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Thoracics Flashcards

1
Q

Architectural patterns of lung adenocarcinoma. Which have poorer prognosis?

A

Lepidic
Acinar
Papillary
Micropapillary*
Solid*
Complex gladular*

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2
Q

Diagnostic criteria and clinical significance for micropapillary adenocarcinoma of the lung

A

Tumor cells grow in papillary tuft lacking fibrovascular cores, appearing to float within the alveolar septae
Must be distinguished from STAS
Micropapillary subtype is poor prognosis for overall survival and recurrence

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3
Q

Significance of TTF1 in lung cancer

A

Poorly differentiated CA: TTF1+ favours adenocarcinoma
AdenoCA: TTF1+ favours lung origin
Neuroendocrine: TTF1+ favours high grade neuroendocrine carcinoma. Usually neg in carcinoids

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4
Q

Definition and clinical significance of STAS

A

Free-floating tumor cell clusters or single tumor cells that are present in air spaces in surrounding lung parenchyma beyond edge of tumor
Represents aerogenous spread and is considered a pattern of invasion. Associated with increased rate of locoregional recurrence for pts who undergo sublobar resection

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5
Q

Main subtypes of SCC

A

Keratinizing
Nonkeratinizing
Basaloid

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6
Q

IHC positive in SCC as opposed to AdenoCA

A

HMWK eg CK5/6, p63, p40

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7
Q

DDx for lung SCC

A

Metastatic SCC
Metastatic urothelial CA
Thymic SCC
Squamous metaplasia

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8
Q

Main histologic features of basaloid SCC

A

Solid and trabecular growth, peripheral palisading, possible rosettes
Abrupt keratinization
Small monomorphic cells, hyperchromatic nuclei, absent/small nucleoli
High mitotic rate
Comedo-type necrosis
Called basaloid SCC if >50% basaloid component

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9
Q

DDx of basaloid SCC

A

High grade Neuroendocrine carcinomas
Poorly diff SCC or adenoCA
Adenoid cystic CA
NUT carcinoma

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10
Q

AIS vs MIS

A

AIS - solitary tumor with pure lepidic growth
- </= 3cm
- No invasion or STAS
- 100% disease free survival if lesion completely resected
MIA - solitary tumor with predominant lepidic growth
- Size </= 3cm
- invasive component </=0.5cm
- Exclusion criteria: invasion of vessels, air spaces, or pleura, tumor necrosis, STAS
- 100% disease free survival if lesion completely resected

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11
Q

Diagnostic criteria for SCCis

A

Full thickness of epithelium, without maturation
Large cells with marked anisokaryosis and pleomorphism are present
Increased NC ratio, coarse chromatin, nuclear angulations/folding
Mitotic figures present throughout full thickness

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12
Q

Diagnostic criteria and clinical significance of DIPNECH

A

Generalized proliferation of pulmonary neuroendocrine cells present in mucosa of airways
Lesions may be incidental or associated with chronic respiratory symptoms
Slowly progressive disease - may form tumorlets or carcinoid tumors

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13
Q

Diagnostic criteria of 4 main neuroendocrine tumors

A

Typical carcinoid: <2mits/2mm^3, no necrosis
Atypical carcinoid: 2-10mits/2mm^3 and/or foci of necrosis
Large cell neuroendocrine carcinoma: neuroendocrine morph and IHC
Small cell CA: small cells, poorly defined cell border, fine chromatin, nuclear molding, absent/inconspicuous nucleoli etc

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14
Q

Define combined small cell carcinoma

A

Admixture of small cell carcinoma with components of any type of NSCLC
For combined small cell and large cell, large ells at least 10% of cells present

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15
Q

Differentiate Large cell neuroendocrine carcinoma, NSCLC with neuroendocrine differentiation, large cell carcinoma with neuroendocrine morphology

A

Large cell neuroendocrine: NSCLC that shows neuroendocrine morphology and expresses NE IHC
NSCLC with neuroendocrine diff: NSCLC without NE morphology but + NE IHC
Large cell carcinoma with neuroendocrine morphology: morphology but neg IHC

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16
Q

Diagnostic criteria for neuroendocrine cell hyperplasia, tumorlet, and carcinoid

A

Neuroendocrine cell hyperplasia: prolif of NE cells confined to epithelium of airways without penetration through basement membrane
Tumorlet: prolif of neuroendocrine cells in bronchioles extending into surrounding tissue, </=0.5cm in size
Carcinoid: prolif of NE cells that forms nodule >0.5cm

