Lower respiratory tract histology Flashcards
What do respiratory bronchioles represent
A transtional zone in the respiratory system
-involved in both air conduction and gas exchange
Composition of respiratory bronchioles
- simple cuboidal epithelium
- initial segments contain ciliated cells and non-ciliated Clara cells
- distal ends contain primarily Clara cells
Clara cells function
Secrete surface active lipoprotein that prevents luminal adhesion
Location of clara cells (how can differentiate them)
Bulge into the air space
Alveoli-position/structure
Scattered thin-walled out pocketings that extend from the lumen of the respiratory bronchials
- terminal air spaces
- principle sites of gas exchange
What does number of alveolus vary with? What is the range?
- 480 M average, range 270 -790 M
- depending on height of subject + total lung volume
Composition of alveolus
- alveolar septa
- lining alveolar epithelial cells
- network of pulmonary capillaries
Alveolar septae
- network of Type IV collagen fibres and elastin fibres
- form a continuum between the different airways
- within this network of fibers will find network of pulmonary capillaries
Composition of alveoli
- Continuous lining of alveolar epithelial cells (pneumocytes)
- on top of a basement membrane
Two types of epithelial cells in alveoli
1) Type I pneumocytes
2) Type II pneumocytes
Type I pneumocytes function
Gas exchange
Type I pneumocytes structure
Joined by tight junctions
- squamous cells
- large surface area
Role of tight junctions of type I pneumocytes
-prevent escape of large molecules such as albumin into the alveolar space
Pneumocytes -abundance
- represent 40% of entire alveolar lining cells
- covers 95% of alveolar surface
Type II pneumocytes structure
-cuboidal cells
Type II pneumocytes location
tend to aggregate around septal junctions
Type II pneumocytes abundance
- 60% of total alveolar cells
- 5% of alveolar space
Role of type II pneumocytes
- secrete surfactant that lines alveoli and reduces surface tension
- also thought to be stem cells from which type I cells arise
Origin of macrophages
- monocytes that enter the pulmonary interstitium
- migrate between type I pneumocytes and enter the lumen of the alveolus
Role of macrophages
scavenge to remove inhaled particulate matter, bacteria and RBCs (that may enter the alveoli during heart failure)
How to identify aveolar macrophages
Engulfed particulate matter
Gomori aldehyde fuchshin stain
- stains elastic elements purple
- stains collagen orange
Two requirements of gas exchange region
1) Thin enough to permit efficient diffusion of O2 and CO2 across alveolar and capillary walls
2) Strong enough to withstand mechanical forces of lung inflantion, deflation and pulmonary blood flow
Ultrathin barrier of gas exchange region
Because type I alveolar epithelium and capillary endothelium are closely apposed with almost no interstitial space (0.3 um barrier width)
- endothelial cells contain flat parts that are void of organelles (except small vacuole)
- have fairly loose junctins that permit passage of large molecules, macrophages and if stimulated WBC
- type I pneumocytes also very thin cells at this site - cytoplasm devoid of organelles (except small vacuoles)
Mechanical resistance of blood -air barrier
Interstital space composed elastin and collagen fibers
Surfactant of type II pneumocytes composition
lipids and proteins
Location of surfactant
osmiophillic granules (lamellar bodies)
Main histological findings of idiopathic pulmonary fibrosis
- regions of interstitial fibrosis
- inflammation
- honeycombing
What is honeycombing
Destroyed and fibrotic lung tissue containing numerous cystic airspaces
Normal wound healing response vs. IPF
- normal = fibrobalsts migrate to the site of injury
- fibroblasts proliferate and transform into myofibroblasts and synthesize ECM
- once structural integrty restoired pro-fibrotic stage switches off and tissues remodelling occurs through ECM resorption and removal of fibroblass
- IPF = imbalance that favours the pro-fibrotic mediators that promote ECM expansion versus anti-fibrotic mediators that drive process of tissue remodeling
- drive for imbalance may be repetitive epithelial injury (smoking, pollution, infection)
