Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
73 Cards in this Set
- Front
- Back
|
Definition of Interstitial Lung Disease (ILD).
|
thickening of alveolar walls by inflammation and fibrosis
|
|
|
What are the most common ILDs?
|
idiopathic
|
|
|
What is the most common of the IIPs?
|
Usual interstitial pneumonia
|
|
|
Name the disease: "plugs" of fibroblasts in airways and consolidation seen on CT
|
bronchilolitis obliterans organized pneumonia (BOOP)
|
|
|
Only disease caused by inhalation of organic particles.
|
Hypersensitivity Pneumonitis (HP)
|
|
|
Abnormal immunological reaction of lung to specific organic antigens
|
Hypersensitivity Pneumonitis
|
|
|
What is the two key factors in determining whether a particle will be inhaled?
|
amount and size, (small enough (5 microns) to get into alveolar space)
|
|
|
Common organic particles seen in HP?
|
fungi, mold, mildew, and avian proteins
|
|
|
Steps in pathogenesis of HP.
|
antigen expoure -> accumulation of inf. cells -> lympocytic alveolitis in more chronic phases -> granuloma formation -> normal repair or fibrosis
|
|
|
Presentation of acute HP.
|
fever, chills, dyspnea, cough w/in hours of exposure
|
|
|
CXR of acute HP.
|
will show infiltrates
|
|
|
HRCT of acute HP.
|
"ground glass opacifications" typically in upper zones of lungs
|
|
|
Presentation of chronic HP.
|
persistent cough, SOB w/ exercise, sputum production (same as someone w/ IPF or fibrotic lung disease)
|
|
|
CT of chronic HP.
|
More fibrosis seen instead of ground glass opacifications
|
|
|
T/F: Removal of pet bird usually fixes the problem in a family with chronic HP.
|
False. Bird antigens can stay in house for a long time.
|
|
|
PFTs seen w/ chronic HP.
|
restrictive pattern (decreased FEV1, FVC, TLC, DLCO)
|
|
|
What is the gold standard for diagnosing HP?
|
lung biopsy
|
|
|
Lung biopsy of acute HP.
|
loose granulomas, mostly around airways -- suggestive but not diagnostic of HP
|
|
|
Lung biopsy of chronic HP.
|
looks like UIP. Honeycombing in lower zones.
|
|
|
Treatment for HP.
|
Removal of aggravating agent, along with possible steroids (if you give them steroids and they stay on the farm, they won't get better)
|
|
|
What is asbestos?
|
naturally occuring mineral w/ thermo-insulating properties
|
|
|
Where is asbestos commonly found?
|
materials that need insulation or is exposed to large amounts of heat.... paint, boilers, brakes
|
|
|
What industries was asbestos commonly used in?
|
shipbuilding, construction, automotive, railroad
|
|
|
What form is the overwhelming majority of asbestos in the US?
|
chrysotile (98%)
|
|
|
Why is chrysotile the more benign form of asbestos?
|
it can't migrate to the outer lung and to the lymphatics
|
|
|
What diseases does asbestos cause?
|
pleural disease, malignant mesothelioma, bronchiogenic cancer, and asbestosis
|
|
|
Definition of abestosis.
|
interstitial pneumonitis and fibrosis caused by exposure to asbestos fiber
|
|
|
What is the latency for asbestos exposure?
|
15-20 years
|
|
|
Two main componenents of the pathogenesis of asbestosis.
|
1) direct toxic effects which kill alveolar cells
2) release of mediators from inflammatory cells causes fibrosis and destruction |
|
|
What is an asbestos body?
|
seen in lung biopsy - asbsestos fibers surrounded by a coating of iron and protein
|
|
|
Physical findings in asbestosis.
|
progressive dyspnea, bibasilar inspiratory crackles (Velcro), clubbing
|
|
|
Radiographic findings in asbestosis.
|
pleural plaques, round atelectasis
predominately a basilar disease |
|
|
Management of asbestosis.
|
remove exposure, smoking cessation, early detection, supportive therapy including oxygen, vaccines, treatment of resp. infections
|
|
|
T/F: Corticosteroids have not been proven to be affective in the treatment of asbestosis.
|
True
|
|
|
Definition of silicosis.
|
chronic fibrosis disease of lungs caused by inhalation of silica dust
|
|
|
Where is silica dust found?
