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Pathophysiology > EXAM 2: F&E > Flashcards

EXAM 2: F&E Flashcards

1
Q

What are electrolytes?

A

substances that dissociate in solution to form a charged particle; electrically charged ions

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2
Q

What are some examples of electrolytes?

A

K, Na, Cl, Ca, Mg, PO

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3
Q

What are the body fluid compartments?

A

intracellular: body cells and blood cells have water
extracellular: plasma and interstitial spaces

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4
Q

This occurs when too much fluid moves from the intravascular space (blood vessels) into the interstitial or “third” space:

A

third spacing (potential space)

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5
Q

Third spacing fluid is:

A
  • trapped in one of the several possible extracellular (transcellular) spaces
  • cannot be used for normal function within the body
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6
Q

How do you relieve fluid in third spacing?

A

letting (cardiocentesis)

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7
Q

What are some examples of third spacing?

A
  • ascites
  • pleural effusion
  • cardio effusion
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8
Q

This condition results in abdominal fluid build up and is associated with right side heart failure

A

ascites

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9
Q

This condition results in fluid (bleeding) and air collecting in the pleural space with s/sx such as SOB and cyanosis and can be caused by trauma and cancer:

A

pleural effusion

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10
Q

What is the normal value for pleural effusion?

A

4 mL (just enough to separate membranes)

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11
Q

What is edema?

A

accumulation of excess interstitial fluid in the extracellular space

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12
Q

What is generalized edema referred to as?

A

anasarca

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13
Q

Where is edema most common?

A

in the feet and legs

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14
Q

This occurs when edema appears in the face, throat, and eyes:

A

anaphylaxis

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15
Q

What are the causes of edema?

A
  • increased hydrostatic pressure
  • lowered plasma oncotic pressure
  • increased capillary permeability
  • lymphatic channel obstruction
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16
Q

What is the lowered plasma oncotic pressure due to?

A

decreased amounts of plasma proteins (albumin)

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17
Q

What reduces the ability to suck fluid from interstitial space back into the capillary?

A

decreased capillary colloidal osmotic pressure

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18
Q

What causes the solutes to leave the capillary, increase the interstitial osmolality and draw more water in the interstitial spaces (causing edema)?

A

increased capillary permeability

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19
Q

What kind of obstruction can be caused by cancer or surgery?

A

lymphatic channel obstruction

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20
Q

What are the functions of body fluids?

A
  • transport gases, nutrients, and wastes
  • help generate the electrical activity needed to power body functions
  • take part in the transformation of food into energy
  • maintain the overall function of the body
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21
Q

What population is at higher risks for function issues?

A

elderly and babies

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22
Q

Fluid intake can be achieved via:

A

oral, IV/IM etc.

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23
Q

Fluid outtake can be achieved via:

A
  • sweating
  • respiratory
  • urinary
  • GIT
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24
Q

This consists of fluid contained within all the cells in the body and is the larger of the two compartments:

A

intracellular compartment (ICF)

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25
Q

The ICF holds how much of the body’s water in healthy adults?

A

2/3

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26
Q

The ICF has a high concentration of which electrolyte?

A

K

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27
Q

This contains the remaining 1/3 of body water and contains all the fluids outside the cells (interstitial + tissue spaces + blood vessels)

A

extracellular compartment (ECF)

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28
Q

The ECF has a high concentration of which electrolyte?

A

Na

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29
Q

This is pushing force exerted by a fluid:

A

hydrostatic pressure

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30
Q

This is pulling force of plasma proteins that cannot pass through the capillary membrane:

A

colloidal osmotic pressure

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31
Q

What does colloidal osmotic pressure assist with?

A

the movement of fluid back into the capillary

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32
Q

What is the total arterial capillary pressure?

A

30 mm Hg

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33
Q

What is the total venous capillary pressure?

A

10 mm Hg

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34
Q

What contributes to outward movement of fluid from the capillary?

A

interstitial fluid that has a negative hydrostatic pressure of about - 3 mm Hg

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35
Q

The composition of the ECF, plasma, and interstitial fluid consists of:

A
  • large amounts of sodium and chloride (and some bicarbonate)
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36
Q

The composition of intracellular fluids (ICF) consists of:

A

large amounts of potassium (with some magnesium)

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37
Q

What is the concentration gradient?

