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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
Types of papillomas in the lung
Squamous papilloma Glandular papilloma Mixed squamous and glandular
26
Cell types in sclerosing pneumocytoma and IHC
Cuboidal surface cells: PanCK+ EMA+ TTF1+ NapsinA+ Round stromal cells: TTF1+ EMA+ PanCK-
27
Growth patterns of sclerosing pneumocytoma
Solid Papillary Sclerosing Hemorrhagic Most tumors have at least 3 of these
28
Define pulmonary hamartoma
Most common benign neoplasm in the lung Usually peripheral, solitary, asymptomatic At least two mesenchymal elements combined with entrapped respiratory epithelium
29
Main forms of PEComatous tumors in liung
Lymphangioleiomyomatosis Clear cell tumor Overlap of both of the above
30
Histopathologic features of pulmonary extranodal MALT lymphoma
Diffuse infiltration of small B cells: CD20+ CD79a+ BCL2+ CD10- CD23- BCL6- Lymphoepithelial lesions
31
Clinical and histopathological features of lymphomatoid granulomatosis
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
32
Clinical, histopathologic, genetic features of pulmonary langerhans cell histiocytosis
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
33
Histopathological features of Erdheim-Chester disease
Lipid-laden foamy histiocytes and giant cells along distribution of pulmonary lymphatics Associated with fibrosis and chronic inflammation BRAF V600E in 50%
34
How to differentiate primary from metastatic adenocarcinoma in the lung other than IHC
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
35
Reporting parameters in lung resection for primary cancer
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
36
Sampling requirements for lung resection for primary cancer
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
37
Rationale for frozen sections in lung nodules
Establish cancer diagnosis to prompt further surgery Evaluate resection margins Confirm or r/o metastatic lesions
38
Parameters for cancer reporting in lung
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
39
IHC marker for thymic epithelium
PAX8 (polyclonal)
40
T staging for lung
* pT1: 7 cm OR invades pther large structures OR separate nodule in ipsilateral different lobe
41
N-staging for Lung
* pN1: ipsilateral peribronchial, hilar, intrapulmonary nodes * pN2: ipsilateral mediastinal, subcarinal * pN3: contralateral regional nodes
42
M-staging for lung
* M1a: Separate tumor nodules in contralateral lung OR pleural/pericardial nodule OR malignant pleural effusion * M1b: single extrathoracic met * M1c: ultiple extrathoracic mets
43
2 situations of pleural extension and their respective staging
* Direct invasion and <4 cm: pT2a * Direct invasion and <7 cm: pT3 * Visceral/pericardial nodule: pM1a
44
# ` How to stage multiple lung CAs
Multiple primary lungs CAs should be staged separately Intrapulmonary mets are staged according to site of metastatic nodule
45
Define visceral pleural invasion
TUmor cells invade visceral pleual beyond external elastic layer
46
Most frequent alterations in EGFR, what type of alterations
Activating mutations * Exon 19 deletion * Exon 21 L858A * Exon 20 insertion of T790M
47
Most frequent alterations in ALK, what type of alterations
Gene rearragement * EML4 fusion * KIF5B fusion * TFG fusion
48
Most frequent alterations in ROS1, what type of alterations
Gene rearragement * CD74 fusion * EZR fusion * SDC4 fusion
49
How is PDL1 testing reported?
