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Pathophysiology > Chapter 27 - Alteration In Pulmonary Function > Flashcards

Chapter 27 - Alteration In Pulmonary Function Flashcards

1
Q

Ventilation

A

Movement of air in and out of lungs

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2
Q

Oxygenation

A

Loading oxygen molecules onto. Hemoglobin

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3
Q

Respiration

A

O2 and co2 exchange of alveoli and systemic capillaries

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4
Q

Perfusion

A

Delivery of blood to a capillary bed in tissue

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5
Q

Dyspnea

A

Breathlessness
-subjective
-work of breathing is greater than actual result

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6
Q

Signs of dyspnea

A

-flaring of nostrils
-use of accessory muscles
-head bobbing in children

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7
Q

Paroxysmal nocturnal dyspnea

A

Pulmonary condition that wakes you up gasping for breath in the middle of the night

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8
Q

Sputum

A

Color provides information about progression of disease
-microscopic appearance allows microorganism identity

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9
Q

Hemoptysis

A

Coughing up blood (usually indicates infection of inflammation of bronchiole)
-if severe can indicate cancer

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10
Q

Normal breathing

A

Rhythmic and effortless
-includes short expiratory pause with each breath

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11
Q

Sighs

A

1.5 to 2 times normal tidal volume

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12
Q

Abnormal breathing patterns

A

Patterns of breathing automatically adjust to minimize WOB

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13
Q

Purpose of sigh

A

-twice tidal volume, 10 times per hour
-help maintain normal breathing
-equals out oxygen consumption and CO2 expulsion

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14
Q

Hyperpnea: kussmaul respiration

A

Occurs with strenuous exercise
-inc ventilation rate and tidal volume
-no pause

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15
Q

Cheyne stokes respiration

A

Alternating deep and shallow breathing
-periods of apnea

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16
Q

Periods of apnea

A

15 to 60 seconds
-followed by inc volume ventilations
-eventually returned to normal, triggering another period of apnea

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17
Q

Cause for cheyne stokes

A

Reduced blood flow to brain
-reduced brain impulses to respiratory center

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18
Q

Both of what can be determined by blood gases

A

Hypoventilation and hyperventilation

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19
Q

Hypoventilation

A

Inadequate ventilation

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20
Q

Hypoventilation issue

A

Co2 removal doesn’t keep up with co2 production

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21
Q

Hypoventilation result

A

Hypercapnia
-inc co2 in blood stream

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22
Q

Hyperventilation

A

Alveolar ventilation exceeding needs

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23
Q

Hyperventilation issue

A

Removal of more co2 than is produced

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24
Q

Hyperventilation result

A

Hypocapnia
-reduced co2 in blood stream

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25
Q

Cyanosis

A

-bluish discolouration of skin

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26
Q

Cause of cyanosis

A

develops when 5 grams of hemoglobin is desaturated

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27
Q

Cyanosis is not evident until is is severe =

A

Insensitive indicator of respiratory failure

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28
Q

Peripheral cyanosis

A

Poor circulation in fingers and toes due to peripheral vasoconstriction
-best seen in nail beds

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29
Q

Central cyanosis

A

Decreased arterial oxidation (low PaO2) from pulmonary disease
-best detected in buccal mucosa membranes and lips

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30
Q

Clubbing

A

Bulbous formations at end of fingertips and toes

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31
Q

Clubbing is from

A

Diseases that disrupt pulmonary circulation causing hypoxemia
-rarely reversible

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32
Q

Pain from pulmonary disorders
-where is it located
-what sound does it make

A

Almost always localized in chest wall
-can be pinpointed by unique sound called pleural friction rub

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33
Q

Pleural friction rub

A

Pleural walls rub together due to reduced fluid in pleural cavity

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34
Q

Pain can be reproduced by

A

Pressing on sternum or ribs

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35
Q

Hypercapnia

A

Increased co2 in blood
-caused by Hypoventilation of alveoli
-increased PaCO2

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36
Q

Hypoventilation causes

A

-decreased drive to breath
-depression of respiratory center
-disease to medulla oblong at a

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37
Q

Effects of Hypoventilation

A

-electrolyte imbalances
-dysrhythmia
-in severe cases comatose

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38
Q

Hypoventilation is often overlooked, why?

