Respiratory - Breathlessness: Airflow Obstruction Flashcards
Overview of mechanical respiration
Inspiration & expiration
Gas conduction
Gas transfer
Exhalation
What does inhalation and exhalation require
Organised MSK function (diaphragm, IC muscles and rib cages) of the thorax to draw in air and return it to atmosphere
Function of pleural space to enable the expansion of the lung
What kind of things compromise inhalation and exhalation
Muscle wasting and neurodegenerative disease
Pleural disease - fibrosis, PTX
Where is the conducting zone
From nose to bronchioles
What is found in conducting zone
Resp type mucosa
Function of conducting zone
Passage of air from environment to lungs Airways protection Air humidification and warming Smell Speech
How does the conducting zone protect the airway
Through mechanical and immunological removal of pathogens
How does the conducting zone allow the passage of air
Made of cartilage and muscle
Allows rigidity but flexibility of airways
Resistant to compression and collapse
Allows expansion during breathing
Why is the trachea C shaped
To allow swallowing
Mechanical (cellular) mechanisms of airway protection by the conducting zone
Cilla and mucus (mucocilliary escalator)
Physical barrier between external environment and tissue
Immunological mechanisms of airway protection by the conducting zone
Identification and removal of pathogens
Mechanical (anatomical) mechanisms of airway protection by the conducting zone
Reflex protection
How does nasal hair protect the airway
Remove larger particulate material
Movement of mucocilairy escalator
Moves mucus up the airways to pharynx to remove particles
What is cilia action independent of
Nervous control
May persist for several hrs after death
What is cilia rate dependent on
Temp (falls when colder)
Mucus secreting cells
Seromucinous glands within submucosa
Goblet cells within epithelium
Comparison of mucus produced by different cells
Seromucinous glands produce more watery, thin mucous whereas the goblet cells and mucous cells produce thicker mucous
When are neuroendocrine cells involved in the growth and envelopment of the airways
In utero
MALT
Mucosa Associated lymphoid Tissue
When is MALT acquired
In response to antigenic stimuli
Why can immunological identification and removal of pathogens occur in the nasopharynx
Dense lymphoid tissue
Serous cell secretions that destroy potential pathogens
Lysosome Lactoferrin Antiprotease IgA Epithelial peroxidase
Examples of reflex airway closure and removal of foreign bodies
Cough reflex
Swallow reflex
Gag reflex
What are pulmonary irritant receptors stimulated by
Both mechanical (light touch) or chemical stimuli
Swallow reflex
Enables epiglottis to cover larynx to prevent aspiration
What nerve is involved in the cough reflex
Vagus nerve
Gag reflex (pharyngeal reflex or laryngeal spasm)
Reflex contraction of back of throat
Prevents foreign bodies entering upper wiarways
Stimulus of gag reflex
Touch from back of throat, tonsils, uvula, roof of mouth or base of tongue
Mucous involvement in smell
Dissolve odours to allow detection
Phases of speech
Respiration - lung function
Phonation - laryngeal function
Articulation - vocal tract (upper airways)
Where does the laryngeal cavity extend from
The tip of the epiglottis to the lower edge of the cricoid cartilage
False vocal cords vs true vocal cords
Resp epithelium vs squamous epithelium
Why do the true vocal cords adjust to a more robust epithelium
True vocal cords are subject to more mechanical trauma from phonation
Barriers to tumour spread in the larynx
Intrinsic and extrinsic connective tissue bands
Thyroid and cricoid cartilage
Intrinsic connective tissue bands in the larynx
Quadrangular membrane
Conus elastics
Extrinsic connective tissue bands in the larynx
Thyroid membrane
Cricothyroid membrane
What is the interstitium
Lungs connective tissue scaffolding
What does interstitial comprise of
Collagen Elastin fibres Fibroblasts Myofibroblasts Pericytes Histiocytes Mast cells Neuroendocrine cells
Where are Clara cells (bronchiolar exocrine cells) most numerous in
Terminal bronchioles
What are Clara cells important in modulating
Bronchiolar infl
What can Clara cells secrete
Endothelin - powerful broncho and vasoconstrictor
Protease inhibitors
Cells found in alveoli
Type 1 pneumocytes Type 2 pneumocytes Alveolar macrophages Pores of Kohn Lambert's canal
Pores of Kohn
Small gaps between alveoli
Lambert’s canal
Tubular connections which connect terminal and resp bronchioles w. adjacent peri bronchial alveoli
Nuclei in pneumoncytes
Type 1 - flattened
Type 2 - larger, darker
What do Type 1 pneumocytes do
Thin for increased gas exchange
Forms a barrier to prevent fluid loss
What do Type 2 penumocytes do
Surfactant protection - reduced surface tension in order to facilitate lung expansion
Pulmonary vasculature
Pulmonary arteries Pulmonary capillaries Pulmonary veins Bronchial arteries Lymphatics
Where do pulmonary veins tend to be found
In the interlobar septa
Blood supply of lungs
Bronchial arteries arising from systemic circulation
Pulmonary arteries
