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a path 3 > HISTO: Gynaecological Pathology > Flashcards

HISTO: Gynaecological Pathology Flashcards

1
Q

Which classification is used for neoplasia in the female genital tract?

A

FIGO - updated every 2 years by WHO

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2
Q

Name two types of congenital anomalies in gynae.

A

Duplication

Agenesis

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3
Q

What is inflammation of diffferent parts of the gynae tracts called?

A
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4
Q

Name 3 infections of the female genital tract that can cause discomfort but no serious complications.

A

Cause discomfort but no serious complications:

–Candida: Diabetes mellitus, oral contraceptives and pregnancy enhance development of infection

–Tichomonas vaginalis: protozoan

–Gardenerella: gram negative bacillus causes vaginitis

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5
Q

Name 3 infections of the female genital tracts that have serious complications,

A

–Chlamydia: major cause of infertility

–Gonorrhoea: major cause of infertility

–Mycoplasma: causes spontaneous abortion and chorioamnionitis

–HPV: implicated in cancer

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6
Q

What are the causes of PID?

A

Gonococci, chlamydia, enteric bacteria –usually starts from the lower genital tract and spreads upward via mucosal surface

Staph, strept, coliform bacteria and clostridium perfringens

  • –secondary to abortion
  • –usually start from the uterus and spread by lymphatics and blood vessels upwards
  • –deep tissue layer involvement
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7
Q

What are the complications of PID?

A
  • Peritonitis
  • Bacteraemia
  • Intestinal obstruction due to adhesions
  • Infertility
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8
Q

What is the aetiology of salpingitis?

A

Ususally direct ascent from vagina

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9
Q

What are the complications of salpingitis, if it remains unresolved?

A

Depending on severity and treatment may result in:

–Resolution

–Complications:

  • Plical fusion
  • Adhesions to ovary
  • Tubo-ovarian abscess
  • Peritonitis
  • Hydrosalpinx
  • Infertility
  • Ectopic pregnancy
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10
Q

Where do most ectopic pregnancies present?

A

Tubal 95%

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11
Q

Name 3 disorders of the cervix.

A
  • Inflammation
  • Polyps
  • Dysplasia and carcinoma
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12
Q

What is shown?

A

Cervical polyp

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13
Q

How common is cervical cancer? What is the mean age?

A
  • 2nd most common cancer affecting women worldwide
  • Mean age 45-50yrs
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14
Q

What is the premalignant phase of cervical cancer?

A

Cervical intraepithelial neoplasia

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15
Q

What are the risk factors for cervical cancer?

A
  • Human Papilloma Virus -present in 95%
  • Many sexual partners
  • Sexually active early
  • Smoking
  • Immunosuppressive disorders
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16
Q

Which are low risk HPVs? What do they cause?

A

Most common types: 6, 11

Other types: 40, 42, 43, 44, 54, 61, 72, 73, 81

Cause:

  • Genital and oral warts
  • Low grade cervical abnormalities
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17
Q

What are the high risk HPVs? What do they cause?

A

Most common types: 16, 18

Other types: 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68,82

Cause:

  • Low & high grade cervical abnormalities
  • Cervical cancer
  • Vulval, vaginal, penile, and anal cancer
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18
Q

What types of cells are present in the ecto and endocervix?

A

SJC = squamo columnar junction

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19
Q

Describe the progression of cervical epithelium to carcinoma.

A
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20
Q

What defines the progression from CIN to carcinoma?

A

Invasion of the basement membrane

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21
Q

Describe the differences between LSIL and HSIL and dyskaryosis.

A
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22
Q

Define CIN. What is the cause?

A

This is the term for dysplasia of cervical cells

  • Epithelial cells have undergone some phenotypic and genetic changes which are premalignant and preinvasive
  • Basal membrane immediately deep to the surface epithelium is intact
  • Squamous epithelium is involved more often than glandular epithelium (CGIN)
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23
Q
A
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24
Q

What defines cervical carcinoma? What are the two types?

