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imed3003 > Pathology of the Uterus > Flashcards

Pathology of the Uterus Flashcards

1
Q

What are the 3 important phases of the menstrual cycle?

A

Proliferative phase: Gland and stromal proliferation due to oestrogen production by ovarian follicles

Secretory phase: 14 days following ovulation, due to combined oestrogen + progesterone production by the corpus luteum.

Menstrual phase: Stromal breakdown following involution of the corpus luteum.

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2
Q

What are the symptoms of endometrial pathology?

A

Abnormal cyclical bleeding (heavy, painful, irregular periods)

Post Menopausal Bleeding

Infertility

Investigations: D and C, pipelle biopsy, hysteroscopy, ultrasound

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3
Q

What does dysfunctional uterine bleeding mean?

A

Bleeding without an underlying organic condition.

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4
Q

What causes dysfunctional uterine bleeding?

A

Anovulatory cycles

Inadequate luteal phase

Irregular or delayed shedding.

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5
Q

What are anovulatory cycles?

A

Commonest cause of dysfunctional uterine bleeding. Typically occurs near menarche/menopause.

Follicles develop with oestrogen production but they don’t get to ovulation due to no progesterone from corpus luteum. As a result follicles regress and there is withdrawal bleeding.

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6
Q

What does histology show with anovulatory cycles?

A

Proliferative endometrium with stromal breakdown.

If prolonged it develops a disordered proliferative organisation. Variably spaced and shaped glands with cystic dilatation. This can eventually lead to hyperplasia/cancer.

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7
Q

How does inadequate luteal phase cause dysfunctional uterine bleeding?

A

Ovulation occurs but inadequate progesterone secretion by corpus luteum to develop the ovule so it leads to failure of ovule to develop or leads to premature regression.

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8
Q

What does histology show with inadequate luteal phase?

A

Secretory changes but less well developed with glands lacking tortuosity, discordant stromal breakdown.

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9
Q

What is a potential consequence of inadequate luteal phase?

A

Can be a cause of infertility/spontaneous abortion.

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10
Q

What causes irregular shedding?

A

Persistent corpus luteum with prolonged progesterone production.

Often see mixture of proliferative and secretory changes, or irregular secretory development, with stromal breakdown.

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11
Q

What is the effect of exogenous oestrogen intake?

A

Proliferative changes + stromal breakdown as endometrium cannot support continued growth

Disordered proliferative endometrium and can eventually lead to hyperplasia/carcinoma

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12
Q

Why are exogenous oestrogens taken?

A

Typically used initially in unopposed HRT.

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13
Q

What is the effect of exogenous progestins?

A

Short term: Leads to secretory glandular changes and stromal decidualistion

Long term leads to downregulation of ER/PR receptors with eventual atrophy.

High dose therapy can lead to superficial necrosis.

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14
Q

Where do exogenous progestins come from?

A

Used in IUCD/Rx, DUB, and hyperplasia.

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15
Q

How is the oral contraceptive pill designed to combat the effects of these exogenous hormones?

A

Usually consists of combined oestrogen/progesterone. The effect of the progesterone dominates.

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16
Q

What does the oral contraceptive pill do?

A

Suppresses ovulation

Simple tubular glands in vascular decidualised stroma +/- stromal breakdown.

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17
Q

What is in the minipill?

A

Progesterone only (depo-provera is intramuscular and has similar effect)

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18
Q

What causes post menopausal bleeding?

A

Can be due to benign or malignant causes:

Benign: Poly, endometritis, hormone therapy, hyperplasia, and atrophy

Malignant: Endometrial carcinoma, sarcoma

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19
Q

What are potential investigations that can be done for post-menopausal bleeding?

A

Ultrasound, hysteroscopy, D and C, endometrial pipelle

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20
Q

When are endometrial polyps most common?

A

In perimenopausal women (Less frequent after 60 years)

Tamoxifen treatment increases the occurrence of these polyps.

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21
Q

What happens in endometrial polyps?

