Interstitial Lung Disease Flashcards

1
Q

what is pneumoconoiosis? what are some explains of disease which fall under this category

A

pneumoconoiosis - group of lung diseases which result from inhaling inorganic dusts –> resulting in chronic fiberosis of the lung
- asbestosis
- silicosis
- coal/coal dust
- beryllium

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2
Q

Parynchymal Asbestosis
what is it
when do you usually see it
what type of expsoures

A
  • a restrictive disease of the lungs diffuse and resulting in fiberosis
  • impairs gas exchange
  • progressive exercision on dyspnea

changes appear on radiography > 10 years after exposure (lays ** dormant for 2-=40 years**)

who is exposed
- ship workers
- mechanincs
- construction
- military
- people whos homes may have asbestos
- household contacts of these workers
- secondary exposures in the workplace

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3
Q

what are the signs and symptoms of asbestosis?

whats seen on chest xray

A
  • dyspnea
  • crackles
  • cyanosis
  • clubbing

chest xray
- thickened pleura
- calcified pleural plaques
- interstitial fibrosis
- “Shaggy heart sign

- normally below hilum and lower you will see these things

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4
Q

what are some abnormalities with asbestosis
- things youll see on xray

A
  • pleural plauques
  • thickened pleura
  • atelectasis
  • benign pleural effusions
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5
Q

what is silicosis? who is at risk? length of exposure? what are they at increased risk for?

A

silicosis: inhalation of silica
from..
- stone workers
- mining
- glass cutters
- cemeting

if expousre is intense –> dont need large periods of exposure

if small –> can be subtle accumulation

at an increased risk of TB!!!

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6
Q

what are some radiographic findings for silicosis?

A
  • diffuse throughout the lung : see opacities
  • **miliary infiltrations (small dots) or consolidation
  • eggshell calcifications!**

normally begins in the upper lobes

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7
Q

how is silicosis diagnosed and treated?

A

diagnosis
- history of significant exposure
- consisten imaging
- excluded other causes of symptoms
- biopsy rarely needed

treatment
- symptomatic: bronchodialotors, abx. if infected, O2 for hypoxia
- transplant if severe

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8
Q

coal workers pneumonitis
what is it
who gets it
what do you see on xray

A
  • deposition of coal mine dust in lungs
  • silicosis can be concurrent infection
  • upper lung fields effected
  • ** WILL LOOK IDENTICAL ON IMAGE AS SILICOSIS MINUS EGGSHELL APPEARACE**
  • smoking makes it worse
  • no treatment
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9
Q

berylliosis
what is it
who gets it
complications
testing
imaging

A
  • heavy metal poisoning due to inhaled beryllium dust
  • who: those who work in aeorspcae or light bulb high tech
  • complications: acute syndrome, chronic granulomatous, lung fiberosis, cancer

test: with a beryllium lymphocyte test

imaging: show nodules along septal lines

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10
Q

Occupational Asthma
- what triggers
- how to dx.
- treatment

A

triggers
- grain/wood dust
- tobacco
-pollen
-dyes
-formaldehyde

dx: spirometry before and after exposure needed for dx.

treat: bronchodilators

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11
Q

industrial bronchitis and byssinosis
what is it
who gets in
symptoms

A
  • miners most common get industrial bronchitis
  • cotton dust is byssinosis
  • like asthma –> chest tightness, dyspnea, and repeated exposure –> chronic bronchitis
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12
Q

hypersensitivity pneumonitis
-what is it
- pathology
- seen on bx.

A
  • inflammation of the alveoli and airways (without bronchospasms)
  • an immune mediated reaction to an inhaled antigen
  • bird droppings !!! and pets!! animals!! - essentially an allergic reaction in the lungs to an inhaled thing

bx: granulomas

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13
Q

etiologies for hypersensitivity pneumonititis

subtypes (based on time)

A
  • moldy hay
  • birds
  • grain dust
  • air conditioning
  • coffee dust
  • cheese workers

subtypes
acute: within 48 hrs. of exposure; ground-glass opacities
subacute: weeks after
chornic: can lead to ILD

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14
Q

treatment of hypersensitivty pneumonitis

A
  • allergey avoidance
  • steroids if severe attack
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15
Q

what is interstitial lung disease?
what can it be a result of (generally)
what is the most commony type

A
  • a GROUP of diseases characterized by the progressive, diffuse fiberosis and inflammation of the lungs (starting usually in intersitium and then impacting the capillaries, alveoli and gas exchange)
  • impacts the airways, vasculature and pleura
  • many types of disease can cause ILD –> MCC is idiopathic plumonary fiberosis
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16
Q

what is the gold standard diagnosis for ILD?

A
  • pulmonary pathology specimens (BIOPOSY)
  • but dx. is often made without as it wont change treatment
17
Q

what are some physiological problems which can result from inflammation and fiberosis of ILD?

A
  • reduced elasticity = stiffened lungs
  • reduced lung capacity (compliance)
  • gas exchange issues

larger airways usually not affected! since theres no “obstruction”

18
Q

what are some radiographic findings you may see on ILD?

A
  • thickened interstitum
  • ** honeycombing of the lungs –> seen in fiberosis
  • traction bronchiectisis (large airspaces of airways)
19
Q

when doing a workup for ILD – what are some key things to be aware of/ask

A
  • through hsitory!! about everything
  • PE may be normal respiratory problems –> look for extrapulmonary signs of other disease processes
  • the goal is to find the underlying conditions and etiologies of ILD!
20
Q

what are some causes (etiology) of ILD

A

Exposures
- smoking
- occupational (asbesosis and silica)
- radiation

medications
- methotrexate
- amioderone
- sulfonamides
- chemos
- heroin, cocain and crack (talc)

connective tissue disease
- RA
- scleroedema
- SLE

Idiopathic fiberosis

granulomatous

histological (idopathic)
- LAM
- PLCH
- PAP
-PPF
-sarcoidosis

infection
-coccidyomycosis
-histoplasmosis

21
Q

specifics of the idopathic interstitial penumonias of ILD (7 subtypes)

A

UIP: think > 65, fiberosis

AIP: acute, very sick, emerpic abx & steroids, high mortality

NSIPS: NON-smokers + connective tissue dz.

RB-ILD: SMOKING

COP: weeks after flu-like, DENSE infiltrates, GET BETTER WITH STEROIDS

22
Q

specificas about idopathic fiberosis of ILD

A
  • fibrosis, diffuse
  • men > women
  • clubbing!!
  • acute exacerbations = steroids to help
  • ## not a great prognosis
23
Q

sarcoidosis and ILD

A
  • non-caseating granulomatous inflammation –> therefore inflammation not tissue destruction
  • blacks> whites
  • NO CRACKLES
  • skin involvement, lungs can be asymptomatic
  • bilateral hilar LAN, reticular in apex of lung

treatment
- STEROIDS = 1st line
- methotrexate and TNF
-

24
Q

Wegener Granulomatosis

A
  • cavitary necrotizing and non-caseating granulomas at the arteries and veins
  • BAL or VATS to get bx.