A

Invasion through the basement membrane defines change from CIN to invasive carcinoma

Two types of cervical cancer

  • Squamous cell carcinoma
  • Adenocarcinoma (20% of all invasive cases)
    • HPV dependent or independent
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25
Q

What types of cervical cancer are these?

A

Squamous cell carcinoma (left)

Adenocarcinoma (right)

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26
Q

What factors does prognosis of cervical cancer depend on?

A
  • Tumour type
  • Tumour grade
  • Tumour stage: FIGO Stage I (90%) – IV (10%) 5 year survival
  • Lymphovascular space invasion
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27
Q

What happens when someone is infected with HPV?

A

Transient infection - For most people, nothing will happen

  • The body’s immune system eliminates HPV
  • HPV becomes undetectable within 2 yrs in ~90%
  • Relatively few will develop symptoms

HPV viral persistence - Persistent infection with high-risk HPV types is associated with pre-cancerous and cancerous cervical changes

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28
Q

What two proteins are encoded by the virus and have transforming genes?

A

Two proteins E6 and E7 encoded by the virus have transforming genes.

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29
Q

What is the pathophysiology of E6 and E7 presence in HPV?

A

E6 and E7 bind to and inactivate two tumour suppressor genes:

  • Retinoblastoma gene (Rb) (E7)
  • P53 (E6)

Both effects interfere with apoptosis and increase unscheduled cellular proliferation both of which contribute to oncogenesis.

Infection is either latent or productive.

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30
Q

What are the two distinct biological states of HPV infection?

A

A- Non productive or latent infection

B- Productive viral infection

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31
Q

What happens in productive viral infection with HPV?

A

Viral DNA replication occurs independently of host chromosomal DNA synthesis.

Large numbers of viral DNA are produced and result in infectious virions.

Characteristic cytological and histological features are seen

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32
Q

What happens in non productive or latent infection of HPV?

A
  • HPV DNA continues to reside in the basal cells
  • Infectious virions are not produced
  • Replication of viral DNA is coupled to replication of the epithelial cells occurring in concert with replication of the host DNA
  • Complete viral particles are not produced
  • The cellular effects of HPV infection are not seen
  • Infection can only be identified by molecular methods
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33
Q

What are the screening intervals for cervical cancer?

A
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34
Q

What is the sensitivity of cervical screening?

A

Cervical cytology has a sensitivity ranging between 50% - 95% and specificity of at most 90% in detecting high grade CIN and SCC.

Now screening is focusing on detection of high risk HPV by molecular genetic approaches.

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35
Q

Which assay is available for detection of HPV?

A

Hybrid Capture II (HC2) HPV DNA Test - a nucleic acid solution hybridization assay with signal amplification that uses long synthetic RNA probes complementary to the DNA sequence of:

  • 5 low-risk HPV types ( types 6, 11, 42, 43 and 44)
  • 13 high risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68).

RNA probe cocktails to the most common cancer-associated HPV types

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36
Q

What are the benefits of the HPV vaccine? What ages is it offered to? How many doses?

A

The vaccine helps protect against cancers caused by HPV, including:

  • cervical cancer
  • some cancers of the anal and genital areas and genital warts
  • some head and neck cancers

Girls and boys aged 12 to 13 years are offered the HPV vaccine as part of the NHS vaccination programme.

In England, they are routinely offered the 1st dose when they’re in school Year 8, and the 2nd dose is offered 6 to 24 months after the 1st dose.

It’s important to have both doses of the vaccine to be properly protected.

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37
Q

What are the layers of the uterine body?

A

Endometrium:

  • Glands
  • Stroma

Myometrium

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38
Q

What are the indications for uterine biopsies?

A

Endometrium:

  • Infertility
  • Uterine bleeding
  • Thickened endometrium on imaging

Uterus or related mass:

  • Lesion identified on imaging
  • As part of a wider resection
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39
Q

List 5 pathologies affecting the uterine corpus.

A
  • Congenital anomalies
  • Inflammation: acute or chronic
  • Adenomyosis
  • Dysfunctional uterine bleeding: e.g. hormonal imbalance
  • Endometrial atrophy and hyperplasia
  • Endometrial polyp
  • Uterine tumours
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40
Q

What are the types of tumours of the uterus?

A
  1. Endometrial epithelial tumours and precursors
  2. Mesenchymal tumours specific to the uterus
  3. Mixed epithelial and mesenchymal tumours
  4. Miscellaneous tumours
  5. Tumour like lesions; e.g. endometrial polyp
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41
Q

What are the causes of endometrial hyperplasia?

A
  • Perimenopause
  • Persistent anovulation
  • Polycystic ovary (PCO)
  • Ovarian Granulosa cell tumours
  • Oestrogen therapy
  • May be associated with atypia
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42
Q

What is the most common gynaecological malignancy in developed countried?

A

Endometrial cancer

43
Q

What are the risk factors for endometrial cancer?

A
  • Nulliparity
  • Obesity
  • Diabetes mellitus
  • Excessive oestrogen stimulation
44
Q

What factors affect prognosis and plan for therapy in endometrial cancer?

A
  • Histological tumour type
  • Tumour grade
  • Tumour stage
  • Lymphovascular space invasion
45
Q

What are the histological subtypes of endometrial cancer?

A
  • Endometrioid
  • Serous
  • Clear cell
  • Undifferentiated
  • Mixed cell
  • Mesonephric
  • Squamous cell
  • Mucinous
  • Mesonephric-like
  • Carcinosarcoma
46
Q

Describe the features of endometrioid carcinoma? What do they depend on? What are they associated with?

A
  • Most common endometrial carcinoma
  • Oestrogen dependent
  • Often associated with atypical endometrial hyperplasia
  • Can be low grade and high grade tumours
  • Develop through the accumulation of mutations of different genes
47
Q

What are the features of serous and clear cell tumours? What are they dependent on? What grade? Who is most affected?

A
  • Less oestrogen dependent
  • High grade by definition, deeper invasion, higher stage
  • Arise in atrophic endometrium
  • Older, postmenopausal
48
Q

What mutations may be implicated in endometrial serous carcinomas and clear cell carcinomas?

A

Endometrial serous carcinoma

  • P53 mutations in 90%
  • PI3KCA mutations in 15% Her-2 amplification

Clear cell carcinoma

  • PTEN mutation
  • CTNNB1 mutation
  • Her-2 amplification
49
Q

What are the most common mutations in these endometrial cancers?

  1. Endometrioid
  2. Clear cell carcinoma
  3. Serous carcinoma
A
  1. Endometrioid - PTEN >50%
  2. Clear cell carcinoma - PTEN 30-40%
  3. Serous carcinoma - P53 90%
50
Q

Which endometrial tumours are high grade?

A
  • serous,
  • clear cell,
  • mixed,
  • undifferentiated,
  • dedifferentiated
  • carcinosarcoma

…are considered high grade.

51
Q

How many grades of endometrioid carcinoma are there?

A

FIGO 3 tier system: grade 1, 2 and 3 depending on

  • Architecture: % of gland formation
  • Cytological atypia

NB: the other types are not graded e.g. serous, clear cell, mixed.

52
Q

Summarise the FIGO staging for carcinoma of the endometrium.

A

Stage I Tumour confined to the corpus uteri

  • IA No or less than half myometrial invasion
  • IB Invasion equal to or more than half of the myometrium

Stage II Tumour invades cervical stroma

Stage III Local and/or regional spread of the tumour

  • IIIA Tumour invades the serosa of the corpus uteri and/or adnexa
  • IIIB Vaginal and/or parametrial involvement
  • IIIC Metastases to pelvic and/or para-aortic lymph nodes
    • IIIC1 Positive pelvic nodes
    • IIIC2 Positive para-aortic lymph nodes with or without positive pelvic lymph nodes

Stage IV Tumour invades bladder and/or bowel mucosa, and/or distant metastases

  • IVA Tumour invasion of bladder and/or bowel mucosa
  • IVB Distant metastases, including intra-abdominal metastases and/or inguinal lymph nodes
53
Q

How was The Cancer Genoma Atlas (TCGA) made? What is its purpose?

