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Supporting life block > COPD: Clincal presentation&pathophysiology > Flashcards

COPD: Clincal presentation&pathophysiology Flashcards

1
Q

What causes COPD?

A
  1. ) Tobacco smoking (active& passive)
  2. )Biomass fuel exposure
  3. ) Occupational exposures (organic&inorganic dusts, chemical agents, fumes)
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2
Q

Oxidative stress may result in the pathological changes of COPD; what can prevent this oxidative stress?

A
  • Antioxidants

- Antiproteases

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3
Q

How can inflammation present in COPD

A
  • Increased neutrophils, macrophages and T cells (CD8>CD4) in the lungs
  • Extent of the inflammation related to the degree of airflow obstruction
  • Inflammatory pattern is markedly different from asthma-eosinophilic inflammation
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4
Q

Describe some inflammatory mediators involved in inflammation

A
  • Leucotriene B4- neutrophil and T cell chemoattractant
  • Chemotactic factors e.g IL-8 and growth related oncogene alpha. Amplify pro-inflammatory responses
  • Pro-inflammatory cytokines e.g TNF-alpha, IL-1Beta and IL-6
  • Growth factors e.g TGF-Beta, cause fibrosis in the airways
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5
Q

What are the sources of oxidative stress contributing to COPD

A
  • cigarette smoke

- reactive oxygen&nitrogen species from inflammatory cells

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6
Q

What is the role of oxidative stress in COPD

A
  • Markers of oxidative stress are increased in stable COPD (further increased in exacerbations)
  • Oxidative stress: inactivates antiproteases; stimulates mucus production; amplifies inflammation by enhancing transcription factor activation (e.g NF kB) and gene expression of pro-inflammatory mediators
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7
Q

Describe the pathophyisology of the airway involved in COPD in terms of mucus hypersecretion

A
  • There’s hypertrophy and hyperplasia of bronchial submucosal glands
  • increased number of goblet cells in bonchioles
  • destruction of cilia, therefore there’s a difficult expectorating as the sputum gets stuck
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8
Q

Describe the pathophyisology of the airway involved in COPD in terms of the airways

A
  • Narrowing of airways: due to remodeling, starting with smaller airways <2mm
  • Increased airways resistance
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9
Q

Why are the smaller airways more susceptible to narrowing?

A

They don’t have cartilage keeping them open.

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10
Q

Describe the pathophyisology of the airway involved in COPD in terms of the lung parenchyma

A
  • Proteolytic enzymes destroy alveolar tissue
  • Elastin &collagen are destroyed (reduced elasticity and structural integrity of the lungs, leading to a loss of elastic recoil.
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11
Q

Airflow obstruction, loss of lung elasticity, loss of alveoli and airway inflammation are all associated with COPD. What presentations of the disease do these bring?

A
  • Expiratory flow limitation
  • decreased elastic recoil of lungs
  • decreased gas exchange
  • Hyperinflation
  • Sputum production
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12
Q

What clinical features does COPD give?

A
  • Dyspnoea
  • Exercise limitation
  • Wheeze
  • Sputum
  • Increased RR
  • Accessory muscle use
  • Reduced chest expansion
  • Barrel chest
  • Reduced breath sounds
  • Asterixis
  • Cyanosis
  • Cor pulmonale
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13
Q

What are the extrapulmonary features of COPD?

A
  • Weight loss
  • Muscle wasting
  • Cardiovascular comorbidities
  • Depression
  • Osteoporosis
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14
Q

What do we use to diagnose COPD?

A
  • symptoms

- spirometry (needs to be obstructive)

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15
Q

How do we assess the severity of COPD?

A
  • %FEV1 predicted

- symptoms

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16
Q

Outline the significance of compliance in various respiratory diseases.

A
  • Stiff lungs have low compliance( high elastic resistance)
  • Lung fibrosis (scarred/stiff)=low compliance, increased lung recoil, reduced FRC
  • Emphysema (tissue destruction/floppy)= high compliance, floppy lungs, reduced lung recoil, increased FRC(barrel chest)
  • Asthma doesn’t usually affect compliance
17
Q

What is FRC

A
  • Functional residual capacity
  • The volume of air present in the lungs at the end of passive expiration.
  • At FRC, the opposing elastic recoil forces of the lungs & chest wall are in equilibrium and there’s no exertion by the diaphragm or other respiratory muscles.
18
Q

What is the likely state of the lungs of a patient with COPD?

