Gynae Flashcards

1
Q

What are fibroids?

A

Benign tumours of the smooth muscle of the uterus that are oestrogen sensitive (grow in response to oestrogen)

Also called uterine leiomyomas

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2
Q

How common are fibroids?

A
  • Very common - 40-60% of women in later reproductive years
  • More common in black women
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3
Q

What are the types of fibroids?

A
  • Intramural: within myometrium
  • Subserosal: just below outer layer of uterus (grow outwards)
  • Submucosal: just below lining of uterus
  • Pedunculated: on a stalk
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4
Q

What is the presentation of fibroids?

A

Often asymptomatic
* Menorrhagia (heavy period)
* Prolonged period (> 7 days)
* Abdominal pain (worse during period)
* Bloating
* Urinary/bowel Sx: due to pelvic pressure/fullness
* Deep dyspareunia
* Reduced fertility

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5
Q

What investigations should be done for fibroids?

A
  • Hysteroscopy: submucosal fibroids presenting with heavy menstruation
  • Pelvic USS
  • MRI before surgery
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6
Q

What is the medical management of fibroids?

A
  • Mirena coil - depending on size & shape of fibroids/uterus
  • NSAIDs and tranexamic acid - Sx management
  • Combined oral contraceptive
  • Cyclical oral progestogens
  • Referral to gynaecology if > 3cm
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7
Q

What is the surgical management of smaller and larger fibroids?

A

Smaller fibroids:
* Endometrial ablation
* Resection of submucosal fibroids
* Hysterectomy

Larger fibroids:
* Uterine artery embolisation
* Myomectomy
* Hysterectomy

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8
Q

What is uterine artery embolisation?

A
  • Catheter inserted into femoral artery, then passed through to uterine artery
  • Once in correct place, particles injected that cause a blockage in the arterial supply to the fibroid: starves it of oxygen causing it to shrink
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9
Q

What medications may be used before fibroid surgery?

A

GnRH agonists e.g. goserelin/leuprorelin
* Used to reduce size of fibroid before surgery by reducing the amount of oestrogen maintaining the fibroid
* Usually only used short-term

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10
Q

What is myomectomy?

A

Surgically removing fibroid via laparoscopic surgery (keyhole) or laparotomy (open surgery)
* Only Tx known to potentially improve fertility in fibroid patients

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11
Q

What is endometrial ablation?

A
  • Used to destroy the endometrium
  • Balloon thermal ablation: inserting specially designed balloon into endometrial cavity & filling it with high-temp fluid that burns the endometrial lining of uterus
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12
Q

What is a hysterectomy?

A

Removing the uterus & fibroids
* May be laparoscopy, laparotomy or vaginal approach
* Ovaries may be removed or left (depends on patient preference, risks & benefits)

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13
Q

What are some complications of fibroids? (7)

A
  • Iron deficiency anaemia (from heavy period)
  • Reduced fertility
  • Pregnancy Cx e.g. miscarriages, premature labour, obstructive delivery
  • Constipation
  • Urinary outflow obstruction/ UTI
  • Red degeneration of fibroid
  • Torsion of fibroid (usually affects pedunculated fibroids)
  • Malignant change to leiomyosarcoma (very rare)
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14
Q

What is red degeneration of fibroids?

A

Ischaemia, infarction & necrosis of the fibroid due to disrupted blood supply
* More likely to occur in fibroids > 5cm during 2nd + 3rd trimester

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15
Q

What are possible causes of ischaemia in red degeneration of fibroids?

A
  • As fibroid rapidly enlarges during pregnancy it outgrows its blood supply
  • Kinking in blood vessels as uterus changes shape & expands during pregnancy
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16
Q

How does red degeneration of fibroids present?

A
  • Severe abdo pain
  • Low-grade fever
  • Tachycardia
  • Vomiting
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17
Q

What is the management of red degeneration of fibroids?

A

Rest, fluid, analgesia

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18
Q

What are ovarian cysts?

A

Cyst = Fluid-filled sac
* Functional ovarian cysts - related to fluctuating hormones of menstrual cycle
* Very common in pre-menopausal women (benign usually)

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19
Q

What is the presentation of ovarian cysts?

A
  • Most are asymptomatic
  • Pelvic pain: if ovarian torsion, haemorrhage or rupture of cyst
  • Bloating
  • Fullness in abdomen
  • Palpable pelvic mass
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20
Q

What are the two types of functional cysts?

A

Follicular cysts (MC):
* Occur when follicle fails to rupture and release egg
* Harmless & tend to disappear after a few cycles
* Typically have thin walls & no internal structures = give reassuring appearance on USS

Corpus luteum cysts:
* Occur when corpus luteum fails to break down & instead fills with fluid
* May cause pelvic discomfort/pain/delayed period
* Often seen in early pregnancy

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21
Q

What are some other types of ovarian cysts (not functional)?

A
  • Serous cystadenoma: benign tumour of epithelial cells
  • Mucinous cystadenoma: same as above but these can become huge & take up lots of space in pelvis/abdomen
  • Endometrioma: lumps of endometrial tissue within ovary (occurs in endometriosis), can cause pain & disrupt ovulation
  • Dermoid cysts/Germ cell tumours: benign ovarian tumours, teratomas (come from germ cells & may contain various tissue types e.g. skin, teeth, hair, bone), associated w/ ovarian torsion
  • Sex Cord-stromal tumours: rare, can be benign or malignantm, arise from stroma or sex cords, several types - includes Sertoli-Leydig cell tumours & granulosa cell tumours
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22
Q

What features of an ovarian cyst history/examination suggest malignancy?

