Obstructive Lung Disease Flashcards
How is the left bronchus vs. the right bronchus?
Left is narrower/longer (5 cm vs. 2 cm)/more horizontal
*meaning foreign bodies more likely to enter the right bronchus
What is the characteristic epithelium of bronchorespiratory?
Pseudostratified ciliated columnar epithelium
What comprise the alveolar wall and what are the fxns?
Type I pneumocytes: cover 95% of alveolar surface
Type II pneumocytes: Produce surfactant and repair alveolar epithelium
What is COPD and what are examples?
Diseases that cause obstruction to outflow out of the lungs
Examples:
Emphysema
Chronic bronchitis
Asthma
Bronchiectasis
Describe Obstructive
Airway disorder- trachea to terminal bronchiole
Increased resistance to air fllow and limited expiratory rate son forced expiration
Reduced FEV1:FVCratio
Describe Restrictive
Parenchymal disorder- respiratory bronchiole alveoli, and alveolar ducts
Decreased expansion with reduced total lung capacity, O2 diffusing capacity, lung volumes, and compliance
Increased FEV1:FVC ratio
What is emphysema
Causes?
Types?
Permanent enlargement of all or part of teh respiratory unit (respiratory bronchioles, alveolar ducts, alveoli) accompanied by wall destruction without obvious fibrosis.
Causes: Smoking/Air pollution/ Alpha1-antitrypsin deficiency
Types: Centriacinar (centrilobular) in 95% of cases and Panacinar
What is the pathogenesis of emphysema?
Increased macorphages, CD8+ T lymphocytes, and neutrophils
Tissue damage (From cigarette smoke) activate neutrophils and macrophages
Elastase and free radicals are then released. (anti-elastase [aka alpha1-antitrypsin] and anti-oxidants go down)
Destruction of elastic tissue
Consequential increased compliance and decreased elasticity
Why is destruction of elastic tissue as seen in Emphysema bad?
Because it keeps airway lumens open by applying traction. It’s destruction collapses airways on expiration.
What type of emphysema do you see in smoking?
Centriacinar emphysema
So the apical segment of upper lobes are affected.
How does smoking cause emphysema?
Free radicals deplete the normal levels of antioxidants in the lung.
This oxidative injury also inactivates native antiproteases (fxnal alpha1-antitrypsin deficiency)
What does alpha1-antitrypsin deficiency cause?
How does it occur?
Where does it happen?
Why does it happen here?
Panacinar emphysema.
This can be genetic (autosomal dominant. Phenotypes assoc with severe deficiency have marked underproduction of the enzyme in the liver)
or
acquired (cigarette smoking)
Affects the lower lobes/all parts of the respiratory unit are affected by elastic tissue destruction
There is total lack of antiproteases throughout the acinus bu thte lower lung distribution is where perfusion and neutrophil numbers are the greatest.
What are clinical findings of Emphysema
Chest x ray findings?
Severe and early onset of dyspnea
Pink puffers
Coexistence w chronic bronchitis (Smoker’s emphysema)
Cor pulmonale-less common than in chronic bronchitis
Diminished breath sounds due to hyperinflation
Increased AP diameter
Hyperlucent lung fields
Vertical heart
Depressed diaphragm
What are other types of emphysema?
Paraseptal emphysema
- Subplueral involvement
- Spontaneous pneumothorax
- No COPD
Irregular emphysema
- Localized, scar associated
- No COPD
What is chronic bronchitis?
What causes it?
What is the pathogenesis?
Chronic Bronchitis is productive cough for at least 3 months for 2 consecutive years
Cause: smoking, Cystic fibrosis
Pathogenesis:
Inhaled smoke/irritant, causes mucous hypersecretion in bronchi, leads to airflow obstruction in termiinal bronchioles (making this more proximal than emphysema) leading to irreversible fibrosis of terminal bronchioles
Then made worse by infections these patients suffer. Maintining this disease and causing acute exacerbations.
Bronchospasms contribute to this process.
What are clinical findings of chronic bronchitis
Chest x ray findings?
Productive cough
Cyanosis
Blue bloaters
Dyspnea
Expiratory wheezing and rhonchi
Cor pulmonale (congestive heart failure occuring earlier in the disease than in emphysema)
in CXR: Enlarged heart, horizontally oriented
Increased bronchial markings
Gross findings in morphology of chronic bronchitis?
Other findings?
Hyperemia, swelling and edema of mucomembranes
Mucinous and mucopurulent secretions
Chronic inflammation of airways and increased mucous glands
Thickening of walls (narrowing of bronchiolar lumina)
What is the Reid index?
Ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage.
In Chronic bronchitis the reid index is closer to one due to the larger mucous gland thickness
What is bronchiectasis
Permanent destruction and dilatation of bronchi and bronchioles. Destruction involves cartilage and elastic tissue
Causes: Cystic fibrosis (one of the main causes)
Infections (TB/Adenovirus/Hinfluenzae/Staph Aureus)
Bronchial obstruction
Primary ciliary dyskinesia
Allergic bronchopulmonary aspergillosis
clinical findings and CXR of bronchiectasis?
Copious sputum
Hemoptysis
Digital clubbing
Cor pulmonale
CXR: **Bronchial markings extending to the periphery of the lungs **
How does cystic fibrosis happen?
Autosomal recessive inheritance, mostly in caucausians few AZN or African americans
Deletion on chromosome 7, with 3 nucleotides coding for phenylalanine.
Defective CF transmembrane conductane regulator for chloride ions
Increased NA and water reabsorption from luminal secretions and decreased Cl secretions from epithelial cells into lumen. This causes dry and thick secretions.
Dehydration of body secretions due to lack of NaCl. (this affects bronchioles, pancreatic ducts, bile ducts, meconium, seminal fluid)
What are clniical findings in Cystic fibrosis?
What ussually happens
Nasal polyps
Respiratory infections (p aeruginosa, staph aureus, h influenzae)
Malabsorption
Type I diabetes mellitus
Infertility in males
Meconium ileus
Secondary biliary cirrhosis
Usually the respiratory infections followed by secondary biliary cirrhosis
GRoss and microscopic findings of Bronchiectasis (cystic fibrosis)
Gross: Bilateral lower lobes, distal bronchi, and bronchioles
Dilated airways which can be followed out to teh pleural surfaces
On cut surface the dilated bronchi appear as cysts filled with mucopurulent secretions
Micro: Intense acute and chronic inflammatory exudate in bronchial walls, necrotizing ulceration
Squamous metaplasia of bronchial epithelium
Lung abcesses may be present
Fibrosis of bronchial walls leading to bronchiolitis obliterans
Cultures are usually postiive
