Pathology of Obstructive Diseases Flashcards
What is atelectasis?
Incomplete expansion of the lung of collapse of previously inflated lung
What is the major issue with atelectasis?
Predisposes to infx
What is the resorptive type of atelectasis? What happens to the mediastinum with this?
Atelectasis that follows complete airway obstruction
Mediastinum will shift toward the affected side
What is compressive atelectasis? What happens to the mediastinum with this?
Excessive air, fluid, blood etc in pleural space causing compression
Mediastinum will shift away from the affected lung
What is patchy atelectasis? What usually causes this?
Loss of surfactant, usually post surgical complication
What is contraction atelectasis?
FIbrosis around the lung causing collapse
Which way does the trachea/mediastinum shift with a tension pneumothorax?
Away from the affected lung
What are the two primary causes of pulmonary congestion and edema?
- Hemodynamic disturbances
- Microvascular injury
What happens in ARDS?
Breakdown of capillary cell walls and lung interstitium usually due to sepsis
What are the hemodynamic disturbances that can cause pulmonary edema?
Increased hydrostatic pressure from heart failure
What are the gross characteristics of pulmonary edema?
Heavy, wet lungs
What are the histological characteristics of hemodynamic pulmonary edema? (3)
- Engorgement of alveolar capillaries
- Intraalveolar HF cells
- Fibrosis
What is transudate?
extravascular fluid with low protein content and a low specific gravity (
What is exudate?
any fluid that filters from the circulatory system into lesions or areas of inflammation.
What is the microvascular injury type of pulmonary edema?
Capillaries of alveolar septa. Either the endothelial cells, or the alveolar epithelial cells
What are the localized forms of microvascular injury type forms of pulmonary edema?
Pneumonia and ALI
What is the systemic form of microvascular injury type forms of pulmonary edema?
ARDS
What are the four major obstructive diseases?
- Emphysema
- chronic bronchitis
- asthma
- bronchiectasis
What is COPD?
Emphysema + chronic bronchitis
What is the main feature of obstructive pulmonary disease?
Air cannot get out of the lung efficiently
What is the main feature of restrictive pulmonary disease?
Air cannot get in the lung efficiently
Which of the obstructive diseases is/are reversible?
Asthma
What is the pathophysiology behind emphysema?
Breakdown of the elastin in alveoli, causing overexpansion
Which airways are primarily affected with emphysema?
Small airways–acinus and respiratory bronchioles
Which airways are primarily affected with chronic bronchitis?
Large airways–trachea and bronchi
What is the pathophysiology with chronic bronchitis?
Airway inflammation, causing mucus plugging
What is the pathophysiology behind asthma?
Bronchial hyperresponsiveness
What part of the airways are primarily affected with bronchiolitis? What happens here?
Bronchioles–fibrosis causes airway obstruction
What is the anatomic site affected with asthma?
Bronchi
What is the anatomic site affected with bronchiectasis? What happens here? Cause?
bronchus–breakdown of the airways due to an excessive inflammatory response. Involved bronchi become enlarged and thus less able to clear secretions
What are the ssx of bronchiectasis?
Productive, purulent cough, fever
In which obstructive lung diseases does tobacco play a major role?
Emphysema
Chronic bronchitis
Bronchiolitis
Which of the obstructive disorders primarily present(s) with wheezing?
asthma
Which of the lung volumes increase in obstructive diseases? What causes this?
Residual volume due to obstruction or loss of recoil (as in COPD)
What happens to the FVC1 with obstructive airway disease?
Decreases
What happens to FVC1/FVC with obstructive lung diseases?
Decreases
What happens to TLC and FVC with obstructive diseases?
Normal to increased
What happens to TLC with restrictive diseases?
Decreases
What happens to FVC with restrictive diseases?
Decreases
What happens to FEV1/FVC in restrictive lung diseases? Why?
Normal–both FEV1 and FVC decrease since there is not a problem with getting air out, just how much that can be held
Ssx of emphysema are not apparent until what fraction of the pulmonary parenchyma are incapacitated?
1/3
What is the definition of emphysema?
Irreversible enlargement of airspaces distal to the terminal bronchioles without fibrosis
What are the two major causes of emphysema?
Smoking and environmental pollutants
What is the pathogenesis of COPD?
Smoking causes PMNs to increase in the lungs, which release elastase.
What is notable about macrophages specifically in the role of COPD?
Macrophage elastase is not inhibited by alpha-1-antitrypsin.
Also release metalloproteases
What is the oxidant model of COPD?
Oxidants in cigarette smoke and free radical formation inhibit antiprotease and cause damage
What is the role of alpha-1-antitrypsin?
Inhibits elastase
What are the cytokines that increase PMNs in the alveoli? (3)
IL-8
LTB4
TNF
What causes the cirrhosis with alpha-1-antitrypsin deficiency?
Buildup of protein in the liver
What is the gene that is mutated in alpha-1-antitrypsin?
PiMM goes to PiZZ
What is the major functional difference between smoking induced COPD and alpha-1-antitrypsin induced?
