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Year 5 Histopathology > 6s: Gynaecological Pathology > Flashcards

6s: Gynaecological Pathology Flashcards

1
Q

2 congenital abnormalities

A

Duplications (i.e. uterus didelphys)

Agenesis

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2
Q

Infections that can cause discomfort with NO serious complications (4)

A

Candida = more common in diabetes, OCP, pregnancy

Trichomonas vaginalis = protozoan

Garenerella = Gram -ve bacillus → vaginitis

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3
Q

Infections that cause SERIOUS complications

A

Chlamydia = major cause of infertility

Gonorrhoea = major cause of infertility

Mycoplasma = spontaneous abortion and chorioamnionitis

HPV = implicated in cancer

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4
Q

PID usual causes and other causes and complications

A

Chlamydia > gonococci, enteric bacteria

  • usually starts at lower genital tract and spreads upwards via the mucosal surface

Other causes = staph/strep, coliform bacterium, clostridium perfringens

  • tend to occur 2o to abortion
  • usually starts in uterus and spreads via lymphatics and blood vessels
  • involves deep tissue layers

Complications

  • peritonitis
  • bacteraemia
  • intestinal obstructions due to adhesions
  • infertility
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5
Q

PID usual causes and other causes and complications

A

Chlamydia > gonococci, enteric bacteria

  • usually starts at lower genital tract and spreads upwards via the mucosal surface

Other causes = staph/strep, coliform bacterium, clostridium perfringens

  • tend to occur 2o to abortion
  • usually starts in uterus and spreads via lymphatics and blood vessels
  • involves deep tissue layers

Complications

  • peritonitis
  • bacteraemia
  • intestinal obstructions due to adhesions
  • infertility
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6
Q

Salpingitis: from where, complications

A

Usually direct ascent from the vagina

Depending on severity and tx, it may result in → resolution or complications:

  • plical fusion
  • adhesions to ovary
  • tube-ovarian abscess
  • peritonitis
  • hydrosalpinx (fallopian filled with fluid)
  • infertility
  • ectopic pregnancy
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7
Q

Ectopic pregnancy

A
  • Normal = ovum fertilised in fallopian tube → moves down fallopian tube → implant in the endometrial lining
  • The ampulla of the fallopian tube is the most common site of ectopic pregnancy
  • Inflammation and formation of obstructions → increase risk of developing an ectopic
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8
Q

Cervical cancer epidemiology and RFs

A

Epidemiology:

  • 2nd most common cancer affecting women
  • Mean age: 45-50 years

Risk factors:

  • Major = HPV (95%)
  • Minor = many sexual partners, sexually active early, smoking, immunosuppression (i.e. HIV)
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9
Q

HPV family: high risk cancer types, low risk quart types

A

High-risk cancer types

  • MOST COMMON = 16 and 18 (others = 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 82)
  • Can cause low- and high-grade cervical abnormalities

Low-risk wart types

  • MOST COMMON = 6 and 11 (other types: 40, 42, 43, 44, 54, 61, 72, 73, 81)
  • Can cause genital and oral warts
  • Low grade cervical abnormalities
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10
Q

Pathogenesis of cervical cancer

A

Most people = nothing (as immune system eliminates HPV  undetectable within 2 years in 90% of cases)

HPV 16, 18 → encode proteins E6 and E7 which bind to and inactivate TSGs:

  • E6 → p53
  • E7 → retinoblastoma
  • Interferes with apoptosis and increased cellular proliferation which contributes to oncogenesis
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11
Q

Latent vs productive HPV infection

A

Latent = HPV resides in cell and only replicates when the cell divides

  • Complete viral particles not produced
  • Cellular changes of HPV not seen

Productive = HPV replicates independently of cell cycle

  • Cellular changes of HPV are seen
  • Halo around the nucleus (koilocyte)
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12
Q

Cervical cancer transformation zone (vulnerable to dyskaryosib)

A
  • Squamocolumnar junction → see picture
  • CIN = mitotic figures at every level (cells look atypical and pleiomorphic)
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13
Q

Disease progression of cervical cancer

A
  • 1 = lower ⅓
  • 2 = lower ⅔
  • 3 = entire epithelium

CIN = dysplasia (pre-malignant changes) in the cervical epithelium

  • invasion through BM = CIN → invasive SCC
  • CIN = dysplastic changes → invasive SCC (80%, most common)
  • CGIN = dysplastic changes → invasive adenocarcinoma
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14
Q

