off, then Mg+ is off

89
Q

hypomagnesemia is commonly seen in what?

A

chronic ETOH abuse (from poor dietary intake)

90
Q

causes of hypomagnesemia?

A

-***chronic ETOH abuse

  • reduced intestinal absorption
  • increased renal excretion
  • excessive GI loss (vomiting, diarrhea)
  • starvation
  • refeeding syndromes (after starvation and after gastric bypass)
91
Q

what are the signs and sx’s of hypomagnesemia?

A
  • lethargy, confusion, tremors, convulsion
  • hyperreflexia, parathesias
  • cardiac arrhythmias
92
Q

what does an EKG look like with hypomagnesemia?

A

widening of QRS, conduction prolongation and ST segment depression

93
Q

what is tx for mild asymptomatic hypomagnesemia?

A

oral replacement with Mg salts

  • Mag-Ox (magnesium oxide)
  • Slow-Mag (magnesium chloride)
  • Mag-Tab (magnesium lactate)
94
Q

precaution with what when treating hypomagnesemia with oral Mg salts?

A

may develop osmotic diarrhea

95
Q

what is tx for severe or symptomatic deficiency of hypomagnesemia?

A

IV replacement
Mg sulfate

  • careful monitoring for rebound hypermagnesemia and arrhythmias
  • caution when giving Mg+ to renal pts
96
Q

caution when giving Mg+ to what pts?

A

renal pts

97
Q

careful monitoring for what when treating severe or symptomatic deficiency of hypomagnesemia?

A

careful monitoring for rebound hypermagnesemia and arrhythmias

98
Q

hypermagnesemia seen in?

A

seen in:

  • renal failure pts
  • supratherapeutic replacement
  • antacid abuse (milk of magnesium)
99
Q

sx’s of hypermagnesemia?

A
  • decreased deep tendon reflexes
  • bradycardia
  • hypotension
  • flaccid paralysis
  • cardiac arrest
  • N, HA
  • hypocalcemia
100
Q

what does an EKG look like with hypermagnesemia?

A
  • tall T’s
  • widened QRS
  • irregular conduction
  • escape beats
101
Q

tx of hypermagnesemia?

A
  • dietary restriction
  • elimination of magnesium containing meds
  • saline + loop diuretics (too pee it out and dilute it)

-hemodialysis

Clin Med 3 (21 decks)

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