Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

O&G > Gynae oncology > Flashcards

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
Q

Treatment of endometrial cancer?

A
  • Surgery (total hysterectomy, BSO, peritoneal washings)
  • Radiotherapy (if unfit for surgery, external beam)
  • Chemotherapy if metastatic
  • Recurrence treated with progesterone
26
Q

Survival of endometrial cancer

A

75% survival at 5 years

27
Q

What is the point of cervical screening?

A

Allows intervention early in pathogenesis

Improves outcome

28
Q

Symptoms of cervical cancer

A
  • Post coital bleeding
  • Intermenstrual bleeding (could also be hormonal, polyps and ectropions)
  • Abnormal discharge
  • Renal failure-> ureters obstructed if locally advanced
29
Q

Treatment of cervical cancer

A
  • 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
Q

Types of vulval cancer

A

Most are SCC
Melanomas
BCC
Adenocarcinoma

31
Q

What are the 2 main causes of vulval cancer?

A

HPV related

Lichen sclerosis related (chronic inflammation, repeated insults)

32
Q

Presentation of vulval cancer

A 
•	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
Q

Diagnosis of vulval cancer?

A

Full examination
Take biopsy from suspicious area in specialist clinic
Punch biopsy/ies
Sufficient concern-> wide local excision for diagnosis and treatment

34
Q

Define gestational trophoblastic disease

A

Disease processes that originate in the placenta

35
Q

Types of gestational trophoblastic disease

A 
Complete hydatidiform mole
Partial hydatidiform mole
Invasive mole
Placental site trophoblastic tumour
Choriocarcinoma
36
Q

Define complete hydatidiform mole

A

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
Q

Define partial hydatidiform mole

A

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
Q

Explain biparental complete hydatidiform mole

A

Ovum from individual with NLRP7 or KHDC3L mutation plus sperm can lead to 46XX or 46XY complete mole

39
Q

Explain a monospermic complete mole

A

X sperm + egg w/no maternal DNA-> sperm DNA duplicates-> 46XX andorgenetic complete mole

40
Q

Explain partial mole formation

A

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
Q

Differences between complete and partial mole

A 
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
Q

Risk factors for hydatidiform mole

A

Extremes of age (teenage/perimenopausal)

43
Q

Presentation of hydatidiform mole

A
  • Irregular PV bleeding
  • Hyperemesis
  • Excessive uterine enlargement
  • Acute abdomen
  • Early failed pregnancy (anembryonic pregnancy)
44
Q

Rare presentation of hydatidiform mole

A
  • 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
Q

What does a hydatidiform mole look like on USS?

A

Snowstorm appearance

Bunch of grapes

46
Q

Describe invasive moles

A
  • 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
Q

5 risk factors for invasive mole

A 
Advanced maternal age
High ßHCG levels
Eclampsia
Hyperthyroidism
Bilateral theca lutein cysts
48
Q

Describe placental site trophoblastic tumours

A
  • 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
Q

Describe choriocarcinoma

A
  • 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
Q

Treatment of molar pregnancies

A
  • 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
Q

Future issues after molar pregnancy?

A
  • Avoid hormonal and IUCD contraception, no pregnancy until 1 yr after chemo
  • 2% recurrence rate
52
Q

Name 9 causes of intermenstrual and post coital bleeding

A 
Cervical ectropion
Cervical polyps
Cervical/endometrial malignancy
Cervicitis
Polyps
Submucous fibroids
Endometrial hyperplasia
Endometritis
Hormonal breakthrough bleeding
53
Q

Causes of PMB

A

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
Q

Define urethral caruncle

A

Prolapse of the urethral mucosa

55
Q

Risk factors for cervical cancer

A 
Early age of 1st intercourse
High number of sexual partners
HPV infection
Lower socioeconomic group
Smoking
Partner with prostatic/penile cancer

O&G (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions