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Gynae Flashcards

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1
Q

Define leukoplakia

A

Opaque, white, plaque like epithelial thickening
Can be due to a variety of non malignant and malignant causes

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2
Q

What is the most common histological type of vulval cancer

A

SqCC

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3
Q

What are the two groups of vulval SqCC. Which is associated with HPV

A

-Basaloid and warty carcinomas; high risk HPV related (HPV16)
-Keratinizing SqCC: non HPV associated. More common, accounting to 70% of cases

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4
Q

What precursor lesions to vulval basaloid and warty carcinomas arise from

A

VIN: vaginal intreaepithelial neoplasia

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5
Q

What are the risk factors for CIN and VIN

A

Early age first sexual intercourse, multiple sexual partners, male partner with multiple sexual partners (all related to early HPV exposure)

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6
Q

What are some histological features of vaginal keratinizing SqCC

A

Keratin pearls
Nests and tongues of squamous epithelium

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7
Q

What abnormalities are typically precursors to keratinizing SqCC of the vulva

A

Lichen sclerosis
Squamous cell hyperplasia
Which lead to differentiated VIN (vulval intraepithelial neoplasia)

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8
Q

What subtype of endometrial carcinoma is most commonly associated with dMMR?

A

Endometrioid

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9
Q

What is the recommended method to test for dMMR

A

IHC for MLH1, MSH2, MSH6, PMS2.
Testing for micro satellite instability is more complicated and expensive

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10
Q

Is endometrial or ovarian cancer more common in women with Lynch syndrome?

A

Endometrial

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11
Q

What testing should be done if there is a loss of MLH1/PMS2 expression on IHC

A

MLH1 promoter methylation.
This is relevant to both endometrial cancer and to colorectal cancer. MLH1 is the MMR gene most commonly affected by epigenetic changes

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12
Q

Why do all 4 endometrial markers need to be tested concurrently

A

They are not mutually exclusive, and it is relevant to know if a patient is a ‘double classifier’

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13
Q

What are the histological subtypes of endometrial carcinoma, and which ones are never classified as low risk

A

Endometrioid

Higher risk:
-serous
-clear cell
-carcinosarcoma
-undifferentiated carcinoma
-mixed

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14
Q

What pathological features are prognostic in endometrial carcinoma

A

Any myometrial invasion
Histological subtype
Grade
LVSI

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15
Q

What are the FIGO grades of endometrial carcinoma

A

Low: grade 1 and 2
High: grade 3

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16
Q

How are cervical pre-invasive lesions classified

A

LSIL (CIN1) low grade squamous intraepithelial lesion
HSIL (CIN2-3) high grade squamous intraepithelial lesion

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17
Q

What is the natural history of cervical LSIL

A

Most cases will regress spontaneously. They do not progress directly to cervical cancer, instead if the progress they will progress to HSIL.
The natural history from high risk HPV infection to cervical cancer usually takes many years/ decades.

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18
Q

What is the highest risk HPV. What percentage of cervical cancer is caused by it

A

HPV16. 60% of cervical cancer

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19
Q

How can HPV viral load be measured in a cervical biopsy

A

In situ hybridisation for HPV DNA

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20
Q

What are the microscopic abnormalities in cervical SIL. How is LSIL distinguished from HSIL

A

Hyperchromatic basal-like cells
Hyperchromatic, Pleomorphic nuclei, Nuclear enlargement
Increased N:C ratio
Cytoplasmic halo around nucleus (koilocytic atypia)
Mitosis
HSIL: loss of differentiation

LSIL has this change only in the basal third of the epithelial thickness. Mitosis confined to lower third

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21
Q

Other than squamous cell carcinoma, what other types of cervical cancer can occur. Which others are HPV associated

A

All are Caused by high risk HPV
Adenocarcinoma (15%)
Neuroendocrine (rare)
Adenosquamous (rare)

Neuroendocrine and adenosquamous have a shorter natural history, and often present with more advanced disease.