Cervical cancer prognosis

A
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15
Q

Cervical screening system

A
  • Part of the squamocolumnar junction is scraped and sent to the pathologists for cytological analysis

Screening Intervals

  • First invitation: 25 years
  • 25-49 = 3-yearly
  • 50-62 = 5-yearly
  • 65+ = only screen those not screened since they were 50 or have recent abnormal tests

Screening approaches:

Cervical cytology (used less now)

  • 50-95% sensitivity
  • 90% specificity

Hybrid Capture II (HC2) HPV DNA Test (molecular genetics are used more)

  • This has been included in the screening programme at many centres
  • Smear is taken and put in fluid that contains RNA probes that match 5 low-risk HPV types and 13 high-risk types → identify HPV strains present and whether they are low or high risk
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16
Q

HPV vaccine: TWO available and to who

A

TWO vaccines available

  • Bivalent (16 + 18)
  • Quadrivalent (6, 11, 16, 18)

The vaccine offers no reduction in disease in women who are already infected

National vaccination programme for girls aged 12 + boys aged 13

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17
Q

Structure of uterine body

A

Structure:

  • Endometrium
    • Glands
    • Stroma
  • Myometrium
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18
Q

Leiomyoma (fibroids) and leiomyosarcoma

A
  • Smooth muscle tumour of the myometrium
    • MOST COMMON (20% of >35yo) uterine tumour
    • Usually multiple
    • May be intramural, submucosal or subserosal
  • Malignant counterpart: leiomyosarcoma
    • RARE and usually solitary
    • Usually post-menopausal women
    • 5-year survival of 20-30%
    • Local invasion and spread via the blood stream
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19
Q

Endometrial hyperplasia: causes

A

There is an increase in stroma and glands (usually driven by oestrogen)

Causes – driven by persistent oestrogen…

  • Peri-menopausal
  • Persistent anovulation (because of persistently raised oestrogen levels)
  • PCOS can also cause persistently elevated levels of oestrogen giving rise to endometrial hyperplasia
  • Granuloma cell tumours of the ovary
  • Oestrogen therapy
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20
Q

Endometrial carcinoma RFs

A
  • MOST COMMON gynaecological malignancy in developed countries
  • Risk factors = OESTROGEN
    • Nulliparity
    • Obesity
    • Early menarche
    • Diabetes mellitus
    • Tamoxifen
    • HRT
    • Late menopause

smoking and COCP are protective

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21
Q

2 types of endometrial carcinoma and their subtypes

A

Type I (85%)

SUBTYPES: endometriosis, mutinous, secretory adenocarcinoma

Younger patients

  • estrogen-dependent
  • associated with atypical EH
  • low-grade tumours that are superficially invasive

Genetic mutations = need accumulation ≥4 different mutations

  • PTEN, PI3KCA, K-Ras, CTNNB1, FGFR2, P53
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22
Q

2 types of endometrial carcinoma and their subtypes: type 1

A

Type I (85%)

SUBTYPES: endometriosis, mutinous, secretory adenocarcinoma

Younger patients

  • estrogen-dependent
  • associated with atypical EH
  • low-grade tumours that are superficially invasive

Genetic mutations = need accumulation ≥4 different mutations

  • PTEN, PI3KCA, K-Ras, CTNNB1, FGFR2, P53
23
Q

2 types of endometrial carcinoma and their subtypes: type 2

A

Type 2: 15%

SUBTYPES: serous, clear cell

Older patients

  • less oestrogen-dependent
  • arise in atrophic endometrium
  • high grade, deeper invasion, higher stage

Genetic mutations

  • Serous = p53, PI3KCA, Her2 amplification
  • Clear Cell = PTEN, CTNNB1, Her2 amplification
  • important for tx choices (e.g. using anti-EGFR)
24
Q

Prognositc factors for endometrial carcinoma

staging and grading

A
  • Type, grade, stage
  • Tumour ploidy (number of chromosomes) – diploid cells have a better prognosis
  • Hormone receptor expression (related to survival and response to treatment)

Grading 1 to 3 depends on

  • pattern = glands vs solid areas
  • degree of cytological aplasia

FIGO staging

  • 1 = limited to uterus
  • 2 = limited to cervix
  • 3 = spread adjacent
  • 4 = distant spread
25
Q

What is another type of endometrial cancer?

