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Module 1 Exam > Fluid > Flashcards

Fluid Flashcards

1
Q

Hydrostatic pressure

A

Pushing force
Pushes fluid out of capillaries
Exerted by pumping of heart

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2
Q

Oncotic pressure

A

Pulling force
Pulls fluid and tissues into capillaries
Exerted by non-diffusible plasma proteins…albumin

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3
Q

Kidneys

A

Adjust urine volume and excrete electrolytes

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4
Q

Anti-diuretic Hormone

A

Created in pituitary gland
Also referred to as Vasopressin
Controls water retention
Adds DA H20
Decreased Urine output
Pressin the BP up
Headaches are priority
Low Na+-seizures-death
Synthetic ADH-Desmopressin, Vasopressin

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5
Q

Renin-angiotensin-aldosterone system

A

Release of renin

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6
Q

Aldosterone

A

Water regulator

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7
Q

Atrial natriuretic peptide

A

Reduces fluid volume by increasing secretion of Na+ and water
Produced and stored in the atria
Stops action of RAAS
Decreases BP by vasodilation

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8
Q

7 functions of kidney

A

A- controlling ACID-base balance
W-Controlling WATER balance
E-maintaining Electrolyte balance
T-removing TOXINS and waste products from the body
B-controlling BLOOD PRESSURE
E-producing the hormone ERYTHROPROTEIN
D- activating VITAMIN D

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9
Q

RAAS

A

water regulator- regulates Na+ and water
Aldosterone causes kidney to retain Na+ and water to excrete K+
Released if Na+ is low and K+ is high

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10
Q

Low aldosterone

A

High K+

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11
Q

High aldosterone

A

Low K+

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12
Q

RAAS increases/excretes what

A

Reabsorption of Na+ (where salt goes, water flows) and the excretion of K+

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13
Q

Hypovolemia

A

Extracellular fluid volume is reduced, results in decreased tissue perfusion
Can be produced by salt and water loss( Vomit, Diarrhea)
Salt and water loss come from Extracellular fluid

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14
Q

Dehydration

A

Water loss alone
Pure water loss come from total body water. only about 1/3 is of ECF
ALWAYS HYPERNATREMIC
Treatment involves free water administration

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15
Q

Electrolytes

A

Ions found in our body fluids
Conduct electricity, energy
Maintain homeostasis
Communicate cell to cell, nerve to nerve, organ to organ

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16
Q

Electrolytes separate into

A

Ions (charged particles) when dissolved in water

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17
Q

Cations

A

(+ charge) Na+, K+, Ca+, Mg+)

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18
Q

Anions

A

CL,HCO3, Phosphate

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19
Q

Depletion of electrolytes

A

Think fluid-where fluid goes….electrolytes follows
Vomiting
Urination
Bowel movement
Sweating

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20
Q

Magnesium

A

Mg+
1.5-2.5 mg/dl

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21
Q

Phosphorus

A

2.4-4.5 mg/L

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22
Q

Potassium

A

K+
3.5-5.0 mEq/L

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23
Q

Calcium

A

Ca+
8.5-10.5 mg/dl

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24
Q

Chloride

A

Cl-
95-105 mq/L

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25
Q

Sodium

A

Na+
135-145 mEq/L

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26
Q

Foods rich in potassium

A

fruits, green leafy vegetables, spinach, salt substitutes

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27
Q

Foods rich in Sodium

A

Table salt, Cheese, spices, canned, processed foods

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28
Q

Foods rich in Magnesium

A

Spinach, almonds, yogurt, green vegetables, Dark chocolate (excellent source)

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29
Q

Foods rich in Phosporus

A

Dairy, meats and beans

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30
Q

Foods rich in Chloride

A

Salty foods and salt substitutes, canned foods. Vegetables such as tomatoes, lettuce, celery, and olives

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31
Q

Sodium Functions

A

Maintains BP
Blood volume
pH balance( acid base)
Controlling nerve impulses
Stimulating muscle contractions
Big impact on body’s fluid balance
major electrolyte in ECF
controls water balance
regulated by ADH and aldosterone, Na+K+ pump

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32
Q

Hyponatremia

A

Caused by dilution of sodium

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33
Q

SIADH

A

impaired water excretion caused by inability to suppress secretion of ADH; water retention causes dilutional hoponatremia

