Gynae oncology Flashcards

1
Q

Cervical cancer subtypes

A

80% SCC, 20% adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the transformation zone

A

Columnar cells from glandular uterus get exposed to vaginal pH they undergo dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Risk factors for cervical cancer

A
  • Smoking (doubles risk)
  • COCP>10 years doubles risk
  • Genetic/FH
  • HPV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathophysiology of HPV

A
  • Binds to tumour suppressor gene (tP53) causing squamous dysplasia
  • HPV 16 & 18 account for 75% cervical cancer
  • HPV 6&11 account for 90% genital warts (non cancerous)
  • Very common, most women get rid of it in <1yr
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the cervical screening programme

A
  • Diagnoses high grade CIN
  • Women aged 25-64 are screened every 3 years to aged 50, 5 yearly smears to 64
  • Saves around 4500 lives
  • Cervical scrape from transformation zone of cervix
  • Liquid based cytology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the stages of colposcopy

A

Inspection
Acetic acid staining
Iodine staining
Cervical screening samples

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does CIN3 look like in colposcopy?

A

Dense, white and irregular, well demarcated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment depending on CIN stage

A

CIN1: observe and repeat in 1 year

CIN2: treat, if young girl manage conservatively

CIN3: treat all cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Treatment of CIN

A

Large loop excision of the transformation zone (LETS)
Local anaesthetic
Diathermy to crater and rim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Risks associated with LETS?

A

Healed after 6 months (infection, pain, bleeding)

Theoretical risk of future miscarriage (risk only after repetitive treatment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What age is ovarian cancer usually diagnosed?

A

Above age 65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Risk factors of ovarian cancer

A
•	Low parity
•	Infertility/use of clomiphene
•	HRT
•	Smoking
•	Obesity
•	Previous cancer treatment
White caucasian
Blood group A
FH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Protective factors for ovarian cancer

A
•	COC pill
•	Breast feeding
•	Hysterectomy
•	Salpingectomy
•	Bilateral salpingo-oopherectomy
•	Tubal sterilisation
Exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What known mutations predispose to ovarian cancer?

A

BCRA1, BRCA2, HNPCC (lynch) mutations

Prophylactic oophorectomy?+/- hysterectomy With HRT until natural age of menopause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

5 subtypes of ovarian cancer

A
  • Epithelial type (60-70%, serous, mucinous, clear cell, endometrioid, undifferentiated, older women)
  • Germ cell tumours (20-30%, esp malignant if age<20yrs)
  • Ovarian sex cord stromal tumour cells (8%)
  • Metastatic secondary tumours (breast, stomach, large bowel, uterus)
  • Borderline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the ovarian cancer protein marker?

A

CA125

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Symptoms of ovarian cancer

A
•	Abdo pain
•	Abdo distention/bloating
•	Change in bowel habit
•	Urinary symptoms
Emergency:
•	Torsion
•	Haemorrhage
•	Rupture
•	Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clinical features of ovarian cancer

A
  • Solid irregular and nodular fixed mass, palpable omental cake
  • Pain and tenderness over mass
  • Bilateral masses
  • Ascites
  • Leg oedema, venous compression and congestion, DVT
  • Lymph nodes (inguinal, supraclavicular)
  • SOB secondary to pleural effusions if advanced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Investigations for a woman with possible ovarian cancer

A
  • FBC, U&Es, LFTs
  • CA 125, CEA
  • B-hCG and AFP (in young women for germ cell tumours)
  • USS of pelvis and transvaginal USS
  • Chest x-ray, CT chest abdo pelvis
  • Ascitic fluid cytology and CT guided biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors for endometrial cancer

A
  • High levels of oestrogen (obesity, e2 therapy unopposed by progesterone in HRT error, oestrogen secreting ovarian tumour)
  • (Fat cells convert adrenal hormones to weak oestrogens)
  • Early menarche, late menopause
  • Genetic predisposition (younger, don’t recognise bleeding as abnormal)
  • PCOS
  • Tamoxifen (anti-oestrogen in breast, mild oestrogenic effect in endometrium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Signs &symptoms of endometrial cancer

A
  • Post menopausal bleeding (if significant bleed or repeated 10% will have endometrial cancer)
  • Continuing menstruation after aged 55
  • Watery vaginal discharge
  • Pelvic mass
  • Glandular abnormalities on cervical smear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What occurs in a PMB clinic?

A
  • Transvaginal USS (<5mm normal)
  • Hysteroscopy (gold standard)
  • Endometrial biopsy (pipelle as outpatient/endometrial curettage in theatre)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name 3 subtypes of endometrial cancer

A
  • Endometrioid (80%)
  • Serous
  • Clear cell
24
Q

How is endometrial cancer staged?

