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YEAR 5: Histopathology AS > Histo: Gynaecological pathology > Flashcards

Histo: Gynaecological pathology Flashcards

1
Q

List some gynaecological infections that cause discomofrt but no serious complications.

A
  • Candida
  • Trichomonas vaginalis
  • Gardnerella
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2
Q

List some gynaecological infections that cause serious complications.

A
  • Chlamydia (infertility)
  • Gonorrhoea (infertility)
  • Mycoplasma (spontaneous abortion and chorioamnionitis)
  • HPV (cancer)
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3
Q

What is the term used to describe infection of the entire female genital tract?

A

Pelvic inflammatory disease

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4
Q

What are the usual causes of pelvic inflammatory disease?

A
  • Gonococci
  • Chlamydia
  • Enterococci
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5
Q

List some complications of pelvic inflammatory disease.

A
  • Peritonitis
  • Intestinal obstruction due to adhesions
  • Bacteraemia
  • Infertility
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6
Q

List some complications of salpingitis.

A
  • Plical fusion
  • Adhesions to the ovary
  • Tubo-ovarian abscess
  • Peritonitis
  • Hydrosalpinx
  • Infertility
  • Ectopic pregnancy
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7
Q

What is an ectopic pregnancy?

A

When the fertilised ovum implants outside the uterus (e.g. in the Fallopian tube)

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8
Q

List some risk factors for cervical cancer.

A
  • HPV
  • Many sexual partners
  • Sexually active early
  • Smoking
  • Immunosuppression
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9
Q

What strains of HPV are considered:

  • High risk
  • Low risk
A
  • High risk = 16, 18
  • Low risk = 6, 11

NOTE: these can cause genital and oral warts and low-grade cervical abnormalities

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10
Q

What is the outcome of HPV infection in most people?

A
  • Undetectable within 2 years in 90% of people
  • Persistent infection is associated with high-risk HPV types
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11
Q

What feature of high-risk HPV viruses are responsible for the carcinogenic effects of HPV?

A
  • E6 protein - inactivates p53
  • E7 protein - inactivates retinoblastoma
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12
Q

What are the two types of HPV infection? Describe them.

A
  • Latent (non-productive)
    • HPV DNA continues to reside within basal cells
    • Infectious virions are not produced
    • Replication of viral DNA is coupled to replication of epithelial cells
    • This means that complete viral particles are not produced
    • Cellular effects of HPV are not seen
  • Productive
    • Viral DNA replication occur independently of host chromosomal DNA synthesis
    • Large amount of viral DNA and infectious virions are produced
    • Characteristic cytological and histological featuers are seen (halo around the nucleus - koilocyte)
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13
Q

What is the cervical transformation zone?

A

This is the point at which the stratified squamous epithelium becomes columnar epithelium.

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14
Q

Describe the classification of cervical intraepithelial neoplasia.

A
  • CIN1 = lower 1/3 of the epithelium
  • CIN2 = lower 2/3 of the epithelium
  • CIN3 = entire epithelium
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15
Q

In which type of epithelium does CIN occur?

A

Usually squamous

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16
Q

What is the term used to describe CIN occurring in columnar epithelium?

A

Cervical glandular intraepithelial neoplasia (CGIN)

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17
Q

What are the two types of cervical cancer?

A
  • Squamous cell carcinoma
  • Adenocarcinoma (20%)
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18
Q

Which staging system is used for cervical cancer?

A

FIGO staging

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19
Q

Outline the screening intervals for cervical cancer screening.

A
  • 25-49 = every 3 years
  • 49-64 = every 5 years
  • 65+ = if no screening since 50 or if abnormal test results
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20
Q

Other than CIN, what else is screened for in some centres?

A
  • High risk HPV using molecular genetic analysis
  • Hybrid captue II (HC2) HPV DNA test - smear is mixed with fluid containing RNA probes that match 5 low-risk and 13 high-risk types of HPV
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21
Q

What are the two HPV vaccines that are currently available?

A
  • Bivalent = 16 + 18
  • Quadrivalent = 6 + 11 + 16 + 18

NOTE: vaccination is done in girls aged 12 years

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22
Q

List some diseases of the uterine body.

A
  • Congenital anomalies
  • Inflammation
  • Adenomyosis
  • Dysfunctional uterine bleeding
  • Enodetrial atrophy/hyperplasia
  • Leiomyoma
  • Endometrial polyp
  • Tumours
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23
Q

What is a leiomyoma? Outline its key features.

A
  • A benign smooth muscle cell tumour in the uterus (MOST COMMON uterine tumour)
  • Present in > 20% of women > 35 years
  • Often multiple
  • Usually asymptomatic
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24
Q

What are the three types of leiomyoma?

A
  • Intramural
  • Submucosal
  • Subserosal
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25
Q

What is endometrial hyperplasia?

A
  • Increase in stromal and glandular tissue of the endometrium
  • Usually driven by oestrogen
  • Usually occurs in the perimenopausal period
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26
Q

List some causes of endometrial hyperplasia.

