Flashcards in Feb 6 - COPD Deck (26):
How many breaths does a healthy person take per minute? How much air per breath?
Resting breath rate of healthy human is 12-15 times per minute
About 500 ml of air is inspired/expired per breath
What part of the lung becomes damaged in COPD?
Alveoli are the key parts of the lung that become damaged in COPD. Eventually the alveoli start looking like rough cauliflower heads, instead of nice round heads
What is COPD?
Chronic obstructive pulmonary disease
It's a chronic cough with excess sputum/mucous production, inflamed airways. It's also characterized by dyspnea (the most troubling complaint), which causes impaired exercise tolerance and contributes to anxiety and depression
Does COPD affect other systems outside of the respiratory system?
COPD can be a significant burden on extra-pulmonary systems (skin, cardiovascular, liver, kidneys, etc.). For example, if you can't exercise, this has negative consequences for your cardiovascular system
What is chronic bronchitis?
It is one type of COPD. The inflamed bronchi produce a lot of mucous. This leads to cough and difficulty getting air in and out of the lungs. Cigarette smoking is the most common cause.
What is emphysema and chronic bronchitis in COPD?
While previously divided into emphysema and chronic bronchitis, emphysema is only a description of lung changes, rather than a disease itself, and chronic bronchitis is simply a descriptor of symptoms that may or may not occur with COPD
What is emphysema?
Chronic lung condition in which the lungs' natural airspaces, called alveoli, become larger but decrease in number. The tissue surrounding the alveoli loses elasticity so that the air spaces can no longer expand and shrink as usual. This reduces the amount of oxygen transferred by the lungs to the blood stream, making it more difficult for you to breathe
What causes emphysema?
It usually results from exposure to toxins like cigarettes as well as air pollution, dust, chemical fumes, and irritants. Older adults are more likely to be affected and many people who have emphysema are not aware that they have it
What is a host factor that can lead to COPD?
A genetic predisposition; alpha1-antitrypsin (AAT) enzyme deficiency
What is AAT deficiency?
It is a congenital lack of lung anti-protease AAT. AAT has a primary role to protect cells, especially those in the lungs. AAT deficiency leads to increased protease-mediated tissue destruction and emphysema in adults (this accounts for less than 1% of COPD cases)
Describe the natural history of COPD
It's variable between individuals. COPD begins decades before symptoms. Smoking, reduced lung size, etc. leads to reduced max lung function in early adulthood. A disease hallmark: accelerated decline in lung function. Progressive disease, especially if smoking continues. Characteristics recurrent exacerbations (increased symptoms)
What is spirometry?
It measures the amount of airflow obstruction present and is generally carried out after the use of a bronchodilator, a medication used to open up the airways. Two main components are measured to make the diagnosis: the forced expiratory volume in one second (FEV1) which is the greatest volume of air that can be breathed out in the first second of a breath and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single breath
Describe the COPD pathophysiology
Chronic inflammation stimulated by exposure to noxious particles and gases. Inflammatory cells and mediators cause structural changes and narrowing of the small airways. Walls of airways become thick and inflamed. Increased mucous production in airways. Airways and alveoli lose elasticity. Walls between many alveoli are destroyed
What are the key cells in COPD? What the key cells in asthma?
COPD: neutrophils and macrophages
Asthma: Eosinophils, mast cells, Th2 lymphocytes
What are the mediators in COPD? What are the mediators in asthma?
COPD: LTB4, IL-8, TNF-alpha
Asthma: LTD4, IL-4/5
What is the glucocorticoid response in COPD? Asthma?
COPD: variable responses
Asthma: inhibited inflammation
What is the major difference between asthma and COPD?
In asthma we have inflammation resulting in narrowing of the airways with pronounced mucous production whereas in COPD we have the same inflammatory events as asthma along with the structural damage to the parenchyma that results in permanent non-recoverable damage to the lung structures
What is the danger of cigarette smoke?
Cigarette smoke increases oxidants such as hydrogen peroxide and nitric oxide which reach with and damage various proteins and lipids, leading to cell and tissue damage, promote inflammation, and exacerbate the protease-antiprotease imbalance by increased protease activity or reduced activity of antiproteases
What are the major physiological outcomes of COPD?
Mucous hyper-secretion and ciliary abnormalities
Airflow limitation and hyperinflation
Gas exchange abnormalities
Describe the mucous hypersecretion and ciliary abnormalitites
Increased mucous present early on in disease
Increased number and size of goblet cells
Decreased airway clearing ability due to ciliary damage
Describe airflow limitations and hyperinflation
Expiratory airflow limitation is hallmark of COPD
Mainly due to remodelling (fibrosis and narrowing)
Less air flows in/out of airways due to increased resistance
Air gets trapped = hyperinflation
Describe gas exchange and abnormalities
Occurs later on in course of disease
Characterized by hypoxemia (low blood oxygen) +/- hyper-capnia (high blood CO2)
Bronchitis (airway limitation, hyperinflation) and emphysema (alveolar damage/loss) causes altered gas exchange
Describe pulmonary hypertension
Increased pressure in the pulmonary artery
Secondary to gas-exchange abnormalities
Can result in right ventricular hypertrophy and ultimate right-sided heart failure (cor pulmonale)
Describe muscle wasting
Also systemic inflammatory processes
Leads to skeletal muscle wasting
Contributes to decreased exercise capacity = reduced overall health status and prognosis
What is COPD Exacerbations?
A sustained worsening of dyspnea, cough or sputum production leading to an increase in the use of maintenance medications and/or supplementation with additional medication