Pathology Of Obstructive And Restrictive Lung Disease

Front 1

T/F: The alveolar walls do not have cells in them normally.

Back 1

True.

Front 2

Name the 4 components of COPD.

Back 2

chronic bronchitis, emphysema, bronchiectasis, and asthma (ABC & E)

Front 3

T/F: One must have all four components to have COPD.

Back 3

False.

Front 4

Pleural lymphatics help to demarcate _____.

Back 4

the pulmonary secondary lobule.

Front 5

Secondary lobule consists of ____ pulmonary acini.

Back 5

5-7

Front 6

How many divisions of the trachea are there?

Back 6

23 (like Micheal Jordan... or Lebron)

Front 7

What is the definition of chronic bronchitis? Hint: Clinical....

Back 7

Production of excess mucus secretion in the bronchial tree occuring on most days for at least 3 months in a year for at least 2 succesive years.

Front 8

Name the two alterations to mucosa seen in CB.

Back 8

1)hyperplasia of glands
2)some degree of inflammation

Front 9

Reid index?

Back 9

Ratio of mucus glands to wall thickness (increased in CB)

Front 10

COPD is usually associated w/ ____ emphysema.

Back 10

centrilobular

Front 11

3 D's of emphysema.

Back 11

Dilation
Destruction
Distal to the terminal bronchioles

Front 12

"Blue bloaters"

Back 12

centrilobular emphysema

Front 13

"Pink puffers"

Back 13

panlobular emphysema

Front 14

Type of emphysema: very focal, near scar. Not associated w/ general symptoms.

Back 14

Paraseptal

Front 15

Type of emphysema: diffuse plate-like scars

Back 15

Irregular

Front 16

T/F: Alveolar damage can cause small airways to collapse.

Back 16

True

Front 17

Why do emphysema patients purse their lips to breathe?

Back 17

create positive pressure to keep their small airways open

Front 18

End stage of emphysema.

Back 18

The dialated areas coalesce forming bullae. Bullae are dead space w/ no gas exchange.

Front 19

What is the most reproducible feature of emphysema, regardless of the type?

Back 19

reduced expiration of air (decreased FEV1)

Front 20

Define bronchiectasis.

Back 20

Permanent state of abnormal airway dilation resulting from chronic necrotizing infection.

Front 21

Three causes of bronchiectasis.

Back 21

1)Pneumonia
2)Obstruction (tumor, etc.)
3)Genetic (CF)
Think about a POG stuck in your bronchiole, dilating it.

Front 22

CF patients tend to present w/ ____ lobe bronchiectasis.

Back 22

upper (mucus defies gravity)

Front 23

Two factors that must occur to get bronchiectasis.

Back 23

1)Obstruction
2)Recurrent infection
"If you have bronchiectasis, then you better go the OR"

Front 24

Two anatomic types of bronchiectasis.

Back 24

1)Cylindroid
2)Saccular
"Think about a penis and scrotum (cylinder and sac)"

Front 25

T/F: Bronchiole stays the same thickness and diameter in a healthy individual.

Back 25

False. Bronchiole tapers normally, but in bronchiectasis there is no tapering (Tram lines). Think about a train driving through your lungs... that would hurt.

Front 26

Define asthma.

Back 26

REVERSIBLE airway narrowing which over time may produce specific morphological changes.

Front 27

Four morphological changes seen in asthma:

Back 27

1)Sputum changes
2)EOSINOPHILS (important)
3)Curshmann spirals
4)Charcot-Leyden crystals
"The SEC is Cool"

Front 28

A cast of airway caused by clamping down on mucus. Seen in asthma.

Back 28

Curshmann spirals.

Front 29

Ashtma is a ____ airway disease.

Back 29

small

Front 30

Four bronchial alterations seen in asthma.

Back 30

1) Thickening of BM
2) Edema
3) Eosinophil infiltration
4) Hypertrophy and hyperplasia of s.m. and glands

Front 31

Name 5 types of asthma:

Back 31

1)Reaginic (immune)
2)Nonreaginic (non-immune)
3)Asprin sensitive
4)Industrial
5)Aspergillosis

Front 32

T/F: Bronchiolitis is an essential component of COPD.

Back 32

False. Not part of COPD.

Front 33

Bronchiolitis is seen more frequently in ___.

Back 33

children

Front 34

Bronchiolitis involves what cells?

Back 34

neutrophils

Front 35

Asthma involves what cells?

Back 35

eosinophils

Front 36

When lung is injured it responds w/?

Back 36

granulation tissue

Front 37

T/F: Granulation is seen in tracheobronchial tree, pleura, and alveolar processes.

Back 37

False. Not seen in alveoli

Front 38

What happens when the alveoli are injured?

Back 38

Fibrosis replaces alveoli w/ hyperplasia of alveolar type II cells.

Front 39

What is the problem with a person w/ pulmonary fibrosis who tries to excercise?

Back 39

unable to sprout new vascular beds, therefore the PaO2 drops

Front 40

Fibrosis is caused by an imbalance in ___.

Back 40

cell mediated factors that favor repair and antibody mediated factors that favor fibrosis.

Front 41

How is a diagnosis of pulmonary fibrosis made?

Back 41

open lung biopsy (good history important)

Front 42

Acute form of restrictive lung disease?

Back 42

Adults Respiratory Distress Syndrome (ARDS)

Front 43

All morphologic forms of restrictive lung disease have?

Back 43

fibrosis or hyaline membranes

Front 44

When dust is inhaled what will cause a reaction to increase fibrosis?

Back 44

silica

Front 45

What cells dictate the response when dust is inhaled?

Back 45

macrophages

Front 46

Inhalation of organic dusts leading to restrictive disease.

Back 46

Pneumoconiosis

Front 47

Antigens from birds leads to granulamatous reaction in lung leading to lung destruction.

Back 47

Hypersensitivity Pneumonitis

Front 48

Pulmonary edema is first ____ and then later ____.

Back 48

interstitial, alveolar

Front 49

T/F: Cardiac and noncardiac pulmonary edema have V/Q mismatch.

Back 49

True.

Front 50

Floating a balloon in lung and measure pressure. This is called ____ and is equivalent to ____.

Back 50

capillary wedge pressure, LA

Front 51

Distinguishing characteristic of cardiac vs. non cardiac pulmonary edema.

Back 51

Increased capillary wedge pressure in cardiac.

Front 52

Will 100% oxygen fix a shunt problem?

Back 52

No. since some of the blood is never oxygenated.