A

Biphasic growth of benign glands + stroma. Usually they are non-functional and may cause abnormal PV bleeding.

May be involved by neoplastic processes.

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22
Q

What are the types of endometritis?

A

May be acute or chronic

Often non-specific

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23
Q

What causes specific forms of endometritis?

A

Neisseria gonorrheae/Chlam (STD)

TB

Post-partum/abort

pyometra

IUCDs

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24
Q

What are potential consequences of endometritis?

A

Variable symptoms

May lead to PID and infertility

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25
Q

What causes adenomyosis?

A

It is a common benign non-neoplastic condition caused by the deep extension of endometrial glands and stroma into the myometrium.

It is associated with muscle hypertrophy and occurs in late reproductive years.

26
Q

What are the complications of adenomyosis?

A

May cause recurrence of symptoms after endometrial ablation therapy.

Can cause abnormal uterine bleeding/pain.

27
Q

What are the types of tumours that can affect the uterus?

A

Endometrial carcinomas

Mesenchymal tumours

Mixed epithelial and mesenchymal tumours

Others (eg lymphomas which are rare)

Metastases (from ovary, breast, and colon)

28
Q

What is the most common gynaecological malignancy?

A

Endometrial carcinoma

29
Q

Who and where in the uterus is most commonly affected by endometrial carcinoma?

A

Usually in post-menopausal women. It is often confined to the uterus at diagnosis.

30
Q

What is the prognosis of endometrial carcinomas like?

A

Overall good prognosis (80 - 90% 5 year survival) because they present relatively early.

31
Q

What are the 2 main types of endometrial carcinomas?

A

Endometrioid - type 1 vs non-endometrioid - type 2

32
Q

How common is endometrial carcinoma in WA?

A

6th most common cancer (excluding skin)

14th cause of cancer death (2%)

33
Q

How is an endometrial carcinoma staged?

A

Stage 1 - Confined to the uterus (subdivided according to depth of myometrial invasion)

Stage 2 - Extension to cervix

Stage 3 - Invasion of serosa, adnexae or positive peritoneal cytology

Stage 4 - Bladder/bowel invasion or distant metastasis

34
Q

How are the types of endometrial carcinomas different?

A

Type 1 is endometrioid in shape, driven by oestrogen, arising in hyperplasia, and seen in women younger than those that get type 2 (perimenopausal + younger post-menopausal women)

Type 2 has a poor prognosis and is often detected later. has high grade serous or clear cell types. associated with p53 mutations.

35
Q

What percentage of endometrial carcinomas are type 1?

A

80 - 85%

36
Q

What molecular changes occur in type 1 endometrial carcinomas?

A

PTEN, beta catenin, MMR gene mutations, K-ras

p53 mutations are RARE

37
Q

What does a endometrial carcinoma look like on histology?

A

No visible stroma in cribiform mass that looks different to surrounding stroma.

38
Q

When do signs of hereditary endometrial carcinomas first appear?

A

Tend to develop 15 years earlier than the carcinoma.

Most have lynch syndrome (HNPCC): Endometrial carcinoma is as common as ColoRectal Carcinoma, 70% lifetime risk.

39
Q

What causes hereditary endometrial carcinoma?

A

Mutations in DNA mismatch repair genes producing MSI

MSH2/6 mutations are most common

Generally type 1 endometrial carcinoma

BRCA patients (increased risk)

40
Q

What are the risk factors for type 1 endometrial carcinoma?

A

Increased oestrogen: Obesity, anovulation (PCOS), hormonal therapy (HRT, tamoxifen), oestrogen secreting ovarian tumours, relative progestogen deficiency.

41
Q

What are the risk factors for endometrial hyperplasia?

A

Precursor lesion to type 1 carcinoma

Oestrogen induced

Typically perimenopausal (anovulatory cycles)

Also younger women (PolyCysticO) or postmenopausal (excess endogenous or exogenous oestrogen)

42
Q

How does endometrial hyperplasia present?