A
  • Abdo bloating
  • Reduced appetite
  • Wt loss
  • Early satiety
  • Urinary Sx
  • Pain
  • Ascites
  • Lymphadenopathy
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23
Q

What investigations are done for ovarian cysts?

A
  • Premenopausal women w/ simple ovarian cyst < 5cm on USS don’t need further Ix
  • Women < 40 years with complex ovarian mass require tumour markers for a possible germ cell tumour (LDH, alpha-FP, HCG)
  • CA125 = tumour marker for ovarian cancer
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24
Q

What are some non-malignant causes of raised CA125?

A
  • Endometriosis
  • Fibroids
  • Adenomyosis
  • Pelvic infection
  • Liver disease
  • Pregnancy
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25
Q

What is the Risk of malignancy index (RMI)?

A

Estimates risk of an ovarian mass being malignant, takes into account:
* Menopausal status
* USS findings
* CA125 level

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26
Q

What is the management of ovarian cysts in pre-menopausal women?

A
  • < 5cm: resolves within 3 cycles (no follow up needed)
  • 5-7cm: routine referral to gynae & yearly US monitoring
  • >7cm: MRI scan/surgical evaluation

Persistent/enlarging cysts: ovarian cystectomy (removing cyst) possibly with oophorectomy (removing affected ovary)

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27
Q

What is the management of ovarian cysts in post-menopausal women?

A
  • Raised CA125/complex cysts: 2-week wait suspected cancer referral
  • Simple cysts/normal CA125: monitor with USS every 4-6 months

Requires correlation with CA125 result

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28
Q

What are the 3 main complications of ovarian cysts when patient presents with acute onset pain?

A
  • Torsion
  • Haemorrhage in cyst
  • Rupture w/ bleeding into peritoneum
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29
Q

What is the triad of Meig’s syndrome?

A
  • Ovarian fibroma
  • Pleural effusion
  • Ascites

  • Typically older women
  • Removal of tumour = complete resolution of effusion & ascites
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30
Q

What is ovarian torsion?

A

MEDICAL EMERGENCY
Ovary twists in relation to the adnexa

(surrounding connective tissue, fallopian tube & blood supply)

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31
Q

What is the pathophysiology of ovarian torsion?

A
  • Usually due to ovarian mass >5cm / normal ovaries in younger girls before menarche (longer infundibulopelvic ligaments that can twist more easily)
  • Twisting of adnexa & blood supply to ovary = ischaemia
  • If torsion persists = necrosis = function lost
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32
Q

What is the presentation of ovarian torsion?

A

Sudden onset severe unilateral pelvic pain
* constant
* gets progressively worse
* associated with N+V
* localised tenderness on exam & maybe palpable mass in pelvis

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33
Q

What investigation is done for ovarian torsion? And what does it show?

A

Pelvic USS shows:
* whirlpool sign
* free fluid in pelvis
* oedema of ovary

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34
Q

What is the management of ovarian torsion?

A

Laparoscopic surgery to either:
* DETORSION = untwist ovary & fix it in place
* OOPHORECTOMY = remove affected ovary

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35
Q

What are the complications of ovarian torsion?

A
  • If left untreated = loss of function of ovary (fertility not typically affected because other ovary can usually compensate)
  • When necrotic ovary isn’t removed = infected/develop abscess/sepsis
  • May also rupture - peritonitis & adhesions
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36
Q

What is Lichen Sclerosus?

A

Chronic inflammatory skin condition that presents with patches of shiny porcelain-white skin
* Autoimmune condition: associated with other AI diseases (T1DM, hypothyroid, vitiligo, alopecia)

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37
Q

Where does lichen sclerosus typically affect?

A
  • Women: labia, perineum, perianal skin
  • Men: foreskin, glans of penis
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38
Q

What is the presentation of lichen sclerosus?

A
  • 45-60 y.o woman complaining of vulval itching & skin changes in vulva
  • Can be asymptomatic
  • itching
  • soreness/pain
  • skin tightness
  • superficial dyspareunia
  • erosions
  • fissures
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39
Q

What is the Koebner phenomenon?

A

When Sx are made worse by friction to the skin
* e.g. lichen sclerosus can be made worse by tight underwear, urinary incontinence & scratching

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40
Q

What is the appearance of lichen sclerosus?

A
  • ‘Porcelain-white’
  • Shiny
  • Tight
  • Thin
  • Slightly raised
  • May be papules/plaques
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41
Q

What is the management of lichen sclerosus?

A

Control Sx with potent topical steroids and follow up every 3-6 months

  • Clobetasol propionate (Dermovate)
  • Emollients should be used regularly
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42
Q

What are the complications of lichen sclerosus?

A
  • 5% risk of developing squamous cell carcinoma of the vulva
  • Pain/discomfort
  • Sexual dysfunction
  • Bleeding
  • Vaginal/urethral openings narrowing
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43
Q

What are the most common types of cervical cancer?

A
  • Squamous cell carcinoma - 80% (MC)
  • Adenocarcinoma
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44
Q

Who does cervical cancer typically affect?

