Obstructive Lung Diseases Flashcards
What is the main problem in obstructive pulmonary disease?
Limitation of airflow in expiration
Increase in resistance due to partial or complete obstruction
How is the FEV1/FVC ratio affected in obstructive diseases?
FEV1 is reduced
What are the four main obstructive pulmonary diseases?
Asthma
Chronic Bronchitis
Emphysema
Bronchiectasis
Which of the obstructive pulmonary diseases are known as COPD?
Chronic bronchitis
Emphysema
Asthma
What is the main problem? Where are how does the obstruction occur?
Intermittent and reversible airway obstruction
Due to a hyperresponsive tracheobronchial tree
Asthma
Symptoms
Wheezing
Breathlessness
Chest tightness
Cough
Why have asthma rates increased dramatically in recent years?
Hygiene hypothesis is one idea (eradication of infections leads to alteration of immune homeostasis)
What are some stimuli that could induce asthma attacks?
Infections Environmental irritants Cold air Stress Exercise
What is Atopic Asthma?
Immune mediated asthma. Type I hypersensitivity rxn involving IgE bound to mast cells.
What is Non-Atopic Asthma?
We don’t know the cause, but it is presumed to be caused by a hyperreactive bronchial tree
What drug may cause drug-induced asthma? What symptoms might this cause?
Aspirin
Recurrent rhinitis and nasal polyps
Urticaria
What may cause occupational asthma?
Need repeated exposure to the irritating agent
Fumes
Organic chemical dusts
Gases
Describe the pathogenesis of Atopic Asthma
Allergen comes in, gets presented to a T cell. Activate a Th2 cell to produce IL-3, IL-5 (Brings in eosinophils), and IL-4 (to induce B cells to make IgE against the allergen)
When the allergen enters again, mast cells with IgE on surface will degranulate quickly, cause bronchoconstriction, and cause mucus cells to release more mucus
What is status asthmaticus?
Prolonged hyperinflation of the lungs
May appear with mucus casts plugging up the entire bronchial tree
What are Curschmann spirals?
Seen in asthma
Degranulated inflammatory cells and dying epithelial cells covered in mucin
Have a spiral architecture
What are Charcot-Leyden crystals?
They are crystals seen on H&E from the degranulation of eosinophils (bi-lobed nuclei, very pink cytoplasm)
In chronic asthma, what histological changes would you expect to see?
Thickening of the basement membrane
Smooth muscle changes and hypertrophy
Eosinophils present
What are some complications of asthma?
Status asthmaticus Emphysema Chronic bronchitis Pneumonia Bronchiectasis Cor pulmonale
What is the clinical definition of Chronic Bronchitis?
Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years
Who is most likely to get Chronic Bronchitis?
Smokers
Urban dwellers (smog)
Middle-aged men
What part of the respiratory system is affected by Chronic Bronchitis?
The larger airways (the bronchi)
Describe the pathogenesis of Chronic Bronchitis
In smokers, the mucociliary escalator will have increased mucus production to trap more irritants. The body will increase production of the glands and they will become thicker. Inflammation and fibrosis occurs. Leads to a productive cough and may lead to obstruction
What are some important consequences of Chronic Bronchitis?
Cor pulmonale with R heart failure
Infections
Bronchogenic carcinoma
What is emphysema?
Destruction of the walls of airspaces distal to the terminal bronchioles, causing PERMANENT ABNORMAL ENLARGEMENT of those airspaces
What are the 4 types of emphysema?
Centriacinar
Panacinar
Distal acinar
Irregular
Centriacinar Emphysema
Who tends to acquire this disease? Where does it happen in the lungs?
Smokers
Upper lobes of the lungs
Panacinar Emphysema
Where does it happen in the lungs?
Lower lobes, more towards the alveolar sacs and alveoli
Panacinar Emphysema
What deficiency is commonly associated with it?
Alpha-1-antitrypsin deficiency
Distal Acinar Emphysema
Where does it happen in the lungs?
Distal acinus, along pleura and lobular septa
Irregular emphysema
Where does it happen in the lungs?
Acini are irregularly involved
No pattern to the dilatations seen
Describe the pathogenesis of Emphysema and the protease-antiprotease theory
Smoking produces free radicals, which activate PMNs. The PMNs release elastase to digest elastin all over the lung. The body’s compensatory mechanism to prevent damage is the release alpha-1-antitrypsin (an anti-elastase). When a person keeps smoking, elastase will be more prevalent than alpha-1-antitrypsin and cause destruction of the acinus and formation of large sac-like structures
How will the alveoli look on histological section with emphysema?
The alveoli will be very distended with large “grocery bag” sacs
Alpha-1-Antitrypsin Deficiency
What is the normal phenotype? What is the abnormal phenotype?
Normal – PiMM
Abnormal – PiZZ
80% of PiZZ pts develop emphysema
Blue bloaters are associated with what disease?
Bronchitis
Pink puffers are associated with what disease?
Emphysema
Bronchitis vs. Emphysema
Which has a productive cough?
Bronchitis (it affects the bronchi, where mucus can be produced)
Bronchitis vs. Emphysema
Which causes more infections?
Bronchitis (more mucus production provides a great place for bacteria to grow)
Bronchitis vs. Emphysema
Which is more likely to cause cor pulmonale?
Bronchitis
Bronchitis vs. Emphysema
Which has worse elastic recoil?
Emphysema
Why do emphysema patients become cachectic?
Pink puffers
Purse their lips for breathing
Work of breathing is increased, so they often get weakness and wasting of the body due to their chronic illness
What is Bronchiectasis?
Permanent dilatation of bronchi and bronchioles caused by destruction of muscle and elastic tissue caused by chronic necrotizing inflammation
Describe the pathogenesis of Bronchiectasis
Obstruction in the airway leads to impaired clearing mechanisms and pooling of secretions distal to that obstruction.
Leads to inflammation of the airway with necrosis, fibrosis, and eventual dilatation
What are two genetic disorders that could lead to Bronchiectasis?
Cystic fibrosis
Kartagener syndrome
What is the pathological issue in cystic fibrosis? How does this cause bronchiectasis?
Chloride channel (CFTR) dysfunction. Cannot bring H2O out into mucus, so you get thick mucus that is difficult to clear from the airways
Autosomal recessive
Kartagener Syndrome
What is the primary pathological issue?
Primary ciliary dyskinesis
Absence/shortening of the dynein arms prevents proper functioning of the cilia