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34
Q

Water intoxication

A

retaining fluid and sodium causing hemodilution of Na+

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35
Q

Psychogenic polydipsia

A

Excessive fluid intake without physiologic stimuli

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36
Q

Hypotonic fluids

A

Shift solutes into Cell

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37
Q

Inadequate sodium intake

A

Fasting NPO status
Low Na+ diet

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38
Q

Increased Na+ excretion

A

4Ds- diarrhea, diuretics , drainage, diaphoresis
Vomiting
Kidney disease
Hypoaldosteronism (Addison’s)

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39
Q

Addison’s

A

Sodium loss and water retention

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40
Q

Three flavors of Hyponatremia

A

Euvolemic
Hypovolemic
Hypervolemic

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41
Q

Euvolemic

A

Low Na+ with ECF volume normal

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42
Q

Hypovalemic

A

Na+ loss with ECF volume depletion

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43
Q

Hypervolemic

A

Na+ loss with increased ECF volume

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44
Q

Patient presentation during severe Hyponatremia

A

seizures, brainstem herniation, respiratory arrest, death

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45
Q

Patient presentation during Moderate Hyponatremia

A

Lethargy, weakness, altered LOC

46
Q

Patient presentation during Mild Hyponatremia

A

headache,nausea, vomiting, fatigue

47
Q

Hyponatremia Interventions

A

Replace Sodium slowly
Stop Sodium wasting diuretics
Provide IV Fluids/Medications

48
Q

Replacing Sodium during Hyponatremia

A

Avoid fluid overload due to fluid shifting with sodium
Can lead to neuro damage if given to rapidly
0.5 mEq/L per hour MAX
6-12 pts in 24- hour period
Check Na+ levels every 2-4 hours

49
Q

Stop sodium wasting diuretics during Hyponatremia

A

loop diuretics; thiazides
may need to switch to spironolactone

50
Q

Provide IV Fluids/Medications during Hyponatremia

A

Hypovolemic-0.9% NS to correct fluid status and Na+
3% NS (Hypertonic solution) used for extremely low Na+
Give through a central line- highly caustic on veins
Hypervolemic- give osmotic diuretics and fluid restriction
Euvolemic-SIADH

51
Q

Mannitol

A

Excretes water but not Na+

52
Q

Hyponatremia Severe interventions

A

Less than 120 mEq/L administer 3% saline IV slowly
Not increase by more than 6-12 mEq/L in first 24 hours
Plan for CVAD (3% saline highly caustic)
Insert indwelling catheter for strict I&O
Perform neurologic checks every 2-4 hours and keep on bedrest

53
Q

If overcorrected severe hyponatremia too quickly

A

Demyelination syndrome causing damage to nerve cells in the brain
Locked in syndrome

54
Q

Symptoms of Inappropriate Anti-Diuretic Hormone

A

Euvolemic
High levels of ADH retain water
Upsets electrolytes, especially sodium
Increased water retention
Decreased sodium

55
Q

Symptoms of Inappropriate Anti-Diuretic Hormone

A

Hyponatremia
Soaked inside
Stop urination
Causes 3 S- Small cell lung cancer, severe brain trauma, sepsis infection of the brain

56
Q

Treatment for SIADH

A

Fluid restriction
Diuretics
Increased oral sodium intake
Daily weight I&O

57
Q

Fluid restriction treatment during SIADH

A

800-1000 ml/day
Demeclocycline- blocks the effect of ADH= more dilute urine

58
Q

Diuretics treatment during SIADH

A

Medications/Caffeine

59
Q

Increased oral sodium intake during SIADH

A

Salt tablets, bacon, processed foods

60
Q

Causes of Hypernatremia

A

Decreased sodium excretion
Increased sodium intake
Decreased water Intake
Increased water loss (hemoconcentration)

61
Q

Decreased Sodium Excretion in Hypernatremia

A

Corticosteroids (Causes kidney to retain fluid)
Cushing’s syndrome (occurs due to prolonged exposure to glucocorticoids (prednisone) or a tumor producing excessive cortisol by adrenals)
Hyperaldosteronism (high sodium and water retention)
Kidney disease

62
Q

Severe Hypernatremia is defined as what sodium levels

A

Greater than 160

63
Q

Increased sodium intake in Hypernatremia

A

Excessive oral sodium ingestion (too many processed foods)
Hypertonic solutions (3% NS or 5% NS)
Alka seltzer, aspirin