A

Younger women, peaking in reproductive years

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45
Q

What is the most common cause of cervical cancer?

A

HPV - types 16 and 18 (responsible for ~70% cervical cancers)

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46
Q

How does HPV cause cervical cancer?

A
  • P53 & pRb = tumour suppressor genes
  • HPV produces two proteins: E6 and E7
  • E6 inhibits p53
  • E7 inhibits pRb
  • Therefore HPV promotes development of cancer by inhibiting tumour suppressor genes
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47
Q

What are the risk factors for cervical cancer?

A
  • Increased risk of catching HPV: early sexual activity, more sex partners, not using condoms
  • Not engaging with screening = later detection of precancerous/cancerous changes
  • Smoking
  • HIV
  • Combined contraceptive pill
  • FHx
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48
Q

What is the presentation of cervical cancer?

A

Non specific:
* Abnormal vaginal bleeding
* Vaginal discharge
* Pelvic pain
* Dyspareunia

Appearances that suggest cervical cancer:
* Ulceration
* Inflammation
* Bleeding
* Visible tumour

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49
Q

What are two prevention strategies for cervical cancer?

A
  • HPV vaccine: HPV strongly associated w/ cervical cancer, so children 12-13 y.o. vaccinated to reduce risk
  • Cervical screening with smear tests: screen for precancerous & cancerous changes to cells of cervix
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50
Q

What is the cervical intraepithelial neoplasia (CIN) grading system?

A
  • Grading system for the levels of dysplasia in the cells of the cervix
  • CIN is diagnosed at colposcopy (NOT with cervical screening)

Grades are:
* CIN I - mild dysplasia
* CIN II - moderate dysplasia
* CIN III - severe dysplasia / cervical carcinoma in situ

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51
Q

What is involved in cervical cancer screening?

A

Aims to pick up precancerous changes in epithelial cells of cervix
* Smear test: speculum exam & collection of cells from cervix
* Cells deposited into preservation fluid & transported to lab for microscopy to check for dyskaryosis (precancerous cervical cells)
* Samples initially tested for high-risk HPV before cells are examined: if HPV negative, the cells are not examined = smear considered negative

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52
Q

How often are smear tests in the cervical screening program?

A
  • Every 3 years for 25-49 y.o
  • Every 5 years for 50-64 y.o.
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53
Q

What is the management depending on the smear test results?

A
  • HPV negative - continue routine screening
  • HPV positive with normal cytology - repeat HPV test after 12 months
  • HPV positive with abnormal cytology - refer for colposcopy
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54
Q

What happens during colposcopy?

A
  • Inserting speculum & using colposcope to magnify cervix (allows epithelial lining of cervix to be examined)
  • Acetic acid / iodine solution stains used
  • Acetic acid = abnormal cells appear white (“acetowhite”): occurs in cells with more nucleic material e.g. cervical cancer cells
  • Schiller’s iodine test = healthy cells appear brown, abnormal areas don’t stain
  • To get tissue sample = punch biopsy/large loop excision of the transformational zone (loop biopsy)
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55
Q

What is a loop biopsy?

A

Using a loop wire with electrical current (diathermy) to remove abnormal epithelial tissue on the cervix by cauterising it
* Bleeding/abnormal discharge can occur for weeks following LLETZ procedure

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56
Q

What is a cone biopsy?

A

Treatment for cervical intraepithelial neoplasia (CIN) & very early-stage cervical cancer
* Under general anaesthetic - cone-shaped piece of cervix removed using scalpel
* Sent to histology to assess for malignancy

Risks include:
* pain
* bleeding
* infection
* scar formation with stenosis of cervix
* increased risk of miscarriage & premature labour

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57
Q

What is the FIGO staging system for cervical cancer?

A
  • Stage 1: confined to cervix
  • Stage 2: invades uterus or upper 2/3 vagina
  • Stage 3: invades pelvic wall or lower 1/3 vagina
  • Stage 4: invades bladder, rectum or beyond pelvis
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58
Q

What is the management of each cervical cancer stage?

A
  • CIN & early-stage 1A: LLETZ / cone biopsy
  • Stage 1B-2A: radical hysterectomy & removal of local lymph nodes w/ chemo + radio
  • Stage 2B-4A: chemotherapy + radiotherapy
  • Stage 4B: combination of surgery, radio, chemo, palliative care
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59
Q

What is pelvic exenteration?

A
  • Removing all/most of pelvic organs (vagina, cervix, uterus, fallopian tubes, ovaries, bladder, rectum)
  • Used in advanced cervical cancer
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60
Q

What is Bevacizumab?

A
  • MAB used in combo with other chemotherapies in treatment of metastatic/recurrent cervical cancer
  • Targets vascular endothelial growth factor A (VEGF-A): responsible for growth of new blood vessels
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61
Q

What is endometrial cancer?

A

Cancer of the uterus lining
* Oestrogen-dependent cancer = oestrogen stimulates growth of endometrial cancer cells

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62
Q

What is the most common type of endometrial cancer?

A

Adenocarcinoma ~80%

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63
Q

What are the risk factors for endometrial cancer?

