week 8 Flashcards
(148 cards)
1
Q
Asthma is
A
chronic inflammatory disorder of the airways characterised by:
Variable and recurring symptoms (wheeze, cough, dyspnoea, chest tightness)
Airflow obstruction (often reversible)
Bronchial hyperresponsiveness
Underlying airway inflammation
2
Q
Asthma Aetiology and Risk Factors
A
Genetic predisposition (e.g., family history of atopy, asthma)
Environmental exposures (e.g., allergens, pollutants, viral infections)
Occupational sensitisers (e.g., chemicals, dust)
Associated comorbidities (e.g., allergic rhinitis, atopic dermatitis)
Social determinants (e.g., poor housing, pollution, systemic racism)
3
Q
epidemiology of asthma
A
2.8 million (11%) people in Australia are estimated to be living with asthma
4
Q
Clinical Manifestations of asthma
A
Classic symptoms: wheezing, dyspnoea, cough (often nocturnal), chest tightness
Symptoms are episodic, often triggered by exercise, allergens, cold air, viral infections
Exacerbations may be life-threatening in severe cases
Physical signs: polyphonic expiratory wheezing, prolonged expiration, accessory muscle use in severe attacks
5
Q
Pathophysiology of asthma
A
- Airway Inflammation- Mast cells & T lymphocytes infiltrate the bronchial mucosa and contribute to inflammation and tissue injury -> Oedema, Increased mucus production, Increased vascular permeability
- Bronchial Hyperresponsiveness (BHR)- exaggerated bronchoconstrictor response to various stimuli (hallmark of asthma)
- Bronchoconstriction- triggered by: Direct exposure to allergens
- Mucus Hypersecretion- Goblet cell hyperplasia leads to excess mucus production. Mucus plugs may form and obstruct bronchioles, worsening airflow limitation.
- Airflow Obstruction
- Reversibility and Variability
- Contributing Systemic Factors
6
Q
- Reversibility and Variability
Asthma is characterised by
A
Reversible airflow limitation
Day-to-day and diurnal variability in symptoms
Symptoms often worse at night or early morning.
7
Q
- Contributing Systemic Factors to asthma
A
Atopy: Strongly associated with asthma, especially early-onset forms. Involves a heightened IgE response to environmental allergens.
Obesity: Independently associated with increased asthma risk and severity, possibly through systemic inflammation and mechanical effects.
Environmental pollutants: May exacerbate inflammation, especially in genetically susceptible individuals.
Smoking and infections: Worsen inflammation and contribute to airway remodeling
8
Q
Bronchoconstriction mechanism
A
Inflammatory mediators (e.g., histamine, leukotrienes) released by mast cells cause smooth muscle contraction
9
Q
Immune Sensitisation and the Role of IgE
A
- In genetically predisposed individuals, asthma often begins with sensitisation to inhaled allergens
- On first exposure to an allergen, dendritic cells present antigen to naïve T helper (Th0) cells, which differentiate into Th2 cells under the influence of cytokines like IL-4
- Th2 cells play a pivotal role in asthma by promoting IgE class switching in B cells
- These B cells then produce allergen-specific IgE antibodies, which bind to FcεRI (high-affinity IgE receptors) on the surface of mast cells and basophils, effectively priming these cells for future allergen exposures
10
Q
Early Phase: Bronchoconstriction and Mast Cell Activation
A
- Upon re-exposure to the allergen, IgE molecules on mast cells, triggering mast cell degranulation
- This results in the rapid release of bronchoconstrictive mediators, including histamine& leukotrienes
- These mediators cause smooth muscle contraction, increased vascular permeability, mucus hyper secretion, and airway narrowing.
11
Q
Late Phase: Inflammatory Cell Recruitment
A
- Several hours later
- recruitment of additional immune cells—particularly eosinophils, basophils, neutrophils, and memory Th2 cells—to the airways, Cytokines released
- The ongoing inflammation leads to epithelial damage, further mucus plugging, and heightened airway responsiveness
12
Q
Airway Hyperresponsiveness (AHR)
A
- hallmark of asthma, airways overreact to a range of triggers
- due to effects of inflammatory mediators and structural changes in the airways
- involves enhanced smooth muscle contractility, increased vagal tone, and greater sensitivity to stimuli.
- It contributes to the variability and reversibility of airflow obstruction seen in asthma.
13
Q
Airway Remodelling to asthma
A
- Hypertrophy and hyperplasia of airway smooth muscle
- Thickening of the basement membrane due to collagen deposition from activated fibroblasts and myofibroblasts
- Goblet cell hyperplasia and increased mucus gland size, leading to mucus overproduction=
- Loss of epithelial integrity and epithelial-mesenchymal transition (EMT)
14
Q
Chronic Obstructive Pulmonary Disease is
A
COPD is a common, preventable and treatable disease characterised by:
Persistent airflow limitation
Progressive and not fully reversible airflow obstruction
Chronic inflammatory response to noxious particles or gases
15
Q
Chronic Obstructive Pulmonary Disease aeitology
A
Cigarette smoking
Air pollution
Occupational exposure to dusts and fumes
Recurrent childhood respiratory infections
Genetic factors: α₁-antitrypsin deficiency
Low socioeconomic status
16
Q
Chronic Obstructive Pulmonary Disease epidemiology
A
- foremost cause of preventable hospitalisations amongst chronic health conditions
- 5th leading cause of death in Australia
- Of the 8.5 million (34%) people in Australia estimated to have chronic respiratory conditions, 2.5% people had COPD
17
Q
Pathogenesis of COPD
A
changes in the lung parenchyma and pulmonary vasculature
* defective macrophages
* chronic bacterial colonization
* fail to carry out efferocytosis and resolve
inflammation
18
Q
Subtypes of COPD
1. Chronic Bronchitis
A
Chronic cough and sputum production for at least three months in each of two consecutive
years in the absence of other conditions that can explain the symptoms
Prominent mucus production, airway narrowing
ABGs: chronic compensated respiratory acidosis in later stages
mucus hypersecretion, an increased number of goblet cells and enlarged submucosal glands
19
Q
Subtypes of COPD
2. Emphysema
A
Enlargement of air spaces distal to terminal bronchioles with destruction of their walls
→ decreased surface area for gas exchange
Hyperinflation and air trapping → barrel chest, dyspnoea
ABGs: hypoxaemia, later hypercapnia with acidosis
affects the structures distal to the terminal bronchiole - respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli - collectively as the acinus
20
Q
Proximal acinar emphysema:
A
abnormal dilation or destruction of respiratory bronchiole, the central portion of the acinus
commonly associated with cigarette smoking and coal workers’ pneumoconiosis
21
Q
Panacinar emphysema:
A
enlargement or destruction of all parts of the acinus.
characteristic of alpha-1 antitrypsin deficiency
22
Q
Ddistal acinar emphysema
A
alveolar ducts predominantly affected
may occur alone or in combination with proximal acinar and panacinar emphysema
23
Q
Pulmonary vasculature from COPD
A
intimal hyperplasia and smooth muscle hypertrophy/hyperplasia, which are thought to be due to chronic hypoxic vasoconstriction of the small pulmonary arteries
24
Q
Chronic Bronchitis Emphysema mainsite
A
CB: Bronchi and bronchioles
E: Alveoli and distal airspaces
25
Chronic Bronchitis Emphysema primary issue
CB: Mucus hypersecretion and inflammation
E: Alveolar wall destruction and ↓ elastic recoil
26
Chronic Bronchitis Emphysema cellular features
CB: Goblet cell metaplasia, neutrophils, CD8+ cells
E: Macrophages, CD8+ cells, elastase-mediated destruction
27
Chronic Bronchitis Emphysema Gas exchange
CB: Mild hypoxaemia, late hypercapnia
E: Significant hypoxaemia with hyperinflation
28
Chronic Bronchitis Emphysema ABG findings
CB: Chronic compensated respiratory acidosis
E: ↓ PaO₂, early normal PaCO₂ progressing to hypercapnia
29
Chronic Bronchitis Emphysema Imaging
CB: Increased markings, cardiomegaly (CXR)
E: Hyperlucency, flat diaphragm, bullae (CXR/CT)
30
COPD CM
Dyspnoea (esp. on exertion)
Chronic cough
Sputum production
31
Functions of the respiratory system
breathing
- moving air in and out of lungs
* Provide an extensive area for gas exchange between and circulating blood
* Provide olfactory sensations to the central nervous system
* Produce sounds involved in phonetics
* Protect respiratory surfaces from dehydration, environmental variations and defending from invasion or pathogens
32
chronic broncitis epidemiology
3% to 7% of healthy adults
33
chronic broncitis CM
Dyspnoea, productive cough, cyanosis
34
Emphysema CM
dyspnoea early in disease, wheeze common, barrel chest
35
Chronic Suppurative Lung Disease and Bronchiectasis def
are clinical syndromes, with respiratory signs or symptoms of a persistent productive cough, dyspnoea, airway reactivity and recurrent chest infections.
