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Semester Two - Nursing 112 > Fluid and Electrolytes > Flashcards

Fluid and Electrolytes Flashcards

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1
Q

What are the three adaptive mechanisms for acid base imbalance?

A
  1. Chemical Buffer System
  2. Respiratory System
  3. Renal system
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2
Q

What is the primary regulator of acid base imbalance?

A

chemical buffer system

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3
Q

How fast is the chemical buffer system?

A

immediate actions

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4
Q

How does the chemical buffer system work?

A

chemicals that combine with acids and bases to minimize pH change

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5
Q

What is this?

A

Acidosis

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6
Q

What is this?

A

Alkalosis

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7
Q

What is the secondary system for acid base imbalance?

A

respirarory system

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8
Q

How long does the respiratory system take to respond?

A

minutes

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9
Q

What is the action of the respiratory system on acid base imbalance?

A

elimination or retention of carbon dioxide

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10
Q

What is the other secondary system for acid base imbalance?

A

renal system

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11
Q

How long does the renal system take to respond to acid base imbalance?

A

2-3 days

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12
Q

What is the renal system’s response to acid/base imbalance?

A

secretion or reabsorption of hydrogen and bicarbonate

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13
Q

How do you determine acid base imbalance?

A

arterial blood gas analysis

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14
Q

What does arterial blood gas assess?

A
  • Acid/Base Balance
  • Need for oxygen therapy
  • Change in oxygen therapy
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15
Q

pH

A

7.35-7.45

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16
Q

paCo2

A

35-45mm Hg

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17
Q

HCO3

A

24-30mEq/L

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18
Q

paO2

A

75-100mm Hg

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19
Q

O2 sat

A

92-100%

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20
Q

What should you remember to indicate with ABG sample?

A

the use of O2

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21
Q

What should you avoid changing 20 minutes prior to obtaining ABG sample?

A

O2 therapy

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22
Q

What syringe should you use for ABG sample?

A

heparinized syringe

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23
Q

Why is it especially important to expel air bubbles with an ABG sample?

A

air bubbles contain gases that can mess with the results of test

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24
Q

What should be done after ABG sample has been taken?

A

put sample on ice and/or transfer immediately to lab

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25
Q

What should you apply after ABG sample?

A

pressure to artery for 5 minutes

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26
Q

Step One of Three Step Method

A

Look at pH

If >7.45 alkalosis

If <7.35 acidosis

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27
Q

Step Two in Three Step Method

A

Look at the pCO2

Respiratory conditions will have a change in the paCo2

Metabolic conditions - no change

Respiratory conditions - opposite pattern

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28
Q

ROME

A

Respiratory Opposite Metabolic Equal

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29
Q

pH UP PCO2 DOWN

A

Respiratory Alkalosis

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30
Q

pH DOWN PCO2 UP

A

Respiratory Alkalosis

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31
Q

pH UP HCO3 UP

A

Metabolic Alkalosis

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32
Q

pH DOWN HCO3 DOWN

A

Metabolic Acidosis

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33
Q

Step Three in Three Step Method

A

Look at the HCO3

Metabolic conditions will have a change in HCO3

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34
Q

Respiratory Acidosis

A
  • Shallow Respirations
    • Pain
    • Narcotics
    • Atelectasis
    • Pneumonia
    • COPD
    • Asthma
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35
Q

Respiratory Acidosis Assessment

A
  • Shallow Respirations
  • Hypoxia
  • Mental Changes
    • Disorientation
    • Drowsiness
    • Dizziness
  • Flushed, Warm Skin
  • Weakness
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36
Q

Respiratory Acidosis Nur Dx

A
  • Impaired Gas Exchange
  • Disturbed Thought Processes
  • Activity Intolerance
  • Risk for injury
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37
Q

Respiratory Acidosis Interventions

A
  • Assess
  • Treat cause of shallow respirations
    • TCDB
    • Ambulate
    • Treat Pain
    • Reduce narcotic dose
    • O2
  • Protect from injury
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38
Q

Respiratory Acidosis

A
  • Fast Respirations
    • Anxiety
    • Fever
    • Respiratory Infections
    • Pain
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39
Q

Respiratory Alkalosis Assessment

A
  • Lightheadedness
  • Confusion
  • Teachycardia
  • Numbness in extremities
  • SOB
  • Anxiety
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40
Q

Respiratory Alkalosis Nur Dx

A
  • Ineffective Breathing Pattern
  • Disturbed Thought Processes
  • Risk for Injury
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41
Q

Respiratory Alkalosis Interventions

A
  • Assess
  • Treat underlying cause of hyperventilation
    • Encourgae slow breathing
    • Breathing into a paper bag
  • Sedatives
  • Protect from injury
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42
Q

Below Waist?

