Obstructive Lung Diseases Flashcards by Tom O

What is the main problem in obstructive pulmonary disease?

Limitation of airflow in expiration

Increase in resistance due to partial or complete obstruction

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How is the FEV1/FVC ratio affected in obstructive diseases?

FEV1 is reduced

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What are the four main obstructive pulmonary diseases?

Asthma
Chronic Bronchitis
Emphysema
Bronchiectasis

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Which of the obstructive pulmonary diseases are known as COPD?

Chronic bronchitis

Emphysema

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Asthma

What is the main problem? Where are how does the obstruction occur?

Intermittent and reversible airway obstruction

Due to a hyperresponsive tracheobronchial tree

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Asthma

Symptoms

Wheezing
Breathlessness
Chest tightness
Cough

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Why have asthma rates increased dramatically in recent years?

Hygiene hypothesis is one idea (eradication of infections leads to alteration of immune homeostasis)

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What are some stimuli that could induce asthma attacks?

Infections
Environmental irritants
Cold air
Stress
Exercise

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What is Atopic Asthma?

Immune mediated asthma. Type I hypersensitivity rxn involving IgE bound to mast cells.

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What is Non-Atopic Asthma?

We don’t know the cause, but it is presumed to be caused by a hyperreactive bronchial tree

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What drug may cause drug-induced asthma? What symptoms might this cause?

Aspirin

Recurrent rhinitis and nasal polyps
Urticaria

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What may cause occupational asthma?

Need repeated exposure to the irritating agent
Fumes
Organic chemical dusts
Gases

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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

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What is status asthmaticus?

Prolonged hyperinflation of the lungs

May appear with mucus casts plugging up the entire bronchial tree

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What are Curschmann spirals?

Seen in asthma
Degranulated inflammatory cells and dying epithelial cells covered in mucin
Have a spiral architecture

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What are Charcot-Leyden crystals?

They are crystals seen on H&E from the degranulation of eosinophils (bi-lobed nuclei, very pink cytoplasm)

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In chronic asthma, what histological changes would you expect to see?

Thickening of the basement membrane

Smooth muscle changes and hypertrophy

Eosinophils present

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What are some complications of asthma?

Status asthmaticus
Emphysema
Chronic bronchitis
Pneumonia
Bronchiectasis
Cor pulmonale

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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