Respiratory Tract And Mediastinum

Front 1

1. What are the two airway compartments? list the cells normally found in each

Back 1

1. Upper: sinonasal region to larynx

ciliated columnar cells

squamous cells

Lower: trachea to lungs

trachea/bronchi:

ciliated columnar cells

goblet cells

basal/reserve cells

neuroendocrine cells

terminal bronchioles:

nonciliated cuboidal/columnar cells (Clara cells)

alveoli:

type I and II pneumocytes

macrophages

Front 2

Back 2

ciliated columnar (bronchial epithelial) cells

1. In what proportion are goblet cells seen? describe the morphology of both.

Hint 2

1. one goblet per six ciliated cells

Goblet: basally located nucleus, cytoplasm distended with mucus, NO cilia

Ciliated columar: basally located nucleus and luminal surface with terminal bar and cilia

Front 3

1. Describe basal/reserve cells.

2. Describe neuroendocrine cells.

3. Describe clara cells.

4. Describe type I and II pneumocytes.

Back 3

1. near the basment membrane; small undifferentiated cells

2. AKA Kulchitsky cells, only seen with special stains or ultrastructural examination; they are argyrophil-positive and have dense core granules

3. line terminal bronchioles, non ciliated cuboidal to columnar cells

4. Both line alveoli

Type I: more numerous, paper thin, cover the gas exchange surfaces

Type II: plump cuboidal, secretes pulmonary surfactant (seen ultrastructurally as osmophilic lamellar bodies) they are type I's reserve or backup cell after injury; resemble macrophages on cytology

Front 4

1. How often is cancer confirmed in atypical and suspicious diagnoses in respiratory specimens?

2. what optimizes the sensitivity of sputum samples?

3. What transport medium can be used?

Back 4

1. Atypical: 40%

Suspicious: 70%

2. collection over several days, early morning deep cough specimens and sputum induction

3. 70% ethanol

Front 5

1. List and describe 4 methods of sputum preparation.

2. Which method requires preparation under a biologic safety hood and why?

3. What determines adequacy of sputum?

Back 5

1. pick and smear: fresh sputum is examined for blood and tissue fragments and smears containing these are fixed in 95% ethanol

Saccomanno: modified version of the above; collected in 50% ethanol and 2% carbowas, homogonized in blender (with dithriothreitol, DTT is better), concentrated with centrifugation, then smears are made

Thin layer

Cell block

2. Saccomanno, risk of infection from aerosolization

3. numerous pulmonary macrophages

Front 6

Back 6

pulmonary macrophages with carbon pigment (arrows) and yellow green cigarette pigment seen in smokers

1. What findings suggest are considered unsatisfactory in a sputum sample? what do they represent?

2. Discuss the sensitivity of sputum to find cancer with increasing samples.

3. What is the specificity, negative and positive predictive values of sputum cytology?

4. The sensitivity of sputum cytology depends on what property of the tumor? discuss.

Hint 6

1. squamous cells with bacteria and candida organisms; oral contamination! or spit haha!

2. 42% with one sample and 91% with five samples

3. specificity: 96-99%

PPV: 100%

NPV: 15%

3. Location in the lungs

Central: 46-77%

Peripheral: 31-77%

Front 7

1. How safe if bronchoscopy? Compare to alternative.

2. List and describe 4 types of specimens generated by this procedure.

Back 7

1. 0.5% major complication and 0.8% minor complication rate; transthoracic biopsy is 6.8% for major!

2. Aspiration: direct aspiration of secretions

Washing: instilling 3-10mL of saline then aspiration

Brushing: Fiberoptic bronchoscopy allows direct visualization of bronchial lesions on which a brush is swabbed

Lavage: the bronchoscopeis wedged into position as deep as possible in distal airways which are then flushed with saline (deep washing kinda)

Front 8

1. How are slides prepared for aspiration and washing specimens?

2. How are slides prepared for brushings?

Back 8

1. fluid is centriuged and the concentrate is use to make smears, thin layer preps and/or cell blocks

2. direct smearing of the brush onto the slide and submersion in 95% ethanol OR spray fixation; brush placed into media for thin layer preps or cell block

Front 9

1. For what is a BAL particularly useful in diagnosing?

2. What features helps distinguish between oral contamination and true infection?

3. Compare the sensitivity, specificity for infection in AIDs and immunocompromised patients.

4. What is the yield of infectious pathogens in a BAL?

Back 9

1. opportunistic infections in immunocompromised patients

2. neutrophils indicate a real infection while squamous cells indicate contamination

3. AIDS: sensitivity is 86% if biopsy is also done jumps to 98% when used in combonation with biopsy

immunocompromised: sensitivity is 82% specificity is 53%

4. 39%

Front 10

1. List the most common infections organisms detected in BALs of HIV patients.

2. What is the sensitivity of BAL for diagnosing malignancy?

3. What cells cause false positive results and in what condiditons?

Back 10

1. Pneumocystic jiroveci (78%)

bacteria (19%)

M. tuberculosis

Atypical mycobacteria

Histoplasma

Cryptococcus

2. 35-70% higher for multifocal or diffuse tumors

3. atypical type II pneumocytess; pneumonia, DAD, bone marrow transplant and chemotherapy

Front 11

Back 11

Pneumocystis jiroveci casts on pap stain

Front 12

Back 12

PCP cast on pap, note the "negative spaces"

Front 13

Back 13

PCP on GMS see crushed ping pong ball or cup shaped organisms

Front 14

Back 14

PCP on Giemsa, blue dot like intracystic bodies are see

Front 15

Back 15

histoplasma organisms inside macrophages

Front 16

Back 16

cryptococcus on giemsa stain

note variation in size and the clear polysacharride capsule

Front 17

1. What is the sensitivity of transbronchial FNA (wang needle) for detecting malinancy? when combined with the previously discussed procedures?

2. What is the specificity, PPV and NPV?

3. What is the most common cause of false negative in transbronchial FNA mediastinal staging? what is a remedy?

Back 17

1. 56%, increases to 72% when combined with brushing, washing and biopsy

2. specificity 74%

PPV 100%

NPV 53-70%

3. specimens without sufficient lymphocytes called negative; if these are called unsatisfactory the NPV increase from 36% to 78%!

Front 18

1. What is the sensitivity and specificity for EBUS TBNA?

2 . What is needed to be considered adequate when sampling a lung mass?