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17
Q

NE immunostains, localization and utility

A

Chromogranin: cytoplasmic, specific but not sensitive for Ne cells. More sensitive in benign than HG tumors
Synaptophysin: cytoplasmic staining, good specificity
CD56: membranous, most sensitive, least specific
INSM1: nuclear, highest sensitivity and spec

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18
Q

Define large cell carcinoma

A

Undifferentiated NCSLC waste basket
Diagnosis of exclusion - it lacks architectural, cytologic immunohistochemical features of SCLC, adenoCA and SCC
Requires resected tumors

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19
Q

Diagnostic criteria of adenocaquamous

A

Admixture of adeno and SCC components
Each component at least 10% of tumor
May be suggested on small specimen but diagnosis requires resected tumors

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20
Q

Pleomorphic CA vs carcinosarcoma

A

Pleomorphic CA: poorly diff CA composed of any type of NSCLC that contains at least 10% spindle and/or giant cells, or a carcinoma consisting only of spindle or giant cells. Expression of epithelial markers helps establish diagnosis. Aggressive tumors, often high stage and associated with poor prognosis
Carcinosarcoma - consists of mixture of NSCLC and sarcoma-containing heterologous elements. Prognosis usually poor

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21
Q

Classic features of pulmonary blastoma

A

Biphasic pattern - primitive epithelial component resembling fetal bronchioles embedded in sarcomatous mesenchyme with embryonic appearance
Tubules lined by pseudostratified, nonciliated columnar cells and have subnuclear or supranuclear vacuoles

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22
Q

Histologic features of lymphoepithelioma-like carcinoma and it’s clinical significance

A

Poorly diff CA with syncytial pattern of growth, large tumor cells with prominent nucleoli, marked lymphocytic infiltrate and pushing borders (sounds like medullary)
IHC squamous
Presence of EBV
Better survival than other carcinomas

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23
Q

Define NUT carcinoma and described it’s clinical, histological, and genetic features

A

Aggressive, poorly diff CA associated with rearrangement in NUT gene
Clinical: large midline mass extending into hilar structures
Histo: sheets and nest of monomorphic cells with prominent nucleoli. Focally abrupt keratinization may be seen, infiltrating neutrophils
IHC: Variable with epithelial markers, SCC more often than TTF1 or NE markers. Diffuse nuclear staining present with NUT antibody
Genetic: translocation NUTM1-BRD3/4

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24
Q

List salivary gland type tumors occuring in the lung

A

Mucoepidermoid CA
Adenoid cystic CA
Epithelial-myoepithelial CA
Pleomorphic adenoma

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25
Q

Types of papillomas in the lung

A

Squamous papilloma
Glandular papilloma
Mixed squamous and glandular

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26
Q

Cell types in sclerosing pneumocytoma and IHC

A

Cuboidal surface cells: PanCK+ EMA+ TTF1+ NapsinA+
Round stromal cells: TTF1+ EMA+ PanCK-

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27
Q

Growth patterns of sclerosing pneumocytoma

A

Solid
Papillary
Sclerosing
Hemorrhagic
Most tumors have at least 3 of these

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28
Q

Define pulmonary hamartoma

A

Most common benign neoplasm in the lung
Usually peripheral, solitary, asymptomatic
At least two mesenchymal elements combined with entrapped respiratory epithelium

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29
Q

Main forms of PEComatous tumors in liung

A

Lymphangioleiomyomatosis
Clear cell tumor
Overlap of both of the above

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30
Q

Histopathologic features of pulmonary extranodal MALT lymphoma

A

Diffuse infiltration of small B cells: CD20+ CD79a+ BCL2+ CD10- CD23- BCL6-
Lymphoepithelial lesions

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31
Q

Clinical and histopathological features of lymphomatoid granulomatosis

A

Rare disorder of immunocompromised pts
EBV-associated lymphoproliferative disorder
Bilateral, multiple, poorly defined pulmonary nodules/masses
Polymorphous lymphoid infiltrate present with 2 key features: angiocentric location with transmural involvement, large EBV+ B cells with RS like features

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32
Q

Clinical, histopathologic, genetic features of pulmonary langerhans cell histiocytosis

