Overview of respiratory pathologies Flashcards
How is the respiratory system divided?
- Divided structurallay and functionally into conducting and respiratory airways.
What is the conducting airways comprised of ?
- The nose, pharynx,larynx,trachea, bronchi and bronhcioles
What are the respiratory airways comprised of?
-Respiratory bronchioles, aleveolar sacs, ducts and alveoli
What is the histology of the respiratory wall?
- Innermost layer = epithelium
- varies in structure depending on location
- In conducting airways epithelium made of pseudostratified columnar ciliated epithelial cells
- Have cilia which help move the mucus and trap the particles in the respiratory tract.
- As the respiratory passages get smaller the epithelial cells transition from pesudo stratified columnar cells to simple columnar epithelium- ideal for facillitation of gas exchange.
Describe the divisions of the bronchial tree.
- Starts at the trachea
- T = 12 cm long . Have hyaline cartilage which provide structural support to prevent trachea from collapsing during inhalation etc.
- Bifurcates into the right and left bronchus
- Right bronchus is usually shorter and wider compared to Left main bronchus
- Right main bronchus bifurcates into secondary bronchi
- Left main bronchus - bifurcates into secondary bronchi TO tertiary or segmental bronchi which gives rise to bronchioles.
Describe the histology of the respiratory bronchioles
- Bronchioles are lined with simple columnar epithelial cells
- These transition to simple cuboidal epithelium in the smaller bronchioles and terminal bronchioles
- The number of cillia will decrease
- Cartilage plates in the bronchus are replaced by smooth muscle
- ## Abscence of the cartilage allows them to be more collapsible and responsive to changes in the smooth muscle tone
What is the respiratory bronchiole?
- A branch from terminal bronchioles
- Each respiratory bronchiole branches into 2-11 alveolar ducts that retain a cuboidal epithelium
- Along the walls of the alveolar = single alveoli and numerous alveolar sacs that comprise 2-4 alveoli
- The space at the entrance from the alveolar duct to an alveolar sac = the atrium
Describe the histology of alveoli
- Alevolar duct branches off into several alveoli
- The walls of the alveoli are made up of a single layer of squamous epithelial cells = type I pneumocytes - very thin = rapid gas diffusion
- Type II pneumocytes- connect two alveolar junctions. Cuboidal epithelial cells. Secrete pulmonary surfactant (Helps prevent surface tension and prevents alveolar collapse).
- Alveolar macrophages - clean and sterilise alveolar spaces
What are some host defence mechanisms ?
Uper airways :
- Nasopharynx = nasal hair , mucocilliary apparatus, IgA secretion
- Oropharynx - Saliva. Sloughing of epithelial cells
Conducting airways :
Trachea, bronchi = cough, epiglotic reflexes
sharp- angled branching of airways . Immunoglobulin production (IgG, IgM, IgA)
Lower respiratory tract - surfactant, alevolar macrophages
What are obstructive dieseases?
- Limit airflow due to obstruction. Causes increased airway resistance
- Airway narrowing (asthma), loss of elsaticity (emphysema) or increased secretions (bronchitis/asthma)
What are restrictive diseases?
- Restrict normal lung movement during respiration
- Reduced expansion of lung parenchyma
- Decreased total lung capacity
What is COPD?
- Chronic bronchitis and emphysema often co-exist
- A chronic inflammatory lung disease that causes obstructed airflow from the lungs, distal respiratory tree
- 4th leading cause of death in the UK
- Due to smoking and urban pollution
- Irreversible disease
- Defined clinically rather than morphologically (persistant cough for 3 consecutive moths in at least 2 consecutive years)
- Mucus hyper-secretion in large airways or small airways
- Inflammed bronchus
What is the pathogenesis of chronic bronchitis 3Hs?
3 HS:
- Hypertrophy, Hyperplasia, Hypersecretion
- Hypertrophy and hyperplasia of mucous glands
- Hypersecretion of mucus- increase in goblet cells in the epithelium
- Inflammation - T cells, neutrophils and macrophages (no eosinophils in contrast to asthma)
What is the pathology of chronic bronchitis?
- Goblet cell metaplasia
- Mucus plugs bronchiolar lumen
- Inflammation
- Bronchiolar wall fibrosis
- Luminal narrowing and airway obstruction
What is emphysema?
- chronic condition where air sacs may be destroyed or narrowed
- Located distal to the terminal bronchioles
- Manifested by:
- Permanent dilation of respiratory bronchioles and alveoli
- Destruction of elastic wall tissue without significant fibrosis
What are the different types of emphysema?
-Centri-acinar ot centrillobular
- Panacinar (PA)/ pan lobular
- Para-septal (distal acinar emphysema or peripheral emphysema)
What is panlobular (acinaar) emphysema?
- Dilated alveoli
- More common in lower lobes
- Hereditary (presents earlier)
- Para-septal (Distal acinar emphysema or peripheral emphysema)
What is the pathology of emphysema?
- Destruction of alveolar walls without fibrosis
- Enlarged air spaces
- Number of alveolar capillaries diminishes
- Deformed terminal and respiratory bronchiles and loss of septa
What is the difference between emphysema with and without bronchitis?
