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Nursing 337 > Unit one and Two > Flashcards

Unit one and Two Flashcards

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1
Q

Normal Sodium Levels

A

135-145 MEq/L

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2
Q

Critical values for sodium

A

less than 120 or greater than 160 mEq/L

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3
Q

Where is sodium normally found?

A

main cation of the ECF

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4
Q

How does sodium move in the body

A

active transport

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5
Q

What hormones influence sodium

A

aldosterone and antidiuretic hormone

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6
Q

what is the primary source of sodium

A

diet

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7
Q

What are the most dangerous problems with sodium imbalances

A

cerebral dehydration and seizure

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8
Q

Serum levels for Hyponaturemia

A

less than 135mEq/L

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9
Q

causes of Hyponatremia

A 
vomiting
Nasogastric suctioning
diarrhea
excessive diaphoresis
wound drainage
medication
renal disease
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10
Q

Serum levels for hypernaturemia

A

greater than 146 mEq/L

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11
Q

Common cause of sodium gain

A

excessive sodium intake
inability to ingest water
hypertonic tube feeding w/o hypertonic IV fluids

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12
Q

Consequences of sodium retention

A

Hyperaldosteronism
Cushing’s syndrome
Corticosteroids
acute renal failure

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13
Q

Common assessment of sodium imbalances

A

confusion, coma, seizures, orthostatic hypotension, muscle weakness,

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14
Q

Common assessment findings of hyponatremia

A

headache, fatigue, apathy, respiratory distress, anorexia, weight loss, nausea, vomiting, abdominal cramps

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15
Q

Common assessment findings of hypernatremia

A

restlessness, irritability, lethargy, dyspnea, tachycardia, dry mucous membranes, dehydration, flushed skin, low urine output

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16
Q

How much of an adult body mass is water?

A

50-60% weight in adults

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17
Q

What affects water content

A

gender (greater in males), body mass( more fat, less water), age

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18
Q

How much water is in the ICF

A

2/3

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19
Q

what is interstitial fluid

A

fluid in spaces between cells

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20
Q

what is plasma

A

liquid part of blood

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21
Q

Transcellular fluid

A

small amount of fluid contained within specialized cavities of the body- CFS, GI tract, pleural

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22
Q

what are electrolytes

A

substances that when dissolved in water separate into charged particle

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23
Q

What are the cations in the body

A

sodium, potassium, calcium, magnesium

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24
Q

what are the anions of the body

A

chloride, phosphate, bicarbonate

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25
Q

What are the major functions of electrolytes

A

regulate water distribution, muscle contraction, nerve impulse transmission, blood clotting, regulate enzyme reactions, regulate acid-base balance

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26
Q

How does ICF and ECF transportation occurs

A 
filtration
diffusion
facilitated diffusion
osmosis
active transport
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27
Q

Diffusion

A

passive movement of particles across a permeable membrane from a higher concentration to a lower concentration

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28
Q

Example of diffusion

A

gas exchange in the alveoli

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29
Q

Facilitated Diffusion

A

movement of specific particles across a cell membrane by a protein carrier
passive

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30
Q

Examples of facilitated diffusion

A

glucose and amino acids entering or leaving the cell

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31
Q

Active Transport

A

movement of particles across a cell membrane from areas of low concentration to areas of higher concentration by combining with a carrier on the outside of the cell membrane and moving the inside of cells
requires energy

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32
Q

Example of active transport

A

sodium/potassium pump

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33
Q

Normal potassium values

A

3.5-5.0 mEq/L

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34
Q

critical value of potassium

A

2.5-6.5 mEq/L

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35
Q

Role of potassium

A

significant role in cardiac muscle, skeletal muscle and smooth muscle activity

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36
Q

How does potassium move

A

active transport with sodium-potassium pump

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37
Q

What hormone enhances kidney excretion of potassium

A

aldoserone

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38
Q

what is the primary source of potassium

A

diet

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39
Q

causes of Hypokalemia (less than 3.5)