3. What is the advantage compared to the wang needle previously discussed?

Back 18

1. sensitivity 78% and specificity 99%

2. pigmented macrophages

3. increases the accessibility to lower staion lymph nodes (Wang does 2-4 and 7; EBUS does 2-4, 7, AND 10-12 and with addition of EUS full accessibility)

Front 19

1. What are the relative contraindications to percutaneous FNA of a peripheral lung mass?

2. What is the most common complication?

3. What are the accuracy values for this procedure?

Back 19

1. COPD, emphysema, uncontrollable coughing, uncooperative patient, bleeding diathesis, severe pulmonary HTN, AV malformation, cardiac disease, suspected echinococcal cyst

2. pneumothorax (10% require chest tube)

3. Sensitivity 89%

specificity 96%

PPV 98%

NPV 70%

false positive 0.85%

false negative 8%

Front 20

1. How often can one distinguish small cell from non and ACA from SCC?

2. List 5 possible normal tissue contaminants for percutaneous lung FNA?

Back 20

1. 95% for non small

88% for ACA versus SCC

2. mesothelial cells (have flat sheets, cohesion, windows)

cutaneous squamous cells

skeletal muscle

fibroconnective tissue

hepatocytes (trans-diaphragm)

Front 21

1. How are receptor tyrosine kinases involved in development of cancer?

2. List two drugs targeted at TKR including the specific kinase and the mechanism of action.

Back 21

1. they stimulate growth, invasion and angiogenesis

2. Bevacizumab: anti-VEGF monoclonal antibody

erlotinib: EGFR inhibitor

Front 22

Fill in the receptor pathway.

Back 22

Front 23

1. For what does EGFR stand and what does it activate?

2. In what percent of cancers is it seen? what type?

3. Relate it to race?

4. Which two drugs (inhibitors) are available?

5. Discuss resistance.

Back 23

1. epidermal growth factor receptor; the PO3K/AKT and RAS/RAF/MEK signaling

2. 30-60% of NSCLC

3. the EGFR tyrosine kinase domain is mutated in >30% of Asians and 10% of Caucasians

4. Erlotinib and gefitinib (improve overall survival)

5. most develop major resistance within a year due to additional mutations (most often) in T790M amino acid substitution in exon 20

Front 24

1. What is MET?

2. With what is it associated? how common?

Back 24

1. a proto-oncogene that encodes hepatocyte growth factor receptor (HGFR) another tyrosine kinase

2. Amplification of MET leads to EGFR inhibitor resistance; this is present in 5-20% of EGFR mutated EGFR resistant NSCLC

Front 25

1. What is VEGF?

2. Describe a drug used to target it.

3. What is it used to treat and why?

4. List two other drugs targeting VEGF and their mechanism of action.

Back 25

1. vascular endothelial growth factor and receptor

2. Bevacizumab; highly effective monoclonal antibody against VEGF which has a role in angiogenesis

3. nonSQUAMOUS NSCLC; because it caused fatal pulmonary hemorrhage in patients with SCC

4. sunitinib and sorafenib which are both tyrosine kinase inhibitors

Front 26

1. What is ERBB-1?

2. How often is it expressed and in what cancers?

3. What can be used to treat cancer with these and what cannot?

Back 26

1. HER2, echinoderm microtubule associated protein;

2 .23% of NSCLC

3. do NOT benefit from single agent anti HER2 therapy; a subset 3-10% have mutation in HER2 kinase domain and anti-HER2 antibodies and kinase inhibitors are in development

Front 27

1. Discuss a translocation found in NSCLC.

2. How common is it?

3. In what population does this occur? discuss related mutations.

4. To what drug do they respond and how is the mutation tested?

5. On what chromosome are these genes located?

Back 27

1. Echinoderm microtubule associated protein like 4/ anaplastic lyphoma kinase (EML4-ALK); the fusion of these two proteins results in the activation of progrowth PI3K/AKT and RAS/RAF/MEK pathways

2. seen in 5-7% of NSCLC

3. young (50s) non-smokers withOUT KRAS or EGFR mutations

4. VERY sensitive to crizotinib! found with FISH (break apart)

5. ALK is on 2p23.2 and EML4 is on 2p21; same chromosome different loci

Front 28

1. What is BRAF?

2. Where are the mutations and how are common are they?

3. What cancer also has a BRAF mutation and how are they related?

Back 28

1. a form of RAF, a serine threonine kinase that activates MEK

2. exons 11 or 15 in kinase domain; 3% of NSCLC

3. melanoma, BRAF V600E; they are NOT related and the same drugs are ineffective MEK inhibitors are in development for lung cancers

Front 29

1. What is IGF-1R?

2. With which cancers is it associated?

3. What does this mutation implhy?

Back 29

1. Insulin like growth factor 1 receptor

2. deregulation of it is seen in SCC

3. Better prognosis!

Front 30

1. What kinds of PIK3CA mutations are seen and how often?

2. What role does this have in therapy?

Back 30

1. 12-17% NSCLC show amplification; 2-13% show activating mutations of the kinase or helix domain in NSCLC

2. associated with resistance to receptor tyrosine kinase inhibitor therapy

Front 31

1. When are KRAS mutations seen and what is the prognosis?

2. What is the patient

population?

3. What drug does NOT work?

4. What treatment is used?

Back 31

1. absent in patient with receptor tyrosine kinase mutation; carry a worse prognosis!

2. smokers

3. patients do worse with erlotinib treatment

4. These are treatment resistant tumors; sorafenib has been shown to have efficacy

Front 32

Back 32

Creola body

1. What is it? what is the main associated disease?

2. What can cause reactive squamous and bronchial epithelial changes?

3. What features exclude ACA in reactive broncheps?

Hint 32

1. large clusters of bronchial cells; asthma!

2. infarction, radiation, chemo, sepsis, DAD

3. cilia and a spectrum of changes rather than 2 distinct population

Front 33

Back 33

Reserve cell hyperplasia

1. What is the pathophysiology?

2. What is the cytomorphology?

3. What malignancy does this mimic? what are the distinguishing characteristics?

Hint 33

1. during lung injury surface epithelia is shed and basal reserve cells proliferate in response

2. tightly packed cells

very small cells

smudged dark chromatin

nuclear molding

scant cytoplasm

NO mitosis or necrosis

3. small cell carcinoma; RCH has much smaller cells, greater cohesiveness and NO mitoses or necrosis

Front 34

1. What does repair represent and under what circumstances?

2. What is the cytomorphology?

3. Most often seen in what specimens?

4. What is the DDX? how can one differentiate?

Back 34

1. reepithelialization of an ulcer created by trauma, burns, radiatioin, pulmonary infarction and infection

2. flat cohesive sheets

abundant cytoplasm

enlarged hypOchromatic nuclei

enlarged nucleoli

mitoses

3. brushings and washings

4. malignancy! malignant cells are less cohesive and orderly and more numerous

Front 35

Back 35

Type II pneumocyte hyperplasia

1. What is the pathophysiology?

2. What are 7 common causes?

3. What is the cytomorphology?

4. What is the best tool to distinguish these cells from malignancy?

Hint 35

1. these are alveolar "reserve cells" that proliferate after lung injury.