A
  • T2DM (increased insulin = stimulates endometrial cells)
  • Obesity (adipose tissue = source of oestrogen)
  • Older
  • Earlier onset of period
  • Late menopause
  • Oestrogen only HRT
  • no/fewer pregnancies
  • PCOS (lack of ovulation)
  • Tamoxifen (anti-oestrogenic effect on breast tissue, but oestrogenic effect on endometrium)

Exposure to unopposed oestrogen (oestrogen without progesterone)

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64
Q

What is the primary source of oestrogen in postmenopausal women?

A

Adipose tissue
* Contains aromatase = enzyme that converts androgens (e.g. testosterone) into oestrogen
* More adipose tissue = more aromatase = more androgens converted

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65
Q

What are 4 protective factors against endometrial cancer?

A
  • Combined contraceptive pill
  • Mirena coil
  • Increased pregnancies
  • Cigarette smoking
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66
Q

What is the presentation of endometrial cancer?

A

Postmenopausal bleeding
* Postcoital bleeding
* Intermenstrual bleeding
* Menorrhagia
* Abnormal vaginal discharge
* Haematuria
* Anaemia
* Raised platelet count

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67
Q

What is the criteria for a transvaginal USS referral for women over 55 years?

A
  • Unexplained vaginal discharge
  • Visible haematuria plus raised platelets/ anaemia/elevated glucose levels
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68
Q

What investigations should be done for endometrial cancer? (3)

A
  • Transvaginal USS for endometrial thickness
  • Pipelle biopsy: highly sensitive for endometrial cancer
  • Hysteroscopy w/ endometrial biopsy
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69
Q

What is the FIGO staging for endometrial cancer?

A
  • Stage 1: confined to uterus
  • Stage 2: invades cervix
  • Stage 3: invades ovaries/fallopian tubes/vagina/lymph nodes
  • Stage 4: invades bladder/rectum/beyond pelvis
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70
Q

What is the management of stage 1 and 2 endometrial cancer?

A

Total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAH and BSO): removal of uterus, cervix & adnexa

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71
Q

What are some other treatment options for endometrial cancer? (not TAH and BSO)

A
  • Radical hysterectomy - also removes pelvic lymph nodes, surrounding tissues & top of vagina
  • Radiotherapy
  • Chemotherapy
  • Progesterone: hormonal Tx to slow progression
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72
Q

What are the types of ovarian cancer?

A
  • Epithelial cell tumours (MC): MC subtype = serous tumours
  • Dermoid cysts/Germ cell tumours: teratomas, benign, may contain various tissue types e.g. teeth, hair, bone
  • Sex cord-stromal tumours: rare
  • Metastasis: from cancer elsewhere
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73
Q

What is a Krukenberg tumour?

A

Metastasis in ovary from GI tract cancer, particularly stomach
* Have ‘signet-ring’ cells on histology

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74
Q

What are the risk factors for ovarian cancer?

A
  • Age (60 y.o. peak)
  • BRCA1 & BRCA2 genes
  • Increased number of ovulations (early onset period, late menopause, no pregnancies)
  • Obesity
  • Smoking
  • Recurrent use of clomifene - medication used for ovulation
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75
Q

What are protective factors for ovarian cancer?

A

Factors that stop ovulation or reduce number of lifetime ovulations reduce the risk:
* Combined contraceptive pill
* Breastfeeding
* Pregnancy

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76
Q

What is the presentation of ovarian cancer?

A
  • Non-specific Sx
  • Abdo bloating
  • Early satiety
  • Appetite loss
  • Pelvic pain
  • Urinary Sx (freq/urgency)
  • Wt loss
  • Abdo/pelvic mass
  • Ascites
  • Referred hip/groin pain (due to ovarian mass pressing on obturator nerve
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77
Q

What is the referral criteria for referring directly to a 2-week-wait for ovarian cancer?

A

If physical exam reveals:
* Ascites
* Pelvic mass
* Abdo mass

78
Q

What is the criteria for carrying out initial investigations in primary care before a referral for ovarian cancer?

A

Women over 50 years presenting with:
* New Sx of IBS/ change in bowel habit
* Abdo bloating
* Early satiety
* Pelvic pain
* Urinary freq/urgency
* Wt loss

79
Q

What investigations should be done in primary care for ovarian cancer?

A
  • CA125 blood test (>35 = significant)
  • Pelvic USS
  • RMI: Risk of Malignancy Index (estimates risk of ovarian mass being malignant)
80
Q

What 3 things does the Risk of Malignancy Index for ovarian cancer take into account?

A
  • Menopausal status
  • USS findings
  • CA125 level
81
Q

What investigations should be done in secondary care for ovarian cancer?

A
  • CT scan
  • Histology
  • Paracentesis (test ascitic fluid: cancer cells)
  • Women < 40y.o with complex ovarian mass require tumour markers for possible germ cell tumour: Alpha-fetoprotein (a-FP) & Human chorionic gonadotropin (HCG)
82
Q

What is the FIGO staging for ovarian cancer?

A
  • Stage 1: confined to ovary
  • Stage 2: spread past ovary but inside pelvis
  • Stage 3: spread past pelvis but inside abdomen
  • Stage 4: spread outside abdomen
83
Q

What is the management of ovarian cancer?

A

Combination of surgery and chemotherapy

84
Q

What is the prognosis of ovarian cancer?

A
  • Often presents late due to non-specific Sx
  • > 70% of patients present after it has spread beyond pelvis
85
Q

What type of cancer is vulval cancer?

A
  • Very rare
  • ~90% = squamous cell carcinomas
  • Less common = malignant melanomas
86
Q

What are the risk factors for vulval cancer?

A
  • Older (>75)
  • Immunosuppression
  • HPV
  • Lichen sclerosus (~5% women with this get vulval cancer)
87
Q

What is vulval intraepithelial neoplasia? (VIN)

A

Premalignant condition affecting squamous epithelium of skin that can precede vulval cancer

88
Q

What are the 2 types of VIN?

A
  • High grade squamous intraepithelial lesion: associated with HPV infection (typically younger - 35-50y.o.)
  • Differentiated VIN: associated with lichen sclerosus (typically older - 50-60y.o.)
89
Q

What is the management of VIN?

A

Biopsy then:
* Watch & wait
* Surgery to remove lesion
* Iquimod cream
* Laser ablation

90
Q

What is the presentation of vulval cancer?

A
  • Vulval lump (irregular mass)
  • Ulceration
  • Bleeding
  • Pain
  • Itching
  • Lymphadenopathy in groin

Usually affects labia majora

91
Q

What investigations are done to diagnose vulval cancer?

A
  • Biopsy of lesion
  • Sentinel node biopsy: demonstrate lymph node spread
  • Further imaging for staging e.g. CT abdo & pelvis
92
Q

What is the management of vulval cancer?

A
  • 2-week-wait urgent cancer referral
  • Wide local excision
  • Groin lymph node dissection
  • Chemotherapy
  • Radiotherapy
93
Q

What is the cause of vaginal cancer?

A

HPV

94
Q

What are the symptoms of vaginal cancer?

A
  • lump in vagina
  • ulcers/skin changes around vagina
  • abnormal bleeding from vagina
  • Dyspareunia
  • smelly/bloodstained discharge
  • dysuria
95
Q

What are the risk factors for vaginal cancer?

A
  • Exposure to HPV infection
  • > 75 y.o.
  • Smoking
  • If mother took diethylstilbestrol when pregnant (once used to prevent miscarriage)
96
Q

What are the types of vaginal cancer?

A
  • Vaginal squamous cell carcinoma (MC)
  • Vaginal adenocarcinoma
  • Vaginal melanoma (rare)
  • Vaginal sarcoma (rare)
97
Q

What investigations are done for vaginal cancer?

A

Colposcopy

98
Q

What is the treatment of vaginal cancer?

A
  • Radiotherapy
  • Surgery
  • Chemotherapy
  • HPV vaccine for prevention
99
Q

What is a hydatidiform mole?

A

Type of tumour that grows like a pregnancy inside the uterus: molar pregnancy

100
Q

What are the 2 types of molar pregnancy?

A

Complete mole:
* two sperm cells fertilise an ‘empty ovum’ (contains no genetic material)
* These sperm combine genetic material - cells start to divide & grow into a tumour
* No fetal material will form

Partial mole:
* two sperm cells fertilise normal ovum (containing genetic material) at same time
* Cell now has 3 sets of chromosomes
* Cell divides & multiplies into a tumour
* Some fetal material may form

101
Q

What signs indicate a molar pregnancy vs a regular pregnancy?

A
  • More severe morning sickness
  • Vaginal bleeding
  • Increased enlargement of uterus
  • Abnormally high hCG
  • Thyrotoxicosis - hCG can mimic TSH & stimulate the thyroid to produce excess T3 and T4

In both types, period stops and hormonal changes of pregnancy occur

102
Q

How is molar pregnancy diagnosed?

A
  • Pelvic USS: shows snowstorm appearance of the pregnancy
  • Dx confirmed with histology
103
Q

What is the management of hyatidiform mole (molar pregnancy)?

A
  • Evacuation of the uterus
  • Referral to gestational trophoblastic disease centre
  • Monitor hCG levels until normal
  • If mole metastasises: systemic chemotherapy
104
Q

What is endometriosis?

A

Ectopic endometrial tissue outside the uterus

105
Q

What is an endometrioma? And give 2 examples of endometriomas in specific locations

A

A lump of endometrial tissue outside the uterus
* If in ovaries: “chocolate cysts
* If in myometrium (muscle layer) of uterus: adenomyosis

106
Q

What is the main theory for the cause of ectopic endometrial tissue?

A

Retrograde menstruation
* during menstruation endometrial lining flows backwards thru fallopian tubes out into pelvis/peritoneum

107
Q

What is the presentation of endometriosis?

A
  • Cyclical pelvic/abdo pain
  • Deep dyspareunia
  • Dysmenorrhoea (painful periods)
  • Infertility
  • Cyclical bleeding from other sites e.g. haematuria
  • Cyclical urinary/bowel Sx if area affected
108
Q

What investigations are done for endometriosis?

A
  • Pelvic USS: large endometriomas & chocolate cysts, but usually unremarkable
  • Laparoscopic surgery = Gold Standard (surgeon can remove deposits of endometriosis, potentially improving Sx)
  • Definitive Dx made with biopsy of lesions
109
Q

What is the staging system to be aware of for endometriosis?

A

American Society of Reproductive Medicine (ASRM)

110
Q

What is the pathophysiology behind pelvic pain in endometriosis?