A

Loss of Base (poop)

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43
Q

Above waist?

A

Loss of acid (throw up)

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44
Q

Metabolic Acidosis

A
  • Loss of intestinal contents
    • Diarrhea
  • Diabetes
  • Renal Failure
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45
Q

Metabolic Acidosis Asessment

A
  • Kussmaul Respirations
  • Weakness
  • Nausea and Vomiting
  • Abdominal pain
  • CNS symptoms
    • Headache
    • Confusion
    • Drowsiness
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46
Q

Nursing Dx Metabolic Acidosis

A
  • Deficient Fluid Volume
  • Risk for Injury
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47
Q

Metabolic Acidosis Interventions

A
  • Assessment
  • Treat underlying cause
  • Give IV sodium bicarbonate
  • Protect from injury
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48
Q

Metabolic Alkalosis

A
  • Loss of gastric acid contents
    • Vomiting
    • NG suction
  • Diuretics
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49
Q

Metabolic Alkalosis Assessment

A
  • CNS Symptoms
    • Dizziness
    • Confusion
    • Irritability
  • Tetany
  • Tingling in extremities
  • Tachycardia
  • Hypoventilation
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50
Q

Metabolic Alkalosis Nur Dx

A
  • Deficient Fluid Volume
  • Risk for Injury
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51
Q

Metabolic Alkalosis Interventions

A
  • Assessment
  • Treat underlying cause
  • IV fluid replacement
  • Protect from injury
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52
Q

What % of the body is water?

A

50-60%

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53
Q

Older adult water %

A

45-55%

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54
Q

Infant water %

A

70-80%

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55
Q

Who is at a higher risk for fluid problems?

A

elderly people and infants

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56
Q

How much body water is located within the cells (intracellular fluid)

A

2/3

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57
Q

What does water do in the body?

A

regulates body temperaturre, lubricates joints and membranes and is a medium for food digestion

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58
Q

How much does one liter of water weigh?

A

2.2 lb or 1 kg

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59
Q

Fluid spacing

A

distribution of water

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60
Q

First Spacing

A

describes the normal distribution of fluid in the ICF and ECF compartments

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61
Q

Second Spacing

A

an abnormal accumulation of interstitial fluid, edema

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62
Q

Third Spacing

A

Occurs when fluid accumulates in a portion of the body (trancellular fluid) from which it is not easily exhanged with the rest of the ECF. Third spaced fluid is trapped and unavailable for functional use

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63
Q

Why are perioperative patients at risk for the development of fluid and electrolyte imbalances?

A

because of restriction of oral intake, GI prep, blood volume loss, fluid shifts

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64
Q

Hypovolemia is

A

ECF deficient

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65
Q

Hypervolemia is

A

ECF excess

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66
Q

Dehydration

A

the loss of pure water alone without corresponding loss of sodium

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67
Q

Why might fluid volume excess occur?

A

excessive intake of fluids, abnormal retention of fluids, or a shift of fluid from interstitial fluid into plasma fluid

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68
Q

What might be forms of therapy for fluid volume excess?

A

diuretics and fluid restriction

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69
Q

ECF volume excess signs and symptoms

A

full, bounding pulse, distended neck veins, increased blood pressure

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70
Q

Mild to moderate fluid volume deficit

A

sympathetic nervous system stimulation of the heart and peripheral vasoconstriction. orthostatic hypotension

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71
Q

Severe fluid volume deficit signs and symptoms

A

weak, thready, pulse that is easily obliterated as well as flattened neck veins, shock

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72
Q

ECF excess respiratory changes

A

pulmonary congestion and pulmonary edema as increased hydrostatic pressure in the pumonary vessels forces fluid into the alveoli

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73
Q

ECF excess resp. symptoms

A

SOB, irritative cough, moist crackles

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74
Q

ECF deficit resp. changes

A

increased resp. rate due to decreased tissue perfusion and resultant hypoxia

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75
Q

ECF excess neurologic changes

A

cerebral edema

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76
Q

ECF deficit neurologic changes

A

alteration in sensorium secondary to reduced cerebral tissue perfusion

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77
Q

Why does edemous skin feel cool?

