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ERS > ERS30 Pathology Of Female Genital Tract > Flashcards

ERS30 Pathology Of Female Genital Tract Flashcards

1
Q

Embryological development

A
  1. Gonads covered by Coelomic epithelium (Mesothelium)
    —> Ovaries
  2. Müllerian ducts
    —> Fallopian tube
    —> Uterus (Corpus + Cervix)
    —> Upper vagina
  3. Urogenital sinus
    —> Lower vagina

(—> Produce similar pattern of diseases?)

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2
Q

Vulva, Vagina, Cervix pathologies

A
  1. Inflammation
  2. Non-neoplastic epithelial disorders
  3. Neoplasia

Clinical presentation:

  • Pruritis vulva
  • Leukoplakia
  • Mass
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3
Q

Vulva + Vagina: Inflammation

A

~ Male genital tract

  1. Non-STD infection
    - UTI
    - Candida albicans
  2. STD
    - e.g. Herpes infection, Syphilis, Gonorrhea
    - Effects and complications ***NOT confined to genital tract (spread to systemic involvement)
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4
Q

Vulva: Non-neoplastic epithelial disorders

A
  1. Prone to many skin disease seen in other body parts
  2. Specific to Vulva
  • ***Lichen Sclerosis (whitish, thin epithelium, band of chronic inflammatory cells)
    —> Atrophic + Friable skin, mucosa
    —> fissures, adhesions, introital (vaginal opening) stenosis
    —> Hyperkeratosis with thinning of epidermis + Flattening of dermo-epidermal junction
    —> Hyalinisation of upper dermal collagen with subjacent band of chronic inflammatory cells
  • ***Squamous hyperplasia
    —> Hyperplasia of stratified squamous epithelium with no specific dermatological diagnosis
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5
Q

Cervix: Non-neoplastic epithelial disorders

A
  • **Endocervical Polyp
  • common lesion
  • single <1cm diameter
  • usually asymptomatic but may result in vaginal bleeding / discharge
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6
Q

Vulva + Vagina + Cervix: Neoplastic

A

Classification:
1. **Squamous Intraepithelial Lesion (SIL)
- VIN (Vulvar) / VAIN (Vagina) / CIN (Cervical)
- Current classification (Cytology: Bethesda system / Biopsy: WHO)
- **Squamous precursor lesions
- Low grade (e.g. Condyloma / Koilocytosis —> CIN grade 1)
- High grade (e.g. CIN grade 2-3)
—> grade depend on ***thickness of epithelium involved by dysplastic squamous cells
- Dysplastic cells show malignant features: ↑ nuclear/cytoplasmic ratio, nuclear pleomorphism, ↑/abnormal mitotic figures
- Regress (some low grade may spontaneously regress) / Progress to invasive carcinoma / Remain stationary

VIN:

  • Classic VIN (associated with high risk ***HPV infection)
  • Differentiated VIN (associated with ***chronic irritation e.g. Lichen sclerosis / Squamous hyperplasia)

CIN:

  • from ***Transformation zone of cervix (Glandular —> Stratified squamous)
  • may progress to ***SCC of cervix over years (basis of cervical cancer screening)

(2. Condyloma (HPV-related changes)
—> Cervical Intraepithelial Neoplasia (CIN: grade 1 —> 3)

  1. Past
    - Normal —> mild dysplasia —> moderate —> severe —> carcinoma-in-situ —> invasive carcinoma)
  • **Types of Neoplasia:
    1. SIL (Preinvasive)
    2. SCC (Invasive)
    3. Adenocarcinoma (Invasive)
    4. Metastatic
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7
Q

***HPV-related Neoplasia + Warts in lower genital tract

A

Warts:

  1. **Condyloma acuminata (anogenital wart)
    - **    papillomatous lesions: covered by ***Stratified squamous epithelium
  2. Condyloma planum (flat)

