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Gynae Flashcards

1
Q

MENSTRUAL CYCLE

Explain the basics of the menstrual cycle up to ovulation

A
  • Multiple follicles develop under presence of FSH + then one dominates causing increased oestrogen conversion which has -ve feedback on FSH/LH
  • Oestrogen rises to a point where it stops inhibiting hypothalamus + causes a spike in LH > ovulation
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2
Q

MENSTRUAL CYCLE

Explain the basics of what happens after ovulation

A
  • Corpus luteum (dominant follicle) produces progesterone which inhibits FSH/LH
  • Egg fertilised = syncytiotrophoblast secretes hCG which maintains it
  • Egg not fertilised = degenerates + so FSH/LH can rise again
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3
Q

1º AMENORRHOEA

What is primary amenorrhoea?

A

Absence of menstruation by –

  • 13y if no secondary sexual characteristics
  • 15y with secondary sexual characteristics (breast buds)
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4
Q

1º AMENORRHOEA

What is the difference between hypogonadotrophic hypogonadism and hypergonadotrophic hypogonadism?

A
  • Deficiency in gonadotrophins (LH + FSH) stimulating ovaries due to abnormal hypothalamus or pituitary so low sex hormones (hypogonadism)
  • Gonads fails to respond to stimulation of gonadotrophins meaning no negative feedback + increasing amounts of FSH/LH
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5
Q

1º AMENORRHOEA

What are some causes of hypogonadotrophic hypogonadism?

A
  • Constitutional delay (temporary delay, no pathology, ?FHx)
  • Kallmann’s (failure to start puberty + anosmia)
  • Excessive exercise, dieting or stress causes hypothalamic failure
  • Endo = Cushing’s, prolactinoma, thyroid
  • Damage (cancer, surgery, radiotherapy)
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6
Q

1º AMENORRHOEA

What are some causes of hypergonadotrophic hypogonadism?

A
  • Gonadal dysgenesis e.g., Turner’s syndrome (XO)
  • Congenital absence of ovaries
  • Previous damage to gonads (torsion, cancer, infections like mumps)
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7
Q

1º AMENORRHOEA

What are some other causes of primary amenorrhoea and how may they present?

A
  • Congenital adrenal hyperplasia = tall, deep voice, facial hair
  • Androgen insensitivity syndrome = 46XY but female phenotype
  • Congenital malformations of genital tract e.g., imperforate hymen = regular painful cycles but amenorrhoea > haematocolpos
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8
Q

1º AMENORRHOEA

What are some initial investigations for primary amenorrhoea?

A
  • FBC + ferritin (anaemia), U+E for CKD, anti-TTG for coeliac, urinary beta-hCG crucial
  • FSH + LH (low = hypothalamic, high = gonads)
  • TFTs, prolactin, free androgens
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9
Q

1º AMENORRHOEA

What further investigations might be useful in primary amenorrhoea?

A
  • XR wrist to assess bone age + Dx constitutional delay
  • Pelvic USS for structural causes
  • Karyotyping for Turner’s syndrome, AIS
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10
Q

1º AMENORRHOEA

What is the management of primary amenorrhoea?

A
  • Constitutional delay = reassurance + observe

- Primary ovarian insufficiency due to gonadal dysgenesis = HRT to prevent osteoporosis

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11
Q

2º AMENORRHOEA

What is secondary amenorrhoea?

A
  • Absence of menstruation for 3–6m in women with previously regular menses, or 6–12m in women with previous oligomenorrhoea
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12
Q

2º AMENORRHOEA
What is the most common cause of secondary amenorrhoea and the non-pathological causes?
What are the pathological causes of secondary amenorrhoea?

A
  • Pregnancy (most common), breastfeeding, menopause (physiological)
  • Pituitary = Sheehan’s syndrome, hyperprolactinaemia (prevents GnRH)
  • Ovarian = PCOS, premature ovarian failure
  • Thyroid = hyper or hypothyroidism
  • Asherman’s syndrome
  • Hypothalamic failure = excessive exercise, stress or eating disorders
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13
Q

2º AMENORRHOEA

What hormonal tests would you do in secondary amenorrhoea?

A
  • Urinary pregnancy test
  • FSH/LH and androgens
  • Mid-luteal (day 21) progesterone to check ovulation happened
  • Prolactin + TFTs if indicated
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14
Q

2º AMENORRHOEA

What other investigations may you do in secondary amenorrhoea?

