Disorders of Fluid, Electrolyte, and Acid-Base Balance Flashcards
1
Q
Edema is
A
Palpable swelling produced by the expansion of interstitial fluid
2
Q
Increased capillary filtration pressure is where
A
As pressure rises, fluid moves into interstitial spaces
3
Q
How does heart/kidney failure and premenstrual sodium retention cause edema?
A
Increased vascular volume
4
Q
How does liver disease/portal vein obstruction, acute pulmonary edema, and venous thrombosis cause edema?
A
Venous obstruction
5
Q
Edema can be __ or ___
A
Localized
Generalized
6
Q
Localized edema is in
A
A limited site/space
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
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
9
Q
Examples of plasma proteins
A
Albumin
Globulins
Fibrinogen
10
Q
Edema is usually a result of
A
Inadequate production or abnormal loss of plasma proteins
*mainly albumin
11
Q
Common causes of edema are
A
Kidney disease
Extensive burns
Sever liver disease
Starvation/Malnutrition
12
Q
Increased capillary permeability is where
A
Capillary pores become enlarged or capillary wall integrity is damaged
**both allow fluid to pass easier
13
Q
When capillary permeability is increased, plasma proteins ___, so fluid __
A
Leak into the interstitial spaces
Moves to the tissue
14
Q
Common causes of increased capillary permeability are
A
Burns
Inflammation
Immune responses
Tissue injury
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
16
Q
A common cause of an obstruction of lymph flow is
A
Disruption or malformation of the lymphatic system
17
Q
Lymphedema is
A
High-protein swelling in an area of the body
18
Q
Edema of what is life-threatening?
A
Brain
Larynx
Lungs
19
Q
Pitting edema occurs when
A
Interstitial fluid accumulation exceeds absorptive capacity of tissue gel
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
21
Q
Ascites is
A
Fluid accumulation in peritoneal space
22
Q
Hydrothorax is
A
Excessive fluid in the pleural cavity
23
Q
Changes in sodium are usually accompanied by
A
Changes in water volume
24
Q
ADH or ___ tells your kidneys __
A
Vasopressin
How much water to conserve
25
ADH is released from __ when
Pituitary
| There is an increase in blood osmolality or decrease in blood volume
26
ADH =
Antidiuretic hormone
Anti - Block
Diuretic - Increased Urination
Blocking Urination
27
DI is
Diabetes insipidus
Or dry inside
28
Pathophysiological mechanisms of DI
Deficiency of ADH or decreased response to ADH
| Unable to concentrate urine
29
Clinical manifestations of DI
Excrete large volumes of urine
Excessive thirst
** Lack of ADH or not responding = lots of pee = Thirsty**
30
SIADH is
Syndrome of inappropriate antidiuretic hormone
Or soaked inside b/c ADH
31
Pathophysiological mechanisms of SIADH
Failure of negative feedback loop that releases/inhibits ADH
Too much ADH released
32
Clinical manifestations of SIADH
```
Water retention
Dilutional hyponatremia (low serum Na+)
Urine osmolality is high
Serum osmolality is low
Urine output is decreased
```
33
Disorders of sodium and water are divided into
Isotonic
| Hyponatremia/hypernatremia
34
Isotonic is a ___ chance in sodium and water
Concentration is ___
Proportionate
Unchanged
35
Isotonic fluid volume DEFICIT is
Decreased fluid volume - proportionate loss of water and sodium
36
Etiology of isotonic fluid volume DEFICIT
- 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)
37
Clinical manifestations of isotonic fluid volume DEFICIT
- 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
38
Isotonic fluid volume EXCESS is
Increased fluid volume
Proportionate increase in water and sodium
39
Etiology of Isotonic fluid volume EXCESS
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)
40
Clinical manifestations of isotonic fluid volume EXCESS
Weight gain
Edema
Increased vascular volume (full and bounding pulse, venous distention, pulmonary edema, shortness of breath, crackles, dyspnea (difficult or labored breathing), cough )
41
HYPOnatremia is
Low serum sodium
42
HYPOnatremia is commonly in
Elderly due to decreased renal function and inability to conserve sodium
43
Etiology of HYPOnatremia
GI losses, vomiting, diarrhea, sweating, diuretics
SIADH
Administering sodium-free IV fluids, enemas, irrigating solution
44
Clinical manifestations of HYPOnatremia
Neurologic affects = water intoxication.
