Obstructive lung disease Blake Briggs, Class of 2017

Introduction Bronchial disease is the second most common type of lung disease in the world. Airway disease is divided up into 2 categories: Obstructive and Restrictive. Obstructive disease: damage is in the bronchioles with impairment of air flow. The inflammation and/or smooth muscle constraction make airways more collapsible and therefore obstructive. Restrictive disease: inflammation and fibrosis is in the lung parenchyma, outside the airways. Restriction of lung expansion due to fibrosis.

Obstructive lung diseases Obstructive: includes asthma, COPD (emphysema, chronic bronchitis), bronchiectasis

Asthma Reversible bronchoconstriction with local inflammation due to some environmental stimulus. Reversible  with acute therapy, inflammation subsides and the airways dilate again. Type I hypersensitivity reaction- IgE binds to mast cells and releases histamine, leukotrienes, and bradykinin- all cause bronchoconstriction. Presentation: cough with wheezing on exam. If the patient is in an acute exacerbation, there will be accessory muscle use and prolonged expiration.

Asthma pulmonary function tests FEV1: The amount of air expired in 1 second after maximally taking in a deep breath. This is decreased because under the high intraluminal pressure of a forced expiration, the weak, inflamed bronchioles will collapse. However, the FEV1 will improve >12% after giving a bronchodilator. This proves that the cause is reversible. FEV1/FVC: This is a ratio between the FEV1 and the FVC, which is the total amount of air expired forcefully after a maximal inspiration. It is normally 70-85% in healthy patients. This will be lowered due to a decrease in FEV1. Tidal Volume: Amount of air inhaled/exhaled at rest. Unchanged or decreased. Total Lung Capacity: Increased. “Air trapping” in lower lungs occurs due to bronchial collapse. Residual Volume and FRC (RV+ERV): Both increased due to air trapping. DLCO: Diffusion capacity. Calculated using carbon monoxide. It measures the ease of exchange at the capillary-alveolar membrane. DLCO is unchanged in asthma. PEF: Peak expiratory flow rate (speed of expiration). <80% means poorly controlled asthma.

COPD: Emphysema Emphysema: destruction of the alveolar air spaces. Pathophysiology: Stressor*  Loss of alpha 1-antitrypsin (degrades elastase)  unregulated elastase destroys elastin  Massive increase in pulmonary compliance *Stressors include: Smoking, inherited Alpha 1 antitrypsin deficiency Diagnosis: hyperinflated “barrel chest” on chest x-ray due to patients breathing at higher lung volumes. Over time the patient will develop a hyperinflated chest that appears to take up the entire chest x-ray picture. Histological pathology: large empty alveoli spaces with loss of type 1 and 2 pneumocytes lining the alveolar walls.

Emphysema PFTs FEV1: decreased and does not reverse with bronchodilators. FEV1/FVC: Lowered. Tidal Volume: Unchanged or decreased. Total Lung Capacity: Increased. “Air trapping” occurs due to alveolar collapse. Residual Volume and FRC (RV +ERV): Both increased. DLCO: Decreased due to loss of alveoli. There will be poor gas exchange as a result.

COPD: Chronic Bronchitis Defined by cough with thick sputum production for a minimum of 3 months within a 2-year period. Pathophysiology: Smoking  hypertrophied mucus glands  mucus hypersecretion which raises airway resistance. Diagnosis: same as emphysematous PFT pattern on previous slide. Histological pathology: high goblet cell count in bronchiole cells. Reid Index: ratio >66% of glands to total bronchial wall thickness.

COPD Treatment Only two therapies to decrease mortality: smoking cessation and O2 therapy When to do home O2 therapy: SaO2 <88% on room air. Therapies which do not reduce mortality but can treat symptoms: albuterol (SABA), LABA, Ach antagonists (“-tropiums”), inhaled steroid. COPD exacerbation: Treatment includes bronchodilators and steroids. Antibiotics are given for moderate/severe exacerbations.

Bronchiectasis Permanent dilation of airways due to chronic inflammation and mucus production. These large, nonreactive airways that are largely clogged with mucus can be a nidus for colonization and infection. Diagnosis: besides symptoms and history, CT will show massively dilated airways. Histological pathology: scarred lung tissue with focal areas of infection and mucus plugs. Causes: Allergic Bronchopulmonary Aspergillosis: Most common in those either immunocompromised or with asthma. Patients will present with brown sputum, and aspergillum fungal ball present on chest x-ray or CT. Treatment: oral steroids, itraconazole Tumor obstruction Infections Cystic Fibrosis (most common cause on boards) Kartagener’s syndrome: Loss of ciliary motility due to defect in dynein. -situs inversus (left side of heart is now on right side of body) -sterility: no sperm motility -bronchiectasis: lack of mucus and particulate clearance

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