Pelvic pain = Main Sx

A
  • Cells of endometrial tissue outside uterus respond to hormones in same way as tissue inside the uterus
  • During menstruation endometrial tissue in uterus sheds lining & bleeds - same happens in endometrial tissue elsewhere in body
  • This causes irritation & inflammation of tissues around sites of endometriosis
  • Results in cyclical, dull, heavy/burning pain that occurs during menstruation
111
Q

How does endometriosis cause adhesions?

A
  • Localised bleeding & inflammation - causes damage and deveopment of scar tissue that binds organs together
  • Adhesions lead to chronic, non-cyclical pain that can be sharp/stabbing/pulling & associated w/ nausea
112
Q

What is the management of endometriosis?

A
  • Analgesia: NSAIDs & paracetamol
  • Hormonal Mx
  • Surgical Mx
113
Q

What hormonal managament options can be tried for endometriosis?

A
  • COCP
  • Progesterone only pill
  • Nexplanon implant
  • Mirena coil
  • GnRH agonists (induce menopause-like state)
  • Depot injection

stop ovulation and reduce endometrial thickening

114
Q

What surgical managament options are available for endometriosis?

A
  • Laparoscopy: excise/ablate endometrial tissue & remove adhesions (adhesiolysis)
  • Hysterectomy
115
Q

What is adenomyosis?

A

Endometrial tissue inside the myometrium
* Hormone-dependent, Sx tend to resolve after menopause (like endometriosis/fibroids)
* Can occur alone, or alongside endometriosis/fibroids
* More common in later reproductive years & those that have had multiple pregnancies

116
Q

What is the presentation of adenomyosis?

A
  • ~1/3 asymptomatic
  • Dysmenorrhoea
  • Menorrhagia
  • Dyspareunia
  • Infertility/pregnancy-related Cx
117
Q

What investigations are done for adenomyosis?

A
  • Transvaginal USS (1st line)
  • MRI/transabdo USS (alternative Ix)
  • Histological exam of uterus after hysterectomy (GS)
118
Q

What is the management of adenomyosis for women not wanting contraception?

  • Mx depends on Sx, age, plans for pregnancy
  • NICE recommend same Tx as heavy menstrual bleeding
A
  • When there’s no associated pain: Tranexamic acid (antifibrinolytic - reduces bleeding)
  • When there’s associated pain: Mefenamic acid (NSAID - reduces bleeding & pain)

Other options:
* GnRH analogues (induce menopause-like state)
* Endometrial ablation
* Uterine artery embolisation
* Hysterectomy

119
Q

What is the management of adenomyosis for women wanting/accepting contraception?

A
  • Mirena coil (1st line)
  • COCP
  • Cyclical oral progesterones

Progesterone only meds e.g. pill, implant, depot may also help

120
Q

What pregnancy complications are associated with adenomyosis?

A
  • Infertility
  • Miscarriage
  • Preterm birth
  • Small for gestational age
  • Preterm PRoM
  • Malpresentation
  • Need for C section
  • Postpartum haemorrhage
121
Q

What is atrophic vaginitis

A

dryness and atrophy of the vaginal mucosa related to a lack of oestrogen.

122
Q

Why does atrophic vaginitis usually occur in menopause

A

LACK OF OESTROGEN during menopause

  • usually Epithelial lining in the vagina and urinary tract responds to oestrogen by getting thicker, producing secretions and being elastic

-less oestrogen means tissue is more prone to inflammation and infection

123
Q

Presentation of atrophic vaginitis

A

Itching
Dryness
Dyspareunia (discomfort or pain during sex)
Bleeding due to localised inflammation

Post menopausal women:
Recurrent UTI
Stress incontinence
Pelvic organ prolapse

124
Q

Upon examination what will be the findings of atrophic vaginitis

A

-pale mucosa
-thin skin
-reduced skin folds
-dryness
-sparse pubic hair
-erythema and inflammation

125
Q

Mx of atrophic vaginitis

A

-Vaginal lubricants e,g SYLK, replens

-topical oestrogen
Estriol cream
Estriol pessaries
Estradiol tablets - once daily
Estradiol ring

126
Q

Topical oestrogen contraindications (4)

A

Breast cancer
Angina
VTE
Endometrial hyperplasia

127
Q

What is menarche

A

Females first episode of menstruation

128
Q

What is the Rotterdam criteria

A

A criteria used for making a diagnosis for polycystic ovarian syndrome of 2 out of three of:

1)Oligoovualtion/anovulation - irregular/ absent periods

2)Hyperandrogenism - characterised by hirsutism and acne

3)Polystic ovaries on Ultrasound

129
Q

Presentation of PCOS (6)

A

-oligomenorrhoea/amenorrhoea (irregular/ absent periods)
-infertility
-obsesity
-hirsutism
-acne
-hair loss in a male pattern

130
Q

Complications of Polycystic ovarian syndrome (7)

A

-insulin resistance + diabetes
-CVD
-obstructive sleep apnoea
-depression and anxiety
-sexual problems
-endometrial cancer
-hypercholesterolaemia

131
Q

What is acanthosis nigrans and why is it seen in PCOS

A

-thickened rough dark skin typically on elbows and armpits
-due to INSULIN RESISTANCE

