Disorders of Fluid, Electrolyte, and Acid-Base Balance Flashcards

1
Q

Edema is

A

Palpable swelling produced by the expansion of interstitial fluid

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2
Q

Increased capillary filtration pressure is where

A

As pressure rises, fluid moves into interstitial spaces

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3
Q

How does heart/kidney failure and premenstrual sodium retention cause edema?

A

Increased vascular volume

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4
Q

How does liver disease/portal vein obstruction, acute pulmonary edema, and venous thrombosis cause edema?

A

Venous obstruction

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5
Q

Edema can be __ or ___

A

Localized

Generalized

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6
Q

Localized edema is in

A

A limited site/space

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7
Q

Generalized edema is in __ due to

Often accumulates in

A

A larger area
Increased vascular volume

Dependent part of the body (gravity)
Nurses wear compression socks because of this

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8
Q

Decreased capillary colloidal osmotic pressure is where ___ exert the ___ needed to pull __ back into the ___ from

A

Plasma proteins exert the osmotic force needed to pull fluid back into the capillary from the tissue spaces

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9
Q

Examples of plasma proteins

A

Albumin
Globulins
Fibrinogen

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10
Q

Edema is usually a result of

A

Inadequate production or abnormal loss of plasma proteins

*mainly albumin

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11
Q

Common causes of edema are

A

Kidney disease
Extensive burns
Sever liver disease
Starvation/Malnutrition

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12
Q

Increased capillary permeability is where

A

Capillary pores become enlarged or capillary wall integrity is damaged

**both allow fluid to pass easier

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13
Q

When capillary permeability is increased, plasma proteins ___, so fluid __

A

Leak into the interstitial spaces

Moves to the tissue

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14
Q

Common causes of increased capillary permeability are

A

Burns
Inflammation
Immune responses
Tissue injury

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15
Q

An obstruction of lymph flow means that ___ cannot be reabsorbed through ___ and need the ___ to get back into the ____

A

Plasma proteins and other large particles
The capillary membrane pores
Lymphatic system
Circulatory system

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16
Q

A common cause of an obstruction of lymph flow is

A

Disruption or malformation of the lymphatic system

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17
Q

Lymphedema is

A

High-protein swelling in an area of the body

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18
Q

Edema of what is life-threatening?

A

Brain
Larynx
Lungs

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19
Q

Pitting edema occurs when

A

Interstitial fluid accumulation exceeds absorptive capacity of tissue gel

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20
Q

Third-spacing is the ____ of ECF into ___

Is the extra fluid helpful?

A

Loss or trapping
Transcellular space
e.g, pericardial sac, peritoneal cavity, pleural cavity

No, doesn’t help with function and can be problematic

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21
Q

Ascites is

A

Fluid accumulation in peritoneal space

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22
Q

Hydrothorax is

A

Excessive fluid in the pleural cavity

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23
Q

Changes in sodium are usually accompanied by

A

Changes in water volume

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24
Q

ADH or ___ tells your kidneys __

A

Vasopressin

How much water to conserve

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25
Q

ADH is released from __ when

A

Pituitary

There is an increase in blood osmolality or decrease in blood volume

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26
Q

ADH =

A

Antidiuretic hormone

Anti - Block
Diuretic - Increased Urination
Blocking Urination

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27
Q

DI is

A

Diabetes insipidus

Or dry inside

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28
Q

Pathophysiological mechanisms of DI

A

Deficiency of ADH or decreased response to ADH

Unable to concentrate urine

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29
Q

Clinical manifestations of DI

A

Excrete large volumes of urine
Excessive thirst

** Lack of ADH or not responding = lots of pee = Thirsty**

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30
Q

SIADH is

A

Syndrome of inappropriate antidiuretic hormone

Or soaked inside b/c ADH

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31
Q

Pathophysiological mechanisms of SIADH

A

Failure of negative feedback loop that releases/inhibits ADH

Too much ADH released

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32
Q

Clinical manifestations of SIADH

A
Water retention
Dilutional hyponatremia (low serum Na+) 
Urine osmolality is high 
Serum osmolality is low 
Urine output is decreased
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33
Q

