L5+6 Respiratory Flashcards
(185 cards)
1
Q
What is the number one cause of COPD?
A
Smoking (80-85% of cases)
2
Q
What two main conditions are included under COPD?
A
Emphysema and chronic bronchitis
3
Q
What characterises COPD?
A
Chronic and recurrent obstruction of pulmonary airways, progressive obstruction accompanied by inflammatory responses to noxious particles or gases
4
Q
How is chronic bronchitis diagnosed?
A
History of chronic productive cough for ≥3 consecutive months in ≥2 or more consecutive years
5
Q
What is emphysema associated with?
A
Destruction of tissue & alveoli, causing enlarged airspaces which leads to gas trapping
6
Q
What is chronic bronchitis associated with?
A
Increased mucus production, small airway obstruction, and a chronic productive cough
7
Q
What causes the barrel chest in some COPD patients?
A
Hyperinflation from trapped air due to alveoli collapse during exhalation
8
Q
Why do some COPD patients breathe through pursed lips?
A
To create positive end-expiratory pressure (PEEP) which helps keep airways open and prevents alveoli collapse
9
Q
What are patients with emphysema often referred to as?
A
“Pink puffers”
10
Q
What are the two recognised causes of emphysema?
A
Smoking and inherited deficiency of α1-antitrypsin (AAT)
11
Q
What is the role of α1-antitrypsin (AAT) in the lungs?
A
It’s a protease-inhibitor which stops the release of elastase, therefore protecting the lung
12
Q
How does smoking damage the lungs in emphysema?
A
Smoking causes neutrophils to release protease enzymes (elastase) that damage healthy lung tissue, particularly alveoli with their thin epithelium
13
Q
What is the pathophysiological foundation for chronic bronchitis?
A
Excess mucus production from goblet cells in response to inflammatory signals and neutrophils releasing elastase
14
Q
Why is there difficulty clearing secretions in chronic bronchitis?
A
Due to poor ciliary function, ineffective cough secondary to respiratory muscle weakness, and reduced peak expiratory flow
15
Q
Define asthma.
A
A chronic inflammatory disorder with acute episodes of obstruction due to bronchospasm, mucosal oedema and excess mucus production, where the airway reacts to various stimuli leading to recurrent episodes of wheezing, breathlessness, coughing, and chest tightness
16
Q
What are the three key elements of asthma?
A
Bronchospasm, increased mucosal oedema, and increased mucus production/plugging
17
Q
What are the two main categories of asthma?
A
Allergic asthma and non-allergic asthma
18
Q
When does allergic asthma typically begin?
A
In childhood
19
Q
What characterises allergic asthma?
A
A typical type 1 hypersensitivity IgE response to an external allergen (typically on inhalation)
20
Q
When does non-allergic asthma typically occur?
A
In adulthood
21
Q
What characterises non-allergic asthma?
A
A reaction to internal factors not associated with the typical type 1 hypersensitivity IgE response; pathophysiology unclear but subsequent inflammatory response is similar to allergic asthma but more severe
22
Q
How does the nervous system affect airway diameter?
A
Bronchial smooth muscle tone is controlled by the autonomic nervous system. The parasympathetic nervous system stimulates bronchial constriction and mucus secretion, while the sympathetic nervous system causes bronchodilation
23
Q
What occurs in the early phase response of asthma (0-2 hours)?
A
Allergen binds to IgE-mediated mast cells and basophils, causing degranulation and release of histamine, cytokines and leukotrienes, resulting in bronchospasm, mucosal oedema, and mucus plugging
24
Q
What occurs in the late phase response of asthma (4-12 hours)?
A
Activated mast cells & helper T cells release cytokines causing eosinophils to migrate and release leukotrienes, resulting in prolonged inflammation, bronchiole constriction, airway oedema, and epithelial damage
25
What does histamine primarily cause in asthma?
Vasodilation and bronchospasm
26
What do leukotrienes primarily cause in asthma?
Mucus secretion
27
What do cytokines primarily cause in asthma?
Airway constriction & mucus secretion
28
What clinical manifestations occur in less severe asthma?
Difficulty exhaling air leading to trapped air and hyperinflation, prolonged wheeze on exhalation, increased breathing effort, and shortness of breath (dyspnoea)
29
What clinical manifestations occur in life-threatening asthma?
