COPD Flashcards

1
Q

Why is there a global increase of asthma?

A

could be because of more diagnosing
or it is actually increasing and we have no reason why

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2
Q

Why is there a global increase in COPD?

A

increased pollution, climate alteration, smoking/ vaping?
Or is it because of more diagnosing?

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3
Q

What do asthma and COPD have in common?

A

They are both airway obstructive
roughly 10% have both asthma and COPD

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4
Q

What are the component of asthma?

A

Reversible

affected site= Large & small airways

Airway hyper-responsiveness

­ Increased mucus

Inflammatory cells
- Eosinophils
- Mast cells
- Th2 lymphocytes

Mediators
- IL-4, -5, cysLTs

Treatment
- Bronchodilators
- Corticosteroids

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5
Q

What are the component of COPD?

A

Irreversible

Affected ‘site’= Airways and lung

Very little AHR
­
Increased mucus

Inflammatory cells
-Neutrophils
- Macrophages
- Tc1 lymphocytes

Mediators
- TNFa, IL-8, LTB4

Treatment, bronchodilators and corticosteroids do not work

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6
Q

What are Tc1 cells?

A

cytotoxic cells (toxic to cells)

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7
Q

What is asthma pathology?

A

bronchoconstriction and mucus

epithelium thrown into folds due to airway constriction

mucus plug in airway lumen

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8
Q

What are the 3 types/ aspects of COPD?

A

chronic bronchitis
Emphysema
Small airway disease

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9
Q

What is chronic bronchitis?

A

mucus hypersecretion
- main bronchus (extrapulmonary) filled with mucus
- smaller diameter airway
- inflammation
- mucus occluded airways

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10
Q

What is another way of saying small airway disease?

A

chronic bronchiolitis

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11
Q

Where else can small airway disease occur?

A

smokers

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12
Q

What is emphysema?

A

destruction of lung parenchyma and alveoli

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13
Q

What does an emphysematous lung look like?

A

no clear defined edges
possibly dark due to cigarette
Self digesting (holes from ‘eating itself’)

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14
Q

When might mucolytic therapy work for COPD patients?

A

mucolytic therapy is thinning of the mucus, so it can be coughed up
- giving temporary relief/ symptom relief (lung function is still bad)

It can work for COPD patients who have more chronic bronchitis than the other aspects of COPD (SAD, emphysema)

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15
Q

What happens during COPD to airways?

A

Mucosal and peribronchial inflammation and fibrosis (obliterative bronchiolitis)

Mucus hypersecretion (luminal obstruction)

Disrupted alveolar attachments (emphysema)

Increase in size of submucosal gland hypertrophal

Goblet cell hyperplasia (more goblet cells)

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16
Q

How many alveolar macrophages per alveoli?

A

1 or 2

17
Q

Do you understand this diagram?

A

protease inhibors are endogenous (we make them ourselves)

18
Q

How does lung function change as someone quits smoking, and does it change depending on when you quit?

A
19
Q

Why is COPD more common in males and the elderly?

A

No link between sex and COPD but men started smoking earlier than women so it’s more common in males

Elderly because you usually start smoking when you’re older

20
Q

What are differences between COPD and asthma?

A

Asthma and COPD are significant causes of morbidity

COPD is a very significant cause of mortality

Asthma is generally an ‘allergic’ disease

COPD associated with cigarette smoking

Each has a particular ‘portfolio’ of inflammatory cells and inflammatory mediators

Current treatment of asthma (bronchodilators and glucocorticosteroids) generally effective

Current treatment of COPD generally poorly effective

21
Q

What is the overall pathology, physiology of COPD?

A

COPD comprises three pathological/pathophysiological features – chronic bronchitis, small airways disease and emphysema

Some features may be more predominant in some patients compared with others

Macrophages, neutrophils, fibroblasts, proteases and oxidants are the ‘major players’ in COPD pathophysiology

Lung function decline in COPD is faster than in non-smokers, and does not return to ‘normal’ upon smoking cessation

22
Q

What are the basic features of asthma?

A

Asthma has airway/bronchial hyperresponsiveness – ‘twitchy’ airways to a variety of ‘triggers’ (e.g. cold air) - as a clinical/pathophysiological feature

Mucus hypersecretion in the airways in asthma may exaggerate airway closure due to bronchoconstriction

Bronchodilators dilate the airways – possibly reducing impact of excessive mucus

23
Q

Describe the linkage between clinical trials and COPD.

A

Clinical trials in COPD require long duration and may have to investigate changes in rate of decline in symptoms (e.g. lung function)

Trials may include different measurement methodologies

Patients would generally have ‘only’ COPD – no comorbidities

Protease inhibitors are in development for COPD because they have theoretical benefit in treatment, but would not be ‘totally’ effective, nor a ‘cure’