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Block 9 week 3 > Obstructive lung disease - Baker and Parks > Flashcards

Obstructive lung disease - Baker and Parks Flashcards

1
Q

Obstructive lung pathology occurs in what part of the lung?

A

The bronchioles and alveoli.

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2
Q

What is FVC?

A

Forced vital capacity - This is the total volume of air expired after a full inspiration. Patients with obstructive lung disease usually have a normal or only slightly decreased vital capacity. Patients with restrictive lung disease have a decreased vital capacity.

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3
Q

What is FEV and FEV1?

A

FEV is forced expiratory volume.

FEV1 =This is the volume of air expired in the first second during maximal expiratory effort. The FEV1 is reduced in both obstructive and restrictive lung disease. The FEV1 is reduced in obstructive lung disease because of increased airway resistance. It is reduced in restrictive lung disease because of the low vital capacity.

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4
Q

What if the FEV1/FVC ratio?

A

This is the percentage of the vital capacity which is expired in the first second of maximal expiration. In healthy patients the FEV1/FVC is usually around 70%. In patients with obstructive lung disease FEV1/FVC decreases and can be as low as 20-30% in severe obstructive airway disease. Restrictive disorders have a near normal FEV1/FVC.

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5
Q

What is the DLCO?

A

(Diffusing Capacity of the Lung for Carbon Monoxide) – Carbon monoxide can be used to measure the diffusing capacity of the lung. Basically measures the ability of the lungs to transfer gas from inhaled air to RBC’s. The diffusing capacity of the lung is decreased in parenchymal lung disease and COPD (especially emphysema) but is normal in asthma.

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6
Q

What is PEF?

A

Peak expiratory flow. is the maximal flow (or speed) achieved during the maximally forced expiration initiated at full inspiration, measured in liters per minute or in liters per second.

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7
Q

What is TLC?

A

Total lung capacity (TLC) is the maximum volume of air present in the lungs.

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8
Q

What is TV?

A

Tidal volume - the amount of air inhaled and exhaled normally at rest.

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9
Q

What is FEF?

A

Forced expiratory flow (FEF) is the flow (or speed) of air coming out of the lung during the middle portion of a forced expiration. Often measured at intervals 25-75 in Liters per second.

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10
Q

What is RV?

A

Residual volume - air in the lungs after forceful expiration.

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11
Q

A full pulmonary function test measures…?

A
  1. spirometry parameters
  2. body plethysmography - uses Boyle’s law to measure total lung capacity. Once you have TLC you can subtract vital capacity to get residual volume.
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12
Q

What is Boyle’s law?

A

States that the pressure exerted by a gas at constant temperature is inversely proportional to the volume of the gas. P=1/V

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13
Q

What is the main problem in obstructive lung diseases?

A

The patient can breath in a normal amount of air but cannot exhale a normal amount.

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14
Q

What parameters of spirometry would change in obstructive lung disease?

A
  1. FEV1 is decreased
  2. FEV1/FVC is decreased
  3. FEF is decreased
  4. normal to increased TLC (may be increased because RV increases)
  5. increased RV
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15
Q

Along with patient information what is important to look at on a spirometry report?

A

The predicted values. These take into account patient information and give expected values for a person in that condition.

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16
Q

Spirometry generates a flow-volume loop where you look at inspiratory and expiratory flow. What is a classic pattern to see in obstructive lung diseases?

A

A scooped pattern in the expiration portion of the loop.

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17
Q

What are some obstructive lung diseases?

A
  1. COPD - including emphysema and chronic bronchitis
  2. asthma
  3. bronchietasis
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18
Q

Is the prevalence of COPD higher for males or females?

A

Females - most likely due to increase in smoking in this population

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19
Q

What is the biggest risk factor for COPD?

A

Smoking - though only about 10-15% of smokers develop COPD.

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20
Q

What is the definition of Emphysema?

A

It is defined anatomically as:

  1. irreversible enlargement of the airspaces distal to the terminal bronchioles
  2. airspace wall destruction without fibrosis
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21
Q

What are the 4 types of Emphysema?

A
  1. Centriacinar - clinically important
  2. Panacinar - clinically important
  3. paraseptal - rare
  4. irregular - rare
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22
Q

Centriacinar emphysema is associated with what?

