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MD3002 > Reproductive pathology: female 2 > Flashcards

Reproductive pathology: female 2 Flashcards

1
Q

What proportion of women are affected by congenital uterine abnormalities ?

A

5% of women

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2
Q

Which groups are uterine congenital abnormalities more common in ?

A

The rate is higher among infertile women, and the highest in women with recurrent pregnancy losses (10%).

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3
Q

What is the embryonic cause of congenital uterine abnormalities ?

A

A uterine malformation is a type of female genital malformation resulting from an abnormal development of the Müllerian duct (i.e. Mullerian malformation)

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4
Q

Which other body abnormalities are Mullerian abnormalities associated with ?

A

Müllerian malformations are frequently associated with abnormalities of the renal and axial skeletal systems.
HOWEVER most müllerian duct anomalies are associated with functioning ovaries and age-appropriate external genitalia.

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5
Q

When are Mullerian abnormalities usually recognised ? How do they present ?

A

• These abnormalities are often recognized after the onset of puberty:

1) In the prepubertal period, normal external genitalia and age- appropriate developmental milestones often mask abnormalities of the internal reproductive organs.
2) After the onset of puberty, young women often present to the gynaecologist with menstrual disorders.

• Late presentations include infertility and obstetric complications.

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6
Q

Define hysterosalpingogram.

A

An x-ray film of the uterus and the fallopian tubes using gas or a radiopaque substance introduced through the cervix to allow visualization of the cavity of the uterus and the passageway of the tubes.

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7
Q

Give examples of Mullerian abnormalities.

A

Bicornuate uterus

Septate uterus

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8
Q

Which types of cancers affect the vulva ? Why ? Where exactly do they form ?

A
  • The vulva is essentially epithelial skin; therefore the main tumour types that affect the vulva are skin-related cancers.
  • About 90% of vulval cancers are squamous cell carcinomas, which typically develop at the edges of the labia majora/ minora or in the vagina.
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9
Q

How fast do vulval cancers grow ? Are they associated with any precursor lesions ?

A

Slow growing

Usually develop from “precancerous”, pre-invasive areas called vulval intraepithelial neoplasia (VIN).

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10
Q

Identify the most common vulvar cancers.

A

Two subtypes of squamous cell vulval cancer:

1) One is more common in younger women and is associated with the human papillomavirus (HPV)
2) the other occurs in older women and is not associated with HPV infection, but is associated with chronic vulval skin changes called vulval dystrophy, including lichen sclerosus.

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11
Q

Identify the main vulval benign disorders, and describe the morphology and neoplastic potential of each.

A

1) Squamous hyperplasia – hyperkeratosis, irregular thickening of ridges. Some neoplastic potential

2) Lichen Sclerosus – hyperkeratosis, flattening of ridges, oedema in connective tissue with chronic inflammation.
Some neoplastic potential. Sometimes white patches ‘leukoplakia’.

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12
Q

Identify any complications of Lichen Sclerosus.

A

Causes pruritis

Excoriation makes things worse

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13
Q

How is Lichen Sclerosus treated ?

A

Treated with potent topical corticosteroids

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14
Q

What age ranges do endometrial cancers usually affect ?

A

It usually affects women in their 50s, 60s and 70s, and is rare in those aged under 40.

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15
Q

Are endometrial cancers increasing or decreasing ? Why ?

A

The incidence is increasing, probably due to increasing population age, obesity and use of HRT.

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16
Q

What is the most commonly diagnosed gynaecological cancer in developed countries ? in developing countries ?

A

Developed: Endometrial cancer
Developing: Cervical cancer

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17
Q

What are the main components of the endometrium ?

A

The endometrium lines the uterine corpus and exhibits two chief constituents - the endometrial glands and endometrial stroma

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18
Q

What epithelium lining the endometrium pre-puberty, and post-menopause ?