A

Tumours were analysed using a variety of modalities, including:

  • Exome sequencing
  • Somatic copy number alteration
  • Whole genome sequencing
  • DNA methylation
  • mRNA expression
  • Protein expression
  • microRNA expression

When this profiling is applied then endometrial cancers are split into 4 distinct categories. It is likely that TCGA classification may become the mainstay of endometrial carcinoma diagnosis in the coming years.

  • Group 1: EEC with mutations in POLE (Polymerase E- ultramutated)
  • Group 2: EEC with MSI (hypermutated)
  • Group 3: EEC with low copy number alterations
  • Group 4: (serous-like) tumours show TP53 mutations and high copy number alterations

NB: the survival with each.

54
Q

How does POLE mutant present in endometrial cancer?

A

Appear to be high grade with poor prognosis at first but actually better prognosis

So important to identify this group

55
Q

What is the role of the mismatch repair system/genes? What happens if dysregulated?

A

A fundamental cellular mechanism for preventing DNA alteration that are created largely during DNA replication

Mutations or silencing by hypermethylation of one of the DNA mismatch repair genes

  • —>results in Microsatellite instability (MSI) (Group 2 TCGA)
  • –> alterations in the length of short, repetitive DNA sequences called microsatellites.
  • —> increase of the rate of mutations contributing to tumorigenesis, again with a high mutation burden.
56
Q

What is the significance of MSI in endometrioid carcinoma?

A

HMLH1 (A), PMS2 (B), MSH2 (C) and MH6 (D) show strong nuclear expression in tumour cells of endometrioid carcinoma.

57
Q

What treatment are EECs exhibiting POLE mutations and MSI sensitive to? Why?

A

EECs exhibiting POLE mutations and MSI are hypersensitive to the immune checkpoint inhibitor, anti-PD-1, monotherapy because,

  • these tumours are characterised by a high mutation load which produces more neo-antigens.
  • they have a higher number of tumour infiltrating lymphocytes.

So TCGA is useful in deciding whether immunotherapy is important.

58
Q

What mutations do TCGA group 4 tumours shown?

A

TP53 mutations and high copy number alterations

Composed mostly of SCs, but also include some EEC; many grade 3 but also some grades 1 and 2

59
Q
A
60
Q

What is the commonest uterine tumour? What does it consist of?

A

Leiomyoma aka fibroids = smooth muscle tumour of myometrium

61
Q

Where can leiomyomas occur? How common are they?

A
  • 20% of women >35yrs
  • Usually multiple
  • May be intramural, submucosal or subserosal
62
Q

What are leiomyosarcomas? How do they present? What is the prognosis?

A

Malignant counterpart of leiomyoma - rare

Usually solitary, postmenopausal

Cause local invasion and blood stream spread –> 5yr survival 20-30%

63
Q

Define endometriosis. How common is it?

A

Presence of endometrial glands and stroma outside the uterus

Common – 10% of premenopausal women

64
Q

What is the aetiology of endometriosis? What are the complications?

A

Origin:

  • Metaplasia of pelvic peritoneum
  • Implantation of endometrium, retrograde menstruation

Ectopic endometrial tissue is functional and bleeds at time of menstruation > pain, scarring and infertility

Can develop hyperplasia and malignancy

(NB: can sometimes be mistaken for bowel cancer if in the bowel)

65
Q

How common is polycystic ovarian disease? What is the consequence on ovulation?

A

3-6% of reproductive age women

Persistent anovulation

66
Q

Name 3 non-neoplastic cysts of the ovary.

A

Non neoplastic cysts:

  • Follicular and luteal cysts
  • Polycystic ovarian disease:
  • Endometriotic cyst
67
Q

How are ovarian tumours classified?

