Gynaecology: Bleeding Disorders and Cancer Flashcards

1
Q

Define Post-Menopausal Bleeding?

A

Vaginal bleeding occurring at least 12 months after the last menstrual period.

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2
Q

What is PMB presumed to be until proven otherwise?

A

Endometrial Carcinoma.

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3
Q

Apart from Endometrial Carcinoma, what are some alternative diagnoses for PMB?

A
  • Endometrial hyperplasia (with or without Atypia or Polyps)
  • Cervical Carcinoma
  • Ovarian Carcinoma
  • Atrophic Vaginitis (diagnosis of exclusion)
  • Cervicitis
  • Cervical polyps
  • Foreign bodies e.g. Pessaries
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4
Q

What initial investigations should be performed for a woman presenting with PMB?

A
  • Bimanual examination
  • Speculum examination
  • Cervical smear (if not already performed through national screening programme)
  • Transvaginal USS
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5
Q

What does TVS show?

A
  • Endometrial thickness
  • Pelvic pathology e.g. fibroids, ovarian cysts
  • Fluid in the endometrial cavity (indicates increased risk of malignancy)
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6
Q

When should a patient with PMB go in for an endometrial biopsy and hysteroscopy?

A

If…

  • Endometrial thickness >4/5mm (depends on the literature) OR
  • Multiple episodes of PMB
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7
Q

What management options tend to follow a presentation of PMB?

A

Generally it’ll be either cancer or atrophic vaginitis…

  • Cancer: surgical management options, chemotherapy
  • AV: Oestrogen cream
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8
Q

What is the most important thing to check when a patient presents reporting PMB?

A

Is the bleeding actually coming from the vagina, rather than the urethra or rectum

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9
Q

What are the first and second line treatment options for heavy menstrual bleeding?

A
  • Tranexamic acid, PO

- Merina coil

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10
Q

Why is post menopausal bleeding such a concern?

A

PM women do not menstruate, therefore any bleeding noticed is pathological.

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11
Q

What questions are important to ask in a PMB history?

A
  • Spotting vs Bleeding vs Flooding
  • Any concurrent bladder or bowel problems
  • Symptoms of cancer
  • RFs for cancer
  • Cervical smear history
  • HPV vaccine history
  • Sexually active/protection
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12
Q

What are the most common risk factors for endometrial cancer?

A

Non-oestrogen related:

  • Smoking
  • HTN
  • Diabetes

Oestrogen related:

  • Obesity
  • PCOS Leads to many follicles, leads to high oestrogen levels)
  • Tamoxifen (stimulates endometrial hyperplasia)
  • Lynch syndrome (genetic mutation which increases risk of bowel and endometrial cancer)

Prolonged Oestrogen exposure:

  • Nulliparity
  • Early menarche
  • Late menopause
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13
Q

What are some causes of PMB?

A

Vaginal:

  • Atrophic vaginitis
  • Vulvar cancer
  • Lichen sclerosis

Cervical:

  • Polyps
  • Ectropion
  • Cancer

Uterus:

  • EM cancer
  • EM Hyperplasia
  • EM polyp
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14
Q

How would you investigate a women with PMB?

A

Visualise the vagina and cervix with an external exam + speculum.

Examine the uterus with a TVUSS within 2 weeks (urgent pathway).

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15
Q

What is an Ectropion?

A
  • Condition in which the glandular cells of the inner cervix begin to develop outside of the cervix, which should be squamous cells
  • Symptoms: clear vaginal discharge, PCB, IMB
  • Area looks red and irritated, can be indistinguishable from cancer so should be investigated
  • Causes include: random congenital, hormone related (common in puberty), pregnancy, while on oral contraceptives
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16
Q

What are you looking at in the TVUSS of a woman with PMB?

A

Endometrial thickness, if greater than 4mm (5 in some hospitals), need hysteroscopy and pipelle biopsy

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17
Q

What would a pipelle biopsy show and how are each managed?

