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Human Pathophysiology > Disorders of Fluid Electrolyte, Acid-base balance and blood flow > Flashcards

Disorders of Fluid Electrolyte, Acid-base balance and blood flow Flashcards

1
Q

Water Balance

Water comprises ?? total body weight.

A

50 - 60%

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2
Q

Water Balance

What are the components of bodily fluids?

A
  • intracellular fluids
  • extracellular fluids
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3
Q

Water Balance

Intracellular fluid makes up ?? of total fluids.

A

2/3

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4
Q

Water Balance

Extracellular fluids make up ?? of total fluids.

A

1/3

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5
Q

Water Balance

What 2 things are in extracellular fluid?
What percentages?

A
  • interstitial fluid (80%)
  • plasma (20%)
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6
Q

Water Balance

Water balance is determined by what 2 things?

A
  • fluid intake
  • fluid loss
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7
Q

Water Balance

Examples of fluid intake.

A
  • food and water
  • metabolism
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8
Q

Water Balance

Examples of fluid loss.

A
  • urine
  • sweat
  • lungs
  • feces
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9
Q

Structure and Function

Capillaries are ?? lying between arteries and veins.

A

vessels

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10
Q

Structure and Function

Capillaries consist of only an ??.

A

intimal layer

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11
Q

Structure and Function

Capillary Function

A

regulate fluid, electrolyte and nutrient exchange between blood and extracellular space

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12
Q

Structure and Function

Capillaries can ?? to help repair injured areas.

A

proliferate

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13
Q

Structure and Function

What 3 factors mediate exchange of nutrients across capillaries?

A
  1. hydrostatic pressure
  2. osmotic pressure
  3. integrity of endothelial cells
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14
Q

Structure and Function

What is osmotic pressure determined by?

A

the amount of proteins in fluid

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15
Q

Structure and Function

Lymph is composed of…

A

water, proteins and white blood cells

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16
Q

Edema

A

accumulation of fluid in tissues

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17
Q

Effusion

A

accumulation of fluid in body cavities

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18
Q

What are the 2 types of edema?

A
  • exudate
  • transudate
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19
Q

What type of edema has high protein?

A

exudate

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20
Q

What type of edema has low protein?

A

transudate

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21
Q

What type of edema is associated with an inflammatory response?

A

exudate

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22
Q

What type of edema is associated with pitting?

A

transudate

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23
Q

Transudate edema is caused by:
- decreased ??
- increased ??

A
  • osmotic pressure
  • capillary fluid pressure
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24
Q

Clinical aspects of edema

Why is edema a problem?

A
  • edema can result of underlying disease
  • range from mild to severe
  • can be fatal
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25
Q

Give two examples of fatal edema.

A
  • cerebral edema
  • pulmonary edema
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26
Q

Types of Edema

Name for edema of the peritoneum.

A

ascites

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27
Q

Types of Edema

Name for severe generalized edema.

A

anasarca

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28
Q

Types of Edema

Name for edema of the lungs.

A

pleural

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29
Q

Types of Edema

Name for edema around the heart.

A

pericardial

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30
Q

Pathogenesis of Edema: Increased Hydrostatic Pressure

Hydrostatic edema may be due to ??.

A

impaired venous return

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31
Q

Pathogenesis of Edema: Increased Hydrostatic Pressure

Hydrostatic edema is often observe in ??.

Why?

A
  • lower extremities
  • gravity, vein function, standing/sitting, lymphatic draining
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32
Q

Pathogenesis of Edema: Alts in Osmotic Pressure

Osmotic edema is typically seen with low albumin; which is caused by?

A
  • liver disease
  • poor nutrition
  • kidney disease
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33
Q

Pathogenesis of Edema: Alts in Osmotic Pressure

Osmotic edema is considered which type of edema?

A

transudate (low protein)

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34
Q

Pathogenesis of Edema: Lymphatic Obstruction

Lymphedema is the build of up fluid when…

A

lymphatics are damaged or blocked

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35
Q

Pathogenesis of Edema: Lymphatic Obstruction

Lymphedema typically has ?? protein levels.