Severe bronchiole obstruction with decreased ventilation to alveoli, increased heart and respiratory rates, increased use of accessory neck muscles, tachypnoea progressing to slow shallow respirations, tachycardia progressing to bradycardia, hypotension, severely decreased O₂ sats, decreased level of consciousness, silent chest, inability to talk
30
List five risk factors for life-threatening asthma.
Previous severe/life-threatening attack, hospital admission in last year, three or more classes of asthma medication, heavy use of β2-agonist, repeated emergency department visits, nocturnal symptoms, previous intubation/ICU admission, cor pulmonale, recent steroid withdrawal, poor perception of airflow limitation, poor adherence to treatment plan (any five)
31
What is a ventilation-perfusion (V/Q) mismatch?
Areas of lung are perfused but not ventilated, or ventilated but not perfused
32
How does asthma cause a V/Q mismatch?
Bronchospasm, mucosal oedema and excess mucus production result in less effective ventilation while lungs remain perfused; in severe cases, hyperinflation can also reduce perfusion
33
What happens to O₂ and CO₂ levels in asthma with V/Q mismatch?
O₂ levels decrease (hypoxia) and CO₂ levels increase (hypercapnia) as patients cannot breathe out trapped gas
34
How does hyperinflation in severe asthma decrease perfusion?
Hyperinflation puts pressure on the vena cava, compressing these thin-walled veins, decreasing blood returning to the heart (venous return), reducing preload and stroke volume, which decreases cardiac output and affects perfusion to the lungs
35
What is cor pulmonale?
Right-sided heart failure due to chronic pulmonary hypertension from lung diseases like COPD or emphysema
36
How can emphysema exacerbate right-sided heart failure?
Decreased surface area for gas exchange causes reduction in capillaries, slowing blood flow through lungs and increasing pulmonary blood flow resistance, making it harder for the right ventricle to pump blood through pulmonary arteries, amplifying symptoms of right-sided heart failure
37
Why must supplemental oxygen be used cautiously in COPD patients?
If oxygen saturation increases above 92%, it can lead to dangerously high carbon dioxide levels and worsening respiratory acidosis due to failure of the hypoxic drive, Haldane effect, reversal of hypoxic vasoconstriction, and nitrogen displacement leading to atelectasis
38
What is COPD?
Chronic Obstructive Pulmonary Disease/Disorder
39
What is emphysema?
Destruction of alveoli walls creating enlarged airspaces and gas trapping
40
What is chronic bronchitis?
Condition with excessive mucus production and chronic productive cough for ≥3 months per year for ≥2 consecutive years
41
What is α1-antitrypsin (AAT)?
Protease-inhibitor that protects lungs by stopping elastase release
42
What are protease and elastase?
Enzymes that break down proteins
43
What is alveolar destruction?
Breakdown of air sacs in lungs
44
What is hyperinflation?
Abnormal increase in lung volume
45
What is barrel chest?
Enlarged chest appearance from chronic hyperinflation
46
What is self-PEEP?
Positive End-Expiratory Pressure created by pursed-lip breathing
47
What is a productive cough?
Cough that produces mucus/sputum
48
What are goblet cells?
Cells that produce mucus in airways
49
What is peak expiratory flow?
Maximum flow rate during forced exhalation
50
What is asthma?
Chronic inflammatory disorder with acute episodes of airway obstruction
51
What is bronchospasm?
Constriction of bronchial smooth muscle
52
What is mucosal oedema?
Fluid accumulation in airway lining
53
What is mucus plugging?
Blockage of airways by excessive mucus
54
What is allergic asthma?
Type I hypersensitivity response to external allergens
55
What is non-allergic asthma?
Response to internal factors not associated with Type I hypersensitivity
56
What is type I hypersensitivity?
Immediate allergic reaction involving IgE antibodies
57
What are IgE antibodies?
Immunoglobulin E, antibodies involved in allergic reactions
58
What are T₂H cells?
Helper T cells that direct immune response
59
What are mast cells?
Immune cells containing granules with mediators like histamine
60
What is degranulation?
Release of contents from mast cells/basophils
61
What does histamine cause?
Vasodilation, bronchospasm
62
What do leukotrienes cause?
Mucus secretion, promote inflammation
63
What do cytokines cause?
