Session 11 Flashcards

1
Q

Imaging techniques used to view reproductive tract and which is best.

A

Ultrasound MRI Fluoroscopy CT in order of most used to least.

CT only really used for cancer as it doesnt give much tissue detail. Radiation exposure to rapidly dividing cells also a malignancy risk.

MRI also good but takes too long so ultrasound used more.

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2
Q

HSG?

A

Hysterosalpingography (HSG) is an X-ray procedure that is used to view the inside of the uterus and fallopian tubes. It often is used to see if the test the patency of the fallopian tubes. Will leak into the peritoneal cavity, non patent tubes will not have the leakage.

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3
Q

Ovarian cysts

A
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4
Q

Describe ovulation and what happens after

A
  • The normal ovary contains over two million primary oocytes at birth
  • 10 of which mature each menstrual cycle
  • Of the 10 Graafian follicles that begin to mature, only one becomes the dominant follicle and grows to a size of 18-20 mm by mid-cycle, when it ruptures to release the oocyte.
  • After release of the oocyte, the dominant follicle collapses, and the granulosa cells in the inner lining proliferate and swell to form the corpus luteum of menstruation
  • Over the course of 14 days the corpus luteum degenerates, leaving the small scarred corpus albicans
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5
Q

Functional cysts

A

Two types:

Follicular cyst

Corpus luteum cyst

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6
Q

Follicular cyst

A
  • A dominant Graafian follicle sometimes fails to ovulate and does not involute
  • When it becomes larger than 3 cm, it is called a follicular cyst
  • Follicular cysts are usually 3-8 cm, but may become much larger
  • On ultrasound follicular cysts present as simple unilocular, anechoic cysts with a thin, smooth wall.
  • Follicular cysts will usually resolve spontaneously on follow-up.
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7
Q

Corpus luteal cyst

A
  • A corpus luteum may seal and fill with fluid or blood, forming a corpus luteum cyst.
  • The characteristic circular Doppler appearance is called the ‘ring of fire’.
  • Remember that women who are on birth control pills usually won’t form a corpus luteum, as birth control pills prevent ovulation.
  • Use of fertility drugs that induce ovulation, increases the chance of developing corpus luteum cysts
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8
Q

Haemorrhagic cysts

A

Occur when you get bleeding into a functional cyst. Should resolve by themselves. Checked with a follow up.

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9
Q

Polycystic Ovarian Syndrome / Hyperandrogenic anovulation

A

Chronic anovulation syndrome associated with androgen excess

  • ovulatory dysfunction (oligo- or anovulation)
  • clinical and/or biochemical hyperandrogenism
  • polycystic ovarian morphology on ultrasound

Need to see roughly 20

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10
Q

Mature cystic ovarian teratoma

A
  • Encapsulated tumours with mature tissue or organ components.
  • They are composed of well-differentiated derivations from at least two of the three germ cell layers (i.e. ectoderm, mesoderm, and endoderm).
  • Contain developmentally mature skin complete with hair follicles and sweat glands
  • Sometimes luxuriant clumps of long hair, and often pockets of sebum, blood, fat (93%), bone, nails, teeth, eyes, cartilage, and thyroid tissue
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11
Q

Ovarian hyperstimulation

A
  • Ovarian hyperstimulation syndrome is a relatively rare condition
  • It is caused by hormonal overstimulation by hCG, and is therefore usually bilateral
  • Hormonal overstimulation can occur in gestational throphoblastic disease, PCOS or in patients receiving hormonal therapy.
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12
Q

Pelvic inflammatory disease

A
  • PID is defined as an acute clinical syndrome associated with ascending spread of micro-organisms, unrelated to pregnancy or surgery.
  • The infection generally ascends from the vagina or cervix to endometrium (endometritis)
  • Then to the fallopian tubes (salpingitis)
  • Then to and/or contiguous structures (tubo-ovarian abscess).
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13
Q