A

Pre-pubertal: inactive endometrium shows a cuboidal to low columnar epithelium that lines the surface and the underlying glands. The appearance greatly resembles the inactive endometrium seen in postmenopausal women, as both prepubertal and postmenopausal endometria do not exhibit any proliferative or secretory changes that are hormone dependent.

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19
Q

Identify the main endometrial benign disorders, and describe the morphology and neoplastic potential of each.

A

Endometrial Hyperplasia

  • Simple
  • Complex
  • Atypical
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20
Q

What are the most common endometrial cancers ?

A

Endometrial Adenocarcinoma
Endometrial stromal sarcoma (arises from endometrial stroma)
Malignant mixed Müllerian tumour

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21
Q

Describe the main features of endometrial adenocarcinoma.

A

-Infiltrates endometrium, then myometrium

Two clinico-pathological types:

1) Endometrioid
2) Non-endometrioid

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22
Q

Describe the main features of enometrioid adenocarcinoma.

A
  • Related to unopposed oestrogen
  • Associated with atypical hyperplasia
  • Associated with polycystic ovary syndrome
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23
Q

Describe the main features of non-enometrioid adenocarcinoma.

A
  • Not associated with unopposed oestrogen
  • Affects elderly post-menopausal women
  • p53 often mutated
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24
Q

What does prognosis of endometrial adenocarcinoma depend on ?

A

Prognosis of endometrial adenocarcinoma is related to stage:

I- Confined to uterus body
II- Involvement of cervix
III- Involvement of ovaries/tubes or extension beyond serosa
IV- spread to other organs

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25
Q

How does endometrial cancer usually present ?

A

With post-menopausal bleeding

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26
Q

Which reproductive cancers are screened for in the UK ?

A

Cervical Cancer (NOT endometrial cancer)

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27
Q

Where do Malignant mixed Müllerian tumours arise from ? How good of a prognosis does it have ?

A

Mixed tumour with malignant epithelial and stromal elements (carcinosarcoma)

Poor prognosis

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28
Q

Identify the main benign and malignant abnormalities of the myometrium.

A

Benign:
1) Adenomyosis

Smooth Muscle Tumours

  • Leiomyoma (Uterine fibroids) (benign)
  • Leiomyosarcoma (malignant)
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29
Q

Describe the main morphological characteristics of adenomyosis. How does it present ?

A

Presence of ectopic endometrial glands and stroma, deep within the myometrium with adjacent reactive myometrial hyperplasia. The disease can be diffuse or focal (adenomyoma).

Causes menorrhagia / dysmenorrhoea

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30
Q

How does leiomyoma of the myometrium present ?

A

Associated with menorrhagia, infertility

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31
Q

Identify a cause of uterine enlargement.

A

Leiomyoma

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32
Q

To what extent can leimyomas undergo degeneration ?

A
  • May undergo degeneration
33
Q

Identify the main types of leimyomas morphologically.

A
  • Intramural
  • Submucosal (e.g. pedunculated appearing in the form of an endometrial polyp)
  • Subserosal (can compress bladder or rectum)
34
Q

Describe treatment for uterine fibroid (uterine Leiomyoma).

A

Uterine Artery Embolisation (UAE): “minimally invasive procedure. This uses a form of real-time x-ray called fluoroscopy to guide the delivery of embolic agents to the uterus and fibroids. These agents block the arteries that provide blood to the fibroids and cause them to shrink.”

35
Q

What is endometriosis ? Where does it occur ?

A

“Condition in which endometrial glands and stroma grow outside the uterine body”

Sites:
– Ovary (‘chocolate’ cyst)
– Pouch of Douglas
– Peritoneal surfaces, including uterus 
– Cervix, vulva, vagina
– Bladder, bowel etc
36
Q

What are possible presentations of endometriosis ?

A

– Pelvic inflammation
– Infertility
– Pain

37
Q

Identify pathologies of the ovaries. What are possible presentations of ovarian pathologies ?