A

EM Hyperplasia w/o Atypia:
- Treat with progesterone

EM Hyperplasia w/ Atypia:
- Hysterectomy (possibly TAH BSO)

EM adenocarcinoma:
- Requires CT CAP for staging
- Staged using FIGO system
- If advanced refer to TAH BSO
- +/- Removal of lymph nodes depending on metastasis
+/- Radiotherapy +/- Chemotherapy (mostly paliative)

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18
Q

What is a TAH BSO?

A

Total abdominal hysterectomy with bilateral salpingo-oophorectomy.

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19
Q

What is the benefit of TAH BSO over just a hysterectomy?

A
  • Prevents future ovarian cancer + need for intervention
  • Prevents development of malignant disease (impossible to tell that early whether or not there are mets in the ovaries).
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20
Q

What are your differentials for Post-Coital Bleeding?

A
  • Infection
  • Cancer
  • Cervical Ectropion
  • Cervical or Endometrial Polyps
  • Vaginal atrophic changes
  • Sexual abuse or trauma
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21
Q

What are your differentials for Inter-Menstrual Bleeding?

A

Don’t forget…

  • Think of PREGNANCY causes e.g. Ectopic, Gestational Trophoblastic Disease
  • Physiological causes (Ovulation, Peri-menopause)
  • Medications e.g. SSRIs, anti-coagulants, Tamoxifen, missed COCP

Vaginal causes:

  • Adenosis
  • Vaginitis

Cervical causes:

  • STIs
  • Polyps
  • Ectropion

Uterine causes:

  • Fibroids
  • Polyps
  • Adenomyosis
  • Endometritis

In all cases CANCER

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22
Q

What is the most likely cause of severe cyclical pain?

A

Endometriosis.

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23
Q

What are the most common causes of Chronic Pelvic Pain?

A
  • PID
  • Endometriosis
  • Ovarian cyst
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24
Q

What are the differential diagnoses for Heavy Menstrual Bleeding?

A

Use the Mnemonic; PALM-NOICE

PALM = structural factors:

  • Polyps (endometrial or cervical)
  • Adenomyosis (look for bulky uterus)
  • Leiomyoma (aka Fibroid)
  • Malignancy (or hyperplasia)

NOICE = non-structural factors:

  • Not classified
  • Ovulatory dysfunction (PCOS or Hypothyroidism)
  • Iatrogenic
  • Coagulopathy
  • Endometrial
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25
Q

How is HMB typically managed?

A

First line:

  • Tranexamic acid (esp. if still trying to conceive!), which can cut down bleeding by up to 60%
  • Mirena coil.

Alternatively:

  • Other hormonal options (POP, implant, Depo, COCP)
  • Surgical managements (discussed later)
  • GnRH analogues can be used to manage fibroids conservatively
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26
Q

What coagulopathy is most commonly associated with HMB? What history features do you look for?

A

Von Willebrand’s disease. Look for:

  • Heavy bleeding since menarche
  • Excessive surgical or dental bleeding
  • Bleeding gums
  • Easy bruising
  • PPH
  • Family history

Other coagulopathies linked to HMB include platelet disorders, leukaemia, thrombocytopenia

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27
Q

How is VWD diagnosed?

A

Von Willebrand antigen, might also look for factor 8 activity

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28
Q

What is considered a normal cycle?

A
  • Length of 24-32 days
  • Regularity (although this drops with age)
  • N.B: if cycle flits between the normal range e.g. one month is 25 days another is 30, this is still considered regular
  • Menstrual blood loss 37-43ml/cycle and mostly in first 48 hours
  • However 10% of women lose more than 80ml, 3/4 of whom are anaemic
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29
Q

What factors affect degree of MBL?

A
  • Age, highest in 40s-50s decade
  • Genetics
  • Parity, more children heavier periods (possibly due to adenomyosis)
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30
Q

What is the difference between menorrhagia and metrorrhagia?

