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Gynae > Cancers and neoplasia > Flashcards

Cancers and neoplasia Flashcards

1
Q

What is CIN?

A

Premalignant atypia in squamous lining of cervix (FIGO stage 0)

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2
Q

What serotypes of HPV are usually implicated in cervical cancer?

A

HPV 16 and 18

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3
Q

What is the peak age range of onset of CIN?

A

25-29 y/o

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4
Q

Risk factors for CIN

A

smoking
multiple sexual partners
early age first intercourse
HIV

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5
Q

HPV vac

A

girls and boys 12-13
gardasil 6,11,16,18

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6
Q

What are the dysplastic epithelial changes that occur in CIN?

A

Increased nuclear to cytoplasmic ratio
Abnormal nuclear shape: poikilocytosis
increased nuclear size
increased nuclear density - koilocytosis - hpv infection
reduced cytoplasm

dyskaryosis - abnormal nucleus

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7
Q

smear schedule

A

under 25 - once
25-50 - every 3 years
51-65 - every 5 years
65+ - only if one of last 3 were abnormal

inadequate
inflammation
age related atrophy
blood on smear
after 3 - colposcopy

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8
Q

Recall the grading system for CIN

A

Grade 1 = mild dysplasia confined to lower 1/3 of epithelium
Grade 2 = Moderate dysplasia affecting 2/3 of epithelial thickness
Grade 3 = Severe dysplasia extending to the upper 1/3 of epithelium

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9
Q

What are the symptoms of CIN?

A

Same as cervical cancer symptoms: PV bleeding. IMB, PCB, PMB

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10
Q

If a smear test revealed CIN grade I, what should be done next?

A

An HPV test: If it’s positive, do a colposcopy, if it’s negative, do a routine recall

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11
Q

What does dyskaryosis mean?

A

Abnormal nucleus appearance

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12
Q

If a smear test revealed suspected invasive cancer, what should be done next?

A

Urgent colposcopy (<2 weeks)

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13
Q

How should CIN grade 1 be managed?

A

Smear in 12 months (conservative)

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14
Q

How can CIN be treated?

A

1st line: Large loop excision of the transformational zone (LLETZ - loop diathermy) - involves a wire loop with current running through that removes cells - however it is heavy on the side effects
Biggest risk = increases risk of miscarriage and preterm delivery

2nd line - core biopsy - only performed if a large area needs to be removed, done under GA

Always do a follow-up test of cure 6 months later - smear and HPV test
-ve - routine recall
+ve - repeat colposcopy

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15
Q

Complications of CIN

A

miscarriage
PTL
Cervical carcinoma (can regress)

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16
Q

What are the subtypes of cervical cancer and their relative prevalences?

A

Squamous (80%) CIN
Adenocarcinoma (20%) CGIN

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17
Q

Aetiology cervical cancer

A

types 16 18
age 45-50

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18
Q

cervical cancer risk factors

A

smoking
many sexual partners
early first intercourse
immunosuppression

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19
Q

What is the staging sysytem used in cervical cancer?

A

FIGO

0 - carcinoma in situ
1 - cervix
2 - vagina not pelvis
3 - lower vagina, pelvis, ureteric obstruction
4 - metastatic

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20
Q

Recall the signs and symptoms of cervical cancer

A

PV discharge
PCB, IMB, PMB
Dyspareunia (deep)
Symptoms of late metastasis (ie SOB, DIC) + FLAWS

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21
Q

To which lymph nodes does cervical cancer metastasise?

A

Iliac (NOT para-aortic)

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22
Q

Other than the screening pathway, how can cervical cancer be investigated?

A

MRI is better than CT-CAP (whereas CT-CAP is better for ovarian cancer)
Bloods to show anaemia, UandEs showing obstructive picture, LFTs may show metastasis, clotting and group and save

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23
Q

Recall all the stages of cervical cancer and their management!

A

Stage Ia1 (microinvasive) - mx = LLETZ/ cone biopsy

Stage Ia2 to IIa - mx =
- Fertility sparing: radical trachelectomy (removal of cervix) + BL pelvic node dissection
- If tumour is <4cm: radical hysterectomy + BL pelvic node dissection (Wertheim’s)
- If tumour is >4cm: chemoradiation

Stage IIb to IVa (locally advanced disease) - mx = chemoradiation

IVb combination chemo - single agent therapy and palliative care

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24
Q

What types of radiotherapy can be useful in cervical cancer?