A

the difference in concentration over a distance

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38
Q

This is the movement of charged or uncharged particles along a concentration gradient from an area of higher concentration to one of lower concentration:

A

diffusion

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39
Q

This is the movement of water across a semipermeable membrane going from a low to high solute concentration:

A

osmosis

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40
Q

What path does water follow during osmosis?

A

water goes from the side of the membrane having a lesser number of particles and greater concentration of water TO the side with the greater number of particles and lesser concentration of water

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41
Q

What is osmolarity?

A

the amount of sodium and other solutes in the blood (majority is sodium)

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42
Q

What is the main source of fluid intake?

A

water

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43
Q

What is the main source of fluid output?

A

urine

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44
Q

What mechanisms maintain proper balance?

A

homeostatic mechanisms

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45
Q

Small amounts of urine results in:

High amounts of urine results in:

A 
highly concentrated urine (too much ADH) 
diluted urine (too little ADH) > results in thirst
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46
Q

What is the osmolarity of the blood plasma (serum) largely determined by?

A

the amount of sodium contained in the plasma

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47
Q

A patient with an elevated sodium serum will have hyper-osmolarity. In this case, what fluid movement would you expect to happen?

A

an increase in plasma sodium (plasma osmolality) attracts water out of the cell, leading to shrinkage of the intracellular volume

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48
Q

This is the tension or effect that the effective osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane:

A

tonicity

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49
Q

In obligatory urine output, how much cc’s are required per 24hours?

A

300-500 cc’s

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50
Q

An hourly urine output assessment is to:

A
  1. increase blood flow by increasing water reabsorption in kidney tubules
  2. increase systemic vascular resistance - vasoconstriction of blood vessels
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51
Q

How can solutions be classified?

A

according to whether or not they cause cells to shrink

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52
Q

These cells neither shrink nor swell and there is an equal loss of water and sodium:

A

isotonic

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53
Q

These cells swell (become lysed) and more Na is lost than water (serum Na is low):

A

hypotonic

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54
Q

These cells shrink (shrivel) and more water is loss than sodium:

A

hypertonic

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55
Q

What is the proper term for dehydrated?

A

fluid volume deficit

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56
Q

Vomiting, diarrhea or misuse of diuretics/lasix’s is an example of what kind of fluid volume deficit?

A

isotonic

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57
Q

Osmotic diuresis, excessive sweating, loss of thirst and being unable to drink fluids is an example of what kind of fluid volume deficit?

A

hypertonic

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58
Q

Excess renal losses of Na and aldosterone deficiency is an example of what kind of fluid volume deficit?

A

hypotonic

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59
Q

What is the recommended treatment for isotonic fluid volume deficit?

A

IV fluid replacement using NS (0.9%)

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60
Q

Who usually suffers from hypertonic fluid volume deficit due to large glucose molecules drawing out fluids while Na ions are maintaining normal filtration levels

A

diabetics

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61
Q

What is the recommended treatment for hypertonic fluid volume deficit?

A

drinking plain water or IV of dextrose 5% in water (D-5-W)

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62
Q

What is the recommended treatment for hypotonic fluid volume deficit?

A

IV of NS or a 3% solution of Na IV

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63
Q

What are some s/sx of a fluid volume deficit?

A
  • dry skin and mucous membranes (tongue)
  • poor skin turgor
  • decrease urine output
  • babies have a decreased fontanel and their eyes appears sunken
  • BP may be decreased with increased HR (orthostatic hypotension)
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64
Q

What are some physiological consequences of fluid volume deficit?

A

inadequate renal perfusion (blood flow)

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65
Q

What mechanisms protect extracellular fluid volume?

A
  1. alterations in hemodynamic variables

2. alterations in sodium and water balance

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66
Q

Alterations in hemodynamic variables results in:

A

vasoconstriction and an increase in heart rate

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67
Q

Alterations in sodium and water balance results in:

A
  • isotonic contraction or expansion of ECF volume

- hypotonic dilution or hypertonic concentration of extracellular sodium brought about by chances in extracellular water

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68
Q

What are the different types of edema?

