Lecture 25 Flashcards
What does injury to the ciliated bronchial epithelium result in
Degeneration, detachment and exfoliation
What does injury to the ciliated bronchial epithelium follows with
- Inflammation, cell proliferation, cell differentiation and repair
What is the exudate like with injury to the bronchi
- Fibrinous, catarrhal, purulent, fibronecrotci
- Chronic inflammation - also goblet cell hyperplasia and excess mucus production
Explain the chronic injury to the bronchi
Can lead to squamous metaplasia of bronchial epithelium -> breakdown of mucociliary clearance
Goblet cell hyperplasia -> chronic catarhal inflammation
What can chronic bronchitis lead to
- Bronchiectasis
- Pathological and permanent dilation of the bronchus from accumulation of exudates
- Partial destruction of the bronchial wall
- Due to proteolytic enzymes and free radicles from neutrophils and macrophages
Severe Bronchiectasis
Why is the epithelium susceptible to injuty
- High vulnerability to oxidants and free radicles
- Presence of club cells righin antioxidants which generate toxic metabolites
- Alevolar macropages and leukocytes accumulate
What is bronchiolitis
- Classified as necrotizing, suppurative, catarrhal of granulomatous
- In severe injury, the exudate becomes infiltrated with fibroblast and forms microscopic polyps inside the bronchiolar lumen
- May block air flow
What are the chronic injury to bronchioles
- Peribronchiolar lymphoid hyperplasia
- Mild persistent injury
- Goblet cells proliferate and change the properties f bronchiolar secretions
- Goblet cell metaplasia
- Mucous needs to be cleared by coughing
- As there is partial or coplete blockage of the lumen of bronchioles by mucus hypersecretion
- Goblet cells proliferate and change the properties f bronchiolar secretions
- Pulmonary emphysema and atelectasis occur
- CHaracteristically seen in chronic obstructive pulmoary disease
- Recurrent airway obstruction = heaves in horses
What is reccurent airway obstruction in horses
- Haves
- Signs
- Recurrent respiratory distress
- Chronic cough
- Poor atletic performance
- Airway neutrophilia and mucous hypersecretion
What is hypothesis of RAO
Dust paticles upregulate production of cytokines by alveolar macrophages which attracts neutrophils
- Neutrophils induce bronchiolar damage
- Goblet metaplasia
- Preibronchial accumulation of lymphocytes and esinophils and interstitial fibrosis
- Peribronchial fibrosis and epithelial cell hyperplasia are inconsistent findings
- Alveolar emphysema may be present
Goblet cell metaplasia
Alcian blue stain to show mucus
ROA - emphysema
ROA - mucous and exudate in airway
RAO - mucous and exudate in airways
What is feline asthma
- Feline allergic bronchitis/bronchiolitis
- Reccurent bronchoconstriction, coughing or dyspnoea
- Poorly understood
Describe Type I pneumocytes
- Very susceptibleto aerogenousand haematogenous injury -> swelling and vacuolation
- Repair is possible as long as the basement membrane is intact
- Cuboidal pneumocytesproliferate
Describe type Ipneumocytes
- Line the denuded alveolar basement membrane and differentiate into Type I pneumocytes
- In diffuse injury, the proliferating Type II pneumonocytes give the appearance of glandualar structure called - epithelialisation
Pulonary epithelialialisation: proliferating Type II pneumonocytes
What injury to the alveoli
- Loss of type I pneumocytes
- Means damage to blood-air barrier and alveolar capillaries leak plasma
- Alveolar macrophages remove fluid and cellular debris
- If injury is persistent, fibroblasts proliferate leading to intra-alveolar fibrosos
- Extensive alveolar fibrosis seen in toxic and allergic pulmonary disease
- Fibrosis has a major effect on lung function
What is the most important leukocyte in lung inflammation
Alveolar macrophages
- Rapid recruitment and migration of leukocytes into alveoli
- Alveolar fulid contains large amounts of inflammatory mediators
- Large capillary network
- Neutrophils recruited into alveolar spaces within minutes of local and systemic inflammatory response
What is pulmonary oedema
- Protein leakage from flasma into alveoli and formation of fibrin can be rapid
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What is the formation of ‘hyaline membranes’
- Plasma proteins mixed with necrotic Type I pneumonocytes and pulmonary surfactant can form eosinophilic membranes along alveolar septa
Hyaline membranes - cows lung
What is chronic inflammation pneumonia
- Shift from neutrophils to mononuclear cells
- Increased in IL-4, interferon-gamma and interferon-inducible protein to attract lymphocytes and mactophages
- Macrophages and lymphocytes release growth factor
- Recruitment and proliferation of fibroblast
- Fibroblasts and fibrocytes
- Synthesise and secrete large amounts of extracellulat matrix
- Causes fibrosis and obliteration of alveolar spaces
What are the systemic effects of pneumonia
Inflammatory mediators from inflammation of the lungs have effects on other tissues and body systems
What is pulomnary hypertension and right sided heart failure due to
- The effects of increased pulmonary blood pressure in chronic alveolar inflammation and
- The effects of inflammatory mediators on the contracibility of smooth muscle of the pulmonary and system vasculature
What is persistent alveolar injury
- Restoration of alveolar structure does not occur
- Lesions can progress to an irreversible stage
- Tissue can be replaced by fibrous tissue