A

PLCH presents as ILD with spontaneous pneumo. Strong association with smoking
Cellular proliferations of Langerhans cells along small airways with rounded stellate nodules
S100+ CD1a+
BRAF V600E

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33
Q

Histopathological features of Erdheim-Chester disease

A

Lipid-laden foamy histiocytes and giant cells along distribution of pulmonary lymphatics
Associated with fibrosis and chronic inflammation
BRAF V600E in 50%

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34
Q

How to differentiate primary from metastatic adenocarcinoma in the lung other than IHC

A

Clinical history of smoking vs another tumor
CT/gross: spiculated and single for primary, demarked/smooth edge and multiple for metastatic
Histo: primary often mixed patterns, may have in situ component
- Metastatic: morphology reminiscent of nonlung primary

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35
Q

Reporting parameters in lung resection for primary cancer

A

Type of resection
Pleural puckering
Presence of any additional tissues or lesions
Tumor location
Tumor size, necrosis, appearance
Tumor relationship with visceral pleura
Tumor relationship with the airways
Distance of tumor to margins
Nontumoral parenchyma
Lymph nodes

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36
Q

Sampling requirements for lung resection for primary cancer

A

Margins - bronchial, vascular, parenchymal
Tumor - well sampled, submit one full tumor slice if possible, any involvement with pleura, parenchyma, airways
Submit all lesions
Submit any additional tissue present
Nontumoral parenchyma
Lymph nodes

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37
Q

Rationale for frozen sections in lung nodules

A

Establish cancer diagnosis to prompt further surgery
Evaluate resection margins
Confirm or r/o metastatic lesions

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38
Q

Parameters for cancer reporting in lung

A

Specimen type, procedure, laterality
Tumor site, focality
Tumor size
Histologic type and grade
Lymphatic and vascular invasion
STAS
Extent of tumor
Resection margin status
Lymph node status
Pathologic stage
Any other pathologic findings
Ancillary studies

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39
Q

IHC marker for thymic epithelium

A

PAX8 (polyclonal)

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40
Q

T staging for lung

A
  • pT1: </=3 cm without invasion into bronchus
  • pT1mi: </=3 cm predominantly lepidic and </=0.5 cm invasion
  • pT2: Tumor 3-5cm OR involves main bronchus OR invades visceral pleura, OR associated with atelectasis or obstructive pneumonitis
  • pT3: 5-7cm OR invades parietal pleura, chest wall, phrenic nerve, parietal pericardium OR separate tumor noduels in same lobe
  • pT4: >7 cm OR invades pther large structures OR separate nodule in ipsilateral different lobe
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41
Q

N-staging for Lung

A
  • pN1: ipsilateral peribronchial, hilar, intrapulmonary nodes
  • pN2: ipsilateral mediastinal, subcarinal
  • pN3: contralateral regional nodes
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42
Q

M-staging for lung

A
  • M1a: Separate tumor nodules in contralateral lung OR pleural/pericardial nodule OR malignant pleural effusion
  • M1b: single extrathoracic met
  • M1c: ultiple extrathoracic mets
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43
Q

2 situations of pleural extension and their respective staging

A
  • Direct invasion and <4 cm: pT2a
  • Direct invasion and <7 cm: pT3
  • Visceral/pericardial nodule: pM1a
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44
Q

`

How to stage multiple lung CAs

A

Multiple primary lungs CAs should be staged separately
Intrapulmonary mets are staged according to site of metastatic nodule

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45
Q

Define visceral pleural invasion

A

TUmor cells invade visceral pleual beyond external elastic layer

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46
Q

Most frequent alterations in EGFR, what type of alterations

A

Activating mutations
* Exon 19 deletion
* Exon 21 L858A
* Exon 20 insertion of T790M

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47
Q

Most frequent alterations in ALK, what type of alterations

A

Gene rearragement
* EML4 fusion
* KIF5B fusion
* TFG fusion

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48
Q

Most frequent alterations in ROS1, what type of alterations

A

Gene rearragement
* CD74 fusion
* EZR fusion
* SDC4 fusion

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49
Q

How is PDL1 testing reported?