Disorders of sodium and water are divided into

A

Isotonic

Hyponatremia/hypernatremia

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34
Q

Isotonic is a ___ chance in sodium and water

Concentration is ___

A

Proportionate

Unchanged

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35
Q

Isotonic fluid volume DEFICIT is

A

Decreased fluid volume - proportionate loss of water and sodium

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36
Q

Etiology of isotonic fluid volume DEFICIT

A
  • Inadequate fluid intake (oral trauma, impaired thirst sensation, unconsciousness)
  • Excessive GI fluid losses (vomiting, diarrhea, draining GI fistula)
  • Excessive renal losses (diuretic therapy, osmotic diuresis (hyperglycemia), adrenal insufficiency (Addison disease))
  • Excessive skin losses (fever, sweating, Burns)
  • Third space losses (Intestinal obstruction, edema, ascites, burns)
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37
Q

Clinical manifestations of isotonic fluid volume DEFICIT

A
  • Weight loss
  • Urine output decrease?
  • Increased thirst, increased hematocrit and BUN (blood urea nitrogen).

Signs of decreased vascular volume

  • BP decreases
  • HR increases
  • pulse weak and thready
  • veins less prominent
  • hypovolemic shock
  • postural hypotension
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38
Q

Isotonic fluid volume EXCESS is

A

Increased fluid volume

Proportionate increase in water and sodium

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39
Q

Etiology of Isotonic fluid volume EXCESS

A

The most common cause seen are heart failure and renal failure.

Inadequate sodium and water elimination (congestive heart failure, renal failure, increased corticosteroid levels, hyperaldosteronism, Cushing disease, liver failure)

Excessive sodium intake in relation to output (excessive dietary intake, excessive ingestion of sodium-containing medications or home remedies, excessive administration of sodium-containing parenteral fluids)

Excessive fluid intake in relation to output (ingestion of fluid in excess of elimination, administration of parenteral fluids or blood at an excessive rate)

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40
Q

Clinical manifestations of isotonic fluid volume EXCESS

A

Weight gain
Edema
Increased vascular volume (full and bounding pulse, venous distention, pulmonary edema, shortness of breath, crackles, dyspnea (difficult or labored breathing), cough)

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41
Q

HYPOnatremia is

A

Low serum sodium

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42
Q

HYPOnatremia is commonly in

A

Elderly due to decreased renal function and inability to conserve sodium

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43
Q

Etiology of HYPOnatremia

A

GI losses, vomiting, diarrhea, sweating, diuretics

SIADH

Administering sodium-free IV fluids, enemas, irrigating solution

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44
Q

Clinical manifestations of HYPOnatremia

A

Neurologic affects = water intoxication.

Apathy, lethargy, headache – can progress to disorientation, confusion, gross motor weakness, and depression of deep tendon reflexes

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45
Q

HYPERnatremia is

A

High serum sodium

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46
Q

HYPERnatremia causes

A

Cellular dehydration

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47
Q

Etiology of HYPERnatremia

A

Excessive water loss: watery diarrhea, excessive sweating, DI

Decreased water intake: oral trauma, impaired thirst

Increased sodium intake: (rapid/excessive administration of sodium-containing parenteral solutions, near drowning in salt water)

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48
Q

Clinical manifestations of HYPERnatremia

A

Polydipsia
Oliguria
Anuria

Signs of dehydration (Dry skin and mucous membranes, Decreased tissue turgor, Tongue rough and fissured, Decreased salivation and lacrimation)

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49
Q

Polydipsia

A

Excessive thirst

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50
Q

Oliguria

A

Small amounts of urine

51
Q

Anuria

A

Absence of any urine output

52
Q

Lacrimation

A

Lack of tears

53
Q

What happens as a result of water moving out of brain cells?

A

Decreased reflexes, agitation, headache, restlessness

54
Q

Signs of decreased vascular volume:

A

Tachycardia (HR 100+/minute)

Weak and thready pulse

Decreased BP

Vascular collapse

55
Q

HYPOkalemia is

A

Low serum potassium

56
Q

Etiology of HYPOkalemia

A

Inadequate intake

Excessive renal losses: #1 cause – potassium wasting diuretics, e.g., furosemide (Lasix)

GI losses: vomiting diarrhea, GI suction

57
Q

Clinical manifestations of HYPOkalemia

A

Neuromuscular: muscle flabbiness, weakness, fatigue, muscle cramps, paresthesia, paralysis.

CV: postural hypotension, cardiac dysrhythmias

CNS: Confusion, depression

58
Q

Paresthesia is

A

any abnormal touch sensation, which can be experienced as numbness, tingling, often in the absence of external stimuli

59
Q

Effect of low potassium on RMP becomes more ___ and in turn takes a greater ___

A

Negative

Stimuli for an action potential

60
Q

HYPERkalemia is

A

High serum potassium

61
Q

Etiology of HYPERkalemia

A

Excessive intake

Loss from intracellular compartment, i.e., burns, tissue trauma, crushing injuries

Not eliminated from kidneys: most common cause is renal function.

