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Pathology - Y5 > Gynaecological Pathology > Flashcards

Gynaecological Pathology Flashcards

1
Q

What are infections of the female genital tract cause discomfort but no serious complications?

A

Candida: Diabetes mellitus, oral contraceptives and pregnancy enhance development of infection.

Tichomonas vaginalis: Protozoan.

Gardenerella: Gram negative bacillus causes vaginitis

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2
Q

What infections of the female genital tract have serious complications?

A

Chlamydia: Major cause of infertility.

Gonorrhoea: Major cause of infertility.

Mycoplasma: Causes spontaneous abortion and chorioamnionitis.

HPV: Implicated in cancer.

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3
Q

How do gonococci, chlamydia and enteric bacteria cause PID?

A

Usually starts from the lower genital tract and spreads upward via mucosal surface.

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4
Q

How do staph, strep, coliform bacteria and clostridium perfringens cause PID?

A

Secondary to abortion.

Usually start from the uterus and spread by lymphatics and blood vessels upwards.

Deep tissue layer involvement.

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5
Q

What are complications associated with PID?

A

Peritonitis

Bacteraemia

Intestinal obstruction due to adhesions

Infertility

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6
Q

What is the sequence of events with salpingitis?

A

Usually direct ascent from the vagina.

Depending on severity and treatment may result in resolution or complications.

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7
Q

What are complications associated with salpingitis?

A

Plical fusion

Adhesions to ovary

Tubo-ovarian abscess

Peritonitis

Hydrosalpinx

Infertility

Ectopic pregnancy

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8
Q

What is this?

A

Salpingitis

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9
Q

What are pathologies which can occur in the cervix?

A

Inflammation

Polyps

Dysplasia and carcinoma

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10
Q

Which HPV types are low risk?

A

Most common types: 6, 11

Other types: 40, 42, 43, 44, 54, 61, 72, 73, 81

Genital and oral warts.

Low grade cervical abnormalities.

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11
Q

Which HPV types are high risk?

A

Most common types: 16, 18

Other types: 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68,82

Low & high grade cervical abnormalities.

Cervical cancer.

Vulval, vaginal, penile, and anal cancer.

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12
Q

What is cervical intraepithelial neoplasia (CIN)?

A

This is the term for dysplasia in this site.

Epithelial cells have undergone some phenotypic and genetic changes which are premalignant and preinvasive.

Basal membrane immediately deep to the surface epithelium is intact.

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

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13
Q

What is cervical carcinoma?

A

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

Two types of cervical cancer:

  • Squamous cell carcinoma.
  • Adenocarcinoma (20% of all invasive cases).

HPV dependent or independent.

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14
Q

What is this?

A

Squamous cell carcinoma (cervical carcinoma)

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15
Q

What is this?

A

Adenocarcinoma (cervical carcinoma)

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16
Q

How does HPV transform cells?

A

Two proteins E6 and E7 encoded by the virus have transforming genes. E6 and E7 bind to and inactivate two tumour suppressor genes:

  • Retinoblastoma gene (Rb) (E7)
  • P53 (E6)

Both effects interfere with apoptosis and increase unscheduled cellular proliferation both of which contribute to oncogenesis. Infection is either latent or productive.

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17
Q

What is the pathophysiology of HPV in non-productive/latent phases?

A

HPV DNA continues to reside in the basal cells.

Infectious virions are not produced.

Replication of viral DNA is coupled to replication of the epithelial cells occurring in concert with replication of the host DNA.

Complete viral particles are not produced.

The cellular effects of HPV infection are not seen.

Infection can only be identified by molecular methods.

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18
Q

What is the pathophysiology of HPV in productive viral infection stages?

A

Viral DNA replication occurs independently of host chromosomal DNA synthesis.

Large numbers of viral DNA are produced and result in infectious virions.

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19
Q

What are the screening intervals for cervical cancer?

A

25 years - First invitation

25-49 years - Every 3 years

50-64 years - Every 5 years

65+ - Only if one of last three was abnormal

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20
Q

What are endometrial indications for uterine biopsies?

A

Infertility

Uterine bleeding

Thickened endometrium on imaging

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21
Q

What are uterine indications for biopsies?

A

Lesion identified on imaging

As part of a wider resection

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22
Q

What are risk factors for endometrial cancer?

A

Nulliparity

Obesity

Diabetes mellitus

Excessive oestrogen stimulation

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23
Q

What are features of endometrioid carcinomas?

A

Are oestrogen dependent

Often associated with atypical endometrial hyperplasia

Low grade and high grade tumours

Develop through the accumulation of mutations of different genes.

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24
Q

What is this?

A

Endometrioid Carcinoma

25
Q

What is this?

A

Endometrioid carcinoma

26
Q

What are serous and clear cell carcinomas associated with?