Histology:
- ***Koilocytes (enlarged nucleus, perinuclear halo, thickened cytoplasmic border)

Neoplasia:

Preinvasive precursors:

  1. Squamous Intraepithelial Lesion (SIL) / Vulvar/Vaginal Intraepithelial Neoplasia (VIN/VAIN)
    - Low / High grade SIL

Invasive cancers:

  1. Invasive SCC
    - Basaloid / Warty SCC from Classific VIN
    - Keratinising SCC from Differentiated VIN
    - extend locally / lymphatic spread —> inguinal —> pelvic LN
    - associated with second malignancy (usually cervical: SIL / Invasive)
  2. Adenocarcinoma
    - Vagina: secondary tumour more common
    - Primary adenocarcinoma in young girls —> associated with Vaginal adenosis, Intrauterine DES (diethylstilboestrol) exposure
    - Vulva: Extramammary Paget’s disease (in-situ adenocarcinoma)
    - Cervix
  3. Others (including metastasis)
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8
Q

Cervical Cancer incidence and Mortality rate

A
  • ↓ in HK
  • 7th commonest cancer in HK female
  • incidence ↑ with age, peak at 40-50 yo
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9
Q

Cervix: Carcinoma

A
  1. ***SCC (most common)

Gross:

  • Early lesions: Focal induration, Shallow ulceration, Slight granularity
  • Advanced lesion: Exophytic / Endophytic (infiltrating into stroma without obvious lesion)

Histology (SCC):
- Keratinising / Non-keratinising

Spread:
- Local:
—> Contiguous pelvic structures
—> Ureteric involvement —> cause obstruction and subsequent renal failure
- Regional / Distant LN
  1. **Adenocarcinoma
    - from **    Endocervical epithelium (Simple columnar: vs Ectocervix: Stratified squamous)
    —> May have Intra-epithelial phase, Glandular dysplasia, Adenocarcinoma-in-situ
    - ***HPV-associated: Abundant intracytoplasmic mucin, Apoptotic bodies, Diffusely positive with p16

HPV status of cervical cancers characterised by:
1. **HPV molecular testing —> detection + genotyping of HPV
2. Surrogate marker **p16 immunohistochemistry
—> more accurate evaluation of impact of HPV testing, HPV vaccination in cervical cancer prevention
—> new classification:
- SCC/Adenocarcinoma, HPV-associated
- SCC/Adenocarcinoma, HPV-independent
- SCC/Adenocarcinoma, Not otherwise specified

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10
Q

Etiology of Cervical carcinoma

A

Risk factors:

  • ***HPV (carcinogen) —> ~99% association
  • Oncogenes
  • early marriage and pregnancy
  • increased parity
  • sexual promiscuity
  • STD
  • smoking
  • low socioeconomic status
  • immunocompromised state
  • Interaction between **HPV oncogenes and host **Tumour suppressor genes (e.g. p53, retinoblastoma gene) is involved
  • Relationship between men with penile warts and presence of SIL in their partners
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11
Q

HPV genotypes

A
  • > 100 types
  • ~30-40 Anogenital

Low risk HPV:
- ***HPV6, 11
- Non-oncogenic
—> lead to Anogenital warts (Condyloma acuminata / planum) + LSIL

High risk HPV:
- ***HPV16 (50% cervical cancer), 18 (20% cervical cancer)
- ~15-20 Oncogenic
—> lead to High grade SIL, SCC, Adenocarcinoma

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12
Q

HPV infection

A
  • Common (nearly all sexually active men / women)
  • Only a portion infected will progress to cancer
  • HPV infection ***necessary but not sufficient factor for Cervical cancer
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13
Q

Prevention of Cervical cancer

A

One of most preventable cancers

Primary prevention (Prevent development of cancer)

