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MD3002 Pathology > Reproductive Pathology: Female 2 > Flashcards

Reproductive Pathology: Female 2 Flashcards

1
Q

What percentage of women have some form of congenital uterine abnormalities?

A

5%

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2
Q

What are mullerian malformations?

A
  • Anomalies caused by errors in müllerian-duct development during embryonic morphogenesis
  • Abnormalities of the renal and axial skeletal systems present
  • Most problems occur after puberty
  • Can be infertile
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3
Q

What is a hysterscopy?

A

Procedure which uses an endoscope to see insode the uterus

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4
Q

What type of cancers are vulval cancers usually?

A

90% are squamous cell

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5
Q

Where do vulval cancers usually develop?

A

Edges of labia majora/minora or in vagina

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6
Q

What do vulval squamous cell cancers develop from?

A

“Precancerous” pre-invasive areas called VUlval intraepithelial neoplasia

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7
Q

What are the 2 subtypes of sq vulval cancer?

A
  • HPV associated (younger women)

- Older women associated with chronic vulval skin changes called vulval dystrophy, including lichen sclerosus

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8
Q

What does squamous hyperplasia show histologically?

A
  • Hyperkeratosis
  • Irregular thickening of ridges
  • Some neoplastic potential
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9
Q

What does lichen sclerosus show?

A
  • Hyperkeratosis
  • Flattening of ridges
  • Oedema in connective tissue with chronic inflammation
  • Some neoplastic potential
  • Sometimes white patches ‘leukoplakia’
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10
Q

What does lichen sclerosis cause?

A

Pruritis

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11
Q

What is lichen sclerosis treated with?

A
  • Potent topical corticosteroids
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12
Q

What percentage of cancers are endometrial?

A

5% of cancers in women

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13
Q

How common is endometrial cancer in relation to other cancers?

A
  • 4th most common

- Causes around 2.5% of cancer deaths

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14
Q

WHat is the lifetime risk of endometrial cancer in women in the UK?

A

2.35%

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15
Q

What is the most common gynaecological cancer?

A
  • Endometrial (UK)

- CErvical (developing)

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16
Q

What are the 2 clinico-pathologicaltypes of endometrial adenocarcinoma?

A 
Endometriod 
- Related to unopposed estrogen 
- Associated with atypical hyperplasia 
- Associated with polycystic ovary syndrome 
Non-endometroid 
- not associated with unopposed estrogen 
- Affects elderly post-menopausal women 
- p53 often mutated
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17
Q

What are the stages of endometrial adenocarcinoma?

A

1 - confined to uterine body
2 - involvement of cervix
3 - Involvement of ovaries/tubes or extension beyond serosa
4 - Spread to other organs

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18
Q

What does endometrial cancer typically present with?

A

Post-menopausal bleeding (post-menopausal bleeding is due to malignancy until proven otherwise)

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19
Q

What are other endometrial tumours other than adenocarcinoma?

A
  • Endometrial stromal sarcoma

- Malignant mixed Mullerian tumour

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20
Q

What are the abnormalities of the myometrium?

A
  • Adenomyosis
    Smooth muscle tumours
  • Leiomyoma (fibroid)
  • Leiomyosarcoma
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21
Q

What is ademyosis?

A
  • Benign disease of uterus due to ectopic endometrial glands and stroma within the myometrium with adjacent reactive myometrial hyperplasia (disease can be diffuse or focal)
  • Causes menorrhagia / dysmenorrhoea
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22
Q

What is leiomyoma?

A
  • Benign SM tumour within the uterus
  • V. common cause of uterine enlargement
  • May undergo degeneration
  • Can be: intramural, submucosal or subserosal
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23
Q

How are fibroids treated?

A
  • Uterine Artery Embolism

- Hysterectomy

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24
Q

What is endometriosis?

A

Endometrial glands and stroma outside the uterine body

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25
Q

What are the sites of endometriosis?

A
  • Ovary ‘chocolate cyst’
  • Pouch of Douglas
  • Peritoneal surfaces, including uterus
  • Cervix, vulva, vagina
  • Bladder, bowel etc
26
Q

What can endometriosis cause?

A
  • Pelvic inflammation
  • Infertility
  • Pain
27
Q

How common are ovarian cysts and when would they be concerning?

A
  • Very common in post-pubertal women

- Would be cause for concern in post-menopausal, pre-pubertal, pregnant or if mean diameter is >3cm

28
Q

What is polycystic ovary syndrome?

A
  • One of the most common endocrine disorders for women of reproductive age
  • May present with hyperandrogenism
  • Can cause type 2 diabetes mellitus, dyslipidaemia, hypertension, CV disease and endometrial carcinoma
  • Not having normal periods
  • Familial
  • Weight gain common
29
Q

What is the treatment for Polycystic Ovary Syndrome (PCOS)?

A
  • Combined oral contraceptive pill - can protect against development of endometrial hyperplasia and cancer and to suppress excessive androgen secretion to control acne and hirsutism
  • Mirena intrauterine system (IUS) - progesterone released very slowly can be good alternative
30
Q

What are women with Polycystic ovary syndrome at higher risk of?