A
  • Hyperinflated
  • FRC& RV are increased
  • so gas trapping occurs in expiration
19
Q

What is the consequence of an expiratory flow limitation (EFL) in tidal breathing?

A
  • RR increases during exercise
  • FRC increases despite expiratory muscle activity
  • Inspiratory capacity and inspiratory reserve volume decreases
20
Q

Outline 3 differences between a healthy lung and a lung of a COPD patient.

A
  • Reduced recoil
  • Reduced tethering
  • Increased airways resistance
21
Q

Describe the limitation of expiratory flow in a COPD patient

A
  • Expiratory flow limitation occurs when flow doesnt increase with increasing expiratory effort
  • In COPD this can occur during tidal breathing
  • Since maximum expiratory flow is reached during tidal breathing, the minimum time for lung emptying is fixed (so you can’t empty lungs faster by pushing harder in expiration)
  • This results in a trapped volume
22
Q

What is dynamic hyperinflation (DH)?

A

a phenomenon that occurs when a new breath begins before the lung has reached the static equilibrium volume.

23
Q

What are the consequences of DH?

A
  • Forces COPD patients to breathe at higher lung volumes
  • Lower lung compliance
  • Higher work of breathing
  • Limitation of tidal volume expansion
24
Q

Describe the neural respiratory drive of a person with COPD

A
  • There’s an increased respiratory load

- There’s a reduced muscle pump capacity(due to hyper inflammation and functional diaphragm weakness)

25
Q

How may someone with COPD present?

A
  • Increased RR
  • Accessory muscle use
  • Wheeze
  • Reduced chest expansion
  • Barrel chest
  • Reduced breath sounds
  • Asterixis
  • Cyanosis
  • Cor pulmonale
26
Q

How may pulmonary hypertension develop in someone with COPD?

A
  • Chronic hypoxia leads to pulmonary vasoconstriction which leads to pulmonary hypertension
  • Muscularisation, intimal hyperplasia,fibrosis and obliteration may also cause pulmonary hypertension
27
Q

What may be the consequence of pulmonary hypertension

A
  • May cause cor pulmonale, leading to death
  • May also result in oedema
  • oedema may also be caused by renal and hormonal changes
28
Q

What is the function of the bronchial mucinous glands?

A
  • Responsible for the production of most of the mucus

- Present in the main bronchi

29
Q

What happens to the bronchial mucinous glands (in the main bronchi) in COPD

A
  • smoke causes exposure to irritants & chemicals

- These irritants and chemicals cause hypertrophy &hyperplasia of the bronchial mucinous glands

30
Q

What is the function of the goblet cells

A
  • mucous production

- Present in the smaller airways

31
Q

What happens to the FEV1/FVC ratio of a COPD pt

A
  • FEV1 decreases significantly more than FVC decreases
  • Result is a much lower FEV1/FVC ratio
  • The normal FEV1/FVC ratio is~ 70-80% in normal adults; a value <70% indicates airflow limitation & possible COPD
32
Q

What is the role of age in COPD

A

-COPD is favoured by age of onset>35yrs

33
Q

How is chronic bronchitis defined

A

chronic cough, sputum production on most days for 3 months of 2 successive yrs

34
Q

Explain the distinction between the terms ‘blue bloaters’ and ‘pink puffers’

A
  1. ) BLUE BLOATERS= mostly chronic bronchitis
    - have a decreased alveolar ventilation
    - low pao2 and high paco2
    - cyanosed
    - not breathless
    - may develop cor pulmonale
    - Their resp. centres are very insensitive to co2
    - supplementary oxygen should be given with care cos they rely on their hypoxic drive
  2. )PINK PUFFERS=mostly emphysema
    - near normal pao2
    - normal/low paco2
    - increased alveolar ventilation
    - not cyanosed
    - breathless
    - may progress to type 1 respiratory failure

Supporting life block (28 decks)

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