A 
vomiting
prolonged gasrtic suctioning
chronic diarrhea
eating disorders 
hemorrhage
medication
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40
Q

causes of hyperkalemia (greater than 5.5)

A 
acute renal failure
chronic kidney disease
glomerulonephritis
addison's disease
medication
excessive of potassium intake
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41
Q

What is calcium

A

the most abundant mineral in human body

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42
Q

where is calcium found

A

99% in bones and teeth

1% in blood stream in bound form and ionized form

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43
Q

What is ionized calcium

A

is the active form of calcium and must be maintained in a narrow range

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44
Q

what is calcium bound to

A

serum proteins, especially albumin

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45
Q

where does calcium get absorped

A

in the intestines and requires active form of vitamin D

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46
Q

What is calcium required for

A

transmission of nerve impulses, cardiac muscle contractility
clotting mechanism
teeth and bone formation

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47
Q

Hypocalcemia serum levels

A

total- < 8.5mg/dl

ionized- < 4.9 mg/dl

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48
Q

what causes hypocalcemia

A 
any condition that decreases the production of parathyroid hormone
surgical removal or injury
pancretitis
multiple blood transfusion
laxative abuse
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49
Q

what happens when serum calcium levels is low?

A

calcium is borrowed from the bones

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50
Q

Why can pancreatitis cause hypocalcemia

A

lipolysis produces fatty acid that combine with calcium ions decreasing serum calcium levels

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51
Q

Why does multiple blood transfusions cause hypocalcemia

A

the citrate use to anticoaguleate blood binds with the calcium

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52
Q

Consequence of hypocalcemia

A

increased nerve excitability and sustained muscle contraction- tetany
- due to decreased calcium level, decreases threshold levels

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53
Q

Consequence of Hypocalcemia

A 
Chvostek 
Trousseau
Laryngeal strigor
Dysphagia
numbness and tingling around mouth
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54
Q

Chvostek sign

A

twitching of the lip and muscles on the side of the face stimulated from a tap over the facial nerve in front of the ear
(cranial nerve VII)

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55
Q

Trousseas sign

A

carpel spasms produced by inflating a blood pressure cuff on the arm

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56
Q

Treatment of hypocalcemia

A

oral/ IV replacement (calcium gluconate or calcium chloride)
Vitamin D
Aluminum hydroxide gel- hyperphosphatemia
Mg for Hypomagnesemia

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57
Q

Hypercalcemia serum levels

A

> 10.5 mg/dL- total

> 5.0 mg/dL - ionized

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58
Q

Critical calcium values

A

12 mg/dL

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59
Q

Causes of hypercalcemia

A 
excess intake 
loss from bones, increased mobilization from bones
steroid therapy
hyperthyroid 
Metastatic Cancer
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60
Q

Treatment of hypercalcemia

A

volume expansion with NS
loop diuretics or corticosteroids
calcitonin and/or mithramycin (prevent bone reabsorption

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61
Q

Phosphorus serum levels

A

2.5-4.5 mg/dL

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62
Q

what does phosphorus assist with

A

muscle contraction, maintaining heart rhythm, kidney function, nerve conduction, acid-base balance, functioning of RBC
metabolism of protein, fat and carbs

63
Q

Phosphorus is a major component of what

A

ATP, DNA, RNA

64
Q

where is most of the phosphorus found

A

85% bound to teeth and bones

rest in cells

65
Q

what regulates phosphorus

A

parathyroid hormone

66
Q

What are phosphorus levels related to

A

glucose intake, insulin administration, hyperventalation

67
Q

Hypophosphatemia serum levels

A

< 2.4mg/dL

68
Q

causes of hypophosphatemia

A 
malabsorption syndrome
recovery from malnutrition or refeeding syndrome
glucose or insulin therapy
TPN
alcohol withdraw
phosphate-binding antacids
respiratory alkalosis
69
Q

serum levels of hyperphosphatemia

A

level greater than 4.4 mg/dL

70
Q

causes of hyperphosphatemia

A 
chemotherapy for leukemia or lymphoma 
excessive milk injetion
excessive use of phosphate containing laxative or enemas
vitamin D excess
chronic kidney disease
acute renal failure
hypoparathyroidism
sickle cell anemia
71
Q

