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Pathology > H+N > Flashcards

H+N Flashcards

1
Q

What are the types of differentiated thyroid carcinoma. What is their IHC profile. What are the differences microscopically.

A

Papillary thyroid carcinoma: branching papillae with fibrovascular stalks. Epithelium covering stalks cuboidal. Psammoma bodies
Follicular thyroid carcinoma: uniform cells forming small follicles containing colloid
Positive: PAX8, TTF1, thyroglobulin, broad spectrum CK
No IHC markers with adequate sensitivity to distinguish papillary from thyroid.

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2
Q

What are the epidemiological differences between papillary and follicular thyroid carcinoma

A

Papillary: most common, 85% of cases. Most common age 25-50. Form most associated with ionising radiation
Follicular: more common in regions of iron deficiency. Females more common 3:1. Age 40-60

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3
Q

What is the cell of origin of medullary thyroid carcinoma. What is the microscopic appearance

A

Parafollicular C cells that normally secrete calcitonin.
5% of thyroid tumours
Large lesions contain haemorrhage and necrosis.
Spindle shaped cells forming nests and trabeculae. Amyloid deposits in stroma (derived from calcitonin polypeptides)

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4
Q

What is the IHC profile for medullary thyroid neoplasms

A

Positive: TTF1, calcitonin, AE1/AE3, neuroendocrine markers. Congo red (amyloid deposits), CEA
Negative: thyroglobulin
Variable: PAX8

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5
Q

What is the microscopic appearance of anaplastic thyroid carcinoma

A

Minimal follicular differentiation, intratumoral necrosis, frequent mitosis.
Pleomorphic giant cells and/or spindle cells.

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6
Q

What is the usual IHC profile of anaplastic thyroid carcinoma

A

Positive: (usually) AE1/AE3, cam5.2
Negative: thyroglobulin, TTF1.
Variable: pax8

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7
Q

What are the normal microscopic appearances and IHC profile of parathyroid tumours

A

Microscopic: uniform cells resembling normal parathyroid cells. Enclosed by dense fibrous capsule.
Cytology unreliable for diagnosing carcinoma vs benign, invasion of surrounding tissues or mets are key features.
IHC: PTH+, GATA3+, neuroendocrine markers +

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8
Q

What is MEN2 syndrome

A

Autosomal dominant
Near 100% incidence of medullary thyroid carcinoma.
Mutation in RET proto-oncogene (RET is a tyrosine kinase): constitutively activated.

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9
Q

What driver mutations are frequent in papillary thyroid carcinoma

A

RET or NTRK gene translocations resulting in gene fusions
BRAF point mutations (gain of function): in 50-80% of papillary cancers. Most common V600E. Associated with lower expression of thyroglobulin and higher recurrence risk

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10
Q

What driver mutations are found in follicular thyroid carcinoma

A

RAS mutations (gain of function). 30-50%. Associated with retained thyroglobulin expression
t(2;3) involving PAX8
PI3K gain of function mutations
PTEN loss of function mutations

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11
Q

What mutations are commonly found in anaplastic thyroid carcinoma

A

TP53 point mutation
B-catenin point mutation
TERT point mutation (related to telomerase)

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12
Q

What is the difference in prognosis and extra thyroid spread patterns of papillary and follicular thyroid carcinoma

A

Papillary: spread to nodes, but Mets less common. Better prognosis, indolent
Follicular: less spread to nodes, Mets to lung and bone. Worse prognosis, but still indolent

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13
Q

What is the typical presentation of anaplastic thyroid cancer

A

20% have history of differentiated thyroid carcinoma
45% distant Mets at presentation. Lung and bone most common
Extremely aggressive, rapidly enlarging neck mass.
Always classified as stage 4

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14
Q

What are the three main patterns of upper aerodigestive tract mucosa abnormal appearances

A

Leukoplakia: white plaque on mucus membrane
Erythroplakia: red plaque. Higher risk of dysplasia
Speckled erythroplakia: mixed red and white plaque

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15
Q

What are common genetic abnormalities in H+N non-HPV SqCC

A

Genomically unstable with chromosome loss or gain
TP53 mutation

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16
Q

How is H+N squamous dysplasia classified

A

Low grade: maintained stratification/maturation. Minimal atypia, rare mitoses

High grade: abnormal cells in at least half of epithelium thickness. Increased mitoses, increased N:C ratio. Conspicuous atypia

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17
Q

What are some features of invasion of H+N conventional SqCC

A

Downward growth of islands
Cords or isolated tumour cells
Irregular interface
Desmoplastic response
LVI
PNI

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18
Q

What is the microscopic appearance of verrucous SqCC of the H+N

A

Dramatic acanthosis. marked “church spire” keratinisation
Well defined pushing invasion. Infiltrative growth would mean conventional SqCC rather than verrucous

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19
Q

What is the prognosis of the following subtypes of H+N SqCC in comparison to conventional SqCC

Verrucous
Spindle cell
Basaloid
Papillary

A

Verrucous: locally destructive, but does not metastasise
Spindle cell: similar prognosis
Basaloid: more aggressive
Papillary: better prognosis

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20
Q

What is the morphological appearance of HPV positive H+N SqCC

A

Non keratinizing
High N:C ratio (Basaloid appearance)
Frequent mitosis
Apoptotic figures
Lymphocytes/lymphocytic stroma