A

because of the fluid accumulation and a decrease in blood flow secondary to the pressure of the fluid

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78
Q

Why should the patient with nasogastric suction not be allowed to drink water?

A

It will increase the loss of electrolytes. Water causes diffusion of electrolytes into the gastric lumen from mucosal cells; the electrolytes are then suctioned away.

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79
Q

What is the main cation of the ECF?

A

sodium

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80
Q

What does sodium do?

A

plays a major role in maintaining the concentration and volume of the ECF

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81
Q

What is the primary determinant of ECF osmolality?

A

sodium. sodium imbalances are typically associated with parallel changes in osmolality

82
Q

What besides ECF osmolality does sodium do?

A

generation and transmission of nerve impulses and the regulation of acid-base balance

83
Q

What absorbs sodium?

A

GI tract from foods

84
Q

How does sodium leave the body?

A

urine, sweat, feces

85
Q

What is the primary regulator of sodium balance?

A

kidneys

86
Q

How do the kidneys regulate the ECF concentration of sodium?

A

excreting or retaining water under the influence of ADH

87
Q

Hypernatremia occurs with

A

water loss OR sodium gain

88
Q

Hypernatremia causes hyper…

A

osmolality. ECF hyperosmolality causes a shift of water out of the cells, which leads to cellular dehydration

89
Q

Primary protection against the development of hyperosmolality

A

thirst

90
Q

What clinical states can produce water loss and hypernatremia?

A
  • a deficiency in the synthesis or release of ADH from the posterior pituitary gland
  • decrease in kidney responsiveness to ADH
  • administration of concentrated hyperosmolar tube feedings and osmotic diuretics
  • hyperglycemia associated with uncontrolled diabetes mellitus
  • excessive sweating
  • increased sensible loss from high fever
91
Q

Symptoms of hypernatremia

A
  • intense thirst
  • lethargy
  • agitation
  • seizures
  • coma
  • postural hypotension
  • weakness
  • decreased skin turgor
92
Q

Hyponatremia results from

A

loss of sodium-containing fluids, from water excess, or a combination of both

93
Q

Common cause of hyponatremia from water excess

A

inappropriate use of sodium-free or hypotonic IV fluids. This may occur in patients after surgery or major trauma, during admistration of fluids in patients with renal failure, or in patients with psychiatric disorders addociated with excessive water intake

94
Q

Symptoms of hyponatremia

A
  • cellular swelling
  • excess water lowers plasma osmolality, shifting fluid into brain cells
  • irritability
  • apprehension
  • confusion
  • seizures
  • coma
95
Q

What is the major ICF cation?

A

potassium

96
Q

What is potassium’s role in the body?

A
  • neuromuscular and cardiac functions
  • regulates intracellular osmolality
  • promotes cellular growth
  • acid-base balance
97
Q

Factors that cause potassium to move from the ICF to the ECF

A
  • acidosis
  • trauma to cells
  • exercise
98
Q

What is the most common cause of hyperkalemia?

A

renal failure

99
Q

Metabolic acidosis is associated with K+ moving…

A

from the ICF to the ECF as hydrogen ions move into the cell

100
Q

Hyperkalemia symptoms

A
  • increased excitability of the cells
  • cramping leg pain
  • weakness
  • paralysis of skeletal muscles
  • ventricular filbrillation
  • cardiac standstill
  • abdominal cramping
  • diarrhea
101
Q

Treatment of hyperkalemia

A
  • Eliminate oral and parenteral potassium intake
  • Increase elimination of potassium VIA diuretics, dialysis, and use of ion exhange resins such as sodium polystyrene sulfonate, increase fluid intake
  • Force K from ECF to ICF by administrating insulin + glucose or IV sodium bicarbonate
  • calcium gluconate IV to reverse the membrane excitability
102
Q

Most common causes of hypokalemia

A
  • diuresis
  • elevated aldosterone levels
  • magnesium deficiency
  • diarrhea
  • laxative abuse
  • vomiting
  • ileostomy drainage
103
Q

Hypokalemia is associated with which acid base imbalance?