Normal magnesium serum levels

A

1.6-2.6 mg/dL

72
Q

what is the major role of magnesium

A 
major role in 300 fundamental enzymatic reactions 
powers the sodium-potassium pump
aids converting ATP to ADP
transmits electrical impulses 
important in skeletal muscle relaxation
maintains heart rate
Necessary for release of PTH
73
Q

Hypomagnesemia serum level

A

1.5 mEq/L

74
Q

Hypomagnesemia causes

A

nutritional or metabolic abnormalities
fluid loss form GI tract
redistribution of body magnesium

75
Q

What inhibits magnesium absorption

A

phytates
oxalates
fat

76
Q

Assessment findings of hypomagnesemia

A 
similar to hypocalcemia or hypokalemia 
muscle twitching
tremors
hyperreactive reflexes
mood changes
nausea, vomiting, diarrhea
seizures, hallucinations
77
Q

What is SIADH

A

syndrome of inappropriate antidiuretic hormone

results in water intoxication and hyponatremia

78
Q

characteristics of SIADH

A 
fluid retention
serum hypoosmolality 
dilutional hyponatremia
hypochloremia
concentrated urine 
common in elderly
79
Q

causes of SIADH

A

Malignant tumor
central nervous system disorders
drug therapy
miscellaneous condition

80
Q

Signs and Symptoms of SIADH

A 
clinical signs and symptoms related to hypovolemia dn hyponatremia are present as mild to severe 
low urine output
dark concentrated urine
thirst 
dulled sensorium
dyspnea
hypertension
81
Q

Osmosis

A

a process by which molecules of solvent tend to pass through a semipermeable membrane from a less concentrated solution into a more concentrated one, thus equalizing the concentrations on each side of the membrane

82
Q

Osmolality

A

concentration of solute per kilogram of water

83
Q

Osmolarity

A

concentration of solutes per liter of solution

84
Q

Serum osmolality

A

measures the body’s water balance

85
Q

Normal values of osmolality

A

275-295 mOsm/Kg

86
Q

Water deficit osmolality

A

value higher than 295 mOsm/kg- concentration of particles is too great or the water is too low

87
Q

Water excess osmolality

A

values lower than 275 mOsm/kg- too little solute for the amount of water or too much water for the amount of solute

88
Q

Conditions that increase serum osmolality-

A

dehydration/sepsis/fever/ sweating burns
Diabetes mellitus
Diabetes Insipidus
Uremia
Hypernatremia
Ethanol, methonal or ethylene glycol ingestion
mannitol therapy

89
Q

Conditions that increase urine osmolaity

A 
dehydration
SIADH
adrenal insufficiency
glycosuria
Hypernatremia
High protein diet
90
Q

Conditions that decrease serum osmolality

A

excess hydration
hyponatremia
SIADH

91
Q

Conditions that decrease urine osmolality

A

diabetes insipidus
Excess fluid intake
acute renal insufficiency
glomerulonephritus

92
Q

Tonicity

A

refers to the osmolality of a solution

93
Q

Isotonic solution

A

fluids with the same osmolality of the cell interior. Remains in the vascular compartment
expanding vascular volume
Normal Saline 0.9%

94
Q

Hypertonic Solutions

A

fluids with solutes more concentrated than in the cell (increased osmolality)
causes a shift from cells into the vascular space, expanding vascular volume
- 3% Normal Saline

95
Q

Hypotonic Solution

A

solutes are less concentrated than in the cell. Helps to move cellular dehydration through shifting out of blood vessels into the cells promotes elimination by kidneys
0.45% normal saline

96
Q

Oncotic Pressure

A

Pressure caused by plasma colloids in a solution
protein is the major colloid in the vascular system
plasma proteins attract water pulls from tissue to vascular space

97
Q

What is the capillary fluid movement determined by?