Smoking merely inhibits antitrypsin, while alpha-1-antitrypsin causes a decrease in antitrypsin
What is the stain that highlights antitrypsin in the liver?
PAS
What is the anatomic site of smoking induced emphysema? How about for alpha-1-antitrypsin?
smoking = centriacinar alpha-1-antitrypsin = panacinar
What are the four anatomic locations of emphysema? Which is clinically insignificant?
Centriacinar
Panacinar
Paraseptal
Irregular*-insignificant
What is paraseptal emphysema?
lesion in the distal acinar, adjacent to areas of fibrosis, scarring, or atelectasis
What is irregular emphysema?
Airspace enlargement with fibrosis
What is centriacinar emphysema?
Respiratory bronchioles are fragmented with loss of septal tissue, creating enlarged areas
Where in the lungs is the greatest damage with centriacinar emphysema?
Apical lungs
What is panacinar emphysema?
Acini are uniformly enlarged from respiratory bronchioles to terminal blind alveoli
Where is the lungs is panacinar emphysema most common?
Basilar portions
Which two types of emphysema commonly occur together?
Panacinar and centriacinar
What is distal acinar (paraseptal) emphysema? Where in the lung is this usually found?
Enlargement with destruction of the distal portion of the acinus, worst in the upper lung zones, adjacent to the pleura
What is distal acinar (paraseptal) emphysema usually associated with? Why?
Spontaneous pneumothorax
d/t cyst like structure that form rupturing
What are the histological characteristics of distal acinar (paraseptal) emphysema?
Scarring, fibrosis, or atelectasis
Cyst like structures
What is irregular emphysema?
Acini are irregularly involved, but are scarred and inflamed
What is bullous emphysema? What is the major complication associated with this?
Subpleural emphysematous spaces that are greater than 1-2 cm in diameter
Can give rise to a pneumothorax
What are the three major causes of death from emphysema?
- respiratory acidosis/coma
- Right heart failure
- Massive pneumothorax
What is the treatment for emphysema?
Bronchodilators
Steroids
What is pink puffer?
Pt with severe emphysema, who overventilation but achieves adequate respiration
What are blue bloaters?
Chronic bronchitis leads to hypercapnia and abundant sputum production
What is the clinical definition of chronic bronchitis?
Persistent cough with production of sputum for at least 3 months of year, for 2 consecutive years
What is the most common cause of chronic bronchitis?
cigarette smoking
What is chronic bronchitis? What is it characterized by?
Chronic inflammation of the airways, characterized by hypertrophy of submucosal glands, and goblet cell metaplasia
What is bronchiolitis obliterans?
obliteration of the lumen of bronchioles secondary to fibrosis from chronic bronchitis
What is the Reid index?
Fraction of the submucosa (from BM to the cartilage) that is taken up by glands.
What are the ssx of chronic bronchitis?
Persistent cough and sputum production, leading to outflow obstruction
What are the non-neoplastic complications of chronic bronchitis?
Pulmonary HTN and HF
What are the neoplastic complications of chronic bronchitis?
Squamous metaplasia and dysplasia of bronchial epithelium
What are the two common infectious bacteria that cause chronic bronchitis?
H. Influenza
Strep Pneumonia
What are the two common infectious viruses that cause chronic bronchitis?
Adenovirus
RSV
How does cigarette smoking predispose patients to chronic bronchitis? (2)
Interfere with mucociliary escalator, and directly damaging the epithelium
What is the elastic recoil like in emphysema? Chronic bronchitis?
Emphysema = low Bronchitis = normal
When does a cough usually present with chronic bronchitis? Emphysema? How does this compare to the SOB with each?
Early with bronchitis
Late with emphysema
Flipped for dyspnea
Which can lead to pulmonary HTN: chronic bronchitis or emphysema?
Bronchitis
What are the CXR findings for chronic bronchitis? Emphysema?
Bronchitis = prominents vessels
COPD= hyperinflation
What are the histological changes with chronic bronchiolitis? (3)
Goblet cell metaplasia with fibrous thickening of the wall and increased smooth muscle
What are the long term complications of asthma?
chronic bronchitis or cor pulmonale
What is status asthmaticus?
Unremitting asthma attack
What are the two important questions to ask patients with asthma Why?
Have you been hospitalized or intubated for it
Increased probability of mortality
What is atopic asthma? Non-atopic?
Atopic = Type I hypersensitivity
Non-atopic = idiopathic
What are the cytokines released by Th2 cells in allergic asthma? (2)
IL-4
IL-5
What is the major immune cell response to asthma?
Th2
What is the early phase of allergic asthma?
antigen exposure causes asthmatic attack within 30 minutes
What is the late phase of allergic asthma?
4-8 hours after initial attack, with new cells binding to left-over IgE triggering another attack
Why is the vagal nerve stimulated to cause contraction in asthma?
Destruction of epithelial cells
What are the two findings of asthma with alveolar lavage? What are each of these?
Curschmann spirals = whorls of shed epithelium
Charcot-Leyden crystals = crystalloids of eosinophilic proteins