COPD Flashcards
What is COPD?
Definition:
Chronic obstructive Pulmonary Disease
(COPD) is a common preventable and
treatable disease that is characterized by
persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.
Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible
• COPD is present only if chronic airflow
obstruction occurs.
• Chronic bronchitis without chronic airflow
obstruction is not COPD.
• COPD may be punctuated by periods of acute worsening of respiratory symptoms, called exacerbations
• In most patients, it is associated with significant concomitant chronic diseases which increase its morbidity & mortality
What does COPD include?
– emphysema, an anatomically defined condition characterized by destruction and enlargement of the lung alveoli;
– chronic bronchitis, a clinically defined condition with chronic cough and phlegm and;
– small airways disease, a condition in which small bronchioles are narrowed.
What is emphysema and Chronic bronchitis?
Chronic bronchitis—Presence of chronic
productive cough on most days for 3 months, in each of 2 consecutive years, and other causes of productive cough have been excluded
• Emphysema—Abnormal, permanent
enlargement of the distal airspaces, distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
Epidemiology of COPD
In 2019 an estimated 391.9 million people
were said to be living with COPD with a global prevalence of 10.3%
• It is currently the 3rd leading cause of death worldwide
• It caused 3.23 million deaths worldwide in
2019.
• It is underdiagnosed
• Affects middle aged (45 years) and the elderly (60 years)
• Male/female ratio is 2:1
• Mortality increases with age, disease severity and socioeconomic disadvantage
Risk factors for COPD: Host factors
• Genetic factors e.g α1 antitrypsin deficiency
• Asthma
• Airway hyperactivity
• Infections
* Severe childhood respiratory infections
* Tuberculosis
* Age 45 and above 65 and above (elderly)
Risk factors for COPD: Exposures
• Tobacco smoking (most common)
• Indoor air pollution e.g. use of biomass fuel for cooking
• Outdoor air pollution
• Occupational dusts & chemicals e.g vapors, irritants & fumes
• Low socioeconomic status
Discuss the Pathogenesis of COPD
Which protein causes loss of lung elasticity when destroyed?
Which proteins contribute to tissue destruction and inflammation when destroyed?
- NOXIOUS AGENT (tobacco smoke, pollutants, occupational agent) in combination with genetic factors or respiratory infections lead to lung inflammation
- Lung inflammation leads to oxidative stress and release of proteinases
Cells involved include:
– Neutrophils:
Release serine protease (which are enzymes that break down proteins and our usually combatted by antiproteases eg alpha 1 antitrypsin):
- elastase (degrades elastin, leading to loss of lung elasticity causing them to enlarge (emphysema)),
- cathepsin G and protease 3 (contribute to tissue destruction and inflammation)
- the reduced structural support results in the bronchioles collapsing and causing air to be trapped causing hyperinflation
– Macrophages: when activated macrophages release cysteine proteases (cathepsin E,A,L,S): break down proteins in the lung matrix and matrix metalloproteases
– T-lymphocytes CD8>CD4:
– Extent of inflammation is related to the degree of the airflow obstruction
– Cells release cytokines and mediators
OXIDATIVE STRESS
– Cigarette smoke
– Reactive oxygen and nitrogen species released from inflammatory cells
What is the Pathophysiology of COPD?
Different pathogenetic mechanism discussed leads to the following pathological changes;
• Mucus hypersecretion: due to increased goblet cells and stimulated secretion from enlarged mucus glands.
- Ciliary dysfunction: due to squamous metaplasia from epithelial cells
• Repeated cycles of inflammation and repair: this leads to remodeling of tissue in the airway resulting in the following changes:
– Inflammation and Edema
– Fibrosis
– Collagen deposition
– Destruction of alveolar support
– Small airway obstruction
• Hyperinflation: Loss of elasticity causes the lung to become floppy and hyperinflated.
– Progressively traps air during expiration causing hyperinflation at rest and dynamic hyperinflation during exercise
– Reduces inspiration capacity and functional residual capacity during exercise resulting in breathlessness and decreased exercise capacity
• Gas exchange abnormality
– Arterial hypoxaemia +/- hypercapnia
– From abnormal distribution of ventilation perfusion ratios
SYSTEMIC EFFECTS OF COPD
• Cachexia - Skeletal muscle wasting and disuse atrophy
• Increased risk of cardiovascular disease
(associated with increased concentrations of C reactive protein)
• Normochromic normocytic anaemia
• Secondary polycythaemia (the body attempts to compensate for the low O2 by making rbc’s)
• Osteoporosis
• Depression and anxiety
How does COPD cause PULMONARY HYPERTENSION?
What would be the symptoms and signs?