A

metabolic alkalosis. causes a shift of potassium into the cells in exchange for hydrogen, lowering the potassium in the ECF

104
Q

Hypokalemia symptoms

A
  • reduced excitability of the cells
  • ventricular dysrhythmias
  • skeletal muscle weakness
  • paralysis
  • weakness or paralysis of respiratory muscles
  • shallow respirations and resp. arrest
  • decreased GI motility
  • decreased airway responsiveness
  • impaired regulation of arteriolar blood flow
  • release of insulin impaired leading to hyperglycemia
105
Q

Can potassium be given IV push?

A

no

106
Q

Calcium balance is controlled by which part of the body?

A

parathyroid (parathyroid hormone, calcitonin and vitamin D)

107
Q

What does PTH do?

A

increases bone resorption (movement of calcium out of bones), increases GI absorption of calcium and increases renal tubule reabsorption of calcium

108
Q

What does calcitonin do?

A

opposes the action of PTH (opposite reactions)

109
Q

What can cause hypocalcemia?

A

any condition that casuses a decrease in the production of PTH (surgical removal or f a portion of or injury to the parathyroid glands during thyroid or neck surgery), acute pancreatitis, multiple blood transfusions, diet low in calcium, increased loss of clacium due to laxative abuse and malabsorption syndromes

110
Q

Trousseu’s sign

A

carpal spasms induced by inflating a blood pressure cuff on arm. The blood pressure cuff is inflated above the systolic pressure. Carpal spasms become evident within 3 minutes if hypocalcemia is present.

111
Q

Chvostek’s sign

A

a contraction of facial muscles in response to a tap over the facial nerve in front of the ear

112
Q

What is the second most abundent IC cation?

A

magnesium

113
Q

How is magnesium regulated?

A

GI absorption and renal excretion

114
Q

What happens with hypomagnesium?

A

neuromuscular and CNS hyperirritatbility

115
Q

What happens with hypermagnesium?

A

depresses neuromuscular and CNS functions

116
Q

When does hypermagnesium usually occur?

A

with an increase in magnesium intake accompanied by renal insufficiency or failure.

117
Q

Major cause of hypomagnesemia

A

prolonged fasting or starvation, chronic alcholism

118
Q

What foods are high in magnesium?

A

green vegetables, nuts, bananas, oranges, peanut butter, chocolate

119
Q

Why do infants and growing children have much greater fluid turnover than adults?

A

high metabolic rate increases fluid loss. infants lose more fluid through the kidneys because immature kidneys are less able to conserve water than adult kidneys. infants’ respiratory rate is much higher than that of adults and their body surface area is proportionately greater than that of adults, increasing insensible loss

120
Q

How much water do fat cells contain?

A

little or no water

121
Q

How much water do lean muscle tissue contain?

A

high water content

122
Q

How much % water women

A

52% adult women’s weight

123
Q

how much % water men

A

60% adult man’s weight

124
Q

Obsese person’s % water

A

30-40% person’s weight

125
Q

Two types of fluid imbalance

A

`isotonic and osmolar

126
Q

Isotonic Imbalances

A

water and electolytes are lost or gained in equal proportions, so that the osmolality of the body fluids remains constant

127
Q

Osmolar Imbalances

A

involve the loss or gain of only water, so that the osmolality of the serum is altered

128
Q

Isotonic Fluid Volume Deficient

A

the body loses both water and electolytes

129
Q

Hypovolemia

A

fluid initially lost from the intravascular compartment

130
Q

Why does fluid volume deficit occur?

A
  • abnormal losses through the skin, GI tract, or kidney
  • decreased intake of fluid
  • bleeding
  • movement of fluid into a third space
131
Q

Third Space Syndrome

A

fluid shifts from the vascular space into an area where it is not readily accessible as extracellular fluid

132
Q

Fluid Volume Excess

A

occurs when the body retains water and sodium in similar proportions to normal ECF

133
Q

Hypervolemia

A

increased blood volume

134
Q

Causes of fluid volume excess

A
  • excessive intake of sodium chloride
  • administering sodium-containing infusions too rapidly, particularly to clients with impaired regulatory mechanisms such as heart failure, renal failure, cirrhosis of the liver and cushing’s syndrome
135
Q

Edema

A

excess interstitial fluid

136
Q

Dehydration

A

hyperosmolar fluid imbalance. occurs when water is lost from the body, leaving the client with excess sodium

137
Q

Overhydration

A

hypoosmolar fluid imbalance, occurs when water is gained in excess of electrolytes, resulting in low serum osmolality and low serum sodium levels

138
Q

1 g of wet diaper weight = how much urine?