A
  • Pelvic USS to Dx PCOS

- MRI head if ?pituitary tumour

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15
Q

MENORRHAGIA

What is menorrhagia?

A
  • Blood loss during menses to the extent in which the woman’s QOL is affected
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16
Q

MENORRHAGIA

What are some causes of menorrhagia?

A
  • Dysfunctional uterine bleeding = no underlying pathology in about half
  • Local = fibroids, adenomyosis, endometrial polyps or cancer, PID, copper IUD
  • Systemic = bleeding disorders (vWD), hypothyroidism
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17
Q

MENORRHAGIA

What are some investigations for menorrhagia?

A
  • FBC for ALL women, ferritin (anaemia), clotting screen
  • Transvaginal USS for underlying causes
  • TFTs, STI screen if clinically indicated
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18
Q

FIBROIDS

What are fibroids?

A
  • Benign tumours of the smooth muscle of the uterus (uterine leiomyomas)
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19
Q

FIBROIDS

What are the different types of fibroids?

A
  • Intramural (most common) = within the myometrium
  • Subserosal = >50% fibroid mass extends outside uterus
  • Submucosal = >50% projection into the endometrial cavity
  • Subserosal + submucosal can be pedunculated (on stalk = risk of torsion)
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20
Q

FIBROIDS
What are some associations with fibroids?
What are some risk factors?

A
  • Grow in response to oestrogen so rare before puberty

- Black ethnicity, increasing age, early puberty, FHx + obesity

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21
Q

FIBROIDS

What is the clinical presentation of fibroids?

A
  • Menorrhagia (#1)
  • Pelvic pain
  • Urinary symptoms (frequency, urgency)
  • Subfertility
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22
Q

FIBROIDS

What are some investigations for fibroids?

A
  • Abdo + bimanual exam = firm, enlarged, irregularly shaped non-tender uterus
  • FBC for ALL women (?IDA)
  • TV USS
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23
Q

FIBROIDS
What is a key complication of fibroids?
How does it present?
How is it managed?

A
  • Red degeneration
  • Growth in pregnancy due to rise in oestrogen so fibroid outgrows blood supply > ischaemia + degeneration
  • Low-grade fever, severe abdo pain + vomiting > analgesia, fluids
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24
Q

FIBROIDS
What is the first line management of fibroids <3cm?
How is the management split after that?

A
  • IUS (cautious if uterus distortion > specialist advice)
  • Non-hormonal = does not want contraception
  • Hormonal = wants contraception
  • Surgical = severe or submucosal for hysteroscopic removal
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25
Q

FIBROIDS

What are the options for non-hormonal management of fibroids <3cm?

A
  • Tranexamic acid (antifibrinolytic) taken during bleeding to reduce it
  • Mefenamic acid (NSAID) to reduce bleeding + pain
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26
Q

FIBROIDS

What are the options for hormonal management of fibroids <3cm?

A
  • COCP

- Cyclical progesterone (norethisterone)

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27
Q

FIBROIDS

What is the management of fibroids >3cm?

A
  • Same medical Mx but surgery offered too
  • GnRH agonists (goserelin) can be given to shrink fibroids by inducing menopausal state (reduced oestrogen) in short-term only (can demineralise bone) for surgery
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28
Q

FIBROIDS

What are the main surgical options for fibroids?

A
  • Uterine artery embolisation
  • Myomectomy
  • 2nd gen endometrial ablation
  • Hysterectomy
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29
Q

FIBROIDS
What is…

i) uterine artery embolisation?
ii) myomectomy?
iii) endometrial ablation?
iv) hysterectomy?

A

i) Injection > blocked arterial supply to fibroid = starves of oxygen + shrinks
ii) Removal of fibroid either laparoscopic, hysteroscopic or laparotomy
iii) Destroys endometrium + superficial myometrium of uterus
iv) Uterus removal, last resort, patient choice, family completed

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30
Q

FIBROIDS

What should you make women aware of before certain surgical procedures?

A
  • Myomectomy is only treatment known to potentially improve subfertility
  • Must AVOID subsequent pregnancy + use effective contraception after endometrial ablation
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31
Q

ADENOMYOSIS
What is adenomyosis?
What is the epidemiology?

A
  • Endometrial tissue inside the myometrium – oestrogen dependent
  • More common in later reproductive years + multiparous
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32
Q

ADENOMYOSIS

How does adenomyosis present?

