COPD, Pneumonia

Question 1

What is COPD a term for?

Answer 1

→ a mixture of chronic bronchitis and emphysema

Question 2

How does lung function decline in healthy people vs people who smoke?

Answer 2

→ Lung function naturally declines with age

→ Lung function decline is accelerated in people who smoke

Question 3

What can the harmful constituents of tobacco smoke cause?

Answer 3

→ Acute damage to respiratory tissue generating an inflammatory response

Question 4

What happens with repeated exposure to tobacco smoke?

Answer 4

→ Inflammation becomes pathological

→ Creates chronic and irreversible dysfunction

Question 5

What are the steps that cause inflammation in COPD?

Answer 5

→ Inhalation of reactive oxygen species and noxious chemicals
→ This causes tissue damage
→ The body responds by initiating an inflammatory response
→ Macrophages and neutrophils are activated
→ They secrete proteases to repair damaged tissue
→ Before damage can be repaired more inflammation occurs by smoking again
→ Increased protease burden which damages healthy tissues
→balance between proteases (enzymes which break down proteins) and anti-proteases (enzymes which inhibit proteases) is disrupted

Question 6

What are the long term effects of inflammation?

Answer 6

→ Impaired mucociliary clearance
→ More vulnerable to respiratory infection
→ Generates more inflammation
→ Tissue remodelling

Question 7

What is the layer of mucus in the airways for?

Answer 7

→ Trapping small particulates/ bacteria or viruses and moving them up the airways to remove them

Question 8

What happens to the mucus with COPD?

Answer 8

→ Hypersecretion of mucus because toxic particles stimulate the production of it
→ They damage the way cilia work so they cannot beat as effectively
→ Mucus is not cleared well and bacteria live in the mucus and can infect lungs

Question 9

What pathological features are present in the airways of someone with COPD?

Answer 9

→ Excess amounts of mucus within the airways
→ Weakened airway structure
→ Impairment of mucociliary clearance
→ Irritation of sensory neurons (coughing)
→ Decreased luminal area

Question 10

What happens to alveoli in emphysema?

Answer 10

→ Decrease in surface area

→ Loss of elastin fibers means increased compliance and decrease in recoil

Question 11

Why is not as much gas exchanged in emphysema?

Answer 11

→ Higher surface area to volume ratio

Question 12

What consequence does emphysema have on breathing in and out?

Answer 12

→ Easier to expand the lungs (breathing in)
→ Harder to expel the air
→ Alveoli do not recoil so accessory muscles have to be used

Question 13

What happens as a result of elastin degradation in COPD?

Answer 13

→ Loss of patency

→ Loss of elastic recoil

Question 14

How can COPD lead to heart failure?

Answer 14

→ Chronic alveolar hypoxia
→ Hypoxic vasoconstriction
→ Pulmonary hypertension
→Right ventricular hypertrophy
→ Heart failure

Question 15

What are 3 conditions that can occur with COPD?

Answer 15

→ Hypoxaemia
→Hypercapnia
→ Acidaemia

Question 16

What is the most effective method of slowing the decline of lung function?

Answer 16

→ Smoking cessation

Question 17

What happens to lung function if you quit smoking?

Answer 17

→ Doesn’t regenerate but slows the decline

Question 18

How can pathophysiology of COPD be modelled in animals?

Answer 18

→ Expose mice to tobacco smoke
→ Measure lung function, airway resistance and compliance
→ Cull animals and take lung samples
→ Measure cytokine and leukocyte levels

Question 19

Apart from smoking, what are other causes of COPD?

Answer 19

genetic disorders such as alpha-1-antitrypsin deficiency

Question 20

What causes right heart hypertrophy in relation to chronic hypoventilation?

Answer 20

→Constriction of the pulmonary vasculature increases vascular resistance
→increasing the force required to pump blood through the system and the pressure of blood within it (pulmonary hypertension).
→requires the heart to work harder to maintain normal blood flow against increased resistance
→increased venous pressure and right ventricular afterload

Question 21

What are the immediate effects of chronic alveolar hypoxia?

Answer 21

→hypoxic vasoconstriction=increased pulmonary vascular resistance
→hypoxaemia, hypercapnia, acidemia
→decreased exercise tolerance fatigue

Question 22

Define pneumonia

Answer 22

an infection of the lung parenchyma (the alveoli and surrounding tissue)

Question 23

How is pneumonia classified?

Answer 23

• The type of pathogen responsible for the infection (bacterial, viral, fungal)
• The specific tissue(s) that are affected, e.g. lobar (the intra-alveoar space), bronchial, and interstitial.
• Where the infection was acquired (e.g. in the community vs. in hospital)

Question 24

Describe the mechanism of pneumonia

Answer 24

→colonisation of the alveoli by pathogens
→activation of alveolar macrophages, leading to release of inflammatory cytokines such as IL-6, IL-8, and TNF-α.
→act as a chemokine stimulus to recruit neutrophils
→they are activated and release further pro-inflammatory cytokines, and reactive oxygen species and proteases to kill the pathogens

Question 25

How oedema caused by pneumonia?

Answer 25

→inflammatory signal and injury to the alveolar wall, basement membrane and capillary endothelium, enables excessive fluid to be drawn into alveoli and surrounding interstitial tissue.

Question 26

Explain hyaline membrane formation…

Answer 26

→ hyaline membrane is when membranes that are normally thin and selectively permeable become thick and relatively impermeable
→damage to the alveolar wall and the accumulation of dead cells and fibrinous waste causes
→impaired gas exchange > hypoxaemia

Question 27

Why is hypercapnia avoided in pneumonia?

Answer 27

due to the combination of high PaCO2 and low PaO2 inducing an immediate reflex increase in ventilation within any remaining parts of the lung that are still relatively functional, removing the excess carbon dioxide.

Question 28

Why is hypoxaemia not resolved increasing ventilation?

Answer 28

due to the resulting VQ mismatch and shunt effect

Question 29

How does acute injury lead to hypoxaemia?

Answer 29

→deposition of dead cells and proteins in alveolar walls- hyaline formation
→basement and endothelium disruption
→fluid accumulates in intestinal and alveoli- cackling sounds
→impaired gas exchange