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Histopathology > Gyanaeocological Pathology > Flashcards

Gyanaeocological Pathology Flashcards

1
Q

What makes up the gynaecological tract

A
  • Vulva
  • Vagina
  • Cervix
  • Uterine body
  • Fallopian tube
  • Ovaries
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2
Q

What are the gynaecological congenital anomalies?

A
  • Duplication
  • Agenesis
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3
Q

What is inflammation of •Vulva

  • Vagina
  • Cervix
  • Uterine body
  • Fallopian tube
  • Ovaries

Called?

A
  • Vulva: vulvitis
  • Vagina: vaginitis
  • Cervix: cervicitis
  • Endometrium: endometritis
  • Fallopian tube: salpingitis
  • Ovary: oopheritis
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4
Q

What do infections of the female genital tract cause?

A
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5
Q

What organisms caused pelvic inflammatory disease?

A
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6
Q

What are the complications of PID?

A
  • Peritonitis
  • Bacteraemia
  • Intestinal obstruction due to adhesions
  • Infertility
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7
Q

What are the sequence of events of salpingitis?

A
  • Usually direct ascent from the vagina
  • Depending on severity and treatment may result in:

–Resolution

–Complications:

  • Plical fusion
  • Adhesions to ovary
  • Tubo-ovarian abscess
  • Peritonitis
  • Hydrosalpinx
  • Infertility
  • Ectopic pregnancy
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8
Q

What is an ectopic pregnancy? What increases the risk?

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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9
Q

What are the diseases of the cervix?

A
  • Inflammation
  • Polyps
  • Dysplasia and and carcinoma
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10
Q

Describe the epidemiology of cervical cancer?

A
  • 2nd most common cancer affecting women
  • Mean age: 45-50 years
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11
Q

What are the risk factor of cervical cancer?

A
  • Major = HPV (95%)
  • Minor = many sexual partners, sexually active early, smoking, immunosuppression (i.e. HIV)
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12
Q

What are the low risk HPVs?

A
  • 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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13
Q

What are the high risk HPVs?

A
  • 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
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14
Q
A
  • Transformation zone (vulnerable to dyskaryosis)
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15
Q
A

High grade dysplasia

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16
Q

How do we measure degrease progression in cervical cancer?

A
  • CIN = mitotic figures at every level (cells look atypical and pleiomorphic)
  • Disease progression:
    • Classification:
    • 1 = lower 1/3
    • 2 = lower 2/3
    • 3 = entire epithelium
    • CIN = dysplasia (pre-malignant changes) in the cervical epithelium

•Basal membrane immediately deep to the surface epithelium is intact

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17
Q

What is CGIN?

A

•Squamous epithelium is involved more often than glandular epithelium (CGIN)

  • CIN = dysplastic changes → invasive SCC [80%; most common]
  • CGIN = dysplastic changes → invasive adenocarcinoma [20%]
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18
Q

What changes CIN to invasive carcinoma?

A

•Invasion through the basement membrane defines change from CIN to invasive carcinoma

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19
Q

What are the types of cervical cancer?

A
  • Two types of cervical cancer
  • Squamous cell carcinoma
  • Adenocarcinoma (20% of all invasive cases)
  • HPV dependent or independent
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20
Q
A
  • Left: SCC
  • Right: Adenocarcinoma
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21
Q

What determines the prognosis of cervical cancer?

A
  • Tumour type
  • Tumour grade
  • Tumour staging: FIGO Stage 1 (90%) to 4 (10% 5-year survival)
  • Lymphovascular space invasion
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22
Q

What are the 2 types of HPV infection?

A
  • Infection is either latent or productive:
    • 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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23
Q

What happens when one is infected with HPV?

A

For most people, nothing will happen

  • The body’s immune system eliminates HPV
  • HPV becomes undetectable within 2 yrs in ~90%
  • Relatively few will develop symptoms

Persistent infection with high-risk HPV types is associated with pre-cancerous and cancerous cervical changes

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24
Q

How does HPV transform cells?

A
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25
Q

What is the cervical screening programme?

A
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26
Q

How is the cervical sample taken?

A
  • Part of the squamocolumnar junction is scraped and sent to the pathologists for cytological analysis
  • 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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27
Q

What is HC2 HPV DNA Tests?

A
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28
Q

Describe the use of the HPV vaccine?

A
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29
Q

What is the uterine body made up of?

A
  • Structure:
    • Endometrium
      • Glands
      • Stroma
    • Myometrium
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30
Q

What are the indications for uterine biopsies?

A

Endometrium: commonest types of specimens

  • Infertility
  • Uterine bleeding
  • Thickened endometrium on imaging

Uterus or related mass:

  • Lesion identified on imaging
  • As part of a wider resection
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31
Q

What goes wrong in the uterine corpus?

