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PULMONARY BOARDS > ILD > Flashcards

ILD Flashcards

1
Q

What is Dermatomyositis associated with?

A

anti MDA-5 (associated with progressive ILD)
Mi1-2
hyperkeratosis and periungal erythema, dilated nail capillaries

Dermatomyositis is characterized by specific skin manifestations and muscle involvement.

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2
Q

Which antibodies are associated with Antisynthetase syndrome?

A

anti-jo-1, anti-PL7, anti-EJ

Antisynthetase syndrome is characterized by myositis and proximal muscle weakness.

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3
Q

What markers are used to identify Langerhans cell histiocytosis?

A

Cd1a, S-100, stellate

These markers are important in the diagnosis of Langerhans cell histiocytosis.

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4
Q

What is a key marker for LAM (Lymphangioleiomyomatosis)?

A

serum VEGF-D, mTOR mutation; HMB-45 stain positive

These findings are critical for the diagnosis of LAM.

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5
Q

What characterizes Birt-Hogg-Dube syndrome?

A

cystic; autosomal dominant, cutaneous fibrofolliculomas, renal adenocarcinoma, stain positive follicular (FLCN)

Birt-Hogg-Dube is a genetic disorder associated with skin lesions and increased cancer risk.

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6
Q

What is Pulmonary Benign Metastasizing Leiomyoma (PBML)?

A

women with history of uterine leiomyoma, spindle cell smooth muscle, can be military, multiple nodules, low or no FDG avidity

PBML is characterized by specific histological features and immunohistochemical positivity.

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7
Q

Fill in the blank: Follicular bronchiolitis is associated with _______.

A

sjogren, lymphoid hyperplasia of bronchial-associated tissue along bronchi vascular bundles

Follicular bronchiolitis can be related to autoimmune conditions.

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8
Q

What are the histological features of Nodular Lymphoid Hyperplasia?

A

interfollicular plasma cell, lymphoid, histiocytes on path, mass like, subpleural, cysts

Nodular lymphoid hyperplasia can present as a mass-like lesion in the lungs.

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9
Q

When does Bleomycin toxicity typically occur?

A

1-6 months after exposure

Risk factors include renal failure, high oxygen levels, and G-CSF administration.

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10
Q

True or False: RA associated lung involvement commonly presents with pleural effusions.

A

True

RA lung involvement can manifest in various forms including nodules and bronchiectasis.

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11
Q

What is the most common form of ILD associated with rheumatoid arthritis?

A

UIP (Usual Interstitial Pneumonia)

NSIP (Nonspecific Interstitial Pneumonia) can also be seen but is less common.

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12
Q

What is the prognosis of UIP related to autoimmune disease?

A

slower to progress and has better prognosis

Compared to other forms of UIP, autoimmune-related UIP tends to have a more favorable outcome.

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13
Q

What is the best treatment for myositis in the context of lung involvement?

A

Mycophenolate is best, but bad for RA joints

Treatment options need to be tailored based on the patient’s specific conditions.

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14
Q

What is the characteristic triad of idiopathic pulmonary hemosiderosis?

A

microcytic anemia, recurring hemoptysis, bilateral alveolar opacities without a clear cause (and bland biopsy without vasculitis)

This condition primarily affects children.

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15
Q

What histological finding is associated with Amiodarone-induced pneumonitis?

A

lipid-laden foamy macrophages in alveolar spaces

This finding is specific to the lung injury caused by Amiodarone.

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16
Q

What condition is characterized by the presence of parotid enlargement, facial nerve palsy, and anterior uveitis?

A

Heerfordt’s syndrome

Heerfordt’s syndrome is associated with sarcoidosis.

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17
Q

Fill in the blank: Lofgren’s syndrome includes _______.

A

EN, bilateral lymphadenopathy, migratory polyarthralgias

Lofgren’s syndrome is a form of acute sarcoidosis that often improves with NSAIDs.

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18
Q

What is the association of Interferon gamma receptor deficiency in young patients?

A

sarcoidosis and NTM

This deficiency can lead to increased susceptibility to certain infections and autoimmune conditions.

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19
Q

What can the end-stage HP resemble?

A

UIP

End-stage hypersensitivity pneumonitis can have similar radiological and pathological features to UIP.

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20
Q

What genetic predispositions are linked to IPF?

