Pathophysiology of COPD

Question 1

what does COPD stand for?

Answer 1

Chronic Obstructive Pulmonary Disease

Question 2

what is COPD?

Answer 2

an umbrella term used for a mixture of chronic bronchitis and emphysema, and encompasses a long-term, progressive, and accelerated decline in respiratory function

Question 3

what % of long long term smokers develop COPD?

Answer 3

30%

Question 4

what % of COPD is associated with long-term tobacco smoke exposure?

Answer 4

90%

Question 5

name some other factors other than smoking that can cause COPD:

Answer 5

• genetic (e.g. Alpha-1 antitrypsin deficiency)

- environmental hazards. (e.g. pollution)

Question 6

Why does smoking harm the respiratory system?

Answer 6

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

Question 7

How does the inflammation observed within the lungs of COPD patients develop?

Answer 7

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

Question 8

why is mucociliary function impaired in COPD?

Answer 8

due to damage to cilia and mucus hypersecretion

Question 9

where do you get impaired mucociliary clearance?

Answer 9

the airways

Question 10

what coats your respiratory airways?

Answer 10

a layer of mucus which is secreted by goblet cells

Question 11

role of the mucus that lines respiratory airways:

Answer 11

• 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

Question 12

what happens to mucus in COPD?

Answer 12

• 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

Question 13

what is the consequence of mucus building up?

Answer 13

• 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

Question 14

what is tissue remodelling?

Answer 14

Long-term consequence of inflammation caused by CODP, because of continuous tissue damage

tissue remodelling basically links to the irreversible changes that occur

Question 15

what does tissue remodelling cause?

Answer 15

an overall decline in respiratory function

Question 16

what 2 things cause hyper secretion of mucus?

Answer 16

• increase in number of goblet cells

- increase in mucus gland activation

Question 17

consequences of airway inflammation

Answer 17

• 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

Question 18

why might patients get a cough?

Answer 18

irritation of sensory neurons

Question 19

predominant effect of COPD?

Answer 19

overall decrease in SA in the lungs

Question 20

why does COPD cause an overall decrease in SA in the lungs?

Answer 20

• 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

Question 21

what is the consequence of this reduced SA?

Answer 21

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

Question 22

Why is simultaneous loss of airway patency (airway being open) and elastic recoil problematic in COPD?

Answer 22

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

Question 23

what happens in chronic bronchitis?

Answer 23

• 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

Question 24

what is an exacerbation and what do COPD exacerbations do?

Answer 24

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

Question 25

hypoxic vasoconstriction is a good adaptation, but why is it not good in COPD?

Answer 25

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

Question 26

chronic alveolar hypoxia also causes hypercapnia, hyperaemia and acidaemia - what is the consequence of this?

Answer 26

hypoxaemia and acidaemia make the person fatigued and decreases their quality of life

Question 27

How effective is smoking cessation at preventing COPD?

Answer 27

• 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

Question 28

what pathological features are observed in chronic smoke-exposed lungs?

Answer 28

air spaces are enlarged, elastin decreases

Question 29

what does chronic alveolar hypoxia lead to?

Answer 29

• hypoxaemia
• hypercapnia
• acidosis
• right heart failure (due to hypoxic vasoconstriction)