Malignant ovarian lesions

A
  • Lesion assessment - US and MRI - Plus CA125 (contrast)
  • Cancer staging
  • Contrast enhanced CT Risk:

Low: premenopausal and no risk factors

High risk: postmenopausal, person of familial history of breast or ovarian cancer, BRCA-1 or 2 carriers, Ashkenazi descent, Lynch-II HNPCC

A Krukenberg tumor refers to a malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast

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14
Q

Endometriosis

A
  • Endometriosis is defined as the presence of endometrial tissue outside the uterine cavity. It is mainly found in the abdominal cavity, most commonly on the surface of the ovaries.
  • It is an estrogen-dependent disease and is estimated to occur in 10% of the female population, almost exclusively in women of reproductive age.
  • The most common symptoms are dysmenorrhea, dyspareunia, pelvic pain, and infertility - although it may also be asymptomatic

Can be divided into superficial and deep infiltrative.

Superficial difficult to find as resolution is good enough, deep infiltrative (involves other organs in peritoneum) iseasier as we have the resolution to see it.

Bimanual transvaginal ultrasound with palpation to check for adhesions. Assessmentwith ultrasoud for endometriosis is very user independent. MRI is much better as the image is better and the image is reproducable so not user dependent.

Kissing ovary sign - strong pelvic adhesions pull ovaries together

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15
Q

Define tumour

A

A tumour is any clinically detectable lump or swelling. A neoplasm is just one type of tumour

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16
Q

Define neoplasm

A

A neoplasm is, “an abnormal growth of cells that persists after the initial stimulus is removed”. For malignant neoplasms the definition needs the following extending: an abnormal growth of cells that persists after the initial stimulus is removed and invades surrounding tissue with potential spread to distant sites.

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17
Q

Vulval cancer? How does vulval cancer spread?

A

Uncommon - only 3% of female cancers

More common in older patients.

Clinical Features:

Lumps, Ulceration, Skin changes

Most common to least - Squamous Cell Carcinoma, Basal Cell Carcinoma, Melanoma, Soft tissue tumours

90% are squamous cell carcinoma - seen wih keratin formation

Vulval Intraepithelial Neoplasia (VIN) = IN SITU - Precursor of vulval squamous cell carcinoma

Atypical cells (no invasion through basement membrane) - big nuclei, pleomorphic, mitotic figure, nucleoli

May or may not develop into SCC

If basement membrane still intact then not SCC

Vulval cancer spread

Direct extension - Anus, Vagina, Bladder

Lymph Nodes - Inguinal, Iliac, Para-aortic

Distant Metastases - Lungs and Liver

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18
Q

Are VIN and Vulval SCC related to HPV?

A

YES and NO

YES: 30% of cases, Usually HPV 16, Peak age of onset = 60s, Risk factors as per cervical carcinoma

NO: 70% of cases, Usually associated with longstanding inflammatory conditions (e.g. lichen sclerosus), Peak age of onset = 80s

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19
Q

Draw cervix

A

Endocervix and ectocervix

Ectocervix is stratified squamous epithelium as its best evolved to deal with environment of vagina.

Endocervix is not exposed and is simple columnar.

After menarche we have more oestrogen, one of its functions is to change the anatomical structure of the cervix by causing it to evert, exposing the coumnar epithelium to the acidic environment causing inflammation forming the ectropian . In response to this we see metaplasia in the cervix so columnar changes to stratified squamous epithelium in the transformation zone.This gives more risk for dysplasia

20
Q

Define dysplasia

A

Dysplasia is a pre-neoplastic alteration in which cells show disordered tissue organisation. It is not neoplastic because the change is reversible. Still see enlarged nuclei, mitotic figures, pleomorphism etc but it may be reversible

21
Q

Human Papilloma Virus (HPV)

A

DNA Virus

Sexually transmitted

Many subtypes:

Low risk (egHPV 6 and 11) -> warts on hands, mouth, genitalia, anus

High risk (egHPV 16 and 18) - Infect transformation zone, Produce viral proteins (E6 and E7) which inactivate tumour suppressor genes p53 and retinoblastoma gene resuting in uncontrolled cellular proliferation