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22
Q

What is the defining feature of endometrial hyperplasia

A

Increased gland to stroma ratio

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23
Q

Which signalling pathway most commonly has mutations in endometrioid endometrial carcinoma

A

PI3K/AKT

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24
Q

What suppressor of the PI3K/AKT pathway is often mutated in endometrioid endometrial carcinoma

A

PTEN

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25
What grade are serous endometrial carcinomas by definition
Grade 3
26
What are the two types of endometrial intraepithelial hyperplasia, and what is the main difference
Typical endometrial hyperplasia Atypical endometrial hyperplasia (nuclear atypia)
27
What is the typical state of a uterus in which serous endometrial carcinoma arises
Atrophic , ie thin layer of endometrium
28
What type of growth pattern does endometrioid endometrial carcinoma have
A glandular growth pattern. -well differentiated: almost entirely well formed glands -moderately differentiated: <50% solid sheets of cells -poorly differentiated: >50% solid sheets of cells
29
What is the typical microscopic growth pattern of serous endometrial carcinoma
Papillary growth pattern Marked cytology all atypia, high nuclear to cytoplasm ratio, atypical mitotic figures, hyperchromasia
30
What are the microscopic features of uterine carcinosarcoma
A mix of adenocarcinoma cells (endometrioid, serous or clear cell) and mesenchymal/ sarcomatoid cells.
31
What are the benign and malignant neoplasms of the myometrium
Benign: leiomyoma (fibromas) Malignant: leiomyosarcoma
32
What is the typical microscopic appearance of lyomyoma?
Smooth muscle cells that resemble normal myometrium Uniform size and shape with small oval nuclei. Scarce mitotic figures
33
What genetic abnormalities do uterine leiomyosarcomas typically have
Complex karyotypes with frequent deletions
34
Microscopically what differentiates a leiomyoma from a leiomyoscarcoma
Nuclear atypia, high mitotic index (10+ mitosis per 10 high power field), necrosis
35
What are the three broad types of ovarian carcinoma based on the ovarian component that they arise from
Surface epithelial-stromal tumours Sex cord-stromal tumours Germ cell tumours
36
What are some examples of ovarian surface epithelial/stromal neoplasms.
Note that within each type they are divided into benign, borderline and malignant neoplasms Malignant types are generally adenocarcinoma -serous (most common) -clear cell -endometrioid -mucinous -adenosarcoma (mixed epithelial-stromal)
37
Which malignant ovarian subtype is most likely to have bilateral tumours.
Serous
38
What are some risk factors for serous ovarian adenocarcinoma
Low parity Family history (inherited mutations)
39
What distinguishes high grade from low grade serous ovarian adenocarcinoma
Degree of nuclear atypia
40
Where are the cells that give rise to high grade serous ovarian adenocarcinoma thought to arise
From the Fallopian tubes
41
Are low grade and high grade serous ovarian adenocarcinoma thought to have the same origins
No. High grade thought to arise from cells of the Fallopian tubes. They tend to have very different mutation profiles. p53 mutation rare in low grade, common in high grade
42
What is the implication of the theorised cell of origin of high grade serous ovarian adenocarcinomas when considering prophylactic surgery for BRCA mutation carriers
A salpingoophrectomy should be performed rather than just an oophrectomy
43
What is a typical pattern of metastatic spread of ovarian cancers
Peritoneal and mental spread (with resulting ascites)
44
What proto-oncogene is mutated in the majority of mucinous ovarian cancers
KRAS
45
What are the three main subtypes of germ cell tumour of the ovary
Yolk sac Teratoma Nongestational Choriocarcinoma
46
What are the three subtypes of teratoma of the ovary
Mature/Benign (dermoid cyst) Immature/ Malignant Monodermal/highly specialised
47
What are the characteristic gross appearances of a dermoid cyst
Cystic structure enclosed in a wall resembling epithelium (with sebaceous glands, hair follicles) Can have areas of tooth, calcification, nerve, muscle etc
48
What is the nature of malignant transformation of benign teratoma
Can transform into a malignancy of any of the cell types it contains. Eg, thyroid cancer, melanoma, SqCC
49
What is the difference between mature and immature teratoma