A

high

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36
Q

Pathogenesis of Edema: Lymphatic Obstruction

Lymphedema is most commonly caused by…

A

the removal of lymph nodes

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37
Q

Pathogenesis of Edema: Lymphatic Obstruction

T/F: Primary lymphedema is clinically more common than secondary lymphedema.

A

FALSE – primary is typically caused by congenital and genetic abnormalities. secondary occurs when there is damage due to external forces

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38
Q

High protein edema is seen with what 2 events?

A
  • observed with inflammation: leaky capillaries release water and plasma protein into interstitial space
  • lymphedema: obstruction of lymphatics
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39
Q

Water Balance

Euhydration

A

optimal state of water content as regulated by the brain

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40
Q

Water Balance

overhydration

A

too much water

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41
Q

Water Balance

What are the risks of overhydration?

A
  • hyponatremia
  • electrolyte imbalance
  • fluid shifts
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42
Q

Water Balance

Dehydration

A

deficiency of body water

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43
Q

Water Balance

Dehydration is caused by?

A
  • insufficient water intake
  • excess water loss
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44
Q

Dehydration severity is categorized by …..

A

relative amount of lost body weight

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45
Q

Mild dehydration percentage

A

2% of body weight lost

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46
Q

moderate dehydration percentage

A

5% of body weight lost

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47
Q

severe dehydration percentage

A

8% of body weight lost

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48
Q

Symptoms of Dehydration

A
  • headache
  • rapid pulse
  • thirst
  • low urine output
  • loss tissue elasticity (tenting)
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49
Q

Who is at greatest risk of dehydration?

A
  • elderly: less water to begin with because loss of mass
  • babies: cant communicated
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50
Q

Tonicity

A

osmolarity of solution relative to cell

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51
Q

Classifications based on electrolytes in fluid loss

Normotonic

A

sweat

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52
Q

Classifications based on electrolytes in fluid loss

Hypotonic

A

urine

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53
Q

Classifications based on electrolytes in fluid loss

Hypertonic

A

diarrhea

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54
Q

Third Spacing characterisitics

A
  • low urine output
  • low BP
  • increased weight
  • puffiness
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55
Q

Third Spacing definition

A

shift of fluid from intrvascular space into another body space or cavity

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56
Q

What can cause third spacing

A
  • ascites
  • severe burns
  • low oncotic pressure
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57
Q

Electrolytes

A

minerals that dissolve in water and carry an electrical charge

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58
Q

electrolytes

Cations (+)

A
  • sodium
  • potassium
  • calcium
  • magnesium
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59
Q

electrolytes

Anions (-)

A
  • bicarbonate
  • chloride
  • phosphate
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60
Q

Hypokalemia hyperpolarizes the membrane:
- cells fire…
- decreases the…
- causes…

A
  • fire less easily
  • excitability of cells
  • cardiac arrhythmias
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61
Q

Hypokalemia is caused by:
1. ?
2. ?

A
  1. diuretics
  2. eating disorders
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62
Q

What does hyperkalemia do to membrane potential?

A
  • depolarizes (brings closer to 0)
  • increases excitability
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63
Q

T/F: Hyperkalemia is common with normal kidney function.

A

FALSE – hyperkalemia is uncommon with normal kidney function

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64
Q

Electrolytes

Sodium function

A
  • main extracellular cation
  • important for controlling water movement
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65
Q

Hyponatremia pathogenesis

A
  • low serum sodium (extracellular fluid hypotonic relative to intracellular fluid)
  • water enters brain cells
  • cerebral edema
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66
Q

pH

A

the measure of hydrogen ion concentration within a solution

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67
Q

extracellular fluid pH

A

7.4

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68
Q

blood pH

A

7.35 - 7.45

69
Q

Death can occur when pH is…

A
  • less than 6.8
  • greater than 8.0
70
Q

Acidosis pH

A

below 7.35

71
Q

alkalosis pH

A

above 7.45

72
Q

Buffering systems

Intracellular – phosphate buffer

A

[H+] + [HPO4 2+] = [H2PO4-]

73
Q

Buffering systems

Plasma

A

carbonic acid-bicarbonate pair

74
Q

Buffering systems

protein buffering (hemoglobin)

