Obstructive Pulmonary Diseases

Question 1

Atelectasis 1.) What is it? 2.) How do you diagnose it

Answer 1

1.) collapse/loss of lung volume - Can be segmental, lobar, or the entire lung 2.) CXR: It will show volume loss and opacification (whitening) of the lung

Question 2

What are the different types of atelectasis?

Answer 2

1. ) Primary atelectasis: incomplete lung expansion at birth (rare) - Inadequate surfactant: premature infants with RDS
2. ) Secondary subtypes: >99% are these
   - Resorptive: pneumonia or poor lung ventilation because your cough reflex or neuromuscular circuit isn’t working –> mucus buildup + air resorption –> collapse
   - Compression: pleural fluid or air or anything else is pushing in on the alvolie
   - Contraction: pulmonary shrinkage due to pleural fibrosis/fibrotic pulmonary interstitial disease

Question 3

Failure to relieve atelectasis casues an increased risk of getting what?

Answer 3

Pneumonia - Need to give prophylaxis after anesthesia because they have not been coughing up mucus –> atelectasis –> pneumonia

Question 4

What does atelectasis look like on CXR?

Answer 4

Like lobar pneumonia! It is a consolidated opacity

Question 5

What are the main obstructive pulmonary diseases?

What is the main problem that is occuring?

Answer 5

Asthma

COPD: Chrconic bronchitis, emphysema

Bronchiectasis

Bronchiolitis

Main problem: Obstruction of expiratory airflow

Question 6

What is asthma?

How is asthma different from COPD?

Answer 6

Asthma is obstruction of expiratory airflow due to hyperresponisve bronchi or inflammation of bronchi

Asthma is different from COPD because the airflow obstruction is reversible by inhaler or spontaneously reverts itself

Question 7

Asthma

What are the majority of asthma cases caused by?

What proportion of occupational lung disease is made up by asthma?

Answer 7

Causes:

• 90% of cases: Triggered by allergic/atopic diseases (IgE mediated)
• 10% of cases: Non-atopic/intrinsic (adverse reactions to drugs (aspirin), inhaled irritants, cold, excercise, etc.)

1/3 of occupational lung diseases are asthma

Question 8

Asthma

Symptoms?

Diagnosis?

PFT results?

Answer 8

Symptoms: Classic triad

1. Chronic cough (can be productive or not)
2. Dyspnea
3. Chronic expiratory and inspiratory wheeze

Diagnosis: Clinical based (won’t see anything on CXR), spirometry, methacholine challenge (occasionaly)

PFT: Spirometry

• See FEV1 <80% with symptoms
• FEV1/FVC < 70%
• FEV1 increases >12% with use of bronchodilator

Question 9

10% of COPD patients have asthmatic features and benefit from prednisone and inhaler treatments, why?

Answer 9

They probably have a coinciding asthma with their COPD

Question 10

What are the three general treatments of asthma?

Answer 10

1. Beta-2-agonist –> relief of bronchoconstriction
2. Inhaled corticosteroid (can take an oral or not) –> control and suppress inflammation
3. Third line drugs for recurring cases

Question 11

How does reactive asthma occur?

Answer 11

1. Dendritic cells in the airway mucosa binds allergens –> activation of TH2 cells to secrete cytokines
   - TH2 secrete IL-5 (eosinophil recruitment) and IL-4 (B-cells –> plasma cells)
2. Plasma cells secrete IgE that is specific for the allergen –> binding to mast cells
3. Mast cells and recruited eosinophils degranulate releasing histamine, major basic protein, and eosinophilic cation protein
   - Histamine binds to H1 receptors –> vasodilation, increased permeability of vasculature (edema), increased mucous secretion, activation of vagal efferents (bronchoconstriction)
   - Major basic protein destroys nearby tissue causing chronic damage
4. Bradykinins and increased acidictivate vagus afferent and efferent nerves –> coughing and increased bronchoconstriction

Question 12

What are the complications of asthma?