A
  • Congenital anomalies
  • Inflammation: acute or chronic
  • Adenomyosis
  • Dysfunctional uterine bleeding: e.g. hormonal imbalance
  • Endometrial atrophy and hyperplasia
  • Endometrial polyp•Uterine tumours
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32
Q

What are the uterine tumours?

A
  • Endometrial epithelial tumours and precursors
  • Tumour like lesions; e.g. endometrial polyp
  • Mesenchymal tumours specific to the uterus
  • Mixed epithelial and mesenchymal tumours•
  • Miscellaneous tumours
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33
Q

What are the commonest type of tumour?

A

Endometrial Epithelial Tumours and Precursors

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34
Q

When do you get endometrial hyperplasia? What may it be associated with?

A

Endometrial hyperplasia

nPerimenopause

nPersistent anovulation

nPolycystic ovary (PCO)

nOvarian Granulosa cell tumours

nOestrogen therapy

nMay be associated with atypia → serious

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35
Q

Describe the epidemiology of endometrial cancer.

A

•Endometrial cancer is the most common gynaecological malignancy in developed countries, causing 6% of new cancer cases in women.

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36
Q

Describe the RFs of endometrial cancer.

A

–Nulliparity

–Obesity

–Diabetes mellitus

–Excessive oestrogen stimulation

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37
Q

What are the factors affecting prognosis and plan of therapy?

A

–Histological tumour type

–Tumour grade

–Tumour stage

–Lymphovascular space invasion

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38
Q

What are the histological subtypes on endometrial carcinoma?

A
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39
Q
A

Endometriod carcinoma

  • Are oestrogen dependent
  • Often associated with atypical endometrial hyperplasia
  • Low grade and high grade tumours
  • Develop through the accumulation of mutations of different genes
40
Q

What are the gene mutations in endometrioid carcinoma, clear cell and serous carcinoma?

A
41
Q

Describe serous and clear cell carcinomas.

A
42
Q

How do we look at tumour grade in endometrial carcinoma?

A
43
Q

What is the distinction between high and low grade endometrial carcinoma?

A
44
Q

What is the FIGO Staging?

A
45
Q

What is TCGA? Why is it relevant in endometrial cancer?

A

The Cancer Genome Atlas (TCGA)

46
Q

What is the prognosis in POLE mutant cases?

A
47
Q

What is the mismatch repair system?

A
  • Mutations or silencing by hypermethylation of one of the DNA mismatch repair genes results in MSI•
  • Microsatellite instability (MSI): Alterations in the length of short, repetitive DNA sequences called microsatellites.
  • This results in an increase of the rate of mutations contributing to tumorigenesis, again with a high mutation burden.
48
Q
A
  • Mutations or silencing by hypermethylation of one of the DNA mismatch repair genes results in MSI•
  • Microsatellite instability (MSI): Alterations in the length of short, repetitive DNA sequences called microsatellites.
  • This results in an increase of the rate of mutations contributing to tumorigenesis, again with a high mutation burden.
49
Q

What are EECs exhibiting POLE mutations and MSI hypersensitive to?

A
50
Q

What are group 4 tumours comprised of?

A
51
Q

What are the main patterns of p53 staining?

A
52
Q

What are leioyomas?

A
  • Smooth muscle tumour of the myometrium
    • MOST COMMON (20% of >35yo) uterine tumour
    • Usually multiple
    • May be intramural, submucosal or subserosal
  • Lay term = fibroid
52
Q

What are leioyomas?

A
  • Smooth muscle tumour of the myometrium
    • MOST COMMON (20% of >35yo) uterine tumour
    • Usually multiple
    • May be intramural, submucosal or subserosal
  • Lay term = fibroid
53
Q

What are leiomyosarcomas?

A
  • Malignant counterpart of leiomyoma
    • RARE and usually solitary
    • Usually post-menopausal women
    • 5-year survival of 20-30%
    • Local invasion and spread via the blood stream
54
Q
A

Fibroid

55
Q
A

Leiomyosarcoma

56
Q
A

Endometrial stromal sarcoma

Low grade, high grade and other

Tumour types

57
Q

What is endometriosis? How common is it? What is the origin?

A

•Presence of endometrial glands and stroma outside the uterus

  • Common – 10% of premenopausal women
  • Origin:–Metaplasia of pelvic peritoneum–Implantation of endometrium, retrograde menstruation
  • Ectopic endometrial tissue is functional and bleeds at time of menstruation > pain, scarring and infertility
  • Can develop hyperplasia and malignancy
58
Q
A

Endometriosis

59
Q

What are the ovarian cysts?