A

endometrial stromal sarcoma

26
Q

What is GTD and it’s types

A

Gestational Trophoblastic Disease – a spectrum of tumours characterised by proliferation of trophoblastic tissue

  • Types:
    • Complete (2.5% = malignancy; 10% = invasive moles) and partial (0% = malignancy) mole
    • Invasive mole
    • Choriocarcinoma
27
Q

Presentation of complete and partial moles

A
  • Prevalence: 1 in 1000 pregnancies
  • Presentation:
    • Spontaneous abortion
    • USS – snowstorm, cluster of grapes
    • Very high hCG
    • Complete moles may persist or recur
    • Chromosomal abnormalities are important
28
Q

Complete vs partial mole

A

Complete = empty egg fertilised by 2 sperm (or 1 which duplicates DNA)

  • 46 XY or 46 XX (paternal origin only)

Partial = normal egg fertilised by 2 sperm (or 1 which duplicates DNA)

  • 69 XXX or 69 XXY (1x maternal and 2x paternal origin)
29
Q

what is choriocarcinoma

A

Incidence: 1 in 20,000-30,000 pregnancies

  • Rapidly invasive, widely metastasising (lung, vagina, brain, liver, kidney)
  • Responds well to chemotherapy
  • 50% arise in moles
  • 25% arise in previous abortion
  • 22% arise in normal pregnancy
30
Q

Endometriosis pathogenesis

A

Endometriosis – presence of endometrial tissue outside the uterus

COMMON - 10% of premenopausal women

Pathogenesis

  • Metaplasia of pelvic peritoneum → implantation of endometrial tissue
  • Another theory suggests that it occurs due to retrograde menstruation (endometrial lining goes up the fallopian tubes and into the peritoneal cavity instead of out of the vagina) which then leads to implantation of this endometrial tissue at a site outside the uterus
31
Q

Endometriosis complications and associations

A

Ectopic endometrial tissue is functional and bleeds at the time of menstruation → pain, scarring and infertility

Associations:

  • Strongly → clear cell (mesonephroid/epithelial) ovarian cancer
  • Less strongly → endometroid (epithelial) ovarian cancer
32
Q

Non-neoplastic functional ovarian cyst

A
  • Follicular and luteal cysts
  • Endometriotic cyst
33
Q

PCOS

A
  • 3-6% of women of reproductive age
  • Patients have persistent anovulation
  • Other features include obesity and hirsutism/virilism
34
Q

RFs for ovarian cancer

A
  • Nulliparity
  • Early menarche
  • Late menopause
  • Genetic predisposition (1%)
  • Infertility
  • Endometriosis
  • HRT
  • Inflammation (PID)
  • FHx ovarian/breast cancer
35
Q

Protective factors for ovarian tumours

A
  • Pregnancy
  • OCP
36
Q

Types of ovarian cancers (4)

A

Benign tumours

  • serous cystadenomas
  • mutinous cyst adenomas
  • cystadenofibromas
  • Brenner tumour

Epithelial = serous, mucinous, endometriosis, clear cell, transitional, mixed types

  • 70% of all ovarian tumours
  • 95% of all malignant tumours

Germ cell tumours = dysgerminoma, choriocarcinoma, teratoma, endodermal sinus tumours

  • age 15-21 AND 65-69 (bimodal peaks)

Sex cord tumours = granuloma cell tumour, fibroma, theca, sertoli-leydig cell

  • most common in PMB women
  • some subtypes in 25-30 year olds
37
Q

What is the most common benign growth in <30 years old

A

TERATOMA (a germ cell tumour)

38
Q

2 types fo epithelial tumour classification

A

Type 1 ovarian carcinoma → LOW-GRADE:

“Less Exciting, More Cancers”

  • Low-grade serous
  • Endometroid
  • Mucinous
  • Clear cell

Low-grade, arise from benign ovarian tumours and endometriosis

Present as large, stage 1 tumours

Mutations: K-Ras, BRAF, PI3KCA, Her2, PTEN, beta-catenin

Type 2 ovarian carcinoma → HIGH GRADE, aggressive

High-grade serous carcinomas

NO precursor lesions

Mutations: p53 (75% of cases), K-Ras, BRAF

39
Q

Epithelial = serous tumours

A

MOST COMMON type, usually cystic, 30-50% bilateral

benign = lined by bland epithelium

borderline = more complex, atypical epithelial lining with papillae

malignant = invasive with poor prognosis

psammoma

40
Q

Epithelial = mucinous

A

10-20% ovarian tumours

secrete mucin (epithelium resemble GI or endocervical epithelium)