Tumor percentage score (TPS) %
50
Subtypes of mesothelioma
Epithelioid Sarcomatoid Biphasic
51
Differentiation of epithelioid meso from atypical mesothelial hyperplasia
Invasion, expansile nodules, complex/disorganized growth, deep cellularity, complex papillae, irregular vessels, necrosis, loss of BAP1
52
Define biphasic mesothelioma
Each component at least 10% of tumor
53
What is primary effusion lymphoma
HHV8+ atypical B cells with immunoblastic appearance and plasma cell like phenotype (CD20- CD138+)
54
Thymoma subtypes
* 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
55
Clinical and histologic features of thymic SCC
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
Common anterior mediastinal tumors
Thymoma, thymic CA, NET, lymphoma, GCT, thyroid, carcinoma mets
57
Differentiate thymic CA and type B3 thymoma
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
What is primary mediastinal large B cell lymphoma
Aggressive large B cell lymphoma arising in anterior mediastinum No widespread extrathoracic LN or BM involvement
59
Pathogenesis of hypersensitivity pneumonitis
Triggered by immunologic reaction to inhaled agents Combination of immune complex (type III) and T-cell mediated (Type IV) hypersensitivity reactions
60
5 exposures that cause hypersensitivity pneumonitis
Moldy hay "farmer's lung" Sugarcane Maple bark fungus Birds Fungi in stagnant water
61
Pathologic changes in hypersensitivity pneumonitis at different stages
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
3 most consistent and diagnostic histologic featuers of hypersensitivity pneumonitis
1. Temporally uniform chronic insterstitial pneumonia with peribronchiolar accentuation 2. nonnecrotizing granulomas 3. Foci of organizing changes
63
3 findings in BAL specimens from patients with hypersensitivity pneumonitis
Marked lymphocytosis with T cell phenotype CD8>CD4 Increased mast cells
64
Clinical definition of chronic bronchitis
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
4 important pathogenetic facots of chronic bronchitis
* Cigarette smoking * Environmental causes * Chronic irritation/inflammation * Infections
66
4 microscopic features of chronic bronchitis
* 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
Define emphysema
Abnormal permanent enlargement of airspaces distal to terminal bronchioles, accompaanied by the destruction of alveolar walls withot obvious fibrosis
68
4 common types of emphysema and definitions
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
Causes of emphysema
* 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
5 examples of nonnecrotizing granuloma
Sarcoidosis Berylliosis Sarcoid reaction Hypersensitivity pneumonitis Foreign body type granuloma
71
5 examples of necrotizing granuloma
TB and typical mycobacteria Mycoses: histo, crypto, blasto, coccidio Bacteria: syphilis Necrotizing sarcoid gran Rheumatoid nodule Vasculitis
72
5 examples of granulomatous vasculitis
Granulomatosis with polyangiitis EGPA Sarcoidosis GCA Takayasu
73
Clinical features of pulmonary LCH
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
Classic radiographic changes of pulmonary LCH
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
4 microscopic features of pulmonary LCH
* 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
4 pos IHC in pulm LCH
S100 CD1a Vimentin CD68
77
Common extrapulm organs involved in LCH
Bone LN
78
Characteristic EM feature of LCH
Birbeck granules
79
Etiology and pathogenesis of CF
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
Pathological findings in CF
* 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
3 gross fidnings of CF in the lungs
Bronchiectasis and purulent airway mucus Atelectasis and pneumonic consolidation Emphysematous changes with bullae formation
82
5 extrapulm lesions of CF
Sinusitis Nasal polyps Pancreatitis Biliary cirrhosis Acrodermatitis
83
2 microorganisms that frequently cause lung infections in CF
S. Auerus H Flu
84
Define diffuse alveolar damage
* 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
Causes of DAD
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
Histologic features of DAD
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
What is LAM
Lymphangioleiomyomatosis - low grade destructive metastasizing neoplasm of PEComa family
88
Clinical presentation of LAM
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
Radiographic features of LAM
Cystic spaces randomly distributed in both lungs Diffuse and bilateral reticular pattern in hyperinflation
90
4 disorders possibly associated with LAM
TSC Micronodular pneumocyte hyperplasia Angiomyolipoma CLear cell sugar tumor
91
Histologic features of LAM
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
Types of idiopathic interstitial pneumonia
* UIP * NSIP * DIP * DAD * COP * RB-ILD * ILD-unclassifiable
93
What is idiopathic pleuroparenchymal fibroelastosis
* 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
95
What is acute fibrinous and organizing pneumonia
* 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
What is UIP
* 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
Common causes of UIP pattern
Idiopathic (IPF) Collagen vascular disease Drug reaction Pneumoconiosis, radiation pneumonitis
98
Histologic features of UIP
* 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
Main pathologic features of NSIP
* 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