2. penumonia

sepsis (DAD)

pulmonary embolus/infarction

chemo

radiation

inhalant damage (oxygen toxicity)

interstitial lung disease

3. isolated cells and 3D clusters

large nuclei

coarse chromatin

prominent nucleoli

scant to abundant cytoplasm

4. Clinical history! these patients have diffuse infiltrates with recent illness; cancer patients are often not acutely ill and have a solitary mass

Front 36

Back 36

Curschmann spiral

1. What are they?

Hint 36

1. coiled strands of inspissated mucus that are purple with pap stain; a totally nonspecific finding that should not be mentioned in the report

Front 37

Back 37

Ferruginous body

1. What is this stain?

2. What is the pathophysiology and association?

3. What is the morphology and what distinguishing characteristics are seen in "classic" cause?

Hint 37

1. Iron stain

2. mineral fibers (classically asbestos) coated in ferroproteins (calcium and iron)

3. dumbell shaped 5-100 micrometer golden yellow to black on pap stain; "asbestos bodies" have distinctive clubbed ends and thin straight lucent cores

Front 38

Back 38

Asbestos body

1. Where can asbestos contamination occur?

2. What specimen is useful in patients with exposure?

3. Discuss morphology of asbestos fibers.

Hint 38

1. Ships and insulation

2. BAL has numerous asbestos bodies

3. not visible by light microscopy despite being more abundant than asbestos/ferruginous bodies

Front 39

Back 39

Charcot Leyden crystals

1. what is the cytomorphology?

1. What is the pathophysiology?

Hint 39

1. rhonboid or needle shaped orangeophilic structures

2. derived from degenerating eosinophils with degranulation in patients with severe allergic disorders like asthma

Front 40

Back 40

Psammoma body

1. What are they?

2. In what conditions are they seen?

Hint 40

1. concentrically laminated calcifications

2. malignant tumors with papillary architecture (pulmonary ACA, mesothelioma, metastatic thyroid or ovarian) benign conditions (pulmonary tuberculosis and alveolar microlithiasis)

Front 41

Back 41

Copora amylacea

1. Describe it the cytomorphology.

2. How are they distinguished from psammoma bodies?

Hint 41

1. acellular spherical (or angulated) structures with circumferential and radiating lines 30-100 micrometers in size sometimes with central pigmented core

2. They are not made of calcium

Front 42

Back 42

amyloid (amyloidosis)

1. What other amorphous protein is seen?

2. What is the cyomorphology of vegetable cells?

Hint 42

1. protein in alveolar proteinosis

2. rectangle, uniform size refractile cellulose wall and some have elongated shapes and large nuclei (which can resemble keratinized squamous cell carcinoma)

Front 43

Back 43

Alternaria

1. What is the clinical relevance?

2. In what specimens can it be seen?

3. List and describe the 2 forms.

Hint 43

1. a contaminating pigmented fungus that is rarely pathogenic

2. Can contaminate almst any specimen including cervicovaginal smears, CSF and urine

3. Conidiophores: slender septate stalks with occasional branches

Conidia: snow shoe shaped with tranverse and longitudinal sepatations (shown in this card)

Front 44

SEE TABLE 2.1 ON PAGE 70 FOR VIRAL INFECTIONS

Back 44

SEE TABLE 2.1 ON PAGE 70 FOR VIRAL INFECTIONS

Front 45

Back 45

herpes

1. What diseases does herpes infection cause?

2. Which patients does it affect?

3. What condition has the same morphology?

4. What can aid in diagnosis if cytology is equivocal?

Hint 45

1. pharyngitis, laryngotracheitis, pneumonia

2. immunocompromised and neonates

3. herpes zoster

4. viral culture, IHC or ISH

Front 46

Back 46

CMV

1. What stain is this and what should be known regarding CMV?

2. What are the symptoms?

3. Which cells are affected?

4. What can aid in diagnosis?

Hint 46

1. DiffQuk, the intranuclear (and cytoplasmic?) inclusions are more obvious on a pap stain

2. fever, dyspnea, cough and diffuse nondular or reticular interstitial infiltrates

3. bronchial, pneumocytes, macrophages endothelial cells and fibroblasts

4. culture, IHC, ISH or PCR

Front 47

Back 47

Measles

1. What virus causes this?

2. What disease is seen in the lungs and in what patient population?

3. What is the cytomorphology?

4. What is another virus that can mimic this? how are the two differentiated?

Hint 47

1. Rubeola

2. pneumonia in immunocompromised children from premature birth, CF, malignancy or immunologic disorder

3. giant cell pneumonia characterized by huge multinucleated cells

4. Respiratory syncitial virus; detection of RSV antigen in BAL specimens

Front 48

Back 48

adenovirus

1. What cells are infected in the lung?

2. list the two types of inclusionss.

Hint 48

1. type II pneumocytes

2. smudge cell (seen here) and eosinophilic (resembling herpes cowdry A)

Front 49

Back 49

Ciliocytophthoria

1. What is this and with what virus is it associated?

Hint 49

1. decapitated cilia and terminal bar from respiratory bronchial/columnar cells; adenovirus

Front 50

1. What is the characteristic response to bacterial pneumonia?

2. List 8 common causes.

Back 50

1. neutrophilic exudate

2. Streptococcus pneumoniae

Staphylococcus aureus

Haemophilius influenzae

Klebsiella pneumoniae

Pseudomonas

Legioniella

Nocardia

Actinomyces

Front 51

Back 51

Actinomyces

1. Where is this normal flora and what significance does this hold?

2. What is the gross appearance?

Hint 51

1. Tonsil! a common contaminant of sputum and bronchial specimens but NOT FNAs; seen as large blue "cotton balls" with no inflammatory response

2. Sulfur granules which are yellow aggregates of bacteria

Front 52

Back 52

Nocardia

1. What are the two stains in this photo?

2. Describe the bacteria and how they're acquired?

3. Which species is responsible for 80% of pulmonary infections ?

Hint 52

1. Fite/modified Kinyoun (needed because they are weakly acid fast) and GMS;

2. aerobic gram positive thin filamentous and beaded with extensive right angle branching (chinese characters) living in soil acquired by inhalation usually in immunocompromised