A

1mL urine

139
Q
A
140
Q

This electrolyte imbalance is most commonly associated with malignancy, hyperparathyroidism, and immoblization

A

hypercalcemia

141
Q

This electrolyte imbalance may result from an injury or removal of the parathyroid gland

A

hypocalcemia

142
Q

This electrolyte imbalance is commonly associated with renal failure and metabolic acidosis

A

hyperkalemia

143
Q

This electolyte can be lost by GI (D/V/NG suction) and renal losses due to diuretics. A decifit of this electrolyte leads to reduced excitability of tissues, especially cardiac tissues

A

hypokalemia

144
Q

A loss of this electrolyte causes a shift of water intracellular due to a low osmolality

A

hyponatremia

145
Q

Clinical manifestation of excess of this electrolyte can lead to cellular dehydration which causes neurological symptoms

A

hypernatremia

146
Q

This electrolyte imbalance would occur in a client with renal failure who ingests maalox

A

hypermagnesemia

147
Q

This electrolyte imbalance is commonly associated with prolonged fasting or starvation but may also be cause by fluid loss from the GI tract, diuretics, or high glucose levels in uncontrolled diabetes mellitus

A

hypomagnesemia

148
Q

3 day old infant fluid requirement

A

250-300mL/24 hours

149
Q

1 year old fluid requirement

A

1150-1300 mL/24 hours

150
Q

2 year old fluid requirement

A

1350-1500mL/24 hours

151
Q

Adult fluid requirement

A

2500mL/24 hours

152
Q

examples of 3rd spacing

A

blister, ascites (fluid in peritoneal cavity), pleural effusion (fluid between the lining of the lungs)

153
Q

Causes Fluid Volume Deficit

A
  • abnormal losses through skin, GI tract or kidneys
  • Decreased fluid intake
  • Bleeding
  • Movement of fluid into a third space
154
Q

Clinical manifestations fluid volume deficit

A
  • dry mucous membranes
  • weight loss
  • increased respiratory rate
  • decreased skin turgor
  • flattened neck veins
  • increased HR, decreased BP
  • orthostatic hypotension
  • restlessness, lethargy, convulsions
155
Q

TNI fluid volume deficit

A
  • monitor VS
  • measure I/O
  • monitor daily weight
  • assess LOC
  • provide fluid replacement
  • encourage PO intake
  • safety precautions
156
Q

Fluid Volume Excess causes

A
  1. Excessive sodium intake
  2. Administering Na-containing infusions too rapidly
  3. Congestive heart failure
  4. Renal Failure
157
Q

Clinical manifestations of fluid volume excess

A
  • Pulmonary edema - moist crackles
  • Weight gain
  • Neck vein distention
  • Full bounding pulse
  • increased BP
  • peripheral edema
  • HA, confusion, lethargy
158
Q

TNIs Fluid volume excess

A
  • Monitor VS
  • Measure I/O
  • Monitor for changes in LOC
  • Decrease intake of H2O and NA
  • Assess Resp. Status/lung sounds
  • Monitor electrolytes
  • Elevate HOB
  • Monitor Weight Daily
  • Safety Precautions
159
Q

Sodium normal range

A

135-145 mEq

160
Q

Sodium Facts

A
  • Major cation in the extracellular fluid
  • Regulation of fluid distribution in the body. Water follows sodium.
  • Maintenance of body fluid osmolarity
  • Transmission of nerve and muscle impulses
  • Regulation of acid-base balance
161
Q

Hyponatremia Etiology

A
  • V/D/Drainage from suction
  • Excessive Sweating
  • Diuretics, excessive urinary output, other renal losses
  • Water gains - hypotonic tube feedings, excessive hypotonic IV, excessive fluid intake
162
Q

Hyponatremia Clinical Manifestations

A
  • Irritability
  • Feelings of impending doom
  • Confusion
  • Exhaustion
  • Seizures
  • Coma
  • Anorexia
  • N/V
  • Abdominal Cramps
  • Muscle weakness and spasms
  • Dry mucous membranes
  • Pale, dry skin
  • Rapid, thready pulse
  • Postural hypotension
163
Q

TNI Hyponatremia

A
  • Correct deficiency slowly
  • Monitor neurological sstatus
  • Restrict or replace fluids as indicated
  • Sodium replacement as indicated
  • Safe environment for client with neuromuscular symptoms
  • Seizure precautions as indicated
164
Q