A
  • Persistant anovulation (due to persistently raised oestrogen)
  • PCOS
  • Granuloma cell tumour of the ovary
  • Oestrogen therapy
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27
Q

List some risk factors for endometrial carcinoma.

A
  • Nulliparity
  • Obesity
  • Diabetes mellitus
  • Excessive oestrogen stimulation
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28
Q

What are the subtypes of type I endometrial carcinoma?

A
  • Endometrioid adenocarcinoma
  • Mucinous adenocarcinoma
  • Secretory adenocarcinoma
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29
Q

What are the key features of type I endometrial carcinoma?

A
  • Younger patients
  • Oestrogen-dependent
  • Often associated with atypical endometrial hyperplasia
  • Low-grade tumours that are superficially invasive
  • Genetic mutations: PTEN, P13KCA, K-Ras, CTNNB1, FGFR2, p53
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30
Q

What are the subtypes of type II endometrial carcinoma?

A

Serous and clear cell tumours

31
Q

What are the key features of type II endometrial carcinoma?

A
  • Older patients
  • Less oestrogen-dependent
  • Arise in atrophic endometrium
  • High grade, deeper invasion and higher stage
32
Q

Which genetic mutations are associated with the two types of type II endometrial carcinoma?

A

Endometrial Serous Carcinoma

  • P53 (90%)
  • P13KCA (15%) Her2 amplification

Clear Cell Carcinoma

  • PTEN
  • CTNNB1
  • Her2 amplification
33
Q

List some prognostic factors in endometrial carcinoma.

A
  • Type
  • Grade
  • Stage
  • Tumour ploidy (diploid has a better prognosis)
  • Hormone receptor expression
34
Q

What is:

  • FIGO Stage I
  • FIGO Stage 4
A
  • FIGO Stage I = confined to the uterus
  • FIGO Stage 4 = Other pelvic organs outside uterus, adnexae and vagina and other distant spread (e.g. distant lymph nodes)
35
Q

What is gestational trophoblastic disease?

A

A spectrum of tumours characterised by proliferation of pregnancy-associated trophoblastic tissue

36
Q

List three types of gestational trophoblastic disease.

A
  • Complete and partial mole
  • Invasive mole
  • Choriocarcinoma
37
Q

What is the prevalence of complete and partial moles?

A

1 in 1000 pregnancies

38
Q

How do complete and partial moles present?

A

Spontaneous abortion

Sometimes detected as abnormal ultrasound

39
Q

What is a characteristic investigation finding in complete and partial moles?

A

Very very high hCG

40
Q

What are the chances of moles progressing to malignancy?

A
  • NO partial moles progress to malignancy
  • 2.5% of complete moles progress to malignancy
  • 10% of complete moles develop into locally destructive invasive moles
41
Q

Describe how complete and partial moles form.

A

Complete mole

  • Occurs when you get fertilisation of an EMPTY egg
  • Reduplication of the 23X from sperm results in a homozygous diploid 46XX genome
  • Can also occur due to fertilisation of an empty egg by 2 sperms with 2 independent sets of 23X or 23Y

Partial mole

  • A normal ovum containing 23X gets fertilised by TWO sperm leading to the presence of 3 sets of chromosomes (2 paternal + 1 maternal)
  • Dispermia → diandry
  • Overdose of male chromosomes driver proliferation
  • Can also occur due to fertilisation of a normal egg by a sperm carrying unreduced paternal genome (46XY)
42
Q

What is choriocarcinoma?

A
  • Rare (1 in 20,000) rapidly invasive and widely metastasising tumour
  • Responds well to chemotherapy
  • 50% arise in moles
  • 25% arise in patients with previous abortion
  • 22% arise in normal pregnancy
43
Q

What is endometriosis?

A

Presence of endometrial tissue outside the uterus

44
Q

Outline the possible pathogenesis of endometriosis.

A
  • Metaplasia of pelvic peritoneum
  • Retrograde menstruation - endometrial lining travels up the fallopian tubes, into the peritoneal cavity and implants outside the uterus
45
Q

Why is endometriosis an issue?

A
  • It is functional and bleeds at the time of menstruation
  • Can lead to pain, scarring and infertility
  • May develop hyperplasia or malignancy
46
Q

What is adenomyosis?

A
  • Ectopic endometrial tissue deep within the myometrium
  • Causes dysmenorrhoea (because it bleeds into the muscle layer and causes pain)
47
Q

List two types of non-neoplastic functional cysts.

A
  • Follicular and luteal cysts
  • Endometriotic cyst
48
Q

What are some manifestations of polycystic ovarian syndrome?

A
  • Persistant anovulation
  • Obesity
  • Hirsutism
49
Q

What three types of tissue do ovaries consist of?

A
  • Surface epithelium
  • Ovarian stroma
  • Germ cells
50
Q

List three types of primary specific ovarian tumour.

A
  • Surface epithelial tumours
  • Sex cord stromal tumours
  • Germ cell tumours
51
Q

List some risk factors for ovarian cancer.