A

Capillary Hydrostatic Pressure
Plasma Oncotic pressure
Interstitial hydrostatic pressure
Interstitial oncotic pressure

98
Q

Which pressures move water out of the capillaries

A

capillary hydrostatic pressure and interstitial oncotic pressure

99
Q

Which pressures moves fluid into the capillaries

A

Plasma oncotic pressure and interstitial hydrostatic pressure

100
Q

Distribution of water

First spacing

A

normal distribution in ICF and ECF

101
Q

Distribution of water

Second Spacing

A

Abnormal accumulation of interstitial fluid

102
Q

Distribution of Water

Third Spacing

A

accumulation of fluid in a part of the body where it cannot be use- fluid is trapped

103
Q

what controls the body’s water balance

A

Needs access to water
Normal thirst and ADH mechanism
Normal functioning kidneys

104
Q

What is the primary protection of hyperosmolality

A

the thirst mechanism

105
Q

How is the thirst mechanism stimulated

A

Stimulated by fluid loses or increases by thirst receptors in the hypothalamus
stimulates ADH and aldosterone release

106
Q

Where are glucocorticoids and mineralcorticoids secreted?

A

by the adrenal cortex

107
Q

What is the function of glucocorticoids and mineralcorticoids

A

regulate water and electrolytes

108
Q

function of glucocorticoids (cortisol)

A

anti-inflammatory effect and increase serum glucose levels

response to physical stress

109
Q

Function of Mineralcorticoidis (aldosterone)

A

enhance sodium retention and potassium excretion

110
Q

What triggers aldosterone release?

A

drop in blood pressure or blood volume

111
Q

action of aldosterone

A

causes kidneys to reabsorb more sodium into the blood increasing serum sodium levels- water follows
- lowers serum potassium levels

112
Q

Atrial Natriurtic Peptide (ANP)

Characteristic

A

Cardiac Hormone found in the atria

released by high blood volume and high blood pressure

113
Q

How does ANP lower blood pressure

A

causes vasodilation and suppressing the RAAS
decreases ADH
Increases GFR

114
Q

Brain Natriuretic Peptide characteristics

A

cardiac hormone, within the ventricles released with increased blood volume and pressure when ventricles are stretched

115
Q

How do BNP decrease blood volume and pressure

A

vasodilation of Arteries and veins
Decrease release of aldosterone
Diuresis- resulting in excretion of both sodium and water

116
Q

What causes fluid deficit?

A 
diarrhea
fistula drainage
hemorrhage
Polyuria
inadequate intake
117
Q

What is the goal of treatment for fluid volume deficit

A

correct cause
replace water and electrolytes
IV fluids 0.9 NS or LR
Blood

118
Q

How is SIADH diagnosed

A

low urine output
high specific gravity
sudden weight gain without edema
decreased serum sodium level

119
Q

What is the treatment of SIADH

A

Treatment of underlying cause
Fluid restriction
gradual weight loss
progressive rise in serum sodium concentration and osmolality, symptom improvement
head of bed flat or no more than 10 degrees- enhance venous return

120
Q

What results in an over production of ADH

A

Syndrome of inappropriate antidiuretic hormone

121
Q

what results in an underproduction of ADH

A

diabetes insipidus

122
Q

What is the osmolarity of patients with SIADH

A

lows osmolarity

123
Q

What are the characteristics of SIADH

A

fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine in the presence of normal or increased intravascular volume and normal renal function

124
Q

what population is SIADH more common?