A

Heavy smoking and chronic bronchitis.

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23
Q

What is the initial pathology in centriacinar emphysema?

A

Dilation of the proximal acinus of the respiratory bronchioles. Later in the disease the distal portions and alveoli are involved too.

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24
Q

What is the initial pathology in panacinar emphysema?

A

Distention of the alveolus and alveolar duct. The bronchioles will become involved later too. So there is no initial sparing as in the centriacinar type.

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25
Q

What is the most common type of Emphysema?

A

Centriacinar - >95%

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26
Q

What areas of the lungs are affected most in centriacinar emphysema?

A

The apical segments of the upper lobes of the lungs.

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27
Q

What does lung tissue look like grossly and histologically with centriacinar emphysema?

A
  1. Grossly -Large air spaces and walls with black pigment. Possible blebbing
  2. Histo - destroyed alveoli septa
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28
Q

Panacinar emphysema is associated with….?

A

Deficiency in alpha1-antitrypsin enzyme.

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29
Q

What areas of the lungs are most affected in panacinar emphysema?

A

The anterior margins of the lower lung lobes - the bases of the lungs.

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30
Q

What does lung tissue look like grossly and histologically with panacinar emphysema?

A
  1. grossly - large air spaces, possibly blebbing

2. histo - destroyed alveoli septa

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31
Q

How does tissue damage occur in emphysema?

A
  1. Affects the protease-antiprotease imbalance
  2. affects the oxidant-antioxidant imbalance

Basically, smoking increases the amount of ROS’s which directly causes damage and leads to inactivation of antiproteases such as alpha1 antitrypsin (reduces elastase). Neutrophils and macrophages are released due to inflammation and they release elastase which breaks down tissue. If there is a congenital deficiency in alpha1 antitrypsin then the effects are worse. Nicotine can also cause direct tissue damage.

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32
Q

Describe the genetics of alpha1-antitrypsin deficiency.

A

This enzyme is a proteinase inhibitor that is located on the Pi allele of chromosome 14. There are M and Z alleles.

  1. two copies of M allele = normal
  2. one copy of M and one copy of Z = heterozygous and will be asymptomatic except if they smoke then risk increases dramatically
  3. two copies of Z allele = can have panacinar emphysema even without smoking due to severe deficiency in alpha1 antitrypsin
33
Q

With smoking and alpha1 antitrypsin deficiency what happens to the alveoli?

A

Neutrophil and macrophage action causes increased elastase which is not reduced so it causes destruction of elastic tissue and the alveoli expand. They lose the ability to collapse back (lose their elasticity) so air cannot get out effectively.

34
Q

Blebs are very large sacs of air surrounded by thin tissue in severely damaged lungs. What can happen if the bleb pops?

A

A pneumothorax.

35
Q

Why does airspace enlargement/alveoli dilation lead to obstructive physiology?

A

Two mechanisms contribute:

  1. loss of elastic recoil
  2. small airway inflammation leads to - goblet cell metaplasia and mucous plugging, inflammatory cell infiltration, smooth muscle hypertrophy and peribronchial fibrosis
36
Q

What is chronic bronchitis?

A

An obstructive lung disease that is defined clinically as a persistent cough with sputum production for at least three months in at least two consecutive years.

37
Q

Describe the pathogenesis of chronic bronchitis.

A
  1. tissue damage leads to inflammatory cell infiltrate - neutrophils, macrophages and lymphocytes which causes increase in proteases
  2. there is hypertrophy of submucosal glands in the trachea and bronchi leading to hyper secretion of mucous in the large airways
  3. in the small airways there is hypertrophy of goblet cells leading to increased mucous in the small airways too
38
Q

Proteases are released in inflammation by neutrophils and macrophages - name some.

A
  1. neutrophil elastase
  2. cathepsin
  3. matrix metalloproteinase
39
Q

Smoking leads to….?

A

Airway remodeling!!!!

  1. mucous gland hyperplasia
  2. squamous metaplasia and loss of cilia
40
Q

What are the clinical features of Emphysema?

A

A COPD disease:

  1. starts with dyspnea
  2. insidious onset - progressive with slow decline in function
  3. may or may not have a cough
  4. weight loss
  5. barrel-chested, with prolonged expiratory phase
  6. sitting forward, hunched over, pursed lip breathing - to try to get air out
41
Q

What are the clinical features of chronic bronchitis?