A

hermansky pudlak, short telomere, autoimmune, surfactant issues, dyskeratosis

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21
Q

VEXAS

A

autoinflammatory disorder in pediatrics leading to ILD later in life

Vacuoles
E1 ubiquitin activating enzyme
on the X chromosome
with Autoinflammation
Somatic (not passed down)

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22
Q

Erdheim-Chester disease

A

histiocytosis syndrome
BRAF V600E mutation
Pro-inflammatory cytokines
Sclerotic lesions of long bones
Skin findings
Retroperitonium involvement (like IgG4 disease)
PET-avid
foamy histiocytes
CD1a negative
MNG histiocytes (touton cells) - giant cells

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23
Q

Ddx of Lymphocytic BAL (>25%)

A
  1. Sarcoidosis
  2. NSIP
  3. HP
  4. Drug-induced
  5. CTD
  6. Radiation
  7. COP
  8. Lymphoproliferative disorders
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24
Q

Ddx for Eosinophilic BAL (>25%)

A
  1. Eosinophilic pneumonias
  2. Drug-induced
  3. BM transplant
  4. Asthma
  5. ABPA
  6. Infectious
  7. Hodgkin
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25
Q

Exogenous lipoid pneumonia TBBx and BAL findings

A

lipid-laden macrophages

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26
Q

PAP stain

A

PAS stain

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27
Q

CD1a stain

A

PLHC (>5%)

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28
Q

Recommended number of pieces to biopsy when doing surgical lung bx in ILD

A

2-3 multi-lobe
From areas of active disease

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29
Q

Factors increasing risk of in-hospital mortality in surgical lung bx in ILD

A

non-elective (16%)
Male sex
increased age
higher comorbidity scores
open vs. VATS
provisional diagnosis of IPF or CTD-ILD

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30
Q

Smoking-related interstitial disease

A

Respiratory bronchiolitis-interstitial lung disease (RB-ILD)
Desquemative Interstitial pneumonia (DIP)
PLCH langerhan’s
AEP Acute eosinophilic pneumonia
CPFE (combined pulmonary fibrosis and emphysema)

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31
Q

Idiopathic pleuroparenchymal fibroelastosis (iPPFE)

A

2/2 systemic disease
Upper lobe predominant fibrosis
Can look like UIP but upper lobe, think iPPFE or burnt out HP

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32
Q

Histology and HRCT of UIP

A

Path: Peripheral patchy fibrosis, FF, honeycombing, +/- inflammation

CT: Subpleural and basal, reticular, traction bronchiectasis, honeycombing. If costophrenic angles are spared, it is not IPF

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33
Q

Histology and HRCT of NSIP

A

Path: Homogenous, chronic interstitial inflammation/fibrosis

CT: homogenous, GGOs/reticular, subpleural sparing

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34
Q

Histology and HRCT of OP

A

PAth Patchy, polypoid granulation tissue plugs

CT: patchy consolidations, GGOs, migrating

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35
Q

Histology and HRCT of RB-ILD/DIP

A

Path: pigmented brownish (smoker’s) macrophages, bronchiolocentric

DIP more busy

CT: vague NODULES patchy to diffuse GGOs

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36
Q

Histology and HRCT of DAD

A

Hyaline membranes, granulation tissue, organizing/fibroproliferative

CT: diffuse consolidation/GGOs

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37
Q

Histology and HRCT of LIP

A

Path: lymphoid, plasma cells (very blue)

CT: patchy GGOs, nodules, cystys

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38
Q

Histology and HRCT of PPFE

A

Path Pleural/subpleural fibroelastosis, septal elastosis

CT: UPPER/subpl fibrosis +/- PTX pneumomediastinum

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39
Q

“Typical” UIP pattern HRCT (4)

A
  1. Honeycombing
  2. Reticular + peripheral traction bronchiectasis/bronchiolectasis
  3. Basal and subpleural
  4. Absence of features insonsistent with UIP pattern (extensive consolidations, GGOs, mosaic attenuation, nodules, cysts)
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40
Q

“Definite” UIP histopathologic pattern

A
  1. Dense fibrosis/architectural distortion +/- honeycombing
  2. PAtchy involvement
  3. Fibroblast foci
  4. Subpleural +/- paraseptal predominance
  5. No features suggesting alternative diagnosis (e.g. granulomas)
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41
Q

Difference between “probable” and “typical” UIP

A

“Probable”: no honeycombing in “probable”
“Intermediate”: diffuse, not basilar or subpleural

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42
Q

Definitive diagnosis of ILD in undetermined type

A

cryobiopsy

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43
Q

“Acute exacerbation” of IPF

A

new widespread alveolar abnormality
often precedes death
antifibrotic therpy may help prevent AE in IPF, steroids not likely helpful

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44
Q

Benefit of antifibrotic therapy

A

Reduces rate of FVC decline (evidence based)

May help with:
- QOL
- Reduce rate of hospitalization

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45
Q

ASCEND Study - Pirfenidone 2014
INPULSIS-1 & 2 - Nintedanib 2014
What did they find?

