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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
What is the cervical screening programme?
26
How is the cervical sample taken?
* 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
27
What is HC2 HPV DNA Tests?
28
Describe the use of the HPV vaccine?
29
What is the uterine body made up of?
* Structure: * Endometrium * Glands * Stroma * Myometrium
30
What are the indications for uterine biopsies?
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
31
What goes wrong in the uterine corpus?
* Congenital anomalies * Inflammation: acute or chronic * Adenomyosis * Dysfunctional uterine bleeding: e.g. hormonal imbalance * Endometrial atrophy and hyperplasia * Endometrial polyp•Uterine tumours
32
What are the uterine tumours?
* 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
33
What are the commonest type of tumour?
Endometrial Epithelial Tumours and Precursors
34
When do you get endometrial hyperplasia? What may it be associated with?
Endometrial hyperplasia nPerimenopause nPersistent anovulation nPolycystic ovary (PCO) nOvarian Granulosa cell tumours nOestrogen therapy nMay be associated with **atypia → serious**
35
Describe the epidemiology of endometrial cancer.
•Endometrial cancer is the most common gynaecological malignancy in developed countries, causing 6% of new cancer cases in women.
36
Describe the RFs of endometrial cancer.
–Nulliparity –Obesity –Diabetes mellitus –Excessive oestrogen stimulation
37
What are the factors affecting prognosis and plan of therapy?
–Histological tumour type –Tumour grade –Tumour stage –Lymphovascular space invasion
38
What are the histological subtypes on endometrial carcinoma?
39
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
What are the gene mutations in endometrioid carcinoma, clear cell and serous carcinoma?
41
Describe serous and clear cell carcinomas.
42
How do we look at tumour grade in endometrial carcinoma?
43
What is the distinction between high and low grade endometrial carcinoma?
44
What is the FIGO Staging?
45
What is TCGA? Why is it relevant in endometrial cancer?
**The Cancer Genome Atlas (TCGA)**
46
What is the prognosis in POLE mutant cases?
47
What is the mismatch repair system?
* 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
* 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
What are EECs exhibiting *POLE* mutations and MSI hypersensitive to?
50
What are group 4 tumours comprised of?
51
What are the main patterns of p53 staining?
52
What are leioyomas?
* 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
What are leioyomas?
* 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
What are leiomyosarcomas?
* **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
Fibroid
55
Leiomyosarcoma
56
Endometrial stromal sarcoma ## Footnote Low grade, high grade and other Tumour types
57
What is endometriosis? How common is it? What is the origin?
•Presence of endometrial glands and stroma outside the uterus ## Footnote * 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
Endometriosis
59
What are the ovarian cysts?
* 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
How do we clasify ovarian tumours?
61
How common are epithelial tumours? What age groups does it affect?
–make up 65% of all ovarian tumours & 95% of malignant ovarian tumours ## Footnote –50% found in 45-65 age group
62
How common are germ cell tumours? What age groups does it affect?
–have bimodal distribution; one peak 15-21 year olds and one peak at 65-69
63
How common are sex cord stromal tumours? What age groups does it affect?
–most commonly seen in post-menopausal women but some sub-types peak in 25-30 year age group
64
What are the different epithelial ovarian tumours?
65
What is the WHO classification of epithelial tumours?
66
What are the benign epithelial tumours?
Serous Cystadenomas Cystadenofibromas Mucinous cystadenomas Brenner tumour
67
What are borderline epithelial tumours?
68
What are the malignant epithelial tumours? Epidemiology RFs?
•Worldwide is the 6th most common cancer in women ## Footnote * 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
What is the hereditary aspect of ovarian cancer?
* HNPCC is responsible for 3% of ovarian carcinomas• * Ovarian cancers associated are mainly of the endometrioid and clear cell types
70
What genetic aberration underlie the different epithelial carcinomas?
71
High grade serous carcinoma
72
What are high grade serous carcinomas?
73
What is the significance of homologous recombination deficiency testing?¿
* 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
What are low grade serous carcinomas?
•Distinct pathogenesis from high grade serous carcinoma. ## Footnote * Low grade, relatively indolent, arise de novo or from borderline ovarian tumours.• * Mutations in *KRAS*, *BRAF*.• * No association with *BRCA* mutations.
75
Low grade serous carcinoma
76
Mucinous tumours * Morphological features similar to mucinous tumours of the gastrointestinal tract. * *KRAS* mutations.
77
What are the secondary ovarian tumours?
* 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
What are the secondary ovarian tumours?
* 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
Endometrioid carcinoma
80
Describe endometrioud carcinomas?
•10-20% associated with endometriosis, but most others thought to be derived from surface epithelium ## Footnote * 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
Clear cell carcinoma
82
Describe clear cell carcinoma
83
What are the types of sex cord-stomal tumours?
* **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
What are the types of sex cord-stomal tumours?
* **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
What are the molecular changes in sex-cord stromal tumours
86
What are the hereditary predispositions to sex cord stroll tumours?
87
What are the hereditary predispositions to sex cord stroll tumours?
88
What are germ cell tumours?
* 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
What is the most common type of germ cell tumours?
89
What is the most common type of germ cell tumours?
90
What are immature teratomas?
91
What are mature cystic teratomas with malignant transformation?
•Malignant transformation is rare occurring in 2% of cases, usually in post menopausal women ## Footnote * Most frequently squamous cell carcinoma * Also carcinoid, thyroid carcinoma, basal cell carcinoma, malignant melanoma, intestinal adenocarcinoma, leiomyosarcoma, chondrosarcoma and angiosarcoma
92
What are other germ cell tumours?
93
What are the prognostic factors in ovarian malignancies
•Stage of Disease•Tumour type•Tumor grade•Size of residual disease•Tumor response to therapy

Histopathology (14 decks)

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