interstitial lung dz Flashcards

1
Q

ILD

A

Accumulation of inflammation in the interstitium; progressive scarring leads to lung/air sac stiffening and once this happens its irreversible

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2
Q

idiopathic chronic multisystemic inflammatory non-caseating granulomatous disease
aka– small patches of swollen tissue (granulomas) develop in organs

A

sarcoidosis

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3
Q

risk factors for sarcoidosis

A

black females

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4
Q

treatment for sarcoidosis

A

prednisone

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5
Q

sx of sarcoidosis

A

50% asymptomatic
* dry cough
* intrathoracic lymphadenopathy
* erythema nosoum or lupus pernio
* eyes involvement

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6
Q

most accurate way to diagnose sarcoidosis vs best initial test

A

tissue biopsy is most accurate
chest radiographs is best initial

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7
Q

finding of sarcoidosis on chest radiographs & PFT

A

bilateral hilar lymphadenopathy on radiographs
restrictive findings (normal or increased ratio)

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8
Q
  • Chronic progressive fibrosing interstitial pneumonia of unknown etiology
A

idiopathic pulmonary fibrosis

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9
Q

risk factors for IPF

A

men over 50
cigarette smoking!!

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10
Q
  • dry cough
  • SOB then fatigue
  • clubbing
  • bibasilar end-inspiratory crackles/rales
A

pulmonary fibrosis sx

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11
Q

“reticular opacities” (honey combing) at lung bases should make you think of?

A

pulmonary fibrosis

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12
Q

life expectancy of IPF

A

3-4yrs

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13
Q

CT scan shoes usual interstitial pneumonia, reticular honeycombing, focal ground-glass opacification & surgical path/histo. shows UIP

A

IPF

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14
Q

tx of IPF (2)

A
  • steroids for exacerbations (can worsen prognosis)
  • lung transplant is only cure
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15
Q
  • chronic fibrotic lung diseases secondary to inhalation of mineral dust
A

pneumoconiosis

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16
Q

4 pneumoconiosis talked about in lecture

A

asbestosis
silicosis
coal workers pneumo.
hypersentivity pneumonitis

17
Q

which asbestos fiber is harder to remove, more toxic and reaches deeper into lungs

A

amphiboles

18
Q

most common form of exposure to asbestos

A

general community exposre

other forms: work, bystander

19
Q

asbestosis pathophys

A
  1. deposition & transmigration of the fibers
  2. macrophage accumulation then fibroblasts
  3. fibrosis increases over time
    - functions as tumor initaiator and promoter
20
Q
  • smoking
  • DOE
  • nonproductive cough
  • bibasilar end-inspiratory rales
  • RHF if advanced
  • clubbing
  • reduced chest expansion
A

asbestosis

NOTE: sx similar to IPF, before imagings use history as guide!

21
Q

PFT and ABG findings with asbestosis

A
  • PFT– restrictive
  • ABG may show resp. Alkalosis
22
Q

CXR: diffuse reticonodular infiltrates at lung bases “shaggy heart borders”
CT: ground-glass, pleural thickening & calcified pleural plaques by border

A

asbestosis findings

23
Q

3 major effects of asbestos exposure

A
  • pleural and pulmonary fibrosis
  • cancers of resp. tract
  • mesothelioma
24
Q

caused by inhaling silica dust

A

silicosis

25
Q

caused by inhaling coal mine dust

A

coal workers pneumoconiosis/black lung dz

26
Q
  • eggshell calcifications on hilar & mediastinal nodes
  • biopsy shows dust-laden macrophages & loose reticulin fibers
  • non specific tx
  • often asymptomatic but can have DOE, dry cough, rales, fatigue
A

silicosis

27
Q
  • chest radiograph: small nodules predominantly in upper lung w/ hyperinflationof lower lobes in obstructive pattern (resembles emphysema)
  • biopsy (not needed) shows black lungs– interstitial pigment deposition and anthracitic macrophage
  • tx includes pulm rehab
A

CWP/black lung

28
Q
  • Results from repeated inhalation of/sensitization to aerosolized organic antigens
A

hypersensitivity pneumonitis

29
Q
  • acute: rapid on set of flu like sxs, fever, chills, cough, dyspnea, myalgias 4-8 hrs after prolonged exposure to antigen
  • chronic: DOE, cough, crackles, insp squeaks
  • farmers lung from moldy hay
  • restrictive component
  • CT– upper lobe predominance, ground glass and fibrosis, honeycombing
A

hypersentivity pneumonitis

30
Q

tx of hypersensitivity pneumonitis

A

avoid exposures
steroids
lung transplant