Grading is not applicable

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21
Q

What is the typical epidemiological pattern of HPV associated SqCC

A

Increasing incidence
Associated with oral sex
Typically white men in 50’s

22
Q

Radiological what is the key feature of HPV positive lymph node Mets

A

Cystic

23
Q

What are different forms of developmental cysts that can present as neck lumps

A

Thyroglossal duct cysts
Branchial cleft cyst: malformations of bronchial apparatus
Thymic cyst: contain thymic tissue
Bronchogenic cyst: lined by respiratory type epithelium

24
Q

What are the microscopic contents of granulomas, and what are different causes

A

Collections of histiocytes and multinucleated cells

Sarcoidosis
TB
Fungal infections

25
Q

How can HPV be tested

A

ISH or PCR

26
Q

What is the differential diagnosis for a laryngeal neoplasm

A

SqCC
-less commonly verrucous

Malignant salivary gland
Small cell carcinoma
Plasmacytoma
Lymphoma
NET
Sarcomas (soft tissue, osteosarcoma, chondrosarc
Malignant melanoma

27
Q

What is the relevance of EGFR in H+N SqCC

A

Frequent over expression
Associated with poor survival

28
Q

What are the histological subtypes of nasopharyngeal carcinoma

A

WHO type 1: keratinising (squamous): sometimes HPV associated. Worst prognosis
WHO type 2: non-keratinizing differentiated (transitional)
WHO type 3: non-keratinizing undifferentiated (lymphoepithelial). EBV associated. Best prognosis
Basaloid: worst prognosis

29
Q

What are the epidemiological patterns of nasopharyngeal carcinoma

A

M >F
Different patterns in EBV endemic countries: China, Hong Kong, SE Asia, North Africa. More WHO type 3, higher rates, median age 50-59
Non-endemic countries: increasing incidence with age. More WHO type 1 (but majority still WHO type 3)

30
Q

What is the typical IHC pattern of nasopharyngeal carcinoma

A

HMWCK+, p40, p63.
CK7-/CK20-
EBER+ (EBV)

Should do IHC to rule out lymphoma, melanoma, rhabdomyosarcoma, SNUC (EBER neg)

31
Q

What are the microscopic features of oncocytes

A

Pink cells due to abundant mitochondria. Granular cytoplasm
Big, polygonal
Prominent nucleoli

32
Q

What are the microscopic features of oncocytoma

A

Biphasic: oncocytes and myoepithelial cells
No significant pleomorphism, mitotic activity or invasive growth

33
Q

What are the three key microscopic elements of warthins tumour

A

Mature lymphoid tissue surrounding;
Bilayered oncocytic epithelium
Cystic to papillary growth

34
Q

What is the microscopic appearance of acinic cell carcinoma

A

Acinar cells
Large polygonal cells
Basophilic granular cytoplasm
Zymogens (enzyme precursors)

35
Q

What is the IHC pattern of acinic cell carcinoma

A

DOG-1 positive
SOX-10 positive

36
Q

What are the microscopic features of adenoid cystic carcinoma

A

2 cell types: myoepithelial, ductal.

Low grade: myoepithelial predominates (p40, SMA)
High grade: ductal predominates (CD117 [but not c-kit mutation], CK)

Myoepithelial cells form pseudocysts of blue glycosaminoglycoglycans or pink basement membrane material .
Almost always have PNI, can track along cranial nerves

37
Q

What does “pleomorphic” refer to in pleomorphic adenoma

A

Architectural pleomorphism
The cells themselves are bland (benign lesion)

38
Q

What are the three components of pleomorphic adenoma

A

Ductal structures
Myoepithelial cells (can be spindled)
Mesenchymal-like tissue with often myxoid stroma

39
Q

What are the microscopic components of mucoepidermoid carcinoma

A

Mucinous cells (stain with mucicarmine and PASD)
Squamous cells
Intermediate cells (scanty cytoplasm)

40
Q

What gene fusion is almost defining for mucoepidermoid carcinoma

A

MAML2 gene fusions

41
Q

What is the microscopic appearance of salivary duct carcinoma

A

Similar appearance to breast invasive ductal carcinoma
Large ducts with comedo necrosis

42
Q

What IHC stains are positive in salivary duct carcinoma

A

Androgen receptors
HER-2

43
Q

What are the microscopic appearances of carcinoma ex pleomorphic adenoma

A

Carcinoma arising within pleomorphic adenoma (often salivary duct carcinoma)

Very pleomorphic, high mitotic rate, necrosis, destructive growth

44
Q

What are salivary gland tumours that fit into the following subtypes
Oncocytic
Basaloid
Spindled cells
Squamoid
High grade

A

Oncocytic: warthins, oncocytoma, intraductal carcinoma, secretory carcinoma
Basaloid: acinic cell carcinoma, adenoid cystic carcinoma
Spindled cells: pleomorphic adenoma
Squamoid: mucoepidermoid carcinoma, SqCC
High grade: salivary duct carcinoma, carcinoma ex pleomorphic adenoma

45
Q

What system is used to predict the risk of malignancy of a salivary gland tumour on FNA

A

Milan system

46
Q

What is the rate of transformation of pleomorphic adenoma to carcinoma ex pleomorphic adenoma

A

5%. The majority are those who have had recurrence of pleomorphic adenoma following surgery

47
Q

What is the risk of recurrence of pleomorphic adenoma

A

50%

48
Q

What is the most common malignant tumour of the parotid gland

A

Muco epidermoid carcinoma

49
Q

What is the most common malignant tumour of the submandibular gland

A

Adenoid cystic carcinoma

50
Q

What is the natural history of adenoid cystic carcinoma

A

Older age, no gender predilection
Locally Infiltrative, but slow growing
Almost always have PNI
Node Mets uncommon
Distant Mets common (lung); can occur many years later

Pathology (16 decks)

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