A

Decrease rate of FVC decline in both studies

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46
Q

True or false, risk of lung ca is increased in IPF

A

true

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47
Q

In Non-IPF ILD (Progressive fibrosing ILD and SSc-ILD), what is the role of antifibrotics

A

Nintedanib can decrease rate of FVC decline (INBUILD trial NEJM 2019 & SENSIS trial NEJM 2019)

Pirfenidone also (maher Lancet 2019) - not as good at decreasing rate of decline of FVC

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48
Q

Classification of “progressive pulmonary fibrosis”

A

Non-IPF
Decline in DLCO >10%
Decline in FVC >5%
Radiologic progression

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49
Q

Indications for Nintedanib and Pirfenidone

A

Nintedanib: IPF, SSc-ILD, Chronic fibrosing ILD with progressive phenotype

Pirfenidone: IPF only

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50
Q

“Familial pulmonary fibrosis”

A
  1. 2 or more relatives who share common ancestry
  2. 10-20% of interstitial pneumonia/pulmonary fibrosis
  3. 25% of familial cases have identifiable gene variant
  4. Should do genetic testing in those with early onset (<50 yo)
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51
Q

Typical HRCT features of PLCH

A

upper lobe
bizarre cystic changes

52
Q

Stains typically seen with PLCH

A

CD1a, S100, Langerin (CD207)

53
Q

Management of PLCH

A

Stop smoking
BRAF inhibitors (vemurafenib) if BRAF-V600E mutation
Cladribine, cytarabine,cobimetinib, MTX

54
Q

CPFE HRCT and PFT findings

A

HRCT: upper lobe lung emphysema with lower lobe fibrosis
PFT: Preserved spirometry and lung volumes with low DLCO
High risk for PH and lung ca

55
Q

RA associated ILD

A

** UIP is most common **
then NSIP
OP

Can also affect airway (constrictive bronchiolitis), vascular, pleural, associated with pulmonary amyloidosis

56
Q

Sjogren-ILD

A

NSIP > LIP > UIP > OP, and amyloid

MALToma

HRCT: cysts and nodules

57
Q

Antisynthetase-ILD antibodies

A

Anti-jo 1
Aminoacyl-tRNA synthetase

58
Q

RA-ILD is highly associated with this high risk behavior

A

smoking

59
Q

Antibody associated with SSc-ILD

A

anti-SCl70, anti-centromere

60
Q

Treatment for SSc-ILD

A

1st line MMF
2nd Tocilizumab
3rd line RTX
4th Cyclophosphamide & Nintedanib
5th HSCT

61
Q

RA-ILD treatment

A

1st Steroids
2nd MMF, AZA
3rd RTX
4th Abatacept
5th Nintedanib

62
Q

Sjogren-ILD tx

A

1st steroids
2nd MMF, AZA
3rd RTX

63
Q

PM/DM-ILD tx

A

1st steroids
2nd MMF, AZA, MTX
3rd Tacrolimus, cyclosporine
4th RTX, IVIG
5th Cyclophosphamide

64
Q

Tx of SLE-ILD

A

1st steroids
2nd AZA
3rd MMF
4th RTX
5th cyclophosphamide

65
Q

Significance of IPAF

A

can’t identify a CTD but they have some positive autoimmune serology
2/3 of clinical or serologic findings

66
Q

Sarcoid tx if asymptomatic

A

No treatment, repeat imaging

67
Q

3 Syndromes of definite sarcoid that do not need biopsy

A
  1. Lofgren: E nodosum, bilateral LN, migratory polyarthralgias
  2. Heerfordt’s: parotid swelling, uveitis, Bell’s palsy)
  3. Lupus pernio
68
Q

Diagnostic options for sarcoidosis

A

Biopsy of most accessible tissue
lymphocytic >15%
CD4/CD8 >4 (highly specific)
EBUS: 80% yield
TBBx 50-90%
Endobronchial bx: 25% yield

69
Q

Tx of sarcoidosis

A

prednisone 20-40 mg
2nd line methotrexate

70
Q

Limit of thickness of cyst wall (to compare to cavities and emphysematous areas)