A

1) Ovarian Cysts (and Polycystic ovary syndrome)
2) Ovarian Tumors
3) Endometriosis

May be present with pain, swelling, and endocrine effects.

38
Q

Which part of the ovary do ovarian cysts arise from ?

A 
• Arise from several elements of ovary:
– Mesothelial 
– Epithelial
– Follicular
– Luteal
– Endometriotic
39
Q

Are ovarian cysts always pathological ? How can we distinguish between those ?

A

Ovarian cysts vary from physiologic, to complex benign, to neoplastic.

Small cystic ovarian structures should be considered normal ovarian follicles unless the patientispre-pubertal,post- menopausal, pregnant, or the mean diameter is >3.0 cm.

40
Q

Define Polycystic ovary syndrome. How does this present ?

A

“Condition characterized by the accumulation of numerous cysts (fluid-filled sacs) on the ovaries”

Women may initially present with symptoms of hyperandrogenism (such as hirsutism, acne, alopecia), menstrual disturbance, infertility, or obesity. HOWEVER, polycystic ovaries can exist without clinical signs of the syndrome that may then become expressed over time, eg with a weight gain.

41
Q

Identify possible long term associations of polycystic ovary syndrome.

A

Possible long term associations may include type 2 diabetes mellitus, dyslipidaemia, hypertension, cardiovascular disease, and endometrial carcinoma.

42
Q

What is the aetiology of polycystic ovary syndrome ?

A

Multifactorial and polygenic (familial to some extent)

43
Q

Describe treatments of Polycystic ovary syndrome

PCOS.

A

1) Combined oral contraceptive pill may be prescribed to women with PCOS for a variety of indications including for contraception, protection against the development of endometrial hyperplasia and cancer, and to suppress excessive androgen secretion to control acne and hirsutism.
2) Alternatives to Combined oral contraceptive pill: Mirena intrauterine system (IUS).

44
Q

Identify possible complications of Polycystic Ovary Syndrome, explaining why they happen.

A

Women with PCOS are at risk of endometrial hyperplasia or adenocarcinoma.
→ due to the unopposed actions of oestrogen in the absence of progesterone that is normally released after ovulation

45
Q

Identify red flags concerning possible endometrial hyperplasia or adenocarcinoma, and the main ways of investigating these.

A

• Withdrawal bleeds or abnormal uterine bleeding: A transvaginal ultrasound should be considered.
An endometrial thickness of less than 7 mm, or an intermenstrual interval of less than three months, are associated with normal proliferative endometrium only (if more, possible hyperplasia or adenocarcinoma).

• A thickened endometrium in an amenorrhoeic / oligomenorrhoeic woman, or the presence of an endometrial polyp: endometrial biopsy and/or hysteroscopy (can also reveal hyperplasia or adenocarcinoma)

46
Q

Identify the main classifications of ovarian neoplasms.

A

Can be solid or cystic, can be benign or malignant. The main ones are:

– Epithelial (90%, including serous adenocarcinoma (mainly), endometrioid adenocarcinoma, mucinous adenocarcinoma)

Neoplasma affecting other parts of ovary (10%):
– Germ cell tumors
– Sex-cord / stromal tumors
– Metastatic
– Miscellaneous
These generally affect younger women and progress more quickly and aggressively

47
Q

Identify the main epithelial ovarian tumors, along with their main characteristics.

A

1) Benign
2) Borderline
– Cytological abnormalities
– No stromal invasion
3) Malignant
– Stromal invasion

48
Q

What are he main ovarian cancer symptoms ?