36
Chronic Suppurative Lung Disease primarily occurs in who
primarily in children characterised by chronic or recurrent wet/productive cough and lower respiratory infections in the absence of radiological evidence of bronchiectasis.
37
Bronchiectasis primarily affects who
in children/adolescents or adults that involves irreversible dilatation of the bronchi due to structural airway injury.
confirmed by high-resolution chest CT revealing bronchial dilatation.
38
Bronchiectasis and CSLD Aetiology ( i have listed 5 but their are more)
the result of various insults that damage the bronchial wall, impair mucociliary clearance, and promote recurrent infections. Key causes include:
Post-infectious
Cystic fibrosis (CF) or CFTR-related disorders
Autoimmune and systemic diseases
Immunodeficiencies
Recurrent aspiration or reflux
39
Pathogenesis
CSLD and bronchiectasis
characterised by a self-perpetuating cycle of airway damage involving infection, inflammation, impaired mucociliary clearance and with bronchiectasis, notable structural lung changes
40
Pathogenesis CSLD and bronchiectasis
steps
1. Initial Airway Insult
2. Impaired Mucociliary Clearance
3. Chronic Infection
4. Neutrophilic Inflammation
5. Structural Lung Damage
6. Contributing Factors and Amplifiers
41
1. Initial Airway Insult
The pathogenic cascade often begins with injury to the airway epithelium, caused by:
Severe lower respiratory infections
Airway obstruction (tumours)
Congenital or acquired immune defects (e.g., CVID)
Impaired host defence mechanisms (e.g., CFTR mutations)
This initial injury: Compromises epithelial integrity Triggers an aberrant immune response
Disrupts mucociliary clearance
42
2. Impaired Mucociliary Clearance
Damage to the ciliated epithelium impairs the mucociliary escalator, leading to mucus stasis. Factors contributing to this impairment include:
- Ciliary damage or dysfunction impairs mucus transport (as in primary ciliary dyskinesia)
- Goblet Cell Hyperplasia: resulting in excessive mucus production
- CFTR dysfunction (seen in cystic fibrosis and CFTR-related disorders) dehydrates the airway surface liquid, increasing mucus viscosity
Stagnant mucus becomes a breeding ground for pathogens, facilitating chronic infections.
43
3. Chronic Infection
Persisting mucus fosters chronic colonisation by pathogens such as:
Pseudomonas aeruginosa
Haemophilus influenzae
Staphylococcus aureus
NTM (e.g., Mycobacterium avium complex)
Fungal elements (e.g., Aspergillus in ABPA)
Key features of chronic infection:
Biofilms → resist immune clearance and antibiotics
Disruption of epithelial repair
Promotion of chronic neutrophilic inflammation
44
4. Neutrophilic Inflammation
Persistent infection activates innate immune cells, especially neutrophils, which release:
Neutrophil elastase
Reactive oxygen species
Myeloperoxidase
Pregnancy zone protein
Neutrophil extracellular traps
These responses:
Promote mucosal ulceration, oedema and angiogenesis
Correlate with disease severity, sputum purulence and exacerbation risk
45
Neutrophil elastase effect
Degrades extracellular matrix (elastin), disrupts tissue
46
Reactive oxygen species effect
Oxidative stress, epithelial damage
47
Myeloperoxidase effect
Enhances oxidative killing but damages host tissue
48
Pregnancy zone protein effects
Associated with P. aeruginosa, correlates with exacerbations
49
Neutrophil extracellular traps effects
Trap pathogens but also damage airway structures
50
change- Transmural inflammation -> what consequence
Ulceration, capillary leakage, neovascularisation
51
change- Loss of structural proteins -> what consequence
Elastin and cartilage degradation → weakened airway walls
52
change- Bronchial dilation and wall thickening -> what consequence
Irreversible distortion seen on HRCT (in bronchiectasis)
53
change- Goblet cell hyperplasia and smooth muscle hypertrophy -> what consequence
Contributes to airflow obstruction and mucus hypersecretion
54
change- Epithelial-mesenchymal transition -> what consequence
Leads to fibrosis and remodeling
55
Hyperconcentrated mucus causes what
↑ DNA, ↑ mucins (esp. MUC5B), ↑ solids → reduced mucus transport
56
IL-1β excess causes what
Promotes mucus hyperconcentration, correlates with disease severity
57
Atopy causes what
Enhances immune reactivity; associated with worse lung function
58
CFTR mutations (heterozygous or homozygous) causes what
Alter ion transport, promote mucus dehydration
59
Vitamin D deficiency causes what
Impaired innate immunity, increased P. aeruginosa colonisation
60
Impaired neutrophil function causes what
Reduced apoptosis, phagocytosis; increased PZP and NETs release
61
Vortex Component- infection
Initial insult may be viral, bacterial, or due to aspiration causing mucosal damage and loss of ciliary function
62
vortex component inflammation
Persistent infection stimulates neutrophilic infiltration, releasing proteolytic enzymes (e.g., elastase), reactive oxygen species, myeloperoxidase, and neutrophil extracellular traps (NETs)
63
vortex components- structural damage
Chronic transmural inflammation leads to loss of elastin, destruction of cartilage, mucosal ulceration, and neovascularisation, causing irreversible bronchial dilation.