A

Primary tumours

  • Epithelial tumours
  • Sex cord-stromal tumours
  • Germ cell tumours
  • Miscellaneous tumours

Secondary tumours

68
Q

What is the most common type of ovarian tumour? When does it usually present?

A

Epithelial tumours

  • 65% of all ovarian tumours & 95% of malignant ovarian tumours
  • 50% found in 45-65 age group
69
Q

What is the epidemiology of germ cell ovarian tumours?

A

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

70
Q

When are sex cord stromal tumours occur?

A

Most commonly seen in post-menopausal women but some sub-types peak in 25-30 year age group

71
Q
A
72
Q

List 3 types of benign epithelial tumours.

A
  • Serous Cystadenomas
  • Cystadenofibromas
  • Mucinous cystadenomas
  • Brenner tumour
73
Q

What is the problem with borderline epithelial tumours of the ovary?

A

Biologic behaviour cannot be predicted on histologic grounds

Low but still metastatic potential but no reliable histological/molecular predictive markers for their behaviour exists

74
Q

Why are malignant epithelial ovarian tumours a common cause of death?

A

Difficult to diagnosis at an early stage

Develops resistance to therapeutic agents

75
Q

What are the risk factors for malignant epithelial tumours of the ovary? What are the genetic risk factors?

A

Nulliparity, infertility, early menarche, late menopause.

Genetic predisposition: Family history of ovarian and breast cancers

3 familial syndromes, all transmitted in an autosomal dominant fashion:

  • familial breast-ovarian cancer syndrome
  • site-specific ovarian cancer
  • cancer family syndrome (Lynch type II)

Familial breast-ovarian cancer and site-specific ovarian cancer syndromes:

  • mutations of the BRCA1 and BRCA2; account for 90% of familial ovarian cancers
76
Q

What % of ovarian cancers are associated with HNPCC? What type of ovarian tumours are these?

A

HNPCC is responsible for 3% of ovarian carcinomas

Ovarian cancers associated are mainly of the endometrioid and clear cell types

77
Q

What mutation is present in virtually all high grade serous carcinomas of the ovary?

A

P53 alterations

Sometimes BRCA1 or BRCA2 abnormalities

78
Q

What is the most common type of malignant tumour of the ovary?

A

High grade serous carcinoma (make up 80% of malignant ovarian tumours)

Aggressive

79
Q

What is the role of BRCA1 and BRCA2 normally?

A

These genes encode proteins that play important roles in DNA repair (homologous recombination).

80
Q

What is the difference in prognosis between BRCA1, BRCA2 and BRCA-negative in high grade serous ovarian cancer?

A

BRCA2 mutations may confer an overall survival advantage

…compared with either being BRCA-negative or having a BRCA1 mutation in high-grade serous ovarian cancer.

81
Q

What is the significance of BRCA mutations in ovarian cancer treatment?

A

Major influence on response to chemotherapy:

Patients can benefit from targeted therapy by PARP inhibitors

82
Q

What mutations are associated with low grade serous carcinomas of the ovary? Where do these tumours arise from?

A
  • Mutations in KRAS, BRAF.
  • No association with BRCA mutations.

Low grade, relatively indolent, arise de novo or from borderline ovarian tumours.

NB: Distinct pathogenesis from high grade serous carcinoma.

83
Q

What mutations are most assocuated with mucinous tumours of the ovary?

A

KRAS

84
Q

Which cancer commonly metastasises to the ovaries?

A

Prone to involvement by metastatic colorectal adenocarcinoma.

  • 4-10% will metastasise to the ovary*
  • Sometimes the ovarian lesions are identified before the primary cancer*
85
Q

What are Krukenberg tumours?

A
  • Bilateral metastases to the ovary composed of mucin producing signet ring cells.
  • Most often of gastric origin or breast.
86
Q

Histopathology of the ovary shows mucin producing signet ring cells. What should you suspect?

