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Reproductive system > Lecture 23- Reproductive tract tumours > Flashcards

Lecture 23- Reproductive tract tumours Flashcards

1
Q

Tumour-

A

any clinically detectable lump or swellingTumour- any clinically detectable lump or swelling

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2
Q

Neoplasm –

A

an abnormal growth of cells that persists after the initial stimulus is removed

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3
Q

Malignant neoplasm-

A

an abnormal growth of cells that persists after the initial stimulus is removed and invades surround tissue with potential to spread to distant sites

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4
Q

Metastasis-

A

malignant neoplasm that has spread to a distant site

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5
Q

Dysplasia-

A

a potentially pre- neoplastic alteration which cells show disordered organisation and abnormal appearances. May be reversible

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6
Q

Metaplasia-

A

conversion in cell type

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7
Q

features of vulval tumours

A
  • External vagina
  • Rare – 3% of female cancers
  • Older people (peak onset 80-84)
  • Skin cancer
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8
Q

vulval cancer is most commonly

A

squamous cell carcinoma (skin cancer)

  • Can also see basal cell carcinoma or malignant melanoma less commonly
  • Rarely see soft tissue tumours
    • From fat cells, blood vessels and nerves
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9
Q

Precursor to vulval squamous cell carcinoma =

A

Vulval intraepithelial neoplasia (VIN)

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10
Q

Vulval intraepithelial neoplasia (VIN)

A
  • In Situ precursor of vulval squamous cell carcinoma
  • In situ= atypical cells which doesn’t invade basement membrane
  • May or may not progress to SCC
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11
Q

presentation of vulval tumours

A
  • Lumps, bumps, ulceration, skin changes (pigmentation, sensation, pain)
  • May be delayed presentation (due to it being in older patients and also due to the intimate nature of the cancer)
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12
Q

are VIN and Vulval SCC related to HPV?

A

30% of cases are/ 70% are not

  • usually HPV 16
  • mostly in pre-menopasual women
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13
Q

Vin and vulval SCC are usually asscoiated with

A

longstanding inflammtory conditions

  • Lichen sclerosus
  • Squamous hyperplasia
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14
Q

what are the layer sof skin from outr to inner

A

epidermis

dermis

subcutaenous

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15
Q

Squamous cell carcinoma histology

A
  • Loss of architecture
    • Cannot distinguish between dermis and epidermis
  • Atypical squamous cells
  • Keratin formation by squamous cells
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16
Q

How does vulval cancer spread? Locally

A
  • Direct extension
    • Anus
    • Vagina
    • Bladder
  • Lymph nodes
    • Inguinal (predominantly)
    • Iliac
    • Para-aortic
  • Distant metastases via blood vessels
    • Lungs
    • Liver
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17
Q

Vulval cancer histology

A
  • Normal tissue laterally and medially
  • Cancer in the middle
    • Architecture completely loss- no distinction between dermis and epidermis
    • Cell look very abnormal
    • Formation of keratin (pink)
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18
Q

Vulval intraepithelial neoplasia (VIN) histology

A
  • Cells look abnormal- no maturation
    • Pleiomorphic
    • Large nuclei (immature)
    • irregular nuclear outline
  • No breaking though basement membrane (IN SITU)
  • May develop into SCC
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19
Q

Vulval cancer treatment

A
  • Definitive surgery would include removing the primary tumour and nodes, with a higher survival rate in smaller lesions.
  • Excision affects cure
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20
Q

before the onset of menstruation the cervix is divisible into 2 parts

A

the ectocervix

endocervix

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21
Q

ectocervix

A
  • communicates with vagina (low pH)
    • Stratified squamous
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22
Q

endocervix

A
  • not in contact with vagina
    • Simple columnar (doesn’t need protecting from acidic vagina)
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23
Q

At menstruation, oestrogen causes an anatomical change in the cervix-

A

eversion of the cervix

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24
Q

eversion of the cervix

A
  • Simple columnar epithelium of the endocervix is now exposed to acidic environment of the vagina –> not v appropriate to cope with acidic environment
    • Inflammation
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25
Q

overtime (e.g. women in her 30s) what will happen to the columnar cells of the endocervix

A

) these columnar cells will undergo metaplasia and become squamous cells, which are better adapted to cope with acidic environment – transformation zone