A

Menorrhagia = HMB

Metrorrhagia = Heavy irregular bleeding

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31
Q

What is Dysfunctional Uterine Bleeding?

A

Heavy menstrual bleeding with no recognisable pelvic pathology, pregnancy or general bleeding disorders

aka Primary Menorrhagia

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32
Q

How do you clinically assess how heavy someone’s periods are?

A

Difficult, can’t strictly rely on subjective reporting of heaviness (50% of menorrhagia have normal loss).

Best judge is based on:

  • Impact on QoL: staying off work, impact on social life, bleeding through clothing, soiling bed, disrupted sleep
  • Anaemia!!!
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33
Q

When is a patient with HMB high vs low risk?

A

Low risk =

  • Below 45
  • No IMB
  • No risk factors for endometrial cancer (e.g. HTN, diabetes, PCOS, fam history, obesity)

High risk =

  • Above 45
  • Or IMB
  • Or risk factors for Endometrial cancer
  • Or Suspected pathology
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34
Q

How do the assessment pathways differ between low and high risk HMB patients?

A

Low risk are deemed to probably not have any serious underlying pathology, therefore only go for:

  • History
  • Examination
  • FBC
  • First line treatment
  • Follow up

High risk patients could well have something sinister, therefore also get:

  • Pelvic USS
  • Possibly Hysteroscopy and Biopsy
  • THEN get first line treatment
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35
Q

What are the surgical management options for HMB?

A

Used for specific conditions e.g.

  • Polyps= Hysteroscopic removal of polyps (MYOSURE system)
  • Fibroids = Myomectomy or Uterine Artery Ablation
  • Endometrial Ablation (NOVASURE- only if family complete!!!)

Can also do a Hysterectomy (definitive management)

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36
Q

How can fibroids/fibroid based HMB be managed?

A

Medically = GnRH analogues (good but tends to only be temporary)

Surgically = Myomectomy or Uterine Artery Embolization

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37
Q

What is the emergency management of HMB?

A

HMB can be managed in the short term using:

  • Norethisterone 5mg PO TDS, up to 7 days
  • GnRH analogues can be given monthly as injections to induce temporary medical menopause
  • GnRH analogues are good for stopping heavy periods while anaemia is corrected in preparation for another, more surgical intervention e.g. in fibroids.
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38
Q

Define Oligomenorrhoea?

A

Infrequent periods. Cycle greater than 35 days in length but still under 6 months in length

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39
Q

Define Amenorrhoea and what are the two types?

A

Primary:
- No menarche by age 16

Secondary:

  • Absent periods for at least 3 months if cycles previously regular
  • Absent periods for at least 6 months if previously oligomenorrhoea
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40
Q

What are the main causes of Oligomenorrhoea?

A
  • Constitutional

- Anovulation (so PCOS, Thyroid disease, Prolactinoma, CAH)

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41
Q

What are the physiological causes of amenorrhoea?

A
  • Prepubertal
  • Pregnancy
  • Menopause
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42
Q

What is Cryptomenorrhoea?

A
  • Menses ae occurring but without external blood flow (e.g. due to imperforate hymen, absent vagina)
  • Haematocolpos (blood build up in vagina)
  • Haematometra (blood build up in uterus)
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43
Q

What are some pathological causes of PRIMARY amenorrhoea?

A
  • Delayed puberty
  • Imperforate hymen
  • Absent vagina
  • Mullerian agenesis
  • Turner’s
  • PCOS
  • CAH
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44
Q

What are some pathological causes of SECONDARY amenorrhoea?

A
  • Pregnancy
  • PCOS
  • Premature menopause
  • Prolactinoma
  • Thyroid disease
  • Cushing’s
  • Eating disorder
  • Exercise induced
  • Asherman’s
  • Sheehan syndrome
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45
Q

How do you distinguish primary and secondary amenorrhoea?