-Without bronchitis :
- Shortness of breath (dysponoea), prolonged expiration
- Barrel chest due to use of accessory muscle
- Prolonged onset> 40 years
- Pink puffer - pursed lips breathing
With bronchitis :
- Shortness of breath less prominent
- Patient retains CO2 - Hypoxic and cyanotic
- Blue bloater -cyanotic and tend to be obese
What is asthma?
- chronic inflammation of the airways which results in hyper-responsive airways
- Characterised by a triad of:
- intermittent and reversible airway obstruction
- Chronic bronchial inflammation with eosinophils
- Bronchial smooth muscle hypertrophy and hyper-reactivity
How is asthma characterised ?
By triggers :
1.) Atopic/extrinsic such as seasonal allergens
2.Non-atopic/ intrinsic such as infection,exercise , drugs
Clinical manifestation = shortness of breath, wheeze, chest tightness and cough as a result of reversible airway
What are early and late reactions of asthma?
Early:
- Bronchoconstriction
- Hypersection of mucus leading to plugging of airways
Late reaction:
- Inflammation - activation of leucocytes
- Mucosal oedema and miscle hypertrophy- narrow the lumen
- Epithelial cells produce chemokines to attract more TH2 cells and eosinopjils
- Repeated inflammatipn leads to airway remodelling
What are morphological changes relating to asthma?
- Excess mucus production by gobley cell and glandular hypertrophy
- Bronchial wall oedema due to inflammatory exudate : eosinophil and mast cell accumulation
- Smooth muscle hypertrophy and fibrosis
What is bronchiectasis?
- Permanent dilation of main bronchi and bronchioles
- From pulmonary inflammation and scarring due to infection, bronchial obstruction or lung fibrosis
- Airways then dilate, as surrounding scar tissue (fibrosis) contracts
- Secondary inflammatory changes lead to further destruction of airways
- Symptoms are a chronic cough with dysponea and production of copious amounts of foul-smelling septum
What are the causes of bronchiectasis?
- Obstruction: tumours/foreign bodies/impaction of mucus
- Infection: Necrotising pneumonia, esp.with virulent organisms (TB mixed flora on culture)
- Congenital/ hereditary:
- Cystic fibrosis : production of abnormally viscoid mucus causes obstructionand predisposes to infection
- Immunodeficiency : immunoglobulin deficiencies - predispose to infection
- Kartagener syndrome (immotile cilia syndrome) - impaired mucociliary clearance-stagnation of secretions
What is the pathogenesis of bronchiectasis ?
- Predisposed by two main factors:
- Interference with drainage of bronchial secretions :
- Obstruction of proximal airway, e.g. tumour, foreign body
- Abnormality in the viscocity of bronchial mucus , e.g. cystic fibrosis
- Immotile cilia syndrome, in which cilia are abnormal
- Recurrent and persistent infection weakening bronchial walls
- Predisoosed to reterntion of secretions
- Immunodeficiency states, particularly hypogammaglobulinemia
- In many cases in adults, no cause can be found (idiopathic bronchiestasis)
What is acute respiratory distress syndrome?
- Caused by diffuse alveolar damage as a result :
- Direct (pneumonia/aspiration of gastric contents)
- Indirect (sepsis/severe trauma) lung injury
- Acute inflammation of alveoli, heavily involving neutrophils, rapidly damages capillaries and epithelium
- Imbalance of pro and anti-inflammatory mediators: uncontrolled inflammatuon
- Acute onset of dyspnea and hypoxemia due to vascular leakiness and loss of surfactant affecting gaseous exchange
- High mortality rate (60%)
What is the pathogenesis of acute respiratory distress?
- Damaging stimulus to lung
- damage to alveolar lining cells
- Damafe to capillary endothelium
- Interstitial edema . High protein exudation into alveoli (hyaline membranes)
- Death in acute phase
- regeneration of Type II alveolar lining cells
- Inflammation of interstitium
- Organisation leading to interstitial fibrosis
- Mild local fibrosis : recovery eith minimal residual respiratory dysfunction (0%)
- Marked interstirial fibrosis (honeycomb lung)
- Death due to chronic severe respiratory impairement (20%)
What is IPF morphology?
- Stimulated fibroblasts deposit collagen and ECM excessively for an extended time
- Patchy innterstitial fibrosis that worsens with time
- Fibroblastic foci- become more collagenous and less cellular
- Causes collapse of alveolar walls and formation of cystic spaces - honeycomb fibrosis/honeycomb lung
What is pneumoconiosis?
- Group of fibrosing diseases resulting from exposure (often occupational) to toxix inhaled particulates:
- Asbestos (asbestpsos), silica (sillicosis), coal dust (coal workers pneumoconios)
- 5-10 um particles don’t distal airways
- Immune response stimulated by particles/macrophages travelling in lymphatics
- Lesions consist of pigmented/pale nodules of particle laden macrophages and dense collagen
What are the types of pneumoconiosis ?
- Develops over a long time (Devades) even after exposure is stopped
- Sillicosis and asbestosis associated with increased risk of cancer
- Asbestos workers + smoking often with increased risk of cancer
- Asbestos workers + smoking often leads to carcinoma possible due tp adsorption of carcinogens onto fibers trapped deep in the lung
Acinus
- functional respiratory unit that consists of the resp bronchioles, alveolar ducts, sacs and the alveoli
- contains all parts of resp airways