A
  • Non-neoplastic functional Cysts
    • Follicular and luteal cysts
    • Endometriotic cyst
  • Polycystic Ovarian Syndrome (PCOS):
    • 3-6% of women of reproductive age
    • Patients have persistent anovulation
    • Other features include obesity and hirsutism/virilism
60
Q

How do we clasify ovarian tumours?

A
61
Q

How common are epithelial tumours? What age groups does it affect?

A

–make up 65% of all ovarian tumours & 95% of malignant ovarian tumours

–50% found in 45-65 age group

62
Q

How common are germ cell tumours? What age groups does it affect?

A

–have bimodal distribution; one peak 15-21 year olds and one peak at 65-69

63
Q

How common are sex cord stromal tumours? What age groups does it affect?

A

–most commonly seen in post-menopausal women but some sub-types peak in 25-30 year age group

64
Q

What are the different epithelial ovarian tumours?

A
65
Q

What is the WHO classification of epithelial tumours?

A
66
Q

What are the benign epithelial tumours?

A

Serous Cystadenomas

Cystadenofibromas

Mucinous cystadenomas

Brenner tumour

67
Q

What are borderline epithelial tumours?

A
68
Q

What are the malignant epithelial tumours?

Epidemiology RFs?

A

•Worldwide is the 6th most common cancer in women

  • 2nd commonest female cancer causing death in women–Difficult to diagnosis at an early stage–Develops resistance to therapeutic agents
  • Risk factors:•–Nulliparity, infertility, early menarche, late menopause.

–Genetic predisposition: Family history of ovarian and breast cancers

69
Q

What is the hereditary aspect of ovarian cancer?

A
  • HNPCC is responsible for 3% of ovarian carcinomas•
  • Ovarian cancers associated are mainly of the endometrioid and clear cell types
70
Q

What genetic aberration underlie the different epithelial carcinomas?

A
71
Q
A

High grade serous carcinoma

72
Q

What are high grade serous carcinomas?

A
73
Q

What is the significance of homologous recombination deficiency testing?¿

A
  • Identification of hereditary cases.•
  • Current data suggests that BRCA2 mutations confer an overall survival advantage compared with either being BRCA-negative or having a BRCA1 mutation in high-grade serous ovarian cancer.
  • BRCA mutation status has a major influence on response to chemotherapy.•
  • Patients can benefit from targeted therapy by PARP inhibitors.
74
Q

What are low grade serous carcinomas?

A

•Distinct pathogenesis from high grade serous carcinoma.

  • Low grade, relatively indolent, arise de novo or from borderline ovarian tumours.•
  • Mutations in KRAS, BRAF.•
  • No association with BRCA mutations.
75
Q
A

Low grade serous carcinoma

76
Q
A

Mucinous tumours

  • Morphological features similar to mucinous tumours of the gastrointestinal tract.
  • KRAS mutations.
77
Q

What are the 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
78
Q

What are the 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
79
Q
A

Endometrioid carcinoma

80
Q

Describe endometrioud carcinomas?

A

•10-20% associated with endometriosis, but most others thought to be derived from surface epithelium

  • Co-existence with endometrioid carcinoma in uterus common•
  • Molecular changes

–CTNNB1 (38%-50%)–PTEN (15-20%)

–KRAS and BRAF (4%-36%)

–MSI (8-38%)

–PIK3Ca in (20%)

–P53 >60% and usually in high Endometriosis is a precursor

81
Q
A

Clear cell carcinoma

82
Q

Describe clear cell carcinoma

A
83
Q

What are the types of sex cord-stomal 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
84
Q

What are the types of sex cord-stomal 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
85
Q

What are the molecular changes in sex-cord stromal tumours

A
86
Q

What are the hereditary predispositions to sex cord stroll tumours?

A
87
Q

What are the hereditary predispositions to sex cord stroll tumours?

A
88
Q

What are germ cell tumours?

A
  • 20% of ovarian tumours; 95% are BENIGN
  • Predominantly occur in <20 years
  • Germ cell tumours are classified on how they differentiate
  • Dysgerminoma – no differentiation
89
Q

What is the most common type of germ cell tumours?

A
89
Q

What is the most common type of germ cell tumours?

A
90
Q

What are immature teratomas?

A
91
Q

What are mature cystic teratomas with malignant transformation?

A

•Malignant transformation is rare occurring in 2% of cases, usually in post menopausal women

  • Most frequently squamous cell carcinoma
  • Also carcinoid, thyroid carcinoma, basal cell carcinoma, malignant melanoma, intestinal adenocarcinoma, leiomyosarcoma, chondrosarcoma and angiosarcoma
92
Q

What are other germ cell tumours?

A
93
Q

What are the prognostic factors in ovarian malignancies

A

•Stage of Disease•Tumour type•Tumor grade•Size of residual disease•Tumor response to therapy

Histopathology (14 decks)

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