64
Q

Decreased water intake in Hypernatremia

A

Fasting
NPO status

65
Q

Increased water loss

A

Dehydration (too much water loss and Na+ gain)
Infection
Diabetes insipidus

66
Q

Hypernatremia Interventions

A

Bring Sodium levels down slowly
Provide IV fluids/Medications
Diuretics
Avoid medications that cause hypernatremia
Restrict sodium and fluid oral intake as prescribed
Free water intake to help with hemodilution
Patient safety (Confused and agitated)
Weigh Daily
I & O
Neurologic precautions/Checks

67
Q

Bringing Sodium levels down in Hypernatremia Intervention

A

Rapid corrections can lead to seizures due to rapid fluid shifts in the brain

68
Q

Providing IV fluids/medications in Hypernatremia Intervention

A

Administer IV infusion in case of fluid loss
Hypotonic Solutions
NS,D5W

69
Q

Diuretics in Hypernatremia Intervention

A

If inadequate renal excretion of sodium, administer diuretics (thiazides, loop diuretics)

70
Q

Patient presentation in Mild Hypernatremia

A

Faint feeling
Muscle Weakness
Fatigue

71
Q

Patient presentation in Moderate Hypernatremia

A

Confusion, Irritability
Swollen and dry tongue
Hyperreflexia
Muscle twitching
Edema
Thirst

72
Q

Patient presentation in Severe Hypernatremia

A

Nausea and Vomiting
Increased muscle tone
Seizures
Coma

73
Q

Diabetes Insipidus

A

= Hypernatremia
ADH deficiency
Dry inside (labs high, increased sodium, diluted urine)
Dehydrated (DIE ADH)

74
Q

Diabetes Insipidus causes

A

Tumors
Damage to brain
Trauma
Polydipsia
Polyuria (Excreted dilute urine greater than 200 mL/hr)

75
Q

Diabetes Insipidus causes body to have

A

Low ADH, Low water in body
High UO, Polyuria
High Sodium
High H&H and serum osmolality from dehydration
Hypovolemic shock risk
TX: DDAVP (ADH)

76
Q

SIADH causes body to have

A

High ADH, water intoxication
Low UO, Oliguria
Low sodium (dilutional)
Low serum. osmolality
Weight gain
Seizure risk
TX: Hypertonic saline

77
Q

Potassium K+ is

A

The king of hearts
Major electrolyte in intracellular fluid
Maintains heart and muscle contraction
Regulated by the kidneys and aldosterone
Acid base Balance ( Increased K+ in cell, H+ moves out. Increased H+ in the cell, K+ moves out)
Diet is main source of K+

78
Q

Hypokalemia is caused by

A

Potassium loss
Inadequate K+ intake
Alkalosis Metabolic

79
Q

Potassium loss in Hypokalemia

A

Diuretics (digoxin toxicity)
Corticosteroids (water retention causing hemodilution)
Increased secretion of aldosterone (higher levels of aldosterone causes more K+ excretion in kidneys)
GI Loss (Vomiting/ diarrhea/prolonged NG suction)
Excessive diaphoresis
Kidney disease

80
Q

Inadequate K+ intake in Hypokalemia

A

Movement of K+ from ECF to ICF (excess insulin-moves k+ into the cell)

81
Q

Alkalosis Metabolic in Hypokalemia

A

H+ and K+ located inside the cell
In alkalosis, there is less H+ in blood- causes H+ to shift out of cell and K+ to shift into cells
Excess Insulin- Moves K+ into the cell

82
Q

Patient presentation in Severe Hypokalemia (Cardiovascular)

A

torsades de pointes
irregular apical HR
lethal dysrhythmias
bradycardia

83
Q

Patient presentation in Severe Hypokalemia(Neuromuscular)

A

Confusion; lethargy
muscle weakness
diminished D TRS

84
Q

Patient presentation in Severe Hypokalemia(GI)

A

Constipation (if bowel sounds are absent, think paralytic ileus-portion of bowel is not moving and can lead to small bowel obstruction)

85
Q

What to check for in Hypokalemia

A

Should check Mg+ level with hypokalemia, if Mg+ is low, it exacerbates K+ losses; correct Mg+ to first to correct K+

86
Q

Long QT is… and what it means

A

Torsades
Means heart is taking longer to electrically charge for the next heartbeat

87
Q

Torsades de Pointes

A

Irregular QRS complexes appearing to wrap around the EKG baseline
IV Mg+ is treatment (slow 2G IVP)