A

It can appear normal
-it is important then to obtain blood gases to confirm

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39
Q

Hypoxemia

A

Decreased PaO2 in arterial blood

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40
Q

What are the two possible causes of hypoxemia

A
  1. Related to issues with delivery of O2 to alveoli and delivery to lung
  2. Thickening of alveolar membrane or destruction of alveoli
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41
Q

Diffusion of O2 from alveoli to blood is dependant upon two factors

A
  1. Amount of air entering alveoli
  2. Amount of blood perfusion capillaries around alveoli
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42
Q

What is the most common cause of hypoxemia

A

Abnormal ventilation/perfusion ratio
(V/Q)

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43
Q

V=

A

Ventilation

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44
Q

Q=

A

Amount of blood perfusion capillaries around alveoli

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45
Q

Shunt

A

Normal perfusion but Inadequate ventilation
-blocked, collapsed alveolus

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46
Q

Alveolar dead space

A

Normal ventilation but inadequate perfusion

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47
Q

Shunt causes

A

Very low V/A
-hypoxemia

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48
Q

Alveolar dead space causes

A

High V/Q
-hypoxemia

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49
Q

Acute respiratory failure: levels of PaO2

A

Is less than 60 mmHg
(TX = supplemental oxygen)

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50
Q

Acute respiratory failure: levels of PaCO2

A

Is greater than 50
(TX = ventilatory support)

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51
Q

Acute respiratory failure: pH levels

A

Less than or equal to 7.25

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52
Q

Normal pH

A

7.40

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53
Q

Acute respiratory failure is a potential complication of

A

Any major surgical procedure

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54
Q

How to prevent Acute respiratory failure:

A

Frequent turning and position changes
-deep breathing exercises
-early ambulating

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55
Q

CWR or chest wall restrictions (cause)

A

Deformity
-obesity, neuromuscular disease

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56
Q

CWR or chest wall restrictions (result)

A

Increased work of breathing
-usually decrease in tidal volume

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57
Q

CWR or chest wall restrictions (surgical/injury complications)

A

Can cause such pain that causes Hypoventilation

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58
Q

CWR:

A

Decreased tidal volume, increased breathing rate, can lead to respiratory failure

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59
Q

Flail chest

A

Fracture of consecutive ribs with or without sternum damage

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60
Q

Result of flail chest

A

Chest wall instability = paradoxical movement of chest when breathing

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61
Q

Paradoxical breathing (inspiration)

A

Unstable portion of chest wall moves inward
-normal movement would be outward

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62
Q

Paradoxical breathing expiration

A

Portion moves outward
-normal movement would be inward

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63
Q

PaO2 rule of thumb for normal ventilation

A

80-100 mmHg

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64
Q

Severe hypoxemia PaO2 levels

A

<40 mmHG

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65
Q

Pneumothorax (cause and result)

A

Air or gas in pleural space
-due to rupture to visceral pleural
-lungs tend to collapse

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66
Q

Pleural effusion

A

Fluid in pleural space
-can be blood or lymph

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67
Q

How do you diagnosis a pleural effusion

A

-chest xray
-thoracentesis (needle aspiration)

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68
Q

Empyema

A

Infected pleural effusion by microorganism

69
Q

What is the indication of empyema

A

Pus in pleural space

70
Q

Cause of empyema

A

Pulmonary lymphatic tissue becomes blocked
-contaminated lymphatic fluid moves into pleural space

71
Q

empyema is the result of

A

Surgery, or bronchial obstruction

72
Q

TX for empyema

A

Antibiotics and drainage of pleural space with chest tube

73
Q

Restrictive lung diseases have difficulty with

A

Inspiration
-expanding lungs

74
Q

Obstructive lung diseases have difficulty with

A

Expiration

75
Q

Restrictive lung diseases

A

Decreased lung compliance
-increased work of breathing at tidal volume

76
Q

Aspiration

A

Passage of fluids or solids into lungs

77
Q

Aspiration caused by

A

Abnormal swallowing mechanism
-cough reflex impaired
-lead to pneumonia

CNS or PNS abnormalities

78
Q

Aspiration TX

A

Bronchoscopy
-failure to remove results in inflammation

79
Q

Atelectasis

A

Collapse of lung

80
Q

Atelectasis: compression

A

Caused by external pressure e
-tumour of fluid

81
Q

Atelectasis: surfactant impairment

A

Decreased production of surfactant

82
Q

Atelectasis tends to occur

A

After surgery when using general anaesthetic

83
Q

Atelectasis: TX

A

Deep breathing exercises promotes ciliary removal of secretion

84
Q

Bronchiectasis

A

Perisistent abnormal dilation of bronchi

85
Q

Obstruction cause in Bronchiectasis

A
  1. Inflammation due to mucus plugs
  2. Chronic inflammation = destruction of elastic/muscular bronchi wall = permanent dilation
86
Q