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26
Q

transitional zone of the cervix

A

risk of dysplasia - cells undergoing metaplasia are at

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27
Q

risk factors for cervical cancer

A
  • Sexual partners with HPV
  • Multiple partners
  • Early age of first intercourse
  • Early first pregnancy
  • Multiple births
  • Smoking
  • Low socio-economic status
  • immunosuppression
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28
Q

Human Papilloma Virus

A
  • DNA virus
  • Sexually transmitted
  • High risk subtypes cause cancer
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29
Q

high risk subtypes of HPV

A

HPV 16 and 18

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30
Q

HPV and cervical cancer MOA

A
  • In the cervix they infect the transformation zone
    • Produces viral proteins (E6 and E7)
    • Inactivates tumour suppressor genes (E6- p53 and E7- Rb)
    • Uncontrolled cellular proliferation (hallmark of cancer)
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31
Q

percursor condition of cervical cancer

A

cervical intraepithelial neoplasia (CIN)

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32
Q

cervical intraepithelial neoplasia (CIN)

A
  • Dysplasia
  • Confined to cervical epithelium (in situ- doesn’t breach basement membrane )
  • Caused by HPV infection (95%)
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33
Q

CIN can be divided into

A

CIN 1/2/3 –> SCC

  • Defined by the thickness of the cervical epithelium
  • If CIN breaches basement membrane – invasive squamous cell carcinoma
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34
Q

CIN histology

A
  • Abnormal cells
  • Loss of maturation
    • Pleomorphic
    • Irregular nuclear membrane
    • Clumps of chromatin within nucleus
    • Abnormal mitosis
  • Full thickness abnormality – CIN3 (hasn’t broken. Through basement membrane
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35
Q

Treatment of CIN

A
  • CIN1
    • Often regresses spontaneously
    • Follow up cervical smear in 1 year
  • CIN 2 and
    • Needs treatment
      • Colposcopy
      • Large loop excision of transformation zone (LLETZ)
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36
Q

prevention of cervical cancer

A
  • screening
  • vaccination
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37
Q

Cervical cancer screening programme

A
  • aged 25-49= eveyr 3 years
  • age 50-64= every 5 years
  • over 65 only if recent abnormality

brush used to scrape cells from transformation zone- tested for HPV

if positive= cells looked at under microscope

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38
Q

what is the HPV vaccine called and which subtypes does it cover

A

Gardasil

  • Recombinant vaccination
  • HPV subtypes 6/11/16/18
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39
Q

who receives the HPV vaccine

A

girls ages 12-13

  • now being given to boys (oral and anul cancer)
  • homosexual sex
  • protect girls
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40
Q

gardasil protects from

A
  • from cervical, vulval, oral and anal cancers
  • lasts 10 years
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41
Q

Invasive cervical cancer

A
  • Squamous cell carcinoma
  • Adenocarcinoma
    • Less common/ arises from endocervical glandular cells
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42
Q

presentation of cervical cancer

A

Presentation

  • Bleeding
    • Post coital
    • Inter menstrual
    • Post menopausal
  • Mass
  • Screening
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43
Q

Cytology: squamous cell carcinoma

A
  • Large nuclei
  • Pleiomorphism
  • Irregular nuclear outlines

Less commonly endocarcinomas

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44
Q

spread pf cervical carcinoma

A
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45
Q

stage 0 cervical cancer

A

carcinoma in situ

100% survival

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46
Q

stage 1 cervical cancer

A

confided to cervix

85% 5 year survival

(most people at this stage at presentation 47%)

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47
Q

stage 2 cervical cancer

A

disease beyond cervix but not pelvic wall or lower 1/3 of vagina

65% survival

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48
Q

stage 3 cervical cancer

A

disease to pelvic wall or lower1/3 of vagina

36% 5 year survival

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49
Q

stage 4 cervical cancer

A

invades bladder, rectum or metastasis

7% survival

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50
Q

Treatment of invasive cervical cancer

  • If advanced:
A
  • Hysterectomy
  • Lymph node dissection
  • Chemoradiotherapy +-
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51
Q

Endometrium is composed of

A
  • Glands- adenocarcinoma
    • Stroma – supporting cells
52
Q

Endometrial hyperplasia

A
  • Increased gland: stroma ratio
  • Thickened endometrium >7mm (biopsy taken)
  • Can be precursor to invasive endometrial cancer
53
Q

Presentation of endometrial hyperplasia:

A

intermenstrual/ postmenopausal bleeding

54
Q

cause of endometrial cancer

A

excessive oestrogen

55
Q

endogenous cause of excessive oestrogen

A
  • Obesity
    • Fat cells convert androgens –> oestrogen
  • Early menarche/late menopause
    • Increased lifetime amount of oestrogen
  • Oestrogen secreting tumours
56
Q

Exogenous cause of excessive oestrogen

A
  • Unopposed oestrogen hormone replacement therapy (manage symptoms of menopause)
  • Tamoxifen
57
Q

Tamoxifen

A
  • Drug used to treat oestrogen receptor positive breast cancer (blocking oestrogen receptors)
  • Stimulates oestrogen receptors in the endometrium
58
Q

excessive oestrogen caused by irregular cycle

A

PCOS

59
Q

Invasive endometrial cancer

A
  • Most common gynaecological tract cancer
  • Typically presents between 60/70
  • Most commonly adenocarcinoma
60
Q

presentation of invasive endometrial cancer

A
  • Bleeding
    • Post menopausal
    • Intermenstrual
  • Mass (palpable if progressed)
61
Q

types of invasive endometrial cancer

A
  • Endometroid adenocarcinoma
  • Serous adenocarcinoma
62
Q

endometrioid adenocarcinoma features and histology

A
  • Most common
  • Resembles normal endometrial glands
  • Commonly arises from hyperplasia
  • Grow back-to-back into each other- cells look atypical
    • Pleiomorphic
    • Irregular nuclear membranes
    • Hyperchromatic
63
Q

spread of endometrioid adenocacrinoma

A

direct invasion

  • Spreads to the cervix, bladder and rectum, through the peritoneal cavity and to regional lymph nodes
64
Q

serous adenoacrinoma features and histology

A
  • Less common
  • More aggressive- worse prognosis
  • Poorly differentiated endometrial gland
    • Big nuclei
    • Hyperchromatic
    • Irregular outlines
    • psammona bodies
65
Q

psammona bodies

A

serous adenocarcinoma feature- assoicates with collections of calcium

66
Q

serous adenocarcinoma spread

A

exfoliates

  • Cells break off from main tumour
  • Travels through fallopian tubes
  • Deposits on peritoneal surface (transcoelomic spread- across serous cavities e.g. peritoneum)
67
Q

normal endometrium histology

A
  • Glands are spaced out
  • Not too tightly packed
68
Q

Endometrial cancer

A
  • Glands growing into one another
  • Too tightly packed
  • Cells of glands look atypical
    • Pleiomorphic
    • Irregular nuclear outline
    • Hyperchromatic
69
Q

another Serous adenocarcinoma histology

*

A
  • Projections of tissues- papillae–. LINED BY ABNORMAL CELLS
    • Pleiomorphic
    • Nuclear look abnormal
    • Cells breaking off- can spread- exfoliate
70
Q

Management of endometrial cancer

A
  • Hysterotomy- removal of cervix and uterus
  • Bilateral salpingo-oophorectomy- removal of fallopian tubes and ovaries
  • +- lymph node dissection
  • +- chemo radiotherapy
71
Q

myometrial tumours can be

A

benign or malignant

72
Q

benign tumour of myometirum

A

fibroids

73
Q

fibroids are more medically known as

A

leiomyoma

74
Q

Fibroid(leiomyoma) features

A
  • Most common tumour of myometrium
  • Benign tumour of connective tissue
    • Pale homogenous, well circumscribed mass
  • Their growth is oestrogen dependent and usually regress after the menopause
75
Q

Presentation of leiomyoma depends on size

*

A
  • Asymptomatic
  • Pelvic pain
  • Heavy periods
  • Infertility
  • Urinary frequency (bladder compression)
    • Multiple leiomyomas can cause massive uterine enlargement and results in pressure symptoms of the pelvis
76
Q

fibroid histology

A
  • Made up of smooth muscle cells
  • Arranged in fascicles which intersect in a 3 dimensional nature
77
Q