A
  • pitting edema (due to extra water, responds well to elevation and diuretics)
  • nonpitting edema (caused by factors other than just fluid, making drainage more difficult)
  • brawny edema (swelling of subcutaneous tissues that cannot be indented easily by compression)
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69
Q

What physiologic mechanisms contribute to edema?

A
  • increase in capillary filtration pressure
  • decrease in capillary colloidal osmotic pressure
  • increase in capillary permeability
  • obstruction to lymph flow
  • localized, general and dependent edema
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70
Q

How can you assess a patient for edema?

A
  • daily weight
  • visual assessment
  • measurement of the affected part
  • application of finger pressure to assess for pitting edema
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71
Q

These physiological mechanisms assist in regulating body water:
>This is primarily a regulator of water intake:
>This is primarily a regulator of water output:

A
  • thirst

- ADH

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72
Q

Both physiological mechanisms respond to changes in:

A

extracellular osmolarity and volume

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73
Q

What regulates effective volume?

A

baroreceptors

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74
Q

The rate of sodium is coordinated by the:

A
  • SNS
  • angiotensin II
  • aldosterone
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75
Q

Water and Na balance modulate:

A

SNS outflow and ADH secretion

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76
Q

How is water and Na gained?

A
  • oral intake and metabolism of nutrients

- foods

77
Q

How much sodium is required per day?

A

<16-18/day

78
Q

How is water and Na loss?

A
  • kidneys
  • skin
  • lungs
  • GIT
79
Q

What is the main regulator for sodium?

A

the kidneys

80
Q

The kidneys monitor arterial pressure, retaining sodium when arterial pressure is ________ and eliminating it when arterial pressure is ________

A

decreased; increased

81
Q

________ may also regulate sodium excretion by the kidney:

A

atrial natriuretic peptide (ANP)

82
Q

What results when serum sodium levels decreases?

A

there is an excess amount of water, which causes:

  • serum osmolarity to fall <280 mOsm/kg
  • thirst to diminish
  • ADH release suppressed
  • renal water excretion increases
  • serum osmolality normalizes
83
Q

What do you assess when assessing body fluid loss in a patient?

A
  • their history of conditions that predispose to Na and water losses and weight loss
  • heart rate
  • BP
  • venous volume/filling
  • capillary refill rate
84
Q

What are the V1 receptors of ADH?

A

vasoconstriction

85
Q

What are the V2 receptors of ADH?

A
  • control water reabsorption

- aquaporins

86
Q

What are some disorders of ADH expression?

A
  • diabetes insipidus

- SIADH

87
Q

These patients have a deficiency or decrease response to ADH and are unable to concentrate urine during periods of water restriction causing them to excrete large volumes of urine

A

diabetes insipidus

88
Q

These patients have a failure of the negative feedback system that regulates the release and inhibition of ADH

A

SIADH (resulting from surgery, pain, stress or temperature changes)

89
Q

Neurogenic diabetes insipidus results from:

A

head injury or surgery

90
Q

Central diabetes insipidus results from:

A

a defect in synthesis or release of ADH

91
Q

What is the goal of treatment to restore fluid volume excess?

A

to restore fluid balance, correct electrolyte imbalances and eliminate or control underlying cause of overload

92
Q

What are the types of fluid volume excesses?

A
  • isotonic over-hydration
  • hypertonic over-hydration
  • hypotonic over-hydration
93
Q

What is isotonic over-hydration?

A

when there is excessive fluid in the EFC causing circulatory overload and interstitial edema

94
Q

What is hypertonic over-hydration?

A

it is rare but may be caused by excessive sodium intake

95
Q

What is hypotonic over-hydration?

A

it is known as water intoxication and occurs when excessive fluid moves in intracellular space and all body compartments expand

96
Q

What are some causes of fluid volume excess?

