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Histopathology > Histopathology 5 - Gynaecological pathology > Flashcards

Histopathology 5 - Gynaecological pathology Flashcards

1
Q

Common infectious organisms of the gynaecological tract

A
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2
Q

What organisms cause PID?

A

Gonococci

Chlamydia

Enteric bacteria

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3
Q

Complications of PID

A
  1. Peritonitis:

Inflammation can spread via the fallopian tubes → peritoneal cavity

  1. Intestinal obstruction due to adhesions:

When healing from inflammation → fibrosis → adhesion in the abdominal cavity → obstruction

  1. Bacteraemia:

Spread of infection via blood stream which → systemic spread of infection

  1. Infertility:

Due to adhesions

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4
Q

Complications of salpingitis

A
  • Infertility
  • Fitz-Hugh Curtis
  • Adhesions
  • Chronic pelvic pain
  • Ectopic pregnancy
  • Plical fusion:
  • The fimbrial ends of the fallopian tubes can start adhering together and to the ovary
  • Hydrosalpinx:
  • fallopian tubes are obstructed
  • → fluid continues (inflammatory and biological fluids) to accumulate in the fallopian tube
  • → tube can swell
  • → enlarged fallopian tube filled with fluid
  • Tubo-ovarian abscess
  • Peritonitis
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5
Q

Where does cervical cancer rank in the common cancers affecting women?

A
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6
Q

What general pathology can affect the cervix?

A

Inflammation

Polyps

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7
Q

Risk factors for cervical cancer

A

Human Papilloma Virus (HPV)- present in 95% of cases

Many sexual partners

Sexually active early

Smoking

Immunosuppressive disorders

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8
Q

Which types of HPV cause which lesions?

A

High risk: 16 and 18- can cause low and high grade carcinoma.

Low risk: HPV 6 and 11. causes oral and genital warts.

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9
Q

Difference between CIN and cervical cancer

A

CIN: abnormal cells have not invaded the basement membrane

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10
Q

What is salpingitis?

A

Infection of fallopian tubes

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11
Q

What are the possible complications of untreated salpingitis?

A

Adhesions
Abscesses
Peritonitis
Ectopic pregnancy

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12
Q

What are the high risk forms of HPV for cervical cancer?

A

16 and 18

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13
Q

Recall the stages of progression from normal cervical cells to cervical carcinoma

A

Normal
T positive HPV (abnormal cells)
CIN 1 (lower 1/3 of cells neoplastic)
CIN 2 (2/3 of cells neoplastic)
CIN 3 (full thickness neoplastic)
Carcinoma

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14
Q

What do CIN and CGIN stand for, and what is the main difference between them?

A

CIN = cervical intraepithelial neoplasia
CGIN = cervical glandular intraepithelial neoplasia
CIN progresses to squamous cell carcinoma
CGIN progresses to adenocarcinoma

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15
Q

How does HPV lead to neoplatic transformation of cervical cells?

A

E6 and E7 viral proteins deactivate p53 and Retinoblastoma (tumour suppressor genes)

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16
Q

What age range is invited to cervical screening?

A

25-64

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17
Q

Which HPV strains are included in the quadrivalent vaccine?

A

6,11,16,18

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18
Q

What is leiomyoma of the uterus?

A

Smooth muscle cell tumour of the uterus

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19
Q

What is a fibroid?

A

Leiomyoma

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20
Q

How are fibroids classified?

A

As either intramural, submucosal or subserosal

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21
Q

What is the biggest risk factor for endometrial hyperplasia?

A

Persistent oestrogen

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22
Q

Which is the most common gynaecological cancer in developed countries?

A

Endometrial carcinoma

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23
Q

WHo is at risk of endometrial hyperplasia?