64
vortex component- Impaired Mucociliary Clearance
Damaged cilia, hyperconcentrated mucus and viscous secretions impair clearance, perpetuating infection.
65
CM Chronic Suppurative Lung Disease (CSLD)
- Chronic wet/productive cough lasting >4 weeks
-Recurrent lower respiratory tract infections
- Dyspnoea on exertion, wheeze, chest tightness (especially during exacerbations)
- Crackles, wheeze, possible chest wall deformity if prolonged
- Fatigue, failure to thrive in children
note: CSLD may be reversible with treatment (especially in children)
66
CM Bronchiectasis
- Chronic cough with daily sputum production, often mucopurulen
- Recurrent respiratory infections and exacerbations with increased sputum volume and purulence
- Dyspnoea, pleuritic chest pain, haemoptysis (in some cases
-Crackles, wheeze, digital clubbing in advanced disease
- Fatigue, malaise, and weight loss in chronic disease
note: Bronchiectasis is typically irreversible once structural changes occur
67
Cystic Fibrosis def
is an autosomal recessive multisystem disorder caused by mutations in the CFTR gene. It is characterised by defective chloride and bicarbonate transport across epithelial surfaces, resulting in dehydrated, thick secretions in the lungs, gastrointestinal tract, pancreas, biliary system, reproductive organs, and sweat glands.
68
CF aeitology
Genetic Basis: Caused by biallelic pathogenic mutations in the CFTR gene
Most Common Mutation: F508del accounts for
Inheritance Pattern: Autosomal recessive
69
Epidemiology of CF
~1 in 2500–3500 live births
70
Pathogenesis of CF
involves abnormal epithelial ion transport and a "vicious cycle" of infection, inflammation, and tissue destruction, especially in the lungs.
1. CFTR Dysfunction
2. Airway Inflammation and Infection
3. Tissue Destruction and Bronchiectasis
4. Extrapulmonary Effects
5. Genetic Modifiers
71
1. CFTR Dysfunction
CFTR protein is a chloride/bicarbonate channel regulated by cAMP/PKA.
Loss of CFTR function → ↓ chloride and bicarbonate secretion, ↑ ENaC sodium absorption → dehydrated airway surface liquid.
Consequences:
Mucus stasis
Ciliary dysfunction
Airway obstruction
72
2. Airway Inflammation and Infection
Early neutrophilic inflammation occurs even before infection in infants.
Persistent colonization with pathogens (e.g., Pseudomonas aeruginosa, Staph. aureus):
Forms biofilms
Increases oxidative stress
Releases proteases (e.g., elastase)
NETs, myeloperoxidase (MPO), and reactive oxygen species (ROS) exacerbate damage.
73
3. Tissue Destruction and Bronchiectasis
Neutrophilic inflammation causes:
Bronchial wall thickening
Irreversible airway dilation (bronchiectasis)
Loss of elastin and airway remodeling
74
4. Extrapulmonary Effects
Pancreatic insufficiency: Thick secretions block pancreatic ducts → enzyme loss → fat malabsorption, malnutrition.
CF-related diabetes (CFRD): Progressive β-cell loss and insulin deficiency.