A
    • heart failure and kidney issues **
  • inadequate Na and water elimination
  • excessive Na intake in relation to output
  • excessive fluid intake in relation to output
  • inadequately controlled IV therapy
  • kidney disease
  • long term steroid therapy
  • rapid infusion of hypertonic-hypotonic solutions
  • excessive sodium bicarbonate therapy
  • SIADH
  • irrigation of wounds and body cavities with hypotonic fluids
97
Q

What assessment findings can you expect with fluid volume excess?

A
    • active weight gain, HTN, bounding pulse, SOB, JVD, edema **
  • tachycardia, HTN, distended neck veins
  • tachypnea, moist crackles
  • altered LOC
  • pitting, dependent edema, diarrhea, ascites
  • polyuria
98
Q

What interventions should be used when treating fluid volume excess?

A
  • administer diuretics
  • restrict Na and fluid intake
  • monitor electrolyte values
99
Q

This drug decreases fluid volume

100
Q

What are the different types of diuretics?

A
  • furosemide (lasix): works in the loop of henle in the kidneys
  • hydrochorothiazide (HCTZ): a thiazide diuretic (gives to AA)
  • spironolactone (aldactone): an aldosterone receptor antagonist that is potassium sparing when K is too low
101
Q

Isotonic fluid volume excess results in:

A

isotonic expansion of the ECF compartment with increases in both interstitial and vascular volumes, increases in total body sodium that is accompanied by proportionate increase in water

102
Q

What are some causes of decreased Na and water elimination?

A
  • renal function
  • heart failure
  • liver failure
  • corticosteroid excess
103
Q

When water and electrolytes are lost in equal proportions, what results?

A

isotonic dehydration

104
Q

When electrolyte loss exceeds water loss, what results?

A

hypotonic dehydration

105
Q

When water loss exceeds electrolyte loss, what results?

A

hypertonic dehydration

106
Q

What are some causes of fluid volume deficits?

A
  • inadequate intake of fluids and solutes
  • excessive perspiration
  • hyperventilation, ketoacidosis
  • prolonged fever, vomiting and diarrhea
  • end stage kidney disease, diabetes insipidus
  • excessive fluid replacement, kidney disease, chronic malnutrition
107
Q

How is isotonic dehydration caused and treated?

A
  • vomiting, diarrhea and misuse of diuretics

- RX: IV fluid replacement w/isotonic (0.9% saline aka normal saline)

108
Q

How is hypertonic dehydration caused and treated?

A
  • osmotic diuresis, excessive sweating, loss of thirst sensation or being unable to obtain or drink fluids
  • RX: drinking plain water or IV dextrose 5% in water (D5W)
109
Q

How is hypotonic dehydration caused and treated?

A
  • excess renal losses of Na, aldosterone (saves or retains Na) deficiency
  • RX: if mild, IV of 0.9 Saline but if severe, a 3% solution of sodium might be ordered
110
Q

What assessment findings can you expect with fluid volume deficit?

A
  • tachycardia, hypotension, tachypnea
  • lethargy to coma state
  • oliguria
  • nonelastic skin turgor, dry skin and mucous membranes
  • decreased bowel sounds, constipation
  • thirst
111
Q

What interventions should be used when treating fluid volume deficit?

A
  • rehydrate client

- administer medications to correct causes

112
Q

What is hematocrit?

A

a blood test that shows the % or proportion of RBCs to the plasma (in dehydrated people, Hct is increased)

113
Q

What is normal hematocrit levels for males and females?

A

males: 42%-52%
females: 37%-47%

114
Q

What does the urine specific gravity test measure?

A

the weight of urine compared to the density of water

115
Q

What is the normal range for USG in adults?

A

1.010-1.025

116
Q

A low USG is seen in what kind of urine?

117
Q

A high USG is seen in what kind of urine?

A

concentrated

118
Q

Dehydration will results in what kind of USG result?

A

high specific gravity (hypertonic urine)

119
Q

What is increased USG caused by?

A

glucose or proteins in the urine (making urine more dense)

120
Q

T/F SG doesn’t change in pt. where the kidneys are unable to concentrate the urine adequately. If the SG is low, it indicates an adequately hydrated pt. due to it being dilute and not
containing solutes.

