Mary COPD Flashcards
Patho of COPD
Emphysema
Characterized by destruction of alveoli leading to reduced surface area for gas exchange and air trapping. This results in hyperinflation of the lungs
Chronic bronchitis
Involves inflammation and thickening of the bronchial walls with increased mucus production leading to airway obstruction amd difficulty in airflow
Signs and symptoms of COPD
Emphysema
Dyspnea ..SOB
prolonged expiration phase and a barrel chest due to overinflation
Cough but less common
Barrel fingers
Pursed lips when breathing
Tripod breathing position
Chronic bronchitis
Persistent cough (>3 months) WITH SPUTUM
wheezing
Cynosis
Difficulty breathing
Signs and symptoms of COPD
Emphysema
Dyspnea ..SOB
prolonged expiration phase and a barrel chest due to overinflation
Cough but less common
Barrel fingers
Pursed lips when breathing
Tripod breathing position
Chronic bronchitis
Persistent cough (>3 months) WITH SPUTUM
wheezing
Cynosis
Difficulty breathing
Diagnosis of COPD
Emphysema
Chest xray
CT scan
Chronic bronchitis
Clinical hx
Pulmonary function testing
Patho of emphysema
Chronic inflammation in alveoli
This leads to oxidative stress and increase in protease
Tissue destruction and breakdown of….
Alveolar cells
Pulmonary capillaries
Elastic fires
Airways collapse
Leaving airspace enlarged…airsacs
Air is retained…hyperinflation
Leading to
Changes in lung volume and capacity
This effects the thoracic cavity
Resulting in increase WOB
Surface are is decreases for gas exchange Leading to
Hypoxia …decreased O2
Hyperopia…increased CO2
This causes respiratory acidosis and pulmonary hypertension
Patho of chronic bronchitis
Chronic inflammation of the bronchi
Swelling
Mucus
Decreased Cillia action
Causes increased airway resistance
Increased WOB
Decreased ventilation
Decreased gas exchange
Increased risk of infection
V/Q mismatch ventilation and perfusion
Floppy lungs
Causes/risk factors that Mary may have had
Smoking
Possible exposure to irritants
Family Hx…genes
3 family members
1 sister aged 50s
1 brother aged 60s
Mother aged 70s
Genetics involved
Alpha-1 anti-trips in (AAT) is a genetic disease when the body doesn’t produce enough AAT. It’s a protein that protects the lungsbajrbl8ver from damage
Smoking
Damages the endothelial. Long term exposure leads to an inflammatory reaction within the respiratory tract
Smoking
Damages the endothelial. Long term exposure leads to an inflammatory reaction within the respiratory tract
Signs and symptoms of COPD
Dyspnoea..SOB
Pursed lips when breathing
Pallor
SoB on exertion
Barrel chest
Increased WOB including increased use of accessory muscles
Tripod position
Flared nostrils
Weight loss
Signs and symptoms of COPD
Dyspnoea..SOB
Pursed lips when breathing
Pallor
SoB on exertion
Barrel chest
Increased WOB including increased use of accessory muscles
Tripod position
Flared nostrils
Weight loss
Complications of COPD
Acute resp failure
Resp acidosis
Metabolic acidosis
Tissue wasting/emaciation
Pulmonary hypertension and cor pulmonale
Mary’s complications
Cynosis
Thin appearance
Ankle oedema…sign of right sided heart failure (cor pulmonale)
Episodes of acute resp failure
Breathing quiet but labored
Rr 20 per min
Poor chest movements
Increased expiration effort
Over use of accessory muscles
Fine and course crackles
Chronic cough
Sputum production
SoB
Assessments and testing
Sputum sample
Chest xray
CT scan
Blood tests
Spirometry
Ecg
Pulse oximetry
Spirometry
Measures how much available air can blow and how well they do it
So it’s a lung/Pulmonary function test
It measures airflow and changes in lung volume
Records inspiratory and expiration lung volume
Speed and ingale/exhale
Reveals residue volume and total lung capacity
Spirometry
Measures how much available air can blow and how well they do it
So it’s a lung/Pulmonary function test
It measures airflow and changes in lung volume
Records inspiratory and expiration lung volume
Speed and ingale/exhale
Reveals residue volume and total lung capacity
Lung function in COPD patients
Increased residual volume
Increased functionality residual capacity volume
Increased total lung capacity
Decreased vital capacity
Decreased force vital capacity
Decreased forced expired volume in 1 second
Lung function in COPD patients
Increased residual volume
Increased functionality residual capacity volume
Increased total lung capacity
Decreased vital capacity
Decreased force vital capacity
Decreased forced expired volume in 1 second
More about marys lung function for chronic bronchitis
Elements of her COPD cause Mucus secretion, narrowing and obstructing the airways.
Airway resistance is increased reducing airflow
This lengthens thr expiration time
Because all thr air can’t be breathed out air becomes trapped
This results in increased residual volume and increased functional residual capacity.
More about marys lung function for chronic bronchitis
Elements of her COPD cause Mucus secretion, narrowing and obstructing the airways.
Airway resistance is increased reducing airflow
This lengthens thr expiration time
Because all thr air can’t be breathed out air becomes trapped
This results in increased residual volume and increased functional residual capacity.
Mary’s Ling function for empysema
Elements of her COPD is associated with a loss of lu g elasticity
Elasticity recoil compresses air in the lungs generating pressures that force the air in the lung out.
Without recoil it’s harder to generate pressures required to drive expiration.
Elastic tissue helps maintain structure
Without this airways are prone to collapse during expiration
This results in premature ending of exhilation and air becomes trapped.
This increases residual volume
Trapped air = increased residual volume plus decreased vital capacity
Mary’s Ling function for empysema
Elements of her COPD is associated with a loss of lu g elasticity
Elasticity recoil compresses air in the lungs generating pressures that force the air in the lung out.
Without recoil it’s harder to generate pressures required to drive expiration.
Elastic tissue helps maintain structure
Without this airways are prone to collapse during expiration
This results in premature ending of exhilation and air becomes trapped.
This increases residual volume
Trapped air = increased residual volume plus decreased vital capacity
Management of COPD
Medications
Supportive care
Low level o2
Management of COPD
Medications
Supportive care
Low level o2
Typical medications
Beta agonists
Bronchodilators the open airways by relaxing bronchial smooth muscle
Anticholinergic
Drug test blocks the action of acetylcholine which prevent bronchoconstricion therefore allow bronchodilation
Corticosteroids
Anti-inflammatory
Oxygen
Low level
Typical medications
Beta agonists
Bronchodilators the open airways by relaxing bronchial smooth muscle
Anticholinergic
Drug test blocks the action of acetylcholine which prevent bronchoconstricion therefore allow bronchodilation
Corticosteroids
Anti-inflammatory
Oxygen
Low level