Biliary cirrhosis: Obstruction of intrahepatic bile ducts.
Male infertility: Congenital absence of vas deferens (CBAVD).
Intestinal obstruction: Meconium ileus, distal intestinal obstruction syndrome (DIOS).
75
5. Genetic Modifiers
Influence phenotype and severity:
TGFB1: ↑ inflammation and lung damage
MBL2: ↑ risk of infection
SLC26A9, TNF, TCF7L2: Affect risk of CFRD and pulmonary progression
76
Clinical Manifestations of CF
common presentations are respiratory or gastrointestinal.
* respiratory: persistent cough, dyspnoea, recurrent or severe pulmonary infection
* gastrointestinal: meconium ileus at birth and malabsorption
* complications of CF: liver disease and cystic fibrosis-related diabetes
77
Bronchiectasis - Pathophysiology
1. Infectious insult and impaired mechanisms
2. Inflammatory Response: immune response involving neutrophils, lymphocytes and macrophages
3. Neutrophils and Elastase: progress airway destruction (microbial colonisation, affect cilia and mucus secretion)
4. Sputum/Mucus: physical properties – tenacious due to higher
concentrations of DNA and mucin
5. Can occur in parallel with COPD and asthma – worse prognosis
78
Bronchiectasis
Clinical manifestations
* Chronic cough
* Sputum
* Exacerbations
* Dyspnoea
* Rhinosinusitis
* Haemoptysis
79
CF aeitology
* inherited genetic disease
* mutation to the CHTR gene
* autosomal recessive pattern 1:4 chance of inheriting if both parents are carriers of CF gene
80
Cystic fibrosis - Imaging
CXR
Thickening of bronchial walls
Irregular shaped bronchioles
Mucus plugging
Widespread ‘patchy’ opacities / mucoid impaction
CT scan
81
Cystic fibrosis - PFTs
shows respiratory function
* Spirometry: decline in FEV1 and FEV1 /FVC
* Lung volumes demonstrate increases in TLC and RV as hyperinflation progresses
* Increase in ratio of residual volume to total lung capacity (RV/TLC)
* Decrease in forced expiratory flow at 25 to 75 percent of lung volume
82
Cystic Fibrosis – gas exchange
* hypercapnia should be evaluated by measuring end-tidal carbon dioxide (CO2 ) or
via arterial blood gas analysis
* as bronchiectasis and airway obstruction become more pronounced, ventilation-
perfusion mismatch leads to hypoxaemia
83
Pneumonia def
inflammation of the lung parenchyma associated with alveolar filling by exudate
84
Pneumonia aeitology
caused by inhalation of bacteria, fungi, viruses or chemical agents (or inhalation of food, liquid or other substances)
85
Pneumonia Clinical manifestations
Fever, chills, productive or dry cough, malaise, pleural pain and sometimes dyspnoea and haemoptysis; Auscultation: consolidation and inspiratory crackles
86
Pathophysiology of Pneumonia
A. Pathogen Entry
Inhalation of airborne droplets (e.g., Streptococcus pneumoniae, influenza)
Aspiration of oropharyngeal flora or gastric contents
Haematogenous spread from extrapulmonary infection sites (rare)
B. Host Defense Mechanisms
Nasal hair, mucociliary clearance, cough reflex
Alveolar macrophages & neutrophils
Surfactant proteins, antimicrobial peptides
C. Failure of Host Defenses
Pathogens bypass barriers or overwhelm the immune system
Risk factors: Smoking, viral infection, chronic illness, elderly age
D. Inflammatory Response
Innate immune activation: Alveolar macrophages detect PAMPs (e.g., LPS, peptidoglycan).
Release of proinflammatory cytokines: IL-1β, TNF-α, IL-6.
Recruitment of neutrophils → phagocytosis of pathogens.
Neutrophil degranulation & ROS production → local tissue injury.
E. Alveolar Damage & Consolidation
Accumulation of neutrophils, exudate, and fibrin in alveoli.