22
Q

Cervical Intraepithelial Neoplasia (CIN)

Risk factors for CIN and Cervical Carcinoma

A

Dysplasia

Confined to Cervical epithelium (in situ)

Caused by HPV infection

Divided into CIN 1 / 2 / 3

Risk of progression to squamous cell carcinoma higher with each stage

Risk factors for CIN and Cervical Carcinoma

•Increased risk of exposure to HPV:

Sexual partner with HPV

Multiple partners

Early age of first intercourse

  • Early first pregnancy
  • Multiple births
  • Smoking
  • Low socio-economic status
  • Immunosuppression

Treatment for CIN :

CIN1

  • Often regresses spontaneously
  • Follow up cervical smear in 1 year

CIN 2 and 3

  • Needs treatment
  • Large Loop Excision of Transformation zone (LLETZ)
23
Q

Cervical Cancer Screening Programme

A

Brush used to scrape cells from transformation zone:

Tested for HPV - If positive –cells looked at under microscope

  • Aged 25 –49 = every 3 years
  • Aged 50 –64 = every 5 years
  • Over 65 –only if recent abnormality
24
Q

Vaccination against HPV

A
  • Gardasil
  • Recombinant vaccination
  • Against HPV (subtypes 6/11/16/18)
  • Given aged 12-13
  • Protects from cervical, vulval, oral, anal cancers
25
Q

Invasive Cervical Cancer

A

Squamous Cell Carcinoma - Most common / CIN = precursor

Adenocarcinoma - Less common / arises from endocervical glandular cells

Presentation: Bleeding (Post coital, Inter menstrual, Post menopausal)

Mass Screening

Spread of Invasive Cervical Cancer - spreads to involve bladder, pelvic wall, rectum, vagina

Staging for cervical cancer is called figo staging

Treatment of Invasive Cervical Cancer:

If advanced: Hysterectomy, Lymph Node Dissection, +/-Chemoradiotherapy

26
Q

Endometrial Hyperplasia

A

Thickened endometrium >11mm

Can be a precursor to endometrial cancer

Presents with inter-menstrual/postmenopausal bleeding

Caused by excessive oestrogen:

Endogenous -Obesity (androgens -> oestrogens via aromatisation) -Early menarche/late menopause -Oestrogen secreting tumours

Exogenous -Unopposed oestrogen hormone replacement therapy -Tamoxifen

Irregular Cycle - most often caused by Polycystic Ovary Syndrome

27
Q

Endometrial Cancer

A

Most common gynaecological tract cancer

Most common at age 70

Presentation: Bleeding (Post menopausal, Inter menstrual) and Mass

28
Q

Types of endometrial cancer

A

Endometrioid Adenocarcinoma - Most common

Resembles normal endometrial glands

Commonly arises from hyperplasia

Serous Adenocarcinoma - Less common

More aggressive

Poorly differentiated cells

29
Q

Spread of endometrial cancer

A

Method of spread also helps to detrmine type of endometrial cancer.

Spread of Endometrioid Adenocarcinoma - Spreads as you would expect - through the myometrium, invades into the cervix and vagina and then other nearby organs and then break off.

Spread of Serous Adenocarcinoma

Exfoliates Travels through Fallopian tubes

Deposits on peritoneal surface (Transcoelomic spread)

Associated with collections of calcium (Psammomabodies)

30
Q

Management of Endometrial Cancer

A

Hysterectomy

Bilateral salpingooophorectomy

+/-lymph node dissection

+/-chemo radiotherapy

31
Q

Leiomyoma

A

Leiomyoma (fibroid)

Most common tumour of myometrium

Benign

Pale, homogenous, well circumscribed mass

Presentation: Asymptomatic, Pelvic pain, Heavy periods, Urinary frequency (bladder compression)

