81 Flashcards
Causes of disease
I DIVINE TIME Congenital/Genetic • Acquired – Infectious – Degenerative – Inflammation/Immune reactions – Vascular – Iatrogenic • Drugs • Surgery • Radiotherapy – Neoplastic – Environmental – Trauma – Idiopathic – Metabolic – Endocrine
Difference between a bronchus and a bronchiole
Bronchioles lack cartilage
Acinus
Respiratory bronchiole
Alveolar ducts
Alveolar sacs
Alveoli
Lobule
3-5 acini
Epithelial lining of airways 1 2 3 4
Tall, columnar, pseudostratified, ciliated.
Goblet cells
Neuroendocrine cells
Basal cells
Cells comprising normal alveoli 1 2 3 4 5
Alveolar macrophages Type I, II pneumocytes Fibroblasts Inflammatory cells Endothelial cells
Examples of obstructive lung disease
1
2
3
Asthma
COPD (chronic bronchitis, emphysema, small airways disease/chronic bronchiolitis
Bronchiectasis
Examples of restrictive lung disease 1 2 3 4
Idiopathic pulmonary fibrosis
Pneumoconiosis
Sarcoidosis
‘Honeycomb lung’
Spirometry of obstructive lung disaese
Decreased FEV1, normal FVC
Spirometry of restrictive lung disaese
Decreased FEV1, decreased FVC
Obstructive lung diseases associated with smoking
Emphysema
Chronic bronchiolitis
Small airway disease
Collectively called COPD
How is asthma diagnosed?
Physiologically and clinically, not histologically
Different types of asthma
1
2
Atopic/allergic (increased serum IgE, specific external allergens)
Non-allergic asthma (normal serum IgE, non-specific triggers)
Acute phase of asthma
1
2
3
Increased vascular permeability leading to oedema
Increased mucus production
Bronchospasm
Late phase of asthma
1
2
3
4-8 hours later.
Chemotaxis of eosinophils, mast cells, lymphocytes, macrophages. This leads to ongoing inflammation.
Epithelial damage
Which aspects of acute phase asthma do bronchodilators work on?
Only on bronchospasm (smooth muscle)
Which aspects of late-phase asthma do bronchodilators work on?
None (patient can have early symptoms relieved, but then get worse when late-phase response begins kicking in)
Short-term complications of asthma
1
2
3
Death
Atelectasis
Spontaneous pneumothorax and/or pneumomediastinum (rare)
Long-term complications of asthma
1
2
Airway remodelling (fibrosis and irreversible obstruction) Chronic hypoxia leads to pulmonary hypertension leads to cor pulmonale
Cor pulmonale
Right heart failure from pulmonary artery hypertension from pulmonary artery constriction in response to hypoxia
Status asthmaticus
Acute severe asthma not responding to bronchodilators
Emphysema
Abnormal, permanent enlargement of air spaces distal to
the terminal bronchiole
From destruction of the alveolar wall
without fibrosis
Types of emphysema 1 2 3 4
Centriacinar (centrilobular, caused by smoking)
Panacinar (panlobular)
Distal acinar (Paraseptal)
Irregular
Aetiology of centriacinar emphysema
Smoking leads to an imbalance between proteases and antiproteases in the lungs.
Smoke leads to recruitment of inflammatory cells which release proteases.
ROS generated by smoke inactivate antiproteases
How does emphysema lead to obstruction?
Loss of elastic recoil
Effect of loss of elastic recoil on the lungs
Loss of supporting elastic tissues around small airways leads to collapse, with dynamic airway collapse on expiration (the harder you try to expire, the more compressed the lungs become)
Complications of emphysema
1
2
3
Hypoxia (caused by airflow obstruction, loss of diffusion capacity (rare, only happens in late emphysema)
Pulmonary hypertension–>Cor pulmonale
Pneumothorax
Bullous emphysema
Emphysema with cysts on the outside of the lung.
Risk of bursting, cause pneumothorax.
More an appearance of the disease, doesn’t tell you anything of pathogenesis
Clinical definition of chronic bronchitis
Persistent cough productive of sputum for
at least 3 months in 2 consecutive years.
No other cause
Pathogenesis of chronic bronchitis
1
2
3
Chronic irritation of large airways by inhaled substances.
Increased mucus production in larger airways.
Airways inflammation, scarring, narrowing in smaller airways.
Histological appearance of chronic bronchitis 1 2 3 4 5
Excessive mucus (hypertrophy of mucus-secreting glands, Reid index over 0.4)
Increased goblet cells
Mild increase in lymphocytes, macrophages and plasma cells, and oedema
Peribronchial fibrosis in small airways
+/-Squamous metaplasia
Complications of chronic bronchitis
Superimposed infective exacerbations (most common complication)
Hypoxia, pulmonary hypertension, cor pulmonale
Squamous metaplasia, squamous dysplasia (premalignant)
Is there squamous epithelium in the lungs?
No. Squamous is tough, impermeable, which is why it’s on the skin, and unsuitable for the lungs
What is small airways disease?
Caused by cigarette smoke
Chronic inflammation, fibrosis, obstruction of terminal bronchioles (<2mm)
Important component of COPD
Differences in parts of lungs affected by COPD diseases
Chronic bronchitis affects large airways.
Emphysema affects acini.
Small airways disease affects very small airways.
Why are bronchodilators often prescribed for COPD?
Because there is a small aspect of bronchospasm to COPD, even though primary problems with COPD are non-responsive to bronchodilators
Two broad types of COPD
Predominant bronchitis and predominant emphysema
Predominant bronchitis
A lot of cough, a lot of sputum, not much shortness of breath.
‘Blue bloaters’ - Tolerate cyanosis better than predominant emphysemics. Become cyanotic, develop cor pulmonale
Predominant emphysema
Not much cough or sputum, a lot of shortness of breath.
Breathe hard, quickly. Look sort of pink because of this (don’t look cyanosed) (‘pink puffers’)
Cause of most smoking-related deaths
COPD
Bronchiectasis
Irreversible, abnormal dilation of bronchi/bronchioles
Appearance of bronchiectasis
Huge, dilated airways present at the lung hila
Pathogenesis of bronchiectasis
1
2
3
Severe destructive inflammation of airways (severe recurrent infection is common)
Loss of surrounding elastic tissue and muscle exceeds contraction of fibrous tissue.
Clearance of organisms and fluid is impaired (bronchiectasis will only get worse)
Causes of bronchiectasis
Necrotising infections (S aureus, influenza, aspergillus)
Obstruction with infection
Cystic fibrosis
Cilia disorders
Contents of dilated airways in bronchiectasis
Pus
Clinical course of bronchiectasis 1 2 3 4 5 6
Severe cough productive of copious amounts of foul-smelling sputum. Episodic fever SOB and cyanosis Cor pulmonale Metastaic infection (rare) Amyloidosis (rare)
Common features of restrictive lung disaese
Chronic, diffuse, non-infectious
Restrictive spirometry
Inflammation and fibrosis in inter-alveolar septa (interstitium)
Idiopathic pulmonary fibrosis
1
2
3
Cause unknown
Interstitial inflammation, fibrosis at varying stages of development.
Mean survival is three years
A restrictive lung disease