A

Tumor percentage score (TPS) %

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50
Q

Subtypes of mesothelioma

A

Epithelioid
Sarcomatoid
Biphasic

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51
Q

Differentiation of epithelioid meso from atypical mesothelial hyperplasia

A

Invasion, expansile nodules, complex/disorganized growth, deep cellularity, complex papillae, irregular vessels, necrosis, loss of BAP1

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52
Q

Define biphasic mesothelioma

A

Each component at least 10% of tumor

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53
Q

What is primary effusion lymphoma

A

HHV8+ atypical B cells with immunoblastic appearance and plasma cell like phenotype (CD20- CD138+)

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54
Q

Thymoma subtypes

A
  • Type A: Epithelial cells blandle spindle cells with few/no immature lymphocytes
  • Type AB: admixture of type A and B thymocytes. Sharp areas of demarcation usually present
  • Type B1: resembles normal thymus with few dispersed epithelial cells without clustering
  • Type B2: Minority of epithelial cells in small clusters
  • Type B3: numerous epithelial cells with solid growth pattern
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55
Q

Clinical and histologic features of thymic SCC

A

Most common subtype of thymic carcinoma
Often poorly efined with invasion of mediastinal structures
Morphologic features of SCC, lacking normal thymic cytoarchitecture
5 year survival 60%, prognosis associated with resection completion and stage

56
Q

Common anterior mediastinal tumors

A

Thymoma, thymic CA, NET, lymphoma, GCT, thyroid, carcinoma mets

57
Q

Differentiate thymic CA and type B3 thymoma

A

Thymoma - lobular growth, pushing invasion, no desmoplasia, no squamous diff, CD5- CD117-, TdT+
SCC - sheets, islands, cords, infiltrative invasion, desmoplasia, squamous diff, CD5+ CD117+ TdT-

58
Q

What is primary mediastinal large B cell lymphoma

A

Aggressive large B cell lymphoma arising in anterior mediastinum
No widespread extrathoracic LN or BM involvement

59
Q

Pathogenesis of hypersensitivity pneumonitis

A

Triggered by immunologic reaction to inhaled agents
Combination of immune complex (type III) and T-cell mediated (Type IV) hypersensitivity reactions

60
Q

5 exposures that cause hypersensitivity pneumonitis

A

Moldy hay “farmer’s lung”
Sugarcane
Maple bark fungus
Birds
Fungi in stagnant water

61
Q

Pathologic changes in hypersensitivity pneumonitis at different stages

A

Acute
* acute alveolitis and bronchiolitis
* DAD (possible)

Subacute
* Lymphocytic intersitital infiltrate
* Poorly formed granulomas
* Focal organizing pneumonia
* Eos/neuts not prominent

Chronic
* Cellular chronic bronchiolitis with peribronchilar intersititial mononuclear cell infiltrate
* Poorly formed nonnec granulomas
* Focal organizing pneumonia
* Eos scant or absent
* Intersititial fibrosis

62
Q

3 most consistent and diagnostic histologic featuers of hypersensitivity pneumonitis

A
  1. Temporally uniform chronic insterstitial pneumonia with peribronchiolar accentuation
  2. nonnecrotizing granulomas
  3. Foci of organizing changes
63
Q

3 findings in BAL specimens from patients with hypersensitivity pneumonitis

A

Marked lymphocytosis with T cell phenotype
CD8>CD4
Increased mast cells

64
Q

Clinical definition of chronic bronchitis

A

Persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in the absence of any other identifiable causes

65
Q

4 important pathogenetic facots of chronic bronchitis

A
  • Cigarette smoking
  • Environmental causes
  • Chronic irritation/inflammation
  • Infections
66
Q

4 microscopic features of chronic bronchitis

A
  • Chronic inflammation of airways
  • Mucus gland hyperplasia in trachea/bronchi
  • Reid index >0.4 - ratio of thickness of mucous gland layer to thickness of wall
  • Marked narroing of bronchioles - mucus plugging, inflammation, fibrosis
67
Q

Define emphysema

A

Abnormal permanent enlargement of airspaces distal to terminal bronchioles, accompaanied by the destruction of alveolar walls withot obvious fibrosis

68
Q

4 common types of emphysema and definitions

A
  1. Centriacinar/centrilobular: distention and destruction involving proximal portion of acinus, mainly respiratory bronchioles
  2. Panacinar/panlobular: distention and destruction involving entire acinus, causing diffuse and bilateral lung involvement
  3. Paraseptal/distal: distention and destruction involving distal portion of acinus, such as alveolar ducts and alveoli often in the subpleural and paraseptal regions
  4. Irrgular: irregular airspace enlargement and tissue destruction associated with scar
69
Q