A
  • Nulliparity
  • Early menarche
  • Late menopause
  • Genetic predisposition (MOST SIGNIFICANT)
  • Infertility
  • Endometriosis
  • HRT
  • Inflammation (PID)
52
Q

List some protective factors for ovarian cancer.

A
  • After pregnancy
  • OCP
53
Q

Outline the classification o epithelial ovarian tumours.

A

Type 1

  • Low grade
  • Relatively indolent and arise from well characterised precursors (benign tumours) and endometriosis
  • Mutations: K-Ras, BRAF, P13KCA, Her2, PTEN, beta-catenin

Type 2

  • HIGH GRADE
  • Aggressive
  • P53 mutation in 75% of cases
  • NO precursor lesion
54
Q

Give examples of Type 1 and Type 2 ovarian tumours.

A
  • Type 1 = low grade serous, endometrioid, mucinous and clear cell
  • Type 2 = mostly serous
55
Q

List some benign ovarian tumours.

A
  • Serous cystadenoma
  • Cystadenofibroma
  • Mucinous cystadenoma
  • Brenner tumour
56
Q

What are borderline tumours?

A
  • Tumours where their biological behaviour cannot be predicted based on histology
  • Low but definite malignant potential
57
Q

What are the key features of serous tumours?

ovarian cancer

A
  • MOST COMMON type of ovarian tumour
  • Usually cystic
  • 30-50% bilateral
  • Benign tumours are lined by bland epithelium
  • Borderline tumours have a more complex, atypical epithelial lining with papillae but no invasion through the basement membrane
  • Malignant tumours are invasive with a poor prognosis
58
Q

What are the key features of mucinous tumours?

ovarian

A
  • 10-20% of ovarian tumours
  • Composed of mucin-secreting epithelium (may resemble endocervical or GI epithelium)
59
Q

What are the key features of endometrioid tumours?

ovarian

A
  • 10-24% of ovarian tumours
  • 10-20% associated with endometrisis
  • Better prognosis than mucinous and serous
60
Q

What are the key features of clear cell tumours?

ovarian

A

Strong association with endometriosis

NOTE: called clear cell because the cytoplasm contains a lot of glycogen

61
Q

List four types of sex cord stromal tumours.

A
  • Fibroma
  • Granulosa cell tumour (may produce oestrogen)
  • Thecoma (may produce oestrogen (rarely androgens))
  • Sertoli-Leydig cell tumour (may be androgenic)
62
Q

What are the key features of germ cell tumours?

A
  • 20% of ovarian tumours
  • 95% are benign
  • Mainly occur in < 20 years
  • Classified based on how they differentiate
63
Q

What are the four main types of germ cell tumour?

A
  • Dysgerminoma - no differentiation
  • Teratoma - from embryonic tissues
  • Endodermal sinus tumour - from extraembryonic tissue (e.g. yolk sac)
  • Choriocarcinoma - from trophoblastic cells which would form the placenta
64
Q

What are the key features of a mature teratoma?

A
  • Most common type of germ cell tumour
  • Benign
  • May show different lines of maturation but all tissues will mature to adult-type tissues
  • Teeth and hair are common
65
Q

What are the key features of an immature teratoma?

A
  • Indicates presence of embryonic elements (most commonly neural tissue)
  • Malignant tumour that grows rapidly, penetrates the capsule and forms adhesions
  • Spreads within peritoneal cavity and metastasis to the lymph nodes, lungs, liver and other organs
66
Q

What is a mature cystic teratoma with malignant transformation?

A

When any type of mature tissue within a teratoma becomes malignant (most commonly squamous cell carcinoma)

67
Q

Name two secondary ovarian tumours.

A
  • Krukenberg Tumour - bilateral metastases composed of mucin-producing signet ring cells (usually from breast or gastric cancer)
  • Metastatic colorectal cancer
68
Q

What proportion of ovarian tumours are familial?

A

Up to 10%

69
Q

List three familial syndromes associated with ovarian cancer.

A
  • Familial breast-ovarian cancer syndrome
  • Site-specific ovarian cancer
  • Cancer family syndrome (Lynch type II)
70
Q

List some specific genetic associations for serous, mucinous and endometrioid carcinoma.

A
  • Serous - BRCA
  • Mucinous and endometrioid - HNPCC
71
Q

What is lichen sclerosus?

A

Thinning of the vulval epithelium with a layer of hyalinisation underneath

72
Q

Name a benign tumour of the vulva.

A

Papillary hidradenoma

73
Q

List some other types of malignant tumour of the vulva.

A
  • Squamous cell carcinoma (85%)
  • Paget’s diase (adenocarcinoma in situ)
  • Adenocarcinoma
  • Malignant melanoma
  • BCC
74
Q

What are some diseases that can affect the vagina?

A
  • Congenital anomalies (e.g. atresia)
  • Tumours (rare)
  • Carcinoma (squamous cell carcinoma)
  • Adenocarcinoma (increased risk of clear cell carcinoma in women with threatened miscarriage treated with diethyl stillbosterol)
  • Rhabdomyosarcoma

YEAR 5: Histopathology AS (20 decks)

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