A
  • Dysmenorrhoea + menorrhagia

- Examination = bulky + tender uterus, “boggy”

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33
Q

ADENOMYOSIS

What is the management of adenomyosis?

A
  • FBC + TV USS first line, may get MRI pelvis

- Manage as per fibroids

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34
Q

ENDOMETRIOSIS

What is the pathophysiology of endometriosis?

A
  • Presence of ectopic endometrial tissue outside the uterus potentially due to retrograde menstruation (Sampson’s theory) which responds to normal menstruation hormones > bleeding + chronic inflammation and scarring
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35
Q

ENDOMETRIOSIS

Where might endometriosis occur and what might this cause?

A
  • Pouch of Douglas = PR bleeding
  • Bladder + distal ureter = haematuria
  • Ovaries = endometrioma (chocolate cyst)
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36
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?
What are some protective factors?

A
  • Early menarche, nulliparity or FHx

- Hence = multiparity and COCP

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37
Q

ENDOMETRIOSIS

What is the clinical presentation of endometriosis?

A
  • Cyclical pelvic pain, deep dyspareunia and secondary dysmenorrhoea (worse 2–3d before menses + better afterwards)
  • Cyclical urinary Sx = dysuria, urgency, haematuria
  • Dyschezia = painful bowel movements
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38
Q

ENDOMETRIOSIS
What are the investigation of endometriosis?
What is the gold standard investigation and what might it show?

A
  • Bimanual = fixed, retroverted uterus 2º to adhesions
  • TVS may reveal endometrioma
  • Diagnostic laparoscopy (white scars or brown spots “powder burn”)
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39
Q

ENDOMETRIOSIS

What are some complications of endometriosis?

A
  • Adhesions 2º to endometriosis or surgery > bowel obstruction
  • Subfertility due to inflammatory damage + tubal adhesions
  • Reduced QOL > depression, anxiety
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40
Q

ENDOMETRIOSIS
What is the first line management of endometriosis?
What is trialled after that?

A
  • NSAIDs ± paracetamol for symptomatic relief

- Hormonal treatments to abolish cycles = COCP or progestogens (POP/implant/injectable/IUS)

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41
Q

ENDOMETRIOSIS

What is the secondary care management of endometriosis?

A
  • GnRH analogues for ‘pseudomenopause’
  • Laparoscopic excision or ablation
  • Ultimately, hysterectomy may be considered
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42
Q

PCOS

What is polycystic ovarian syndrome (PCOS)?

A
  • Heterogenous endocrine disorder which emerges at puberty due to a combination of hormone imbalances e.g., insulin resistance, raised LH + hyperandrogenism
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43
Q

PCOS

How does insulin resistance contribute to PCOS?

A
  • Low sex hormone-binding globulin (SHBG) which usually binds to testosterone so more testosterone is unbound in blood
  • Raised androgens
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44
Q

PCOS

What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism = hirsutism, acne + male pattern baldness
  • Oligo or amenorrhoea
  • Insulin resistance (obesity, acanthosis nigricans)
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45
Q

PCOS
How does hirsutism present in PCOS?
What are some differentials of hirsutism?

A
  • Growth of thick, dark hair often in male pattern (facial hair)
  • Androgen-secreting ovarian/adrenal tumours, CAH, Cushing’s
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46
Q

PCOS

What diagnostic criteria is used in PCOS?

A

Rotterdam criteria (≥2) –

  • Oligo- or anovulation
  • Hyperandrogenism (biochemical or clinical)
  • Polycystic ovaries (≥12) or ovarian volume >10cm^3 on USS
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47
Q

PCOS

What blood tests may be used in PCOS diagnosis and what would they show?

A
  • Testosterone (normal/raised)
  • SHBG (low)
  • LH (raised) + raised LH:FSH ratio (LH>FSH)
  • Prolactin + TFTs (exclude causes), OGTT (screen for T2DM)
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48
Q

PCOS
What is the gold standard for visualising the ovaries?
What might it show?

A
  • TVS
  • “String of pearls” appearance
  • Can also visualise endometrial thickness
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49
Q

PCOS

What are some complications of PCOS?

A
  • Metabolic = T2DM, CVD (screen for) + OSA
  • Subfertility
  • Mental health = depression, anxiety
  • Endometrial cancer = unopposed oestrogen from no progesterone as no ovulation
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50
Q

PCOS

What is the most crucial part of PCOS management?

A
  • Healthy lifestyle + weight loss as can improve overall condition + complications
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51
Q

PCOS

How is endometrial cancer risk managed in PCOS?