Immature teratoma contains tissues resembling immature embryonal/ fatal tissues. Can have areas of necrosis and haemorrhage. Grade of immature teratoma is based on the percentage of immature neuroepithelium.
50
What tumour of the ovary is the equivalent of testicular seminoma. What group of tumour markers do they express
Dysgerminoma Express stem cell markers. Activating KIT mutations
51
What is a key difference in treatment response of placental/gestational vs ovarian/nongestational choriocarcinoma
Non-gestational is very resistant to chemotherapy and usually fatal
52
What is the utility of WT1 in ovarian malignancy
Positive in serous ovarian carcinoma, negative or positive in serous endometrial carcinoma Negative in other subtypes of endometrial cancer
53
What is a pan-positive marker in tumours of gynae tract
PAX8 Ie tumours of mullerian origin
54
How are HSIL and LSIL of the cervix distinguished microscopically
LSIL involves immature squamous cells in the lower 1/3 of the epithelium thickness only
55
What is the precursor lesions to adenocarcinoma of the cervix
Adenocarcinoma in situ
56
What is the typical microscopic appearance of cervical SqCC
Nests and tongues of malignant squamous epithelium Either keratinizing or not Invade underlying cervical stroma
57
What are the four main families of ovarian tumours
Surface/epithelial (70%) Germ cell (10%) Sex cord-stromal (15%) Metastasis (most commonly GI tract)
58
What are the 5 types of ovarian germ cell tumours
Dysgerminoma (equivalent of testicular seminoma) Yolk sac Choriocarcinoma Teratoma Embryonal carcinoma
59
What are the 5 types of ovarian epithelial/surface tumours
Clear cell -a/w endometriosis Mucinous- must consider GI Mets Brenner/transitional- resembles nests of bladder cells in fibrous stroma Endometrioid- resembles endometrial glands. a/w endometriosis Serous - resembles fallopian tubes -low grade (BRAF/KRAS) -high grade (p53/ genetic instability)
60
What are the three sublassifications of ovarian surface/epithelial tumours
Benign: Cystadenoma & adenofibroma Borderline/low malignant potential Malignant: Carcinoma All of these come in the different types of epithelial tumour. Eg mucinous cystadenoma/adenofibroma
61
What must be done during pathological work up to distinguish borderline from malignant ovarian epithelial tumours
Must be well samples: more than 1 slice per cm
62
What is the natural history of the development of low grade serous ovarian tumours
Usually arise from serous borderline tumours Present at younger age to high grade. (50’s vs 60’s) Share the same IHC profile: ER/PR positive. KRAS/BRAF mutations. PAX8+, P53 wild type. Don’t respond well to platinum chemo
63
What is the natural history of high grade serous ovarian carcinoma
Strong association with BRCA 1/2 mutation Most originate in fallopian tube, then spread to ovary Normal tube -> p53 mutation -> serous tubal intraepithelial carcinoma -> invasive high grade serous carcinoma of tube -> spreads to ovary
64
What are the microscopic features of high grade serous ovarian carcinoma
High mitotic rate Pleomorphic nuclei Irregular chromatin Solid to papillary architecture with slit like spaces
65
What IHC stains can be used to distinguish a mucinous ovary tumour as primary vs metastatic from GI tract
CK7: strong positive ovarian, variable GI tract (sensitive but not specific for ovarian) SATB2 strong positive lower GI tract, negative ovarian (sensitive and specific for GI) PAX8: variable ovarian, always negative GI tract (specific but not sensitive for ovarian) CDX2 variable in both CD20 variable in both
66
What is the IHC profile of high grade serous ovarian carcinoma
p53 over expression or null WT1 positive p16 block positive ER +/- CK7 + CD20- PAX8 +
67
What IHC profile will an ovarian Brenner/transitional tumour have
Urothelial immunophenotype. Positive: P40, p63, HMWCK, CK20/7, uroplakin III
68
What is the difference between testicular and ovarian germ cell tumours
Not much! Use the same microscopic and IHC features. Dysgerminoma = seminoma, both most common germ cell tumour for male/ female = germinoma when in arises in the CNS, still same morphological features
69
What is the rate of progression from acute hpv infection to persistent infection to precursor lesions (LSIL) to invasive cervical carcinoma
10% rule. 10% risk of progression of each (But once 10% of LSIL progress to HSIL the majority (70%) will then progress to invasive disease
70
What makes HPV 16/18 high risk for causing cancer compared to low risk variants such as 6/8