121
Q

What is the intracellular concentration of potassium and the extracellular concentration?

A

intracellular: 140-150 mEq/L
extracellular: 3.5-5.0 mEq/L

122
Q

What is body stores of K related to and where is K derived from?

A
  • related to body size and muscles mass

- derived from dietary sources

123
Q

What two mechanisms are plasma K regulated through?

A
  • renal mechanisms that conserve or eliminate K

- a transcellular shift b/w the ICF and ECF compartments

124
Q

What are noneletrolytes?

A

substances that don’t dissociate into charged particles (glucose)

125
Q

During interstitial fluid exchange, what occurs when capillary filtration pressure is pushing fluid out?

A
  • the tissue hydrostatic pressure is acting against the interstitial space
  • if you have a lot of water in the IS space, it will push into the vascular space
126
Q

During interstitial fluid exchange, what occurs when capillary colloidal (albumin) osmotic pressure is pushing fluid back into the blood stream?

A

water is pulled from IS space back into the capillary

127
Q

Interstitial Pressure opposes the movement of water out of the capillary, resulting in:

A

the arterial end being higher pressure than venous end of capillaries
> 120 mmHg in the LV and pushes the blood all the way to the capillaries (it is at its lowest point the rt. atrium)

128
Q

This reflects the kidneys ability to produce concentrated/dilute urine

A

osmolality

129
Q

How is osmolality measured?

A

by serum osmolality and the need for water conservation/excretion

130
Q

Why do diuretics cause a “hypo” electrolyte imbalance?

A

because water follows sodium (therefore water is loss)

131
Q

What are the causes of hyponatremia?

A 
○ Increase in Na secretion
○ Inadequate intake
○ Diluted serum Na
○ Excess ADH
○ Vomiting
○ Hypotonic irrigations (enemas)
○ Excessive water intake
○ Near drowning (freshwater)
132
Q

What are the s/sx of hyponatremia?

A

○ Change in pulse and BP
○ Shallow respirations
○ Inc. GI motility (hyperactive bowel sounds)
○ Polyuria (dec SG)
○ Diminished deep tendon reflexes
○ Muscle/abdominal cramping and weakness
○ N/V
○ Suppression of thirst reflex
○ HA, confusion, lethargy, seizures, coma, death
most sxs. Are manifestations from the brain!!!*
Neuro sxs

133
Q

What drug can cause hyponatremia?

A

Diuretics because it induces sodium loss to reduce water concentrations

134
Q

How is hyponatremia diagnosed?

A

○ Serum sodium level = below 135
○ Serum osmolality below 280
○ Urine Specific Gravity below 1.010
○ Elevated Hct & plasma proteins

135
Q

How is hyponatremia treated?

A

○ Treat the underlying cause and monitor systems related to impact
○ If client taking lithium, monitors levels (can cause diminished lithium excretion resulting in toxicity)
○ Fluid restriction
○ Oral or IV of saline solution (NS)
○ Eat high sodium foods

136
Q

How is severe hyponatremia treated?

A

▪ Neurological symptoms such as seizures (serum sodium <110)
▪ Treated with hypertonic solution (3-5%) to increase sodium levels and return to normal
> Too much treatment with hypertonic solution can cause a rapid shift of water out of the
brain cells and cause permanent brain damage (Karev)

137
Q

This condition results in sodium levels above 145 mEq/L and serum osmolality about 295

A

Hypernatremia

138
Q

What are the causes of hypernatremia?

A 
○ Dec. Na secretion
○ Inc. Na intake
○ Dec. H2O intake
○ Inc. H2O loss 
○ Tube feedings
     ▪ Some of the canned foods for tube feedings are high in sodium (need to dilute them)
○ Watery diarrhea
○ IV infusion of hypertonic solution
○ Near drowning (salt water)
○ Inability to respond to thirst  
   ▪ They are relatively hypernatremic due to low fluid levels
139
Q

What are the s/sx of hypernatremia?