A

Primary = never had a period

Secondary = No periods in 6 months or 3 cycles

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46
Q

What is Sheehan’s syndrome?

A
  • Massive PPH
  • Hypovolaemia
  • Under-perfusion of the pituitary
  • Becomes non functional
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47
Q

How can you distinguish between infrequent/absent periods caused by the Hypothalamus/Pituitary vs Ovaries vs Uterus

A

Blood test for FSH and Oestrogen:

  • Hypo or Pit causes have low both
  • Ovarian causes have high FSH but low oestrogen
  • Uterine causes will have normal bloods
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48
Q

How would you investigate a patient with PRIMARY amenorrhoea?

A
  • History and exam
  • Check for normal pubertal developments
  • Pregnancy test +/- b-hCG
  • TSH
  • Prolactin
  • LH, FSH
  • Pelvic USS if FSH normal
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49
Q

What are the differentials in a patient with primary amenorrhoea with LOW FSH?

A

Caused by lack of stimulation from pituitary:

  • Constitutional delay
  • Eating disorder
  • Exercise induced amenorrhoea
  • Stress induced (common in famine or war victims)
  • Chronic illness
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50
Q

What are the differentials in a patient with primary amenorrhoea with HIGH FSH?

A

If test high FSH, pituitary is working but ovaries are not responding, have to send for karyotyping

  • 46XX = primary ovarian failure (or premature menopause)
  • 46XO = Turner’s syndrome
51
Q

What is the next step in the investigation of a patient with primary amenorrhoea with NORMAL FSH?

A

Require a Pelvic USS, check for presence of uterus.

If present, it’s either:

  • imperforate hymen
  • vaginal agenesis
  • transverse septum

If absent, send for karyotyping, it’s either:

  • 46 XX = Mullerian agenesis
  • 46 XY = Androgen insensitivity
52
Q

What are the three important tests for primary amenorrhoea and what do they most commonly indicate?

A

FSH:

  • Low = Pituitary dysfunction (constitutional delay, eating disorder)
  • High = Ovarian dysfunction (Primary ovarian failure, Turner’s)
  • Normal = something else

Pelvic USS:

  • Absent uterus = Genetic conditions = Mullerian agenesis, androgen insensitivity
  • Present uterus = imperforate hymen, vaginal agenesis

Karyotyping exists to identify the genetic conditions which can cause amenorrhoea (if necessary) e.g. Turner’s. Mullerian…

53
Q

How do you investigate a patient with amenorrhoea?

A
  • History and exam
  • Pregnancy
  • TSH
  • Prolactin
  • FSH (more diagnostic)
  • Pelvic USS (if FSH normal)
54
Q

How would you interpret FSH results in a patient with secondary amenorrhoea?

A

If low = Pituitary = eating disorder, exercise or stress induced, chronic illness, Sheehan syndrome.

If high = Ovarian = premature ovarian failure, Turner mosaic

If normal = PCOS/Uterine so need Pelvic USS or Hysteroscopy. Most likely uterine cause is adhesions.

55
Q

What is PCOS?

A
  • Heterogenous endocrine disorder with unknown aetiology (link to diabetes)
  • Clusters in families and accounts for 90% of amenorrhoea cases.
  • Usually emerges in adolescence
56
Q

What are the features of PCOS?

A

Hyperandrogenism:

  • Acne
  • Hirsutism (hair growth)
  • Obesity

Anovulation:

  • Oligo/amenorrhoea
  • Infertility

Also commonly get psych issues e.g. depression

57
Q

What conditions can present similarly to PCOS?

A
  • Hypothyroidism
  • Hyperprolactinaemia
  • Cushing’s disease

Less closely:

  • Simple obesity
  • CAH
  • Androgen secreting tumour
  • Primary ovarian failure
58
Q

How do you diagnose PCOS?