A
  • Occurs in perimenopausal women
  • It can occur in women with persistent anovulation e.g. PCOS:Because in menstrual cycle:
    • there is a surge in oestrogen then ovulation
    • → oestrogen drops and progesterone rises
    • No ovulation:
    • oestrogen surge continues driving proliferation and hyperplasia of endometrium
  • Women with polycystic ovary disease are at risk
  • Granulosa cell tumours from the ovary can produce oestrogen which may result in this
  • Oestrogen therapy (alone i.e. HRT) can also lead to this
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24
Q

Risk factors for endometrial carcinoma

A

Nulliparity

Obesity

DM

Excessive oestrogen stimulation

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25
Q

What is the difference between type 1 and 2 endometrial carcinomas?

A

Type 1: adenocarcinomas (endometroid, mucinous and secretory adenocarcinomas)

  • happen in younger patients
  • are oestrogen dependent

Type 2: Serous/ clear cell carcinoma

  • happen in older women (post menopausal)
  • less oestrogen dependent
  • happen in atrophic endometrium
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26
Q

What is the relative prevelance of type 1 vs type 2 endometrial carcinoma?

A

Type 1 = 80-85%
Type 2 = 10-15%

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27
Q

Recall the genetic associations of serous and clear cell endometrial carcinomas

A

Serous: p53 mutation
Clear cell: PTEN mutation

10 before 53

c before s

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28
Q

Which type of endometrial carcinoma is high grade and which is low grade?

A

Type 1 = low grade
Type 2 = high grade

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29
Q

Which type of endometrial carcinoma is most likely to arise in atrophic endometrium?

A

Type 2

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30
Q

Recall the FIGO stages of endometrial cancer

A

Stage 1: Confined to uterus
Stage 2: Spread to cervix
Stage 3: Spread to adnexa, vagina, local lymph nodes (pelvic/ para-aortic)
Stage 4: Distant metastases

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31
Q

Recall the different types of gestational trophoblastic disease

A

Partial/ complete mole
Invasive mole
Choriocarcinoma

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32
Q

How does gestational trophoblastic disease usually present?

A

As spontaneous abortion

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33
Q

Genetics of complete mole

A

Fertilisation of empty egg by:

  1. one sperm that duplicates its genetic material once fertilised with the egg
  2. 2 sperm

Possible genotypes: 46XX, 46XY (but for some reason not 46YY…)

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34
Q

Genetics of partial mole

A

Egg fertilised by 2 sperm or 1 sperm that hasn’t split

Possible genotypes: 69XXY, 69XYY, 69XXX

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35
Q

Difference between invasive mole and choriocarcinoma

A

Invasive mole: partial or complete mole that invades the uterine wall and beyond

Choriocarcinoma:

  • This is a malignancy of trophoblastic disease
  • RARE: 1 in 20,000-30,000 pregnancies
  • It is rapidly invasive, widely metastasising
  • Responds well to chemotherapy
  • 50% arise in moles
  • 25% arise in previous abortion
  • 22% arise in normal pregnancy
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36
Q

Describe the prognosis of choriocarcinoma

A

Very aggressive but also very responsive to treatment

37
Q

What is endometriosis?

A

Presence of endometrial glands and stroma outside of the uterus - bleeding of ectopic material is painful

38
Q

What is adenomyosis?

A

Ectopic endometrial tissue within the myometrium

39
Q

What is the main symptom of adenomyosis?

A

Dysmennorhoea

40
Q

What are the 3 layers of the ovary?

A

Surface epithelium

Germ cells (this is in the middle)

Sex cord stromal cells (this is what surrounds the germ cells)

41
Q

Primary and secondary neoplastic tumours of the ovaries

A

Primary:

a) specific- epithelial, germ cell, sex cord stromal
b) non-specific- lymphoma, sarcoma

Secondary:

metastasis from intestines, stomach, breast, lymphoma, sarcoma

42
Q

Epidemiology of primary ovarian tumours (**from the lecture**)

A

•Epithelial tumours:

–make up 65% of all ovarian tumours & 95% of malignant ovarian tumours

–50% found in 45-65 age group

•Germ cell tumours:

–have bimodal distribution; one peak 15-21 year olds and one peak at 65-69

•Sex cord stromal tumours:

–most commonly seen in post-menopausal women but some sub-types peak in 25-30 year age group (eg granulosa cell tumours)

43
Q

What type of tumour are 95% of ovarian neoplasms?

A

Epithelial tumours

44
Q

Describe the classification of ovarian epithelial tumours

A

SMEC

45
Q

What type of epithelium are most ovarian carcinomas derived from?

A

Serous

46
Q

Which types of ovarian carcinoma are associated with endometriosis?

A

Endometrioid and clear cell carcinoma (both types of Type 1 epithelial carcinomas)

47
Q

Recall the 4 types of sex cord stromal tumours, and the malignant potential of each.

Which one is associated with endometrial hyperplasia?

A

Fibromas (from fibroblasts) = benign
Granulosa cell tumours = variable behaviour
Thecoma (thecal cells) = benign
Sertoli-Leydig cell tumours = variable behaviour

Granulosa cell tumours are associated with endometrial hyperplasia as they produce oestrogen

48
Q

In what age group of women are germ cell tumours seen?

A

<20s

49
Q

Recall the different types of germ cell tumour in women

A

Undifferentiated germ cells: dysgermioma
Tumour of extra-embryonic tissue: endodermal sinus tumour
Trophoblast tumour: choriocarcinoma
Cancer of embryonic tissue: teratoma

50
Q

Which is the most common malignant ovarian germ cell tumour?

A

Dysgerminoma

Associated with Turner’s syndrome

51
Q

Epidemiology of ovarian cancer

A

6th most common cancer affecting women

2nd most common cause of cancer death in women

52
Q

Risk factors for ovarian cancer

and what decreases risk?

A

1) MOST significant risk factor is genetic predisposition:

Up to 10% of epithelial ovarian cancer cases are familial

10% with ovarian carcinoma are carriers of a breast/ ovarian cancer susceptibility gene

2) Increased oestrogen exposure:

Nulliparity/ Infertility

Early menarche

Late menopause

Hormone replacement therapy

3) Family history of ovarian and breast cancers
4) Endometriosis
5) Inflammation:

pelvic inflammation exposes the lining of the ovary to toxic mediators (lots of cytokines and growth factors)

and makes cells quickly turnover

Both may be mutagenic

RISK DECREASED BY: OCP, PREGNANCY

53
Q

Two types of ovarian cancer

A

Type 1 (low grade) - 20% of tumours. Arise from precursor lesions. Mutations - k-ras.

Type 2 (high grade)- 80% of tumours. Mostly serous. Arise de novo (not from pre-cursor lesions). Mutations - p53

**basc opposite of endometrial cancer

54
Q

Which 3 familial syndromes are related to ovarian cancer?

A

– familial breast-ovarian cancer syndrome (BRCA1 and BRCA2)

– site-specific ovarian cancer

– cancer family syndrome (Lynch type II)

55
Q

What is the significance of BRCA1 and BRCA2 with prognosis for ovarian cancer?

A

in HIGH GRADE serous carcinoma- having BRCA2 mutation confers survival advantage over having no BRCA mutations or BRCA1 mutation

**low grade serous carcinoma doesn’t show association with BRCA1 and BRCA2

56
Q

Which ovarian tumour is lynch syndrome associated with?

A

endometroid and clear cell

**same as those associated with endometriosis

57
Q

Recall 2 types of cancer that commonly metastasise to the ovary

A

Krukenburg tumours- from gastric or breast mucosa
Colon cancer

58
Q

Which site in female genital tract receives the most metastases?

A

Ovaries

59
Q

Do most leiomyosarcomas arise de novo or from precursor lesions?