A

proteins have negative charges, so thay can serve as buffers for H+

75
Q

buffering systems

renal buffering

A

secretion of H+ in the urine and reabsorption of HCO3-

76
Q

buffering systems

ion exchange (between ICF and ECF)

A

exchange of K+ for H+ in acidosis and alkalosis

77
Q

4 categories of acid-base imbalances

Respiratory acidosis

A

elevation of pCO2 as a result of ventilation depression

78
Q

4 categories of acid-base imbalances

Respiratory alkalosis

A

depression of pCO2 as a result of alveolar hyperventilation

79
Q

4 categories of acid-base imbalances

metabolic acidosis

A

depression of HCO3- or an increase in noncarbonic acidds

80
Q

4 categories of acid-base imbalances

metabolic alkalosis

A

elevation of HCO30 usually caused by an excessive loss of metabolic acids

81
Q

What is the principal effect of acidosis?

A

depression of the CNS through decreases in synaptic transmission

82
Q

What are the major concerns of deranged CNS function due the acidosis?

A
  • disorientation
  • coma
  • death
83
Q

Respiratory Acidosis

Carbonic acid excess caused by elevated…

A

blood levels of CO2 (hypercapnia)

84
Q

Respiratory acidosis

hypercapnia may be due to:

A
  • depression of respiratory center in brain that controls breathing rate - drugrs or head trauma
  • paralysis of respiratory or chest muscle
  • emphysema
85
Q

respiratory acidosis

?? compensates for repiratory acidosis by eliminating ?? and retaining ??.

A
  • the kidneys
  • hydrogen ions
  • bicarbonate ions
86
Q

Metabolic Acidosis

Metabolic acidosis is caused by:
1. ??
2. ??

A
  1. losss of bicarbonate through diarrhea or renal dysfunction
  2. accumulation of acids (lactic acid or ketones)
87
Q

Metabolic Acidosis

compensation?
1. ??
2. ??

A
  1. increased ventilation
  2. renal excretion of hydrogen ions is possible
88
Q

Alkalosis causes…

A

over excitability of the central and peripheral nervous systems

89
Q

alkalosis can lead to:

A
  • nervousness
  • muscle spasms or tetany
  • convulsions
  • loss of consciousness
  • death
90
Q

respiratory alkalosis is due to…

A

low pCO2 (hypocapnea)

91
Q

primary cause of respiratory alkalosis?

A

hyperventilation

92
Q

what are other causes of respiratory alkalosis?

A
  • oxygen deficienfy at high altitudes
  • pulmonary disease and congestive heart failure
  • acute anxiety
  • fever
  • early salicylate intoxication
  • cirrhosis
  • gram-negative sepsis
93
Q

How can respiratory alkalosis be compensated?

A
  • kidneys conserve hydrogen ions
  • excrete bicarbonate ion
94
Q

Metabolic alkalosis is caused by…

A
  • excess vomiting = loss of stomach acid
  • certain diuretics
  • endocrine disorders-hyperaldosteronism
  • heavy ingestion of antacids
  • severe dehydration
95
Q

T/F: metabolic alkalosis most commonly occurs with renal dysfunction.

A

TRUE - the body cannot rely of kidneys to combat metabolic alkalosis

96
Q

Why is respiratory compensation difficult for metabolic alkalosis?

A

hypoventilation risks hypoxia

97
Q

Which pH correction mechanism works the fastest?

A

buffer function works almost instantaneously

98
Q

Which pH correction mechanism take minutes to hours?

A

respiratory mechanisms

99
Q

Which pH correction mechanism take hours to days?

A

renal mechanisms

100
Q

T/F: Kidneys can conserve and produce bicarb ions.

A

TRUE – most effective regulator of pH; if kidneys fail, pH balance fails

101
Q

active hyperemia

A

dilation of arteriols
- blushing, exercise, inflammation

102
Q

passive hyperemia (congestion)

A

due to impaired venous outflow
- heart failure: pulmonary edema

103
Q

hemorrhage

A

the escape of blood into the tissue

104
Q

hemostasis stops hemorrhage by using…

A

vascular factors, platelets, and coagulation factors

105
Q

When is blood coagulation considered pathological?