A
  1. External beam radiotherapy
  2. Internal radiotherapy
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25
Q

What are the main complications of Wertheim’s hysterectomy to be aware of?

A

Bladder dysfunction (common, may require self-catheterisation), sexual dysfunction (due to vaginal shortening), lymphoedema - manage with leg elevation, good skin care + massage

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26
Q

Recall some side effects of radiotherapy for gynaecological cancer

A

Fatigue, skin erythema, infertility, dysuria, urgency, dyspareunia (due to vaginal stenosis), diarrhoea, incontinence

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27
Q

On what tissues is tamoxifen oestrogenic, and on which tissues is it anti-oestrogenic?

A

Oestrogenic on uterus and bone, anti-oestrogenic on breast

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28
Q

What are the risk factors for endometrial hyperplasia?

A

Oestrogen: so early menarche, late menopause, nulliparity, tamoxifen, HRT, COCP
PLUS
Increasing age, high insulin levels, obesity, smoking, FHx for ovarian Ca

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29
Q

What are the symptoms of endometrial hyperplasia?

A

PV bleeding, usually PMB

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30
Q

How should potential endometrial hyperplasia be investigated?

A

1st line = TVUSS - if more than 4mm, –> hysteroscopy + biopsy
2nd line (and gold standard) = hysteroscopy + pipelle biopsy

31
Q

How does presence/ absence of atypia in endometrial hyperplasia guide management?

A

If there is no atypia, <5% will become malignant in 20 years so it’s pretty chill, if there is atypia, that’s more suboptimal

Without atypia: 1st line = progestogens (either LNG-IUS (mirena) or oral non-cyclical), 2nd line = possible hysterectomy - review in 3-6 months

If there is atypia: 1st line is a hysterectomy, but if fertility needs to be spared then use progestogens - endometrial surveillance with biopsy every 3 months

32
Q

Which symptom signals endometrial cancer until proven otherwise?

A

PMB

33
Q

What are the subtypes of endometrial cancer?

A

Type 1 (85%) - secretory, endometrioid, mucinous (SEM) carcinoma
Type 2 (15%) - uterine papillary Serous carcinoma, Clear cell carcinoma (SC)

34
Q

What are the main differences between the different types of endometrial cancer?

A

Type 1 = younger patients, oestrogen-dependent, superficially invade, lower grade
Type 2 = older patients, less oestrogen-dependent, deeper invasion, higher grade

35
Q

Describe the genetic components of each type of endometrial Ca

A

Type 1 - need to acquire >= 4 mutations, most importantly PTEN and PI3KCA

Type 2 - P53 is very associated with SCC, Her-2 amplification is associated with both

36
Q

To which lymph nodes does endometrial cancer metastasise?

A

Para-aortic LNs

37
Q

Recall the general FIGO staging of Endometrial Ca

A

I - limited to uterus
II - spread to cervix
III - spread to adjacent
IV - distant spread

38
Q

Which investigations are appropriate in endometrial Ca?

A

Similar to EH
1st line = TVUSS - >4mm –> hysteroscopy + biopsy
2nd line - hysteroscopy

39
Q

What is the most useful investigation for deciding FIGO stage of ovarian cancer?

A

CT CAP (better than MRI in this case)

40
Q

Recall the management of endometrial Ca depending on stage

A

Stage 1 - total abdominal hysterectomy, BL salpingoophrectomy + peritoneal washings
Stage 2+ - radical hysterectomy + radiotherapy adjunct

41
Q

What are some protective factors against ovarian tumours?

A

Pregnancy, COCP

42
Q

What are some risk factors for ovarian tumour?

A

More ovulations eg nulliparity, early menarche, late menoapuse
Increasing age (obviously)
Endometriosis
Talcum powder?!

43
Q

Recall some genetic associations of ovarian Ca

A

Lynch syndrome (Autosomal dominant HNPCC), BRCA1/2
Type 1 epithelial ovarian tumours: PTEN/P13KCA
Type 2 epithelial tumours: p53 mutation present in 95%

44
Q

What is the most common type of ovarian cancer?

A

Tumour of epithelial origin - most of which are benign

45
Q

Recall the type 1 ovarian epithelial tumour types

A

These are low-grade
Mnemonic = Less Exciting, More Cancers
L: low-grade serous
E: endometrioid
M: mucinous
C: clear cell tumour (only one that’s not solid or cystic)

46
Q

Recall the subtypes of type 2 ovarian epithelial tumours

A

High grade serous (solid or cystic)

47
Q

If an ovarian tumour is malignant, what type is it most likely to be?