What is the pleura
A pair of serous membrane lining the thoracic wall (parietal) and lungs (visceral)
Structure of pleura
Meosthelial cell lining
Connective tissue sub mesothelium
Elastin layer variation in visceral and parietal layers of pleura
Visceral layer is double and thicker - account for lung movement
Parietal - single layer and thinner
What is the most readily preventable cause of death in humans
Smoking
Which components of tobacco have a carcinogenic effect
Tar
Polycyclic aromatic hydrocarbons
Nitrosamine
What causes the a/c effects of smoking
Nicotine - increase in HR and BP, CO and elevation of cardiac contractility
Effects of smoking in resp system
Mucosal irritant —> bronchitis & RBILD/ DIP
Destruction of alveolar walls —> emphysema
Carcinogenesis –> lung cancer
RBILD
Resp bronchial ILD
DIP
Desquamative interstitial pneumonia
What diseases are included in COPD
C/c bronchitis
Emphysema
(a/c obstructive bronchiolitis but diff pathology)
Main risk factor of COPD
Smoking - 80% of cases are smokers
Oher risk factors for COPD
Environmental/ occupational pollution
Airway hyper-responsiveness
Genetic factors
Zones affected in COPD
Conducting zone
Gas exchange zone
How is the conducting zone affected in COPD
C/c bronchitis - hypersecretory
Obstructive bronchiolitis - obstructive
These pathological processes may lead to cyanosis
How are large airways affected in c/c bronchitis
Mucus hyper secretion
Infl
How are small airways affected in c/c bronchitis
Peribronchiolar fibrosis
Airway obstruction - infl thickening
Goblet cell hyperplasia
Loss of Clara cells
How is the gas exchange zone affected in COPD
Emphysema - loss of elastic recoil in alveoli
Symptoms of a blue bloater (c/c bronchitis)
C/c productive cough Purulent sputum Haemoptysis Cyanosis (due to hypoxia) Peripheral oedema Crackles, wheeze
Complications of c/c bronchitis
Pulmonary HTN Cor pulmonale (form c/c pulmonary HTN)
Symptoms of a pink puffer (emphysema)
Dyspnoea Minimal cough Pink skin, pursed lip breathing Accessory muscle use Cachexia Hyperinflation (barrel chest) Tachypnoea
Complications of emphysema
PTX (due to bullae)
Wt loss
Change in mucin type in c/c bronchitis
Thicker, more viscous
Increased seromucinous glands
Change to goblet cells in c/c bronchitis
Hyperplasia - reduced capacity to remove mucus (increased susceptibility to infection)
Emphysema
Irreversible abnormal increase in the size of air spaces beyond the terminal bronchioles w/ destruction of air space walls w/ out obvious fibrosis
What do proteases cause
Tissue degeneration
What does elastase do
Break down elastin
Why must there be a balance between proteases and antiproteases
Allows any tissue damage which may have occurred to be removed and repaired in a controlled manner whilst limiting damage to surrounding tissue
Pathogenesis of emphysema
Smoking causes antiprotease inactivation and causes uncontrolled activity of proteases –> destruction of elastin causes alveoli to become brittle preventing deflation on expiration
Process of emphysema development
Harmful particles from smoking trapped in alveoli
Infl response triggered
Infl chemicals dissolve alveolar septum
Large air cavity filled w/ carbon deposits formed
Patterns of emphysema
Centrilobular
Paracinar
Paraseptal
Irregular
Centrilobular emphysema
Central/ proximal alveolar unit involved, distal alveoli spared
Most commonly seen in smokers
More severe in upper lobes
Paracinar emphysema
Whole alveolar unit involved
More commonly in lower lobes
Associated w/ alpha1-antitrypsin deficiency
Paraspetal emphysema
Proximal alveolar unit normal, emphysematous change more evident near the pleura, along septa and margins of lobules
Seen in upper half of lungs
Emphysema histology
Airspace enlargement
Fractured alveolar walls
+/- infl
Smoking related ILD
Resp bronchiolitis
Resp bronchiolitis associated ILD
DIP
Resp bronchiolotis vs resp bronchiolitis associated ILD
Pts may not be symptomatic w/ resp bronchiolitis and wont always develop RBILD
Pts are symptomatic w/ resp bronchiolitis associated ILD - persistent cough and/ or mild breathless
Lung function test in resp bronchiolitis associated ILD
Normal or mildly restrictive defect
Mx of resp bronchiolitis associated ILD
Resolves completely on quitting smoking
May require corticosteroids
Typical pts of DIP
Middle-aged cigarette smokers who complain of breathlessness and cough of insidious onset
Prognosis of DIP
Responds well to steroid and smoking cessation but can progress to interstitial fibrosis
Effects of tobacco in epthelial lining of resp tract
Metaplasia
Dysplasia
Carcinogenesis
Metaplasia in the resp tract
Noxious tobacco smoke not tolerated by columnar epithelium
Squamous epithelium more resistant to thermal and chemical damage
Consequences of metaplasia in resp tract
Reduced function
Increased propensity for malignant transformation
Is metaplasia in the resp tract reversible
Yes on smoking cessation
What is squamous dysplasia in the resp tract a precursor lesion for
Squamous cell carcinomas
What is squamous dysplasia in the resp tract characterised by