A

Krukenberg tumour - secondary ovarian tumour usuallyof gastric or breast origin

87
Q

What do endometrioid carcinomas of the ovary commonly co-exist with? What condition are they associated with?

A

Common co-existence with endometrioid carcinoma in uterus

Only 10-20% associated with endometriosis; most others thought to be derived from surface epithelium

88
Q

What is the most common mutation in endometrioid carcinoma of the ovary?

A

P53 >60% and usually if high endometriosis is a precursor

CTNNB1 (38%-50%)

89
Q

What condition is clear cell carcinoma of the ovary most associated with? What is the most common mutation?

A

Strong association with endometriosis

  • MSI (6-21%)
  • PIK3Ca (20-25%)
90
Q

What are the types of sex cord-stromal tumours of the ovary?

A
  1. Pure stromal tumours: e.g. Fibroma, Thecoma, microcystic stromal tumour
  2. Pure sex cord cells: e.g. Adult type and juvenile granulosa cell tumour
  3. Mixed sex cord-stromal tumours: e.g. Sertoli Leydig cell tumour
91
Q

Which sex cord stromal tumours of the ovary have endocrine production? What hormones?

A
  1. Thecal cells: Thecoma: benign, may secrete oestrogen, or rarely androgens
  2. Granulosa cells: Granulosa cell tumor: variable behaviour, may produce estrogen
  3. Sertoli-Leydig cells: Sertoli-Leydig cell tumor: variable behaviour, may be androgenic
  4. Fibroblasts: Fibromas: benign, no endocrine production
92
Q

What mutation is common in adult type granulosa cell tumour? What is the role of this mutation?

A

97% of adult GCT show somatic mutation of the Forkhead transcription factor FOXL2

FOXL2 = master transcription factor that regulates cell proliferation and apoptosis. Can be used to confrim diagnosis.

93
Q

What mutation is most common in microcystic stromal tumour of the ovary?

A

CTNNB1

Strong nuclear positivity for beta-catenin

94
Q

Name 2 herediatry syndromes which predispose to sex cord-stromal tumours. What mutation is associated with each?

A

DICER1 Syndrome = germline mutation in DICER1, a gene encoding an RNAse III endoribonuclease.

Peutz Jeghers syndrome = germline mutations of STK11

95
Q

What are the clinical features of DICER1 syndrome? Which SCST is it associated with?

A

Familial multinodular goitre with sertoli / leydig cell tumour, and tumour susceptibility includes pleuropulonry blastoma in childhood.

Found in up to 60% of seroli-Leydig cell tumours.

96
Q

What types of ovarian SCST occur in Peutz Jeghers syndrome?

A
  • Sex cord stromal tumour with annular tubules
  • Usually show indolent behaviour
97
Q

When do germ cell tumours usually occur? Are the mostly benign or malignant?

A
  • 20% of ovarian tumours
  • 95% benign

predominantly occur in first or second decade

98
Q

What are the features of a mature teratoma(dermoid)?

A
  • Benign
  • Solid or cystic
  • May show many lines of differentiation but all mature adult type tissues
  • Teeth and hair very common
99
Q

What are the features of immature teratomas e.g. appearance, growth, invasion?

A

Presence of embryonic elements, neural tissue particularly conspicuous

A malignant neoplasm that grows rapidly, penetrates the capsule and forms adhesions to the surrounding structures

100
Q

Where do immature teratomas spread to and how? Where do they metastasise to?

A

Spreads in the peritoneal cavity by implantation

Metastasis to lymph nodes, lung, liver and other organs

101
Q

What is grading of immature teratomas based on?

A

According to amount of primitive elements - three tier grading system

102
Q

How common do mature cystic teratomas undergo malignant transformation? What type of carcinoma results?

A

Rare occurring in 2% of cases, usually in post menopausal women

Most frequently squamous cell carcinoma

103
Q

What are the prognostic factors used in ovarian malignancies?

A
  • Stage of Disease
  • Tumour type
  • Tumor grade
  • Size of residual disease
  • Tumor response to therapy
104
Q
A

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