3. N. asteroides

Front 53

Back 53

Legionella

1. Describe this organism.

2. What species most commonly causes infections?

3. Which stains highlight the organisms?

4. What can be used to identify specific organisms?

Hint 53

1. aerobic gram negative

2. L. pneumophila

3. Silver stains like Steiner, Warthin Starry and Dieterle

4. IHC or immunoflourescence

Front 54

Back 54

Epithelioid granuloma

1. Commonly associated with what pulmonary infection?

Hint 54

1. Mycobacterium tuberculosis

Front 55

Back 55

M. Tuberculosis

1. What stain is this?

2. What other method is used to identify this bacteria?

3. Discuss the utility of cell blocks with this and related organisms.

4. Name and describe a test method for this organism.

5. How are these organisms visualized on Romanowsky type stains?

Hint 55

1. Ziehl Neelson

2. culture

3. Limited with M. tuberculosis because one or a FEW organisms are present; M. avium intracellulare in contrast yields innumerable acid fast organisms (in immunocompromised patients like HIV+)

4. Mycobacterium Tuberculosis Direct Test (MTD) has 93% sensitivity and 99% specificity; sputum is analyzed by the assay via PCR amplification of ribosomal RNA

5. as negative images

Front 56

SEE TABLE 2.2 ON PAGE 72 PULMONARY FUNGAL INFECTIONS

Back 56

SEE TABLE 2.2 ON PAGE 72 PULMONARY FUNGAL INFECTIONS

Front 57

Back 57

Cryptococcus neoformans

1. From what is this infection acquired?

Hint 57

1. bird droppings and soil

Front 58

Back 58

Histoplasma capsulatum

1. What cell and location does this organism inhabit?

2. Where does it live and how is it acquired?

3. May clinically mimic what and why?

Hint 58

1. histiocytes in the cytoplasm

2. soil, inhalation of spores

3. tuberculosis because it may cause peripheral nodular lesions and mediastinal lymphadenopathy

Front 59

Back 59

Blastomycosis

1. What is the specific organism?

2. What does it inhabit?

3. What is one of the main morphological clues to this organism?

Hint 59

1. blastomyces dermatitidis

2. wooded terrain

3. The size! its big!

Front 60

Back 60

Coccidoidomycosis

1. What is the causative organism?

2. List the two forms.

3. What is the endemic area?

4. What is the preferred method of cytologic detection?

5. What is the buzz word for these?

Hint 60

1. Coccidoides immitis

2. spherules (which contain) endospores

3. southwest and west US

4. transhoracic FNA because BAL detects <50% of culture positive cases

5. Fractured ping pong ball for the spherules in a background of granular eosinophilic debris

Front 61

Back 61

Paracoccidioidomycosis

1. What it the most common organism and what is it's nick name? Why?

2. Where is it endemic and what does it cause?

3. What reaction does it cause that may lead to an erroneous malignant diagnosis?

4. What is the sensitivity of organism detection on a cell block?

5. What is the buzz word for the shape of this fungus?

Hint 61

1. P. braziliensis; called south american blastomycosis because of broad based budding

2. latin america, lungs and mucocutaneous areas of healthy persons; the most common mycosis

3. squamous metaplasia over granulomas which may lead to diagnosis of SCC

4. 50-90% on sputum

5. Captain's, ship's or mariners wheel

Front 62

Back 62

Sporotrichosis

1. What is the most common organism?

2. What infections does it cause? what is a susceptible patient population?

3. What other yeasts does it resemble? so how is it diagnosed?

Hint 62

1. Sporothrix schenkii

2. "rose gardeners" disease; rarely causes pulmonary disease and only in immunocompromised especially alcoholics and diabetics

3. cryptococcus, histoplasma, candida; culture of flourescent antibody staining is needed because it can't be morphologically distinguished from the above.

Front 63

1. List 3 groups of invasive fungal species.

2. What do they invade?

Back 63

1. Aspergillus

Zygomycetes: Mucor, Absidia, Cunninghamella and Rhizopus

Candida

2. pulmonary tissue and blood vessels of immunocompromised patients

Front 64

Back 64

Aspergillus niger

1. What is seen here?

2. What characterizes pulmonary disease caused by aspergillus ?

3. What is seen in cavitary lung lesions when these sporulate?

4. What do these have in common with paracoccidioides?

Hint 64

1. The fruiting body! most are not black like niger

2. bronchopulmonary aspergillosis is characterized by mucus plugs with fungal organisms, numerous eosinophils and charcot Leyden crystsals

3. fruiting heads and polarizable calcium oxalate crystals

4. May cause severe squamous atypia remniscent of SCC

Front 65

Back 65

zygomycosis

1. What characterizes this group of fungi?

2. What are the 4 species and what is the characteristic form?

3. What is suggestive of candida pnumonia rather than contamination in a BAL?

Hint 65

1. aseptate (arrow in pic b/c nothing is 100% so rare septae)

2. mycelia forming! Absidia, mucor, cunninghamella, and rhizopus

3. Elevated Candida antigen

Front 66

Back 66

Pneumocystis jiroveci

1. Describe this structure on pap stain.

2. Describe the appearance on GMS and giemsa.

3. How are the distinguished from histoplasma on GMS?

4. What is the preferred diagnostic method?

Hint 66

1. the organisms are not visible but masses of them enmesh in proteinaceous material resulting in green, foamy alveolar casts that are more circumscribed than debris or lysed RBCs

2. GMS (or other silver stains): cup shaped 5-7 micrometer with central dark zone

Giemsa: cysts seen as negative images but the 8 1.5 micrometer intracystic bodies or trophozoitses are stained as discrete blue dots

3. No budding in PJP

4. direct immunoflourescence with 92% sensitivity, noninvasive and highly accurate!

Front 67

Back 67

Strongyloides stercoralis

1. How are the lungs infected?

2. How is identified in sputum?

3. What is dog heartworm and how is it transmitted to humans?

4. What is seen in sputum of echonococcus infection? what is the other name for this condition?

5. Why may aspiration of the above cysts be hazardous?

Hint 67

1. hematogenous micgration nof filariform larva from gut or skin

2. large size, differentiated from other hookworms by a notched tail and short buccal cavity

3. mosquitos resulting in entrapment within small pulmonary vessels leading to infarction

4. the scoleces if they hydatid cysts rupture; AKA Hydatid disease

5. anaphylactic shock

Front 68

Back 68

Sarcoidosis

1. What characterizes this disease?

2. Where is the most common site of involvement?

3. What are the arrows showing?

4. List the 3 cytomorphologic characteristics of sarcoidosis.

Hint 68

1. noncaseating granulomas

2. LUNG!

3. the tendency of the process to track along veins in a lymphatic distribution

4. aggregates of epithelioid histocytes

multinucleated giant cells

lymphocytes

Front 69

Back 69

granuloma

1. what are the nuclear and cytoplasmic characteristics of (epithelioid) histiocytes?

