copd Flashcards
a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity of in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases
definition of copd
What are the three hallmarks of copd?
emphysema
chronic bronchitis
combination of both
Deaths from ________ continue to rise
3rd Leading Cause of Death in the US
Annual cost of ________ -approximately $49.9 billion
People with ________ typically become symptomatic during the middle adult years
Although certain aspects of lung function normally decrease with age (vital capacity and forced expiratory volume), ________ accentuates and accelerates these physiologic changes
COPD
Chronic Inflammation and Body’s Attempts to Repair It
Changes and Narrowing of the Airway
Ongoing injury-and-repair process causes scar tissue formation and narrowing of the airway lumen
Alveolar wall destruction = loss of alveolar attachments and a decrease in elastic recoil
Chronic inflammation affects pulmonary vasculature and causes thickening of the lining of the vessel and hypertrophy of the smooth muscle = could lead to pulmonary hypertension
copd
copd starts with ____________, If you have an increased blood pressure in lungs it is difficult for blood circulation to occur. Will have chronic inflammation in response to noxious particles that get into the lungs (windy days, or smoking). the trachea and bronchi –they have increase number of goblet cells, large submucosal glands. inflammation is causing thickening of the airway wall causing fibrosis and exudate in the airway causing airway narrowing.
with all this stuff going on, it will lead to left sided heart failure .
may have imbalance of protease which causes issues with proteins
if there’s a lac of antiprotease it can cause emphysema
pulmonary hypertension
Imbalances of proteinases and antiproteinases
When activated by chronic inflammation proteinases and other substances may be released damaging the ______ of the lung
Contribute to airflow limitation
parenchyma
Inflammation of the bronchi and bronchioles due to chronic exposure to irritants
chronic bronchitis
Often … smoke or other environmental pollutants irritate the airways inflammation and hypersecretion of mucus
Constant irritation increase in mucus-secreting glands and goblet cells increased mucus production
Mucus plugging the airways reduces ciliary function
Bronchial walls become thickened = narrowing of bronchial lumen
Alveoli near the bronchioles may become damaged and fibrosed = altered function of the alveolar macrophages
Increased susceptibility to respiratory infection
chronic bronchitis
Loss of lung elasticity and hyperinflation of lung tissue
emphysema
Inflammation of the bronchi and bronchioles due to chronic exposure to irritants
chronic bronchitis
Causes destruction of the overdistended alveoli leading to decreased surface area for gas exchange, carbon dioxide retention and respiratory acidosis
Destruction of alveoli is the end stage of a long process accelerated by recurrent infections
As alveoli are destroyed, the alveolar surface area in direct contact with pulmonary capillaries continually decreases = impaired oxygen diffusion hypoxemia
emphysema
Carbon dioxide elimination is impaired = increased CO2 in arterial blood (hypercapnia) leading to respiratory acidosis
Alveolar walls continue to break down = pulmonary capillary bed is reduced in size pulmonary hypertension = increased pressure in pulmonary artery
Hypoxemia increases pulmonary pressures further right-sided heart failure congestion, dependent edema, distended neck veins, pain in the liver area (suggests development of cardiac failure)
later stages of emphysema
corpulmonale is?
right sided heart failure
hypercapnia is ?
high co2 levels
destruction of the bronchiole, alveolar duct and alveolus
a. All air-spaces within lobule are enlarged
b. Little inflammatory disease
c. Have hyperinflated (hyperexpanded) chest, marked dyspnea on exertion and weight loss
d. To move air in and out of lungs, require negative pressure during inspiration and must have an adequate level of positive pressure during expiration
e. Expiration is not an active response and requires muscular effort
panlobular emphysema
Have hyperinflated (hyperexpanded) chest, marked dyspnea on exertion and weight loss
Expiration is not an active response and requires muscular effort
panlobular emphysema
pathologic changes take place mainly in the center of the secondary lobule
a. Frequently, there is derangement of ventilation-perfusion rations chronic hypoxemia, hypercapnia, polycythemia, right-sided heart failure
b. Leads to central cyanosis and respiratory failure
C. Develops peripheral edema (treated with diuretics)
centrilobular emphysema
CIGARETTE SMOKING! (and Second Hand Smoking!)
Smoking depresses the activity of scavenger cells and affects the respiratory tract’s ciliary cleansing mechanism which keep breathing passages free of inhaled irritants, bacteria and other foreign material
With a damaged cleaning system, airflow is obstructed and it becomes trapped behind the obstruction alveoli greatly distend, diminishing lung capacity
Also, smoking irritates the goblet cells and mucous glands causing increased mucous resulting in increased irritation and so on
Carbon Monoxide (byproduct of smoking) combines with hemoglobin = carboxyhemoglobin cannot carry oxygen efficiently!
risk factor for copd
Alpha1-antitrypsin (AAT) deficiency
1 in 6 with COPD have never smoked involves a gene-environment interaction
This enzyme protects lung parenchyma from injury
Need to modify environmental risk factors
Need genetic counseling
if they want kids
Need Alpha-protease inhibitor replacement therapy (slows progression of disease
Exposure to Air Pollution
risk factors for copd
What are the three risk factors for copd?
smoking
AAT deficiency (alphal antitrypsin deficiency)
air pollution
dyspnea, cough, hypoxemia, hypercarbia (increased co2), respiratory acidosis, compensatory metabolic acidosis, crackles are heard a lot, wheezing can be heard, breath very quickly but also very shallow, use all of their accessory muscles, will have a barrel chest, hyper resonance in the lungs (trapped air), breathing could be asynchronous, thin or skinny extremities and a really thick neck, can see secondary edema,
in late disease process, pale, clubbed nails,
s/s of copd
wheezing
pused lip breathing
chronic cough
barrel chest
dyspnea
prolonged expiratory time
digital clubbing
thin in appearance
cor pulmonale (late disease)
easily fatigued
frequent respiratory infections
use of accessory muscles to breathe
orthopneic
s/s of copd
What are the three primary symptoms of copd?
chronic cough
sputum production
dyspnea on exertion
chronic cough and sputum production often happen years before ______ in copd, weight loss is common as it gets worse, super high risk for respiratory infection, increased risk for acute and chronic respiratory failure.
dyspnea with exertion
