COPD, Pneumonia Flashcards
(29 cards)
What is COPD a term for?
→ a mixture of chronic bronchitis and emphysema
How does lung function decline in healthy people vs people who smoke?
→ Lung function naturally declines with age
→ Lung function decline is accelerated in people who smoke
What can the harmful constituents of tobacco smoke cause?
→ Acute damage to respiratory tissue generating an inflammatory response
What happens with repeated exposure to tobacco smoke?
→ Inflammation becomes pathological
→ Creates chronic and irreversible dysfunction
What are the steps that cause inflammation in COPD?
→ 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
What are the long term effects of inflammation?
→ Impaired mucociliary clearance
→ More vulnerable to respiratory infection
→ Generates more inflammation
→ Tissue remodelling
What is the layer of mucus in the airways for?
→ Trapping small particulates/ bacteria or viruses and moving them up the airways to remove them
What happens to the mucus with COPD?
→ 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
What pathological features are present in the airways of someone with COPD?
→ Excess amounts of mucus within the airways
→ Weakened airway structure
→ Impairment of mucociliary clearance
→ Irritation of sensory neurons (coughing)
→ Decreased luminal area
What happens to alveoli in emphysema?
→ Decrease in surface area
→ Loss of elastin fibers means increased compliance and decrease in recoil
Why is not as much gas exchanged in emphysema?
→ Higher surface area to volume ratio
What consequence does emphysema have on breathing in and out?
→ Easier to expand the lungs (breathing in)
→ Harder to expel the air
→ Alveoli do not recoil so accessory muscles have to be used
What happens as a result of elastin degradation in COPD?
→ Loss of patency
→ Loss of elastic recoil
How can COPD lead to heart failure?
→ Chronic alveolar hypoxia → Hypoxic vasoconstriction → Pulmonary hypertension →Right ventricular hypertrophy → Heart failure
What are 3 conditions that can occur with COPD?
→ Hypoxaemia
→Hypercapnia
→ Acidaemia
What is the most effective method of slowing the decline of lung function?
→ Smoking cessation
What happens to lung function if you quit smoking?
→ Doesn’t regenerate but slows the decline
How can pathophysiology of COPD be modelled in animals?
→ Expose mice to tobacco smoke
→ Measure lung function, airway resistance and compliance
→ Cull animals and take lung samples
→ Measure cytokine and leukocyte levels
Apart from smoking, what are other causes of COPD?
genetic disorders such as alpha-1-antitrypsin deficiency
What causes right heart hypertrophy in relation to chronic hypoventilation?
→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
What are the immediate effects of chronic alveolar hypoxia?
→hypoxic vasoconstriction=increased pulmonary vascular resistance
→hypoxaemia, hypercapnia, acidemia
→decreased exercise tolerance fatigue
Define pneumonia
an infection of the lung parenchyma (the alveoli and surrounding tissue)
How is pneumonia classified?
- 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)
Describe the mechanism of pneumonia
→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