E7/E6 from low risk variants have lower affinity for Rb and p53
71
What is the rate of progression from cervical HSIL to invasive carcinoma
70% progression at 5 years old
72
What is the IHC pattern of cervical SqCC
p16+ Keratin+ P53 loss of expression (due to E6) P63+ CK5/6+ CEA+
73
What is the typical IHC pattern of cervical adenocarcinoma, how does this differ from endometrial carcinoma
Cervical: p16+, CEA+ (100%), ER/PR- or weak, CK7+/CK20-, vimentin- Endometrial carcinoma: CEA-, p16-, ER/PR+, vimentin +, CK7+/CK20- Both PAX8 positive
74
What is the differential diagnosis for a cervical mass
Malignant: -SqCC -Adenocarcinoma -adenosquamous -small cell carcinoma (NETs extremely rare) -lymphoma, melanoma, sarcoma, adenoid cystic Benign: -endocervical polyp -cyst -glandular hyperplasia -endometriosis
75
What is the microscopic appearance of cervical metaplasia
Can closely resemble HSIL, but difference is: p16-ve Uniform chromatin Minimal nuclear contour irregularities More likely to have residual mucinous epithelium
76
What is the p16 status of cervical LSIL, and why
p16 negative Because HPV DNA has not integrated into the host DNA in LSIL, and therefore E7 is not being over produced. Note: p16 negative SIL extending 1/3-2/3 of epithelial thickness is classified as LSIL
77
What is the microscopic appearance of cervical squamous cell carcinoma
Keratinisation (but majority are non keratinizing) Sheet like growth, bands and single cells Desmoplastic/inflammatory stroma
78
What are the microscopic and IHC features of cervical adenocarcinoma in situ
Cell crowding, pseudostratification, mucin depletion Enlarged, variable nuclei “Floating” atypical mitosis p16 diffuse positivity Loss of ER/PR staining
79
What is the microscopic appearance of endocervical adenocarcinoma
Most well to moderately differentiated Cribriform to papillary architecture Mucin-poor glands Psudostratified, enlarged, hyperchromatic nuclei Frequent mitosis and apoptosis
80
What non HPV related adenocarcinoma can occur at the cervix
Gastric type Much worse prognosis than hpv associated
81
Compare the microscopic appearance of usual type VIN versus differentiated VIN
Usual type: HPV associated; therefore most of the same appearances as cervical HSIL. Koilocytes etc. can get warty or basaloid subtypes Differentiated: lichen sclerosis associated. Very subtle atypia. No viral associated atypia
82
What are malignant differentials for vulva lesions
SqCC (keratinizing or verrucous) Bartholins gland adenocarcinoma Melanoma Merkel cell carcinoma Sebaceous carcinoma Rhabdomyosarcoma
83
Which type of VIN is more likely to progress to invasive malignancy
Differentiated VIN. Usual type VIN left untreated has a 10-16% risk
84
What are the two aetiological pathways of development of vulval SqCC
HPV dependent: usual type VIN. Younger patients. Associated with basaloid subtype HPV independent: differentiated VIN. p53 associated. Worse prognosis. Associated with verrucous subtype. Verrucous cause firm masses, well demarcated tumours lined by well differentiated squamous epithelium. Minimal atypia
85
What are two patterns of growth of vulval SqCC associated with higher risk disease
Spray pattern: fingers of tumour extending deeper than main tumour Diffuse pattern: connected tumour of >1mm in dimension
86
What is the most common site of metastasis of vulval SqCC
Lung
87
What are the microscopic features of lichen schlerosus
An autoimmune condition most commonly affecting post menopausal women -hyalinization of papillary dermis (homogenised collagen) -band like lymphocytic infiltrate deep to homogenised collagen -epidermal atrophy
88
What is the single most important risk factor for vulval SqCC
Lymph node involvement
89
What are the two main histological types of vulval SqCC
Keratinizing: associated with differentiated VIN (HPV neg) p16- p53 abnormal. Univocal Basaloid: usual type VIN/ HPV associated. p53 neg, p16+. Histologically basal cells. Both: desmoplasia or inflamed stroma (ie same as cervical SqCC)
90
What are the patterns of myometrial invasion for endometrial cancer
Single gland pattern (diffusely Infiltrative): most common, poor prognosis, a/w LVSI, high grade Pushing/expansile pattern: good prognosis, difficult to distinguish from in situ Adenomyosis-like pattern: good prognosis MELF: microcystic, elongated and fragmented pattern, commonly associated with low grade endometrial

Pathology (16 decks)

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