Airway constriction & mucus secretion
64
What is the early phase response?
Initial reaction occurring 0-2 hours after allergen exposure
65
What is the late phase response?
Secondary reaction occurring 4-12 hours after initial phase
66
What is airway remodelling?
Structural changes in airways from chronic inflammation
67
What is the V/Q ratio?
Ventilation (V) ÷ Perfusion (Q)
68
What is the normal V/Q ratio?
0.8-1
69
What is a high V/Q ratio?
Areas with good ventilation but poor perfusion
70
What is a low V/Q ratio?
Areas with poor ventilation but good perfusion
71
What is the emphysema pathophysiology cascade?
Smoking/Irritants → Neutrophil activation → Protease release → AAT inadequacy → Alveolar destruction → Loss of elasticity → Air trapping → Hyperinflation → Barrel chest
72
What is the chronic bronchitis pathophysiology cascade?
Smoking/Irritants → Inflammatory response → Goblet cell hyperplasia → Excess mucus production → Ciliary dysfunction → Mucus accumulation → Airway obstruction → Infection risk
73
What is the asthma early phase cascade?
Allergen exposure → IgE-mediated mast cell activation → Degranulation → Release of histamine, leukotrienes, cytokines → Bronchospasm, mucosal oedema, mucus production → Airway narrowing
74
What is the asthma late phase cascade?
Cytokine release → Eosinophil recruitment → Leukotrienes release → Prolonged inflammation → Epithelial damage → Airway remodelling
75
What is the cor pulmonale development?
Chronic hypoxia → Pulmonary vasoconstriction → Increased pulmonary vascular resistance → Right ventricular pressure overload → Right ventricular hypertrophy → Diastolic dysfunction → Right-sided heart failure
76
77
What are the two layers of the pleura?
Visceral pleura (covers lung) and parietal pleura (lines thoracic cavity)
78
How does the structure of airways change as they branch deeper into the lungs?
Cartilage decreases while smooth muscle and elastic fibres increase
79
What are the two sources of blood supply to the lungs?
Pulmonary circulation (for gas exchange) and bronchial circulation (for nutrition to airways)
80
What effect does parasympathetic stimulation have on the airways?
Causes bronchoconstriction and increases glandular secretion
81
What effect does sympathetic stimulation have on the airways?
Causes bronchodilation, blood vessel constriction, and inhibits glandular secretion
82
What is the primary stimulus for breathing in normal conditions?
Rising CO₂ levels detected by central chemoreceptors
83
Why is intrapleural pressure normally negative?
To help keep elastic alveoli open and prevent lung collapse
84
What happens to intrapulmonary pressure during inspiration?
It becomes negative relative to atmospheric pressure, allowing air to flow in
85
What is transpulmonary pressure?
The difference between intrapulmonary and intrapleural pressures
86
What is the normal V/Q ratio?
Approximately 0.8
87
How does V/Q ratio vary from apex to base of the lung?
Higher at apex (more ventilation than perfusion), lower at base (more perfusion than ventilation)
88
What are the three vital components for oxygenating blood?
Ventilation, oxygenation, and perfusion
89
What happens to the diaphragm during inspiration?
It contracts and flattens, increasing thoracic volume
90
What is alveolar ventilation?
Exchange of gases within the gas exchange portion of the lung
91
What structures form the mediastinum?
Heart, major blood vessels, trachea, esophagus, and other central thoracic structures
92
What are the two main types of respiratory failure?
Hypoxemic respiratory failure and hypercapnic/hypoxemic respiratory failure
93
What causes hypoxemic respiratory failure?
Failure of gas exchange leading to low arterial O₂ levels
94
What are the two major pathophysiological factors in hypoxemic respiratory failure?
Ventilation-perfusion mismatch and impaired diffusion
95
What causes hypercapnic respiratory failure?
Insufficient ventilation to clear CO₂ and maintain normal O₂ levels (hypoventilation)
96
Why is high-flow oxygen potentially dangerous for COPD patients with respiratory failure?
It may eliminate their hypoxic respiratory drive, leading to reduced breathing effort
97
What is bronchiectasis?
An uncommon form of COPD with permanently dilated bronchi and bronchioles
98
What are common causes of bronchiectasis?
Previous pneumonia, viral infections, bacterial infections, noxious chemical inhalation, or damage from conditions like cystic fibrosis
99
How does bronchiectasis affect gas exchange?
Reduced airway diameter, mucus accumulation, fibrosis, and V/Q mismatch impair gas exchange
100
What happens to blood pH when CO₂ levels increase?
pH decreases (becomes more acidic) as CO₂ combines with water to form carbonic acid
101
What defines respiratory acidosis?
pH < 7.35, PaCO₂ > 45 mmHg due to impaired alveolar ventilation
102
What physiological effects occur in respiratory acidosis?
Sympathetic response, cerebral vessel dilation, tachycardia, peripheral vasoconstriction, sweating
103
What defines respiratory alkalosis?
pH > 7.45, PaCO₂ < 35 mmHg due to increased pulmonary ventilation
104
What physiological effects occur in respiratory alkalosis?
Cerebral vessel constriction causing dizziness, light-headedness, tingling and numbness of extremities
105
What is the relationship between hyperventilation and pH?
Hyperventilation reduces CO₂, leading to increased pH (alkalosis)
106
What is the relationship between hypoventilation and pH?
Hypoventilation increases CO₂, leading to decreased pH (acidosis)
107
What is a pulmonary embolism?
A blood-borne substance lodging in a pulmonary artery branch, obstructing blood flow
108
What is the most common cause of pulmonary embolism?
Thrombus (blood clot), typically from deep vein thrombosis
109
What other substances can cause pulmonary embolism?
Air, fat (from fractures), amniotic fluid, or externally introduced sources
110
What happens to the right ventricle with a large pulmonary embolism?
Increased afterload leading to potential right heart failure (Cor pulmonale)
111
Which type of shock can result from a large pulmonary embolism?
Obstructive shock
112
What is the difference between pulmonary embolism and airway obstruction?
PE obstructs blood flow to the lungs, not airflow through the respiratory tract
113
What is pneumonia?
Inflammation of parenchymal structures of the lung involved in gas exchange
114
What structures are involved in pneumonia?
Alveoli, alveolar ducts, and terminal/respiratory bronchioles
115
What is the most common bacterial cause of pneumonia?
Streptococcus pneumoniae
116
What is the difference between typical and atypical pneumonia?
Typical involves bacterial infection multiplying extracellularly in alveoli; atypical involves viral or mycoplasma infection of alveolar septum and interstitium
117
How does pneumonia affect gas exchange?
Inflammation causes fluid accumulation in alveoli, reducing surface area and increasing diffusion distance
118
What is pleurisy?
Inflammation of the membranes (pleurae) that surround the lungs and line the chest cavity
119
What is the characteristic symptom of pleurisy?
Sharp chest pain during breathing as inflamed pleural layers rub against each other
120
What is a pleural effusion?
Abnormal collection of fluid in the pleural cavity that impairs breathing by limiting lung expansion
121
What is the difference between a transudate and an exudate?
Transudate is fluid pushed through capillaries due to pressure changes; exudate is fluid leakage caused by inflammation
122
What is a haemothorax?
Accumulation of blood in the pleural cavity
123
What makes a large haemothorax life-threatening?
Blood loss causing hypovolaemic shock and respiratory compromise from lung compression
124
What is a pneumothorax?
Presence of air in the pleural space causing partial or complete lung collapse
125
What is a tension pneumothorax?
A pneumothorax where intrapleural pressure exceeds atmospheric pressure due to a one-way valve effect
126
How does a tension pneumothorax cause obstructive shock?
Increasing pressure causes mediastinal shift, compressing the heart and major vessels, reducing venous return and cardiac output
127
What is mediastinal shift?
Deviation of mediastinal structures (heart, trachea, major blood vessels) toward one side of the chest
128
What conditions commonly cause mediastinal shift?
Tension pneumothorax, large pneumothorax, massive haemothorax, large pleural effusion
129
What is cardiac tamponade?
Compression of the heart due to fluid, blood, or pus accumulation in the pericardial sac
130
What three signs make up Beck's triad?
Hypotension, jugular venous distension, and muffled heart sounds
131
Is tachycardia part of Beck's triad?
No, tachycardia is commonly present in cardiac tamponade but is not part of Beck's triad
132
What is an alveoli?
Tiny air sacs in the lungs where gas exchange occurs
133
What are bronchi?