A
  • IUS (continuous endometrial protection)

- COCP or cyclical progestogens (medroxyprogesterone) with withdrawal bleed every 3–4m

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52
Q

PCOS

How is infertility managed in PCOS?

A
  • Weight loss #1 if appropriate
  • Clomifene first line to induce ovulation
  • Metformin may be used ± clomifene
  • Laparoscopic ovarian drilling or IVF afterwards
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53
Q

PCOS

How is hirsutism managed in PCOS?

A
  • Co-cyprindiol COCP with anti-androgen effects but increased VTE risk so used <3m
  • Hair removal cream, topical eflornithine for facial hair
  • Spironolactone (mineralocorticoid anatagonist with anti-androgen effects)
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54
Q

PCOS

How is acne managed in PCOS?

A
  • Co-cyprindiol COCP

- Standard treatments e.g., retinoids, lymecycline

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55
Q

BREAST CANCER
What is the pre-malignant form of breast cancer?
How is it detected?
What is the pathology?

A
  • Non-invasive ductal carcinoma in situ (DCIS) = not invaded basement membrane
  • Asymptomatic on screening
  • Microcalcification on mammography, unifocal lesion in one area of breast
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56
Q

BREAST CANCER

What are the 2 most common histological types of invasive breast cancer?

A
  • Invasive ductal carcinoma (70%) = abnormal proliferation of ductal cells, invaded basement membrane
  • Lobular carcinoma (10%) = more diffuse + frequently impalpable
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57
Q

BREAST CANCER

What are some other types of breast cancer?

A
  • Inflammatory breast cancer (presents like mastitis, no Abx response)
  • Medullary cancers (younger, BRCA1)
  • Paget’s disease of nipple
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58
Q

BREAST CANCER
What is Paget’s disease of the nipple?
When would you expect it and how is it managed?

A
  • Eczematous change of nipple due to underlying malignancy (invasive #1 or in-situ)
  • Suspect if nipple eczema unresolved with 2w of steroid or anti-fungal cream
  • Triple assessment
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59
Q

BREAST CANCER

What is the epidemiology of breast cancer?

A
  • 1 in 8 women will develop breast cancer in their lifetime

- Most common cancer in women + second most common cause of death

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60
Q

BREAST CANCER

What are some modifiable risk factors of breast cancer?

A
  • Obesity, smoking, alcohol, not breastfeeding
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61
Q

BREAST CANCER

What are some non-modifiable risk factors of breast cancer?

A
  • Increased hormone exposure = early menarche, late menopause, nulliparity, COCP or combined HRT
  • Genetic = FHx, female, BRCA1, BRCA2, TP53 (Li Fraumeni), Peutz-Jeghers
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62
Q

BREAST CANCER

What are some protective factors of breast cancer?

A
  • Breastfeeding
  • Multiparity
  • Late menarche + early menopause
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63
Q

BREAST CANCER
What are the two most common genetic associations with breast cancer?
What are they?

A
  • BRCA1 #1 = mutation of C17, 60-80% lifetime risk
  • BRCA2 = mutation of C13, 45% lifetime risk
  • Tumour suppression genes that act as inhibitors of cellular growth
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64
Q

BREAST CANCER

What are some other genetic mutations associated with breast cancer?

A
  • TP53 (Li Fraumeni)

- Peutz-Jeghers

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65
Q

BREAST CANCER

What is the classic clinical presentation of breast cancer?

A
  • Palpable painless lump (upper outer quadrant) = hard, irregular, tethered to chest wall
  • Visually = nipple inversion, bloody nipple discharge, peau d’orange (oedema + pitting due to blockage of lymphatic drainage)
  • Palpable lymphadenopathy (axillary > supraclavicular)
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66
Q

BREAST CANCER
What warrants an urgent 2ww cancer referral?
What happens under the 2ww referal?

A
  • ≥30 with unexplained breast lump ± pain
  • ≥50 with discharge, retraction or other change of concern
  • Triple assessment
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67
Q

BREAST CANCER

What is the triple assessment?

A
  • Clinical assessment = Hx + Examination
  • Imaging = <40 USS as dense tissue, >40 USS + mammography, ?MRI
  • Biopsy = with core needle biopsy (or fine needle aspiration)
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68
Q

BREAST CANCER

What imaging choices are there for investigating breast cancer and what would influence your choice?