41
Q

Epithelial = endometrioid tumours

A
  • 10-24% of ovarian tumours
  • Associations:
    • Endometriosis (10-20% associated with endometriosis)
    • Endometrioid carcinoma co-existence in uterus
  • Better prognosis than mucinous and serous
42
Q

Epithelial = clear cell carcinoma

A

Strong association with endometriosis

Called ‘clear cell’ because their cytoplasm is clear due to the presence of a lot of glycogen

  • Glycogen dissolves when the sample is processed for microscopy leaving an empty space)
43
Q

4 types of sex cord stroll tumours

A

Fibromas (arising from fibroblasts):

  • Benign
  • No endocrine production

Granulosa cell tumour:

  • Variable behaviour
  • May produce oestrogen

Thecoma (arising from thecal cells):

  • Benign
  • May secrete oestrogen (rarely secretes androgens)

Sertoli-Leydig Cell Tumour

  • Variable behaviour
  • May be androgenic
44
Q

Germ cell tumours: epidemiology and 4 types

A
  • 20% of ovarian tumours; 95% are BENIGN
  • Predominantly occur in <20 years
  • Germ cell tumours are classified on how they differentiate

dysgerminoma, teratoma, choriocarcinoma, endodermal sinus tumour

45
Q

Dysgerminoma

A

no differentiation

46
Q

three types of teratoma

A

Mature Teratoma (most common type of germ cell tumour)

  • Benign; solid or cystic
  • Tissues all MATURE to adult-type tissues (teeth and hair are very common)

Immature Teratoma

  • Indicates presence of embryonic elements (most commonly neural tissue)
  • This is a MALIGNANT tumour that grows rapidly, penetrates the capsule and forms adhesions
    • Spreads within the peritoneal cavity
    • Metastasises to the lymph nodes, lungs, liver and other organs

Mature Cystic Teratoma with Malignant Transformation:

  • Rare; most frequently SCC
  • Any type of the mature tissue within the teratoma can become malignant → so, it can give rise to carcinoid, thyroid cancer, BCC, melanoma etc.
47
Q

Choriocarcinoma is from

A

trophoblastic cells (form placenta) → choriocarcinoma

48
Q

Endodermal sinus tumour is from

A

extraembryonic tissues (e.g. amniotic sac) → endodermal sinus tumours

49
Q

Other germ cell tumours

A

yolk sac tumour

choriocarcinoma

embryonal carcinoma

50
Q

Name 2 secondary ovarian tumours

A

Krukenberg Tumour:

  • Bilateral metastases composed of mucin-producing signet ring cells
  • Most often from gastric or breast cancer

Metastatic Colorectal Carcinoma

  • Ovaries are prone to metastatic spread of colorectal cancer
51
Q

three familial syndromes of ovarian cancer (10`% of ovarian cancers are familial)

A
  • Familial breast-ovarian cancer syndrome BRCA1 association
  • Site-specific ovarian cancer BRCA1 association
  • Cancer family syndrome (Lynch type II)
52
Q

specific associations of susceptibility genes and ovarian tumours

A
53
Q

3 conditions of the vulva

A

Lichen sclerosus (thinning epithelium with a layer of hyalinisation underneath)

  • This is sometimes associated with epithelial dysplasia and development of malignancy

Papillary Hidradenoma (benign tumour)

Malignant Tumours:

  • Squamous cell carcinoma (85%) – risk factors…
    • HPV or lichen sclerosus
    • VIN (vulval intraepithelial neoplasia)
  • Invasive adenocarcinoma or adenocarcinoma in situ (Paget’s disease)
  • Malignant melanoma
  • BCC
54
Q

Vagina pathology

A
  • Congenital anomalies (e.g. absence or atresia)
  • Tumours (RARE; 1%)
  • Carcinoma (squamous cell carcinoma)
  • Adenocarcinoma
    • Children of women with threatened abortion treated with diethyl stilbosterol → risk of clear cell carcinoma
  • Rhabdomyosarcoma

Year 5 Histopathology (10 decks)

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