COPD Flashcards
What is COPD?
Chronic air trapping from damaged lungs = lung hyperinflation
What are the main risk factors?
SMOKING is the main
GENETICS - a deficiency of AAT.
Why is smoking a cause/risk factor?
Chronic exposure to the irritants associated with SMOKING results in inflammatory reaction within the respiratory system.
In ALVEOLI, this causes a protease anti protease imbalance and increased oxidants enhancing the tissue/protein breakdown resulting in enlarged air spaces and decreased surface area for gas exchange.
In UPPER RESP TRACT, the inflammation leads to bronchial oedema, impaired cilia and increased mucous production. This narrows the airways and increased airway resistance.
S+S of COPD? FUCC DIBS
FINGER CLUBBING
USE OF ACCESSORY MUSCLES
CYANOTIC
CHRONIC COUGH
DYSPNOEA
INCREASED EXPIRATORY EFFORT
BARREL SHAPED CHEST
SOBOE
PURSED LIP BREATHING
What are the 2 types of COPD?
Emphysema and chronic bronchitis
What is emphysema?
Emphysema is the permanent enlargement of air spaces
So if the inflammation is in the alveoli, then this will cause a protease and anti protease imbalance, and increases oxidants, both enhancing the tissue and protein breakdown, causing and enlargement of air sacs and decreases the surface area available for gas exchange. This is the inflammatory destruction of the alveoli and capillaries and includes the breakdown of elastin decreasing expiratory airflow resulting in air trapping and further reduction in volume of exchangeable air
What is chronic bronchitis?
Narrowed bronchioles causing airway resistance.
Inflammation happens in the bronchioles leading to bronchial oedema, increase mucous production and decrease ciliary action. This increases airway resistance decreasing volume of air flowing in/out of the lungs for gas exchange.
S+S of emphysema? PINK
Any others?
P-ink skin and pursed lip breathing
I-ncreased chest (barrel)
N-o chronic cough - minimal
Keep tripoding to get air exchanged.
Other:
Clubbed fingers = chronic hypoxia = vasodilation to compensate decreased O2.
SOB AR
Prolonged expiration
S+S of chronic bronchitis? BLUE
B-ig and blue skin - cyanosis - hypoxia
L-ong term chronic cough and sputum
Unusual lung sounds
Edema peripherally.
Why oedema in CB?
Due to col pulmonale
RHF
Bc R) side of heart struggles to pump blood into rly hard fibrotic lungs
S+S = JVD or weight gain.
What’s the pathophysiology for Mary’s COPD? Consequence?
Firstly she experienced both Emphysema and Chronic bronchitis. She had both narrowed airways and floppy lungs.
The exposure to toxic particles such as smoking, trigger an inflammatory response in the lungs and overtime, this repeated exposure leads to chronic inflammation.
If the inflammation reaches the BRONCHI, it causes bronchial edema, impairs the cilia and increases mucous production causing narrowed airways and also decreasing the airflow when inhaling and exhaling
There is an inflammatory destruction of the alveoli and capillaries causing a protease and anti protease imbalance and increased oxidants increasing the tissue and protein breakdown enlarging the air sacs and decreasing the surface area available for gas exchange. This destruction includes the breakdown of elastin decreasing expiratory airflow resulting in air trapping and further reduction in volume of exchangeable air. Continuation of smoking also results in the formation of carbon deposits within air spaces of lungs
One of the consequences can be from the alveoli damage where the air spaces enlarge and air is trapped in the lungs at the end of expiration. The residual volume will increase causing HYPERINFLATION of lungs. This hyperinflation of the lungs flattens the diaphragm which regulates the pleural pressures for efficient breathing. When flattened, it cannot regulate the pleural pressures so to compensate, the chest and neck muscles work harder increasing the WOB. This will make the pt suffer from dyspnoea. They often hyperventilate in effort to ventilate their lungs normally but the retention of CO2 will eventually put the body in an acidotic state.
Relevant diagnostic tests?
Expected lab tests = sputum sample, ABG and pH
Expected investigations = CXR, pulmonary function tests, ECG
Physical examination = Checking for S+S like cyanosis, barrel chest, check the pts breathing if it’s laboured. Listen to their lungs and check their weight for and fluid gain. Check for mental status change.
What would you expect from blood test or ABG? Complications possible just from seeing results? Why PCO2 and PO2 change?
For COPD I would expect there to be an increase in hemoglobin levels and an increase in both RBC and hemocrit. This reflects the body’s attempt to compensate for the lower PO2 by increasing the O2 carrying capacity of blood. So anemia would not be common.
But this is a complication from COPD called polycythemia where the increased RBC count will only cause a traffic jam in the blood vessels instead of perfusing the body in blood vessels increasing the risk of forming a deadly clot that could cause a stroke.
For ABG i expect to see an increase in PCO2 levels meaning it’s chronic respiratory acidosis. The PCO2 levels can be so high that instead of being a respiratory stimulant, the CO2 becomes a CNS depressant causing Respiratory acidosis. The PCO2 and PO2 change is associated with this complication. Basically respiratory acidosis is having excess carbonic acid in the blood. Since COPD makes the lung unable to remove enough CO2, CO2 will accumulate in the blood and combines with H2O becoming HCO3. This dissociates into hydrogen ions and bicarbonate ions decreasing blood pH = more acidic.
COPD pts are prone to acute respiratory infection and may cause respiratory failure.
What is the spirometry? What are the expected results?
It’s a common pulmonary function test and records inspiratory and expiratory lung volumes and how fast you can inhale and exhale.
Can be used to monitor or diagnose conditions like COPD, asthma or cystic fibrosis.
I expect the residual volume and total lung capacity to increase bc of COPD.
But if the residual volume (RV) and total lung capacity (TLC) increase proportionally, the vital capacity will appear normal. BUT! RV increases to a greater extent than TLC making the vital capacity to decrease.
In short
Increased RV, functional residual capacity, TLC
Decreased VC, forced vital capacity, forced expired volume in 1 second.
What about X ray?
I expect to see the lungs to take up a lot more of the chest capacity pushing the heart out of position by the hyperinflated lungs. I also should see the clavicles to be pulled superiorily due to the increased action of the accessory muscles to breathe.