Hint 69

1. nuclei: round, oval, curved or boomerang shaped, or spindle-shaped

cytoplasm: translucent and vacuolated

Front 70

Back 70

Wegeners granulomatosis

1. What is the triad?

2. What 3 histologic findings are seen?

3. Describe the cytomorphology.

4. What is the classic blood test used to support this diagnosis?

Hint 70

1. necrotizing angiitis

aseptic necrosis of upper respiratory tract and lungs

focal glomerulonephritis

2. necrosis

granulomatous inflammation vasculitis

3. neutrophils

giant cells

necroti collagen "pathergic necrosis"

epithelioid histiocytess

4. antineutrophil cytoplasmic antibody in a cytoplasmic pattern (c-ANCA, but neither this or perinuclear p-ANCA si entirely sensitive or specific)

Front 71

Back 71

pulmonary alveolar proteinosis

1. What is in the globules?

2. What is the cause? secondary causes?

3. What are the characteristic gross and microscopic findings?

4. What 4 things are on the DDX?

Hint 71

1. lipid rich material

2. impaired macrophage function due to production of neutralizing autoantibodies to GM-CSF (granulocyte macrophage colony stimulating factor); HIV lung transplantation

3. gross: opaque milky BAL specimen

micro: large acellular eosinophilic PAS-positive blobs and pulmonary macrophages filled with it

4. PJP pneumonia

pulmonary edemea

acute silicosis

alveolar mucinosis

Front 72

Back 72

Organizing pneumonia

1. What are the cytomorphologic characteristics?

2. What 4 diseases have cytologic overlap in this DDX?

Hint 72

1. tissue fragments of fibroblasts and collagen

masson bodies ( polypoid plugs of loose organizing connective tissue)

pulmonary macrophages with hemosiderin

lymphocytes

pneumocytes

2. organizing pneumonia

cyryptogenic organizing pneumonia (COP formerly BOOP)

DAD

transplant rejection

Front 73

Back 73

pulmonary hamartoma (pap stain)

1. Why is this a misnomer?

2. What is the cytomphology?

3. What are the most common misdiagnoses?

Hint 73

1. because it is a neoplasm with a recurrent clonal rearrangement of HMGA1 gene on 6p21

2. benign glandular cells

immature fibromyxoid matrix with bland spindle cells

mature cartilage with chondrocytes in lacunae

adipocytes

3. carcinoid tumor, adenocarcinoma and small cell carcinoma

Front 74

Back 74

Inflammatory myofibroblastic tumor

1. Previous name?

2. What is the molecular alteration?

3. Patient population?

4. List two variant molecular alterations.

5. What is an effective medication for this tumor and why? what other tumor?

6. What is the cytomorphology?

7. DDX?

Hint 74

1. inflammatory pseudotumor

2. ALK (2p23) translocations with TPM3 (1q25) and TPM4 (19p13.1)

3. under age 40!

4. clathrin heavy chain (17q23, CLTC) and

ATIC (2q35)

5. crizotinib (ALK inhibitor); EML4-ALK NSCLC

6. spindle cells, storiform pattern, polymorphous inflammatory cells, minimal (if any) necrosis

7. organizing pneumonia and sarcomatoid carcinoma

Front 75

Back 75

Granular cell tumor

1. What is the cell of origin?

2. Cytomorphology?

Hint 75

1. Schwann cells

2. small clusters of macrophage like cells

abundant granular cytoplasm

small uniform round/oval nuclei

Front 76

1. What is the presumed precursor of pulmonary adenocarcinoma?

2. What malignancy has similar morphologic features?

3. Describe the morphology.

4. List 3 epidemiological facts about lung cancer.

Back 76

1. atypical adenomatous hyperplasia

2. nonmucinous adenocarcinoma of lepidic type

3. alveoli lined by cuboidal cells with features of clara cells and type II pneumocytes without ciliated and mucinous cells; often with intranuclear inclusions and binucleation

4. most common cancer in the world

more common in developed countries due to tobacco

most common fatal malignancy in men (29%) and women (25%)

Front 77

1. List genetic alterations that play a role in lung cancer tumorogenesis.

2. Describe the histologic heterogeneity of lung cancer.

Back 77

1. 3p deletion (common in neuroendocrine tumors)

p53 (17p)

K-ras (12)

p16 (CDKN2 on 9.21)

2. almost 50% contain more than one histologic type!

Front 78

1. What is the mechanism behind a p53 mutation related to smoking?

2. List other substances linked to lung cancer.

3. What four types account for 95% of lung cancer?

4. Which one has a unique treatment? describe it.

Back 78

1. G-C to T-A transversion induced by cigarette smoke

2. Asbestos (smoking + asbestos increases lung cancer risk 50 fold!), radon, crystalline silica, nickel compounds, organic compounds (benzene and vinyl choride)

3. SQC, ACA, LCC, SmCC

4. SmCC is treated with systemic chemo because it's usually metastatic at the time of detection

Front 79

Back 79

Squamous cell carcinoma

1. These account for what proportion of lung tumors?

2. What is the typical location?

3. This subtype is most commonly associated with what clinical symptom?

Hint 79

1 . 1/3

2. 2/3 are centrally located and the rest are in smaller bronchi

3. Hemoptysis

Front 80

1. What s a Pancoast tumor?

2. List 4 histologic variants.

Back 80

1. SQCs in the superior sulcus characterized by posterior rib destruction and neural invasion causing severe pain and Horner syndrome (enopthalmos, ptosis, miosis and ipsilateral decreased sweating)

2. papillary, clear cell, small cell basaloid

Front 81

1. List the cytomorphology of well-differentiated SQC.

2. List the cytomorphology of moderate and poorly-differentiated SQC.

3. List the DDX of SQC.

Back 81

1. abundant noncohesive cells

polymorphoic cell shapes (polygonal, rounded, elongated "fiberlike" and tadpole)

dense cytoplasmic orangeophilia on pap stain

pyknotic nuclei

frequent anucleate cells

2. large cohesive clusters of spindle cells

rare/absent keratinization

large nuclei

coarse chromatin texture "Idaho potato"

+\- prominent nucleoli

3. squamous metaplasia

degenerative changes

reactive atypia (aspergilloma)

vegetable cells

upper airway cancer

adenocarcinoma

large cell carcinoma

small cell carcinoma

NUT midline carcinoma

Mets

Front 82

1. What happens to make squamous metaplasia in sputum mimic SQC?

2. When should one exercise caution in diagnosing SQC to avoid false positive diagnosese?

3. What are nuclear and cytoplasmic features to distinguish SQC and ACA?

Back 82

1. Degenerative changes cause a pyknotic condensed nuclear appearance

2. few cells, poorly visualizeed, degenerated, associated with stoma or fungal infection or severe lung injury

