Pathophysiology of COPD Flashcards
what does COPD stand for?
Chronic Obstructive Pulmonary Disease
what is COPD?
an umbrella term used for a mixture of chronic bronchitis and emphysema, and encompasses a long-term, progressive, and accelerated decline in respiratory function
what % of long long term smokers develop COPD?
30%
what % of COPD is associated with long-term tobacco smoke exposure?
90%
name some other factors other than smoking that can cause COPD:
- genetic (e.g. Alpha-1 antitrypsin deficiency)
- environmental hazards. (e.g. pollution)
Why does smoking harm the respiratory system?
there are many harmful constituents of tobacco smoke which cause acute damage to respiratory tissue, generating an inflammatory response.
with repeated exposure, the inflammation becomes pathological and generates chronic and irreversible dysfunction
How does the inflammation observed within the lungs of COPD patients develop?
Person breathes in tobacco smoke into the lungs and the toxic constituents cause local injury/tissue damage, which generates inflammation-the body responds to the injury by attracting various immune cells (alveolar macrophages, neutrophils, secretion of cytokines)
While this is happening the person smokes again causing further tissue damage before its properly repaired
Increase protease burden is where the immune cells secrete too many proteases, which are now starting to damage and digest the tissue within the airways and lungs
At the same time, some of the constituents within tobacco smoke also inhibit the activity of enzymes which are supposed to stop this process happening, eg. anti-protease inactivation so proteases build up. Becomes a vicious cycle
Chronic and irreversible long-term changes to the structure of the airways and lung tissue
why is mucociliary function impaired in COPD?
due to damage to cilia and mucus hypersecretion
where do you get impaired mucociliary clearance?
the airways
what coats your respiratory airways?
a layer of mucus which is secreted by goblet cells
role of the mucus that lines respiratory airways:
- used to trap small matter and infectious organisms like bacteria and viruses
- during inhalation, they get trapped in the mucus, and the cilia wafts the mucus up the airways in 1 direction, where it is eventually spat out or swallowed- prevents the infectious organisms/particles getting to the lung tissue or gaining access to the body
what happens to mucus in COPD?
- chronic damage eg. in COPD, causes hyper secretion of mucus as well as damage to cilia function (so they can’t waft as effectively)
- so, you get too much mucus which is then not wafted properly
what is the consequence of mucus building up?
- bacteria gets trapped in the mucus, starts to live there and infects the individual - makes them more vulnerable to respiratory (bacterial) infection
- this generates more inflammation and more tissue damage which makes situ worse
-airways logged with mucus means there is an obstruction, making airflow more difficult
what is tissue remodelling?
Long-term consequence of inflammation caused by CODP, because of continuous tissue damage
tissue remodelling basically links to the irreversible changes that occur
what does tissue remodelling cause?
an overall decline in respiratory function
what 2 things cause hyper secretion of mucus?
- increase in number of goblet cells
- increase in mucus gland activation
consequences of airway inflammation
- swelling, long-term changes to structure which both affect the size of the lumen
- overall weakened airway structure due to degradation of some of the structural proteins (elastin) within the wall of the airway
- less able to maintain patency and structural integrity
- airway starts to collapse when placed under too much pressure
why might patients get a cough?
irritation of sensory neurons
predominant effect of COPD?
overall decrease in SA in the lungs
why does COPD cause an overall decrease in SA in the lungs?
- chronic inflammation and degradation of alveoli structure and proteins within it causes alveoli to fuse together
- loss of elastin in some of the fibres so the lungs don’t recoil as effectively and it becomes easier to expand them during inspiration but harder to recoil during expiration
- so overall there is an increase in lung compliance and decrease in recoil
what is the consequence of this reduced SA?
if the lungs aren’t recoiling the patient gets to a point where they have to use their respiratory muscles to push their lungs closed, like you normally would during a forced expiration, except this time it’s just at rest
Why is simultaneous loss of airway patency (airway being open) and elastic recoil problematic in COPD?
you need to compress your lungs harder during expiration because they don’t recoil on their own so you have to push the airways shut
but, by exerting more pressure in order to compress your lungs during expiration, you are also compressing your airways, and ultimately obstruct them
what happens in chronic bronchitis?
- airway obstruction and air “trapping”, which leads to decreased ventilation and alveolar hypoxia and increased CO2
- “air trapping” means you get increased residual volume and a decrease in vital capacity
- decrease in lung recoil means increased respiratory effort
- so, the amount of air that you are able to breathe in and out decreases
- net effect = decreased level of ventilation, decreased gas exchange and overall hypoxaemia
- less o2 getting into the blood and hypercapnia (build-up of co2 within the blood
what is an exacerbation and what do COPD exacerbations do?
throughout the course of the disease you get points called an exacerbation
- person gets a respiratory infection and sudden worsening in respiratory function
- after the infection stops it gets a little bit better, but not back to where it was before
- generally, there is a risk of death, or it will just contribute to the overall rate of decline overall.
exacerbations temporarily and drastically reduce lung function + contribute to decline
hypoxic vasoconstriction is a good adaptation, but why is it not good in COPD?
in cases like COPD there are large areas of the lung which are hypoxic, so the majority of blood vessels within lung vasculature start to vasoconstrict
means the RHS of the heart has to work harder because blood has to be forced through constricted blood vessels (increased RV after load)
causes problems like pulmonary hypertension because resistance in blood vessels increases - right ventricular hypertrophy
hypertrophy damages the function of the lung in the long-term, leads to heart failure
chronic alveolar hypoxia also causes hypercapnia, hyperaemia and acidaemia - what is the consequence of this?
hypoxaemia and acidaemia make the person fatigued and decreases their quality of life
How effective is smoking cessation at preventing COPD?
- most effective method of slowing the decline, however lung function doesn’t regenerate and decline continues (just not as rapidly)
- so, all it does is slow the acceleration- this might be enough to prevent the patient from doing from COPD, but it’s not like the respiratory function is going to back what it would have been if the patient had never smoked
what pathological features are observed in chronic smoke-exposed lungs?
air spaces are enlarged, elastin decreases
what does chronic alveolar hypoxia lead to?
- hypoxaemia
- hypercapnia
- acidosis
- right heart failure (due to hypoxic vasoconstriction)