Potassium-sparing diuretics

62
Q

Clinical manifestations of HYPERkalemia

A

Risk of cardiac arrest due to impact on cardiac conduction!

Paresthesia (pins and needles)

Generalized muscle weakness

Dyspnea

High serum potassium level

Nausea/vomiting

Intestinal cramps

Diarrhea

Dizziness

Muscle cramps

Changes in ECG

63
Q

In HYPERkalemia, rate of repolarization is

A

More rapid

64
Q

What effect does vitamin D have on calcium absorption?

A

Increases calcium absorption in the intestine

65
Q

PTH stand for

A

Parathyroid hormone

66
Q

PTH is a major regulator of

A

Plasma calcium and phosphorus

67
Q

When plasma calcium is high, PTH is ___ and calcium is deposited ___

A

Inhibited

In the bones

68
Q

When plasma calcium is low, PTH is ___ and calcium is mobilized ___

A

Increased

From the bones

69
Q

HYPOparathyroidism is

A

Decreased PTH secretion > hypocalcemia

70
Q

Etiology of HYPOparathyroidism

A

Congenital absence of parathyroid glands.

Acquired after neck surgery.

71
Q

Clinical manifestations of HYPOparathyroidism

A

Associated with decreased calcium: tetany with muscle cramps, carpopedal spasm, convulsions

Parethesias

72
Q

HYPERparathyroidism is

A

Increased PTH secretion > hypercalcemia

73
Q

Etiology of HYPERparathyroidism

A

Primary disorder: hyperplasia, adenoma, rarely carcinoma of parathyroid glands.

Secondary disorder: Chronic renal failure, chronic malabsorption of calcium

74
Q

Clinical manifestations of HYPERparathyroidism

A

Hypercalciuria>develop kidney stones

Diffuse demineralization of bones, pathologic fractures and bone lesions. TOO MUCH CALCIUM!

75
Q

HYPOcalcemia is

A

Low serum calcium

76
Q

Etiology of HYPOcalcemia

A

Unable to mobilize calcium from bone (hypoparathyroidism)

Decreased intake or absorption (Malabsorption, Vitamin D deficiency, Liver or kidney disease, Medications that impair activation of vitamin D)

Abnormal renal loss (renal failure)

77
Q

Clinical manifestations of HYPOcalcemia

A

Cardiovascular:
Hypotension
Signs of cardiac insufficiency

Skeletal:
Osteomalacia
Bone pain, deformities, fracture

Neuromuscular:  
Paresthesia 
Skeletal muscle cramps 
Abdominal spasms and cramps 
Hyperactive reflexes 
Tetany 
Positive Chvostek and Trousseau signs
78
Q

HYPERcalcemia is

A

High serum calcium

79
Q

Etiology of HYPERcalcemia

A

Increased bone reabsorption (increased PTH, malignant neoplasms, prolonged immobilization)

80
Q

Clinical manifestations of HYPERcalcemia

A

Urine and kidney: polyuria, polydipsia, kidney stones (flank pain)

Pay special attn. to
Neuromuscular (decreased neuromuscular excitability):
Muscle weakness and atrophy
Ataxia, loss of muscle tone

Skeletal:
Osteopenia
Osteoporosis

CNS:
Lethargy
Personality and behavioral changes
Stupor and coma

CV:
Hypertension
Atrioventricular block on ECG

81
Q

The normal pH of ECF is

Is maintained through mechanisms that

A

7.35-7.45

Generate, buffer, and eliminate acids and bases

82
Q

The three major mechanisms of pH regulation are

A

Chemical buffer systems
Lungs
Kidneys

83
Q

Chemical buffer systems in body fluids immediately

A

Combine with excess acids or bases to prevent large changes in pH

84
Q

The chemical buffer system works how quickly?

A

Immediately

85
Q

The chemical buffer system works while waiting for

A

Renal and respiratory system to become effective

86
Q

What are the three buffer systems?

A

Bicarbonate buffer system
Proteins
Transcellular H/K exchange system

87
Q

Which of the three buffer systems is the most powerful?

A

Bicarbonate buffer system

88
Q

The bicarbonate buffer system

A

Exchanges weak acids for strong acids and weak bases for strong bases

89
Q

Which of the three buffer systems is the largest?