A
  • Biopsy for grade
  • MRI for invasion/lymph node status/metastatic involvement
  • Surgical staging allows further assessment
25
Treatment of endometrial cancer?
* Surgery (total hysterectomy, BSO, peritoneal washings) * Radiotherapy (if unfit for surgery, external beam) * Chemotherapy if metastatic * Recurrence treated with progesterone
26
Survival of endometrial cancer
75% survival at 5 years
27
What is the point of cervical screening?
Allows intervention early in pathogenesis | Improves outcome
28
Symptoms of cervical cancer
* Post coital bleeding * Intermenstrual bleeding (could also be hormonal, polyps and ectropions) * Abnormal discharge * Renal failure-> ureters obstructed if locally advanced
29
Treatment of cervical cancer
* LETS is enough in 1a disease * Tissue diagnosis via LETS or pinch biopsy * MRI/CT imaging to look for metastatic disease * Cervical and hysterectomy is best * Fertility sparing, just cervix * Chemo and radiotherapy if metastatic
30
Types of vulval cancer
Most are SCC Melanomas BCC Adenocarcinoma
31
What are the 2 main causes of vulval cancer?
HPV related | Lichen sclerosis related (chronic inflammation, repeated insults)
32
Presentation of vulval cancer
``` • Incidentally with PMB • During follow up for lichen sclerosis • Thickened, discoloured skin • Persistent burning of itching of the vulva • Lump/wart like growth • Ulcer • Anal problems Particularly if lesion is excessively hyperkaratotic or woman is immunospuressed ```
33
Diagnosis of vulval cancer?
Full examination Take biopsy from suspicious area in specialist clinic Punch biopsy/ies Sufficient concern-> wide local excision for diagnosis and treatment
34
Define gestational trophoblastic disease
Disease processes that originate in the placenta
35
Types of gestational trophoblastic disease
``` Complete hydatidiform mole Partial hydatidiform mole Invasive mole Placental site trophoblastic tumour Choriocarcinoma ```
36
Define complete hydatidiform mole
A pregnancy within the uterus consisting of a multivesicular mass of trophoblastic tissue with hydropic changes (bunch of grapes) and no evidence of a fetus. Usually formed by mono/dispermic fertilisation of an oocyte which has deleted all maternal genetic material. All genes are therefore usually paternal.
37
Define partial hydatidiform mole
A pregnancy within the uterus consisting of some trophoblastic proliferation and some hydropic change, where a fetus (usually non-viable) may also be seen. Formed by dispermic fertilisation of an oocyte resulting in triploidy. Genes are therefore maternal and paternal.
38
Explain biparental complete hydatidiform mole
Ovum from individual with NLRP7 or KHDC3L mutation plus sperm can lead to 46XX or 46XY complete mole
39
Explain a monospermic complete mole
X sperm + egg w/no maternal DNA-> sperm DNA duplicates-> 46XX andorgenetic complete mole
40
Explain partial mole formation
23X sperm + 23Y sperm + 23X egg-> 23X 23X 23Y -> 69XXY Triploid biparental partial mole Or 23X sperm duplicates-> 46XX + 23X egg-> 69XXX Tetraploidy can also occur
41
Differences between complete and partial mole
``` Complete: Partial Diploid: Triploid Androgenetic usually: biparental No fetal tissue: presence of fetus ßHCG>100,000: ßHCG<100,000 15-20% invasive: <5% invasive ```
42
Risk factors for hydatidiform mole
Extremes of age (teenage/perimenopausal)
43
Presentation of hydatidiform mole
* Irregular PV bleeding * Hyperemesis * Excessive uterine enlargement * Acute abdomen * Early failed pregnancy (anembryonic pregnancy)
44
Rare presentation of hydatidiform mole
* Hyperthyroidism * Early onset pre-eclampsia * Abdo distension due to theca lutein cysts * Acute respiratory failure (embolisation of trophoblastic tissue) * Neuro symptoms (seizures) more likely to be metastatic disease
45
What does a hydatidiform mole look like on USS?
Snowstorm appearance | Bunch of grapes
46
Describe invasive moles
* 20% of women with a complete mole develop trophoblastic malignancy, 2-3% of partial moles * Mortality rate is essentially zero * Classified as invasive if there is destructive invasion of the myometrium and/or metastases * Perforation of the uterus may occur * Persistent elevation of ßHCG levels seen after evacuation of molar pregnancy
47
5 risk factors for invasive mole
``` Advanced maternal age High ßHCG levels Eclampsia Hyperthyroidism Bilateral theca lutein cysts ```
48
Describe placental site trophoblastic tumours
* Least common * Slow growing * Can follow normal pregnancy, non-molar abortion, complete and partial moles * hCG levels are elevated (but less than choriocarcinoma/moles) * Spread by local infiltration and lymphatics * If presents after 2 yrs from causative pregnancy, 6 yr prognosis
49
Describe choriocarcinoma
* Can occur after a miscarriage/live birth/molar pregnancy * Usually after complete moles * Usually present within year of pregnancy * Presents with distance metastases (liver/lung/brain) * Due to high ßHCG, thyrotoxicosis and ovarian theca luteal cysts also present * Can cross placenta to fetus
50
Treatment of molar pregnancies
* Surgical evacuation (NO misopristol due to venous embolisation, syntocin only if necessary, NO cervical prep) * Register with centre (Charing Cross) * Follow up with weekly ßHCG levels until normalised, F/U extra 6 months * Methotrexate/IV chemo may be needed * If chemotherapy indicated due to invasive disease, F/U 1 yr after normalisation of ßHCG
51
Future issues after molar pregnancy?
* Avoid hormonal and IUCD contraception, no pregnancy until 1 yr after chemo * 2% recurrence rate
52
Name 9 causes of intermenstrual and post coital bleeding
``` Cervical ectropion Cervical polyps Cervical/endometrial malignancy Cervicitis Polyps Submucous fibroids Endometrial hyperplasia Endometritis Hormonal breakthrough bleeding ```
53
Causes of PMB
Ovary (cancer, oestrogen secreting tumour) Uterus (submucous fibroid, atrophic changes, polyp, cancer) Cervix (atrophy, SCC, adenocarcinoma) Vagina (atrophy) Urethra (caruncle, haematuria) Vulva (vulvitis, dystropy, malignancy)
54
Define urethral caruncle
Prolapse of the urethral mucosa
55
Risk factors for cervical cancer
``` Early age of 1st intercourse High number of sexual partners HPV infection Lower socioeconomic group Smoking Partner with prostatic/penile cancer ```