A 
○ Changes in pulse and BP
○ Irregular muscle contraction 
○ Diminished to absent deep tendon
○ Altered cerebral function 
○ Thirst
○ Oliguria (inability to form urine)
○ Decrease in skin turgor, salivation and moisture 
Neuro sxs: 
     ▪ HA, agitation, poor reflexes, seizures, coma, death
140
Q

How do you assess for hypernatremia?

A

Inspect for drugs containing sodium bicarbonate or IV NaCl

141
Q

What are the nursing interventions for hypernatremia?

A

▪ Monitor neuro status, seizures, I&O, and Vitals
▪ Instruct to avoid high Na+ foods
▪ Administer IV fluids (if due to fluid loss)
▪ Administer diuretics

142
Q

How is hypernatremia diagnosed?

A

○ Serum sodium above 145
○ Serum osmolality above 295/300
○ Urine specific gravity will be high (dehydrated) = 1.025+

143
Q

How is hypernatremia treated?

A

○ Treat the underlying CAUSE
○ Replace fluids, slowly and carefully
▪ Can be done orally or IV but gradually to avoid Cerebral Edema

144
Q

Some examples of high sodium foods include?

A
  • bacon
  • butter
  • canned foods
  • luncheon meats
  • table salt
145
Q

What are the normal potassium levels?

146
Q

What are good food sources of potassium?

A
  • Fruits (think bananas, oranges, etc.)
  • Meats
  • Vegetables
147
Q

What causes hypokalemia?

A 
○ Inadequate Dietary Intake:
(also due to poor eating habits -> anorexia, NPO, unbalanced diet)
○ Excess Renal, GI, Skin losses
○ Movement of K from ECF to  ICF
○ Dilution of serum K
148
Q

What are considered potassium wasting diuretics?

A
  • lasix

- thiazides

149
Q

What are GI secretions high in and what occurs during hypokalemia?

A

GI secretions are high in K+, therefore unusual wasting can cause hypokalemia

150
Q

What are the s/sx of hypokalemia?

A

○ Thready, weak pulse and orthostatic hypotension
○ Changes in ECG (ST depression and flat or inverted T wave)
○ Shallow respirations
○ Lethargy to coma state
○ Skeletal muscle weakness, deep tendon hyporflexia
○Polyuria, decreased urine specific gravity
○ GI, Neuromuscular, renal, & Cardiovascular systems are mostly effected

151
Q

What effect does hypokalemia have on the cardiovascular system?

A

Due to K+ acting on the electrical activity of excitable tissues, heart dysrhythmias occurs causing a decreased T-wave

152
Q

What effect does hypokalemia have on the GI system?

A

It causes abdominal distention, constipation, and diminished bowel sounds (abnormal peristalsis) due to the K+ deficiency acting on the bowels’ contractility

153
Q

What effect does hypokalemia have on the neuromuscular system?

A
  • muscles weakness

- paralysis

154
Q

How is hypokalemia diagnosed?

A 
> By lab results such as:
     ▪ Urine specific gravity
     ▪ K+ serum level
     ▪ Serum osmolality 
> Presence of T-wave depression
155
Q

How do we treat hypokalemia?

A

○ Place client on a heart monitor
○
○ High K+ foods, oral supplements, or IV (take precaution)
○ Using the drugs K-Dur & IV Potassium Chloride
○ Patient can NOT take oral K supplements on a empty stomach

156
Q

What must be done before giving a potassium IV and why?

A

K+ must be diluted when given IV or it will stop the heart. It also needs to be infused not pushed

157
Q

What are some food sources for potassium?

A
  • Fruits (oranges, bananas, apricots and cantaloupe)
  • Meats
  • Vegetables
  • Dried fruit, nuts and seeds
  • Chocolate
158
Q

What causes hyperkalemia?

A

○ MOST COMMON CAUSE IS DECREASED RENAL FUNCTION
○ Excess IV administration of K+ or excessive oral ingestion of supplements
○ Decreased excretion due to K+ sparing diuretics (spironolactone)
○ Shift of K+ from intracellular to extracellular (ICF -> ECF)

159
Q

How does hyperkalemia cause a decrease in renal function?

