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FunMed: Pulmonology > Restrictive Interstitial Lung Disease > Flashcards

Restrictive Interstitial Lung Disease Flashcards

1
Q

Common Presentation

A

Dyspnea

Dry, Nonproductive Cough

Inspiratory Crackles on Exam (except Sarcoidosis)

May or may not have digital clubbing

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2
Q

Common Chest X-ray and CT Findings

A

nodular oppacties - diffuse white spots

reticular opacities - irregular spider webs that represent scarring

honeycombs (CT) - alveoli are broken and surrounded by thick scar tissue, limiting the passage of gasses across the alveolar-capillary barrier

traction bronchiectasis (CT) - too much negative pressure pulls tissue away from bronchioles

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3
Q

FVC

A

low

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4
Q

FEV1/FVC

A

normal to high

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5
Q

DLCO

A

low

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6
Q

TLC

A

low

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7
Q

Common Pathophysiology

A

injury and damage occurs to the alveolar epithelial or capillary endothelial cells leading to inflammation (alveolitis) and eventually fibrosis

the inflammation and scarring limits the passage of gases across the alveolar-capillary barrier

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8
Q

Lungs with interstitial lung disease …

A

show areas of fibrosis (irreversibly enlarged, damaged bronchioles and distorted alveoli) that alternate with areas of normal lung

the areas of fibrosis between the alveoli greatly decreases the gas exchange, reducing oxygen transferred to the bloodstream

honeycombing results – clustered cystic air spaces

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9
Q

Idiopathic Pulmonary Fibrosis

A

also called Usual Interstitial Pneumonia

fibrotic scarring of the lung interstitium of unknown cause

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10
Q

Idiopathic Pulmonary Fibrosis: Epidemiology

A

men

55-60 yo

white

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11
Q

Idiopathic Pulmonary Fibrosis: Signs and Symptoms

A

insidious onset of dry, hacking cough

SOB

inspiratory crackles on exam

slow onset; may seem normal to patient

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12
Q

Idiopathic Pulmonary Fibrosis: Characteristic Histologic Pattern

A

alternating areas of normal lung, interstitial inflammation, fibroblast focial, and honeycomb change (+/-)

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13
Q

Idiopathic Pulmonary Fibrosis: Chest X-Ray

A

reticular opacities with a basilar predominance (lower lobes)

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14
Q

Idiopathic Pulmonary Fibrosis: CT

A

basilar and subpleural areas of reticular changes, honeycombing, and traction bronchiectasis

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15
Q

Idiopathic Pulmonary Fibrosis: Diagnosis

A

must rule out other insterstitial diseases in order to be truly idiopathic

can be made on H&P and imaging alone as long as all features are present

may require tissue pathology via Bronchoalveolar Lavage or Transbronchial Biopsy or Surgical Lung Biopsy

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16
Q

Idiopathic Pulmonary Fibrosis: Treatment

A

none; lung transplant is definitive with a 50% 5 year survival rate

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17
Q

Sarcoidosis

A

a multisystem granulomatous disorder of unknown etiology

multisystem inflammatory disorder characterized by noncaseating granuloma formation

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18
Q

Sarcoidosis: Epidemiology

A

geographical and familial clusters

10-20 per 100,000

African Americans

Female

20-30 yo

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19
Q

Sarcoidosis: Signs and Symptoms

A

pulmonary findings in 90%: onset of dry hacking cough and shortness of breath can be subacute (weeks to months) or chronic (months to years)

NO inspiratory crackles

Imaging: reticular opacities are in the middle and upper lungs

hilar adenopathy

extrapulmonary findings

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20
Q

Sarcoidosis: Extrapulmonary Findings

A

may have fatigue, malaise, fever, or weight loss

skin lesions

cervical lymphadenopathy

visual changes, dry eyes

dry mouth, parotid swelling

joint pain and swelling

muscle weakness

hepatomegaly and tenderness

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21
Q

Sarcoidosis: Diagnosis

A

based on H&P (no historical features indicative of other similar presenting disorders) and imaging findings

MUST have tissue pathology that shows noncaseating granulomas

CBC to rule out lymphomas

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22
Q

Sarcoidosis: Treatment

A

glucocorticoids (Prednisone)

immunosuppressive therapy if ineffective (Methotrexate)

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23
Q

Pneumoconiosis

A

occupational lung disease secondary to inhalation of inorganic dusts

a group of chronic fibrotic lung diseases that result from inhalation of inorganic dusts typically associated with specific occupations

treatment is supportive

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24
Q

Coal Miners Lung Disease: Pathophysiology

A

coal dust is ingested by macrophages, which then become coal macules that show as 2-5 mm radio-opaque nodules on chest x-ray

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25
Q

Coal Miners Lung Disease: Chest X-Ray

A

2-5 mm radio-opaque nodules that are primarily in the upper lung fields in “simple”

may become more widespread in “complicated coal worker’s pneumoconiosis” with progressive massive fibrosis

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26
Q

Coal Miners Lung Disease: Treatment

A

supportive care; no other treatment is shown to help; prevent further exposure

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27
Q

Asbestos Pneumoconiosis

A

secondary to inhalation of asbestos fibers, which contain fibrous magnesium silicate

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28
Q

Who is most at risk for developing Asbestos Pneumoconiosis?