3. Nuclear:

SQC: coarse chromatin

ACA: fine chromatin

Cytoplasmic:

SQC: dense

ACA: thin, foamy, vacuolated, transparent

Front 83

1. If a tumor demonstrates positivity for TTF-1 AND p63 what is the diagnosis?

2. What percent of ACAs are positive for p63? Alternative stain?

3. What is NUT midline carcioma?

Back 83

1. Same population: adenocarcinoma

Different population: NOS, comment about adenosquamous

2. 30% at least focally, so can use p40

3. a subtype of SQC, that (grows midline and) has a rearrangement of NUTM1 (15q14) to fuse to BRD4 or BRD3; Nuclear protein in testis (NUT) can be used to stain it and is 100% specific and 87% sensitive OUTSIDE of the testis

Front 84

SEE TABLE 2.3 ON IHC OF SCC AND ACA

Back 84

SEE TABLE 2.3 ON IHC OF SCC AND ACA

Front 85

1. What is the most common type of lung cancer?

2. How does it present?

3. What are the (new) four groups of classification for this tumor?

Back 85

1. adenocarcinoma

2. a peripheral mass with desmoplasia causing pleural puckering; often discovered indidentally; rarely cavitary (like SQC)

3. preinvasive (AAH and AIS) minimally invasiveinvasivevariants of invasive

Front 86

1. How is AIS defined and what are the two types?

2. What are the five patterbs of invasive ACA?

3. Which has a worse prognosis?

4. What is included under "variants of ACA"?

Back 86

1. growth along alveolar septa (lepidic growth, formerly BAC) without destruction of the alvolar architecture; mucinous and nonmucinous

2. lepidic predominant (also formerly nonmucinous BAC)

acinar predominant

papillary predominant

micropapillary predominant

solid predominant with mucin production

3. micropapillary

4. Fetal

Colloid

Mucinous

Enteric

Front 87

1. What are 3 former variants that are now non-distinct?

2. Describe fetal variant.

3. What mutations does mucinous varian have and with what tumor can it be confused?

Back 87

1. mucinous cystadenocarcinoma

clear cell

signet ring

2. resembles epithelial component of pulmonary blastoma

3. KRAS in 76%! lacking EGFR

metastatic colorectal because it often is CK20+ and CK7- and TTF-1-

Front 88

Back 88

Adenocarcinoma

1. What are the cytomorphologic features?

2. What is the size of atpical adenomatous hyperplasia?

Hint 88

1. honeycomb like sheets, 3D clusters, acini or papillae

eccentric round or irregular nuclei

fine chromatin

large nucleoli

mucin vacuoles

translucent foamy cytoplasm

2. <5mm

Front 89

1. What are features seen in mucinous ACA (invasive or in situ)?

2. What is the DDX of ACA?

3. Which preparation can mimic micropapillary ACA?

Back 89

1. honeycomb sheets, pale optically clear nuceli, inconspicuous nucleoli, nuclear grooves and pseudoinclusions

2. reactive bronchial cells

creola bodies

reactive pneumocytes

AAH

Mesothelial cells (on FNA)

vegetable cells

hamartoma

SQC

Large cell carcioma

small cell carcinoma

epithelioid hemangioendothelioma

epithelioid angiosarcoma

mets

3. Liquid based methods

Front 90

Back 90

Mesothelial cells

1. Seen in what specimens?

2. What characteristics identify them as mesothelial?

3. What distinguishes vegetable cells and pulmonary hamartomas as mimics?

4. What features confuse EHE and angiosarcomas with ACA?

5. What stain can further confuse the above issue?

Hint 90

1. Percutaneous FNA

2. cohesion, slit like "windows" separating them from one another

3. vegetable cells have a prominent capsule; hamartomas have fragments of chondromyxoid matrix

4. intracytoplasmic vacuoles and intranuclear inclusions

5. Cytokeratin positivity is seen in 30%

Front 91

Back 91

Large cell carcinoma

1. How common is it?

2. How is it diagnosed?

3. What are histologic variants?

4. What is the cytomorphology?

Hint 91

1. 9% of all lung cancers

2. diagnosis of exclusion based on absence of squamous glandular or small cell features and ONLY diagnosed on resection specimens

3. basaloid

lymphoepithelioma-like

clear cell

LCC with rhabdoid phenotype

LCNEC

4. syncitial clusters and dispersed cells

irregular nuclei

striking chromatin clearing

prominent multiple nucleoli

ill defined feathery cytoplasm

Front 92

1. What cytologic features are seen in LCNEC?

2. Which feature is shared with the basaloid variant and how are the two differentiated?

3. What is the DDX for large cell carcinoma?

Back 92

1. nuclear palisading, molding and rosettes

2. palisading; with LCNEC having positivity for a neuroendocrine stain and basaloid is positive for 34betaE12 (which includes cytokeratins 1, 5, 10 adn 14)

3. reactive

ACA

SQC

sarcomatoid carcinoma

epithelioid angiosarcoma

non-Hodgkinlymphoma

mets

melanoma

Front 93

1. What are the 5 categories within sarcomatoid carcinoma?

2. Why are these important to recognize?

Back 93

1. pleomorphic carcinoma

spindle cell carcinoma

giant cell carcinoma

pulmonary blastoma

Carcinosarcoma

2. They have a worse prognosis

Front 94

1. What is the definition of pleomorphic carcinoma?

2. What is the definition of spindle cell carcinoma?

3. What is the definition of giant cell carcinoma?

Back 94

1. poorly differentiated ACA, SQC or LCC with at least 10% spindle or (no differentiated sarcomatous elements) giant cell morphology

2. consists ONLY of spindle shaped malignant cells with no differentiated spindle cell elements

3. enormous multinucleated cells with NO foci of ACA, SQC or LCC

Front 95

1. What is the morphology of pulmonary blastoma?

2. What is the patient population?

3. What is the cell of origin and molecular alteration?

4. What stains are used?

5. What is cytologic pitfall?

6. How do carcinosarcomas differ?

Back 95

1. biphasic neoplasm composed of two primitive elements resembling fetal lung:

glandular: tubules of cuboidal to columnar cells, sub- and supra- nuclear vacuoles containing glycogen with a "piano key' appearance mimicking endometrial ACA

stromal: spindle cells showing myxoid, chondroid, osteoid or rhadbdomyoblastic differentiation