Main pathologic features of DIP
* 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
Main pathologic features of RB-ILD
* 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
Causes of organizing pneumonia
Idiopathic (COP) Collagen vascular disease Drug reaction Infection Nonspecific reaction adjacent to other lesions (abscess, neoplasm, infarct) Others - viral infection, rads, hemorrhage
103
Microscopic features of OP
* 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
Conditions associated with OP pattern
COP Collagen vascular disease Drug reaction Hypersensitivity pneumonitis Infection Rads Hemorrhage Nonspecific reaction adjacent to other lesions - tumor, abscess, infarct, obstruction
105
Etiology of acute interstitial pneumonia
Idiopathic
106
Histologic findings of acute interstitial pneumonia
Identical to DAD
107
Disorders associated with asbestos exposure
Asbestosis Benign asbestos effusion Hyaline pleural plaques Rounded atelectasis Lung CA Mesothelioma
108
Methods for identify or quantifying asbestos fibres in the lungs
* 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
Histologic criteria for diagnosis of asbestosis
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
WHO classification of pulmonary hypertension
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
Etiology of pulmonary arterial hypertension
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
5 Histologic changes of primary pulmonary arterial hypertension
* medial hypertrophy and muscularization of arterioles * Cellular proliferatin of intima and concentric intimal fibrosis * Angiomatoid lesions * plexiform lesions * Fibrinoid necrosis
113
Histologic changes in pulmonary venooculsive disease
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
Types of pulmonary aspergillosis
* Colonization of aspergillus to form fungus ball/mycetoma * Hypersensitivity reaction * Invasive aspergillosis
114
Examples of hypersensitivity reaction to aspergillosis
* Allergic bronchopulmonary aspergillosis * Bronchocentric granulomatosis * Mucoid impaction * Hypersensitivity pneumonitis * Eosinophilic pneumonia
115
Clinical manifestations related to invasive aspergillosis
* Acute invasive aspergillosis * Chronic necrotizing aspergillosis * Necrotizing pseudomembranous tracheobronchitis * Empyema * Bronchopleural fistula
115
Pathogenesis of silicosis
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
5 disorders associated with silica exposure
* Acute silicoproteinosis * Nodular silicosis * Silicotuberculosis * Rheumatoid pneumoconiosis * Mixed dust fibrosis, diffuse interstitial fibrosis, and pleural fibrosis
117
Characteristic histology of nodular silicosis
* 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
What is sarcoidosis
* Multiorgan disease of nonnecrotizing granulomatous inflammation with unknown etiology * Young adults 20-40s, slight female predominance * Swedes, Danes, African americans
119
Histologic findings of sarcoidosis in the lungs
* 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
DDx sarcoidosis
* Fungal infection * mycobacterium * Hypersensitivity pneumonitis * Berylliosis and other inhaled substances (talc, aluminum) * sarcoidal reaction - seen in malignancys, collagen vascular disease, vasculitis syndromes
121
5 extrapulm sites involved in sarcoidosis
LN Liver Eyes Spleen Skin
122
Causes of pulmonary edema
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
Histologic changes of pulmonary edema
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
Types of asthma
* Extrinsic/atopic * Intrinsic * Occupational * Others - drug (aspirin) reolatd, obstructed, persistent
125
Histologic findings of asthma
* 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
What are charco-leyden crystals and curshman spirals
* 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
4 main groups of disorders that predispose to cor pulmonale
* Pulmonary parenchymal disorders * pulmonary vascular disorders * Disorders affecting chest wall movement * Disorders inducing pulmonary arterial constriction
128
2 acute causes of cor pulmonale
Massive pulmonary embolism Exacernation of chronic cor pulmonale
129
2 gross changes of the heart in cor pulmonale
* Dilatation right ventricle * Right ventricle hypertrophy
130
Synonyms for primary ciliary dyskinesia
Immotile cilia syndrome Kartagener syndrome
131
Ultrastructural features of primary ciliar dyskinesia
* Absent or shortened dynin arms * Absence of radial spokes * Absence, transposition or disarragement of microtubules * Presence of compound cilia and ciliary disorientation
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Conditions associated with pulmonary alveolar proteinosis
Idiopathic Associated with: * infection * inorganic dust * immunodeficiency * Lymphoma/leukemia
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What is bronchogenic granulomatosis
Destructive granulomatous lesion of the bronchi and bronchioles Generally believed to represent a nonspecifric response to a variety of types of airway injury
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Causes of bronchogenic granulomatosis and associated disorders
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
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Histologic changes of bronchogenic granulomatosis
* 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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