Causes of emphysema

A
  • Smoking - most common cause of centriacinar emphysema
  • Chronic inflammation
  • A1AT-def - most common cause of panacinar emphysema
  • Scarring - most common cause of irregular emphysema
  • Others - IVDU, Marfan
70
Q

5 examples of nonnecrotizing granuloma

A

Sarcoidosis
Berylliosis
Sarcoid reaction
Hypersensitivity pneumonitis
Foreign body type granuloma

71
Q

5 examples of necrotizing granuloma

A

TB and typical mycobacteria
Mycoses: histo, crypto, blasto, coccidio
Bacteria: syphilis
Necrotizing sarcoid gran
Rheumatoid nodule
Vasculitis

72
Q

5 examples of granulomatous vasculitis

A

Granulomatosis with polyangiitis
EGPA
Sarcoidosis
GCA
Takayasu

73
Q

Clinical features of pulmonary LCH

A

History of smoking
Variabl presentation from asymptomatic to rapidly progressive disease
Dyspnea, cough, chest pain, fatigue, pneumothorax
Extrapulm involvment in 10-15%
LCH can occur in children either as usolated lung dz or multisystem
Reduced DLCO

74
Q

Classic radiographic changes of pulmonary LCH

A
  1. Symmetric, bilat nodular/reticulonodular pattern more prominent in centrilobular regions of upper and middle zones
  2. Often, small cystic changes with bizarre shapes
75
Q

4 microscopic features of pulmonary LCH

A
  • Multiple nodular lesions centered on bronchioles with stellate border
  • Lesions composed of langerhans cells with moderate eosinophilic cytoplasm, indistinct cell border, bean shaped nuclei, prominent grooved nuclear membranes
  • Variable number of eos
  • Spectrum of disease process from infiltrate to stellate fibrotic tissue
76
Q

4 pos IHC in pulm LCH

A

S100
CD1a
Vimentin
CD68

77
Q

Common extrapulm organs involved in LCH

A

Bone
LN

78
Q

Characteristic EM feature of LCH

A

Birbeck granules

79
Q

Etiology and pathogenesis of CF

A

CFTR gene located on chromosome 7
CFTR expressed in epithelium of lung, GI tract, pancreas
Mutations result in inability of airway epi cells to secrete salt, excessive reabsorption of salt and water with dessication of luminal secretions
Mucus plugging and decreased clearance predispose affected individuals to bacterial growth, resulting in recurrent infection

80
Q

Pathological findings in CF

A
  • Acute and chronic bronchitis, bronchiolitis, pneumonia
  • Purulent mucous plugging
  • Bronchiectasis and bronchostenosis
  • Constrictive bronchiolitis and peribronchiolar scarring
  • Abscess formation
  • Atelectasis
  • Emphysema/air trapping
  • Interstitial inflammatory cell infiltrat and fibrosis
81
Q

3 gross fidnings of CF in the lungs

A

Bronchiectasis and purulent airway mucus
Atelectasis and pneumonic consolidation
Emphysematous changes with bullae formation

82
Q

5 extrapulm lesions of CF

A

Sinusitis
Nasal polyps
Pancreatitis
Biliary cirrhosis
Acrodermatitis

83
Q

2 microorganisms that frequently cause lung infections in CF

A

S. Auerus
H Flu

84
Q

Define diffuse alveolar damage

A
  • Histologic pattern of aut lung injury that occurs in a variety of clinical settings
  • Clinically, often presents as ARDS
  • Histologically, hyaline membrane formation and/or intersitial organizing changes are present
85
Q

Causes of DAD

A

Infection
Shock
Trauma - lung contusion, fat embolism, head injury
Inhalation injury
Aspiration of gastric contents
Drugs
Metabolic disorders - pancreatitis, uremia
Radiation
Heme disorders - DIC, transfusion associated
Idiopathic - “acute interstitial pneumonia”
Others - burns, high altitude, near drowning, air embolism, IV contrast

86
Q

Histologic features of DAD

A

Acute/exudative phase - pulmonary congestion, interstitial and intraalveolar edema, fibrin deposition, damage to alveolar walls, hyaline membrane formation
Organizing/proliferative phase - Type 2 pneumocyte prolif, interstitial fibroblast prolif with edematous change, fibrotic thickening of septae
Fibrotic/chronic phase - Interstitial fibrosis, honeycomb changes