A

asbestos mining and milling workers are most at risk, but also people doing insulation work, shipbuilding, construction, pipe fitting, and textile work

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29
Q

Asbestos Pneumoconiosis: Symptoms

A

dry, nonproductive cough; dyspnea; and inspiratory crackles that presents decades after exposure

30
Q

Asbestos Pneumoconiosis Imaging

A

reticular and small nodular opacities in the lower lung field

calcified pleural plaques in the lower lungs

pleural effusions

31
Q

Asbestos Pneumoconiosis: Pathology Lab

A

pathology is not necessary but can aid diagnosis by identifying asbestos fibers and ferruginous bodies

32
Q

Asbestos Pneumoconiosis: Complications

A

respiratory failure for a minority of patients

Malignancy: bronchogenic adenocarcinoma, malignant mesothelioma, concomitant smoking increases risk

33
Q

Asbestos Pneumoconiosis: Treatment

A

supportive and preventative; O2

34
Q

Silicosis Pneumoconiosis

A

secondary to inhalation of crystalline silica (SiO2) in quartz, grant, or sandstone

can be acute or chronic

35
Q

Who is most at risk for developing Silicosis Pneumoconiosis?

A

occupations at risk include mining, quarrying, drilling, potters, masonry, and sandblasting

36
Q

Acute Silicosis Pneumoconiosis

A

rare; after exposure to high concentrations of crystalline silica

symptoms begin within a few weeks to years

appears like chronic silicosis on radiograph, but shows sooner

poor prognosis: progresses to complicated and frequently respiratory failure

less than four year survival rate from onset of symptoms

37
Q

Chronic Silicosis Pneumoconiosis

A

often decades after cessation of job associated with exposure

includes Simple Silicosis, which can progress to Complicated Silicosis (Progressive Massive Fibrosis)

can be asymptomatic and only noted on chest x-ray

insidious onset of cough and dyspnea with inspiratory crackles on exam

38
Q

Silicosis Pneumoconiosis: Imaging

A

Simple Silicosis appears as innumerable, small, rounded opacities (<10mm) in the dorsal, upper lung fields

Complicated Silicosis shows larger nodules (>1cm) that evolve into conglomerate masses

the small nodules of simple have coalesced

conglomerate masses can appear like malignancies

39
Q

Berylliosis Pneumoconiosis

A

a chronic, immunologically mediated, granulomatous disease caused by exposure to beryllium

your body makes an antibody to beryllium, and the immune response leads to disease

40
Q

Beryllium

A

a metal used in a number of industrial applications

41
Q

Who is at most risk for developing Berylliosis Pneumoconiosis?

A

occupations at risk include metal and metal allow machine shops, electronics manufacture and assembly, defense industry, beryllium extraction, automotive industry, computer industry, aerospace industry (more often)

42
Q

Berylliosis Pneumoconiosis: Symptoms

A

insidious onset of dry, nonproductive cough; shortness of breath; crackles in the lungs on exam

inhalation causes pulmonary pathology, but skin contact can also cause cutaneous nodules

cutaneous nodules are on exposed areas of skin and smaller than those in Sarcoidosis

onset of exposure to symptoms varies from 3 months to 30 years

43
Q

Berylliosis Pneumoconiosis: Imaging

A

varies, but more common in the upper lung fields

44
Q

Berylliosis Pneumoconiosis: Special Testing

A

Beryllium Lymphocyte Proliferation Test (BeLPT)

blood test, low sensitivity, high specificity

repeat negative or borderline

two negatives is a ‘negative;

also perform Bronchoalveolar Lavage (BAL) effluent

45
Q

Berylliosis Pneumoconiosis: Tissue Pathology

A

shows noncaseating granulomas

46
Q

Berylliosis Pneumoconiosis: Management

A

mild disease or Beryllium sensitization but no frank Berylliosis: None

with onset of bothersome dyspnea or decrease in lung volumes: Prednisone chronically

if fail glucocorticoids then may try Methotrexate or other immunosuppressive agents but no clear evidence showing efficacy

47
Q

Berylliosis Pneumoconiosis: Prognosis

A

course is variable; may live chronically on glucocorticoids

some patients experience progressive deterioration of lung function and development of pulmonary fibrosis

no increased risk of cancer

48
Q

Hypersensitivity Pneumonitis

A

an immunologic reaction to an inhaled organic antigen that is often animal or plant related, such as agricultural dusts, bioaerosols, reactive chemical species

requires initial exposure to sensitize the immune system; subsequent exposures can then result in disease

49
Q

Occupations and hobbies most at risk for Hypersensitivity Pneumonitis are related to….