A

<2 mm

71
Q

5 cystic lung diseases

A

LAM
BHD
PLCH
LIP
Amyloidosis

72
Q

HMB-45 staining cells correlates with that disease

A

LAM

73
Q

Threshold of serum VEGF-D to dx LAM

A

> 800 pg/mL

74
Q

PFT in LAM

A

obstructive, low DLCO

75
Q

Diagnosis of LAM needs these

A
  1. CT
  2. LAM on biopsy
  3. renal AML
  4. chylothorac
  5. TSC OR elevated serum VEGF >800
76
Q

treatment of LAM

A

sirolimus
lung transplant

77
Q

Birt-Hogg-Dube mutation

A

FLCN gene

78
Q

Distribution of cysts in BHD

A

lower to mid lung fields

79
Q

If thinking LIP, what serology should you send

A

workup for Sjogren
HIV
dysproteinemia (polyclonal)

80
Q

Cysts and nodules, think ___

A

LIP
Amyloidosis
Follicular bronchiolitis (less cysts) - favorable prognosis

81
Q

Light Chain deposition disease vs. amyloid

A

Non-amyloid deposits, does not stain congo red
no zonal predilection

82
Q

Follicular bronchiolitis

A

Hyperplastic lymphoid follicles with reactive germinal centers along bronchovascular bundles

Associated with CVID, COPA (cell trafficking issue), and sjogren’s

83
Q

Tx of light chain deposition disease

A

chemotherapy
HSCT

84
Q

Most frequent types of Amyloidosis

A

AL (primary) - light chain

AA (secondary) - chronic inflammatory disorders - infrequent
Infrequent with ATTR (familial)

85
Q

Manifestations of Amyloidosis in the lungs

A
  • Diffuse thickening tracheobronchial tree (posterior membrane NOT spared), foci of calcification
  • pulmonary parenchyma - nodules (amyloidomas), reticular pattern, predominantly cystic, can be calcified
    localized/diffuse pattern
  • pleural effusion
  • intrathoracic adenopathy
  • OSA from microglossia
86
Q

Management of pulmonary amyloidosis

A

tracheobronchial: bronchoscopic laser and external beam therapy

Nodules: observe

Diffuse parenchymal: treat underlying plasma cell dyscrasia

87
Q

IgG4 disease diagnosis

A

Histopathological: (2 of 3 major feature)
1. Dense lymphoplasmacytic infiltrate
2. Fibrosis, at least focally storiform (cart-wheel like)
3. Obliterative phlebitis

Immunohistochemical: Increased IgG plasma cells AND IgG4 to IgG cell ratio

AND

Clinical context (serum IgG4 level 70-80%); response to steroids

88
Q

Treatment of IgG4 disease

A

steroids 30-60 mg/d then taper
Rituximab

89
Q

IBD-related bronchiolitis tx

A

corticosteroids (inhaled or systemic)
JAK2 inhibitor (prob not on the boards)

90
Q

PAP etiology (primary)

A

autoimmune (90%)
GM-CSF production disruption or receptor (anti-GSM-CSF antiboties) –> decreased surfactant

91
Q

Causes of secondary PAP

A

acquired macrophage dysfunction (silicoproteinosis, fentanyl patch smoking, hematologic dyscrasias, infections)

92
Q

Tx of PAP

A

whole lung lavage (benefit 15 mo)
GM-CSF SQ daily, nebulized BID q other week
Rituximab
?Statin

PAP can recur after lung transplant

93
Q

WHat is pulmonary alveolar microlithiasis

A

intraalveolar deposition of concentrically lammellated calcium phosphate spheres

Dx teen-50yr

CT: calcific micronodular infiltrate on imaging; “sandstorm” with black pleural line

AR genetic: mutation SLC34A2 for typeIIb sodium phosphate cotransporter

Tx lung transplant

94
Q

Long bones pain, ILD, think ___

A

Erdheim-Chester Disease

95
Q

Diffuse Pulmonary Lymphangiomatosis

A

present with chyloptysis, cough, wheezing
HRCT: septal thickening that is smooth, GGOs, mediastinal infiltration
Dx SLBx
Management sirolimus? bevacizumab? propranolol?