A

Rotterdam Criteria- Need 2/3 of…

  • Oligomenorrhoea or anovulation
  • Clinical and/or biochemical signs of hyperandrogenism (acne, hirsutism, obesity)
  • Polycystic ovaries on imaging (12 follicles or more)
59
Q

What blood tests should be ordered in potential PCOS cases?

A

To rule out differentials:

  • TSH (Hypothyroidism)
  • Serum prolactin (Hyperprolactinaemia)

Classic PCOS picture =

  • Raised testosterone
  • Raised LH
  • Normal FSH
  • Low Progesterone
  • Low Sex Hormone Binding Globulin (SHBG)

Use Test and SHBG to calculate free androgen index (FAI), raised = classic of PCOS

60
Q

What are the management options for PCOS?

A

Conservative:

  • Weight loss is the primary intervention for PCOS! (especially good if trying to get pregnant)
  • Encourage generally healthy lifestyle
  • Offer screening for impaired glucose tolerance (diabetic link)
  • Ask about mental wellbeing and refer appropriately

Specific management depends on what woman wants

61
Q

What specific intervention would you offer a woman with PCOS who wants regular periods?

A

COCP or Cyclical Progestogens

62
Q

What specific intervention would you offer a woman with PCOS who wants to conceive?

A
  • Reduce BMI below 30
  • Folic acid
  • Fertility assessment + partner’s semen
  • Refer to fertility services
  • May require ovulation induction
63
Q

What specific intervention would you offer a woman with PCOS who wants to manage their acne?

A

Acne:

  • COCP is good for this as well, will cause periods to return
  • If not should go under dermatology care for retinoids, antibiotics (nice)

Hirsutism:

  • Waxing
  • Laser treatment
64
Q

What are the long term implications of PCOS?

A
  • Higher risk of type 2 diabetes
  • CVD
  • Obstructive sleep apnoea
  • Infertility
  • Recurrent miscarriages
  • Infertility (normally resolves with treatment)
  • Increased chances of complications in pregnancy e.g. pre-eclampsia and diabetes
  • Anxiety, depression
65
Q

How do you define HMB?

A

Clinically, the definition is 80mls+

In reality its based on symptomatic anaemia and impact on QoL

66
Q

How does PCOS present (menstruation wise)?

A

Fluctuation between HMB and Amenorrhoea

67
Q

What is the most important contraindication of Tranexamic acid?

A

DVTs and PEs, as its a pro-clotting agent

68
Q

What are the 5 common interventions for HMB?

A

1) Tranexamic Acid (for bleeding) +/- Mefenamic Acid (for pain)
2) Hormonal therapy: Mirena, COCP, POP, Depo…
3) Endometrial Ablation (e.g. Novasure)
4) IF Polyp Uterine Artery Embolisation
5) If all else fails, Hysterectomy

69
Q

How do you take Tranexamic acid?

A

When the bleeding occurs, 1g, 3 times a day.

70
Q

What is crucial to check before sending a patient in for endometrial ablation?

A
  • Is there family complete, EA can be sterilising
  • Pregnancy is absolutely contraindicated following
  • Must have taken an endometrial biopsy, can’t miss cancer.
71
Q

What is the classic Endometriosis presentation and what is the diagnostic gold standard?

A

CYCLICAL pain + pain on pooing, intercourse + irregular menstruation

72
Q

What are the main management options for Endometriosis?

A

Medical:
- Mefenamic Acid (for pain)
- Mirena, COCP, POP…
(a good option is COCP trycycling, where they take it for 90 days straight)

Surgical:

  • Diathermy
  • Resection
  • Hysterectomy
73
Q

What is essential to test before performing a hysterectomy for endometriosis?

A

GnRH analogue test. Puts patients into a pseudo menopausal state which should cure their pain. IF it doesn’t something else is going on and it would be worthwhile to address that before removing the uterus.

74
Q

What are the most common gynae cancers in the UK?

