Diffuse and Interstitial Lung Disease Flashcards

1
Q

Diffuse vs interstitial

A

Diffuse - involving parenchyma of both lungs

interstitial - diffuse lung dz that preferntially involves lung interstitium

Lung is either sole organ or might be part of multisystem

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2
Q

Ground glass opacification

A

Airspace filling less dense than consolidation

Alveolitis
Edema
Alveolar hemorrhage
Alveolar proteinosis

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3
Q

When to think of

Pneumocysttis
Alveolar hemorrhage

A

Fever, HIV risk

Hemoptysis

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4
Q

Ground glass

Reticular pathology

A

Alveolitis (after infectious pnuemonia, edema, hemorrhage and alveolar proteinosis excluded)

Collagen deposition/intersitital inflammation/interstitial edema/lymphatic process

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5
Q

Small nodules
Honeycomb
Traction bronchiec

A

Granuloamtous inflammation/infection/inhaled dust/neoplastic spread

End-stage lung fibrosis

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6
Q

Sarcoidosis
DIP
Alveolar proteinosis

Patho findings

A

Non-necortizing, well-formed granulomas…expect nodules

Desquam interstitial pneumonitis…ground glass opacities by imaging

PAS material filling alveolar without cells

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7
Q

IPF

Age, mutation, radio, patho

A

50s

Telomerase gene mutation (familal version)

Basilar, sub-pleural predominant reticular infiltrates

No associated PE or thoracic LN enlargement

Low titer ANA and RF may be present

Heterogeneity in extent and appartent age of lesions with little inflammation

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8
Q

IPF dx

A

Typical presentation and HRCT OR surgivcal biopsy

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9
Q

Asbestosis dx

A

Similar to IPF but with a plaque

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10
Q

Rheumatoid contrasted with IPF, HP, silicosis

A

Will have extra-pulm findings

Chronic HP will be upper lobe involvement

Silicosis is nodular and upper-lung

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11
Q

Pneumoconiosis

A

Respirable particles must be small enough to reach alveoli but large enough to not be breathed out

Most spherical except asbesots fibers

Look for ferruginous bodies in asbestos

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12
Q

Patho of silocosis vs. sarcoidosis, vs coal miners

A

All going to be upper lobe predominant

Carbon laden macrophages - CWP

Silicotic nodules - silliociss

Sarcoidosis - well-formed granuloma with multinucleated giant cells

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13
Q

Silicosis and CWP similarities and differences

A

Upper and mid zone predom nodular infiltrates

Simple and PMF varieites

Thoracic adenopathy may calcify

Diffs***

Silicotic nodule vs. macule

Silica polarizble

Silica has acute varient that mimics alveolar proteinosis

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14
Q

Asbestosis

A

Lower zone reticular infiltrates (mimics IPF)

NO adenopathy

PLeural plaques

Ferruginous bodies

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15
Q

Pneumonoconiosis dx by

A

Appropritate hx and imaging (maybe with path)

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16
Q

Sarcoidosis including dx

A

MULTIsystem disorder by non-caseating granulomatous infalmmation

Mimicked by berylliosis

dx - demonstration of non-caseating granulomas in 2 or more organs…exclude other dx

Will be nodular

May get hilar adenopathy

17
Q

COP Path
Hx
Dx

A

Exuberant lung repair occurring in response to insult

Very important clinical hx - cough, dyspnea, fever of weeks-months

Recognitionf of syndrome as less acute than bacterial, evaluating potnetial predisposing condiions, characteristic lung patho, negative cultures

18
Q

Alveolar hemorrhage syndromes

A

Hemoptysis with dyspnea

Urinalysis shows RBCs

Bilateral symmteric aispace filling (GGO)

Patho shows diffuse capillaritis

GPA - diagnositc is ANCA (proteinase 3)

Anti-glomerular basement membrane antibody disease - GBM antibody (cross reacts with alveolar basement membrane)…has linear glomerular distribtuion of IgG

Both are pulm-renal syndromes

19
Q

Alveolar proteinosis

A

Chronic, non-infectious airspace opacities

Antibody to GM-CSF leads to excess surfactant production

SLowly progressive dyspnea and cough

IMaging is bilateral airspace opac with crazy paving

Dx by lavage or biopsy (PAS)

Therapy is whole-lung lavage plus GM-CSF

20
Q

Goodpastures vs. GPA

A

Goodpastures has no ENT findings (or findings outside of the pulm-renal system)

21
Q

HP is

A

Parenchymal lung dz resulting from inhlaation of an antigen to which pt has been previously sensitized

22
Q

Patho of HP

A

Inhlaed antigen stimulates TLR (Th1 and Th17)

23
Q

Smoking and ILD

A

SMokers get - respiratory bronchioltis - ILD
Desquamative interstitial pneumonia
Langerhands

Non-smokers get - HP and sarcoidosis…difference is that sarcoisosi does NOT have crackles

24
Q

Acute
SUbactue
Chronic HP

A

Acute- non-specific bilateral airspace dxz with ground glass

Subactue- ground glass, centrilobular nodules, mosaic

Chronic - looks like IPF

25
Q

Radiation pneumonitis and fibrosis

A

Fibrosis more than pneumonitis

Crackles, dry cough, dyspnea

Dx made by hx and imagingin…patho is diffuse alvolar damage and organziing pneumonia

26
Q

IPF important

A

Peripheral, basilar, reticular with honeycombing

Finger clubbing

Heterogenous fibrosis admixed with more normal lung

27
Q

DIP important

A

Begins as GGO with little interstitial thickening

SMokers dz

Uncommonly progresses to end-stage fibrosis

28
Q

Sarocidosis

A

Multisystem and granulomatous with thoracic adenopathy and nodular

Endemic fungi

Beryllioss is exact mimic

29
Q

Pneumoconisosi

A

Silicosis and CWP are upper, nodular and have thoracic adenopathy

Asbestor - lower lobe, reticular, no adenopathy and honeycombing

30
Q

COP

A

Airspace that radiographically looks more like pneumonia but clinically indolent

Inflam change with myxomatous granulation

Steroid responsive

31
Q

Alv hemorrhage

A

Airspace dx caused by cpaillaritis - ANCA vasculitis and anti-GBM dz

32
Q

ALveolar proteinosis

A

Airspace

AB to GM-CSF and macros can;t remove surfactant

PAS+ material in alveolar space

Unusla infections occur

33
Q

HS penumonotis

A

3 types

Chronic - IPF mimic
Subacute - sarcoidosis mimic
Antibides not part of patho

34
Q

Radiation

A

2 forms

Over 40 Gray dose

Pneumonits about 8 weeks after XRT conclusion

Dx by history and sharp bordered