Whorled, intersecting fascicles of benign smooth muscle cells seen on microscope

32
Q

Leiomyosarcoma

A

Malignant tumour of smooth muscle

Atypical cells

Doesn’t arise from a leiomyoma

Tend to metastasise to lung

33
Q

Ovarian Cancer

A

Presentation

Early symptoms - Vague and non-specific leading to Delayed diagnosis

Later symptoms - Abdominal pain, Abdominal distension, Urinary symptoms, Gastrointestinal symptoms, Hormonal disturbances,

Ca-125 Serum marker –diagnosis/monitoring recurrence

BRCA1/2 - Tumour suppressor genes

Associated with high grade serous cancers

Prophylactic salpingo-oophrectomy often done to reduce risk

34
Q

Cells that make ovaries at risk of specific tumours

A

Lined by epithelium • Epithelial tumours

Contains germ cells • Germ cell tumours

Contains stromal cells • Sex cord stromal tumours

Is also a site for metastatic spread

35
Q

Ovarian Epithelial Tumours

A

Often present as cystic masses

Histological subtypes: (adenocarcinoma) -Serous -Mucinous -Endometrioid

Can all be:

  • Benign
  • Borderline -Increased atypia, no stromal invasion
  • Malignant
36
Q

Ovarian Serous Adenocarcinoma

A

Highly atypical cells

Often show Psammoma Bodies

Often spreads to peritoneal surface

37
Q

Ovarian Mucinous Adenocarcinoma

A

Atypical epithelial cells

Secreting mucin

38
Q

Ovarian Endometrioid Adenocarcinoma

A

Glands resembling endometrium

May arise in endometriosis

May have synchronous endometrial endometrioid adenocarcinoma

39
Q

Teratoma

A

Most common germ cell tumour

Three subtypes:

  • Mature(benign)
  • Immature(malignant)
  • Monodermal (highly specialised) - commonly thyroid tissue

Mature Teratoma (Dermoid Cyst) - Contain fully mature, differentiated tissue from all germ cell layers - Can be bilateral - Often contains skin + hair structures

Immature Teratoma - Contains immature, embryonal tissue

Malignant

40
Q

Other Germ Cell Tumours

A

Dysgerminoma (equivalent of seminoma in testis)

Choriocarcinoma

Embryonal Carcinoma

Yolk Sac Tumour

All malignant

41
Q

Sex Cord Stromal Tumours

A

From ovarian stroma

Sex Cord ->

Testes - Sertoli Cells and Leydig Cells

Ovaries - Granulosa Cells and Theca Cells

Tumours resembling ALL the above cell types can arise in the ovary

42
Q

Theca and Granulosa Cell Tumours

A

Produce Oestrogen

Patient pre-puberty - Precocious puberty

Patient post-puberty - Breast cancer, Endometrial hyperplasia, Endometrial carcinoma

43
Q

Sertoli-Leydig Tumours

A

Produce testosterone

Patient pre-puberty - Prevents normal female pubertal changes

Patient post-puberty - Sterility, Amenorrhoea, Hirsuitism, Male pattern baldness, Breast atrophy

44
Q

Metastases to Ovary

A

Breast cancer

Krukenberg Tumour • Metastatic GI tumour • Often gastric • Signet cells

Gastrointestinal cancers

Other Gynaetumours • Endometrial • Other ovary • Fallopian Tube

45
Q

Testicular Cancer

A

Risk factor: -Cryptorchidism (undescended testicle)

Presentation: -Mass+/-pain

Investigations: -Scans -Tumour markers

Tumour Markers:

Useful in germ cell tumours Diagnosis/response to treatment/monitoring for recurrence

β hCG - Choriocarcinoma

Alpha fetoprotein (AFP) - Yolk Sac Tumours

46
Q

Subtypes of Testicular Cancer

A
47
Q

How do we image prostate cancer?

A

MRI as ths reduces bipsies. PSA test used prior. PSA density looked at. Then use PI-RADS to determine likelihood of cancer.

MRI can be used in conjunction with ultrasound for biopsy guidance.