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KK RESPII Exam 1 > Gomez - Obstructive vs Restrictive Pulm Disease > Flashcards

Gomez - Obstructive vs Restrictive Pulm Disease Flashcards

1
Q

How is obstructive airway disease defined in terms of FEV1 and FVC

A

FEV1/FVC is reduced (<0.7)

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2
Q

What are the four classes of emphysema?

A

Centriacinar/centrilobular (most common)

Panacinar/panlobular

Distal acinar/paraseptal

Irregular/paracicatrical

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3
Q

Describe centriacinar/centrilobular emphysema

A

Most common form of emphysema, > 95% of cases

Found in smokers

Mainly upper lobes/apices are involved

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4
Q

Describe panacinar/panlobular emphysema

A

Associated with α-1 antitrypsin deficiency

Smoking will result in earlier onset

Mostly in lower lobes

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5
Q

Describe distal acinar/paraseptal emphysema

A

Genetic component

Happens in relatively young adults

Associated with formation of subpleural blebs

Blebs can burst and result in pneumothorax

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6
Q

Describe irregular/paracicatrical emphysema

A

Most common, but most clinically insignificant

Occurs anywhere there has been scarring of lung

Causes relatively few symptoms because of small, localized areas of damage

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7
Q

What is the eitology of emphysema?

A

Proteolytic digestion of alveolar walls

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8
Q

What causes proteolytic digestion of alveolar walls?

A

Inflammatory cells like neutrophis secreting neutrophil elastase

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9
Q

What inhibits neutrophil elastase?

A

α-1 antitrypsin

Deficiency will cause increased and earlier onset of emphysema

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10
Q

How does tobacco contribute to the abundance of neutrophil elastase?

A

Tobacco induces formation of free radicals

Free radicals inactivates α-1 antitrypsin

This inactivation results in upregulation of neutrophil elastase

Leads to emphysema

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11
Q

What is the clinical picture of emphysema?

A

Breathing out becomes more difficult

Sx develop after damage to about 1/3 of lung tissue

Low FEV1/FVC, high TLC and RV

Gas exchange is initially adequate

Pts purse their lips to increase back-pressure upon expiration to keep bronchi inflated - “pink puffers”

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12
Q

Why do lungs transplanted into emphysema pts not become emphysematous?

A

Pt placed on immunosuppresive drugs post transplant

These reduce presence of inflamatory cells

Few to no neutrophils present in lungs to secrete elastase

Therefore it doesn’t matter if pt has α-1 antitrypsin deficiency or not, there are no inflammatory cells to cause destruction

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13
Q

Describe compensatory hyperinflation

A

Enlarged airspaces due to loss of adjacent tissue

No alveolar damage

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14
Q

Describe obstructive overinflation

A

Obstruction that allows air in upon inspiration, but occludes airway upon expiration

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15
Q

What is the definition of chronic bronchitis?

A

3 months of productive cough per year over two consecutive years

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16
Q

What is bronchiolitis obliterans?

A

Destruction of small airways

17
Q

Why do pts with chronic bronchitis develop cor pulmonale?

A

Possible explanation:

Fibrosis due to recurrent infectious processes affects blood vessels, preventing their expansion

This leads to increased pressures which can lead to pulmonary HTN

Eventually causes R heart strain and cor pulmonale

18
Q

Why do bronchitis pts have hypoxemia?

A

Increased mucus presence in alveoli impairs gas exchange

Results in pts who are very short of breath and can’t exercise much

Called “blue bloaters” due to cyanosis

19
Q

What is the Reid index?

A

Ratio of thickness of glands to the thickness of the wall

Normal should be .4 or less

20
Q

Describe asthma

A

Chronic inflammatory airway disorder

Episodic in nature

Partially reversible attacks

21
Q

What type of hypersensitivity is atopic asthma classified as?

A

Type I hypersensitivity

22
Q

What is the role of IL-13 in asthma?

A

Stimulates submucosal gland hyperplasia

More mucus production

23
Q

What is a classic cause of drug-induced asthma? What is the mechanism?

A

Aspirin

Because ASA inhibits COX, but not lipoxygenase, there is a shunt, so more leukotrienes produced

Increased leukotrienes causes bronchoconstriction

24
Q

What are common morphologic changes observed in pts with Type I asthma?

A

Airway remodeling resulting in:

Epithelial injury

Fibrosis

Eosinophilic inflammation in bronchial wall

Submucosal gland hyperplasia and increased goblet cells

25
Q

What are Charcot-Leyden crystals?

A

Precipitates of galectin-10 containing crystalloid

Galectin-10 comes from eosinophils

26
Q

What are Curschmann spirals?

A

Strip of dead epithelial cells that have been shed off

27
Q

What is bronchiectasis? What causes it?

A

Permanent dilation of bronchi and bronchioles

Caused by tissue destruction by infection, resulting in large quantities of foul smelling mucus

28
Q

What conditions are associated with bronchiectasis?

A

Cystic fibrosis

Obstruction

Infection

Pulmonary sequestration

KK RESPII Exam 1 (9 decks)

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