|
foundry work, tunneling, sandblasting, pottery making, manufacturers of glass, tiles, and brick
|
|
|
Three clinical types of silicosis:
|
1) simple/chronic - low conc. over 20 years or more
2) accelerated - moderately high conc. over 4-8 years 3) acute - massive exposure, presents similarly to ARDS |
|
|
Pathogenesis of silicosis.
|
Deposited in distal airways -> ingested by macrophages -> macrophages activated -> inf. mediators released -> inf. and fibrosis
|
|
|
Clinical presentation of silicosis.
|
most asymptomatic, abnormal CXRs, restrictive PFTs, 10-15% develop "progressive massive fibrosis"
|
|
|
Typical CXR for silicosis.
|
micronodular opacities in the UPPER zones
|
|
|
How does one differentiate the diagnoses of asbestosis and silicosis?
|
asbestosis usually found in lower zones while silicosis is typically found in upper zones
|
|
|
Silicotic nodule
|
silicotic area surrounded by inflammation.. if you polarize you can see the sand
|
|
|
Associated illnesses w/ silicosis.
|
mycobacterial infections, especially TB
CTD occur more frequently, especially scleroderma lung cancer |
|
|
Why are silicosis patients susceptible to TB?
|
alveolar macrophages are filled w/ silica so they can't eat the bugs
|
|
|
Management of silicosis.
|
remove from environment, yearly screening for TB, smoking cessation, supportive therapy including oxygen and bronchodilator therapy
|
|
|
What causes coal worker's pneumonconiosis?
|
excessive inhalation of coal dust and silica
|
|
|
Why is the underground more hazardous for inhalation?
|
more concentration of particles
|
|
|
What is the typical presentation for coal worker's pneumoconiosis?
|
mostly asymptomatic w/ small nodular opacities on CXR, no lung area affected more than another
|
|
|
Lung biopsy of coal worker's pneumoconiosis.
|
normal lung w/ very thin alveolar walls
|
|
|
What causes the damage in ILD associated w/ CTDs?
|
pathogenic auto-Abs and immune complexes
|
|
|
Prevalence of ILD w/ lupus.
|
rare
|
|
|
Prevalence of ILD w/ scleroderma.
|
frequent
|
|
|
True/False: ILD never precedes systemic manifestations of CTDs.
|
False. ILD precedes in 30% of cases.
|
|
|
List some problems that CTDs can cause in the chest.
|
bronchiolitis, airway problems, pleural disease, resp. muscle dysfunction, pulmonary HTN, bleeding into alveolar space
|
|
|
What is the correlation btwn RF titers and likelihood of ILD.
|
The higher the RF titers, the higher the likelihood of ILD.
|
|
|
Who is ILD caused by rheumatoid more common in ?
|
men w/ severe disease
|
|
|
Infiltrates in ILD from RA are typically found in the ?
|
bases
|
|
|
Mean survival for ILD from RA.
|
5 years
|
|
|
Most common manifestatoin of ILD from RA.
|
pleural
|
|
|
What is scleroderma?
|
accumulation of CT in skin and visceral organs
|
|
|
In the diffuse cutaneous form of scleroderma, 40% have ?
|
antitopoisomerase 1 Ab (Scl-70)
|
|
|
In the limited cutaneous form of scleroderma, 60-80% have?
|
anticentromere Ab
|
|
|
Most lung abnormalities in ILD related to scleroderma are found?
|
in the base
|
|
|
What is a common symptom of scleroderma that can makes fibrosis worse?
|
esophageal dysmotility causing aspirations
|
|
|
What is the most common cause of death in scleroderma?
|
lung disease
|
|
|
If DLCO<40% what is the 5 year survival in ILD related to scleroderma?
|
less than 10%
|
|
|
The risk of ? is increased in ILD related to scleroderma.
|
bronchogenic cancer
|
|
|
Two common manifestations seen in Polymyositis/dermatomyositis?
|
heliotrope rash (around eyes) and Gottron's sign (reddish discoloration in knuckles)
|
|
|
ILD is a side effect w/ what types of drugs?
|
cytotoxic agents (chemotherapy), risk of ILD may be associated w/ concomitant use of radiation
|
|
|
ILD due to Bleomycin is ____ dependant.
|
dose
|
|
|
ILD due to cyclophosphamide/methotrexate is ? dependent.
|
time
|
|
|
Anti-arrythimia drug that can cause ILD.
|
amiodarone (more common if used >400 mg/day)
|
|
|
Treatment of amiodarone induced ILD.
|
stop the drug, and give prednisone.
|
