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Pulmonology > Restrictive Lung Disease > Flashcards

Restrictive Lung Disease Flashcards

1
Q

Restriction” in lung disorders always means what?

What else may be reduced?

What is increased or normal?

A

a decrease in lung volume (FVC)

TLC and FEV1

FEV1/FVC

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2
Q

What is the cause of Asbestosis?

A

inhalation of asbestos fibers

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3
Q

What are the two categories of fibers?

Which is less toxic and more common?

A

chrysotile and amphibole

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

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4
Q

Asbestosis disease manifestations?

What can it lead to? 2

A

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)
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5
Q

Asbestosis pathogenesis?

2

A
  1. direct toxic effect of the fibers on pulmonary cells and
  2. release of mediators from inflammatory cells
    (inflammatory to fibrous scaring)
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6
Q

Clinical findings for Asbestosis?
3

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

A
  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

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7
Q

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

2 (3 and 4)

A

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
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8
Q

Bronchiolitis Obliterans (BO) pathogensis?

A

Chronic airway rejection in lung transplant patients

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9
Q

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

A
  1. Episodes of acute rejection
  2. Primary graft dysfunction
  3. CMV pneumonitis
  4. Noncompliance w/ immunosuppressive meds
  5. Lymphocyte bronchitis or bronchiolitis
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10
Q

What can BO develop from?

A

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

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11
Q

BO presentation

4

A
  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
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12
Q

Diagnosis of BO requires what?

A

Requires transbronchial biopsies with BAL

Need a good bronchoscopy technique and adequate bronchio-alveloar lavage

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13
Q

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

What do we have to rule out?

A

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

infection

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14
Q

Treatment of BO?

4

A
  1. Changing anti-immune medications
  2. Photopheresis
  3. Retransplantation
  4. Prevention!
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15
Q

What is hypersensitivity pneumonitis also know as?

A

extrinsic allergic alveolitis

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16
Q

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

What kind of agent usually?
Where does it occur?

A

immunological reaction

Usually an organic antigen

Occurring within the pulmonary parenchyma

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17
Q

Inciting agents include for HP include?

3

A

Agricultural dusts
Bioaerosols
Reactive chemical species

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18
Q

What is associated with a decreased risk of HP?

Increased risk?

A

smoking

genetic factors

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19
Q

HP Etiologic Agents

A

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

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20
Q

Presentation types of HP?

3

A

Acute
Subacute or intermittent
Chronic progressive

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21
Q

Acute presentation of HP? 2

Onset?
Symtpoms? 4

PE findings? 2

Treatment? 1

A
  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

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22
Q

What would an XRAY look like for HP?

Labs to order?

A

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

CBC to rule out infection maybe

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23
Q

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

A

Low level exposure over time

Gradual development of

  1. productive cough,
  2. dyspnea, fatigue,
  3. anorexia and
  4. weight loss
24
Q

Subacute HP PE findings? 2

Lab findings? 2

PFT findings? 2

Xray findings? 2

Treatment?2

A

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
Q

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

A

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
Q

Differential Diagnosis for HP?

5

A
  1. Inhalation fever
  2. Organic dust toxic syndrome
  3. Chronic bronchitis
  4. Asthma
  5. Chronic airflow limitation
27
Q

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

What tests would we use to diagnose HP?
3

A

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
Q

HP treatment?

2

A

Antigen avoidance

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

29
Q

How would we prevent HP?

4

A
  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
Q

Definition of interstitial lung disease?

2

A
  1. Diffuse parenchymal lung diseases

2. Most of these disorders are associated w/ extensive alteration of alveolar and airway architecture

31
Q

Short term side effects of steroids

4

A
  1. insomia
  2. stomach upset
  3. high blood pressure and blood sugars
  4. psychosis
    take in the morning and noon
32
Q

Long term side effects of steroids

7

A
  1. osteoporosis
  2. immunosuppression
  3. adrenal axis suppression (give them more for trauma)
  4. ulcers
  5. weight gain
  6. cataracts
  7. diabetes
33
Q

What is Idiopathic Pulmonary Fibrosis?

Affects adults of which age?

Cause?

A
  1. Chronic, relentlessly progressive fibrotic disorder of the lower respiratory tract
  2. Affects adults > 40YO
  3. Precise factors that initiate and maintain inflammatory and fibrotic responses in IPF are unknown
34
Q

Risk factors for IPF?

4

A

Smoking
Infections
environmental pollutants
chronic aspiration and drugs

35
Q

Early in IPF alveolitis is dominated by inflammatory cells including:
5

A
  1. Alveolar macrophages—secrete proinflammatory and profibrotic cytokines which affect mesenchymal cell proliferation and promote collagen depositions
  2. Neutrophils
  3. Eosinophils
  4. Lymphocytes
  5. Increased numbers of basophils and mast cells are also found
36
Q

IPF presentation

3

A
  1. Dyspnea on exertion
  2. Persistent nonproductive cough
  3. Abnormal CXR
37
Q

Diagnosis of IPF?

4

A
  1. Routine blood tests including serologic studies and autoimmune testing to r/o other diseases
  2. Radiographs, HRCT
  3. PFTs—restrictive pattern
  4. Bronchoalveolar lavage (looking for neutrophilia)
38
Q

Treatment of IPF
2

Meds?
3

A
  1. Prognosis of the disease dismal
  2. Trials have no proof that prognosis of the disease is dismal
  3. Glucocoricoids
  4. Immunosuppressives:
    Azathiprine
    Cyclophosphamide
    Methotrexate
  5. Antioxidants:
    Acetylcysteine
39
Q

Definition of sarcoidosis?