A

farming, bird and poultry handling, and ventilation and water-related contamination

50
Q

Farming Environmental Source and Causative Agent related to Hypersensitivity Pneumonitis

A

moldy hay, grain, and silage

thermophilic actinomycetes

51
Q

Poultry Handling Environmental Source and Causative Agent related to Hypersensitivity Pneumonitis

A

parakeets, budgerigars, pigeons

droppings, feathers, serum proteins

52
Q

Ventilation and Water-Related Environmental Sources and Causative Agents related to Hypersensitivity Pneumonitis

A

humidifier fever – thermoactinomyces

hot-tub lung – myobacterium complex

lifeguard lung – endotoxin from pool-water sprays

53
Q

Acute Hypersensitivity Pneumonitis: Symptoms

A

abrupt onset (w/in 4-6 hrs) of fever, chills, malaise, nausea, cough, chest tightness, dyspnea; exam with basilar crackles and tachypnea

54
Q

Acute Hypersensitivity Pneumonitis: Imaging

A

CXR frequently normal

55
Q

Acute Hypersensitivity Pneumonitis can be confused with?

A

potentially confused with a viral or bacterial infection and given antibiotics

56
Q

Acute Hypersensitivity Pneumonitis: Treatment

A

remove from environment where exposure occurred and not return

symptoms subside within 12hrs to several days.

disease may recur with re-exposure

57
Q

Subacute Hypersensitivity Pneumonitis: Symptoms

A

gradual development of productive cough, dyspnea, fatigue, anorexia and weight loss; exam with tachypnea and diffuse crackles

58
Q

Subacute Hypersensitivity Pneumonitis: PFTs

A

restrictive pattern and decreased DLCO

59
Q

Subacute Hypersensitivity Pneumonitis: Imaging

A

CXR normal to micronodular or reticular opacities; HRCT with diffuse micronodules

60
Q

Subacute Hypersensitivity Pneumonitis: BAL

A

Bronchalveolar Lavage (BAL) often performed and shows marked lymphocytosis

61
Q

Subacute Hypersensitivity Pneumonitis: Tissue Pathology

A

shows noncaseating granulomas

62
Q

Subacute Hypersensitivity Pneumonitis: Treatment

A

removal from exposure; glucocorticoids may be required.

improvement in symptoms and function takes weeks to months

63
Q

Chronic Hypersensitivity Pneumonitis: Symptoms

A

insidious onset of cough, dyspnea, fatigue, weight loss

64
Q

Chronic Hypersensitivity Pneumonitis: Imaging

A

similar to IPF; differentiation from IPF may be difficult

65
Q

Chronic Hypersensitivity Pneumonitis: BAL

A

Bronchoalveolar Lavage (BAL) is often necessary - low CD4 to CD8 ratio

66
Q

Chronic Hypersensitivity Pneumonitis: Tissue Pathology

A

noncaseating granulomas, destruction of alveoli, bronchiolitis obliterans

67
Q

Chronic Hypersensitivity Pneumonitis: Treatment

A

chronic glucocorticoids

removal from exposure still necessary but doesn’t help as much

68
Q

Byssinosis

A

an obstructive, asthma-like, disorder caused by inhalation of cotton fibers

presents with chest tightness, cough, wheezing and dyspnea

usually worse on Mondays or first day back after a break/vacation

if left untreated and without job change, could lead to chronic bronchitis/COPD

69
Q

Sillo-filler’s Disease

A

toxic lung injury due to nitrogen dioxide inhalation

bacterial conversion of nitrates in fresh grains produces N02; his gas is heavier than air and accumulates in silos

inhalation of large amounts causes toxic injury to airways and alveoli

leads to increased tissue permeability → pulmonary edema

70
Q

Sillo-filler’s Disease: Symptoms

A

dyspnea, cough, crackles on exam, occasionally wheezing as well

71
Q

Sillo-filler’s Disease: Treatment

A

glucocorticoids ASAP to prevent progression to bronchiolitis obliterans, a common late complication.

FunMed: Pulmonology (6 decks)

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