COPD Flashcards
what are risk factors for COPD?
In general and for Mary
In general:
- smoking (main one)
- genetics- AAT deficiency
- environmental/ air irritants
- asthma
For Mary:
- smoking
- genetics- AAT deficiency
- exposure to environmental/ air irritants
pathophysiology of COPD
exposure to toxins –> narrowed airways –> oxidative stress –> damage to the alveoli –> enlarged airspaces –> chemicals dissolve alveolar wall
exposure to noxious particles trigger an inflammatory response in the lungs. Overtime, repeated exposure leads to chronic inflammation. If this occurs in the bronchi, inflammation leads to the airways becoming permanently narrowed (chronic bronchitis) and inflammation in the alveoli leads to destruction of lung tissue with the loss of the normal lung elasticity (emphysema). Cycles of inflammation and repair are associated with excess mucus production, fibrosis and protein breakdown. Continued noxious particles lead to the formation of carbon deposits within the air spaces of the lungs. This leads to alveolar tissue damage, air spaces enlarged and air becomes trapped in the lungs at the end of expiration. Overtime, residual volume increases which leads to hyperinflation which flattens the diaphragm causing it to become less effective at regulating pleural pressures- this is necessary for efficient breathing.
pathophysiology of emphysema and chronic bronchitis
Emphysema:
chronic inflammation in the alveoli which leads to oxidative stress and an increase in proteases (enzymes that break down protein). This causes tissue breakdown- the alveolar cells, pulmonary cells and fibre cells break down. This creates an enlarged airspace and a collapsed airway. this means there is decreased alveolar surface area which leads to decreased gas exchange. There is also increased air retention in the alveoli and hyperinflation so more air remains behind in the lungs. This air is non exchangeable which leads to increased residual volume (air left in the lungs after exhalation) and this effects the thoracic cavity and breathing becomes harder.
Chronic bronchitis:
chronic inflammation in bronchi/ bronchioles which creates swelling, increased mucus production and decreased cilia action. This creates an increase in airway resistance and a decrease in ventilation/ airflow which leads to decreased gas exchange.
signs and symptoms of COPD
In general and for Mary
In general:
- barrel chest
- chronic cough
- pursing lips when breathing
- shortness of breath
- use of accessory muscles
- laboured breathing
- finger clubbing
- blue tinged lips
- wheezing
For Mary:
- shortness of breath (main one)
- laboured breathing
- pursed lips
- use of accessory muscles
- barrel chest
- tinged lips (bluish)
- increased expiratory effort
what are the complications of COPD
In general and for Mary
it causes decreased gas exchange which means;
- decreased oxygen in the blood which means decreased oxygen in the tissues which increases anaerobic respiration and leads to metabolic acidosis
- increased carbon dioxide in the blood which leads to respiratory acidosis
- diaphragm flattens and alterations in the thoracic cavity shape –> barrel chest
- increased use of accessory muscles= increased work of breathing= fatigue= tissue wasting
- tissue wasting from increased fatigue and metabolic acidosis
- alveolar collapse (atelectasis)
- Right sided heart failure (cor pulmonale)
For Mary;
- decreased oxygen (cyanosis) shown by blue tinged lips
- occasional ankle oedema- a sign of right sided heart failure
- episodes of acute respiratory distress
- appears thin
what are routine clinical investigations for COPD
laboratory tests for COPD
- blood gases and PH
- sputum sample
expected investigations for COPD
- chest x-ray
- ECG
- pulmonary function tests
what is the management of COPD
In general and for Mary
management involves various medications alongside supportive care e.g activity and nutrition guidance
medications;
1. beta-agonists- bind to the beta 2 adrenergic receptors on the bronchiole smooth muscle, stimulating bronchodilation. This relaxes the muscles of the airways and results in easier breathing
2. anticholinergics- block muscarinic acetylcholine (mACh) receptors on the bronchiole smooth muscle leading to bronchodilation
3. corticosteroids- anti inflammatory agents that change the genes that cause inflammation. They are used to decrease the inflammatory response
4. oxygen- low level oxygen therapy used to maintain adequate oxygen saturation
For Mary
1. salbutamol- short acting beta-agonist bronchodilator
2. seretide- long acting beta-agonist bronchodilator and corticosteroid
3. Spiriva- anticholinergic used for bronchodilation
4. oxygen therapy
what was shown in Mary’s physical examination
- she was thin
- face was a dusky colour
- lips had a bluish tinge
- breathing was laboured- respiratory rate was 20 breaths/min
- chest movements poor but symmetrical
- listening to her chest showed quiet breathing sounds. occasional crepitations and scattered course crackles
- heart rate was 82bpm
What are some tests that are used to assess lung function and why are they used
there are various tests available for assessing aspects of respiratory function including blood tests and pulmonary tests to evaluate aspects of ventilation, lung volume and gas exchange. These tests provide useful information about the individuals lung function and can help diagnose lung disorder, monitor the disease severity and assess the efficiency of the treatment
- arterial blood gas- checks oxygenation status and acid balance
- pulse oximetry- estimates 02 content in arterial blood using light
- peak expiratory flow- measures how quickly you can exhale
- body plethysmography- measures thoracic volume and airway resistance
- forced expiratory volume- tests how much air you can exhale in 1 second
- diffusing capacity- tests oxygen transfer from the alveoli to circulation
- sputum culture- used to diagnose bacterial lung infection
why are blood tests done to diagnose COPD
blood tests will often reveal an increased haemoglobin level with increased red blood cell count and a raised hematocrits in COPD patients. It reflects the bodyies attempt to compensate for low P02 (the amount of oxygen in the blood) by increasing 02 carrying capacity of the blood. The raised PC02 (carbon dioxide in the blood) results in chronic respiratory acidosis. These patients are prone to respiratory infections.
Why is spirometry used to diagnose COPD and what were Mary’s spirometry results
Spirometry is the most common pulmonary function test used. It assesses the lung function by measuring airflow and the corresponding changes in lung volumes. It records inspiratory and expiratory lung volumes, and how fast the patient can inhale/ exhale.
These tests reveal that residual volume and total lung capacity are usually increased in COPD. Residual volume (air remaining in the lungs after expiration) increases to a greater extent than total lung capacity (the maximal amount of air in lungs after a big inhalation) and therefore vital capacity is decreased (the greatest volume of air that can be exhaled from the lungs)
Mary’s results showed
- increased residual volume
- increased functional residual capacity
- increased total lung capacity
- reduced vital capacity
- reduced forced vital capacity and forced expired volume in 1 second
measures related to lung volumes are increased and those related to air flow are decreased. More air os trapped in the lungs and Mary finds it harder to move air in and out of her lungs
how does Mary’s chronic bronchitis and emphysema elements of COPD affect her breathing
The chronic bronchitis element of her COPD causes mucus secretion, narrowing, and obstruction of the airways. As a result, Mary M’s airway resistance is increased, reducing air flow and lengthening her expiration time. Because Mary M is unable to properly expire air from the lungs, air becomes trapped, resulting in increased residual volume and increased functional residual capacity.
Mary M’s emphysema is associated with a loss of lung elasticity. Elasticity plays an important role in expiration. Elastic recoil compresses air in the lungs, generating pressures that force air out. Without this elastic recoil, it is harder for Mary M to generate the pressures required to drive expiration. Elastic tissue also helps maintain airway structure, preventing involuntary airway closure during expiration. Loss of this elastic tissue means that Mary M’s airways are prone to collapse during expiration. This also results in expiration ending prematurely, and air becoming trapped in the lungs. This trapped air increased Mary M’s residual volume, which is correlated with a decrease in vital capacity.