Hypernatremia Etiology

A
  • Excessive parenteral administration of saline solutions
  • Hypertonic tube feeding with inadequate H2O supplements
  • Excessive intake of salt
  • Excessive insensible H2O loss
    • Hyperventilation
    • High Fever
    • Heat Stoke
  • Decreased H2O intake
165
Q

SALT

A

HYPERNATREMIA

Skin flushed

Agitation

Low-grade fever

Thirst

166
Q

Clinical Manifestations of hypernatremia

A
  • Intense thirst
  • Dry swollen tongue
  • dry, sticky mucous membranes
  • Flushed skin
  • Elevated T
  • Restlessness, agitation, twitching
  • Disorientation
  • Seizure
  • Coma
167
Q

TNIs Hypernatremia

A
  • Fluid replacement as indicated
  • Meticulous oral care prn
  • Restrict foods high in Na as ordered
  • Maintain a safe environment for clients with neuromuscular symptoms
  • Seizure precautions prn
  • 5 and 20 rule
168
Q

Physiological Role of Potassium

A
  • Major cation in the intracellular fluid
  • Regulation of fluid volume within the cell
  • Promotion of nerve impulse transmission
  • Contraction of skeletal, smooth and cardiac muscles
169
Q

Potassium Normal Range

A

3.5-5.0

170
Q

Hypokalemia Etiology

A
  • Diarrhea
  • Laxative overuse
  • Prolonged gastric suctioning
  • Vomiting
  • Prolonged starvation or fasting
  • Potassium wasting diuretics
  • Inadequate intake of potassium
  • K shift into tissue cells from plasma
    • increase insulin
    • alkalosis
171
Q

Hypokalemia Clinical Manifestations

A
  • Weak, thready pulse
  • Dysrhythmias
  • Enhanced digitalis effect
  • Bradycardia
  • Fatigue
  • Muscle weakness, leg cramps
  • Diminished deep tendon reflexes
  • Soft, flabby muscles
  • Paresthesia
  • Confusion, lethargy, can progress to coma
  • Hypoactive BS
  • anorexia, N/V
  • Ileus
172
Q

A Sick Walt

A

Hypokalemia

  • Alkalosis
  • Soft, flabby muscles
  • Ileus
  • Confusion
  • K-replace cautiously
  • Weakness
  • Arrhythmias
  • Lethargy
  • Thready Pulse
173
Q

TNI Hypokalemia

A
  • Careful VS and ECG monitoring
  • Protect client from injury due to weakness
  • Potassium replacement
  • Salt substitues can be used as a supplement
  • IV potassium replacement (high alert med)
  • Monitor clients receiving digitalis closely
174
Q

Liquid, soluble granule, soluble powder or soluble tablet form of potassium replacement

A

This medicine must be completely dissolved in at least one half glass of cold water or juice to reduce gastric irritation

175
Q

IV Potassium Replacement

A
  • High Alert Med
  • Never IV PUSH
  • Periperal line acess rate should not exceed 10mEq/50-100mL infuses over one hour
  • central line access rate 20mEq 50-100 mL with EID over 1 hour
  • Dilution should never exceed 40mEq/L
  • Always use EID
176
Q

Peripheral Line Access Potassium

A

10mEq/50-100 mL over one hour

177
Q

Central Line Acess Potassium

A

20mEq/50-100 mL over 1 hour

178
Q

Hyperkalemia Etiology

A
  • Excessive or rapid parenteral administration
  • K containing drugs
  • K containing salt substitutes
  • Decreased K excretion (renal failure)
  • K shift out of tissue cells into plasma
    • massive cell damage
    • burns
    • acidosis
179
Q

Mad Red

A

Hyperkalemia

  • Muscle Weakness
  • Acidosis
  • Dysrhythmias
  • Renal Failure
  • EKG changes
  • Diarrhea
180
Q

Clinical Manifestations of Hyperkalemia

A
  • Tachycardia leading to bradycardia
  • Dysrhymias
  • Cardiac arrest
  • EKG changes
  • Muscle twitching
  • Muscle Cramps
  • Weakness
  • Flaccid paralysis
  • Abd cramping
  • hypermotility with hyperactive BS
  • Diarrhea
181
Q

