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Flashcards in Restrictive Lung Disease Deck (57)
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1

Restriction” in lung disorders always means what?

What else may be reduced?

What is increased or normal?

a decrease in lung volume (FVC)

TLC and FEV1

FEV1/FVC

2

What is the cause of Asbestosis?

inhalation of asbestos fibers

3

What are the two categories of fibers?

Which is less toxic and more common?

chrysotile and amphibole

Chrysotile less toxic
and accounts for 90% of asbestos use in U.S.

4

Asbestosis disease manifestations?


What can it lead to? 2

Characterized by slowly progressive (years), diffuse pulmonary fibrosis

-Malignancies: non-small cell and small cell carcinoma of the lungs
-malignant mesothelioma (cancer of the pleural lining of the lungs)

5

Asbestosis pathogenesis?
2

1. direct toxic effect of the fibers on pulmonary cells and
2. release of mediators from inflammatory cells
(inflammatory to fibrous scaring)

6

Clinical findings for Asbestosis?
3

If cough, sputum production, or wheezing are present more likely secondary to what?

1. most patients asymptomatic for 20-30 yrs after initial exposure:
2. Dyspnea on exertion
3. Progresses to fine bibasilar end expiratory crackles and clubbing



smoking

7

How do we diagnose asbestosis and what would these tests show?

2 (3 and 4)

PFTs:
1. Reduced lung volumes—VC and TLC
2. Decreased pulmonary compliance
3. Absence of airflow obstruction (normal ratio of FEV1 to FVC)

Radiographs
1. Begins in lower lung zones w/ small parenchymal opacities w/ a multinodular or reticular pattern
2. Often associated pleural abnormalities
3. “Shaggy” heart and “ground” glass appearance
4. Honeycombing and upper lobe involvement late stage disease

8

Bronchiolitis Obliterans (BO) pathogensis?

Chronic airway rejection in lung transplant patients

9

BO: Chronic airway rejection in lung transplant patients is due to what? 5

1. Episodes of acute rejection
2. Primary graft dysfunction
3. CMV pneumonitis
4. Noncompliance w/ immunosuppressive meds
5. Lymphocyte bronchitis or bronchiolitis

10

What can BO develop from?

lung transplant (5 years out 45% of recipients develop BO)-slowly progressing

11

BO presentation
4

1. Usually indolent symptoms similar to URI
2. Exertional dyspnea and decline in spirometry
3. Initially radiographs and exam only help exclude other illnesses
4. Advanced stages see bronchioectasis w/ obstruction and hyperinflation, often colonized w/ pseudomonas

12

Diagnosis of BO requires what?

Requires transbronchial biopsies with BAL

Need a good bronchoscopy technique and adequate bronchio-alveloar lavage

13

Transbronchial biopsies with BAL are usually made on a pt who presents with what?

What do we have to rule out?

Usually made on a patient who presents w/ declining spirometry without an acute illness

infection

14

Treatment of BO?
4

1. Changing anti-immune medications
2. Photopheresis
3. Retransplantation
4. Prevention!

15

What is hypersensitivity pneumonitis also know as?

extrinsic allergic alveolitis

16

Hypersensitivity pneumonitis represents what kind of response to an inhaled agent?

What kind of agent usually?
Where does it occur?

immunological reaction

Usually an organic antigen

Occurring within the pulmonary parenchyma

17

Inciting agents include for HP include?
3

Agricultural dusts
Bioaerosols
Reactive chemical species

18

What is associated with a decreased risk of HP?

Increased risk?

smoking

genetic factors

19

HP Etiologic Agents

Farming, vegetable and dairy cattle workers
Ventilation and water-related contamination
Bird and poultry handling (exposure to down)
Veterinary work and animal handling
Grain and flour processing and loading (grain can become colonized w/ microorganisms and insects, grain is easily aerosolized so exposure to antigens can occur easily)
Lumbar milling, construction, wood stripping etc.: mold exposure
Plastic manufacturing
Painting
Electronics industry

20

Presentation types of HP?
3

Acute
Subacute or intermittent
Chronic progressive

21

Acute presentation of HP? 2

Onset?
Symtpoms? 4

PE findings? 2

Treatment? 1

1. May follow heavy exposure to antigen
2. May be confused w/ viral or bacterial infection

Abrupt onset (4-6 hrs after exposure) of:
1. fever and chills
2. Nausea
3. chest tightness and dyspnea
4. without wheezing

PE: tachypnea and diffuse fine rales

TX: Removal from antigen—symptoms subside in 12 hrs to several days/disease may recur w/ re-exposure

22

What would an XRAY look like for HP?

Labs to order?

may show a micronodular, interstitial pattern, frequently normal; sometimes do HRCT

CBC to rule out infection maybe

23

How is it acquired?
Describe the onset of subacute or intermittent HP?
4

Low level exposure over time

Gradual development of
1. productive cough,
2. dyspnea, fatigue,
3. anorexia and
4. weight loss

24

Subacute HP PE findings? 2

Lab findings? 2

PFT findings? 2

Xray findings? 2

Treatment?2

PE: tachypnia, diffuse rales
Lab: lymphocytosis on bronchial alveolar lavage, mild hypoxemia
PFTS: restriction pattern or mixed restriction/obstruction pattern
X-rays: normal or reticular opacities in middle and upper lung zones
TX: removal from antigen and glucocorticosteroids, takes weeks to months to resolve

25

Chroic progressive HP generally has no report of what?

Insideous onset of what things? 4

PE findings? 1

What will it be hard to differentiate from? 1

Lab findings? 3

PFT findings? 3

Xray findings? 3

Generally no report of acute episodes

Insidious onset of
1. cough,
2. dyspnea,
3. fatigue
4. wt. loss

PE:
1. digital clubbing may be seen

Differential from idiopathic pulmonary fibrosis is difficult

Lab: lymphocytosis, also neutrophilia or eosinophilia on BAL

PFTs: restrictive, obstructive often seen with it, resting and exertional hypoxemia

X-rays:
1. fibrotic changes,
2. loss of lung volume,
3. emphysema pattern changes

26

Differential Diagnosis for HP?
5

1. Inhalation fever
2. Organic dust toxic syndrome
3. Chronic bronchitis
4. Asthma
5. Chronic airflow limitation

27

What would give us a high index of expoure for an HP diagnosis?

What tests would we use to diagnose HP?
3

Careful review of patient's occupational, avocational and domestic exposures

1. A normal CXR doesn't rule it out
2. Inhalation challenge by re-exposure
3. HRCT and BAL

28

HP treatment?
2

Antigen avoidance

Glucocorticoids used to accelerate initial recovery, however, the long-term outcome is relatively unchanged

29

How would we prevent HP?
4

1. Reduction of antigenic burden (wetting compost)

2. Design facilities: maintain humidity less than 60%, avoid having stagnant water or carpet that is likely to get moist

Maintenance: routinely inspect all heating, ventilation, an air conditioning equipment that it is clean and water is drained daily from humidifiers and vaporizers

Protective devices: masks, filters

30

Definition of interstitial lung disease?
2

1. Diffuse parenchymal lung diseases
2. Most of these disorders are associated w/ extensive alteration of alveolar and airway architecture