A

Usually de novo lesions rather than from fibroid precursor

60
Q

Classification of ovarian tumours: path guide

A

1) epithelial (70%)

  • endometroid
  • serous
  • mucinous
  • clear cell

2) sex cord stromal (20%)

  • fibroma
  • thecoma
  • sertoli-leydig cell tumour
  • (granulosa)

3) germ cell (10%)

  • dysgerminoma
  • teratoma
  • yolk sac
  • choriocarcinoma

4) metastatic
* krukenburg tumour

61
Q

Histopathology of serous cystadenomas

A
62
Q

Mucinous cystadenoma histology

A
63
Q

What is pseudomyxoma peritonei?

A

Presence of mucin in the peritoneal cavity

caused by mucinous cystadenomas

64
Q

Which is the most common oestorgen secreting ovarian tumour?

A

Mucinous cystadenoma

65
Q

Which mutation is found in mucinous cystadenoma of the ovary?

A

K-ras mutation in 75%

66
Q

Serous vs mucinous cystadenoma of the ovary

A

Serous: columnar epithelium (mimics tubal), psammoma bodies, affects women in 30s-40z

Mucinous: mucin secreting cells (mimcis endocervical mucosa), no psammoma bodies, affects younger women

67
Q

Which ovarian tumour is endometriosis a risk factor for?

A

Endometroid

68
Q

Clear cell tumour of the ovary: histology

A

Abundant clear cytoplasm - intracellular glycogen

Hobnail appearance

69
Q

What is the prognosis of clear cell tumours of the ovary?

A

Malignant with poor prognosis

70
Q

What is dysgerminoma?

A

Female counterpart of testicular seminoma

*rare, but most common ovarian malignancy in young women senistive to radiotherapy

71
Q

What is the most common malignant germ cell tumour?

A

Dysgerminoma

72
Q

What is the most common ovarian tumour in young women? (15-21)

A

Teratoma

73
Q

Two types of teratomas

A

Mature: aka demroud cyst. 95% of teratomas. Benign, usually cystic. Differentiate into mature tissues (skin, hair, teeth). Usually bilateral, aasymptomatic.

Immature: malignant, usualy solid, contains immature, embryonal tissues. secrete AFP

74
Q

What are the 4 sex cord stromal tumours and their distinguishing features?

A
75
Q

What is normal vulval histology?

A

Squamous epithelium

76
Q

Which HPV causes VIN?

A

HPV-16

77
Q

Two types of VIN

A

1) usual type
- women aged 35-55y
- associated with warty/basaloid SCC
2) differentiated type
- common in older women
- higher risk of malignant transformation

78
Q

Describe the normal cervical epithelium

A

Outer cervix covered by squamous epithelium; endocervical canal lined by columnar glandular epithelium. The squamocolumnar junction (SCJ) separates them.

79
Q

What is the transformation zone?

A

Transformation zone (TZ): the area where columnar epithelium transforms into squamous cells (=squamous metaplasia). This is a normal physiological process. This area is susceptible to malignant change

80
Q
A
81
Q

How do you define CIN?

A

Dysplasia at the TZ as a result of infection by HPV 16 & 18.

82
Q

Cytology vs histology of CIN

A

Graded mild, moderate or severe dyskaryosis on cytology, but graded CIN 1-3 on histology (from biopsy).

● CIN 1 = dysplasia confined to lower 1/3 of epithelium

● CIN 2 = lower 2/3

● CIN 3 = full thickness, but basement membrane intact

83
Q

Cervical cancer epidemiology

A

2 peaks in incidence

one at 30-39 y

one at 70+ y

84
Q

Which ovarian tumour is associated with Meig syndrome?

A

Fibroma

Meig syndrome: ascites + pleural effusion

85
Q

Powder burn spots

A

Endometriosis

86
Q
A
87
Q

Which ovarian tumour has psammoma bodies?

A

Serous cystadenoma

88
Q

What syndrome are fibromas associated with?

A

Meig’s syndrome

Right sided pleural effusion + ascites + fibroma

Histopathology (18 decks)

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