87
Q

What is LAM

A

Lymphangioleiomyomatosis - low grade destructive metastasizing neoplasm of PEComa family

88
Q

Clinical presentation of LAM

A

Most often sporadic but also in TSC
YOung women of childbearing age, Caucasians
Dyspnea, cough, chest pain
Spontaneous PTX, hemoptysis, chylothorax, chyloperitoneum, chyluria, chylopericardium

89
Q

Radiographic features of LAM

A

Cystic spaces randomly distributed in both lungs
Diffuse and bilateral reticular pattern in hyperinflation

90
Q

4 disorders possibly associated with LAM

A

TSC
Micronodular pneumocyte hyperplasia
Angiomyolipoma
CLear cell sugar tumor

91
Q

Histologic features of LAM

A

Variable sized cystic spaces lined with plaque-like or nodular aggregates of smooth muscle-like spindle cells
Spindle ceclls possibly admixed with more rounded epithelioid cells

92
Q

Types of idiopathic interstitial pneumonia

A
  • UIP
  • NSIP
  • DIP
  • DAD
  • COP
  • RB-ILD
  • ILD-unclassifiable
93
Q

What is idiopathic pleuroparenchymal fibroelastosis

A
  • Interstitial fibroelastotic change in pleural/subpleural region, predominantly in upper lobes
  • Median age 57 with no sex prediliction
  • Half have recurrent pulmonary infections
  • Minority of FHx of ILD
  • Histo - pleural/subpleural and intraalveolar fibroelastosis
94
Q
A
95
Q

What is acute fibrinous and organizing pneumonia

A
  • Histologic pattern that can occur in the clinical spectrum of DAD and OP
  • Maybe be idiopathic or associatd with collagen vascular disease, HP or a drug reaction
  • Main CT findings bilateral basal opacities and areas of consolidation
  • Histo - intraalveolar fibrin deposition with OP, typical hyalind membranes of DAD are absent
96
Q

What is UIP

A
  • Specific form of chronic fibrosing interstitial lung disease
  • seen in variety of clinical sittings including collagen vascular disease and drug reaction
  • Histo correlate of IPF
97
Q

Common causes of UIP pattern

A

Idiopathic (IPF)
Collagen vascular disease
Drug reaction
Pneumoconiosis, radiation pneumonitis

98
Q

Histologic features of UIP

A
  • Patchy lung involvement with peripheral/paraseptal predominance and intervening preserved normal alveolar architecture
  • Temporally heterogeneous appearance with dense collagen fibrosis, fibroblastic foci, and honeycomb change
  • Interstitial inflammation, focal smooth muslce prolif, focal alveolar macrophage accumulation, lymphoid aggregates
99
Q

Main pathologic features of NSIP

A
  • Diffuse and temporally uniform disease process
  • Dense or loose interstitial fibrosis with various degrees of interstitital chronic inflammatory cell infiltrate and type 2 pneumocyte hyperplasia
  • preserved alveolar architecture usually
  • 2 possible patterns - cellular (better) and fibrotic
  • No granulomatous inflammation, inconspicuous or absent fibroblastic foci, no sig eos or alveolar macs
100
Q

Main pathologic features of DIP

A
  • Diffuse and temporally uniform disease process
  • Mild to mod alveolar septal thickening with interstitial fibrosis and mild chronic inflammatory cell infiltrate
  • Prominent accumulation of alveolar macs
  • Lack of lung architecture remodelling or honeycombing
  • inconspicuous or absent fibroblastic foci or organizing pneumonia
101
Q

Main pathologic features of RB-ILD

A
  • Focal and patchy disease process near small airways
  • Accumulation of brown alveolar macs within resp bronchioles and adjacent alveolar spaces
  • Possible interstitial fibrosis involving the walls of the respiratory bronchiles and surrounding alveolar septa
  • No gran inflammation or organizing changes
102
Q

Causes of organizing pneumonia

A

Idiopathic (COP)
Collagen vascular disease
Drug reaction
Infection
Nonspecific reaction adjacent to other lesions (abscess, neoplasm, infarct)
Others - viral infection, rads, hemorrhage

103
Q

Microscopic features of OP

A
  • Intraluminal organizing fibrosis with fibroblastic polyps/plugs in distal airspaces including bronchioles, alveolar ducts, and alveoli
  • Uniform temporal appearance and patchy distribution
  • Mild instersitial chronic inflammation
  • Preservation of lung architecture
104
Q