A

when it occurs inside of the vessel

106
Q

What are the phases of normal hemostasis?

A
  1. vascular system: vasoconstriction
  2. platelet plug
  3. coagulation-clot
107
Q

First Phase: Vasoconstriction

Injury to endothelial cell promote localized clot formation which start with:

A
  • narrowing the lumen to minimize blood loss
  • bringing hemostatic components of blood closer to vessel wall
108
Q

Second Phase: Platelets

Platelets are cell fragments of?

A

megakaryocytes

109
Q

Second Phase: Platelets

How long do platelets circulate in the blood?

A

approximately 10 days

110
Q

Second Phase: Platelets

Platelet function at rest?

A

minimal interaction with other blood components or the vessel wall
- intact endothelial cells normally inhibt platelet adherence and blood coagulation

111
Q

What activates platelets?

A

contact with basement membrane

112
Q

Activated platelet function?

A
  • plug the defect = round and sticky aggregation (hemostatic plug)
  • release secretions
  • cause more platelets to aggregate
113
Q

What do platelets secrete?

A
  • ADP
  • vasoactive amines
  • thromboxane A2
114
Q

Platelet secretion

ADP function

A
  • shape change
  • granule release
  • thromboxane A2 production
115
Q

Platelet secretions

vasoactive amines example

A

epinephrine

116
Q

platelet secretions

Thromboxane A2 structure and function

A
  • metabolite of arachodonic acid
  • amplifies the initial aggregation of platelets into a large platelet mass
117
Q

Von Willebrand factor can be described as…

A

the framework for platelets

118
Q

Third Phase: Coagulation

Define coagulation.

A

clot formation

119
Q

Third Phase: Coagulation

What are the 2 pathways?

A
  • intrinsic
  • extrinsic
120
Q

Third Phase: Coagulation

What 2 molecules are needed for coagulation?

A
  • calcium
  • vitamin K
121
Q

T/F: Platelets and coagulation factors are the same thing.

A

FALSE – mutually dependent but complimentary

122
Q

Coagulation inhibitors

A

tissue plasminogen activator (TPA) activates plasminogen to plasmin
- plasmin dissolves fibrin

123
Q

hemmorrhage size classification (small to large)

A
  • petechiae
  • purpura
  • ecchymosis
  • hematoma
124
Q

Hemrrhage: bleeding from large vessels

A
  • trauma
  • coagulation deficiency
125
Q

Hemorrhage: bleeding from capillaries

A
  • low platelet count
  • vasculitis
126
Q

Consequences of hemorrhage

massive hemorrhage

A

blood loss, hypovolemic shock, death

127
Q

Consequences of hemorrhage

hematoma

A

compression of tissues

128
Q

Consequences of hemorrhage

intracerebral hemorrhage

A

stroke, death

129
Q

Consequences of hemorrhage

chronic hemorrhage

A

slow blood loss, iron deficiency anemia

130
Q

What are the 4 types of abnormal hemostasis?

A
  • abnormalities of small blood vessels
  • abnormality of platelet formation
  • deficiency of one or more plasma coagulation factors
  • liberation of thromboplastic material into circulation
131
Q

Reduced Platelet Numebrs or Function

thrombocytopenia is caused by…

A
  • genetic
  • acquired (radiation)
  • disease (leukemia)
  • autoimmune
  • hypersplenism
132
Q

deficiencies of blood coagulation

A

usually hereditary and relatively rare
- hemophilia A
- hemophilia B
- von Willebrand’s disease

133
Q

Hemophilia:

A
  • x-linked hereditary disease affecting males
  • most common and best known
134
Q

hemophilia A

A
  • classic hemophilia = factor VIII (antihemophilic factor)
135
Q

hemophilia B

A

christmas disease = factor IX

136
Q

charateristics of hemophilia A

A
  • spontaneous or traumatic subcutaneous bleeding
  • blood in the urine
  • bleeding in the moth, lips, tongue
  • bleeding to the joints, CNS, GI
137
Q

