Pathophysiology of Respiratory Diseases - COPD and Pneumonia Flashcards

1
Q

What is Chronic Obstructive Pulmonary Disease (COPD)?

A
  • Umbrella term for patients with respiratory diseases e.g emphysema
  • Characterised by a progressive, long-term decline in respiratory function
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2
Q

Outline three possible causes of COPD

A
  • Smoking
  • Exposure to pollution
  • Genetic disorders e.g alpha-1-antitrypsin deficiency
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3
Q

Why is smoking considered dangerous?

A
  • Contains harmful chemicals which cause acute damage
  • Repeated exposure can cause irreversible injury
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4
Q

Outline COPD inflammation.

A
  • Tobacco smoke causes acute local inflammation due to tissue damage
  • Immune cells, such as neutrophils and macrophages, are attracted to damaged tissues
  • These cells release proteolytic enzymes to breakdown dead cells and attempt to resolve inflammation. However these enzymes can also degrade structural proteins
  • Smoke contains chemicals that inactivate antiproteases. Protease burden increases and tissue damage also increases.
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5
Q

What is the effect of an impairment in mucociliary clearance due to smoking?

A
  • Cilia are damaged
  • Increased secretion of mucus
  • Increases likelihood of further respiratory infections - causing further inflammation
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6
Q

What is the effect of long-term tissue damage?

A

Tissue remodeling
- Reduced ventilation and gas exchange

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7
Q

What is chronic bronchitis?

A

Long-term inflammation of the airways

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8
Q

What is the main effect of chronic bronchitis?

A
  • Coughing due to irritation of sensory neurons
  • Mucus hypersecretion due to stimulation of mucus glands
  • Weakened airway structure due to degradation of elastin by proteases
  • Decreased luminal area - increased resistance to airflow.
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9
Q

Why are asthma treatments such as salbutamol less effective for COPD?

A
  • In asthma, airway lumen size is reduced by smooth muscle contraction
  • In COPD, airway lumen size is reduced by inflammation, mucus secretion. Smooth muscle contraction only plays a limited role
  • Salbutamol works by causing a relaxation in smooth muscle of the airways. This would have very little effect in COPD.
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10
Q

Define emphysema

A
  • Pathological enlargement of alveolar airspaces
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11
Q

What is the effect of emphysema?

A
  • Loss of elastin causing compliance to increase and recoil to decrease
  • Reduced surface area and damage to pulmonary vasculature (reduced gas exchange)
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12
Q

Why is COPD considered progressive?

A
  • Patients usually suffer frequent exacerbations of symptoms
  • Lung function fails to return to previous levels which can cause respiratory failure
  • Smoking cessation only slows, not stops decline in function
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13
Q

Outline the way in which COPD places burden on the CVS - PART 1

A
  • Alveoli are hypoventilated
  • This causes hypoxic vasoconstriction
  • Vascular resistance rises so force and pressure at which blood is pumped rises - pulmonary hypertension
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14
Q

Outline the way in which COPD places burden on the CVS - PART 2

A
  • Increased RV afterload. Greater effort required to maintain normal blood flow against increased resistance. RV hypertrophy occurs
  • Heart eventually unable to cope with increased burden. Causes heart failure/myocardial infarction.
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15
Q

What is pneumonia an infection of?

A

Alveoli and surrounding lung tissue

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16
Q

Outline the steps involved in the development of pneumonia.

PART 1

A
  • Pneumonia follows weakening of host defences e.g immune suppression, HIV
  • Alveoli become colonised by pathogens
  • Alveolar macrophages are activated and release cytokines, such as IL-6 and IL-8
17
Q

Outline the steps involved in the development of pneumonia.

PART 2

A
  • IL-6 and IL-8 recruit neutrophils to the lungs, releasing pro-inflammatory cytokines
  • They also recruit reactive oxygen species to kill the pathogens
  • However, this will injure surrounding tissues such as the alveoli
18
Q

Outline the steps involved in the development of pneumonia.

PART 3

A
  • The damage causes an ‘acute lung injury’
  • Inflammation signal and injury to alveolar walls and capillary endothelium causes fluid to be drawn into alveoli and interstitial tissue
  • This causes oedema. Diffusion distance increases so rate of gas exchange decreases
19
Q

Outline the steps involved in the development of pneumonia.

PART 4

A
  • Damage to alveolar walls and accumulation of dead cells cause a hyaline membrane to form
  • The hyaline membrane is thick and impermeable. This also reduces diffusion distance.
  • These changes causes hypoxaemia.
20
Q

Why is simultaneous loss of airway patency and elastic recoil problematic in COPD?

A
  • The airways are connected to the surrounding lung tissue.
  • These connections help keep the airways open (as they are joined by various elastin).
  • So the lungs increase in size and the airways are compressed (during expiration).
  • In COPD the airways begin to lose patency
  • Due to loss of elastic recoil, lungs need to be compressed harder during expiration