Conditions associated with OP pattern

A

COP
Collagen vascular disease
Drug reaction
Hypersensitivity pneumonitis
Infection
Rads
Hemorrhage
Nonspecific reaction adjacent to other lesions - tumor, abscess, infarct, obstruction

105
Q

Etiology of acute interstitial pneumonia

A

Idiopathic

106
Q

Histologic findings of acute interstitial pneumonia

A

Identical to DAD

107
Q

Disorders associated with asbestos exposure

A

Asbestosis
Benign asbestos effusion
Hyaline pleural plaques
Rounded atelectasis
Lung CA
Mesothelioma

108
Q

Methods for identify or quantifying asbestos fibres in the lungs

A
  • H&E and PPB stains
  • Counting asbestos bodies in lung-tissue digest preps
  • Counting uncoated asbestos fibres in lung-tissue digest preps
  • Counting uncoated asbestos fibres with EM
109
Q

Histologic criteria for diagnosis of asbestosis

A

Presence of both of the following:
1. Pulmonary interstitial fibrosis resembling UIP or NSIP patterns with or without associated pleural fibrosis
2. Asbestos bodies

110
Q

WHO classification of pulmonary hypertension

A
  1. Pulmonary arterial hypertension
  2. Secondary to left sided heart disease
  3. Secondary to lung disease/hypoxia
  4. chronic thromboembolic pulmonary hypertension (CTEPH)
  5. Unclear or multifactorial: hematologic d/o, systemic d/o, Metabolic d/o, misc
111
Q

Etiology of pulmonary arterial hypertension

A

Subgroup 1: Idiopathic
Subgroup 2: heritable
Subgroup 3: Drug and toxin induced
Subgroup 4: conditions with known localization of lesions in th small pulmonary arterioles

112
Q

5 Histologic changes of primary pulmonary arterial hypertension

A
  • medial hypertrophy and muscularization of arterioles
  • Cellular proliferatin of intima and concentric intimal fibrosis
  • Angiomatoid lesions
  • plexiform lesions
  • Fibrinoid necrosis
113
Q

Histologic changes in pulmonary venooculsive disease

A

Pulmonary veins and venules
* Obstructive intimal fibrosis, initially of a loose texture
* Recanalization and septa formation
* Scarcity of recent thrombi
* Medial hypertrophy and arterialization

Pulmonary arteries
* Somtimes intimal fibrosis, often with recent thrombi
* Sometimes medial hypertrophy

Lung parenchyma
* Prominent hemosiderosis, focal congestion, and interstitial fibrosis

114
Q

Types of pulmonary aspergillosis

A
  • Colonization of aspergillus to form fungus ball/mycetoma
  • Hypersensitivity reaction
  • Invasive aspergillosis
114
Q

Examples of hypersensitivity reaction to aspergillosis

A
  • Allergic bronchopulmonary aspergillosis
  • Bronchocentric granulomatosis
  • Mucoid impaction
  • Hypersensitivity pneumonitis
  • Eosinophilic pneumonia
115
Q

Clinical manifestations related to invasive aspergillosis

A
  • Acute invasive aspergillosis
  • Chronic necrotizing aspergillosis
  • Necrotizing pseudomembranous tracheobronchitis
  • Empyema
  • Bronchopleural fistula
115
Q

Pathogenesis of silicosis

A

Silica particles are inhaled and deposited in lung tissue
Particles damage lung tissue vis direct toxicity or by production of oxidants and other pro-fibrotic mediators

116
Q

5 disorders associated with silica exposure

A
  • Acute silicoproteinosis
  • Nodular silicosis
  • Silicotuberculosis
  • Rheumatoid pneumoconiosis
  • Mixed dust fibrosis, diffuse interstitial fibrosis, and pleural fibrosis
117
Q

Characteristic histology of nodular silicosis

A
  • Early/cellular - aggregation of dust laden macs producting centriacinar dust macules
  • Silicotic nodules are composed of discrete nodular dense collagen fibrosis, which may become calcified or hyalinized, or develop central degenerative changes
  • Polarized light reveals weakly birefringent silica particles and more strongly birefrigent silicate particles within the nodules and in surrounding dust filled macs
  • May be accompaied by progressive massive fibrosis and diffuse intersititial fibrosis may occur
118
Q