Symptoms for Bronchiectasis

A

Chronic productive cough
-large amount of foul smelling sputum

87
Q

Bronchiolitis

A

Inflammatory obstruction of small airways

88
Q

Bronchiolitis obliterans

A

Fibrosis of airways = scaring

89
Q

BOOP

A

Alveoli becomes filled with connective tissue

90
Q

Manifestations of Bronchiolitis

A

Rapid ventilatory rate and dry non productive cough

91
Q

Pulmonary fibrosis

A

Excessive amount of fibrous and connective tissue at alveoli

92
Q

Pulmonary fibrosis cause

A

Scar tissue left from previous disease
-example tuberculosis

93
Q

Result of Pulmonary fibrosis

A

Decreased lung compliance and external respiration (O2/CO2 exchange)
-due to multiple injuries at different lung sites associated with abnormal healing

94
Q

Symptoms of Pulmonary fibrosis

A

Dyspnea on exertion

95
Q

Pulmonary Edema

A

Excessive water on lungs
-normal lung is dry

96
Q

Cause of pulmonary edema

A

Left side heart disease

-reduced CO, blood backed up from heart into lungs, inc bp in pulmonary capillaries, fluid into interstitial space, fluid flow exceeds lymph system = pulmonary edema

97
Q

COVID 19

A

Manifested as viral pneumonia induced acute respiratory distress syndrome

98
Q

Post mortem studies of COVID 19

A

Mortality patients had undetectable viral loads
-cytokines effects of virus not main cause of death
-death caused by hosts runaway immune response

99
Q

Management of COVID 19

A

Incubation

100
Q

Restrictive lung disease have difficulty with

A

Inspiration

101
Q

Obstructive lung diseases have difficulty with

A

Expiration

102
Q

S/s of obstructive lung diseases

A

Dyspnea and wheezing

103
Q

Asthma

A

Chronic inflammatory disorder of bronchial mucosa

104
Q

Asthma inflammation =

A

Restriction of airways
-hyper immune response to irritants

105
Q

Early asthmatic attack: classic immune response

A

Dendritic cells, helper T cells, B cell

106
Q

Result of early asthmatic attack

A

Inflammation, inc capillary permeability, inc fluid

107
Q

Late asthmatic attack

A

Begins 4-8 hours after early attack
-latent release of inflammatory mediators from original site

108
Q

Result of late asthmatic attack

A

Inc damage of epithelial cells = scaring
-inc mucus forming plugs and airway resistance

109
Q

Manifestation of asthma

A

Individuals normal between attacks
-pulmonary function tests are normal

110
Q

If bronchospams are not reversed by usual treatment they are considered

A

Status asthmaticus

111
Q

If PaCO2 (asthma) is greater than ___ it means

A

70 mm HG
-sign of impending death

112
Q

TX asthma

A

-short acting inhalers, or inhaled corticosteroids

113
Q

asthma (1)

A

Inhaled antigen passes epithelial layer

114
Q

Asthma (2)

A

Antigen binds to mast cells
-releasing mediators

115
Q

Asthma (3)

A

Mediators
-mucus production in airway
-bronchi spams
-edema from inc capillary permeability

116
Q

Asthma (4)

A

Dendritic cels present antigen to helper T cells
-activate B cells, and release antibodies

117
Q

Asthma (5)

A

Helper T cells also activate eosinophil
-neutrophils activated
-inflammation from both results in airway obstruction

118
Q

COPD

A

Composed of chronic bronchitis and emphysema
-most common

119
Q

Characteristics of COPD

A

-persistent airflow limitation
-chronic inflammatory response to noxious partials or gas
-progressive

120
Q

COPD: chronic bronchitis defined

A

As hypersecretion of mucus
-chronic cough for at least 3 months of the year for 2 consecutive years

121
Q

Cause of COPD: chronic bronchitis

A

Inspired irritant-> inflammation and thickening of mucous membrane
-reduced radius of airways causing obstruction

122
Q

Initially COPD: chronic bronchitis affects

A

Large airways and eventually all airways

123
Q

COPD: chronic bronchitis airways collapse

A

Early in exhalation
-air trapped in distal portions of lungs
-hyperinflation = Hypoventilation

124
Q

COPD: emphysema

A

Permanent enlargement of gas exchange airways
-destruction of alveolar walls
-obstruction due to destroyed walls of alveoli

125
Q

COPD: emphysema does not

A

Mucus production of inflammation

126
Q

COPD: emphysema destruction =

A

Large alveolar spaces = greatly inc diffusion distance between alveoli and capillary

127
Q

Result of COPD: emphysema

A

-reduced O2 and CO2 diffusion
-expiration becomes difficulty because of loss of recoil of normal alveoli

