Pathology Of Obstructive And Restrictive Lung Disease

Front 1

What are the main types of COPD

Back 1

Chronic bronchitis
Emphysema
Bronchiectasis
Asthma

Front 2

Define chronic bronchitis

Back 2

Production of excessive mucus in the bronchial tree on most days for at least 3 months a year for 2 successive years

Front 3

Describe the changes in chronic bronchitis

Back 3

1. increased size of mucus glands
2. Increased Reid index (ratio of thickness of mucus glands to thickness of bronchial wall)
3. some inflammation

Front 4

Features of chronic bronchitis

Back 4

-mostly older men
-cigarette smokers or dusty occupations
-frequently associated with centrilobular emphysema
-inflammation

Front 5

Define emphysema

Back 5

3Ds: dilation and destruction distal to the terminal bronchiole

Front 6

4 types of emphysema

Back 6

1. centriloular- blue bloaters
2. panlobular- pink puffers
3. paraseptal- very focal, near scar. not associated with general symptoms
4. irregular- diffuse plate-like scars in lungs

Front 7

Centrilobular

Back 7

-No fibrosis; alveolar wall is large and dilated.
-When the alveolar wall is knocked out, the alveolar capillaries and the ability to do diffusion are knocked out
-small airways are supported by alveolar walls. When the alveoli are knocked out, small airways collapse prematurely- proximal damage
-looks like "popcorn
-destruction is confied to the terminal and respiratory bronchioles
-prefers apex of lungs

Front 8

Panacinar

Back 8

-terminal bronchioles, respiratory bronchioles, and alveoli are dilated and destroyed
-no regional preference in lungs

Front 9

Hallmarks of emphysema

Back 9

-normal septae but loss of uniform architecture
-no fibrosis
-when the dilated and destroyed areas coalesce they form bullae which are dead spaces and no gas exchange takes place there

Front 10

How do you diagnose emphysema

Back 10

x-ray studies and pulmonary function studies

Front 11

What is bronchiectasis

Back 11

permanent state of abnormal airway dilation resulting from chronic necrotizing infection.
-You lose the natural taper-off = "tram lines"

Front 12

Causes of bronchiectasis

Back 12

1.bronchial obstruction- tumor, foreign body, mucus impaction
2. hereditary or congenital conditions- CF
3. Some sort of necrotizing pneumonia with tissue destruction (TB)

Front 13

Two factors that must happen to get bronchiectasis

Back 13

1. obstruction
2. recurrent infection

Front 14

What are the anatomic types of bronchiectasis

Back 14

Cylindroid and Saccular

Front 15

Define asthma

Back 15

Reversible airway narrowing which over time can produce specific morphological changes. Increased irritation of the tracheobronchial tree leads to paroxysmal narrowing of bronchial airways, may reverse with treatment

Front 16

Morphological changes associated with asthma

Back 16

1. Curshmann Spirals- mucus casts of small airways
2. Eosinophils
3. Charcot-Leydon Crystals- casts of eosinophil membranes
4. bronchial structural alterations- thickening of bronchial epithelial basement membrane, edema, infiltration of bronchial walls by eosinophils, hypertrophy of submucosal glands, and hyperplasia of bronchial smooth muscle.
5. Mucus plugging may be common

Front 17

Someone dies and the have hyperinflated lungs. why did they die?

Back 17

Could be status asthmaticus. they would be hyperinflated from mucus plugging. people die due to the work of breathing

Front 18

Types of asthma

Back 18

1. Immune and non-immune are the most common
2. Aspirin sensitive
3. Industrial
4. Asperigillosis

Front 19

Bronchiolitis

Back 19

Interplay of cellular infiltrate and mesenchymal reaction that works at the small airway. Neutrophilic. Bronchiole swelling can occur upstream. Can get fibrous plugs in bronchiolitis.

Front 20

Spectrum of bronchiolitis

Back 20

Asthmatic type changes. Chronic bronchitis/emphysema-associated bronchiolar changes. Cellular bronchitis. Bronchiolitis obliterans.

Front 21

End stage restrictive interstitial fibrosis

Back 21

-Honeycomb appearance
-When lung is injured it responds with granulation tissue (fibroblasts and new capillaries). When alveoli are injured, they respond with fibrosis

Front 22

Restrictive Lung Disease

Back 22

Principal morphological change is thickening of the alveolar wall or interstitial space either by cellular infiltrate or by fibrosis
-Move air in and out quickly since airways are held open.
-Maximum ventilatory capacity is very high
-With fibrosis, new vascular beds can't be recruited so a drop in PaO2 with exertion occurs

Front 23

Current idea on cause of idiopathic interstitial fibrosis

Back 23

An imbalance between cell-mediated factors that improve tissue restoration and those antibody-mediated factors that lead to fibroblast activity and matrix deposition in the interstitium.

Front 24

How do you diagnose restrictive lung disease

Back 24

Open lung biopsy

Front 25

What is the temporal profile with restrictive lung disease

Back 25

There is an acute type with diffuse alveolar damage and a chronic type

Front 26

Cell mediated versus antibody mediated response in lung

Back 26

Cell-mediated involves TH1 and leads to tissue restoration while antibody-mediated involves TH2 and leads to fibrosis via fibroblast activity. IFN gamma is TH1

Front 27

Define pneumoconiosis

Back 27

Pulmonary diseases caused by inhalation of inorganic dusts. Silica, Asbestos, and coal dust

Front 28

Pathophys of pneumoconiosis

Back 28

When dust is first inahled, alveolar macrophages dictate the response. there will be a reaction that increases fibrosis of alveolar wall and alveolus. This can lead to restrictive lung disease

Front 29

How do you diagnose pneumoconiosis

Back 29

tissue or xray

Front 30

Hypersensitivity pneumonitis

Back 30

an immune response in the lungs to inhaled antigens. example is bird antigens causing granulomatous rxn in lungs

Front 31

Define pulmonary edema (cardiac)

Back 31

extrusion of edema fluid, initially in the interstitium, and then in the alveolar filling phase, produced by cardiac failure. causes an increase in V/Q mismatch. You diagnose it by history, physical exam and xray. may be in a few minutes or chronic.

Front 32

Pulmonary edema (noncardiac)

Back 32

the destruction of the alveolar epithelium or endothelium resulting in interstitial edema and alveolar filling edema in the setting of normal cardiac function. Caused by injury to alveolar endothelium or epithelium. There is an exudative phase (first week), then a proliferative phase (weeks one to three), then a fibrotic phase (week three on)

Front 33

How do you distinguish cardiac and noncardiac pulmonary edema

Back 33

Compare the pressures. In non-cardiac edema, the heart pressures are fine while they are not fine in cardiac edema.