COPD Flashcards

1
Q

Give three disease processes of COPD

A

Airway inflammation
Mucus hypersecretion
Tissue damage

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2
Q

Explain the disease process in COPD

A

Cigarette smoke
Alveolar macrophage production
Release of neutrophil chemotactic factors, cytokines (IL-8), mediators (LTB4), oxygen radicals between macrophages and neutrophils
Neutrophils produce proteases
Causes alveolar wall destruction (emphysema) and mucus hypersecretion (chronic bronchitis)

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3
Q

Give the clinical aspects of COPD

A
Chronic symptoms (not episodic)
Smoking 
Non-apotic
Daily productive cough
Progressive breathlessness
Frequent infective exacerbations
Chronic bronchitis - wheezing
Emphysema - reduced breath sounds
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4
Q

What are the elements of the chronic cascade in COPD?

A
Progressive fixed airflow obstruction
Impaired alveolar gas exchange
Respiratory failure 
Pulmonary hypertension
Right ventricular hypertrophy/failure
Death
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5
Q

What non-pharmacological treatment can be given for COPD?

A
Smoking cessation
Physical activity
Stent
Venesection
Lung volume reduction surgery 
Oxygen - domiciliary 
Immunisation
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6
Q

What pharmacological treatment could be given for COPD?

A
SAMA/LAMA - ipratropium/tiotropium
SABA/LABA - salbutamol/salmeterol
LAMA/LABA combination
LABA-ICS combination
PDE4I - Roflumilast 
Mucolytic - carbocisteine
Antibiotics
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7
Q

Name the cells that secrete the main component of mucus

A

Goblet cells

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8
Q

Give 2 types of emphysema

A

Centriacinar and Panacinar

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9
Q

As emphysema advances what does the increase in PaO2 cause?

A
Dyspnoea and increased respiratory rate
Pulmonary vasoconstriction (and pulmonary hypertension)
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10
Q

In what rare genetic condition are there high rates of emphysema?

A

a (alpha) 1 antitrypsin deficiency

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11
Q

What enzymes produced by neutrophils and macrophages is elastic tissue in the lung sensitive to?

A

Elastases

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12
Q

Give 4 affects of tobacco smoke on the body

A

Increases the number of neutrophils and macrophages in the lung
Slows the transit of these cells
Promotes neutrophil degranulation
Inhibits a (alpha) 1 antitrypsin

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