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COPD.docx

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School
Department
Health Science
Course
HLSC 2461U
Professor
Otto Sanchez
Semester
N/A

Description
COPD  Chronic Obstructive Pulmonary Disease Prevalence: 600,000 Canadians [1.7% of pop.] Mortality: 5 cause in men [4.5 per 100,000] 4 in women [2.8 per 100,000] Smoking in 80-90% of individuals with COPD 50% of smokers have sub-clinical COPD  Smoking “increases” your risk for lung cancer but doesn’t cause it  Smoking causes COPD  Whenever we get a cold we get an obstruction of the airways but this is acute, in COPD cases it is chronic, which can eventually lead to heart disease  Person with COPD has an airway problem (can be reversible) and a pulmonary problem (irreversible most of the time) Steps of COPD Step 1: Smoking Step 2: Chronic bronchitis Step 3: Emphysema Step 4: Chronic hypoxemia Step 5: Cor pulmonale  this all takes YEARS to develop but we only start seeing it happen in the 50’s because of irreversible pulmonary disease Step 2 – Chronic Bronchitis  The first thing is that it injures epithelial cells in the bronchi. When cells get attacked they are injured and the epithelial cells have glands (secret mucous) that react to fight and protect. That’s why you see that the first thing that happens when you start smoking is that you start losing more secretions because this is a defense mechanism in the airway.  Chronic smoking causes many of the cells to die.  The danger is in the ones that adapt. The respiratory epithelium is ciliated. When these cells are attacked they become metaplasia. The respiratory epithelium becomes squamous epithelium. This epithelium does have any cilia, therefore when you get a cold it’ll take a lot longer to get over the cold. This can also cause infection.  Smoke has carcinogens so many of the cells that adapt will be defected.  Chronic bronchitis is airways that are full of mucous all the time.  If you stop smoking the dysplasia will disappear and most of the cilia will come back.  Air trapping is a big problem for people with chronic bronchitis  The second thing that happens is something that is called bronchiectasis. This is dilation of the bronchi. This is because chronically inflamed walls can become permanently dilated. This will cause turbulence and mucous, fungi and bacteria, biofilms will form there (people will have infections all the time).  Once you have weakened bronchial walls, it’ll never go away (if you stop smoking). Step 3 – Emphysema  is pulmonary damage caused by obstruction called emphysema.  It is basically a lung with a lot of holes. If these holes break (pleura) the lungs might collapse this is called pneumothorax.  Air trapping will increase the pressure inside all of the alveolar sacs.  Whenever you smoke you are inducing inflammation in the alveolar walls and eventually this wall will be destroyed and that’s how these holes happen.  The alveolar walls are essential for gas exchange and they have the capillaries that come from the pulmonary arteries.  If you started smoking, it would damage your alveolar walls. The roll of macrophages is to phagocytosis anything that comes through the air. So if you smoke the macrophages will try to eat the  Whenever you smoke the deeper you inhale the more stuff will get into your alveolar walls and this will cause acute inflammation.  Elastase is an enzyme that is released to clean up the inflammatory cells. These are very bad in the lungs because they will be destroyed and this will cause the alveolar walls to become weaker.  Some families have more anti-elastase and protection, and some of them have inherited alpha1 antitrypsin which neutralized elastase which protects them against COPD and emphysema. Step 4- Chronic Hypoxemia  This shows why hypoxemia occurs  In smokers you get impaired ventilation, collapsed alveoli or alveolar dead space (although air goes in there is no blood going in)  When the venous blood bypasses the lungs is it called shunting (short cut that the blood takes so it doesn’t get oxygenated) the more emphysema the more shunting.  Whenever this person gets an infection that they will go into respiratory acidosis and they will be chronically hypoxemic.  Because the alveolar walls are required to remove CO2 then CO2 will not be removed causing hypercapnia (person will breath more, look like they’re in distr
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