128
Q

Symptom difference between chronic bronchitis and emphysema

A

B- frequent couch with mucus

E- shortness of breath

129
Q

Acute bronchitis

A

Acute infection and inflammation of airways
-self limiting
-occurs due to viral infection

130
Q

Symptoms of acute bronchitis

A

Similar to pneumonia
-non productive cough, aggravated by cold, dry, dusty air

131
Q

TX for acute bronchitis

A

Rest, aspirin, cough, suppressant, antibiotics

132
Q

Pneumonia

A

Infection of lower respiratory tract caused by microorganisms

133
Q

HAP pneumonia

A

Hospital acquired pneumonia

134
Q

CAP pneumonia

A

Community acquired pneumonia

135
Q

HAP or CAP is the second most common health care associated infection

A

HAP

136
Q

Pneumonia most common pathogen

A

S.pneumoniae

137
Q

Pathophysiology of HAP pneumonia

A

In hospitals suctioning tubes can become colonized with bacterial biofilms and suction results in seeding lungs with bacteria

138
Q

Guardian cells of lower respiratory tract

A

Cellular alveolar macrophages

139
Q

Macrophages present antigens to

A

Adaptive immune system = activation T and B cells

140
Q

resulting immune response can

A

Fill alveoli with debris

141
Q

Further damage is caused when

A

Microorganisms release toxins

142
Q

Tuberculosis

A

Infection caused by M.tuberculosis
-leading cause of death although curable

143
Q

How is TB spread

A

person to person via airborn droplets

144
Q

TB pathophysiology

A

-pathogen reaches lung and is engulfed by macrophages
-survives and multiplies
-reproduction causes chemotactic response and more macrophages respond causing tubercul formation

145
Q

Macrophage start to die and release (TB)

A

Pathogen, this form a centers in tubercle (dormant stage)

146
Q

Tubercle center enlargens… (TB)

A

Enlargement fills with air, aerobic pathogen starts to multiply outside macrophage

147
Q

Liquifidcation continues (TB)

A

Tubercle ruptures and pathogen sdisseminate throughout lung

148
Q

Pulmonary vascular diseases

A

Pulmonary blood flow disrupted causing occlusions
-destroys vascular bed

149
Q

When pulmonary blood flow is disrupted it causes

A

Dramatic alterations in perfusion and ventilation ratios

150
Q

Pulmonary embolism

A

Occlusion of portion of pulmonary vascular bed by embolus

151
Q

Effect of pulmonary embolism depends on

A

-extent of pulmonary blood flow
-size
-nature of embolus
-secondary effects

152
Q

Pulmonary artery hypertension

A

Mean pulmonary artery pressure greater than 25 mmHG at rest

153
Q

Endothelial dysfunction (pulmonary artery hypertension)

A

Overproduction of vasoconstrictiors

154
Q

pulmonary artery hypertension: increased growth factors

A

=fibrosis=thickening of vessel walls=narrowing of vessels and gas exchange is reduced

155
Q

pulmonary artery hypertension: inc pulmonary artery pressure

A

Increased pressure in right ventricle = right ventricle hypertrophy = failure

156
Q

Cor pulmonale

A

Right ventricle enlargement due to hypertrophy or dilation or birth
-result of pulmonary artery hypertension

157
Q

In cor pulmonale there is an increased

A

Work of right ventricle = increased hypertrophy of normally thin walled heart muscle

158
Q

pulmonary artery hypertension: pressure overload

A

=dilation/hypertrophy= failure of right ventricle

159
Q

Laryngeal cancer: Primary risk factor

A

Smoking
-increased when smoking combined with alcohol consumption

160
Q

What pathogen is linked to laryngeal cancer

A

HPV or human papilloma virus

161
Q

Pathphysioloy of laryngeal cancer

A

Carcinoma of vocal cords (most common site)
-metastsis occurs in lymph nodes, but distant is rare

162
Q

Manifestation of laryngeal cancer

A

Hoarseness, dyspnea, cough
-cough following swallowing

163
Q

Diagnosis and TX for laryngeal cancer

A

Biopsy, radiation, chemotherapy

164
Q

Lung cancer

A

Tumours on respiratory tract in epithelium
-leading cause of death in Canadians

165
Q

Msot common cause of lung cancer

A

Smoking, gas exposure, second hand smoke exposure

166
Q

Pathophysiology of lung cancer

A

Bronchial mucosa suffers hits from tobacco smoke = epithelial damage
-metastasis to brain, bone marrow and liver

167
Q

Tobacco smoke

A

Contains 30 carcinogens
-90% of lung cancers

168
Q

Tumour in lung cancer is result of

A

Growth factors and free radicals

Pathophysiology (20 decks)

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