+/- Squamoid morules

2. M>F 4th decade

3. Totipotent precursor with identical p53 mutation in the glandular and stromal components

4. keratins for glands and SMA for spindle component

5. stroma misinterpreted as small cell carcinoma

6. patient population usually 65yrs

Front 96

1. What are the 4 WHO categories of neuroendocrine tumors?

2. What commonalities do they share?

Back 96

1. carcinoid

atypical carcinoid

large cell neuoendocrine (LCNEC)

small cell carcinoma

2. electron microscopy: cytoplasmic dense core membrane bound granules

stains: reactive to 1+ synaptophysin, chromogranin A (most specific) and CD56 (least specific)

Front 97

SEE TABLE 2.4 CYTOLOGIC FEATURES OF NEUROENDOCRINE TUMORS

Back 97

SEE TABLE 2.4 CYTOLOGIC FEATURES OF NEUROENDOCRINE TUMORS

Front 98

Back 98

Carcinoid tumor on pap

1. What is the critical feature separating these from the other 3 categories? explain.

2. How do these relate to gastroenteric and pancreatic neuroendocrine tumors?

3. How is MIB-1/Ki67 index used?

4. What is the staining profile?

Hint 98

1. mitotic rate!

Carcinoid: <2 per HPF

Atypical carcinoid: 2-10

LCNEC: >10, median 70

SmCC: >10, median 80

2. Mitotic rate cutoff's apply but vary by location

3. <25% in carcinoid/atypical carcinoid and >50% in SmCC

4. Most carcinoids/atypical carcinoids are CK positive (20% negative), and up to 1/3 of carcinoids are TTF-1+

Front 99

Back 99

Carcinoid tumor DiffQuik

1. How common?

2. What is the metastatic potential?

3. what is the cytomorphology?

4. Cell block morphology?

5. DDX of carcinoid?

6. What feature is NEVER seen in typical carcinoid tumors?

Hint 99

1. 2-3% of all pulmonary tumors

2. 10-15% with regional lymph node involvement and 5-10% with distant metastases; 90-98% 5 year survival with surgery

3. loosely cohesive groups and single cells

rosettelike structures

round, plasmacytoid, elongated cells

uniform nuclei with "salt and pepper" chromatin

branching capillaries

few mitoses

no necrosis

inconspicuous nucleoli

4. solid nests, trabeculae (ribbons), papillae and rosettes

5. benign bronchial cells

adenocarcinoma

lymphomoa

SmCC

atypical carcinoid

6. Necrosis!

Front 100

Back 100

Atypical carcinoid

1. What is the 5 year survival rate?

2. Cytomorphology?

Hint 100

1. 61-73%, more aggressive than typical carcinoids

2. cells/architecture like typical carcinoid

focal necrosis

increased mitoses (2-10 per HPF)

prominent nucleoli

Front 101

Back 101

Small cell carcinoma

1. How common is it? Location?

2. Prognosis and associations?

3. What is the cytomorphology?

Hint 101

1. 20-25% of primary lung carcinomas; 90% are centrally located

2. 80% male smokers; <10% 5 year survival

3. small cells (2x lymphocytes)

carrot shaped nuclei

even powdery chromatin

nuclear molding

small/indistinct nucleoli

paranuclear blue bodies

mitoses (>10/ HPF)/ apoptosis

scant cytoplasm

nuclear debris/crush artifact

Front 102

Back 102

1. What is this phenomenon called and how does it occur?

2. How does morphology look in sputum?

3. What are paranuclear blue bodies? in what preparation are they seen?

Hint 102

1. Azzopardi effect; nuclear encrustation of vascular walls by tumor nuclei; characteristic of SmCC

2. streams of small hyperchromati cells in loose aggregates; less preserved than brushing or FNA specimens

3. solitary round, light or dark blue homogeneous spheres that indent the nucleus; only in air dried Romanowsky-type stains NOT on pap or H&E

Front 103

1. What is the DDX of SmCC?

2. What are the most helpful features distinguishing SmCC from NSCLC?

3. What is the most common tumor arising from the submucosal glands of the trachea? prognosis?

Back 103

1. reserve cell hyperplasia

lymphocytes

carcinoid

atypical carcinoid

non small cell carcinoma

NUT midline carcinoma

Ewing sarcoma

Neuroblastoma

Wilm's tumor

rhabdomyosarcoma

pulmonary blastoma

2. powdery chromatin, inconspicuous nucleoli, prominent nuclear molding and scant cytoplasm

3. Adenoid cystic carcinoma; accounts for 25-30% of tracheal malignancies; 80% dead in 20 years

Front 104

1. How common are mucoepidermoid tumors of the lung? what is the molecular alteration?

2. What location are adenoquamous carcinomas seen?

Back 104

1. NOT; 0.2% of lung tumors arising in cartilage containing airways; t(11:19) forming MECT1-MAML2 fusion transcript

2. at the lung periphery beyond a recognizable bronchus

Front 105

1. Describe morphology, origin and staining profile of clear cell tumor of the lung? AKA?

2. Which sarcomas are seen in the lung? List the most common first.

Back 105

1. originate from perivascular epithelioid cells (AKA PEComas and Sugar Tumors), with bland polygonal and spindle-shaped cells with central oval or elongated nucleus and clear glycogen-rich cytoplasm; + for HMB-45 and Melan-A while negative for CKs and CEA

2. leiomyosarcoma> fibrosarcoma, SFT, chondrosarcoma, kaposi sarcoma, angiosarcoma, EHE, rhabdomyosarcoma, MPNST and synovial sarcoma

Front 106

1. Cytomorphology of sarcomas?

2. DDX of sarcomas?

3. How common are primary and secondary lung lymphomas?

4. What are the most common primary non-hodgkin lung lymphomas?

5. List two very aggressive much less common primary lung lymphomas.

Back 106

1. sheetlike, cellular aggregates

single highly atypical spindle cells

2. spindle cell carcinoma

spindle cell carcinoid tumor

spindle cell thymoma

sarcomatoid mesothelioma

melnoma

3. <10% are primary non-Hodgkin lymphomas; while 20-50% of patients have secondary involvement during clinical course (same with Hodgkins!)

4. 70-90% extranodal marginal zone B-cell lymphoma of he mucosa associated lymphoid tissue (MALT, 90% 5 year survival)> DLBCL

5. lymphomatoid granulomatosis and EBV associated T-cell rich B-cell lymphoproliferative disorder both have median survival <2 years

Front 107

1. DDX for pulmonary lymphoma/leukemia?

2. Which patient population is at increased risk for primary lung involvement of hodgkin lymphoma?

Back 107

1. inflammatory lesions

SmCC

LCC

melanoma

2. it's 2x more common in women who present with cough and B-type symptoms

Front 108

1. How common are metastases to the lungs?

2. What specimen often finds

them?