96
Q

Timing of radiation pneumonitis

A

4-12 weeks after radiation

97
Q

Timing of radiation FIBROSIS

A

6-12 mo after irradiation (straight line effect)

98
Q

Timing of radiation OP

A

1-12 mo (usually within 6 mo)
OUTSIDE of the radiation field
Responds well to glucocorticoids
Seen in women with breast ca

99
Q

Constrictive bronchiolitis (BOS)

A

allograft recipients
Severe obstructive lung diasease
inhalational injury - fumes, vaping
DIPNECH
Swyer James McLeod (idiopathic constrictive bronchiolitis after infection, UNILATERAL)

100
Q

What is DIPNECH (what, imaging, dx, tx)

A

Diffuse infiltrative pulmonary neuroendocrine cell hyperplasia
Associated with constrictive bronchiolitis
mosaic pattern HRCT - tiny nodules
Dx lung biopsy
Tx: somatostatin?

101
Q

Constrictive bronchiolitis

A

obstructive
if very severe, insp/exp CT will not be too different due to extent of hyperinflation

102
Q

Management of constrictive bronchiolitis

A

Macrolides, inhaled ICS-formoterol?
Transplant

103
Q

recurrent infection, lower lobe L>R consolidations, think ___

A

Bronchopulmonary sequestration

104
Q

usually 1st year of life, recurrent pulm infections, multiple cysts, connected to tracheobronchial tree, pulmonary arterial supply. Dx?

A

Congenital pulmonary airway malformation (CPAM)

105
Q

What is TGF-beta associated with

A

fibroblasts and IPF

106
Q

WHat is IL-13 associated with

A

T-cells, IgE, asthma

107
Q

What is IL-2 associated with

A

T cells, B cells, melanoma, renal cell Ca

108
Q

Which stage of ABPA is when pt achieves remission

A

Stage II (sx resolution, reduced IgE)

Other stages:
1 - acute (elevated IgE, asthma, eosinophilia, opacities, precipitating Ab)
3- Exacerbation (increased IgE and sx recurrence)
4- steroid dependent asthma, elevated IgE
5- fibrotic lung disease

109
Q

Tx of ABPA

A

corticosteroids
Itraconazole for ~16 weeks; or vori
Limited evidence for omalizumab

110
Q

Loeffler Syndrome

A

simple pulmonary eosinophilia from PARASITES
(Ascaris, hookworms, strongyloides)
Migratory opacities
Pathology: eos infiltrates
usually self-limited, may need corticosteroids but CAUTION if you think it’s strongy

111
Q

Timing of drug-induced AEP

A

febrile illness <5d
BAL >25% eos or eosinophilic pneumonitis on bx

112
Q

Idiopathic acute eosinophilic pneumonia is associated with ___

A

recent onset of smoking
Dust
Environmental stimuli
WTC
vaping

113
Q

Chronic eosinophilic pneumonia is associated with ___

A

asthma
Microabscesses and non-caseating granuloma on path

114
Q

% of eos on BAL in CEP is usually ___

A

> 30-40%

115
Q

Typical age of hypereosinophilic syndrome

A

young middle aged males

116
Q

Dx of hypereosinophilic sd

A

Unexplained eosinophilia >1500 for >6 mo or on 2 exams >1 mo apart
and/or
End-organ dysfunction due to eosinophils

117
Q

Tx of HES

A

steroids
IFN-alpha
Chemotherapy
Hydroxyurea
Imatinib
Mepolizumab

118
Q

3 phases of EGPA

A

Does not always progress and not all always present:
- asthmatic (8-10 years) with allergic rhinitis, atopy
- eosinophilic: peripheral and tissue eosinophilia (lung, GI skin)
- vasculitic - necrotizing vasculitis of small & medium vessels; extravascular granulomas- constitutional sx

119
Q

Mononeuritis multiplex (foot drop) and asthma, think ___

A

EGPA

120
Q

EGPA dx

A

4/6 criteria:
1. Asthma
2. Peripheral eos >10% or >1500
3. Paranasal sinus abnormalities
4. Mononeuropathy or polyneuropathy
5. Migratory pulmonary opacities (nodules, GGO, cavitation
6. Extravascular eos on biopsy

121
Q

Serology in EGPA

A

pANCA, MPO 40-60% - more of the vasculitic phase
if ANCA negative – more eosinophilic phase

122
Q

Tx EGPA

A

corticosteroids
Ritux
Azathioprine
MTX
Leflunomide
Mepolizumab

123
Q

What is Five Factor Score for EGPA

A

Age >65
Cardiac involvement
Renal
GI
Absence of ENT involvement

(0-2 with 1 point/factor)

If FFS 2 or more, or organ infiltration, need stronger medications

124
Q

Asteroid body

A

sarcoid

125
Q

Treatment of refractory checkpoint inhibitor pneumonitis

A

Steroids –>

Infliximab or mycophenolate

PULMONARY BOARDS (9 decks)

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