A

A COPD disease:

  1. persistent cough with sputum production for at least 3 months in at least two consecutive years initially
  2. productive cough alone for many years and then….. dyspnea on exertion, hypercapnea, hypoxemia, mild cyanosis
  3. often overlapping symptoms with emphysema
42
Q

What are COPD exacerbations?

A

A sudden worsening of COPD symptoms (shortness of breath, quantity and color of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants.

43
Q

How do exacerbations effect the course of COPD?

A

Lung function can decline significantly before symptoms appear. Symptoms can appear faster and the disease can progress faster with many exacerbations.

44
Q

What criteria are used to define COPD?

A

The GOLD criteria - Global Initiative for Chronic obstructive lung disease.

45
Q

What are the GOLD criteria used for defining COPD?

A
  1. a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases
  2. exacerbations and comorbidities contribute to the overall severity in individual patients.
46
Q

Describe how COPD is diagnosed.

A
  1. while suspected clinically, spirometry must be used to make the diagnosis
  2. includes a post-bronchodilator FEV1/FVC ratio of less than 0.70
  3. there are classifications of COPD
47
Q

What are the classifications of COPD?

A

All have an FEV1/FVC ratio of less than 0.7

  1. mild - with predicted FEV1 of greater than or equal to 80
  2. moderate - with a predicted FEV1 between 50-80
  3. severe - with a predicted FEV1 between 30-50
  4. very severe - with a predicted FEV1 of less than 30
48
Q

How are patients at risk for COPD classified?

A

A patient who is at risk has an FEV1/FVC ratio of greater than 0.7 and a predicted FEV1 of greater than or equal to 80. They also have clinical findings of smoking or exposure to pollutants, cough, sputum or dyspnea and a family history of respiratory disease.

49
Q

Can the progression of COPD be slowed?

A

Yes, smoking cessation can slow down the progression - there are always benefits to smoking cessation.

50
Q

How is asthma defined?

A
  1. a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyper responsiveness and underlying inflammation
  2. symptoms are often reversible - unlike COPD
51
Q

Asthma is more prevalent in which sex amongst children?

A

Males. In adulthood prevalence is equal among sexes.

52
Q

When does asthma diagnosis peak?

A

Usually around 3 years of age but can present at any age. Prevalence decreases in adolescence but for some it will return in adulthood.

53
Q

Is asthma progressive?

A

Not usually. If it is mild when it presents it is mild for life, if severe at presentation then it is severe for life.

54
Q

Describe the presentation of an acute asthma exacerbation.

A
  1. Typically lasts several hours unless treated
  2. in some cases may lead to status asthmaticus
  3. presents with chest tightness, wheezing, dyspnea, cough w or w/o sputum production
55
Q

What is status asthmaticus?

A

An asthmatic exacerbation with persistent symptoms lasting for days to weeks. Can result in such severe obstruction as to lead to severe cyanosis and even death.

56
Q

Describe some lab findings in asthma.

A
  1. peripheral blood eosinophilia
  2. Charcot-Leyden crystals in sputum (crystals due to granules released when eosinophils break down)
  3. Curschmann spirals in sputum (whorls of shed epithelium forming spiral shaped mucous plugs)
57
Q

What are the two types of Asthma?

A
  1. atopic

2. non-atopic

58
Q

Describe atopic asthma.

A
  1. most common
  2. Type I hypersensitivity reaction
  3. usually have positive skin tests or RAST for specific allergens
  4. usually have a positive family history
59
Q

Describe non-atopic asthma.

A
  1. less common
  2. associated with hyper irritability of the bronchial tree
  3. usually have negative allergy testing
  4. less likely to have family history
  5. typically more severe and persistent symptoms
60
Q

Describe the early part of the Type I hypersensitivity reaction associated with atopic asthma.

A
  1. within the first 5-30 minutes of TH-4 cell stimulation cytokines are released
  2. IL-4, IL-5 and IL-13 are released and lead to inflammation, IgE production, release of granules from mast cells
  3. overall effects are bronchoconstriction, increased mucous, vasodilation, increased vascular permeability, decreased integrity of the mucous membranes
61
Q

Describe the later part of the Type I hypersensitivity reaction associated with atopic asthma.