3. What is the breakdown of mets by most common?

Back 108

1. Seen in 30-50% of autopsies with extrapulmonary cancers

2. diagnosed in sputum in up to 70% of cases

3. 40% SQC from site adjacent to aerodigestive tract

34% metastatic ACA (Breast, kidney and colon)

8% hematopoetic

Front 109

1. What are the most common mets on transthoracic FNA from two different studies?

2. What mimics mucinous lung ACA?

3. Besides staining, what is the significance of TTF-1 in lung cancer?

Back 109

1. melanoma (27%) urinary/male genital tract (17%), breast (15%), female genital tract (13%) GI (10%) in one study and in another breast>colon>renal cell> bladder> melanoma

2. PTC

3. 12% have molecular amplification of TTF-1 so pathogenisis also

Front 110

1. What are 3 zones of the mediastinum?

2. Which is the most likely to harbor malignancies?

3. Describe the anatomy of the above compartment?

4. What is the "four Ts" mnemonic?

Back 110

1. anterior middle and posterior

2. Anterior! 59% are malignant

3. laterally by pleura, superior thoracic inlet and inferior diaphragm

4. Thymoma

Teratoma (germ cell tumor)

Terrible lymphoma

Thyroid disease (goiter ect.)

Front 111

1. What is the DDX of anterior mediastinum?

2. What is the most common neoplasm of the anterior mediastinum?

3. What are the paraneoplastic syndromes associated with the above neoplasm?

4. What is the accuracy of FNA versus core biopsy for epithelial origin tumors in this location?

Back 111

1. thymoma

thymic carcinoma

germ cell tumor

lymphoma

parathyroid adenoma

intrathoracic goiter

lipoma

lymphangioma

aortic aneurysm

NUT midline carcinoma

2. thymoma, 20% of adult tumors

3. myasthenia gravis, hypogammaglobulinemia

pure RBC aplasia

4. 80% FNA

100% core biopsy

Front 112

Back 112

Thymoma

1. What two cellular components comprise this neoplasm?

2. How is thymic carcinoma differentiated?

3. What are the 5 WHO types of thymoma?

Hint 112

1. epithelial and lymphocytic

2. it has unequivocally malignant cells

3. A: bland spindle-shaped or ovoid cells

B: round/polygonal cells plus:

1: rich in lympocytes

2: tweener

3: rich in epithelial cells (mild atypia, poorest prognosis)

AB: mix of spindle and polygonal cells

Front 113

1. What stain is seen in thymomas that can confuse the diagnosis? What stain can help differentiate?

2. What stains do the two cell types in thymoma stain for?

3. What stains are positive in thymic carcinomas?

Back 113

1. 43% are calretinin positive confusing them with mesothelial cells; but thymomas are WT1 negative

2. epithelial: p63 and CK5

lymphocytes: TdT, CD3 and CD99; they're T-cells

3. CD5 and c-kit (CD117)

Front 114

1. What are the subroups of thymic carcinoma?

2. How common are primary mediastinal lymphomas?

3. What are the most common types?

Back 114

1. SQC, NEC, mucoepidermoid, basaloid SQC, undifferentiated lymphoepithelial-like CA

2. Less common than secondary comprising only 10%

3. Hodgkin (50-70%), primary mediastinal LBCL, lymphoblastic lymphoma

Front 115

1. Which hodgkin lymphoma is the most common and in what patient population?

2. What patient population is affected by primary mediastinal large B cell lymphoma?

3. From what cells is the above derived?

4. What is its flow cytometry and immunoprofile?

Back 115

1. Nodular sclerosis, women in 3rd decade

2. women 2x more than men; average presentation 37 years

3. thymic B-cells

4. Negative: Bcl-6, surface immunoglobulin, CD5 (mantle) and CD10 (follicular)

Positive: CD45, CD19, CD20

Front 116

1. What is the morphology of primary mediastinal LBCL?

2. What is the DDX? how are they differentiated?

Back 116

1. indistinguishable from DLBCL

2. anaplastic large cell lymphoma (CD30+, way more pleomorphic, T cells), acute lymphoblastic lymphoma (blast morphology, T-cells)

Front 117

1. Which patient population is affected by acute lymphoblastic lymphoma/leukemia?

2. What is the origin of the above?

Back 117

1. kids, one of top 3 lymphomas

2. T-cell origin in 80% with immunopheotype like mature thymic T-cells; but the lymphoblasts are usually 1.5 to 2x larger than normal T-cells

Front 118

1. How common are germ cell tumors of the mediastinum?

2. What patient population?

3. What are the 3 general types?

4. Which population is more affected by malignant germ cell tumors?

Back 118

1. comprise 15% of adult mediastinal tumors, second most common after thymoma

2. young adults

3. seminoma, teratoma and nonseminomatous germ cell tumor

4. MEN 90% of cases :(

Front 119

Back 119

Seminoma

1. What is the patient population and frequency?

2. Prognosis compared to other GCTs?

3. Describe the cytomorphology.

4. What is the background appearance called and how is it formed?

Hint 119

1. men 20-40yrs, most common malignant germ cell tumor of the mediastinum

2. responds well to treatment (radiation +/- chemo) with 85% 5 year survival rate compared to 48% with nonseminomatous tumors (intensive chemo alone)

3. hypercellular, loose clusters and single cells, round/oval nuclei, coarse chromatin, single large nucleolus, background of small mature lymphocytes, moderate to abundant glycogenated cytoplasm (vacuoles & blebs)

4. Tigroid made from dispersal of glycogen vacuoles due to cell disruption

Front 120

1. What is the general appearance of the nonseminomatous GCTs?

2. What stains are most GCTs positive for?

3. What stains are used to distinguish non-seminomatous tumors?

Back 120

1. large malignant cells with large nucleoli, moderate to abundant cytoplasm formingloose or tight 3D clusters with papillary or gland-like features with a necrotic background

2. PLAP, NANOG and OCT3/4

3. SOX2, CD30, AFP (yolk sac and embyomal), inhibin and beta-HCG (choriocarcinoma)

Front 121

1. Which structure is most commonly involved by NUT midline carcinoma?

2. What molecular alteration defines it?

3. What is survival?

4. Diagnosis made by?

Back 121

1. The mediastinum!

2. rearrangment of NUT gene (NUTM1) on chromosome 15 which is fused to BRD4 on chromosome 19

3. Terrible, median 6.7 months NO cure

4. NUclear protein in Testis IHC which is 100% specific and 87% sensitive outside of the testis