  1. ***HPV vaccination
  2. Avoid risk factors

Secondary prevention

  1. ***Cervical Exfoliative cytology —> then Colposcopy and Biopsy
  2. ***HPV test screening
  • Detect pre-invasive lesion (i.e. SIL)
    —> ***treatment of SIL
    —> prevent further progression to invasive cancer
  • Detect early invasive cancer
    —> slow progression
    —> ***reduce complications, improve clinical outcomes

N.B.:

  • HPV vaccines will affect preventive strategy for cervical cancer
  • ***Screening should be continued as Vaccines will not protect against HPV types not covered in vaccines
  • Implementation of HPV vaccination in young women will not impact older groups initially
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14
Q

Detection of cervical cancer

A
  1. ***Exofoliative cytology of cervical squamous epithelial cells (塗片檢查)
    - “Pap smear”
    - convenient, inexpensive
    - scrape squamo-columnar junction
    - taken from Transformation zone —> between Endocervix (Glandular) and Ectocervix (Stratified squamous)
    - Screening
    —> if have HSIL in cytology —> referred for Colposcopy / Biopsy
  2. **Colposcopy and **Biopsy (Cone/Lip biopsy to excise Transformation zone)
    - by Gynaecologist
    - Observe changes in surface epithelium, vascular pattern
    - Directed biopsies
    - Assess ***extent of disease
    - Diagnosis
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15
Q

Success of cervical cytology screening

A

Screening index ↑ —> Incidence ↓

Reasons:
1. Cervix ***easily accessible to cytological sampling (vs other inaccessible organs e.g. ovaries)

  1. ***Long period of progression from precursor lesion to invasive cancer
    - from LSIL (CIN1) to HSIL (CIN2, 3) (progressive dysplasia) (CIN3: carcinoma-in-situ in old days) (absence of stromal invasion / dissemination)
    —> take many years
  2. ***Cost effective cytology test
  3. ***Early treatment is effective
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16
Q

Natural history of SIL

A

Stationary / Regress / Progress to invasive SCC (within 2-10 years)

LSIL: **60% regress, 30% persist, 10% progress
HSIL: 30% regress, **60% persist, 10% progress

17
Q

HPV vaccination

A
  1. ***Prophylactic vaccines (prevent HPV (re)infection, but cannot cure/remove HPV-infected individuals)
  • **Bivalent / Tetravalent vaccines:
  • protect against HPV 16, 18 (i.e. 70% of CA cervix)
  • **9-valent (Nonavalent) HPV vaccines:
  • Oncogenic: 16, 18, 31, 33, 45, 52, 58 (90% CA cervix)
  • Non-oncogenic but cause most Condyloma: 6, 11 (***包埋Condyloma HPV)
  1. Therapeutic vaccines (in clinical trials)
18
Q

Uterine Corpus pathologies

A

Endometrium:

  1. Inflammation
    - Acute / Chronic (plasma cell infiltrate)
    - related to abortion, parturition, retained products of gestation, pelvic inflammatory disease, IUD users, TB
  2. Endometrial polyp
    - local overgrowth of endometrium —> may cause abnormal bleeding
    - rare malignant change
  3. ***Endometrial hyperplasia
    - see next
  4. ***Endometrial carcinoma
    - see next
  5. Tumour of endometrial stroma
    - tumours with pure endometrial stromal features (e.g. Stromal Sarcoma)
    - tumours with a combination of stromal (sarcoma) + epithelial (carcinoma) elements (e.g. Mixed Mullerian tumours)
  6. Gestational Trophoblastic Disease (GTD)
    - heterogeneous group of diseases arising from Trophoblasts
    - complete / partial hydatidiform mole, invasive mole, choriocarcinoma, placental site trophoblastic tumour (PSTT), epitheloid trophoblastic tumour (ETT)
    - Choriocarcinoma, PSTT, ETT are frank malignant tumours
    - Hydatidiform mole may just be abnormal placentas prone to malignant transformation

Myometrium:

  1. Adenomyosis
  2. Leiomyoma (common)
  3. Sarcoma (rare) (e.g. Leiomyosarcoma)
19
Q

Endometrial hyperplasia

A

Diffusely / Focally involved

Associated with ***↑ Estrogen

  • ***endogenous Estrogen: Ovarian cyst / tumour (functioning Theca cell, Granulosa cell tumour), Repeated anovulatory cycles
  • ***exogenous Estrogen: Tamoxifen (for breast cancer, estrogenic at endometrium)

Risk factors: obesity, diabetes, hypertension, infertility

2 types:

  1. Hyperplasia without atypia (low risk of progression to carcinoma)
  2. ***Atypical hyperplasia (considered as carcinoma precursor)
    - cytological atypia present
    - risk of progressing to carcinoma
20
Q

Endometrial Cancer incidence and Mortality rate

A

↑ significantly in HK (esp. in Type 1 cancer category)

21
Q

Endometrial cancer

A

2 types:
1. **Endometrioid (Type I) (90%)
- look like normal endometrium
- indolent
- Localised polypoid masses / Diffusely involve endometrial surface
- arise from **Atypical hyperplasia
—> often **Estrogen dependent (Associated with ↑ Estrogen: endogenous/exogenous)
- Risk factors: Tamoxifen, **Obesity, diabetes, hypertension, infertility
- Genetic: ***HNPCC syndrome (involve DNA repair genes) (prone to Endometrial cancer as well on top of Colorectal cancer)
- Spread:
—> Local: myometrium, parametrium, Fallopian tubes, ovaries, vagina, pelvis
—> LN: Para-aortic LN involvement (early)

  1. Special variants (Type II)
    - Clear cell
    - Serous
    —> Estrogen-independent
    —> Aggressive tumour with poor prognosis
22
Q

Polycystic Ovaries and Endometrial cancer

A

Polycystic ovaries (Follicular cysts)
—> **Many Granulosa cells produce Estrogen
—> **High Estrogen
—> stimulate ***proliferation of endometrium
—> cancer development

23
Q

Myometrium pathologies

A
  1. **Adenomyosis
    - Nests of **    Endometrium (gland + stroma) embedded in Myometrium
    —> these nests no communication with uterine cavity
    —> **blood accumulation
    —> painful symptoms, palpable mass
    - Uterus enlarged with faintly whorled look on cut surface
    - Small **    blood-containing cysts spaces may be present
    - Menorrhagia / Dysmenorrhea present

Smooth muscle tumours

  1. Leiomyoma (benign, common)
    - one of most common tumours
    - multiple
    - subserosal / submucosal / intramural sites
    - **effect on fertility / pregnancy
    - ↑ in size during pregnancy, ↓ after menopause
    - well-circumscribed spherical nodules + white whorled appearance
    - **    bundles of smooth muscle + some fibrous tissue
  2. Leiomyosarcoma (malignant, rare)
    - less well-demarcated
    - necrosis + haemorrhage
    - ↑ cellularity, cytological atypia, mitotic figures
24
Q

Fallopian tube patholgies

A
  1. Salpingitis (Inflammation)
    - impair fertility
    - predispose to ectopic pregnancy
    - Acute (ascending infection via uterine cavity) / Chronic / Granulomatous (TB Salpingitis due to haematogenous spread)
  2. Ectopic pregnancy
    - surgical emergency (rupture of tubal pregnancy —> bleeding)
    - at Ampulla (most common)
    - Chorionic villi of placenta, Trophoblast (Cytotrophoblast + Syncytiotrophoblast) proliferation seen in Fallopian tube —> permeate tubal wall
  3. Endometriosis
    - abnormal foci of endometrial glands, stroma in tubes (not supposed to be there)
  4. Carcinoma (cause of cancer spreading to ovary / peritoneum)
    - Primary carcinoma rare
    —> Must exclude Metastasis from genital / extragenital sites
    - often diagnosis made only at Laporatomy
    - usually Papillary Adenocarcinoma
25
Q