A

May present with abnormal bleeding.

Macroscopically thickened endometrium

43
Q

How is hyperplasia classified in endometrium?

A

Hyperplasia without atypia (low cancer risk): simple or complex

Atypical hyperplasia (increased cancer risk): Simple or complex, atypia classified as mild, moderate, and severe.

Endometrial Intraepithelial Neoplasia (EIN): monoclonal, premalignant

44
Q

What does histology show in endometrial hyperplasia?

A

Simple hyperplasia without atypia: Increased gland to stroma ratio, variable sized and shaped glands, often dilated, cytologically resembles normal proliferative.

Atypical hyperplasia: Usually complex, very crowded glands with complex infoldings, nuclear enlargement, rounding , nucleoli, increased chance of progressing to cancer.

45
Q

How is hyperplasia treated?

A

Surgery - hysterectomy

Progestins - simple hyperplasia, patients with atypical hyperplasia who are poor surgical candidates or preserving fertility.

46
Q

What risk factors are associated with type 2 endometrial carcinoma?

A

No association with raised oestrogen/hyperplasia

Older patients (post-menopausal)

Often high grade serous or clear cell types

p53 mutations common

47
Q

What is prognosis like in type 2 endometrial carcinomas?

A

Often has extrauterine spread and so prognosis is generally poor

48
Q

What percentage of endometrial carcinomas are stage 2?

A

10 - 15%

49
Q

What are the associated precursor lesions in type 2 endometrial carcinoma?

A

Endometrial intra-epithelial carcinom (EIC)/serous carcinoma in situ.

Similar molecular pathology to invasive serous carcinoma.

50
Q

What is the pathogenesis like in type 2 endometrial carcinoma?

A

Relatively subtle; non-invasive replacement of endometrial surface or glandular epithelium by one or more layers of malignant serous cells.

51
Q

How is endometrial carcinoma managed?

A

Surgically (hysterectomy, BSO)

High grade cases have associated lymph nodes removed and omental sampling.

Post operative radiotherapy and chemotherapy is undertaken.

52
Q

What are the most common mesenchymal tumours of the uterus?

A

Smooth muscle tumours: Leiomyoma, and leiomyosarcoma.

Endometrial stromal tumours.

53
Q

How are smooth muscle tumours detected?

A

Very common, often incidental finding.

54
Q

What are the features of smooth muscle tumours?

A

Vast majority are benign

Often multiple

Typically they are hormone dependent.

55
Q

What are malignant smooth muscle tumours called?

A

Leiomyosarcoma

56
Q

What are the features of leiomyosarcoma?

A

Rapid growth, especially post menopausal

Macro: Often single, large, variegated, haemorrhage, necrosis.

Micro: High cellularity, cellular atypia, infiltrative, mitotic activity, tumour necrosis.

Aggressive

Not responsive to therapy.

57
Q

How are endometrial stromal tumours classified?

A

Endometrial stromal nodule - circumscribed

Endometrial stromal sarcoma (low grade)

Endometrial stromal sarcoma (high grade)

Undifferentiated stromal sarcoma - no resemblance to endometrial stroma

58
Q

Are endometrial stromal tumours common?

A

No they are relatively rare.

59
Q

What are the features of low grade endometrial stromal sarcoma?

A

Most common of the stromal tumours.

Composed of cells resembling endometrial stroma.

Infiltrative growth

Indolent growth, late recurrence, can metastasize.

60
Q

How are low grade endometrial stromal sarcomas treated?

A

Surgery and high dose progestins.

61
Q

What are carcinosarcomas?

A

Biphasic tumours with an epithelial component and a mesenchymal component.

They are polypoid masses with serous epithelial component.

62
Q

What are the risk factors and molecular findings most similar to in carcinosarcomas?

A

Share some molecular findings and risk factors (eg post-menopausal women) with type 1 endometrioid carcinoma. Epithelial component is often serous

Homologous or heterologoous stroma.

imed3003 (48 decks)

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