Answer 12

1. Status asthmaticus: Severe bronchoconstriction that can result in death if you don’t reverse it soon enough
2. Allergic bronchopulmonary aspergillosis: You inhaled A. Fumigatus spores (gungus) and are having an eosinophil reaction that results in plugging of the bronchioles. Eventually it leads to bronchiectasis.
3. Chronic eosinophilic pneumonia

Question 13

What is the definition of COPD?

What is the progression of COPD?

What is COPD overwhelmingly associated with?

Answer 13

1. Definition: Expiratory airflow obstruction that is not fully reversible
2. This is a slowly progressive disease with acute exacerbations intermixed
3. Smoking; 80-90% of those with COPD also smoke
   - Of those who chronic smoke, 15-20% develop COPD

Question 14

What are the two diseases that make up COPD?

How do they relate to asthma?

Answer 14

1. Chronic bronchitis and emphysema
2. These all cause airflow obstruction however COPD does it through irreversible damage to the airways while asthma does it through reversible hypersensitivity reactions

Question 15

What is the etiology of COPD?

Answer 15

Abnormal inflammatory responses to noxious gases and particles (smoking) results in overproduction of mucous secreting cells, damage to the small and distal airways, and bronchoconstriction of the small and distal airways

These factors all come together to create narrowed bronchi/bronchioles that are plugged with mucous constantly. At the same time there can be destruction of the alveoli causing increased reduction in the capacity of airways to work.

Question 16

What are the different patterns of emphysema?

How does this alveoli damage happne?

Answer 16

1. Centriacinar: This is alveolar destruction in the middle of the lobes, typically in the upper lobes.

• *Vast majority of cases

2. Panacinar: Throughout the entire lobe in both the upper and lower lobes

• This can happen in two cases, advanced emphysema or alpha1-antitrypsin deficiency

3. Subleural blebs: This is where the alveoli begins to become hyperinflated and can lead to pneumothorax or a space-occupying mass effect (pushes down on neighboring alveoli)

Alveoli destruction: when neutrophils and macrophages invade the alveoli due to noxious gases/inflammation, they release elastolytic prteinases that destroy the acinar –> large air space enlargements

Question 17

What are the mechanisms of airflow obstruction in …

1. Predominantly bronchitis COPD?
2. Predominantly emphysema COPD?

Answer 17

1. Bronchitis mechanism: Inflammation leads to chronic mucus production –> plugging of alveoli and airways
2. Emphysema mechanism: The respiratory bronchioles’ alvoli have lost their elastic tehring to the bronchioles and the bronchioles collapse as you breath out –> air trapping in the alveoli and unable to recoil –> hyperinflation.

*Most of the time you get a mix of the plugging and gas trapping due to componenets of both bronchitis and emphysema in COPD

Question 18

What are the clinical presentations of COPD?

Answer 18

1. Sedentary lifestyle: The patient will try to avoid exertional dyspnea
2. Gradually progressive dyspnea on exertion: The patient will slowly increase their mucus production and alveoli destruction giving decreased diffusion of gases and clogging of the air
3. Cough with sputum production: Due to mucus production and irritation of the airways from constant inflammation

4. Acute chest illness: due to air trapping and increased mucus buildup but with lack of ciliary movement (the cilia are paralyzed from smoking)

5. Episodic wheezing that resembles asthma, CHF, or bronchiectasis

Question 19

What do you find on physical exam with COPD?

Answer 19

Systemic wasting/weight loss

Hyperinflated lungs with barrel chest –> decreased lung sounds

Use of accessory muscles to breath (neck and intercostals)

Cyanosis

Right heart failure: Chronic hypoxemia –> vasoconstriction of the pulmonary arteries –> increased vascular pressure and cor pulmonale. Shows with peripheral/pedal edema, enlarged/tender liver, and increased JVP

Question 20

How do you diagnose COPD?