A

Uterus and Ovarian and Cervical.

Vulval and Vaginal less common.

75
Q

What is the respective 10 year survival rates for Uterine, Ovarian and Cervical cancers?

A

Uterine (78%) and Cervical (63%) quite good.

Ovarian quite poor, 35%.

76
Q

Which gynae cancers are largely preventable?

A

Generally, the more common two (Uterine and Ovarian) are not preventable.

The least common three (Cervical, Vulval and Vaginal) are mostly preventable.

77
Q

At what age does endometrial cancer generally present?

A

Women aged 64-74, risk rapidly declines after age 80

78
Q

What are some risk factors and protective factors for endometrial cancer?

A

RFs:

  • Obesity
  • Oestrogen exposure (early menarche, late menopause, nulliparity, unopposed oestrogen, tamoxifen)
  • PCOS
  • Previous breast/ovarian cancer
  • BRCA 1/2
  • Endometrial polyps
  • Diabetes
  • Parkinson’s

PFs:

  • Continuous HRT
  • COCP
  • Smoking
  • Physical activity
  • Coffee
  • Tea
79
Q

How do women with EMB present?

A

Pre-menopausal:

  • Prolonged and frequent bleeding
  • IMB

Post-menopausal:

  • PMB!!!
  • Can see blood stained watery and/or purulent discharge but this is less common.
80
Q

What is endometrial hyperplasia and how is it managed?

A
  • Pre-malignant endometrial growth

- Can be with or without atypia

81
Q

How common is cancer progression in EH with atypia?

A
  • 25-50% of the time malignancy co-exists

- 20% develop Ca within 10 years

82
Q

How do you manage endometrial hyperplasia?

A

Ideally surgery (TAH BSO). Can use prostagens.

83
Q

What are the two types of endometrial carcinoma?

A

T1 = Endometrial Adenocarcinoma (80%)

T2 = Papillary Serous, Clear cell, Carcinosarcoma (20%)

Endometrial Sarcoma is incredibly rare.

84
Q

Outline the FIGO staging of endometrial cancer?

A

1 = Limited to myometrium

2 = Cervical spread

3 = Uterine serosa/ ovaries/ tubes/ vagina/ pelvis/ para-aortic lymph notes

4 = Bladder/ bowel/ distant mets

Survival = 80, 60, 40, 20%

85
Q

How is endometrial cancer investigated and diagnosed?

A

TV USS: Useful before clinic to measure endometrial thickness in a woman with PMB, 5mm is cut off for risk.

Gold standard = Hysteroscopy w/ Endometrial sampling by Pipelle biopsy

86
Q

What investigations can be used to look for metastasis in endometrial cancer?

A

All patients should receive blood tests (FBCs, Us and Es, LFTs)

If seriously concerned about mets risks:

  • CT CAP (looks at peritoneum, lungs, bones and brain)
  • MRI Pelvis
87
Q

What is the preferred management of endometrial cancer and what influences this decision?

A

Surgery (TAH BSO + peritoneal washing) (can be laparoscopic or open)

Stage, grade, age, fitness for surgery, patient preference

85% of patients go for surgery.

88
Q

What are the main non surgical alternatives for endometrial cancer?

A
  • Long term progestogens therapy with supervision

- Radiotherapy (also given as adjuvant therapy if high risk of recurrence)

89
Q

What options are available if surgery is counter-indicated, disease is inoperable or too advanced?

A
  • Chemotherapy
  • Radiotherapy
  • Hormonal therapy (aromatase inhibitors)
  • Palliative care
90
Q

What should be offered to a woman presenting to primary care with PMB?

A

Referral to one-stop PMB clinic for:

  • History and Exam by consultant gynaecologist
  • FBC
  • TV USS
  • Hysteroscopy + Endometrial biopsy
91
Q

What is the peak age for Ovarian cancer?

A

70-74 years of age.