A

Because the kidney is unable to excrete potassium into urine like normal

160
Q

The shift of potassium from intracellular to extracellular ICF -> ECF is due to things such as:

A

▪ Crushing injuries or burns that cause cell death and release K into the ECF

161
Q

What are the s/sx of hyperkalemia?

A

○ First symptom is paresthesia (numbness/tingling)
○ HEART DYSRHYTHMIAS (cardiac conduction is blocked which is shown through the peaked/elevated T-waves, widened QRS complexes and prolonged PR intervals)
○ Slow/weak pulse/hypotension
○ Muscle twitching changes to weakness, and decreased neuromuscular excitability
○ Respiratory failure (SOB)
○ Inc. GI motility

162
Q

How is hyperkalemia diagnosed?

A

by looking at lab values, medical history (renal failure, etc.), & EKG findings

163
Q

How is hyperkalemia treated ?

A

○ Limit IVs, supplements & sparing meds (spironolactone)
○ Administer medications that will remove K from body by renal excretion
○ Education client to avoid foods high in K
○ Need to monitor EKG for hypokalemia (flattened T-wave, etc.)
○ Inc. cellular uptake

164
Q

What medications will remove K from the body?

A

▪ Sodium polystyrene (Kaexalate)

▪ Calcium gluconate

165
Q

What does sodium polystyrene (Kaexalate) do?

A

It is a resin drug that exchanges potassium for sodium, lowering the K+ level

166
Q

What does calcium gluconate do?

A

Calcium antagonizes the reduced membrane excitability caused by excess K+, and returns excitability/membrane potential to normal. It is a short-lived solution and thus combined with something that can reduce the ECF concentrations of K+ (insulin)

167
Q

In severe cases of hyperkalemia, what can be used in severe cases in those with renal failure?

A

hemodialysis

168
Q

What effect does sodium bicarbonate have on K disorders?

A

it will cause K to move to ICF

169
Q

What effect does insulin have on K disorders?

A

it will decrease ECF K concentration

170
Q

What is the normal range for calcium?

A

8.6-10.2 mg/dl

171
Q

What is the most common cause of hypocalcemia? What are some other causes?

A 
○ Lactose intolerance
○ Inadequate oral intake or intake of vitamin D
○ Immobility
○ 
○ Most common cause is Renal Failure
○ Hypoparathyroidism
○ Pancreatitis which causes fat necrosis
○ GI wound drainage/Chronic diarrhea (inhibits ability to absorb Ca++ from the GIT)
172
Q

Why is renal failure a cause of hypocalcemia?

A 
Because of the decreased production of activated Vitamin D and hyperphosphatemia
     □ Vitamin D is activated in 
     the Kidneys
     □ Without active Vitamin D, 
     calcium cannot be absorbed 
     from the GIT
     □ Phosphate and Calcium 
     have an inverse relationship
     □ Increased phosphate 
     (hyperphosphatemia) results 
     in hypocalcemia
173
Q

What is normally the first s/sx of hypocalcemia?

A

NEURO/MUSCLE PROBLEMS (Increased Neuromuscular Excitability)

174
Q

What are some other s/sx of hypocalcemia?

A 
▪ Prolonged ST interval
▪ Inc. GI activity 
▪ Neuromuscular irritability
▪ Cramping
▪ Hyperactive reflexes
▪ Paresthesia
▪ Tetany (spasms in face, hands, feet)
▪ Heart dysrhythmias Heart dysrhythmias
175
Q

How is hypocalcemia diagnosed?

A 
○ Chvostek Sign 
     ▪ Stimulating facial nerve 
     by tapping and observing 
     for tetany
○ Trousseau Sign 
     ▪ Inflating BP cuff to 10 mm 
     above systolic and 
     watching for tetany in 
     hands/fingers
176
Q

How is hypocalcemia treated?

A

○ Calcium chloride (IV)
▪ warm injection to body temp. prior to administering
▪ administer slowly
▪ monitor for ECG changes
▪ observe for infiltration
▪ monitor for signs of hypercalcemia
○ Calcium gluconate (10%) - restores functional integrity of the neuromuscular sys.
○ Reduce environmental stimuli
○ Initiate seizure precautions
○ Monitor for s/sx of fractures ○ Eat more cheese, milk, soy, sardines, spinach, tofu, low fat yogurt

177
Q

What is the cause of hypercalcemia?

