4 - Chronic Obstructive Lung Disease Flashcards
What is the acinus in the lung?
Distal to the terminal bronchiole.
What are pores of kohn?
Small holes that you can only see on EM.
They allow communication between alveolar spaces.
What is the definition of obstructive lung disease? What are obstructive lung diseases?
Diseases that cause increased resistance to airflow out of the lungs.
Types:
- emphysema
- chronic bronchitis
- asthma
- bronchiectasis
Asthma and bronchietasis are both related to smoking.
What is emphysema? How common is it?
Permanent enlargement of all or part of the respiratory unit (respiratory bronchioles, alveolar ducts, alveoli).
Accompanied by wall destruction without obvious fibrosis.
Affects 5-8% of the US pop, men more than women.
What are the cuases of emphysema? What are the types?
Causes: smoking, air pollution, a1-antitrypsin deficiency
Types:
- centriacinar (centrilobular) - 95% of cases, related to smoking
- panacinar (involved entire respiratory acinus)
What cellular changes occur in emphysema?
Increased number of macrophages, CD8+ T lymphocytes, and PMNS.
PMNs and macrophages are activated by tissue damage from cigarette smoke.
Elastase and free radicals are derived from PMNs and macrophages.
- increased elastase and decreased antielastase (a1-antitrypsin)
- increased oxidants and decreased antioxidants
Destruction of elastic tissue and increased compliance and decreased elasticity.
What happens to elastic tissue in emphysema?
Elastic tissue normally keeps the airway lumen open by applying traction > elastic destruction causes collapse of airways on expiration and prevents exit of air (airflow obstruction).
Describe the difference btween pacinar and centriacinar (centrolobular) emphysema?
Panacinar emphysema: thorughout the whole lung we see dilation. No areas of sparingl; Affects whole acinar unit.
Centra-acinar: scattered foci with dilation of the alveolar spaces and areas of sparing in between; Dark pigment is depositions in the lungs secondary to smoking.
What cause centriacinar vs panacinar?
Centriacinar:“smokers emphysema”; occurs in apical segments of upper lobes (where smoke primarily goes)
Panacinar: a1-antitrypson deficiency, autosomal dominant. PiZZ phenotype associated with severe disease and underproduction of functional antiproteinase in the liver. Affects lower lobes of the lung (increased # of PMNs which make elastase)
What can be seen on liver biopsy and be a clue to an a1-antitrypsin deficiency?
With coexisting liver disease wioth emphysema, you will see globules in hepatocytes.
These are globs of a1-antitrypsin that get trapped in the liver so they have lower levels in other parts of the body such as the lungs.
What are clinical findinds of emphysema? What is seen on CXR?
Clinical findings: dyspnea, pink puffers (hyperventilation to compensate for poor ventilation and typically don’t get deoxygenated), coexistence with chronic bronchitis.
CXR:
- increased AP diameter
- hyperlucent lung fields
- vertical heart
- depressed diaphragm
What do the air spaces look like in emphysema?
Enlargement of air spaces/enlargement of the pores of kahn due to tissue obstruction.
What is chronic bronchitis? How common is it? What are causes?
Productive cough for at least 3 months for 2 consectutive years. Affects 4-5% of the US pop.
Causes: smoking and air pollutants.
What is the pathogenesis of chronic bronchitis?
Inhaled smoke is an irritant causing mucus hypersecretion in bronchi. This leads to airflow obstruction in terminal bronchioles (more in proximal than in emphysema)
Infection can maintain the disease and cause acute exacerbations.
Bronchospasm can occur.
What are clinical findings seen in chronic bronchitis?
- Productive cough
- Cyanosis: due to decreased O2 saturation from hypoxemia
- “Blue bloaters”
- Expiratory wheezing
- Cor pulmonae (enlarged heart)
CXR: enlarged heart and horizontally oriented, increased bronchial markings because of bronchial inflammation
What are the gross findings in chronic bronchitis?
Hyperemia, swelling and edema of mucous membranes.
Mucinous and mucopurulent secretions.
What is seen on histology in chronic bronchitis?
Chronic inflammation of the airways: inflammatory infiltrate - lymphocytes and plasma cells. Increased mucous glands.
What is the reid index? How does it change with chronic bronchitis?
Ratio of thickeness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage (normally 0.4).
With chronic bronchitis there’s thickening of the walls and narrowing of the bronchiolar lumina due to hyperplasia; therefore, the ratio is larger.
What is seen grossly in asthma? What is seen histologically?
Autopsy - hyperinflated lungs. Plump and full because of obstruction of air flow out of the lungs. Also large mucus plugs that obstruct the larger airways.
Microscopically:
- Microscopic mucus plugs in the smaller airways called curshmann spirals.
- Eosinophils
- Charcot leyden crystals - made of protein granules from eosinophils
How does the airway remodel in reasponse to chronic asthma?
Causes increased number of mucus cells, hyperplasia of smooth muscles around bronchiole wall. Increased fibrotic tissue.
What are gross findings of bronchiectasis?
Lower lobes
Dilated airways can be followed to pleural surfaces (usually don’t go out this far)
What are microscopic findings are seen in bronchiectasis?
- Intense acure and chronic inflammatory exudate in bronchial walls, necrotizing ulceration
- Squamous metaplasia of bronchial epithelium
- Hyperplasia of mucus cells
- Lung abcesses may be present
- Fibrosis of bronchial walls leading to bronchiolitis obliterans