A
  1. 2-24 hours after reaction begins
  2. can last for days without additional exposure because inflammatory cascade is set off
  3. increased inflammatory cells - eosinophils, basophils, neutrophils, lymphocytes
  4. continued airway constriction and epithelial destruction
62
Q

Describe the remodeling of the airways that occurs with asthma.

A

Inflammation leads to goblet cell hyperplasia (increased mucus) and smooth muscle hyperplastia (contributes to bronchoconstriction).

63
Q

Non-atopic asthma is immunopathologically the same as atopic but presents differently - how?

A
  1. symptoms often more severe and persistent
  2. typically adult onset
  3. often presents with Samter’s triad
  4. also has local production of IgE - the same as atopic.
64
Q

What is Samter’s triad?

A

Nasal polyps, Asthma and Aspirin sensitivity.

65
Q

What ar some examples of asthma triggers?

A 
allergens
viral infections
medications such as aspirin, beta blockers
exercise
cold air
laughing
weather changes
strong smells
certain food 
air pollution
occupational exposures
hormonal factors - including premenstrual factors, hypo and hyperthyroidism
66
Q

What tools are used to diagnose asthma?

A
  1. Clinical suspicion - symptoms/signs of variable and intermittent airway obstruction
  2. Confirmed by spirometry - decreased FEV1, FEV1/FVC ratio, decreased PEF
  3. symptoms are reversible - 12% and 200 mL improvement in FEV1 15 minutes post-inhalation of beta2 agonist
67
Q

What is a tool that can be used if a patient’s asthma is hard to trigger in the office?

A

Methacholine challenge - give methacholine to reduce the FEV1 by 20% and have the patient exercise, conduct spirometry. Then give beta2 agonist and conduct spirometry again.

68
Q

What are some symptoms of asthma that are used to determine severity?

A
  1. how often are symptoms present
  2. number of nighttime awakenings due to asthma
  3. how often short acting beta2 agonists are used for symptom control
  4. to what extent is normal activity limited
  5. lung function - tested by spirometry
  6. number of exacerbations requiring use of oral systemic corticosteroids
69
Q

Can a person have normal lung function but have asthma?

A

Yes, it they have symptoms- called intermittent asthma.

70
Q

What is bronchiectasis?

A
  1. Permanent dilation of the bronchi and bronchioles
  2. caused by destruction of the muscle and elastic tissue
  3. associated with necrotizing infections
71
Q

Bronchiectasis is associated with ….?

A

Obstruction - possibly by thick mucus, tumor or foreign body. This leads to secretions and bacteria not being cleared. The secretions pool and there is infection and inflammation with destruction of smooth muscle and elastic fibers.

72
Q

Bronchiectasis usually occurs where?

A

Lower lobes and more vertical airways. Can be localized if due to local issue like a tumor.

73
Q

Bronchiectasis leads to….?

A

Dilated airways and cystic appearance of lungs with mucopurulent secretions.

74
Q

What are some conditions that are associated with bronchiectasis?

A 
cystic fibrosis
primary ciliary dyskinesia/Kartagener syndrome
RA
SLE
IBD
post-transplant
bronchial obstruction - foreign body, tumor, mucous
necrotizing pneumonia
75
Q

What are some causes of necrotizing pneumonia?

A
  1. bacterial - TB, Staph aureus, H. flu, pseudomonas
  2. viral - adenovirus, influenza, HIV
  3. fungal - aspergillus
76
Q

What are the clinical features of bronchiectasis?

A
  1. Cough
  2. foul-smelling and sometimes bloody sputum
  3. cough frequent in the mornings because position changes lead to drainage
  4. obstructive symptoms such as dyspnea and cyanosis
  5. orthopnea
  6. occasional severe hemoptysis (is life-threatening)
  7. multiple positive cultures
77
Q

What are some morphological changes associated with bronchiectasis?

A
  1. acute and chronic inflammation in walls of bronchi and bronchioles
  2. desquamation of epithelium
  3. ulcerations
  4. fibrosis
78
Q

Treatment of bronchiectasis often includes what?

A

Chronic, prophylactic antibiotics.

Block 9 week 3 (5 decks)

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