132
Q

What are DDX for hirsutism

A

-PCOS
-ovarian/adrenal tumours
-cushings
-congential adrenal hyperplasia
-medications e.g phenytoin, ciclosporin, anabolic steroids, corticosteroids, artificial testosterone

133
Q

How does insulin resistance occur in PCOS

A

Insulin resistance is both a symptom and a driver for PCOS

-Insulin resistance means pancreas has to produce more insulin to get the same response

-insulin also promotes androgen release e.g testosterone + suppresses sex hormone binding globulin which usually suppresses androgens

-this can lead to hyperandrogenism in women with PCOS and poor development of follicles in the ovaries

134
Q

Ix for PCOS

A

Blood tests:
-raised LH
-raised LH-FSH ratio (high LH compared to FSH)
-raised testosterone
-raised insulin
-normal/raised oestrogen
-low sex hormone binding globulin

Exclude other pathology
-prolactin
-TSH

Pelvic ultrasound

GOLD STANDARD - Transvaginal ultrasound for observing ovaries - string of peals appearance

2hr oral glucose tolerance test- test for insulin resistance

135
Q

Diagnostic criteria on transvaginal ultrasound for PCOS diagnosis

A

12 or more developing follicles in one ovary

Ovarian volume of more than 10cm3

136
Q

Risk factors for PCOS

A

Obesity
Lack of excercise
History of gestational diabetes
FHx

137
Q

General management of PCOS

A

-Weight loss - can be aided with orlistat (lipase inhibitor)
-Low glycaemic index, calorie-controlled diet
-Exercise
-Smoking cessation
-Antihypertensive medications where required
-Statins where indicated (QRISK >10%)

138
Q

How does PCOS increase the risk for endometrial cancer

A

-in PCOS patients dont experience regular menstruation

-so endometrial lining continues to proliferate under the influence of oestrogen and does not shed

-resulting in endometrial hyperplasia a pre cancerous stage of endometrial cancer

139
Q

Management of the risk of endometrial cancer in PCOS

A

Mirena coil: thin the lining of the uterus

Inducing a period:
-cyclical progestrogens e.g medroxyporgesterone acetate once a day For 14 days

-COCP

140
Q

How do you manage the infertility in PCOS

A

First step: Weight loss

If this fails:
Clomifene - increases FSH and LH levels
Laparscopic ovarian drilling
IVF
Metformin - increases insulin sensitivity

141
Q

Management for hirsutism in PCOS

A

Weight loss

Co-Cyprindiol- COCP for the treatment of hirsutism and acne

Topical eflornithine - 6/8 weeks

Electrolysis
Laser hair removal
Spironolactone
Finasteride - decreases testosterone
Flutamide
Cypoterone acetate - anti androgen and progestin

142
Q

Management of acne in PCOS

A

first line - COCP

Co-cyprindiol may be the best option as it has anti-androgen effects

Topical adapalene
Topical Abx
Topical azelaic acid
Oral tetracycline

143
Q

Major side effect of using co cyprindiol

A

Significantly increased risk of VTE

144
Q

What is ashermans syndrome

A

Where adhesions form within the uterus following damage

145
Q

What can lead to ashermans syndrome (4)

A

-post pregnancy

-dilatation and curettage procedure e.g Tx of retained product of conception

-uterine surgery

-recurrent pelvic infection(Endometritis)

146
Q

Presentation of ashermans syndrome

A

Secondary amenorrhoea (absent periods)

Lighter periods

Dysmenorrhoea (painful periods)

Infertility

147
Q

Diagnosis for ashermans syndrome (4)

A

GOLD STANDARD - Hysteroscopy

Hysterosalpingography - contrast is injected into the uterus and imaged with X-ray

Sonohysterography - uterus filled with fluid and seen pelvic US

MRI scan

148
Q

Mx of ashermanns syndrome

A

dissecting the adhesions during hysteroscopy

149
Q

Where do the female reproductive tract develop from embryologically

A

Müllerian ducts

150
Q

What is a bicornuate uterus

A

A congenital structural abnormality in the uterus causing it to be heart shaped

151
Q

What complications are there for bicornuate uterus

A

Miscarriage
Premature birth
Malpresentation - poor position of baby in uterus

152
Q

What is an imperforate hymen

A

where the hymen at the entrance of the vagina is fully formed, without an opening.

153
Q

Tx of imperforate hymen

A

Surgical incision to create the opening

154
Q

Complications for imperforate hymen

A

Retrograde menstruation leading to endometriosis - due to the debris remaining in the pelvic cavity

155
Q

What is transverse vaginal septae

A

Where the septum wall form transversely across the vagina
Can be perforated or imperforated

156
Q

Treatment of transverse vaginal septae
Complications of the treatment

A

Surgical correction

Complications:
Vaginal stenosis
Recurrence of the septae

157
Q

What is vaginal hypoplasia

A

abnormally small vagina

158
Q

What is vaginal agenesis

A

absent vagina

159
Q

What is the reason for vaginal hypoplasia and vaginal agenesis

A

Failure of the Müllerian ducts to properly develop

160
Q

Mx of vaginal hypoplasia and agenesis

A

Vaginal dilator for prolonged periods

Vaginal surgery

161
Q

What is pelvic inflammatory disease

A

Inflammation and infection of the organs of the pelvis - caused by spreading of infection up through the cervix

162
Q

What are the different types of pelvic inflammatory disease (5)