Answer 20

1. PFT: Key diagnostic evaluation (do this for all patients with chronic cough, sputum production, or dyspnea at rest/exercise)

FEV1/FVC < 70% + FEV1 < 80%

Does not improve with an inhaler

2. CXR Poor sensitivity
3. CT/HRCT: much more sensitive to detect air space destruction, bleb formation, etc.
4. ABGs:
   - Mild COPD –> mild/moderate hypoxemia (respiratory acidosis) whithout hypercapnia
   - Severe COPD –> worsening hypoxemia with hypercapnia
5. Hemogram: Hypoxemia stimulates erythropoietin production –> polycythemia
   - These patients with chronic hypoxemia might need to be phlebotimized

Question 21

As COPD progresses there are periodics acute exacerbations where bronchiole inflammation is worsened and there is increased cough, dyspnea, and sputum production. What causes these exacerbations?

Eventually the patients can develop cor pulmonale (right heart failure not created by left heart failure), why?

Answer 21

1. 50% of the exacerbations are caused by bacterial pneumonia
   - Moraxella, H. influenza, and Strept. pneumonia are the major organsims that do this
   - Other 50% is triggered by viral infection or miscelaneous insults (increased noxious gases?)
2. Chronic hypoxemia induces pulmonary vasoconstriction –> hypertension –> pulmonary stenosis –> increased right heart pressure –> right heart failure (cor pulmonale)

Question 22

COPD Treatment

1. What are the main principles of chronic treatment?
2. What do you use for acute exacerbations?
3. What is the prognosis for patients > 65 admitted to the ICU with COPD?

Answer 22

1. Main principles of chronic treatment:
   - Smoking cessation*
   - Bronchodilators
   - Inhaled steroids
   - Supplemental O2 if there is hypoxemia
   - Pulmonary rehabilitation
2. Treatment of acute COPD exacerbations: Bronchodilators, antibiotics as indicated, systemic glucocorticoids, O2 supplementation, assisted ventilation
3. 15-30% mortality rate in those >65 years of age admitted to the ICU for COPD (60% mortality at 12 months)

Question 23

Bronchiectasis

1. What is it?
2. What are the symptoms?

Answer 23

1. Bronchiectasis = Permanent dilation of the bronchi/bronchioles
   - Cigarettes do not have a definite causal role!
   - They think that constant bronchial infection allows impairment of drainage/airway obstruction and decrease in host defense
2. Symptoms: Cough, daily mucopurulent sputum for months-years
   - May have dyspnea/wheezing due to the airways collapsing on expiration
3. Associations: Rhinosinusitis and hemoptysis

Question 24

Bronchiectasis

1. What do you see on CT?
2. What are classic disease associations of bronchiectasis?
3. If you see a child with >1 month of respiratory symptoms that you can’t explain, what should you start thinking it is?

Answer 24

1. In the CT scan you would see dilated bronchi (diffuse or focal)
2. Classic associations:
   - Cystic fibrosis presenting in adulthood (mucus plugs everything up)
   - Airway obstruction from foreign body in kids
   - Tumor
   - Chronic/recurrent aspiration
3. A foreign body that has been aspirated into the kid’s lungs

Question 25

What causes the constant infection that forms bronchiectasis?

Answer 25

1. Primary ciliary dyskinesia (Kartagener’s syndrome): the cilia aren’t beating properly –> increased risk of bacteria making it into the epithelial cells/lung parenchyma
2. Pulmonary infection straight up: Mycobacteria, bacteria, viral
3. Connective tissue disease (Rheumatoid arthritis, Sjorgens): Don’t know why
4. Immune deficiencies: Primary or secondary (puts you at risk of allergic bronchopulmonary aspergillosis)

5.Uncertain/unkown (25-50% of cases)

Question 26

How do you treat bronchiectasis?

What is the course like if left untreated?

Answer 26

1. Treatment: Long term antibiotics as indicated
   - Bronchial hygeine is key (making sure their airways are cleared out)
   - If there is acute eacerbation you can try using systemic steroids
   - Surgery for localized disease (tumor)
2. Course if left untreated is grim
   - dyspnea with cyanosis, occasional massive hemoptysis, cor pulmonale, amyloidosis, brain abscess