A
  • Its insidious onset means that up to 75% of patients present with symptoms of advanced disease due to the mass effects of the tumour.
  • Non-specific GI symptoms such as bloating or indigestion (often misdiagnosed as Irritable Bowel Syndrome IBS).
  • Gradually increasing abdominal distension (often misdiagnosed as “middle-aged spread”).
  • Increasing tumour size results in pressure effects causing chronic abdominal, pelvic or back pain, urinary frequency/urgency (pressure on bladder), constipation/altered bowel habit/bowel obstruction (pressure on bowel), leg swelling and DVT/PE (pressure on pelvic veins).
  • Abnormal vaginal bleeding can also be a symptom.
  • Symptoms of metastatic disease include pleural effusion, ascites, weight loss and fatigue.
  • Less commonly, sudden torsion, rupture or infection of the tumour in early disease can present with acute abdominal or pelvic pain – this is a blessing in disguise as it can lead to early diagnosis.
49
Q

Describe management of ovarian cancer.

A
  • Surgical management is generally the mainstay of treatment: exploratory laparotomy for tumour debulking and formal surgical staging. This is a major procedure which generally comprises total abdominal hysterectomy (TAH) and bilateral salpingo- oophorectomy (BSO), infracolic omentectomy, pelvic and para- aortic lymph node sampling, peritoneal biopsies, multiple pelvic washings, sampling of ascites.
  • Adjuvant chemotherapy (intraperitoneal chemotherapy improves survival) is given to all patients >stage Ic.
  • Response to treatment can be monitored using CA-125 levels, which decrease if treatment is effective and increase if there is a relapse

• Advanced metastatic cancer (which is unfortunately very common) requires individualised palliative treatment.
—–
POTENTIAL:
• Biological immunotherapy is emerging as a potential new treatment – specific monoclonal antibodies.

50
Q

Why isn’t radiotherapy used for ovarian cancers ?

A

Radiotherapy is not really used in the management of ovarian cancer as the tumours tend to be very radioresistant.

51
Q

Identify the main examples of ovarian Germ Cell Tumors.

A
  • Dysgerminoma (Counterpart of male seminoma) (undifferentiated tumor)
  • Teratoma
  • Extraembryonic:
    a) Yolk sac tumour
    b) Choriocarcinoma
52
Q

Which populations do dysgerminomas usually occur in ?

A

– Young women

53
Q

Which cells do Teratoma affect ?

A

Teratoma

– Contains elements from all three embryonic germ cell layers

54
Q

What are the main kinds of ovarian teratomas ?

A

1) Mature cystic teratoma common (Dermoid Cyst)
2) Immature teratoma rare
3) Monodermal - commonest is struma ovarii (thyroid tissue)

55
Q

Describe the main features of yolk sac tumors (extraembryonic ovarian germ cell tumor).

A

Young (<30 years)
Produces alpha fetoprotein
Highly malignant but treatable

56
Q

Describe the main features of Choriocarcinoma (extraembryonic ovarian germ cell tumor).

A

Pure variety is rare
Usually seen as part of a teratoma
Different from gestational choriocarcinoma

57
Q

Identify the main kinds of ovarian Sex Cord / Stromal Tumours, and state their main features.

A

1) Fibroma/Thecoma
– Benign
– May produce oestrogen, causing uterine bleeding

2) Granulosa cell tumour
– All are potentially malignant
– May be associated with oestrogenic
manifestations

3) Sertoli-Leydig cell tumours
– Rare
– May produce androgens

58
Q

Identify the main sites of metastases of ovarian tumors.

A

– Stomach
– Colon
– Breast
– Pancreas

59
Q

Define Gestational trophoblastic disease.

A

A generic term for a group of pregnancy-related disorders that arise from the trophoblast and clinically range from banal (e.g., hydatidiform mole) to aggressively malignant (e.g., metastatic choriocarcinoma). These include:

  • Hydatidiform mole (complete or partial)
  • Invasive mole
  • Choriocarcinoma
  • Placental-site trophoblastic tumour
  • Epithelioid trophoblastic tumour
60
Q

What cells do Choriocarcinomas consist of ?

A

Choriocarcinomas consist of admixed syncytiotrophoblastic and cytotrophoblastic elements.

61
Q

Which women are more at risk of molar pregnancy ?