Leiomyosarcoma features

A
  • Malignant tumour of smooth muscle
  • Atypical cells
    • Pleiomorphic cells
    • Irregular nuclear
  • Doesn’t arise from leiomyoma
  • Metastasis to lungs and then systemically
  • Similar symptoms to fibroids
78
Q

types of cells within the ovary and associated tumours

A
  • Lined by epithelium
    • Epithelial tumours
  • Contains germ cells
    • Germ cell tumours
  • Contains stromal cells
    • Sex cord stromal tumours
79
Q

the ovaries are a good site for

A
80
Q

Ovarian cancer presentation

*

A
  • Early symptoms
    • Vague and non-specific
    • Delayed diagnosis
  • Later symptoms (mass effect)
    • Abdominal pain
    • Abdominal distension
    • Urinary symptoms
    • GI symptoms
    • Hormonal disturbances
81
Q

Risk factors for ovarian cancer

A
  • Number of pregnancy
  • COCP
  • Family history
  • BRCA 1/ 2
    • Tumour suppressor genes
    • Associated with high grade serous cancers
    • Prophylactic salpingo-oophrectomy
82
Q

BRCA 1/2

A
  • Tumour suppressor genes
  • Associated with high grade serous cancers
  • Prophylactic salpingo-oophrectomy
83
Q

Serum marker for ovarian cancer

*

A
  • Ca-125
    • Diagnosis
    • Monitoring recurrence
84
Q

ovarian epitheilal tumours

A
  • Most common ovary cancers- often present as cystic masses
85
Q

histological subtypes of obvarian epitheilial tumours

A
  • Serous adenocarcinoma
  • Mucinous adenocarcinoma
  • Endometroid adenocarcinoma
86
Q

ovarian epitheil tumours can be further divided based on being

A
  • Benign (top photo)
  • Borderline- increased atypia, no stromal invasion
  • Malignant (bottom photo- complex architecture)
87
Q

Ovarian serous adenocarcinoma histology

A
  • Highly atypical cells
  • Often shows Psammoma bodies (calcium collections)
  • Spreads to the peritoneum due to exfoliation of cells
    • Common first presentation of serous andeocarcinoma- can constrict the intestine
88
Q
A
89
Q

Ovarian mucinous adenocarcinoma

A
  • Atypical epithelial cells
  • Look like goblet cells- produce mucin (push nuclei to the side of the cell)
90
Q

Ovarian endometrioid adenocarcinoma

A
  • Glands resembling endometrium
  • May arise in endometriosis
  • May have synchronous endometrial endometrioid adenocarcinoma
    • In both the endometrium and the ovary
91
Q

germ cell tumours

A

dysgerminoma

yolk sac

embryonal carcinoma

choriocarcinoma

teratoma

92
Q

most common type of germ cell tumour

A

teratoma

93
Q

teratoma subtypes

A
  • Three subtypes
    • Mature (benign)- the scarier it looks
    • Immature (malignant)
      • E.g. primitive neuroepithelium
      • Risk for intra-abdominal spread
    • Monodermal (highly specialised)
94
Q

mature teratoma

A

benign

  • Contain fully mature, differentiated tissue from all 3 germ cell layers
    • GI tissue
    • smooth muscle
    • hair shafts and keratin
    • cartilage
  • Can be bilateral
  • Often contains skin and hair structures
95
Q

Sex cord stromal tumours of the ovary

A

testes

  • sertoli cells
  • leydig cells

ovaries

  • granulosa cells
  • theca cells
96
Q

sex cord stromal tumour- can sertoli and leydig cells tumours occur in women

A

Tumours resemble all the above cell types can arise in the ovary (e.g. you can get Sertoli or Leydig cells in the ovary)

These are derived from the ovarian stroma, which in turn is derived from the sex cords of the embryonic gonad.

97
Q

Theca and granulosa cell tumours

A
  • Produce oestrogen
  • Symptoms depend on age of development
    • Patient pre-puberty = Precocious puberty
    • Patient post puberty
      • Breast cancer
      • Endometrial hyperplasia
      • Endometrial carcinoma
98
Q

Sertoli-Leydig tumours

A
  • Produce testosterone
  • Rare
  • Symptoms depend on age
    • Pre-puberty
      • Prevents normal female pubertal changes
    • Post puberty
      • Infertility
      • Amenorrhoea
      • Hirsutism
      • Male pattern baldness
      • Breast atrophy
99
Q

metastases to the ovary

A
  • breast cancer
  • GI cancers
  • Krukenberg tumour
  • other gynae tumours (endometrial, other ovary, fallopian tube)
100
Q

krueknberg tumour

A

metastatic GI tumour

  • ofte gastric
  • signet cells
101
Q

. Most common origin of ovary metastases

A

they are from tumours derived from Müllerian epithelium, i.e., from the uterus, Fallopian tubes, contralateral ovary or pelvic peritoneum.

