OBSTRUCTIVE lung disease Flashcards
2 major causes of airflow obstruction
1) intrinsic airway narrowing (bronchospasm, plugging, inflame/edema)
2) “floppy airways- decr radial tethering or decr airway integrity
relationship of Airways resistance with airway radius
airway resistance = 1 / airway radius ^ 4
Work of breathing is combination of 2 things
Work against elastic recoil work against airflow resistance
Elastic work and resistive work graph

In obstructive disease are you
incr/decr O2 consumption
incr/decr CO2 conusmption
easier/harder to move air in and out
incr O2 consumption
incr CO2 consumption
harder to move air in and out
How does airflow obstruction incr lung volume
Incomplete emptying of alveoli
incr TLC (breath stacking, gas trapping)

How does diaphragm change in obstructive disease
diaphragm gets flattened because pressure builds up and pushes down

How does hyperinflation and obstructive disease affect
RV
ERV
IC
incr RV
incr ERV
incr FRC
decr IC

How does flattening of diaphragm in obstructive disease affect inspiration?
why?
less inspiratory pressure because incr radius of curvaure
so diaphragm must generate more tension
Lung disease assoc with
Trachea
Bronchi
Bronchioles
Respiratory bronchioles
Alveolar sacs
Trachea = upper airway obstruction
Bronchi = bronchitis
Bronchioles = asthma, bronchiectasis
Respiratory bronchioles = bronchiolitis
Alveolar sacs = emphysema
Asthma
1) describe
2) symptoms
3) assoc with ?
4) physical exam
1) chronic inflamm of airways; reversible
2) airway hyperresponsive
wheezing
breathlessness
chest tightness
dyspnea
cough at night/morning
3) exercise, cold air, allergens, infection
4) maybe normal in stable
incr RR, accessory muscle use
expiratory wheezing
Two types of asthma
1) extrinsic = allergic
IgE
2) Intrinsic = nonseasonal, non allergic
chronic and persistent
= Post viral (epithelail injury causing bronchial narrowing)
- incr leukotrienes, decr porstaglandins
Factors that influence development of asthma
1) genetic predisposition
2) enviornmental (allergens, animals, infection, occupation, smoke)
Molecular underlying causes of asthma1
1) airway hypertrophy of smooth muscle cells
2) mucous plugging
3) incr Th2 pathway so incr mast cells, eosinophils
Th2 process of asthma
1) allergen picked up by macrophage/dendritic cell
2) Th2 cell
3) eosinophil and mast cell release histamine
4) mucous plugging and smooth muscle hypertrophy
PFTs of asthma
normal if no symptoms
normal to incr DLCO
bronchoprovocation with methacholine (airway irritant) shows hyperreactivity
3 Different courses of asthma
1) chronic inflamm = mild persistent
2) incr airway obstruction = moderate persistent
3) irrev airway obstruction = severe
Signs of acute asthma
Hyperinflation
Unable to exhale fully before next breath = incr TLC
Decr tension by shortened diaphragm
Accessory muscle use
incr work of breathing
Molecular changes in acute asthma
1) inflammation, cellular infiltrates
2) epithelial desquamation
3) smooth muscle hypertrophy
4) mucous plugging
P-V curve of asthma
Same shape just raised up

Vocal cord dysfunction
1) describe
2) airflow vs. volume curve
3) symptoms
4) coexists with?
1) inappropriate vocal cord motion –> airflow obstruction
2) variable extrathoracic pattern from closing up of vocal cords with inspiration
3) symptoms same as asthma EXCEPT INSPIRATORY STRIDOR
4) asthma

How do you use bronchoprovocation studies in VCD?
How do you treat?
VCD may worsen with bronchoprovocation BUT NO CHANGES IN FEV1 OR PC20 BECAUSE NOT EXPIRATORY
acute treatment = anxiolytics, H2-O2 mix
long term = speech therapy
COPD
1) Define
2) PFT
3) major cause
1) fixed airflow obstruction
2) FEV1/FVC < 0.7
3) tobacco smoke