What is sarcoidosis

A
  • Multiorgan disease of nonnecrotizing granulomatous inflammation with unknown etiology
  • Young adults 20-40s, slight female predominance
  • Swedes, Danes, African americans
119
Q

Histologic findings of sarcoidosis in the lungs

A
  • Well for nonnec grans which may become confluent and hyalinized
  • Distribution along lymphatic routes
  • May be accompanied by vasculitis
  • may contain inclusion bodies - schaumann bodies, asteroid bodies, crystalline inclusions
120
Q

DDx sarcoidosis

A
  • Fungal infection
  • mycobacterium
  • Hypersensitivity pneumonitis
  • Berylliosis and other inhaled substances (talc, aluminum)
  • sarcoidal reaction - seen in malignancys, collagen vascular disease, vasculitis syndromes
121
Q

5 extrapulm sites involved in sarcoidosis

A

LN
Liver
Eyes
Spleen
Skin

122
Q

Causes of pulmonary edema

A
  1. Increased hydrostatic/pulmonary venous pressure
  2. Decreased oncotic pressure
  3. Infectiojn
  4. Inhaled gases
  5. Aspiration
  6. Drugs/chemicals
  7. shock/trauma
  8. rads
123
Q

Histologic changes of pulmonary edema

A

Alveolar capillaries engorged
Alveolar spaces filled with homogeneous or very fine granular pink material
Hemosiderin laden macs
FIbrosis and alveolar wall thickening in chronic cases

124
Q

Types of asthma

A
  • Extrinsic/atopic
  • Intrinsic
  • Occupational
  • Others - drug (aspirin) reolatd, obstructed, persistent
125
Q

Histologic findings of asthma

A
  • Thickening of bronchial/bronchiolar basement membranes and subbasement membrane fibrosis
  • Increase in size of submucosal glands
  • Goblet cell hyperplasia
  • Hypertrophy and/or hyperplasia or bronchial wall smooth muscle
  • mucus plugs with eos
126
Q

What are charco-leyden crystals and curshman spirals

A
  • Charcot-leyden crystals - slender, rhomboid shaped orangeophilic structures dervied from the breakdown products of eo granules
  • Crushmann spiral s- couled or corkscrew shaped casts of bronchioles formed by inspissated mucus
127
Q

4 main groups of disorders that predispose to cor pulmonale

A
  • Pulmonary parenchymal disorders
  • pulmonary vascular disorders
  • Disorders affecting chest wall movement
  • Disorders inducing pulmonary arterial constriction
128
Q

2 acute causes of cor pulmonale

A

Massive pulmonary embolism
Exacernation of chronic cor pulmonale

129
Q

2 gross changes of the heart in cor pulmonale

A
  • Dilatation right ventricle
  • Right ventricle hypertrophy
130
Q

Synonyms for primary ciliary dyskinesia

A

Immotile cilia syndrome
Kartagener syndrome

131
Q

Ultrastructural features of primary ciliar dyskinesia

A
  • Absent or shortened dynin arms
  • Absence of radial spokes
  • Absence, transposition or disarragement of microtubules
  • Presence of compound cilia and ciliary disorientation
132
Q

Conditions associated with pulmonary alveolar proteinosis

A

Idiopathic
Associated with:
* infection
* inorganic dust
* immunodeficiency
* Lymphoma/leukemia

133
Q

What is bronchogenic granulomatosis

A

Destructive granulomatous lesion of the bronchi and bronchioles
Generally believed to represent a nonspecifric response to a variety of types of airway injury

134
Q

Causes of bronchogenic granulomatosis and associated disorders

A

Allergic reaction
* allergic bronchopulmonary fungal disease
* Allergic aspergillosis

Infectious
* myocobacterial
* funga
* parasitic
* influenza A

Noninfectious
* GPA
* RA
* Ank spon
* Chronic granulomatous disease
* Diabetes inspidius

Idiopathic

135
Q

Histologic changes of bronchogenic granulomatosis

A
  • airway infiltration of neuts, eos, and necrotic debris surrounded by foreign body giant cells
  • Necrotizing granulomatous inflammation, involving and destroying the bronchial and/or bronchiolar walls with a palisaing histiocytic reaction
  • Fragmented elastic tissue
  • Distal lung parenchyma may show obstructive pneumonia and scattered granulomas
  • No fibrinoid necrosis of the vessels

RC (20 decks)

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