Fouty: pathophys of chronic bronchitis and emphysema Flashcards
chronic bronchitis + emphysema
COPD
at the end of normal expiration (most effort independent out of all PFTs)
functional residual capacity (FRC)
when you blow up a balloon, what is the pressure needing to overcome
elastic recoil
when the lung is not present, what does the chest wall do
springs outwards
___ and ___ are held at equilibrium at FRC
the lung and chest wall
at ____ volume, still some air in lungs requiring some pressure to keep it there
residual volume
what sets the residual volume
characteristics of chest wall (can’t go lower than a certain point)
when the springs are equal tension on both sides
FRC
Inward recoil of the lung=outward recoil of chest wall
FRC
takes____ to move respiratory system away from functional residual capacity
work
work being done to inflate the lungs is required to overcome what 2 things
elastic recoil of lungs and chest wall and airflow resistance
low at high volumes
higher at low volumes
resistive work (airflow resistance)
high at higher volumes (takes more work to keep lungs expanded)
low at lower lung volumes
elastic work
spot of least resistance when breathing
RR of 12-18
volume of 400 mL
pressure of elastic recoil of chest wall and lungs + pressure to overcome resistance to airflow
total pressure (work of breathing)
lung is less stiff and easier to distend (high compliance)—lost its elastic recoil; takes very little pressure to move air in
emphysema
lung is much stiffer, (harder to put air in)—takes more work to distend lung
fibrosis
neonate with no surfactant has to generate what to try and distend lung
generate a lot of negative pressure
is based on the compliance of the chest wall and the lung (effort independent)
FRC
FRC goes down
restrictive disease
FRC goes up
obstructive disease
Provides a reservoir of air in the lung during breathing
FRC
Increases The Resistance To Airflow And Thus Increases The Work Required To Overcome Airway Resistance
obstructive disease
airway resistance is greatest in what airways
large (like river opening up into delta (small airways–more of them)
anything that’s being carried such as tobacco smoke in the lungs gets deposited in the area around the _____
terminal bronchioles
centrilobar/centriacinar emphysema means..
where the respiratory bronchioles transition off the terminal bronchioles
airflow obstruction (<LLN)
increases Lung Volumes And Impairs Airflow
emphysema
flattening of _____ decreases ability to generate pressure
diaphragm
Pressure you can generate is _____ related to radius
inversely (smaller radius, can generate more pressure)
how would this person breathe effectively since they have flattened diaphragm
accessory muscles (external intercostals, sternocleidomastoid, scalenes)
RV higher than normal, FRC higher
obstructive lung disease
TLC is higher in this obstructive lung disease
emphysema
TLC stays the same in this obstructive lung disease
asthma
bronchi filled with mucus and causes luminal narrowing
chronic bronchitis
destruction of elastin; dilated airspaces (bronchioles easily compressible)
emphysema
airflow obstruction that is not fully reversible; emphysema and chronic bronchitis
COPD
Tobacco, work exposures to fumes, secondhand smoke, air pollution, vaping
can lead to COPD
major cause of COPD worldwide
smoking, air pollution, indoor cooking w/ wood
smoker’s cough present for atleast 3 months; excessive sputum production
chronic bronchitis
Narrowing of lumen due to mucous glands and smooth muscle cell hyperplasia
chronic bronchitis
more mucous is being secreted into the airways which impairs airflow obstruction (due to mucous gland hyperplasia)
chronic bronchitis
marked increase in mucous glands
chronic bronchitis
alveolar wall destruction w/ irreversible enlargement of the air spaces distal to terminal bronchioles
emphysema
can cause permanent enlargement of the acinus
emphysema
pan-acinar emphysema (in lower lobes)
A1AT deficiency
centri-acinar emphysema
smokers
Loss of elastic recoil; airways and alveoli lost elasticity that allows them to stay open (easy to collapse); gas trapping
emphysema
destruction of elastic fibers
air trapping
emphysema
“moth eaten”
emphysema
destroys alveolar-capillary bed
emphysema
DLCO decreased in this
emphysema
purse lip breathing
emphysema
emphysema
chronic bronchitis
minimal reversibility
normal to slightly decreased DLCO
chronic bronchitis
marked hyperinflation
no reversibility
decreased DLCO
emphysema
dyspnea
mucus production
wheezing
cough
COPD
Pursed lip breathing
Wheezing
Decreased lung sounds
Barrel chest
Cyanosis
physical exam for COPD
Hb desaturated (hypoxemia)
R heart failure (peripheral edema)
GOLD normal (based on FEV1)
stage 0 COPD
GOLD (based on FEV1) >/= 80%
stage I COPD
GOLD (based on FEV1) 50-79%
stage II COPD
GOLD (based on FEV1) 30-49%
stage III COPD
GOLD (based on FEV1) <30%
stage IV COPD
BMI
obstruction
dyspnea
exercise capacity
BODE index for COPD
treatment of COPD
stop smoking, vaccines
peak age for FEV1
25
worst MMRC stage
D (high risk and high symptoms)
bronchodilators
steroids
O2
PDE4 inhibitors
Rx COPD
decreased exacerbations of COPD by 27%
Azithromycin
Increased dyspnea above baseline
Increased sputum production
Deterioration in arterial blood gas
Increased requirements of bronchodilators
Visits to ER/hospitalization
acute exacerbations of COPD (marker for more severe disease)
most common cause of COPD exacerbations
infection
main 3 bacterial infections for smokers with COPD exacerbation
Haemophilus influenzae
Streptococcus pneumoniae
Moraxella catarrhalis
main virus for COPD exacerbation
rhinovirus
causes of death from COPD
resp. failure
R ventricular failure (cor pulmonale)
pneumonia
spontaneous pneumothorax
must have airway obstruction w/ emphysema and/or chronic bronchitis
COPD