Hemophilia A treatment

A
  • transfusion
  • treated with missing factor
138
Q

partial thrombloplastion time (PTT)

A
  • measures time it takes for blood plasma to clot after adding artificial surface
  • intrinsic and overall eficiency
139
Q

prothrombin time (PT)

A
  • time to clot after addition of tissue factor
  • extrinsic pathway
140
Q

thrombin time = fibrinogen assay

A

measures the level of fibrinogen

141
Q

Anti-coagulants

warfarin (caumadin)

A
  • reduced amount of vitamin K availability
  • decrease risk of clot formation
142
Q

anti-coagulants

heparin

A

inactivates thrombin

143
Q

anti-platelets

aspirin

A

inhibits thromboxane A2 formation

144
Q

Anti-platelets

plavix

A

inhibits ADP

145
Q

thrombosis

A
  • inappropiate acitvation of the hemostatic procss in an uninjured or slightly injured vessel
  • never normal, always pathological
146
Q

virchow’s triangle in regards thrombosis formation

A
  • endothelial injury
  • abnormal local blood flow
  • hypercoaguability
147
Q

where do thrombi form?

A
  • usually in large veins or arteries damaged by athersclerosis
  • bifurcations
148
Q

steps in formation of a thrombus?

A
  1. platelet aggregation
  2. blood coagulation-fibrin
  3. further platelet agglutination
  4. WBC adhere to platelets
  5. clot grows larger
149
Q

Thrombus outcomes

A
  • grows by adding clot
  • break loose and become embolus
  • dissolve
  • re-channel
150
Q

ischemia

A
  • lack of O2 to tissue
  • due to obstruction
151
Q

ischemia can be due to things other than vascular occlusion:

A
  • torsion
  • drowning
  • CO
152
Q

define infarct

A

ischemic necrosis

153
Q

white infarction

A
  • bloodless
  • arterial obstruction in dense, solid tissue (liver, heart)
154
Q

red infarction

A
  • bloody
  • occurs in loose spongy tissue
  • dual blood supply
155
Q

Factors that influence the development of an infarct

Single or dual vascular supply

A
  • tissues with dual supply will take longer to develop in infarct
  • lungs and liver
156
Q

Factors that influence the development of an infarct

rate at which obstruction develops

A
  • atherosclerosis takes a lifetime to develop into serious blockage
  • an embolus can form instantaneously
157
Q

Factors that influence the development of an infarct

sensitivity of downstream tissue to ocygen deprivation

A
  • neurons die within minutes of hypoxia
  • fibroblast can last hours without oxygen
158
Q

Factors that influence the development of an infarct

oxygen content of blood

A

higher oxygen content will take longer for infarct to develop

159
Q

Shock

A

inability of the cardiovascular system to meet the O2 demands of the body

160
Q

Shock can signify the final stage of:

A
  • severe hemorrhage
  • bacterial sepsis
  • burns
  • MI
  • severe soft tissue damage
161
Q

What it the typical end result of shock?

A

multi-organ failure and death

162
Q

Types of shock

A
  • cardiogenic
  • hypovolemic
  • anaphylactic
  • obstructive
  • septic
163
Q

obstructive shock

A

fluid in the pericardium

164
Q

cardiogenic shock

A
  • pump failure
  • cannot maintain perfusion pressure
165
Q

Disseminated intravascular coagulation (DIC)

A
  • widespread clotting inside vessels
  • can obstruct small blood vessels
  • causes hemorrhaging bc of consumption of clotting factors and platelets
  • always secondary to some other pathology
166
Q

septic shock is associated with…

A

systemic bacterial infection = sepsis
- LPS, endotoxins

167
Q

Stages of shock

A
  • non-progressive
  • progressive
  • irreversible
168
Q

characcteristics of irreversible shock

A
  • circulatory collapse
  • marked hypoperfusion of vital organs
  • loss of vital functions
  • multiorgan failure
  • death
169
Q

complications of shock

A
  • acute respiratory distress syndrome
  • acute renal dailure
  • GI complications
  • disseminated intravascular caogualation
  • multiple organ dysfunction syndrome

Human Pathophysiology (4 decks)

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