copd

Question 1

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

Answer 1

definition of copd

Question 2

What are the three hallmarks of copd?

Answer 2

emphysema
chronic bronchitis
combination of both

Question 3

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

Answer 3

COPD

Question 4

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

Answer 4

copd

Question 5

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

Answer 5

pulmonary hypertension

Question 6

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

Answer 6

parenchyma

Question 7

Inflammation of the bronchi and bronchioles due to chronic exposure to irritants

Answer 7

chronic bronchitis

Question 8

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

Answer 8

chronic bronchitis

Question 9

Loss of lung elasticity and hyperinflation of lung tissue

Answer 9

emphysema

Question 10

Inflammation of the bronchi and bronchioles due to chronic exposure to irritants

Answer 10

chronic bronchitis

Question 11

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

Answer 11

emphysema

Question 12

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)

Answer 12

later stages of emphysema

Question 13

corpulmonale is?

Answer 13

right sided heart failure

Question 14

hypercapnia is ?

Answer 14

high co2 levels

Question 15

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

Answer 15

panlobular emphysema

Question 16

Have hyperinflated (hyperexpanded) chest, marked dyspnea on exertion and weight loss

Expiration is not an active response and requires muscular effort

Answer 16

panlobular emphysema

Question 17

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)

Answer 17

centrilobular emphysema

Question 18

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!

Answer 18

risk factor for copd

Question 19

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

Answer 19

risk factors for copd

Question 20

What are the three risk factors for copd?

Answer 20

smoking
AAT deficiency (alphal antitrypsin deficiency)
air pollution

Question 21

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,

Answer 21

s/s of copd

Question 22

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

Answer 22

s/s of copd

Question 23

What are the three primary symptoms of copd?

Answer 23

chronic cough
sputum production
dyspnea on exertion

Question 24

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.

Answer 24

dyspnea with exertion

Question 25

cyanotic
recurrent cough and increased sputum production
hypoxia
hypercapnia
respiratory acidosis
high hemoglobin
high resp rate
exertional dyspnea
common in cigarette sokers
digital clubbing
cardiac enlargement
use accessory muscles to breathe
leads to right sided heart failure

Answer 25

chronic bronchitis (blue bloater)

Question 26

decreased co2 retention
minimal cyanosis
purse lip breathing
dyspnea
minimum cough
hyperresonance on chest percussion
orthopneic
barrel chest
exertional dyspnea
prolonged expiratory time
speaks in short jerky sentences
anxious
use of accessory muscles to breathe
thin appearance

Answer 26

pink puffer for emphysema

Question 27

Pulmonary Function Tests
compares forced expiratory volume to forced vital capacity
Chest X-ray
will see a lot of hyperinflation and flattened diaphragm , will get worse as disease progresses
Arterial Blood Gases (ABGs)
how much co2, oxygen, ph is –monitors resp status
will see increased CO2 and decreased O2 level
will see respiratory acidosis and metabolic alkalosis
Pulse Oximetry
ABG is good but cant do it constantly.
will see less than normal pulse oxes
Peak Expiratory Flow Meters
see what normal is and use it as a measurement as to where you are

AAT levels
Hemoglobin and Hematocrit
look for polycythemia (overproduction of red blood cells)
Sputum Cultures
White Blood Cell Counts
Chest Physiotherapy

Answer 27

diagnostic tools for copd

Question 28

copd patients constantly have high co2 levels in their bodies, respiratory drive for COPD patiets comes from low ______levels

in healthy patients it is bc of high ______ levels, not their ______ levels

if you give a COPD patient too much oxygen, it will make it where they don’t want to breath bc their drive center is not there.

titrate oxygen to keep them in range

Answer 28

oxygen , co2, oxygen

Question 29

History of cigarette smoking
Passive smoking exposure
Age
Rate of decline of FEV1
Hypoxemia

Pulmonary artery pressure
Resting heart rate
Weight loss
Reversibility of airflow obstruction

Answer 29

factors that determine outcome of copd

Question 30

Respiratory insufficiency and failure
May be chronic or acute
Other complications
Pneumonia
Chronic atelectasis
Pneumothorax
Pulmonary arterial hypertension (cor pulmonale)

Answer 30

complications that happen bc of copd