TNI Hyperkalemia

A
  • Protect client from injury
  • Monitor ECG/VS
  • Diuretics
  • Sodium polysyrene sulfonate
    • exchanges sodium for potassium in GI tract leading to increased elimination of K
    • slow onset
    • may be given orally or rectally
  • Glucose and insulin
  • Sodium bicarbonate
  • Dialysis
  • Calcium gluconate
182
Q

Normal Level Calcium

A

9-11 mg/dl

183
Q

Physiological Role of Calcium

A
  • Maintaining skeletal elements
  • Regulating neuromuscular activity
  • 99% of body’s calcium reside in bones and teeth
  • Parathyroid hormone regulates calcium levels
184
Q

Etiology Hypocalcemia

A
  • Inadequate secretion of parathyroid hormone
  • Surgical removal of parathyroid gland
  • Vitamin D decifiency
185
Q

CATS

A

Hypocalcemia

  • Chvostek’s Sign
  • Arrhythmias
  • +Trousseau’s Sign, Tetany
  • Spasm (laryngeal)
186
Q

Clinical Manifestations of Hypocalcemia

A
  • Numbness and tingling of extremities and around mouth
  • Muscle Cramps
  • Hyperactive deep tendon reflexes
  • Postive Trousseau’s sign
  • Postive Chvostek’s Sign
  • Tetany
  • Seizures
  • Confusion
  • Laryngeal Spasm
  • Decreased BP
  • Dysrhythmias
  • Reduction in prothrombin time
  • Blood doesn’t clot normally
187
Q

TNI Hypocalcemia

A
  • Monitor resp status
  • Monitor ECG
  • Administer calcium supplements as directed
  • Oral calcium carbonate , IV calcium Gluconate
  • Protect client from injury
  • Close monitoring of thyroid or neck surgery clients in immediate postoperative period
    *
188
Q

Etiology Hypercalcemia

A
  • Muscle Weakness
  • Incoordination
  • Lethargy
  • Bone Pain
  • Pathological fractures
  • Depressed reflexes
  • Confusion
  • Dysrhymias
  • Anorexia
  • Constipation
  • N/V
  • Flank Pain due to calcium stones in the kidney
189
Q

FAR

A

Hypercalcemia

  • Fractures
  • Anorexia
  • Renal Colic, Reflexes depressed
190
Q

TNI Hypercalcemia

A
  • Encourage weight bearing exercises
  • Promote Ca excretion
  • Diuretics
  • 3000-4000mL fluid per day
  • Handle client gently to prevent fractures
  • Administer calcitonin as ordered
191
Q

Normal Magnesium

A

1.5-2.5mEq/L

192
Q

Physiological Role of Magnesium

A
  • Second most abundant intracellular cation
  • Regulation of neuromuscular activity
  • Regulation of electrolyte imbalance, facilitates transport of Na and K across cell membrane, influence utilication of calcium and potassium
  • Regulated by GI absorption and renal excretion
193
Q

Clinical Manifestations Hypomagnesemia

A
  • Hyperactive reflexes
  • Tremors
  • Confusion
  • Seixures
  • Dysrhythmias
  • Increased potential for digitalis toxicity
194
Q

RAT

A

Hypomagnesemia

  • Reflexes hyperactive
  • Arrhythmias
  • Tremors
195
Q

TNIs Hypomagnesemia

A
  • Monitor for digitalis toxicity
  • Oral - magnesium citrate
  • IV- magnesium sulfate
  • Monitor reflexes. Absent or knee jerk reflex is a sign of Mg toxcitiy
196
Q

Etiology Hypermagnesemia

A
  • Decreased urinary output
  • Renal Failure
  • Overuse of Magnesium containing antacids or laxatives
197
Q

Clinical Manifestations Hypermagnesemia

A
  • Hypoactive deep tendon reflexes
  • lethargy
  • drowsiness
  • hypotension
  • dysrhythmias
  • cardiac and respiratory arrest
198
Q

TNI hypermagnesemia

A
  • IV fluids to increase urinary output
  • diuretics for mg excretion
  • creased mg intake
  • emergency treatment administer calcium gluconate, provide myocardial protection against effects of hypermagnesemia
    *
199
Q

Etiology Hypomagnesemia

A
  • Prolonged fasting
  • Starvation
  • Chronic Alcoholism
  • NG suction
  • Prolonged Diarrhea
  • Ileostomy
  • Diuretics
  • Osmotic diuresis secondary to uncontrolled diabetes
200
Q
A

Semester Two - Nursing 112 (90 decks)

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