92
Q

How are ovarian tumours classified?

A
By malignancy status:
- Benign
- Borderline
- Malignant
(no pre-malignant stage therefore no screening)

By cell line:

  • Surface epithelium (90%) –> Serous, Mucinous, Endometrioid, Clear cell, Brenner tumours
  • Germ cells
  • Stroma or Sex cord
  • Mets, Lymphomas
93
Q

How do ovarian tumours spread?

A

Through the peritoneum, therefore normally present with quite advanced disease

94
Q

What are the most common forms of ovarian cancer?

A

Epithelial line:

  • Serous (can be benign or malignant)
  • Mucinous (can be benign or malignant)

Germ cell line:
- Teratoma (benign or very rarely malignant)

95
Q

What are the risk and protective factors for ovarian cancer?

A

RFs:

  • Obesity
  • Oestrogen exposure (nulliparity, early menarche, late menopause, unopposed oestrogen)
  • Family history and BRCA 1/2
  • Endometriosis

PFs:

  • COCP
  • Pregnancy
  • Breastfeeding
  • Hysterectomy
  • Oophorectomy
  • Sterilisation
96
Q

How does Ovarian cancer present?

A
  • Non-specific symptoms
  • Can be incidental finding

Symptoms:

  • Abdominal swelling
  • Pain
  • Anorexia, N, V, Weight loss
  • Vaginal bleeding
  • Pressure symptoms on bowel and bladder
97
Q

What investigations should be ordered for a woman with suspected ovarian cancer?

A
  • Pelvic exam
  • USS
  • FBC, Us and Es, LFTs

CA125!!!

  • Cytology of ascitic tap
  • CXR/CT to look for mets
  • Can do surgical exploration
98
Q

Outline the stages of Ovarian cancer?

A
1 = Limited to ovaries
2 = Spread to pelvic organs
3 = Spread to rest of peritoneal cavity, or omentum, or lymph notes
4 = Lung mets, Liver mets, Distant parenchyma
99
Q

How is epithelial ovarian cancer managed?

A

Epithelial cancer (90% of cancers):

  • Staging Laparotomy
  • TAH + BSO + Debulking
  • Chemo: Cisplatin + Paclitaxel
  • (if woman is of reproductive age and still wants kids, consider oophorectomy only)
100
Q

How is non-epithelial ovarian cancer managed?

A

Non-epithelial tumours:

  • Very chemo sensitive
  • Often treated with combination of conservative surgery and chemo
101
Q

What chemo regime is used for Ovarian cancer?

A

Cisplatin/Carboplatin + Paclitaxel

102
Q

What should be ordered for a woman presenting with suspected ovarian cancer (e.g. abdo distention, anorexia, change in bowel habit in a woman with risk factors)?

A

Refer to gynae clinic:

  • History and exam with consultant gynaecologist
  • Ca125
  • Abdominal or Pelvic USS
103
Q

What women are at greatest risk of cervical cancer?

A

Bimodal age distribution:

  • 30s
  • 80s

More common in women of lower SES due to reduced uptake of screening programmes.

104
Q

What are the RFs and PFs of cervical cancer?

A

RFs:

  • Young age at first intercourse
  • Multiple partners
  • No barrier contraception
  • Smoking
  • Long term COCP use
  • Immunosuppression

Only recognised PFs are vaccination and compliance to screening programmes

105
Q

What are the high risk (oncogenic) HPV types?

A

16 and 18 are the two the vaccine works against, others are rarer e.g. 31, 33, 34, 35…

Produce proteins E6 and E7 which suppresses the p53 tumour suppressor gene.

106
Q

How common is HPV infection?

A

Most women will be infected at some point in their life, commonest in teens and early 20s, infection lasts about 8 months.

Cervical cancer should be viewed as a rare complication of a common infection.

107
Q

What is CIN?