Disrupted gas exchange → hypoxia
87
Bronchopneumonia
bronchi and bronchioles to lower lobes
* patchy areas of consolidation - neutrophil collection in alveoli and bronchi
88
Lobar pneumonia
exudative inflammation of entire lobe
89
Lobar pneumonia 4 classical stages of inflammatory response if left untreated
* congestion/consolidation in the first 24 hours in which the lungs are heavy, red, and boggy
* red hepatization/early consolidation begins 2 to 3 days after consolidation - firm liver-like
consistency. Fibrin strands replace oedema fluid
* grey hepatisation/late consolidation occurs 2 to 3 days following - gray with liver-like
consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells
* resolution and restoration of pulmonary architecture by eighth day. Macrophages are
predominant cells which contain engulfed neutrophils and debris
90
Tuberculosis is
An infectious, inflammatory systemic disease affecting the lungs however
may also disseminate to other organs
91
bacterial pathogen is
Mycobacterium tuberculosis
92
TB risk factors
Age, immunosuppression, alcohol and illicit drug use, smoking tobacco, malnutrition, diabetes mellitus, health-care work and incarceration; migration
93
TB CM
coughing, fever, weight loss and night sweats.
94
Pathophysiology of TB
A. Transmission & Initial Infection
Airborne droplet nuclei inhaled → reach alveoli.
MTB phagocytosed by alveolar macrophages but resists intracellular killing.
B. Immune Evasion
MTB inhibits phagosome-lysosome fusion and acidification.
Survives within macrophages using complex lipids (cord factor, sulfolipids).
C. Adaptive Immunity Activation (Weeks Later)
Antigen presentation triggers Th1 response.
IFN-γ activates macrophages → improved killing.
Formation of granulomas: central infected macrophages (some become multinucleated giant cells), surrounded by T-cells and fibroblasts.
D. Latent vs. Active TB
Latent TB: Controlled infection; MTB dormant within granulomas.
Reactivation: Granuloma breakdown → caseous necrosis → MTB spreads to lung/apex and systemically.
95
SARS-CoV-2 Coronavirus
- a single-strand RNA virus - attaches to a receptor, penetrating cell membrane and
undergoing replication of RNA, which are released from infected cell
- SARS-CoV-2 binds to angiotensin-converting
enzyme (ACE2) receptor in epithelial cells in
respiratory tract Angiotensin II increases inflammation, tissue damage and cell death in alveoli
96
Pathophysiology of covid
A. Viral Entry
Spike (S) protein binds to ACE2 receptor on type II alveolar cells.
Viral entry facilitated by TMPRSS2 protease.
B. Viral Replication & Evasion
Replication within host cells → cell lysis.
Evasion of innate immune detection via suppression of interferon (IFN) pathways.
C. Dysregulated Immune Response
Release of proinflammatory cytokines (IL-6, TNF-α, IL-1β) → cytokine storm in severe cases.
Massive monocyte and neutrophil infiltration.
Endothelial activation → microvascular thrombosis and capillary leak.
D. Lung Injury
Diffuse alveolar damage (DAD): characteristic of ARDS.
Hyaline membrane formation, alveolar edema, pneumocyte desquamation.
Thrombosis: Common in severe COVID-19, especially in small pulmonary vessels.
E. Long-term Sequelae
Post-COVID fibrosis, persistent inflammation, long COVID symptoms
97
typical and atypical pnuemonia
Typical pneumonia: Lobar consolidation (e.g., S. pneumoniae).
Atypical pneumonia: Patchy interstitial infiltrates
98
TB Pathological Hallmarks
Caseating necrosis.
Cavitation in advanced disease.
Miliary TB: Hematogenous spread → tiny nodules in multiple organs.
99
covid cm
- Acute respiratory distress syndrome (ARDS)
- Thromboembolic events
- Multisystem inflammatory syndrome (MIS)
- Post-acute sequelae (Long COVID
100
What is an X-ray
electromagnetic radiation with a shorter wavelength and higher frequency (hence higher energy) than visible light. They are a type of ionizing radiation, which means they have the potential to cause damage to DNA.
101
why use an xray
Identifies infiltrates, effusions, masses, hyperinflation and structural abnormalities for example:
Diagnosis of conditions affecting the chest.
Pre-operative assessment.
Checking the correct position of medical therapies such as intravenous lines, chest drains (ICCs), endotracheal tubes (ETT), and nasogastric tubes (NGT).
Assessing the effectiveness of therapies.
102
Limitations of Chest X-rays
- A CXR provides a 2D view of a complex 3D structure, which can limit the understanding of the spatial relationships of different structures.
- This often necessitates multiple views to visualise structures adequately
- Low sensitivity for early interstitial lung disease (ILD) or pulmonary embolism.
