Obstructive Lung Disease

Question 1

What are the shared features of obstructive lung disease?

Answer 1

Decreased rate of forced expiratory air volume due to EITHER increased airflow resistance OR decreased outflow pressure

Question 2

Morphological differences between emphysema due to Cig smoking vs alpha antitrypsin deficiency

Answer 2

centrilobar vs panlobar emphysema (with excess PAS stained globules in hepatocytes)

Question 3

What’s the definition of emphysema?

Answer 3

COPD with permanently enlarged air spaces, destruction of their walls WITHOUT fibrosis

Question 4

What are potential pathological mechanisms that lead to emphysema?

Answer 4

increased pulmonary proteolysis

decreased ANTIproteolysis

Question 5

How can cigarette smoke lead to decreased alpha-antritrypsin function?

Answer 5

Cig–>chemotaxis, netruophils, macs in alveoli–>release of elastase, proteases and ROS–>increased elastolytic activity and oxidation of alpha-antitryps

Question 6

What do we see with centrilobular emphysema?

Answer 6

primarily respiratory bronchioles involved, more severe in upper lung fields, usually b/c of cig smoking

Question 7

If we see uniform destruction of pulmonary lobule, what are we looking at?

Answer 7

Panlobular emphysema due to alpha antitrypsin deficiency (or end stage centrilobar), more severe in lower lobes

Question 8

What type of emphysema is adjacent to areas of fibrosis?

Answer 8

paraseptal

Question 9

Why are those with emphysema described as PINK PUFFERS?

Answer 9

Lungs are hyper inflated so barrel chest AND normal hemoglobin saturation (not hypoxemic)

Question 10

What is the definition of chronic bronchitis?

Answer 10

presence of persistent productive cough without apparent cause for at least 3 months in at least 2 years

Question 11

What are the two major causes of chronic bronchitis?

Answer 11

chronic exposure to toxic inhalants and recurrent respiratory tract infections

Question 12

whats the pathogenesis of chronic bronchitis?

Answer 12

chronic exposure leads to increased mucus production and epithelial squamous metaplasia (both impair clearance) leads to chronic airflow obstruction and predisposition to pulmonary infections

Question 13

How does chronic bronchitis manifest on the bronchial/bronchiolar level?

Answer 13

• Hyperplasia of goblet cells and hyperplastic glands
• increased ratio of thickness of mucous glands to the airway wall
• increased smooth muscle
• inflam infiltrate

Question 14

Why are patients with chronic bronchitis known as blue bloaters?

Answer 14

Marked vent-perf mismatch so hypoxemic (cyanotic) and vasoconstrict in lung leads to pulmonary hypertension leads to peripheral edema (bloat)

Question 15

Gross appearance of lungs in an asthmatic?

Answer 15

distended, overinflated, multiple airways obstructed by viscoid mucous plugs

Question 16

Airway remodeling in asthma patients?

Answer 16

Too many goblet cells! subepithelial mucous gland hyperplasia!
BM fibrosis! too thick
Smooth muscle hyperplasia!
eosinphohil influx

Question 17

What do to the luminal mucous plugs (asthma) “contain?”

Answer 17

Curschmann spirals, eosinophils, Charcot-Leyden crystals

Question 18

What is Bronchiectasis?

Answer 18

Permanent airways dilatation due to recurrent infections with necrosis (dilated but floppy so act as obstruction)

Question 19

what are the pathological features of bronchiectasis? both gross and micrscopic

Answer 19

markedly dilated PERIPHERAL airways extending out to pleura, especially within lower lobes, mixed inflamm cell infiltrate associated wit ulceration, necrosis, scarring.

Question 20

complete airway obstruction might lead to…

Answer 20

acquired atelectasis! resportion of trapped o2 –> alveolar collapse

Question 21

Besides obstruction, what other way can we get acquired atelectasis?

Answer 21

Compression (due to accum in pleural cavity), contraction (pulmonary fibrosis), patchy (loss of sufactant- RDS)