A

When HPV is not cleared by the body, persists, it causes…

Cervical Intraepithelial Neoplasia, an asymptomatic pre-malignant condition affecting the Transformation Zone. 60% CN1 regresses spontaneously, 30% CN3 progresses to invasive cancer over the next 5-10 years.

108
Q

How is CIN classified?

A

Based on degree of infiltration of basement membrane: CN1, CN2, CN3.

Histological diagnosis.

109
Q

How does Cervical cancer present?

A

PCB, PMB, IMB, Blood stained vaginal discharge.

50% of cases have had zero smears.

110
Q

How is Cervical cancer staged?

A

1 = Confined to cervix

2 = Beyond cervix but not pelvic side wall or lower third of vagina

3 = Pelvic spread, reaches side wall or lower third of vagina

4 = Distant spread or invades adjacent organs

111
Q

How is Cervical cancer managed?

A

Depends on stage:

  • Micro-invasive carcinoma can be managed conservatively, cone biopsy if concerns about fertility. If family complete, hysterectomy is appropriate
  • Stages 1b-2a: Wertheim’s radical hysterectomy OR chemoradiotherapy
  • Beyond stage 2a: Chemoradiotherapy
  • Post-Op Radiotherapy can be offered

Ideally patients only have one of surgery or CR, both has too many side effects.

112
Q

What form of hysterectomy is used in cervical cancer?

A

Wertheim’s

113
Q

What are the general complications of gynaecologic oncology surgeries?

A
  • Infection
  • VTE
  • Haemorrhage
  • Vesicovaginal fistula
  • Bladder dysfunction
  • Short vagina
114
Q

What are some common complications of gynae radiotherapy?

A
  • Vaginal dryness
  • Vaginal stenosis
  • Radiation cystitis
  • Radiation proctitis
  • Loss of ovarian function
115
Q

How frequently is cervical cancer smeared for?

A
  • First invitation at age 25
  • 3 yearly between 25 and 50
  • 5 yearly between 50 and 65
  • After 65 only selected patients
116
Q

How are the results from a cervical smear interpreted?

A

Normal = Routine recall

Moderate or Severe Dyskaryosis = Colposcopy + Histology

Borderline or Mild Dyskaryosis = Require HPV test (if negative, routine recall, if positive, Colposcopy + Histology)

117
Q

What is looked for on colposcopy?

A

Features suggestive of CIN or invasion:

  • Abnormal vascular pattern (mosaicism, punctuation)
  • Abnormal staining of the tissue (aceto-white, brown iodine)
118
Q

How is CIN treated?

A

Excisional options:

  • LLETZ (large loop excision of the transformation zone)
  • Cold knife cone

Destructive options:

  • Cryocautery
  • Diathermy
  • Laser vaporisation
119
Q

Summarise the screening process for cervical cancer?

A

Smear cytology detects DYSKARYOSIS
–>
Colposcopy, opinion based on visual assessment, treatment or biopsy as directed
–>
Biopsy provides histological diagnosis of CIN 1/2/3/Invasion

120
Q

How does vulval cancer present?

A

Ulcerative or raised lesion on vulva.

VIN (premalignant condition) can present as:

  • Asymptomatic
  • Itching, burning, pain
  • Same as CIN mostly resolved but can progress to cancer
121
Q

How is VIN managed?

A

Conservatively: Antihistamine for symptom management

Medically: Imiquimod

Surgically: Excision

122
Q

What are the RFs for vulval cancer?

A
  • HPV
  • HSV Type 2
  • Smoking
  • Immunosuppression
  • Chronic vulvar irritation
  • Lichen Sclerosus
123
Q

What type of cancer is vulval cancer?

A

SCC, normally caused by high rates of skin turnover in an infection (e.g HPV) or a chronic skin disease (e.g. Lichen Sclerosis)

124
Q

How is vulval cancer managed?

A

Surgical excision (with anatomical considerations), Radiotherapy, Chemo