A 
○ Overconsumption of Vitamin D
     ▪ Results in excessive 
     absorption of Calcium and 
     increased serum Ca++ levels 
○ Hyperparathyroidism
     ▪ Excess release of PTH, 
     thus excessive Ca++ release 
     from bones 
○ Bone tumors can also cause increased Ca++ release from bones 
○ Hemoconcentration 
○ Immobility
178
Q

What are the s/sx of hypercalcemia?

A 
○  Early signs = Tachycardia and shortened ST interval
○ Impaired respiratory movement
○ Renal calculi formation 
○ Hypoactive bowel sounds 
○ Decreased neural excitability & impaired cardiac and smooth muscle fxn
○ Muscle weakness
○ Neuromuscular-
     ▪ Headache, stupor, fatigue
○ Anorexia, constipation, N/V
     ▪ Think of the decreased 
     smooth muscle ability
○ Cardiac dysrhythmias (ventricular)
     ▪ Ca++ is the primary ion 
     responsible for cardiac 
     conduction… too much 
     causes deadly
     Ventricular Arrhythmias
179
Q

How is hypercalcemia treated?

A

○ Correct the underlying cause of the serum Ca++ excess
○ Promote urinary excretion of Ca++
▪ The excretion of Na+ is
accompanied by Ca++
▪ Diuretics!!
○ Calcitonin- decrease osteoclast activity/calcium release from bone
○ Position and monitor mobility
○ Monitor for signs of renal calculi and pathological fractures

180
Q

What is the normal range for magnesium?

A

1.5-2.5 mg/dl

181
Q

What is the cause of hypomagnesemia?

A

○ Malnutrition and chronic alcoholism
○ Diabetic Ketoacidosis
○ Diuretic therapy
○ Hyperparathyroidism
○ Vomiting, diarrhea, celiac disease, chrohns disease
○ Hyperglycemia, insulin administration, sepsis

182
Q

What is the s/sx of hypomagnesemia?

A 
○ Hyperactive NEUROMUSCULAR activity
Tetany
     ▪ Nystagmus- following the 
     finger back and forth with 
     pupil (tracking without 
     fluttering)
     ▪ Choreiform movements 
     (dyskinesia)
     ▪ Positive Trousseau and 
     Chvosteks  signs
     ▪ + Babinski test- reflex and 
     the bottom of the foot
○ Peaked T wave, depressed ST segment 
○ Shallow respirations
○ Personality changes
183
Q

How is hypomagnesemia treated?

A

○ Initiate seizure precautions
○ Monitor for reduced deep tendon flexes
○ Magnesium replacement
▪Magnesium hydroxide
(Milk of Magnesia)
▪ Magnesium sulfate
* Route of administration depends on the severity of the hypomagnesemia *

184
Q

What is the cause of hypermagnesemia?

A 
○ Renal Disease/failure
○ Excessive intake of drugs containing magnesium
     ▪ IV administration
     ▪ P.O. meds- antacids, 
     supplements, laxatives
185
Q

What are the neuromuscular and cardiac s/sx of hypermagnesemia?

A

○ Muscle weakness / hyporeflexia
▪ Due to magnesium
decreasing the
acetylcholine release at
the neuromuscular
junction
○ Lethargy, confusion, coma
○ Cardiac arrest, arrhythmias, hypotension (prolonged PR interval)
▪ Due to the Calcium channel blocking effect of magnesium
○ Respiratory arrest, complete heart block, and cardiac arrest (think of the lack of muscular excitability)

186
Q

How is the hypermagnesemia treated?

A

○ Stop administration of magnesium
○ Administer calcium chloride or gluconate (direct antagonist of magnesium)
○ Administer dieuretics
○ Restrict magnesium in the diet
○ Educate client to avoid laxatives and antacids containing magnesium

187
Q

What is the normal range for potassium?

188
Q

What is the normal range for chloride?

189
Q

What is the normal range for sodium bicardbonate?

Pathophysiology (10 decks)

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