A
  • Mammography, high resolution USS (good at Dx + targeting biopsy)
  • MRI (good assessment of implants, dense breasts or high-risk screening)
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69
Q

BREAST CANCER
If someone has breast cancer, what would you like to check now?
What might this tell you about prognosis?

A
  • Oestrogen receptor (ER) = presence good prognosis (and vice versa)
  • Human epidermal growth factor 2 (HER2) = presence bad prognosis (and vice versa)
  • Progesterone receptor
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70
Q

BREAST CANCER
How is breast cancer staged?
How can you work out someone’s prognosis?
What tumour marker is used in breast cancer?

A
  • CT CAP for TNM staging
  • Nottingham prognostic index scoring system
  • Ca 15-3 = monitor response to treatment + disease recurrence
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71
Q

BREAST CANCER
What is the NHS breast screening programme?
What is the process?

A
  • Women 50–70 invited triennially for dual-view (cranio-caudal + medio-lateral oblique) mammography
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72
Q

BREAST CANCER

What are the pros and cons of breast cancer screening?

A
  • Earlier detection, reduces mortality, detects asymptomatic cancers before present, not overly invasive
  • Some cancers missed, false positive distressing, ionising radiation risk
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73
Q

BREAST CANCER

What are some reasons that a woman may be recalled for further views, USS or biopsy?

A
  • Mass
  • Microcalcification (DCIS)
  • Asymmetrical density
  • Clinical or technical recall
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74
Q

BREAST CANCER

What is the high risk screening for breast cancer?

A
  • BRCA1/2 = annual MRI from age 30 + mammography from 40
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75
Q

BREAST CANCER
What are some complications of breast cancer?
How might this be managed?

A
  • Locally advanced breast cancer = rare presentation

- Metastatic disease (2Ls 2Bs) = Lungs, Liver, Bones, Brain > bone mets = spinal radiotherapy or bisphosphonates

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76
Q

BREAST CANCER

What is the management of breast cancer prior to surgery?

A
  • Women with no palpable axillary lymphadenopathy = pre-op axillary USS
  • Women with clinically palpable lymphadenopathy = axillary node clearance indicated at primary surgery
  • Neoadjuvant chemotherapy (FEC-D) to downstage a primary lesion
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77
Q

BREAST CANCER
What are some potential complications of axillary node clearance?
How can that be managed?

A
  • Functional arm impairment

- Lymphoedema (compression bandages, massages)

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78
Q

BREAST CANCER

What are the two main surgical options for breast cancer management and when are they indicated?

A
  • Wide local excision/lumpectomy = solitary lesion, peripheral tumour, small lesion in large breast, DCIS <4cm
  • Mastectomy = multifocal or central tumour, large lesion in small breast, DCIS >4cm
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79
Q

BREAST CANCER
When is radiotherapy indicated in breast cancer management?
What are some side effects?

A
  • Whole breast radiotherapy if wide-local excision to reduce recurrence
  • Radiotherapy if T3-4 tumours or ≥4 +ve axillary nodes if mastectomy
  • Breast tissue fibrosis, fat necrosis, fatigue
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80
Q

BREAST CANCER

What endocrine therapy might be used in breast cancer

A
  • ER +ve and pre/peri-menopause = tamoxifen (SERM)
  • ER +ve and post-menopause = aromatase inhibitors (e.g., anastrozole, letrozole)
  • HER-2 +ve = trastuzumab (Herceptin)
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81
Q

BREAST CANCER
What is the mechanism of action of…

i) tamoxifen?
ii) anastrozole?

A

i) Selective oestrogen receptor modulator = inhibits oestrogen receptors on breast cancer cells
ii) Inhibits aromatase which converts androgens to oestrogen

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82
Q

BREAST CANCER
What are some side effects of…

i) tamoxifen?
ii) aromatase inhibitors?
iii) trastuzumab?

A

i) Menopausal Sx, VTE + endometrial cancer
ii) Hot flushes, osteoporosis, fatigue
iii) Cardiac dysfunction + teratogenicity

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83
Q

BREAST CANCER
When considering the surgical management of breast cancer, what else might be offered and when?
Give some examples

A
  • Breast reconstruction surgery either primary (immediate) or delayed
  • Latissimus dorsi flap, implant based, transverse rectus abdominis flap
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84
Q

BENIGN BREAST DISEASE

What are some differentials for breast lump?

A
  • Breast cancer
  • Fibroadenoma
  • Fibrocystic breast disease
  • Breast cysts
  • Fat necrosis
  • Duct papilloma
  • Breast abscess
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85
Q

BENIGN BREAST DISEASE
What are the features of fibroadenoma?
What is the epidemiology?
What is the management?