A
  • Endometrial hypeplasia
  • Adenocarcinoma
  • 3 fold increased risk for endometrial cancer
31
Q

What type of imaging technique should be considered for PCOS? (or in presence of abnormal uterine bleeding e.g absence of withdrawal bleeds)

A

Transvaginal US (endometrial thickness of more than 7mm should be biopsied, often with hystoscope)

32
Q

How can ovarian neoplasms be classified?

A
  • Epithelial (90%), derived from surface coelomic epithelium
  • Germ cell
  • Sex-cord / stromal
  • Metastatic
  • Miscellaneous
33
Q

How do epithelial ovarian tumour progress?

A
  • Benign
  • Borderline (cytological abnormalities with no stromal invasion)
  • Amilgnant with stromal invasion
34
Q

What are the symptoms of ovarian cancer and what makes it hard to diagnose?

A
  • Insidious onset means that up to 75% of patients present with synmptoms of advanced disease due to mass effects of the tumour
  • Non-specific GI symptoms such as bloating or indigestion (often misdiagnosed as IBS)
  • Gradually increasing abdo distension
  • Pressing on other things -> pelvic + back pain, urinary frequency, constipation, leg sweeling, DVT
  • Symptoms of metastatic disease include pleural efusion, ascites, weigt loss and fatigue
  • Sudden torision, rupture or infection (Less common)
35
Q

What percentage of ovarian neoplasms are serous adenocarcinoma?

A

50 - 80%

36
Q

How is ovarian cancer treated?

A
  • Surgical management: Exploratory laparotomy for tumour debulking and formal surgical staging
  • MAjor procedure which comprises total abdominal hysterectomy and bilateral salpingo-oopherectomy (BSO), infracolic omentectomy, pelvic and para-aortic lymph node sampling, peritoneal biopsies, multiple pelvic washings, sampling of ascites
  • Adjuvant chemotherapy (>stage1c), often intraperitoneal
37
Q

How can response to ovarian cancer treatment be managed?

A

Monitored using CA-125 levels, decrease if treatment is effective and increase if there is relapse

38
Q

What common cancer treatment is not used in ovarian cancer?

A

Radiotherapy as tumours tend to be very radioresistant

39
Q

What are the types of germ cell tumours?

A
  • Dysgerminoma (undifferentiated)
  • Teratoma (contains all 3 embryonic germ cell layers) (mature cystic teratoma = dermoid cyst)
  • Extraembryonic (yolk sac tumour)
  • Choriocarcinoma
40
Q

What can arise as a result of gestational trophoblastic disease?

A

Choriocarcinoma

41
Q

What is the most common monodermal teratoma?

A

Struma ovarii (thyroid tissue)

42
Q

What feature in ovarian teratomas is different to testicular ones usually?

A

Ovarian are usually benign

43
Q

What are different types of sex cord/stromal tumours?

A
  • Fibroma / Thecoma
  • Granulosa cell tumour
  • Sertoli-Leydig cell tumours
44
Q

Where can metastases on the ovary come from?

A
  • Stomach
  • Colon
  • Breast
  • Pancreas
    (always to be considered especially if bilateral)
45
Q

What are different gestational trophoblastic diseases?

A
  • Hyadiform mole
  • Invasive mole
  • Choriocarcinoma
  • Placental-site trophoblastic tumour
  • Epithelioid trophoblastic tumour
46
Q

How common are molar pregnancies?

A

1 for every 714 live births

47
Q

What are the 2 types of Hydatidiform mole?

A
  • Complete hydatidiform mole - sperm cells fertilise empty egg cell
  • Partial hydatidiform mole - 2 sperms fertilise normal egg (non-viable fetus)
48
Q

What is an invasive mole?

A

Hydatidiform mole that has grown into the myometrium

49
Q

What type of Hydatidiform mole is more liekly to become invasive?

A
  • Complete moles more often become invasive than partial
50
Q

How often do invasive moles develop in those who have had a complete mole removed?

A

1 out of 5

51
Q

Women with hydatidiform moles will have higher levels of what hormone compared with normal pregnancy?

A

hCG (can cause extreme morning sickness)

- Test can tell whether it has been completely removed

52
Q

What tissue produces hCG?

A

Trophoblastic tissue

53
Q

What does a hydatidiform mole look like on US?

A

Grapes

54
Q

What is the malignant form of gestational trophoblastic disease called?

A

Choriocarcinoma

55
Q

What percentage of choriocarcinomas start off as molar pregnancies?

A

50%

56
Q

What can increase the risk of choriocarcinoma?

A

Miscarriage, abortion, normal pregnancy (around 50% develop from this)

57
Q

What type of cancer can non-gestational choriocarcinoma develop into?

A

May develop in ovaries, testes, chest or abdomen -> mixed germ cell tumor

58
Q

What is an ectopic pregnancy?

A
  • Implantation of a conceptus outside the endometrial cavity
  • Often ruptures causing fatal intra-abdominal haemorrhage
59
Q

Where is the site of an ectopic pregnancy?

A
  • Commonest site is ampulla of fallopian tube

- May occur in ovary or peritoneum

60
Q

When should ectopic pregancy be considered?

A

Any female of reproductive age with amenorrhoea and acute hypotension or an acute abdomen

61
Q

How is ectopic pregancy treated?

A
  • Methotrexate

- Laparascopic surgical extraction

MD3002 Pathology (19 decks)

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