Who does it typically affect?
And it presents with one or more of the following: (3)

A

It is characterized pathologically by the presence of noncaseating granulomas in involved organs (multisystem granulomatous disorder)

Typically affects young adults, initially presents w/ one or more of the following:

  1. Bilateral hilar lymphadenopathy
  2. Pulmonary reticular opacities
  3. Skin, joint and/or eye lesions
40
Q

Sarcoidosis presentation?

3

A

Dyspnea
Cough
Chest pain

41
Q

Treatment of pulmonary sarcoidosis:

Many pts experience remission how?

Why is it dificult to guide treatment and follow progression of the disease?

What is the cause of the disease?

A

A large number of patients undergo spontaneous remission or have a benign clinical course

No easy way to assess dz activity and severity, so predicting clinical course and prognosis of disease is difficult
Marked variability in presentation and clinical course make it difficult to develop treatment guidelines

The cause of the dz is unknown so no specific treatment exists

42
Q

Indications for treatment of pulmonary sarcoidosis? 3

What would we treat with?

A
  1. Worsening pulmonary sx: cough, dyspnea, chest pain or discomfort, and hemoptysis
  2. Deteriorating lung function
  3. Progressive radiographic changes

Daily glucocorticoids
If improvement slow taper
If reactivation of disease increase to last effective dose and treat for 3-6 months, some patient’s require maintenance dose

43
Q

Describe the pic on slide 58 of the lecture that shows a stage two sarcoidosis. What two things characterize it as this?

A

Bilateral pleural effusions and hilar lymphadanopathy

44
Q

Eosinophilic pneumonias presents how many days after the drug has started?

What are the symtpoms? 4

What will the radiograph show? 2

A

Present 2-10 days after drug started
Symptoms: dry cough, fever, chills and dyspnea

Radiograph: eosinophilic pleural effusion + patchy or diffuse pulmonary infiltrates

45
Q

What drugs are associated with this?

8

A 
Nitrofurantoin          
 -Tricyclic antidepressants
Sulfonamides           
-Hydralazine
Penicillin                 
 -Isonaizid
Thiazides                
 -Gold salts
46
Q

What are the two types of radiation induced lung injury?

Both are seen in patient’s who have undergone thoracic radiation for ? 6

How is it limited?

A

Radiation pneumonitis
Radiation fibrosis

breast cancer
lung cancer
lyphoma
esophygeal cancer
stomach cancer
pancreatic

dose wise

47
Q

Pathogenesis of radiation induced lung injury?

A

Ionizing radiation localized release of sufficient energy to break strong chemical bonds and generate highly reactive free radical species

48
Q

What does radiation induced lung injury result from?

The cytotoxic effect is largely due to what?

A

Radiation-induced lung injury results from the combination of

  1. direct cytotoxicity upon normal lung tissue and the
  2. development of fibrosis triggered by radiation-induced cellular signal transduction

DNA damage that causes clonagenic death in normal lung epithelial cells

49
Q

Many factors affect the development of radiation-induced lung disease:
6

A
  1. Method of irradiation
  2. Volume of lung irradiated
  3. Dosage of radiation
  4. Time-dose factor
  5. Concurrent chemotherapy
  6. Induction chemotherapy
50
Q

Radiation-induced Lung Injury clinical manifestations?

5

A
  1. Early nonproductive cough
  2. Dyspnea on exertion or inability to take a deep breath
  3. Low grade fever
  4. Chest pain: pleuritic, substernal
  5. Malaise and weight loss may be seen
51
Q

Radiation-induced Lung Injury PE findings?

5

A
  1. Fine crackles or a pleural rub, sometimes normal
  2. Pleural friction rib
  3. Dullness to percussion
  4. Tachypnea,
  5. cyanosis or signs of pulmonary HTN (severe)
52
Q

Radiation-induced Lung Injury:
Need to distinguish from other pulmonary dz such as?

5

A
  1. Infection
  2. Lymphangitic or direct extension of tumor
  3. Drug-induced pneumonitis
  4. Hemorrhage
  5. Cardiogenic edema
53
Q

Radiation-induced Lung Injury:
Chest XRAy findings?
4

A
  1. May be normal
  2. Patchy alveolar filling defects
  3. Straight line effect, not conforming to anatomical units but to confines of radiation port is diagnostic (square matching radiation field)
  4. Small pleural effusions
54
Q

Treatment of Radiation-induced Lung Injury?

2

A

Corticosteroids

Inhibition of collagen synthesis

55
Q

Pneumoconiosis definition?

Examples?
3

A

nonneoplastic reaction of the lung to inhaled mineral or organic dust

Silicosis
Coal workers
Can be complicated by infection

56
Q

Coal Worker’s Pneumoconiosis presents how initially?

What may it eventually cause (2) and how does this change the diagnosis?

What will the Xray show?

A

Asymptomatic

May cause chronic bronchitis and COPD so is then known as industrial bronchitis and is compensable

Radiographically: small opacities can progress to larger opacities and fibrosis

57
Q

Things that are very vascular are usually suspected as what?

A

cancer

Pulmonology (16 decks)

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