The presence of disordered squamous epithelium w/ loss of pleomorphism
Most frequently diagnosed major cancer in the world
Lung cancer
Also most common cause of cancer mortality worldwide
What % of lung cancers are in active smokers or those who’ve stopped recently
80%
What age is lung cancer most common in
40 and 70yrs w/ peak incidence in 50s/60s
Prognosis of lung cancer
Poor - survival <50%
Other factors affecting lung cancer
Industrial exposure - asbestos, uranium , arsenic, nickel Radiation Air pollution Molecular genetics EGFR mutations
Types of lung tumours
90-95% are carcinomas
5% carcinomas
2% mesenchymal and other types
Classical features of squamous cell carcinomas
Malignant cells w/ keratinisation and intercellular bridges
Pathological feature for lung adenocarcinomas
Gland or duct formation w/ mucin
Lung tumours of seromucinous glands
Salivary type tumours such as mucoepidermoid carcinoma and adenoids cystic carcinoma
Lung tumours of blood vessels
Haemoangiomas
Lung tumours of mesothelium
Mesothelioma
Determining if a lung mass is a metastasis
Lung is a common site
Can see single lesions but often multiple, well circumscribed nodules
Common cancers that may metastasise to lung
Colorectal Renal Breast Melanoma Direct spread from oesophagus
Dx of lung cancer
Bronchial washings and brushings
EBUS TBNA
Lung biopsy
Bronchial biopsy
EBUS TBNA
Endobronchial ultrasound guided transbronchial (fine) needle aspirations
Reporting of lung excisions - providing prognostic info
Type of tumour Size Margins Pleural involvement Vascular invasion Involvement of adjacent structures e.g. hearts, pericardium, diaphragm Lymph node involvement
Types of air movement in lung
Convection
Diffusion
What part of the conducting zone is most susceptible to collapse during expiration
Bronchioles and alveolar ducts
What does the pulmonary arteries carry
Deoxygenated mixed venous blood from RV to alveoli of lungs
Where does blood drain from the lungs
Pulmonary vein and azygous vein
Minority of blood in bronchial veins
Systems innervating resp tract
Cholinergic
Adrenergic
Peptidergic
Cholinergic effect on smooth muscle of bronchioles
Constrict
Adrenergic effect on smooth muscle of bronchioles
Dilate
Petidergic effect on smooth muscle of bronchioles
Dilate
Spirometry
Method for studying pulmonary ventilation
Tidal volume
Volume of air inspired or expired w/ each normal breath (500ml)
Inspiratory reserve volume
Extra volume of air that can be inspired over and over normal TV (2500ml)
Expiratory reserve volume
Extra volume of air that can be expired by forceful expiration after end of normal TV (1100ml)
Residual volume
Volume of air remaining in lungs after most forceful expiration (1200ml)
Calculating total lung capacity
IRV + TV + ERV + RV
Factors affecting IRV
Current lung volume Lung compliance Muscle strength Comfort Flexibility of the skeleton Posture
Lung compliance
Measurement of lung expandability
Does all the air that is breathed in reach gas exchange area
No - some fills resp passages
Dead air space - 150mls
Intrapulmonary pressure
Pressure in alveoli, which rises and falls during respiration but always equalises w/ atmospheric pressure
Muscles that arise from the rib cage
External IC
Sternocleoimastoid
Anterior serrati (lift many ribs)
Scaleni (lift 1st 2 ribs)
Muscles moving lower rib cage
Abdominal recti
Internal IC
In which ways can lungs be expanded and contracted
Downward (inspiration) and upward (expiration) movement of diaphragm
Elevation and depression of the ribs to increase the diameter of chest cavity
Transpulmonary pressure
Pressure difference between alveoli and pleura
What is lung compliance determined by
Elastic force of the lung tissue itself
Elastic fibres caused by surface tension of fluid lining alveoli
Lung compliance in pulmonary fibrosis (restrictive lung disease)
Decreased –> smaller changes in lung volume for small changes in trans pulmonary pressure
How does decreased lung compliance affect pts breathing
More shallowly and rapidly
How does decreased lung compliance affect spirometry measurements
Decreases seen in RV, FRC, TLC
How does lung compliance change in emphysema
Increases –> larger changes in lung volume for small changes in trans pulmonary pressures
How does increased lung compliance affect pts breathing
Pts breathe more slowly and deeply
How does increased lung compliance affect spirometry measurements
Increases seen in RC, FRC, TLC
Lung compliance in c/c bronchitis
Normal but will still see increases in RV, FRC and TLC
If 2 alveoli are connected but have diff diameters, where will the air flow
From small to large
Alveolar macrophages and surfactant
Help degrade surfactant
Type II pneumocytes take up rest and recycle or destroy it
Role of lung surfactant
Increased lung compliance so easier to inflate
Reduces pressure and fluid accumulation in alveoli
Helps keep alveoli’s size relatively uniform during resp cycle
How does airway resistance change w/ disease
Increases in disease
At any given lung volume, resistance in COPD is higher
What is the glottis formed by
Vocal cords (folds)