Ovary pathologies

A
  1. Inflammation
  2. ***Non-neoplastic cysts
    - commonest cause of ovarian enlargement
    - often asymptomatic
    - torsion may occur —> haemorrhagic infarction + pain
    - rupture —> hemoperitoneum
    - abnormal production of Estrogen / Gonadotropic hormones —> hormonal effects
  • Germinal inclusion cysts, Follicular cysts, Corpus luteum cysts, Theca lutein cysts
    —> lined by Simple epithelium / Granulosa cells / Theca cells
    —> without / without Luteinisation

Example:

  • **Ovarian endometriotic cyst (lined by endometrial gland, stroma —> able to respond to hormone and proliferate —> shedding —> bleeding —> collection of altered blood in cyst: **“Chocolate cyst”)
  • **Follicular cyst (lined by Granulosa cells —> can **produce Estrogen —> Endometrial cancer)
  1. Endometriosis
  2. Ovarian neoplasia
    - **Epithelial tumours (Coelomic epithelium) (60% overall, 80% primary malignancy)
    - **    Germ cell tumours
    - Sex cord-Stromal tumours
    - Miscellaneous e.g. Lymphoma, Tumours of mesenchymal origin (affect other parts of body)
    - Metastatic tumours
26
Q

Epithelial tumours of Ovaries

A

60% overall, 80% primary ovarian malignancy

Young patients:

  • mostly Benign / Borderline tumours
  • invasive tumours less common <40 yo

Clinical presentation:

  • Pelvic mass S/S
  • Early detection by screening is difficult

Staging:
- depends on presence of capsular / contralateral ovary involvement, malignant ascites, nodal, pelvic, intraperitoneal / distant metastasis

2 Broad groups:

  1. ***Type I carcinoma (Mucinous, Endometrioid, Clear cell, Low grade Serous)
    - Develop from benign / borderline tumour
  2. **Type II carcinoma (High grade Serous)
    - Arise De novo, may develop from tubal fimbrial epithelium
    - harbours **    p53 mutations
    - more associated with ***BRCA mutations
Classification:
Type of malignancy:
1. Benign
2. Borderline
3. Malignant
  • **Histological:
    1. Mucinous (~Endocervix: glandular epithelium)
  • ~ Endocervical glandular epithelium
  • associated with Pseudomyxoma peritoneii +/- Co-existing Appendiceal lesion
  • see next
  1. Serous (~Tube)
    - ~ Fallopian tube +/- Psammoma bodies (calcified spherules)
    - Bilateral +/- Peritoneal lesions
    - Low / High grade
    - see next
  2. Endometrioid (~Corpus)
    - ~ Endometrium
    - +/- Co-existing Endometriosis / Concurrent Endometrioid carcinoma of endometrium
  3. Brenner (~Urinary tract)
    - Benign form (commonest): round masses of ***Transitional epithelium surrounded by Ovarian stroma
  4. Clear cell
    - in form of Clear cell carcinoma
    - Poorer prognosis
  5. Seromucinous
  6. Undifferentiated
27
Q

Ovarian cancer risk factors

A

Genetic predisposition:

  1. Breast and Ovarian cancer syndrome (***BRCA1/2 mutation: tumour suppressor genes)
  2. ***HNPCC syndrome (DNA repair genes) (lower risk)

Environmental:
Obesity (less strong association than Endometrial cancer)

28
Q

Borderline tumour

A

Distinct entity, Good prognosis

Different from benign tumour:

  • Presence of epithelial budding
  • Increased mitotic activity
  • Nuclear stratification and Atypia

Different from malignant tumour:
- Absence of destructive stromal invasion

29
Q

Serous Epithelial tumours of Ovaries

A

Classification:
1. Benign
- Serous cystadenoma / adenofibroma / surface papilloma
—> Fallopian Tube-like

