Obstructive Pulm B&B

Question 1

pulmonary obstruction vs restriction

Answer 1

obstruction = air can’t get OUT of lungs (trapped inside)

restriction = air can’t get INTO lungs

Question 2

how does the slope of the spirometry graph change in restrictive and obstructive pulmonary disease, respectively?

Answer 2

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

Question 3

how are FEV1 and FVC affected by obstructive vs restrictive pulmonary disease, respectively?

Answer 3

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

Question 4

which of these values can spirometry NOT measure?
a. FVC
b. RV
c. IRV
d. ERV
e. FRC

Answer 4

spirometry CAN measure FVC, IRV, ERV

cannot measure RV, FRC

Question 5

the work of breathing is proportional to…

Answer 5

… 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

Question 6

how does airflow resistance vs elastic resistance change with breathing, respectively?

Answer 6

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)

Question 7

how does residual and total lung volume change in pulmonary obstruction vs restriction?

Answer 7

obstruction (air trapped): residual and total lung volume go UP

restriction (less filling): residual and total lung volume go DOWN

Question 8

how is chronic bronchitis characterized?

Answer 8

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]

Question 9

describe the physiology of chronic bronchitis

Answer 9

hypertrophy of mucus secreting glands —> mucous plugging and increased risk of infection

—> poor ventilation —> hypoxic vasoconstriction —> pulmonary HTN —> cor pulmonale (right heart failure)

[obstructive]

Question 10

how do patients with chronic bronchitis present?

Answer 10

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]

Question 11

what are 2 possible causes of emphysema? how do they differ?

Answer 11

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]

Question 12

how does emphysema develop?

Answer 12

destruction of alveoli causes loss of elastic recoil, and small airways collapse on exhalation

air gets trapped in lungs (obstructive disease)

Question 13

how does smoking cause the development of emphysema?

Answer 13

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]

Question 14

how do patients with emphysema present?

Answer 14

dyspnea, cough (less sputum than chronic bronchitis), hyperventilating, weight loss (expending a lot of energy to breathe), cor pulmonale, barrel chest

“Pink puffers”

Question 15

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?

Answer 15

emphysema (destruction of alveoli from smoking - obstructive)

Question 16

acinus

Answer 16

bronchiole + alveoli

Question 17

blue bloater vs pink puffer

Answer 17

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]

Question 18

how is alpha1 anti-trypsin deficiency inherited, and what is the consequence of this?

Answer 18

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)

Question 19

how do patients with alpha1 anti-trypsin deficiency typically present?

Answer 19

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!

Question 20

what occurs in asthma?

Answer 20

reversible bronchoconstriction (obstructive disease)

usually allergic stimulus (Type 1 hypersensitivity)

but can also be triggered by stress, exercise, cold, aspirin, URI (upper resp. infection)

Question 21

how does aspirin sometimes trigger asthma?

Answer 21

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)

Question 22

how is asthma diagnosed?

Answer 22

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)

Question 23

what are 2 classic findings of asthma sputum pathology?

Answer 23

1. Curschmann’s spirals: sloughed endothelial cells
2. Charcot-Leyden crystals: eosinophils

Question 24

what occurs in bronchiectasis?

Answer 24

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)

Question 25

what are some symptoms of bronchiectasis?

Answer 25

bronchiectasis: obstructive disease, airways permanently dilated

—> recurrent infections, foul smelling sputum, amyloidosis, cor pulmonale, hemoptysis

Question 26

how can Kartagener’s syndrome cause bronchiectasis? how does it classically present?

Answer 26

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]

Question 27

describe allergic bronchopulmonary aspergillosis (ABPA)

Answer 27

hypersensitivity rxn to aspergillus (opportunistic fungus) - primarily asthma or CF patients

—> high Th2 CD4+ cells, interleukins, eosinophilia, IgE

form of bronchiectasis (obstructive)

Question 28

how will patients with allergic bronchopulmonary aspergillosis (ABPA) present?

Answer 28

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)]