SFP: obstructive lung disease Flashcards
Describe FVC, FEV1, and FEV1/FVC ratio in obstructive lung diseases
FVC is usually normal, FEV1 is decreased, and the ratio is decreased.
In obstructive lung diseases, people have issues with breathing air ___
Out
What is atelectasis?
Collapse or loss of lung volume due to inadequate airspace expansion aka collapsed lung.
What is resorption atelectasis?
Those in which obstruction prevents distal aeration (mucus plugs).
What is compression atelectasis?
Caused by air or pleural effusions, often in CHF.
What is contraction atelectasis?
They’re adjacent to local or generalized lung scarring; this one is not reversible.
What is asthma?
Acute episodes of bronchospasm; it is episodic.
What is the clinical presentation of asthma?
Episodic dyspnea, cough, wheezing, expiratory whistle.
Describe intrinsic asthma.
Typically develops later in life and is characterized by hyperresponsive airways that respond abnormally to non-immune things like exercise, air pollution, infection, and virus.
Describe extrinsic asthma.
Involves type 1 hypersensitivity to exogenous allergen. It is IgE mediated. Eosinophils and mast cells are the key players!!
What is gross morphology of asthma?
Hyperinflation, bronchial mucus plugs, bullae in severe cases.
What do we see in microscopic morphology of asthma?
- Inflammation: Edema, EOSINOPHILS, other white cells
- Hyperplasia of mucus glands and goblet cells
- Hypertrophy of smooth muscle in airways
- Thickened basement membrane
- Elevated IgE in extrinsic.
When are curshmann spirals and Charcot Leyden crystals seen?
Sometimes seen in asthma.
What is status asthmaticus?
Acute asthma attack that won’t quit; hypercapnia (high CO2 in the blood), acidosis, and hypoxia may occur. This can be fatal.
What is emphysema?
Enlargement of airspaces distal to terminal bronchiole with destruction of the walls.
What is a major cause of centriacinar emphysema?
Smoking.
What is centriacinar emphysema?
Widened airspace in centrilobular region.
What is panacinar emphysema?
Involves the entire acinus.
What genetic deficiency leads to panacinar emphysema?
a1AT deficiency.
What is the inheritance pattern of a1AT deficiency?
Autosomal codominant.
What is the function of a1AT?
It is an enzyme made in the liver that protects tissues from enzymes of inflammatory cells, particularly neutrophil elastase.
Which is more destructive: panacinar or centriacinar emphysema?
Panacinar.
A patient has emphysema, obstructive breathing pattern, and liver dysfunction. What do they likely have?
a1AT deficiency.
What are bullae?
Balloon-like structures bulging out of lungs. Often seen in emphysema or asthma.
What is the presentation of chronic bronchitis?
Productive cough and airway inflammation.
Chronic bronchitis often co-exists with…
Emphysema.
What is required for diagnosis of chronic bronchitis?
Cough with phlegm for 2 years in a row with 3 months in a row each year.
What happens to FEV1 in chronic bronchitis?
It is often reduced.
What is the pathology of chronic bronchitis?
Hyperplasia of mucus secreting glands and increased mucin gene and neutrophil elastase.
What is bronchiectasis?
Permanent distortion/dilation of airways.
What causes bronchiectasis?
Chronic obstruction of bronchi and/or chronic persistent infection.
What are some congenital causes of bronchiectasis?
CF, Ig deficiencies, ciliary immotility syndromes.
What would be microscopic presentation of bronchiectasis?
Peribronchiolar fibrosis and destroyed walls, as well as mixed flora in sputum. Will probably include pseudomonas if it is a CF patient.
What are clinical presentations of bronchiectasis?
Clubbing, hypoxemia, pulmonary HTN.
What is bronchiolitis?
Airway disease occurring in the bronchioles.
What is the microscopic morphology of bronchiolitis?
Edema, fibrosis around and inside the airway, mucus metaplasia (goblet cells appear).
Bronchiolitis is usually caused by…
Viral infection.