Large airways that lead from the trachea into the lungs
134
What are bronchioles?
Smaller branches of the bronchi without cartilage
135
What is pleura?
Thin membrane covering the lungs (visceral) and lining the chest cavity (parietal)
136
What is mediastinum?
Central compartment of thoracic cavity containing heart, major vessels, trachea
137
What is diaphragm?
Dome-shaped muscle separating thoracic and abdominal cavities
138
What is trachea?
Windpipe, main airway supported by C-shaped cartilage rings
139
What is ventilation?
Movement of air in and out of lungs
140
What is perfusion?
Blood flow through pulmonary capillaries
141
What is oxygenation?
Transfer of oxygen from alveoli to blood
142
What is compliance?
Measure of lung expandability
143
What is resistance?
Opposition to airflow in airways
144
What is elastic recoil?
Tendency of lungs to return to resting position after expansion
145
What is bronchoconstriction?
Narrowing of airways due to smooth muscle contraction
146
What is bronchodilation?
Widening of airways due to smooth muscle relaxation
147
What is hypoxemia?
Low arterial oxygen level
148
What is hypoxia?
Insufficient oxygen at tissue level
149
What is hypercapnia?
Elevated CO₂ levels in blood
150
What is hypocapnia?
Reduced CO₂ levels in blood
151
What is acidosis?
pH below normal range (< 7.35)
152
What is alkalosis?
pH above normal range (> 7.45)
153
What is an embolus?
Foreign material circulating in bloodstream
154
What is atelectasis?
Collapse of lung tissue
155
What is consolidation?
Solidification of lung tissue
156
What is effusion?
Abnormal fluid collection
157
What is pneumonia?
Inflammation of lung parenchyma
158
What is pleurisy?
Inflammation of pleural membrane
159
What is pneumothorax?
Air in pleural space
160
What is tension pneumothorax?
Air trapped in pleural space under pressure
161
What is haemothorax?
Blood in pleural space
162
What is pleural effusion?
Fluid in pleural space
163
What is pulmonary embolism?
Blockage of pulmonary artery
164
What is bronchiectasis?
Permanent dilation of bronchi and bronchioles
165
What is cardiac tamponade?
Compression of heart due to fluid in pericardial sac
166
What is cor pulmonale?
Right heart failure due to pulmonary hypertension
167
What is hypovolaemic shock?
Shock due to fluid/blood loss
168
What is obstructive shock?
Shock due to mechanical obstruction of blood flow
169
What is cardiogenic shock?
Shock due to pump failure
170
What is distributive shock?
Shock due to abnormal distribution of blood
171
What is Boyle's Law?
P₁V₁ = P₂V₂ (as volume increases, pressure decreases)
172
What is the Henderson-Hasselbalch equation?
pH = 6.1 + log([HCO₃⁻]/[0.03 × PCO₂])
173
What is Fick's Law of Diffusion?
V = (A × D × ΔP) / T
## Footnote
V = volume of gas diffused
A = surface area for diffusion
D = diffusion coefficient
ΔP = partial pressure gradient
T = membrane thickness
174
What is the oxygen content equation?
(1.34 × Hb × SaO₂) + (0.003 × PaO₂)
175
What is Minute Ventilation?
VE = Tidal Volume × Respiratory Rate
176
What is transpulmonary pressure?
Intrapulmonary pressure - Intrapleural pressure
177
What is the normal V/Q ratio?
~0.8
178
What does V/Q = 0 indicate?
Shunt (perfusion without ventilation)
179
What does V/Q = ∞ indicate?
Dead space (ventilation without perfusion)
180
What is respiratory acidosis?
↑PCO₂ → ↓pH
181
What is respiratory alkalosis?
↓PCO₂ → ↑pH
182
What is the bicarbonate-carbonic acid equilibrium?
CO₂ + H₂O ⟷ H₂CO₃ ⟷ H⁺ + HCO₃⁻
183
What is Beck's triad?
Hypotension + Jugular venous distension + Muffled heart sounds = Cardiac tamponade
184
What is Total Lung Capacity?
VC + RV (~5700 mL in adults)
185
What are normal respiratory pressures?
- Atmospheric: 760 mmHg
- Intrapulmonary: 760 mmHg (at rest)
- Intrapleural: ~756 mmHg (-4 mmHg relative to atmospheric)