88
Q

EKG in Hypokalemia

A

Increased amplitude and width of P wave
T wave flattening and inversion
Prominent U waves
Apparent Long QT intervals due to merging of T and U wave

89
Q

Main EKG changes in Hypokalemia

A

T wave inversion
ST depression
Prominent U wave

90
Q

Main EKG changes in Hyperkalemia

A

Peaked T waves
P wave flattening
PR prolongation
Wide QRS complex

91
Q

Hypokalemia Interventions

A

Monitor Cardiac and and Respiratory status
Administer K+ supplements orally or IV (slowly, can be lethal)
If patient is taking a diuretic, may need to stop (spironolactone-K+ sparing diuretic)
K+ rich foods (if orally, must take with food and monitor for digoxin toxicity)

92
Q

Digoxin toxicity

A

Low K+ causes dig toxicity; caution using diuretics with digoxin= increased risk for hypokalemia

93
Q

Potassium is never administered through

A

IV push, IM, or Sub Q
IV potassium is always diluted and administered using an infusion pump

94
Q

Hyperkalemia is caused by

A

Excess K+ Intake
Decreased K+ excretion
Adrenal insufficiency
Kidney disease
Acidosis Metabolic
Traumatic burns

95
Q

Decreased K+ excretion in Hyperkalemia

A

K+ sparing diuretics (spironolactone)
Ace inhibitors
NSAIDS (decreased renal perfusion)

96
Q

Adrenal insufficiency in Hyperkalemia

A

Addisons= low aldosterone=retention of K+
Hyperaldosteronism causes large amounts of sodium excretion and retains K+ (Addisons= destruction of adrenal gland)

97
Q

Kidney disease is the #1 cause of what

A

Hyperkalemia
Decrease in urine and increase in K+

98
Q

Acidosis metabolic in Hyperkalemia

A

H+ and K+ located inside the cell
in acidosis, there is more H+ in blood=causes H+ to shift into the cells and K+ to shift out in the cells

99
Q

Patient presentation in Hyperkalemia(Cardiovascular)

A

Low BP
dysrhythmias-V fib and cardiac standstill

100
Q

Patient presentation in Hyperkalemia(GI)

A

increase motility=hyperactive bowel sounds diarrhea

101
Q

Patient presentation in Hyperkalemia(Muscle weakness)

A

can result in paralysis and respiratory arrest

102
Q

EKG and potassium(hyperkalemia)

A

peaked narrow T wave
ST segment depressed
prolonged PR interval, bradycardia

103
Q

Mild hyperkalemia

A

Monitor cardiac rhythm changes
Restrict K+ in diet
Diuretics
Cation exchange resins (sodium polystyrene sulfate(Kayexalate) po or rectal=explosive diarrhea
Stop medications causing increase in K+
Dialysis

104
Q

Emergency medical treatment for severe hyperkalemia

A

Ca+ Gluconate 10% IV
Hypertonic glucose & insulin
NaHCO3

105
Q

Ca+ Gluconate 10% IV EMT for Hyperkalemia

A

Protects heart from myocardial irritability
It does not lower potassium
must be given over 3-5 minutes
place on monitor for dysrhythmias, monitor BP and HR

106
Q

Hypertonic glucose and Insulin EMT in Hyperkalemia

A

Move excess K+ into the cells

107
Q

NaHCO3 EMT in Hyperkalemia

A

K+ shifts into the cells and raises pH

108
Q

Calcium function

A

Calcium help with function of Mg+ when Mg+ is low (CA+ and Mg+ are best friends- when one goes up, the other follows)
Keep the 3 Bs strong

109
Q

Calcium (3 Bs)

A

Bone-90% of the body’s calcium
Blood clotting
Beat (HR) myocardial contraction
Regulated by 3 hormones

110
Q

Calcium is regulated by which 3 hormones

A

Parathyroid hormone-parathyroid gland makes and releases when Ca+ levels are low
Calcitonin- regulated by thyroid; released when Ca+ levels are high to lower Ca+ and put back into the bone
Calcitriol-Vitamin D analog; controls blood calcium by suppressing release of PTH

111
Q

PTH does what

A

Increases blood calcium levels; calcitonin decreases blood calcium levels

112
Q

Ionized calcium

A

Calcium in blood not attached to proteins(free calcium)
Most accurate test for assessing true calcium status
Important if abnormal levels of proteins
May be drawn if signs of bone, kidney, liver or parathyroid disease

Module 1 Exam (6 decks)

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