A

Proteins

90
Q

Proteins as a buffer system can act as

How quickly does it work?

A

Acids or bases depending on what is needed

Delayed for several hours

91
Q

Two major protein buffers are

A

Albumin

Plasma globulins

92
Q

In the Transcellular H/K exchange system,

A

H+ and K+ are positively changed ions and trade places between intracellular and extracellular spaces.

** if there are excessive H+ ions in blood, K+ ions move into intracellular space which reduces K+ in blood)

93
Q

What is the second line of defense against acid-base imbalances?

A

Respiratory control mechanisms

94
Q

The respiratory control mechanisms involves

A

Involves the lungs, which control the elimination of CO2

Increased ventilation decreases PCO2 and decreased ventilation increases PCO2

95
Q

What happens when H+ ions concentration is above normal?

A

Respirator system is stimulated and ventilation is increased

96
Q

In the respiratory control mechanisms, when does control of pH occur? Max out?

A

Within minutes and is maximal within 12 to 24 hours

97
Q

What is the third defense against avid-base imbalances?

A

Renal control mechanisms

98
Q

The Renal control mechanisms work in three ways

A

Excrete H+
Reabsorption of HCO3
Production of new HCO3

99
Q

When do renal mechanisms kick in? How long?

A

In hours and continue to function for days until the pH has returned to normal/near-normal range

100
Q

Acidosis =

A

Excess of H ions

101
Q

Alkalosis =

A

Loss of H ions

102
Q

Metabolic disorders produce alteration in

A

The plasma HCO3-concentration

103
Q

Respiratory disorders produce an alteration in

A

PCO2

104
Q

Primary disturbance is the

A

Initiating event causing the imbalance

105
Q

Compensatory mechanisms provide a means to

A

Control pH when correction is impossible or cannot be achieved immediately

106
Q

Kidneys can compensate for

A

Respiratory-induced acid-base imbalances

107
Q

Lungs can compensate for

A

Metabolic-induced acid base imbalances

108
Q

Do kidneys or lungs work faster? (compensate)

A

Lungs - take minutes to hours

109
Q

Metabolic Acidosis alterations

A

PH – decreased

HCO3 – decreased

110
Q

Causes of metabolic acidosis

A

Excess metabolic acids: Lactic acidosis (sepsis)

Ketoacidosis (Assoc. with diabetes)

Salicylate (aspirin) toxicity

Decreased renal function > can’t secrete urine

Bicarbonate loss (loss of intestinal secretions (high in H+) due to diarrhea, vomiting, intestinal suction)

111
Q

Metabolic acidosis compensatory responses

A

Respiratory: increased rate and depth of respiration

K+: hyperkalemia

Urine: Acid urine, increased ammonia in urine

112
Q

Metabolic alkalosis alterations

A

PH – increased

HCO3 – increased

113
Q

Causes of metabolic alkalosis

A

Increased bicarbonate or alkali (ingestion of antacids, IV administration of lactate (“lactated ringers”))

Loss of H+ (vomiting, gastric suction, binge/purge, hypokalemia)

114
Q

Metabolic alkalosis compensatory responses

A

Respiratory: decreased rate and depth of respiration

Urine: increased urine pH

115
Q

Respiratory acidosis alterations

A

PH - decreased

CO2 – increased

116
Q

Causes of respiratory acidosis

A

Depression of resp. center, (drug overdose or head injury)

Lung disease: asthma, emphysema, bronchitis

Airway obstruction (resp. muscle paralysis, chest injuries)

117
Q

Respiratory acidosis compensatory responses

A

Urine: acid urine

118
Q

Respiratory alkalosis alterations

A

PH – increased

CO2 – decreased

119
Q

Causes of respiratory alkalosis

A

Excessive ventilation (anxiety and psychogenic hyperventilation)

Hypoxia and reflex stimulation of ventilation 
Lung disease  
Encephalitis 
Fever 
Salicylate toxicity 
Elevated blood ammonia level 
Mechanical ventilation
120
Q

Respiratory alkalosis compensatory responses

A

Occurs so quickly, compensatory mechanisms don’t have a chance to kick in

121
Q

pH is high, CO2 is low

A

Resp. Alkalosis

122
Q

pH is high, HCO3 is high

A

Met. Alkalosis

123
Q

pH is low, CO2 is high

A

Resp. Acidosis

124
Q

pH is low, HCO3

A

Met. Acidosis