A

Those under 16 and over 45 + women of Asian backgrounds

62
Q

Define Hyatid mole. What are the main types of Hydatidiform mole ?

A

A vesicular or polycystic mass resulting from the proliferation of the trophoblast, with hydropic degeneration and avascularity of the chorionic villi.

1) Complete Hydatidiform Mole
2) Partial Hydatidiform Mole

63
Q

Distinguish between complete and partial Hydatidiform moles.

A
  • A complete hydatidiform mole most often develops when either 1 or 2 sperm cells fertilize an egg cell that contains no nucleus or DNA (an “empty” egg cell). All the genetic material comes from the father’s sperm cell. Therefore, there is no foetal tissue.
  • A partial hydatidiform mole develops when 2 sperm fertilize a normal egg. These tumours contain some foetal tissue, but this is often mixed in with the trophoblastic tissue. It is important to know that a viable foetus is not being formed.
64
Q

Define invasive hydatidiform mole. Are these associated with complete or partial hydatidiform moles ?

A

Hydatidiform mole that has grown into the muscle layer of the uterus.

• Invasive moles can develop from either complete or partial moles, but complete moles become invasive much more often than do partial moles.

65
Q

Identify risk factors for invasive hydatidiform moles.

A
  • There is a long time (more than 4 months) between the last menstrual period and treatment.
  • the uterus has become very large.
  • the woman is older than 40 years.
  • the woman has had gestational trophoblastic disease in the past.
66
Q

Describe the main hormonal changes which occur in invasive hydatidiform moles, explaining why these occur.

A

• Women with a hydatidiform mole usually have higher-than-average levels of the pregnancy hormone human chorionic gonadotrophin (hCG) compared with women with a normal pregnancy.
→ This hormone is produced by the trophoblastic tissue. The high levels of hCG occur because there is an excessive amount of trophoblastic tissue with a hydatidiform mole. The high hCG levels are responsible for some of the symptoms.

67
Q

How do trophoblastic gestational diseases affect fertility ?

A

Almost all women with malignant gestational trophoblastic disease can be cured with preservation of reproductive function.

68
Q

Which of the gestational trophoblastic diseases grow quickly and spread to organs away from the uterus ?

A

Choriocarcinoma

69
Q

What proportion of all gestational choriocarcinomas start off as molar pregnancies ?

A

Half

70
Q

Can Choriocarcinoma occur outside of pregnancy ?

A

Non-gestational choriocarcinoma (rarely)

71
Q

Where are non-gestational choriocarcinoma found ?

A

These can be found in areas other than the uterus, and can occur in both men and women. They may develop in the ovaries, testicles, chest, or abdomen. In these cases, choriocarcinoma is usually mixed with other types of cancer, forming a type of cancer called a mixed germ cell tumor.

72
Q

Which of gestational or non gestational choriocarcinoma has a worse prognosis ?

A

Non-gestational choriocarcinoma can be less responsive to chemotherapy and may have a less favourable prognosis than gestational choriocarcinoma.

73
Q

Describe the treatment for molar pregnancies.

A

Suction Curettage

74
Q

Define Ectopic Pregnancy.

A

Implantation of a conceptus outside the endometrial cavity.

75
Q

What are the most common sites for ectopic pregnancies ?

A

Commonest site is Fallopian tube.

May occur on ovary or peritoneum.

76
Q

What are possible complications of ectopic pregnancies ?

A

Often ruptures.

May cause fatal haemorrhage.

77
Q

What are the main red flags for ectopic pregnancy ?

A

Women of reproductive age with amenorrhoea and acute hypotension or an acute abdomen.

78
Q

Are ectopic pregnancies ever successful ?

A

It is rare for these pregnancies to continue beyond a few months and it is exceptional for the pregnancy to reach a stage of viability.

79
Q

Describe treatment for ectopic pregnancy.

A
  • Laparascopic surgical extraction of ectopic (tubal) pregnancy.
  • Methotrexate (to stop pregnancy growing)

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