103
systematic approach to interpreting CXRs including
Technical Details and Orientation: Patient name, DOB, date/time of film, medical record number, side marker (L or R), patient position
Quality: Rotation/alignment (assessing position of spinous processes relative to clavicles), level of inspiration (assessing rib count)
Lung Fields: Mostly black appearance with thin lung markings (vessels) extending to the edges, equal density in both lungs, and noting any extra shadowing (opacity) which could indicate pathology
Extra-thoracic Structures: Upper limb girdle (clavicles, scapulae, humerus), spine abnormalities, ribs (count, fractures),
Intrathoracic Structures: Trachea and bifurcation (around T5-T7), hilar regions (pulmonary arteries, major bronchi
104
Types of CT
Helical (spiral): Continuous scanning, fast, high-resolution
High-Resolution CT (HRCT): Step-and-shoot, excellent parenchymal detail
105
Principles of CT
CT scans utilise X-rays but employ more sophisticated technology to create cross-sectional images of the chest.
Thin, multislice scanners (up to 320 slices) imaging offer detailed view of lung parenchyma
106
uses of CT
more detailed 3D visualisation of the lungs and surrounding structures compared to the 2D image provided by a CXR
Essential in evaluating ILD, bronchiectasis, emphysema, lung nodules
107
Disadvantages of CT
Effective radiation dose for CT of the chest varies between 1 and 10 mSv, which is approximately 10 to 100 times more than radiography
108
Chest MRI advantages
Less ionising radlation than CT scan so useful for those sensitive to radiation, such as pregnant individuals or children, or if repeated imaging is anticipated
109
chest mri uses
To investigate or diagnose specific conditions eg birth defects of the heart, blood vessel problems,
Assessment of the lung apices, diaphragm, and spinal column
Evaluation of pleural disease
Assessment of local tumour extension,
Metastatic invasion of bone marrow
110
Hilar region
the angle formed by the decending upper lobe veins as they cross behid the lower lobe arteries
* Pulmonary arteries
* Major bronchi
* Lymph nodes (not visible unless abnormal)
111
Cardiothoracic ratio (CTR)
difference is distance from the widest thoracic width to the distance of the heart
both verticle measurements
112
Pulmonary Function Tests
is important for evaluating respiratory function in patients with suspected or known lung disease and in individuals with risk factors for lung disease.
113
The major types of PFTs include
Spirometry
Spirometry before and after a bronchodilator
Lung volumes
Quantitation of diffusing capacity for carbon monoxide (DLCO)
114
PFTs are indicated for evaluating symptoms like
chronic cough, wheezing, and dyspnoea
assessing bronchodilator therapy
evaluating workplace exposures
assessing surgical risk
objectively assessing respiratory impairment
monitoring disease progression
115
Spirometry
Spirometry is a key diagnostic test that measures the volume of air exhaled at specific time points during a forceful and complete exhalation after a maximal inhalation
116
Forced Vital Capacity (FVC)
is the maximum volume of air forcefully expired after a maximal inspiration (measured in Litres)
117
Forced Expiratory Volume in one second (FEV1)
is the volume of air forcefully expired in the first second of a FVC manoeuvre (measured in Litres)
118
FEV1/FVC ratio is FEV1 expressed as a fraction or percentage of FVC.
It is important for distinguishing between obstructive and restrictive lung diseases. A reduced ratio suggests obstructive disease
119
Slow vital capacity (SVC)
the maximal amount of air exhaled in a relaxed expiration from full inspiration to residual volume. It may be useful when FVC is reduced and airway obstruction is present
120
Peak expiratory flow (PEF)
the highest flow achieved from a maximum forced expiratory manoeuvre started without hesitation from a position of maximal lung inflation (measured in Litres/sec)
121
Obstructive Lung Diseases spiriotermy
A reduced FEV1/FVC ratio defines obstructive airway diseas
122
Restrictive Lung Diseases spiriomety
A reduced FVC with a normal or increased FEV1/FVC ratio suggests restrictive disease, which needs confirmation with lung volume measurements
123
Monitoring Respiratory Diseases Spirometry
Spirometry is used to monitor asthma, COPD, interstitial lung disease, and neuromuscular diseases
124
Spirometry Upper Airway Obstruction
Flow-volume loops, including inspiratory and expiratory manoeuvres, are useful in detecting upper airway obstruction. A plateau during forced inhalation may indicate variable extra thoracic obstruction
125
respiratory Muscle Weakness spiormetry
A decrease in supine vital capacity (VC) >10 percent compared to sitting suggests diaphragmatic weakness.