  1. Borderline
    - Serous borderline tumour
  2. Malignant
    - Low-grade serous carcinoma
    —> **Low proliferation (MIB1)
    —> **    Wild type p53
    —> Do not respond well to platinum-based chemo
- High-grade serous carcinoma
—> ***High proliferation (MIB1)
—> ***p53 mutation often exists
—> ***Associated with BRCA loss
—> Usually respond well to platinum-based chemo (recurrence may occur)
30
Q

Mucinous Epithelial tumours of Ovaries

A

Benign / Borderline / Malignant

Associate with Pseudomyxoma Peritonei:

  • Difficult to treat
  • Peritoneal cavity filled with abundant mucin (histology show mucinous epithelium)
31
Q

Germ cell tumour of Ovaries

A

2nd largest group of Ovarian neoplasms behind Epithelial neoplasms

  • **Heterogenous group of tumours (combinations may occur in a patient):
    1. ***Teratoma (Mature, Immature, Malignant transformation)
  • see next
  1. Dysgerminoma
    - ~ Seminoma
    - young women
  2. Embryonal carcinoma
    - usually combined with other germ cell tumours
  3. Choriocarcinoma
    - usually combined with other germ cell tumours
  4. Yolk sac tumour / Endodermal sinus tumour
    - young female
  5. Mixed

Children, Adolescents: >60% of Ovarian neoplasms, 1/3 Malignant
Adults: mostly Benign: ***Mature cystic Teratoma (most common germ cell tumour)

Germ cell (Oogonia —> Dysgeminoma)
—> Totipotent cell
—> (Embryonal carcinoma: transition state between primitive / differentiated tumour)
—> Extra-embryonic tissue
1. Trophoblast (placenta) (Choriocarcinoma)
2. Yolk sac / Endodermal sinus (Yolk sac tumour / Endodermal sinus tumour)
OR
—> Embryonic tissue (i.e. Ectoderm, Mesoderm, Endoderm) (***Teratoma —> major difference in Male / Female)

32
Q

Teratoma of Ovary

A

Vs Teratoma of Testes

  • Similar morphologically
  • Different clinically from Teratoma of Testes

Male Teratoma: Malignant
Female Teratoma: ***Mature Cystic Teratoma —> Benign

  1. Mature Cystic Teratoma (most common germ cell tumour)
    - still need to be treated ∵ complications e.g. torsion, rupture, malignant change (2%, usually SCC)
  2. Immature Teratoma
  3. Teratoma with malignant transformation e.g. SCC
33
Q

Sex cord-Stromal tumour

A

Sex cord:

  • Sertoli cells (Seminiferous tubules)
  • Granulosa cells (Graafian follicles)

Stroma:

  • Leydig cells
  • Theca cells
  1. **Granulosa cell tumour
    - Low grade
    - Indolent
    - all ages, most commonly after menopause
    - Solid / Cystic tumour with Granulosa cells forming follicles / trabeculae
    —> Grooved nuclei “coffee-bean appearance”
    —> can produce **    excessive Estrogen
    —> Children: Precocious puberty, Adult: Endometrial hyperplasia / adenocarcinoma
  2. Thecoma-Fibroma
    - Benign
    - from Ovarian stromal cells
    - Spindle cells ~ Fibroblasts / Polygonal cells ~ Theca cells
  3. Ovarian Sertoli Leydig cell tumour
    - Malignant
    - ***Androgen secreting
    —> Virilisation, Breast atrophy, Hirsutism, Amenorrhea, Receding hairline

These tumours can be found in BOTH testes / ovaries

34
Q

Metastatic tumour of Ovaries

A

Most commonly from Breast, Lower genital tract, GI tract

Extra-genital sites
- colon
- stomach
—> Krukenberg tumour: metastatic adenocarcinoma from stomach, Mucin-filled Signet ring cells
- breast
- lung
- etc.

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