A

Endometritis - inflammation of the endometrium

Salpingitis - inflammation of the fallopian tubes

Oophoritis - inflammation of the ovaries

parametritis - inflammation of the parametrium, which is the connective tissue around the uterus

Peritonitis - inflammation of the peritoneal membrane

163
Q

What are the most common causative organisms for pelvic inflammatory disease (3)

A

Sexually transmitted

-Neisseria gonorrhoeae
-chlamydia trachomatis
-mycoplasma genitalium

164
Q

Risk factors for pelvic inflammatory disease (6)

A

-not using barrier contraception
-multiple sexual partners
-younger age
-previous PID
-having an IUD - e.g copper coil
-having existing STI

165
Q

Presentation of Pelvic inflammatory disease

A

Pelvic/lower abdo pain + tenderness
Vaginal discharge - can be purulent
Abnormal bleeding - intermenstrual or after sex
Dyspareunia
Fever
dysuria
Cervical motion tenderness - movement of cervix causes unpleasant sensation

166
Q

Investigations for Pelvic inflammatory disease

A

-NAAT swabs for gonnorhae/chlamydia/mycoplasma genitalium

-HIV test

-syphilis test

-vaginal swab -look for bacterial vaginosis/candiasis + look under microscope to look for pus cells

-CRP+ESR - raised

-pregnancy test - rules out ectopic pregnancy

167
Q

Mx of Pelvic inflammatory disease

A

-Abx started empirically before swabs obtained

168
Q

Complications for pelvic inflammatory disease

A

Sepsis
Abcess
Infertility
Chronic pelvic pain
Ectopic pregnancy
Fitz Hugh Curtis syndrome

169
Q

What is fitz hugh Curtis syndrome

A

complication of pelvic inflammatory disease

Inflammation + infection of the **liver capsule ** leading to adhesion between peritoneum and liver

170
Q

Treatment of fitz Hugh Curtis syndrome

A

Laparoscopy + adhesiolysis

171
Q

Main symptoms of fitz hugh Curtis syndrome

A

RUQ pain
Shoulder tip pain if diaphragmatic involvement

172
Q

What are prolactinomas

A

Tumours of the pituitary gland that secrete excesssive prolactin

173
Q

What condition is associated with prolactinomas

A

Multiple endocrine neoplasia type 1

174
Q

What is the difference between micro and macro prolactinomas

A

Micro - less than 10mm
Macro - more than 10mm

175
Q

Give 5 Symptoms of prolactinomas

A

Bitemporal hemianopia
Headache
Osteoporosis
Galactorrhae
Amenorrhae
Gynocomastia
ED
Infertility
Decreased libido

176
Q

Investigations for prolactinomas

A

MRI - to visualise the prolactinoma
Serum prolactin - raised

177
Q

Tx for prolactinomas

A

Medication - dopamine agonist e.g cabergoline/ bromocriptine

Surgery transphenoidal removal of pituitary tumour - only really for macroprolactinomas or if medication doesnt work

178
Q

What is menopause

A

When a woman has had no periods for 12 months retrospectively

179
Q

What is classed as premature menopause

A

Menopause before the age of 40

180
Q

What are the changes to the sex hormones during menopause

A

Oestrogen - low
Progesterone - low

LH + FSH - high due to lack of negative feedback

181
Q

What is the physiology of menopause

A

begins with a decline in the development of the ovarian follicles.

Without the growth of follicles, causes reduced production of oestrogen.

Oestrogen has negative feedback effect on the pituitary gland, suppressing the quantity of LH and FSH produced.

As the level of oestrogen falls in the perimenopausal period, there is an absence of negative feedback on the pituitary gland, and increasing levels of LH and FSH.

Leads to irregular menstrual cycles

182
Q

Give 5 perimenopausal symtoms (8)

A

Hot flushes
Emotional lability or low mood
Premenstrual syndrome
Irregular periods
Joint pains
Heavier or lighter periods
Vaginal dryness and atrophy
Reduced libido

183
Q

What does menopause increase the risk of

A

Lack of oestrogen leading to:

Cardiovascular disease and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence

184
Q

Mx of perimenopausal symtoms

A

Help with vaginal dryness
Vaginal oestrogen - creams/ tablets
Vaginal moisturisers

Testosterone - help with libido

Help with mood
CBT
SSRI antidepressants - fluoxetine

HRT
Tibolone - acts as HRT
Clonidine

185
Q

What are endometrial (uterine) polyps?

A

Non-cancerous growth attached to endometrium

186
Q

What are the causes of endometrial polyps?

A
  • Perimenopausal or postmenopausal
  • Obese
  • Taking tamoxifen
187
Q

What are possible symptoms of endometrial polyps?

A
  • Irregular periods
  • Heavy periods
  • Postmenopausal bleeding
  • Infertility
188
Q

How are endometrial polyps diagnosed?

A
  • Transvaginal USS
  • Hysteroscopy
  • Endometrial biopsy
189
Q

What is the management of endometrial polyps?

A
  • Watch and wait
  • Hormonal meds (progestins & GnRH agonists to lessen Sx)
  • Surgery
190
Q

What is PCOS

A

Condition affecting women due to imbalance in hormones particularly an increase in androgens, which leads to disruption in egg release and menstruation aswell as other systemic sx