A

Epithelial

48
Q

Which type of germ cell ovarian tumour is most likely to be benign?

A

Teratoma

49
Q

Which types of germ cell ovarian tumour are most likely to be malignant?

A

Dysgerminoma
Endodermal sinus tumour
Choriocarcinoma

50
Q

What are the different types of sex-cord stromal tumour, and which of these are most likely to be benign?

A

Fibroma and thecoma (likely to be benign)
Granulosa cell/ sertoli-Leydig cell tumour

51
Q

Which type of ovarian tumour is associated with endometriosis?

A

Clear cell

52
Q

How does the maturity of teratoma affect prognosis?

A

Mature = benign
Immature = malignant

53
Q

What is Meig’s syndrome?

A

Triad of benign ovarian fibroma, ascites and right-sided pleural effusion

54
Q

What is the krukenberg tumour?

A

BL metastasis from breast/ gastric cancer - mucin producing signet ring cell

55
Q

How are the symptoms and signs of ovarian and endometrial cancer different?

A

Ovarian: adnexal mass and no PV bleeding
Endometrial: uterine mass and PMB

56
Q

Recall the FIGO staging for ovarian tumours

A

Stage 1 = confined to ovary
Stage 2 = tumour within pelvis but outside ovary
Stage 3 = Outside pelvis but within abdomen
Stage 4 = distant metastasis

57
Q

Describe the appropriate investigations for Ovarian tumour

A

1st line = Ca125 tumour marker: >35IU/mL –> 2ww referral to O and G and TVUSS
TVUSS –> size, consistency, solid elements? UL/BL? Ascites?
Risk of malignant index (RMI) calculated from menopausal status, USS features and Ca125
Score >250 is considered hig
Do not biopsy - this can cause dissemination of maligant tissue

58
Q

With what scan is ovarian Ca staged?

A

CT CAP

59
Q

How should Ovarian Ca be managed?

A

1st line is surgery and chemo, 2nd line is just chemo
Chemo = platinum compound (usually carboplatin) with paclitaxel
Follow up with CT scan and Ca125 to assess response to treatment

60
Q

How does platinum treat ca?

A

Cross linkage of DNA –> cell cycle arrest

61
Q

What is the MOA of Paclitaxel?

A

Causes microtubular damage –> prevention of cell division

62
Q

What should be given alongside paclitaxel and why?

A

Pre-emptive steroids given - this reduces hypersensitivity reactions

63
Q

Recall some side effects of paclitaxel

A

Total loss of body hair, peripheral neuropathy, neutropaenia and myalgia

64
Q

Which drug is available for the treatment of recurrent Ovarian Ca and what is its MOA?

A

Bevacizumab
Monoclonal Ab directed against VEGF to inhibit angiogenesis

65
Q

Describe the surgical intervention in ovarian Ca

A

Laparotomy
Total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH-BSO)
Plus omentectomy
Plus extra debulking

66
Q

In what ovarian tumours is chemotherapy not useful?

A

Sex cord stromal tumours - so surgery is the mainstay

67
Q

What is the 5 year survival rate for ovarian Ca?

A

46% (stage 1 = 90%, stage 3 = 30%)

68
Q

What staging system is used for vulval Ca?

A

FIGO

69
Q

What type of cancer is the majority of vulval cancers?

A

SSC (95%)

70
Q

Recall some risk factors for usual and differentiated types of vulval Ca

A

Usual type (warty/ basaloid) - VIN (HPV 16), immunosuppression, smoking

Differentiated (keratinised SCC) - lichen sclerosus

71
Q

What is the usual aetiology of vulval Ca?

A

Progression of certain vulval dermatoses or progresssion of VIN

72
Q

How is VIN classified?

A

Low grade squamous, high-grade squamous and differentiated VIN

73
Q

Recall some symptoms of vulval Ca

A

Vulvar swelling, pruritis, pain, bleeding, discharge
May be a nodule or ulcer visible on vulva (usually labia majora)
Inguinal lymphadenopathy

74
Q

What is the management for vulval ca?

A

Vulvectomy and BL inguinal lymphadenectomy
For stage 1a: wide local excision (10mm clear margin)
For >1a: radical vulvectomy + BL inguinal lymphadenectomy
Sentinel node can be identified using dye and radioactive nucleotide

If unsuitable for surgery, ra

Gynae (4 decks)

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