Apathy, lethargy, headache – can progress to disorientation, confusion, gross motor weakness, and depression of deep tendon reflexes
45
HYPERnatremia is
High serum sodium
46
HYPERnatremia causes
Cellular dehydration
47
Etiology of HYPERnatremia
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)
48
Clinical manifestations of HYPERnatremia
Polydipsia
Oliguria
Anuria
Signs of dehydration (Dry skin and mucous membranes, Decreased tissue turgor, Tongue rough and fissured, Decreased salivation and lacrimation)
49
Polydipsia
Excessive thirst
50
Oliguria
Small amounts of urine
51
Anuria
Absence of any urine output
52
Lacrimation
Lack of tears
53
What happens as a result of water moving out of brain cells?
Decreased reflexes, agitation, headache, restlessness
54
Signs of decreased vascular volume:
Tachycardia (HR 100+/minute)
Weak and thready pulse
Decreased BP
Vascular collapse
55
HYPOkalemia is
Low serum potassium
56
Etiology of HYPOkalemia
Inadequate intake
Excessive renal losses: #1 cause – potassium wasting diuretics, e.g., furosemide (Lasix)
GI losses: vomiting diarrhea, GI suction
57
Clinical manifestations of HYPOkalemia
Neuromuscular: muscle flabbiness, weakness, fatigue, muscle cramps, paresthesia, paralysis.
CV: postural hypotension, cardiac dysrhythmias
CNS: Confusion, depression
58
Paresthesia is
any abnormal touch sensation, which can be experienced as numbness, tingling, often in the absence of external stimuli
59
Effect of low potassium on RMP becomes more ___ and in turn takes a greater ___
Negative
| Stimuli for an action potential
60
HYPERkalemia is
High serum potassium
61
Etiology of HYPERkalemia
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
Clinical manifestations of HYPERkalemia
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
In HYPERkalemia, rate of repolarization is
More rapid
64
What effect does vitamin D have on calcium absorption?
Increases calcium absorption in the intestine
65
PTH stand for
Parathyroid hormone
66
PTH is a major regulator of
Plasma calcium and phosphorus
67
When plasma calcium is high, PTH is ___ and calcium is deposited ___
Inhibited
In the bones
68
When plasma calcium is low, PTH is ___ and calcium is mobilized ___
Increased
From the bones
69
HYPOparathyroidism is
Decreased PTH secretion > hypocalcemia
70
Etiology of HYPOparathyroidism
Congenital absence of parathyroid glands.
Acquired after neck surgery.
71
Clinical manifestations of HYPOparathyroidism
Associated with decreased calcium: tetany with muscle cramps, carpopedal spasm, convulsions
Parethesias
72
HYPERparathyroidism is
Increased PTH secretion > hypercalcemia
73
Etiology of HYPERparathyroidism
Primary disorder: hyperplasia, adenoma, rarely carcinoma of parathyroid glands.
Secondary disorder: Chronic renal failure, chronic malabsorption of calcium
74
Clinical manifestations of HYPERparathyroidism
Hypercalciuria>develop kidney stones
Diffuse demineralization of bones, pathologic fractures and bone lesions. TOO MUCH CALCIUM!
75
HYPOcalcemia is
Low serum calcium
76
Etiology of HYPOcalcemia
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
Clinical manifestations of HYPOcalcemia
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
HYPERcalcemia is
High serum calcium
79
Etiology of HYPERcalcemia
Increased bone reabsorption (increased PTH, malignant neoplasms, prolonged immobilization)
80
Clinical manifestations of HYPERcalcemia
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
The normal pH of ECF is
Is maintained through mechanisms that
7.35-7.45
Generate, buffer, and eliminate acids and bases
82
The three major mechanisms of pH regulation are
Chemical buffer systems
Lungs
Kidneys
83
Chemical buffer systems in body fluids immediately
Combine with excess acids or bases to prevent large changes in pH
84
The chemical buffer system works how quickly?
Immediately
85
The chemical buffer system works while waiting for
Renal and respiratory system to become effective
86
What are the three buffer systems?
Bicarbonate buffer system
Proteins
Transcellular H/K exchange system
87
Which of the three buffer systems is the most powerful?
Bicarbonate buffer system
88
The bicarbonate buffer system
Exchanges weak acids for strong acids and weak bases for strong bases
89
Which of the three buffer systems is the largest?
Proteins
90
Proteins as a buffer system can act as
How quickly does it work?
Acids or bases depending on what is needed
Delayed for several hours
91
Two major protein buffers are
Albumin
| Plasma globulins
92
In the Transcellular H/K exchange system,
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
What is the second line of defense against acid-base imbalances?
Respiratory control mechanisms
94
The respiratory control mechanisms involves
Involves the lungs, which control the elimination of CO2
**Increased ventilation decreases PCO2 and decreased ventilation increases PCO2**
95
What happens when H+ ions concentration is above normal?
Respirator system is stimulated and ventilation is increased
96
In the respiratory control mechanisms, when does control of pH occur? Max out?
Within minutes and is maximal within 12 to 24 hours
97
What is the third defense against avid-base imbalances?
Renal control mechanisms
98
The Renal control mechanisms work in three ways
Excrete H+
Reabsorption of HCO3
Production of new HCO3
99
When do renal mechanisms kick in? How long?
In hours and continue to function for days until the pH has returned to normal/near-normal range
100
Acidosis =
Excess of H ions
101
Alkalosis =
Loss of H ions
102
Metabolic disorders produce alteration in
The plasma HCO3-concentration
103
Respiratory disorders produce an alteration in
PCO2
104
Primary disturbance is the
Initiating event causing the imbalance
105
Compensatory mechanisms provide a means to
Control pH when correction is impossible or cannot be achieved immediately
106
Kidneys can compensate for
Respiratory-induced acid-base imbalances
107
Lungs can compensate for
Metabolic-induced acid base imbalances
108
Do kidneys or lungs work faster? (compensate)
Lungs - take minutes to hours
109
Metabolic Acidosis alterations
PH – decreased
HCO3 – decreased
110
Causes of metabolic acidosis
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
Metabolic acidosis compensatory responses
Respiratory: increased rate and depth of respiration
K+: hyperkalemia
Urine: Acid urine, increased ammonia in urine
112
Metabolic alkalosis alterations
PH – increased
HCO3 – increased
113
Causes of metabolic alkalosis
Increased bicarbonate or alkali (ingestion of antacids, IV administration of lactate (“lactated ringers”))
Loss of H+ (vomiting, gastric suction, binge/purge, hypokalemia)
114
Metabolic alkalosis compensatory responses
Respiratory: decreased rate and depth of respiration
Urine: increased urine pH
115
Respiratory acidosis alterations
PH - decreased
CO2 – increased
116
Causes of respiratory acidosis
Depression of resp. center, (drug overdose or head injury)
Lung disease: asthma, emphysema, bronchitis
Airway obstruction (resp. muscle paralysis, chest injuries)
117
Respiratory acidosis compensatory responses
Urine: acid urine
118
Respiratory alkalosis alterations
PH – increased
CO2 – decreased
119
Causes of respiratory alkalosis
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
Respiratory alkalosis compensatory responses
Occurs so quickly, compensatory mechanisms don’t have a chance to kick in
121
pH is high, CO2 is low
Resp. Alkalosis
122
pH is high, HCO3 is high
Met. Alkalosis
123
pH is low, CO2 is high
Resp. Acidosis
124
pH is low, HCO3
Met. Acidosis