A

older adults

125
Q

what are the Causes of SIADH

A

malignant tumors, drug therapy, CNS disorders, hypothyroidism, lung infection, COPD

126
Q

what are the affects of ADH

A

increase the permeability of renal distal tubule and collecting duct- leads to reabsorption of water , ECF volume increases, GFR increases, sodium levels decline

127
Q

how is the diagnosis of SIADH made

A

by the simultaneous measurements of urine and serum osmolality

128
Q

what should a nurse look for in patients at risk for SIADH?

A

low urine output with high specific gravity
sudden weight gain without edema
decreased serum sodium levels
Monitor I&O, vital signs, heart and lung sounds
signs of hyponatremia

129
Q

What is the treatment of SIADH

A
  • avoid medications that stimulate ADH release
    fluid restriction
    position the head of bed flat or elevated 10 degrees
130
Q

why would you position the bed of a patient with SIADH at 10 degrees or flat?

A

because it enhances venous return to the heart and increase left atrial filling pressure, thereby reducing the release of ADH

131
Q

what is the fluid restriction of a patient with chronic SIADH

A

800-100 mL of water daily

132
Q

What medication is often given to patients with chronic SIADH

A

Demeclocycline

133
Q

what are the actions of demeclocycline

A

blocks the effects of ADH on the renal tubules resulting in more dilute urine

134
Q

What causes diabetes insipidus(DI)?

A

caused by a deficiency of production or secretion of ADH or decreased response to ADH

135
Q

what is the most common cause of DI?

A

central DI

136
Q

What is the etiology of central DI

A

results from an interference with ADH synthesis, transport or release
-brain tumor, head injury

137
Q

what is the etiology of nephrogenic DI

A

results from inadequate renal response to ADH despite presence of adequate ADH

138
Q

primary DI

A

results from excessive water intake

139
Q

what are the clinical manifestation of DI

A

polyuria and polydipsia

140
Q

what are the phases of onset for central DI

A

acute phase- polyuria
interphase- urine volume normalize
third phase- central DI is permanent- 10-14 days after surgery

141
Q

what is the nursing management of DI

A

early detection
maintenance of adequate hydration
patient teaching

142
Q

what is the treatment of central DI

A

fluid and hormone therapy

- IV hypotonic saline or dextrose 5%

143
Q

What is the treatment of nephrogentic DI

A

dietary measures and thiazide diuretics, and in some cases taking indomethacin (NSIAD that increases sensitivity to ADH)

144
Q

When does hypovolemic shock occur?

A

after a loss of intravascular fluid volume

145
Q

what is absolute hypovolemia

A

results when fluid is lost through hemorrhage, gastrointestinal loss, fistula drainage, diabetes insipidus, or diuresis

146
Q

what is relative hypovolemia

A

fluid volume moves out of the vascular space into extravascular space (third spacing) burns.

147
Q

what is a consequence of decreased intravascular volume

A 
decreased venous return
decreased preload
decreased stroke volume
decreased CO 
decreased tissue perfusion and impaired cellular metabolism
148
Q

What is the clinical presentation of hypovolemic shock?

A 
tachypnea -> bradypnea
decreased urine output
pallor, cool clammy skin
Decreased cerebral perfusion (anxiety, confusion, agitation)
Absent bowel sounds
149
Q

Diagnostic lab findings of hypovolemic shock

A 
hematocrit
hemoglobin
lactate
urine specific gravity
changes in electrolytes
150
Q

How much fluid may a patient compensate for?

A

up to 15% of total blood volume

151
Q

A loss of 15-30% of total blood loss results in what?

A

sympathetic nervous system mediated response

152
Q

What happens in a sympathetic nervous system mediated response?

A

increased HR
Increased CO
Increased respiratory rate and depth
The stroke volume, central venous pressure is decreased

153
Q

How is hypovolemia corrected?

A

by crystalloid fluid replacement

Nursing 337 (9 decks)

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