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Respiratory > COPD > Flashcards

COPD Flashcards

1
Q

What is the definition of COPD?

A

COPD is characterised by airflow obstruction
- airflow obstruction os usually progressive, not fully reversible and does not change markedly over several months
This disease is commonly caused by smoking

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2
Q

What are the effects of smoking on the airway?

A

Reduction in cilial motility is reduced
Airway inflammation
Mucous hypertrophy and hypertrophy of goblet cells
Increased protease activity, anti-proteases inhibited
Oxidative stress - neutrophils in COPD inflammation, release free radicals which destroy the airway
Squamous metaplasia -> higher risk of lung cancer

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3
Q

What genetic abnormality can cause COPD in families (1-3% of COPD cases)?

A

Alpha-1 antitrypsin deficiency
- lack of a serine protease inhibitor
- SS and ZZ homozygous have clinical disease
Unable to counterbalance the destructive action of neutrophil-protease enzymes in the lung
Smokers get emphysema earlier than non-smokers with this condition (non-smoker = 30-40s)

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4
Q

What is the clinical syndrome of COPD?

A

Chronic bronchitis
- the production of sputum on most days for at least 3 months in at least 2 years
Emphysema
- abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles

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5
Q

What is the pathogenesis of chronic bronchitis?

A

Chronic inflammation and swelling of the bronchial mucosa resulting in scarring, increased fibrosis of the mucous membrane, hyperplasia and hypertrophy of the bronchial mucosal glands and goblet cells, loss of interstitial support (collapsible airways) and increased bronchial wall thickness (obstruction of airflow)

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6
Q

What is bronchiolitis?

A

Chronic bronchitis of the small airways (airways of 2-3mm or less)
- an early sign of COPD
Narrowing of the bronchioles due to mucous plugging, inflammation and fibrosis

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7
Q

Chronic bronchitis is inflammations of the airways, so what cells/mediators cause airway inflammation?

A

Macrophages, CD8 and CD4 lymphocytes and neutrophils
TNF, IL-8 and other chemokines
Neutrophil elastase, proteinase 3, cethepsin G - from neutrophils
Elastase and MMPs - from macrophages
Reactive oxygen species

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8
Q

What are the three types of emphysema?

A

Centri- acinar - damage around the respiratory bronchioles (more in the upper lobes)
Pan-acinar - uniformly enlarged from the level of the terminal bronchioles distally and can cause large bullae
Paraseptal - just affects the peripheral lobules

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9
Q

Which type of empysema is associated with alpha-1 antitrypsin deficiency?

A

Pan-acinar

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10
Q

Name four mechanisms of airway obstruction in COPD.

A

Loss of elasticity and alveolar attachments due to emphysema (airway collapse on expiration) - causes air trapping and hyperinflation
- increased work to breathe causing breathlessness
Goblet cell metaplasia causes mucous to plug the lumen
Inflammation of the airway wall
Thickening of the bronchiolar wall
- smooth muscle hypertrophy and peribronchial fibrosis

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11
Q

How can COPD be recognised on an X-Ray?

A

It appears more black as some of the lung has been destroyed leaving large air pockets
More ribs can be seen above the diaphragm
The diaphragm appears lower and more flattened

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12
Q

What are some of the signs and symptoms of COPD?

A

Anyone who smokes/used to smoke, who is over the age of 35 with the following symptoms

  • exertional breathlessness
  • chronic cough
  • regular production of sputum
  • frequent winter bronchitis
  • wheeze
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13
Q

What would be seen on spirometry to indicate COPD?

A

FEV1/FVC ratio of less than 70% (both of them being reduced)

An FEV1 of 80% or less of the percentage predicated value

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14
Q

List the pharmacological treatments available for COPD?

A

Inhaled bronchodilators for symptom control
- long acting: salmeterol, tiotropium
- short acting: salbutamol
Inhaled corticosteroids - only used in combination with beta2 agonists
- Budesonide and fluticason - combination inhaler
- oxygen therapy
Oral theophyllines - to open the airway
Mucolytics - carbocysteine
Nebuliser therapy

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15
Q

What ‘Endotypes’ could a person have that would direct their COPD treatment?

A

If they have

  • Persistent systemic inflammation
  • Eosinophilic or Th2 high COPD
  • Persistent pathogenic bacterial colonisation
  • Alpha-1 anti-trypsin deficiency
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16
Q

What ‘Phenotypes’ could a person have that would direct their COPD treatment?

A

They could have

  • Frequent exacerbations
  • Persistent breathlessness
  • Chronic bronchitis
17
Q

What is the only intervention that has been shown to alter the progression of COPD?

A

Smoking cessation

- stopping smoking at any age will slow down the progression of COPD and it’s associated complications

18
Q

Describe the natural history of COPD, once the FEV1 percentage predicated value has dropped below 80% and as it continues down.

A 
Dyspnoea  - 75%
Exacerbations - 45%
Deconditioning - 45%
Hospitalisation - 30%
Systemic effects - 30%
Hypoxaemia - 20%
Pulmonary hypertension - 15%
19
Q

What are the main causes of pink puffer and a blue bloater respiratory failure respectively?

A

Pink puffer - normally caused by emphysema

Blue bloater - normally caused by chronic bronchitis

20
Q

What are the signs and symptoms of blue bloater type respiratory failure?

A

Low respiratory drive (type 2 respiratory failure)
- decreased PaO2 and increased PaCO2 concentrations
Cyanosis
Warm peripheries
Bounding pulse
Flapping tremor (increased carbon dioxide concentrations)
Confusion, drowsiness
Right heart failure
Oedema, raised JVP

21
Q

What are the signs and symptoms of pink puffer type respiratory failure?

A

High respiratory drive (type 1 respiratory failure)
- decreased PaCO2 and decreased PaO2 concentrations
Desaturated on exercise
Pursed lip breathing
Use of accessory muscles - fixing the shoulder and the neck
Wheeze
Indrawing of the intercostal
Tachypnoea

22
Q

Pathologically speaking, what is the difference between COPD and asthma?

A

COPD counts as emphysema, chronic bronchitis and/or asthma that limits airflow
- asthma-COPD overlap syndrome (ACOS) can occur when the definition is unsure

23
Q

What are the different inflammatory processes in COPD and asthma?

A

Asthma - reaction to a sensitising agent (reversible)
- T-helper cells
- eosinophilis
COPD - reaction to a noxious agent (irreversible)
- T-killer cells
- Neutrophils
- Macrophages

24
Q

COPD, or asthma: chronic productive cough.

A

COPD

25
Q

COPD, or asthma: breathlessness?

A

COPD - persistent and progressive

Asthma - variable

26
Q

COPD, or asthma: night time waking with breathlessness and/or wheeze?

A

Asthma

27
Q

COPD, or asthma: significant diurnal or day to day variability of symptoms.

A

Asthma

Respiratory (12 decks)

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