• Develops late in COPD at the time of severe gas exchange abnormalities
• Can result in RVH and subsequent cor pulmonale
• Contributing factors
– Pulmonary artery constriction
– Endothelial dysfunction
– Remodeling of the pulmonary arteries (smooth muscle hypertrophy and hyperplasia)
– Destruction of pulmonary capillary bed
• Wheeze
• A barrel shaped chest*
• Loss of the normal cardiac and liver dullness*
• Poor chest expansion*
• Use of accessory muscles of respiration,
• Sitting in the characteristic “tripod” position
• Cyanosis
• Hoover’s sign^
• Oedema and signs of right heart failure^
CLINICAL FEATURES of COPD
• Symptoms include;
– Cough productive of sputum (particularly in the morning)
– wheeze and;
– Progressive dyspnoea
• Physical examination is normal in early stages
• In more severe disease, findings include;
• Tachypnoea
• Prolonged expiration
• Wheeze (usually during expiration)
• A barrel shaped chest*
• Loss of the normal cardiac and liver dullness*
• Poor chest expansion*
• Use of accessory muscles of respiration,
• Sitting in the characteristic “tripod” position
• Cyanosis (CB)
• Hoover’s sign^
• Oedema and signs of right heart failure^
DIAGNOSIS
How to find history of aetiology?
What would the FEV1/FVC be?
What is FEV1/FVC used to diagnose?
• COPD should be considered in any patient
with dyspnoea, chronic cough and sputum
production and/or a history of exposure to risk factors of the disease
• Any precipitant that caused an acute exercebation?
* Exposure to risk factor (active or passive cigarette smoke or biomass fuels)?
• Diagnosis is confirmed by Spirometry which reveals, a post bronchodilator FEV1/FVC < 0.7
* FEV1/FVC used to differentiate between restrictive (pulmonary fibrosis, pneumonia, lung cancer, sarcoidosis): FEV1/FVC > 0.7 and obstructive (eg. COPD and asthma): FEV1/FVC < 0.7 lung diseases?
SUPPORTIVE INVESTIGATIONS
• Chest X-ray: is often normal, even when disease is advanced. Classic features: over-inflation of the lungs with low, flattened diaphragms, and sometimes the presence of large bullae.
• FBC: can be elevated as a result of persistent hypoxaemia (secondary polycythaemia; high wbc count (to rule out infections), anemia
• Pulse oximetry and arterial blood gases: may be helpful to determine if there is any evidence of respiratory failure.
• Sputum m/c/s (in exacerbations): may reveal Strep. pneumoniae, H. influ-enzae and Moraxella catarrhalis, which can cause infective exac-erbations. Many acute episodes are viral in origin
• ECG: is often normal. If a patient has pulmonary hypertension secondary to COPD, the P wave is tall (P pulmonale), and there may be a right bundle branch block and evidence of right ventricular hypertrophy
• Echocardiography: is useful to assess cardiac function where there is disproportionate dyspnoea.
• α1-Antitrypsin levels: levels and genotype are worth measuring in premature disease or life-long non-smokers
X-ray signs of COPD
• low flat diaphragm
• Increased retrosternal air space
• Tear drop shaped heart
• Signs of Oligaemia
– Diminution of the caliber of pulmonary vessels with rapidity of tapering distally.
• Bullae
– Radiolucent area >1cm in diameter and surrounded by air line shadow.
Overall aims of treatment of COPD
• Reduce symptoms
• Improve exercise tolerance
• Improve health related quality of life
• Prevent exacerbations
• Provide package of care that meets the patient’s needs
• Provide treatment that minimises the risk of adverse effects
• Reduce mortality
• Prevent disease progression
What is the pharmacologic treatment of COPD?
- Bronchodilators
– Beta-agonists (short and long acting)
– Anticholinergics (short and long acting muscarinic antagonists)
– Methylxanthines - Glucocorticoids
– Inhaled
– Systemic - Phosphodiesterase-4 inhibitors e.g. roflumilast
- Combination medications
- Long term oxygen therapy (reduces the progression of heart failure eg. Cor pulmonale)
NON PHARMACOLOGIC
• Pulmonary rehabilitation
• A multidisciplinary programme of care for
patients with chronic respiratory impairment that is individually tailored and designed to optimise physical and social performance and autonomy
– Exercise training
– Education
– Nutritional advise
• Immunisation
– Pneumococcal
– influenza
• Mental health status
• Surgery
– Bullectomy,
– lung volume reduction
– Lung transplantation
• Multidisciplinary care
TREATMENT OF EXACERBATIONS
• Bronchodilators
• Antibiotics
• Corticosteroids (systemic, short course)
• Supplemental oxygen
Precipitants of acute exacerbation
Chest infections
Pleuritic chest pain
Poor drug compliance
Pneumothrax (sudden worsening of breathlessness)
Pulmonary embolism (sudden worsening of breathlessness)
Differentials
Bronchial asthma
Pulmonary TB (chronic cough and weight loss)
Pneumonia (acute cough, breathlessness,
ABPA: allergic bronchopulmonary aspergillosis (cough, weight loss, wheeze)
Left ventricular failure
Congestive cardiac failure with pulmonary edema
Bronchogenic cancer
Bronchiectasis
How would you administer Oxygen for a patient with COPD?
Low dose O2 (1-2L/min) in COPD (because the hypoxia drives the respiration)
High dose O2 15L/min in Pneumonia
Complications
Type 2 respiratory failure
Hypoxemia, low o2 retention , hypercapnia
CO2 retention (a hyper dynamic state): headache, increased lacrimation, papilledema, warm palms, bounding pulse, brisk reflexes?(hyperreflexia), plethora, tachycardia, asterisked, bilateral pedal edema.
Malnutrition
Osteoporosis
Cushing
Polycythemia (which causes the plethora)
Hypoxic encephalopathy
Atrial fibrillation
Depression (most chronic conditions)