126
Bronchoprovocation Challenge spiormetry
Spirometry assesses airway hyperresponsiveness to various challenges
127
Tidal Volume (VT):
Volume of one normal breath
128
Inspiratory Reserve Volume (IRV)
Extra air that can be inhaled beyond tidal volume (1.9 - 3.1 L).
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Expiratory Reserve Volume (ERV)
Extra air that can be exhaled beyond tidal volume (0.9 - 1.2 L).
130
Residual Volume (RV)
Air remaining in the lungs after maximal exhalation (1.1 – 1.2 L). Air trapping is indicated by increased RV or RV/TLC.
131
Inspiratory Capacity (IC) equation
VT + IRV (2.4 - 3.6 L).
132
Functional Residual Capacity (FRC)
RV + ERV (1.8 – 2.4 L). Increased FRC can suggest hyperinflation.
133
Vital Capacity (VC)
IRV + VT + ERV (3.1 – 4.8 L). Can be measured as FVC or SVC.
134
Total Lung Capacity (TLC)
VC + RV (4.2 – 6.0 L). Decreased TLC is key for determining restriction
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Diffusing Capacity for Carbon Monoxide (DLCO)
measures the ability of the lungs to transfer gas from inhaled air in the alveoli to the red blood cells in pulmonary capillaries
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Clinical Indications to use a Diffusing Capacity for Carbon Monoxide (DLCO)
DLCO is used to identify causes of dyspnea or hypoxaemia
monitor interstitial lung disease progression
identify pulmonary hypertension
assess emphysema severity
evaluate restrictive lung disease and pulmonary vascular disease
predict postoperative risk after lung resection
evaluate the need for oxygen therapy.
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Obstructive Disease in re to DLCO
Low DLCO is indicative of emphysema in smokers with airway obstruction
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Restrictive Disease in re to DLCO
Low DLCO with reduced lung volumes suggests interstitial lung disease.
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Pulmonary Vascular Disease
Isolated decreased DLCO with normal spirometry can suggest pulmonary vascular disease like pulmonary hypertension or emboli.
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Low DLCO with Normal Spirometry
Other causes include early interstitial lung disease, anemia, and hepatopulmonary syndrome.
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KCO (DLCO/VA)
is an index of the efficiency of alveolar gas transfer
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What is Pulse Oximetry
- A non-invasive method to estimate oxygen saturation (SpO₂) in arterial blood
- It shows how much oxygen is bound to haemoglobin without needing a blood sample
- Used widely in hospitals, clinics, emergency care, exercise testing and home monitoring.
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How Pulse Oximetry Works
The device emits red and infrared light through the skin
Oxygenated haemoglobin absorbs more infrared light
Deoxygenated haemoglobin absorbs more red light
A sensor detects the changing light absorbance with each arterial pulse to calculate SpO₂
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Components of a Pulse Oximeter
Light source: Red and infrared LEDs.
Photodetector: Measures light that passes through tissue.
Processor: Calculates oxygen saturation percentage.
Display screen: Shows SpO₂ and pulse rate.
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Normal Pulse Oximetry Values - SpO₂ (%)
95–100% Normal oxygenation
Target for COPD patients: 88–92% to avoid worsening CO₂ retention
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Clinical Uses of Pulse Oximetry
Monitoring oxygenation during anesthesia and surgery.
Tracking patients in intensive care units (ICUs).
Assessing respiratory conditions (COPD, asthma, pneumonia).
Screening for sleep disorders (e.g., obstructive sleep apnea).
Evaluating oxygen needs during exercise testing.
Home monitoring for chronic respiratory diseases and COVID-19 recovery
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Advantages of Pulse Oximetry
Non-invasive: No blood sample required
Painless and quick
Portable: Small handheld or clip-on devices
Continuous monitoring: Real-time tracking of SpO₂
Early detection: Identifies hypoxaemia before symptoms worsen
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Limitations and Sources of Error
Poor perfusion: Shock, hypothermia can cause low readings
Motion artefact: Patient movement affects accuracy
Nail polish/artificial nails interfere with light detection
Skin pigmentation: May slightly overestimate SpO₂ in dark-skinned individuals
Carbon monoxide poisoning: Falsely normal SpO₂ readings
Anaemia: Normal SpO₂ but reduced true oxygen-carrying capacity.