A

Older, postmenopausal

Less oestrogen dependent

Arise in atrophic endometrium

High grade, deeper invasion, higher stage

27
Q

Which mutations are associated with endometrial serous carcinomas?

A

P53 mutations in 90%

PI3KCA mutations in 15% Her-2 amplification

28
Q

Which mutations are associated with endometrial clear cell carcinoma?

A

PTEN mutation

CTNNB1 mutation

Her-2 amplification

29
Q

What is this?

A

Endometrial serous carcinoma

30
Q

What is this?

A

Endometrial clear cell carcinoma

31
Q

What is the 2009 FIGO Staging for Carcinoma of the Endometrium?

A

Stage I: Tumour confined to the corpus uteri.

Stage II: Tumour invades cervical stroma.

Stage III: Local and/or regional spread of the tumour.

Stage IV: Tumour invades bladder and/or bowel mucosa, and/or distant metastases.

32
Q

What is this?

A

HMLH1 (A), PMS2 (B), MSH2 (C) and MH6 (D) show strong nuclear expression in tumour cells of endometrioid carcinoma.

33
Q

What are mesenchymal tumours (leiomyoma)?

A

Smooth muscle tumour of myometrium.

Commonest uterine tumour

20% of women >35yrs

Lay term is fibroid

Usually multiple

May be intramural, submucosal or subserosal

34
Q

What is this?

A

Leiomyoma

35
Q

What are leiomyosarcomas?

A

Malignant counterpart of leiomyoma - rare.

Usually solitary.

Usually postmenopausal.

Local invasion and blood stream spread.

5yr survival 20-30%.

36
Q

What is this?

A

Leiomyosarcoma

37
Q

What is this?

A

Endometrial stromal sarcoma

38
Q

What is this?

A

Endometrial stromal sarcoma

39
Q

What is this?

A

Serous Epithelial Ovarian Tumour

40
Q

What is this?

A

Mucinous Epithelial Ovarian Tumour

41
Q

What is this?

A

Endometrioid Epithelial Ovarian Tumours

42
Q

What is this?

A

Clear cell Epithelial Ovarian Tumours

43
Q

What is this?

A

Brenner Epithelial Ovarian Tumours

44
Q

What is this?

A

Serous borderline tumour

45
Q

What is this?

A

Mucinous borderline tumour

46
Q

What are high grade ovarian serous carcinomas?

A

Most common type of malignant tumours (80%).

Aggressive.

  • Alteration in P53, in virtually all.
  • BRCA1 or BRCA2 abnormalities (germline and somatic mutations; BRCA1 promoter methylation).

These genes encode proteins that play important roles in DNA repair (homologous recombination).

47
Q

What are low grade ovarian 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.

48
Q

Where are common origin sites for secondary ovarian tumours?

A

Metastatic colorectal carcinoma:

  • Ovaries, an anatomic site prone to involvement by metastatic colorectal adenocarcinoma.
  • 4-10% of CRC go to ovary.
  • Ovarian lesions are identified prior to the primary tumor in 14-32% of cases.

Krukenberg tumours:

  • Bilateral metastases composed of mucin producing signet ring cells.
  • Most often of gastric origin or breast.
49
Q

What are different categories of sex-cord stromal tumours?

A

Pure stromal tumours: e.g. Fibroma, Thecoma, microcystic stromal tumour.

Pure sex cord cells: e.g. Adult type and juvenile granulosa cell tumour.

Mixed sex cord-stromal tumours: e.g. Sertoli Leydig cell tumour.

50
Q

What is this?

A

Fibroblasts: Fibromas:

Benign, no endocrine production

51
Q

What is this?

A

Granulosa cells: Granulosa cell tumor

Variable behaviour, may produce estrogen

52
Q

What is DICER1 Syndrome?

A

Germline mutation in DICER1, a gene encoding an RNAse III endoribonuclease.

Familial multinodular goitre with sertoli/leydig cell tumour, and tumour susceptibility includes pleuropulonry blastoma in childhood.

Found in up to 60% of seroli-Leydig cell tumours.

53
Q

What is Peutz-Jegher’s Syndrome?

A

Germline mutations of STK11

Sex cord stromal tumour with annular tubules

Cases occurring in PJS usually show indolent behaviour.

54
Q

What are immature teratomas?

A

Indicates presence of embryonic elements.

Neural tissue particularly conspicuous.

A malignant neoplasm that grows rapidly, penetrates the capsule and forms adhesions to the surrounding structures.

Spreads in the peritoneal cavity by implantation.

Metastasis to lymph nodes, lung, liver and other organs.

55
Q

What is this?

A

Dysgerminoma

56
Q

What is this?

A

Yolk sac tumour

57
Q

What is this?

A

Embryonal carcinoma

58
Q

What is this?

A

Choriocarcinoma

Pathology - Y5 (59 decks)

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