Obstructive Pulm B&B Flashcards
pulmonary obstruction vs restriction
obstruction = air can’t get OUT of lungs (trapped inside)
restriction = air can’t get INTO lungs
how does the slope of the spirometry graph change in restrictive and obstructive pulmonary disease, respectively?
restrictive graph/ slope looks similar to normal, but smaller (working with less oxygen because it can’t get into lungs) - decreased plateau (FVC), decreased FEV1
obstructive slope is much less steep and also smaller (can’t get air out of lungs) - decreased plateau (FVC), decreased slope, MUCH smaller FEV1, reduced FEV1/FVC
how are FEV1 and FVC affected by obstructive vs restrictive pulmonary disease, respectively?
restrictive: can’t get air INTO lungs —> similar slope as normal but smaller, decreased FEV1 and FVC
obstructive: can’t get air OUT of lungs —> decreased slope, decreased FVC, VERY decreased FEV1, reduced FEV1/FVC
*note that FVC decrease is similar between restrictive and obstructive diseases
which of these values can spirometry NOT measure?
a. FVC
b. RV
c. IRV
d. ERV
e. FRC
spirometry CAN measure FVC, IRV, ERV
cannot measure RV, FRC
the work of breathing is proportional to…
… airflow resistance and elastic resistance
airflow resistance: slower you breathe, less resistance (less turbulence)
elastic resistance: faster you breathe, less resistance (alveoli don’t have to deflate and reflate all the way)
breaths per minute fall at intersection of these
how does airflow resistance vs elastic resistance change with breathing, respectively?
airflow resistance: slower you breathe, less resistance (less turbulence)
elastic resistance: faster you breathe, less resistance (alveoli don’t have to deflate and reflate all the way)
*breaths per minute fall at intersection of these (graphically)
how does residual and total lung volume change in pulmonary obstruction vs restriction?
obstruction (air trapped): residual and total lung volume go UP
restriction (less filling): residual and total lung volume go DOWN
how is chronic bronchitis characterized?
chronic cough with productive sputum for at least 3 months over 2 years, with no other cause of cough present
strongly associated with smoking
[obstructive]
describe the physiology of chronic bronchitis
hypertrophy of mucus secreting glands —> mucous plugging and increased risk of infection
—> poor ventilation —> hypoxic vasoconstriction —> pulmonary HTN —> cor pulmonale (right heart failure)
[obstructive]
how do patients with chronic bronchitis present?
cough (w/ sputum), wheezing, crackles, dyspnea, cyanosis (due to capillary shunting)
mucous plugging —> increased risk of infection, poor ventilation, pulmonary HTN —> cor pulmonale (right heart failure)
[obstructive]
what are 2 possible causes of emphysema? how do they differ?
smokers (most common): too many proteases overwhelming anti-proteases, mostly upper lung damage (think of smoke rising), centriacinar damage
alpha1 anti-trypsin deficiency (rare): ineffective anti-proteases, lower lobe damage, panacinar damage
[acinus = bronchiole + alveoli]
how does emphysema develop?
destruction of alveoli causes loss of elastic recoil, and small airways collapse on exhalation
air gets trapped in lungs (obstructive disease)
how does smoking cause the development of emphysema?
smoke activates macrophages, which recruit neutrophils
proteases are released, which overwhelm homeostatic level of anti-proteases
destruction of alveoli occurs (centriacinar), esp. in upper lung (think of smoke rising)
[obstructive]
how do patients with emphysema present?
dyspnea, cough (less sputum than chronic bronchitis), hyperventilating, weight loss (expending a lot of energy to breathe), cor pulmonale, barrel chest
“Pink puffers”
Pt is a 48yo M with 20 year history of smoking 2 packs a day, presenting with dyspnea, productive cough, weight loss, and hyperventilation. CXR shows a barrel chest.
What is your diagnosis?
emphysema (destruction of alveoli from smoking - obstructive)
acinus
bronchiole + alveoli
blue bloater vs pink puffer
blue bloater = chronic bronchitis: cyanosis from shunting (blue) and air trapping (bloated)
pink puffer = emphysema: loss of alveoli/surface area for O2 absorption causes hyperventilation (puffer) which initially maintains perfusion (pink)
[both obstructive diseases]
how is alpha1 anti-trypsin deficiency inherited, and what is the consequence of this?
autosomal co-dominant inheritance of decreased/dysfunction alpha1 anti-trypsin, which balances naturally occurring proteases in lung
higher levels of elastase in alveolar macrophages/neutrophils causes panacinar emphysema —> lower lung damage (obstructive)
also may cause liver cirrhosis (abnormal alpha1 builds up)
how do patients with alpha1 anti-trypsin deficiency typically present?
alpha1 anti-trypsin deficiency: causes panacinar emphysema with lower lung damage (obstructive)
COPD symptoms (cough, sputum, wheeze) in younger patients (40s)
smoking for these patients would be disastrous!
what occurs in asthma?
reversible bronchoconstriction (obstructive disease)
usually allergic stimulus (Type 1 hypersensitivity)
but can also be triggered by stress, exercise, cold, aspirin, URI (upper resp. infection)
how does aspirin sometimes trigger asthma?
AERD: aspirin exacerbated respiratory disease (asthma, chronic rhinosinusitis, nasal polyposis)
due to dysregulation of arachidonic acid metabolism leading to overproduction of leukotrienes
(treat with leukotriene receptor antagonist - Montelukast, Zafirlukast)
how is asthma diagnosed?
methacholine challenge: muscarinic agonist, causes bronchoconstriction - administered small amounts via nebulizer and use spirometry to see when FEV1 falls significantly
if FEV1 falls at a low dose —> positive test
(asthma is obstructive disease)
what are 2 classic findings of asthma sputum pathology?
- Curschmann’s spirals: sloughed endothelial cells
- Charcot-Leyden crystals: eosinophils
what occurs in bronchiectasis?
bronchiectasis: chronic/recurrent airway inflammation causes large airways to become permanently dilated and small/medium airways to have thickened bronchial walls
obstructive pulmonary disease (less air getting out)
what are some symptoms of bronchiectasis?
bronchiectasis: obstructive disease, airways permanently dilated
—> recurrent infections, foul smelling sputum, amyloidosis, cor pulmonale, hemoptysis
how can Kartagener’s syndrome cause bronchiectasis? how does it classically present?
Kartagener’s syndrome = primary ciliary dyskinesia: AR mutation in dynein
classic case: child with recurrent ear/sinus infections and cough, showing bronchiectasis on chest CT (permanent airway dilation - obstructive disease)
[can also cause male infertility and situs inversus]
describe allergic bronchopulmonary aspergillosis (ABPA)
hypersensitivity rxn to aspergillus (opportunistic fungus) - primarily asthma or CF patients
—> high Th2 CD4+ cells, interleukins, eosinophilia, IgE
form of bronchiectasis (obstructive)
how will patients with allergic bronchopulmonary aspergillosis (ABPA) present?
classically asthma or CF patient with recurrent episodes of cough/fever
brownish mucus plugs, hemoptysis, eosinophilia, IgE, bronchiectasis on imaging (airway dilation)
[form of bronchiectasis (obstructive)]