102
Q

Testicular cancer is the most

A

Most common tumour in men aged 15-34

103
Q

classification of testicular tumours

A
  • Germ cell tumour
    • Seminomatous
    • Non seminomatous
  • Non germ cell
    • Sex cord stromal
    • Others .e.g lymphoma or metastases
104
Q

Risk factors

A

Risk factors

  • Cryptorchidism (undescended testicles)
    • even more likely if both testicals havent descended
105
Q

presentation of testicualr cancer

A

Mass +- pain (usually no pain)

106
Q

investigations for testicular cancer

A

scan tumour markers

107
Q

testicular tumour markers are useful in monitoring and diagnosisn

A

germ cell tumours

  • BhCG
  • Alpha fetoprotein (AFP)
108
Q
  • BhCG (beta-human chorionic gonadotropin (hCG)

positive

A

choriocarcinoma

109
Q
  • Alpha fetoprotein (AFP)
A
  • Yolk sac tumours
  • Not specific – also produced in liver cancer
110
Q

subtypes of testicular cancer

A
111
Q
A
112
Q

non germ cell tumours

A

sex cord stromal tumours

other

113
Q

Sex cord-stromal tumours

A

are a type of non-germ cell tumour, and the most common types seen in the testes are Sertoli or Leydig cell tumours. These are uncommon and are benign.

114
Q

other non germ cell tumours

A

lymphoma and metastases

115
Q

Germ cell tumours features

A

In postpubertal males, 95% of testicular tumours arise from germ cell tumours and all are malignant. The aetiology of germ cell tumours is unknown, although a familial predisposition is well recognised and furthermore cancer in one testis is associated with an increased risk of cancer in the other testis. In addition, there is a three to five times increased risk of testicular cancer in cryptorchidism (failure of testicular descent into the scrotum). In 10% of cases of testicular cancer there is a history of cryptorchidism. This increased risk affects both the descended and the undescended testis. Orchiopexy (surgical placement of the undescended testis into the scrotum) before puberty decreases this risk of cancer.

116
Q

types of germ cell tumours

A

Seminomas

Nonseminomatous germ cell tumours (NSGCTs)

117
Q

Seminomas

A

Approximately 50% of germ cell tumours are seminomas. The peak age for development of a seminoma is 40-50 years. Seminomas often remain confined to the testis for long periods of time. When they do metastasise it is by the lymphatics, most commonly to the iliac and paraortic lymph nodes. Further spread is rare.

118
Q

Nonseminomatous germ cell tumours (NSGCTs)

A

Pure NSGCTs are classified as yolk sac tumours, embryonal carcinomas, choriocarcinomas and teratomas. However many NSGCTs are mixed tumours and contain at least two of the pure NSGCT components.

119
Q

NSGCTs metastasises

A

NSGT metastasise early and do so both via lymphatics and blood vessels- sometimes metastasised before mass even apparent

120
Q

NSGTs- yolk sac tumour

A

Yolk sac tumours occur in young children and have a very good prognosis. Almost all of them produce alpha fetoprotein (AFP) which can be detected in the blood as a tumour marker

121
Q

NSGCTs- Embryonal carcinomas, choriocarcinomas and mixed NSGCTs occur in

A

young adults. All choriocarcinomas are associated with elevated serum concentrations of the tumour marker beta- human chorionic gondatropin (hCG). Most mixed NSGCTs are associated with elevated serum concentrations of both AFP and hCG.

122
Q

NSGCTs- Teratomas

A

Teratomas occur in men of all ages. If they arise in prepubertal men they are usually benign, however if they occur in postpubertal men they are malignant. Of note approximately 10% of seminomas are also associated with raised serum concentrations of hCG. In these seminomas syncytiotrophoblastic cells that produce hCG are present.

123
Q

management of testicular cancer

A
  • Radical orchiectomy
  • Further treatment depends on whether the tumour is a seminoma or NSGCT
124
Q

seminomas management

A
  • very radiosensitive and treated with radiotherapy
    • Best prognosis
125
Q

NSGCTs management

A

after surgery treated with aggressive chemo

Reproductive system (28 decks)

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