A
  • Firm, mobile, well-circumscribed + smooth lump
  • Common in younger women <30
  • Triple assessment, removal if ≥3cm
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86
Q

BENIGN BREAST DISEASE

What is fibrocystic breast disease?

A
  • Connective tissues, ducts + lobules respond to cyclical hormonal changes becoming fibrous (irregular + hard) + cystic (fluid filled)
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87
Q

BENIGN BREAST DISEASE
What are the features of fibrocystic breast disease?
What is the epidemiology?
What is the management?

A
  • Bilateral “lumpy” breasts, mastalgia, Sx worsen with menstrual cycle
  • Common in women 25–50y
  • Re-examine after menses, exclude cancer, supportive bra, NSAIDs, heat
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88
Q

BENIGN BREAST DISEASE
What are breast cysts?
What is the epidemiology?
Give an example of a specific type

A
  • Benign fluid-filled lumps
  • # 1 cause, 30–50y, small increased risk of breast cancer
  • Galactocele = blocked lactiferous duct (painless lump beneath areola)
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89
Q

BENIGN BREAST DISEASE
What are the features of breast cysts?
What is the management?

A
  • Smooth, well-circumscribed, mobile, fluctuant lumps

- Exclude cancer, aspiration/excision if pain

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90
Q

BENIGN BREAST DISEASE
What is fat necrosis?
What is the epidemiology and causes?

A
  • Benign inflammatory reaction to adipose tissue damage
  • Following trauma, radiotherapy or breast surgery
  • Common in obese
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91
Q

BENIGN BREAST DISEASE
What are the features of fat necrosis?
What is the management?

A
  • Painless, non-mobile mass with overlying skin inflammation and bruising
  • Triple assessment as similar appearance to cancer, often no intervention
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92
Q

BENIGN BREAST DISEASE
What are the features of duct papilloma?
What is the management?

A
  • Bloody nipple discharge, usually no palpable mass

- Triple assessment, microdochectomy

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93
Q

BENIGN BREAST DISEASE
What is duct ectasia?
What are the features?
What is the management?

A
  • Inflammation + dilation of large breast ducts
  • Nipple retraction, creamy/green discharge
  • Troublesome = microdochectomy (young) or total duct excision (older)
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94
Q

BENIGN BREAST DISEASE
What is the associations with periductal mastitis?
What are the features?
What is the management?

A
  • Presents younger than duct ectasia with strong association with smoking
  • Inflammation, abscess or mammary duct fistula
  • Abx, if abscess > draining
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95
Q

BENIGN BREAST DISEASE
What is mastitis?
What are the features?

A
  • Inflammation of the breast, associated with lactation in postpartum women
  • Localised pain, tenderness, erythema + warmth, systemic illness (fever, rigors, fatigue), unilateral
96
Q

BENIGN BREAST DISEASE

What is the management of mastitis?

A
  • Reassurance to continue breast feeding
  • Analgesia
  • Advice on milk removal (manual expression)
  • ?Abx
97
Q

BENIGN BREAST DISEASE

What antibiotics would you give in mastitis and what criteria would you follow?

A

PO flucloxacillin and give if –

  • Systemically unwell
  • Nipple fissure
  • Sx do not improve 12–24h after effective milk removal
  • Culture = infection
98
Q

BENIGN BREAST DISEASE
What is breast abscess?
What are the features?
How is it managed?

A
  • Complication of untreated mastitis
  • Fluctuant, tender mass with overlying erythema + systemically unwell
  • USS = pus collection, incision + drainage with Abx
99
Q

BENIGN BREAST DISEASE
What is cyclical mastalgia?
What are the features?

A
  • Breast tenderness which fluctuates with menstrual cycle
  • Pain starts day before period + subsides by end
  • May be associated with fibrocystic changes = breast lumpiness
100
Q

BENIGN BREAST DISEASE
What is gynaecomastia?
What are some causes?

A
  • Enlargement of glandular tissue in males
  • Puberty = oestrogen/testosterone imbalance
  • Obesity = aromatase in adipose tissue
  • Chronic liver disease
  • Drugs = spironolactone #1, anabolic steroids, cannabis, GnRH agonists
  • Testicular tumour (Leydig cell > oestrogen) or failure (mumps)
101
Q

BENIGN BREAST DISEASE

What is the management of gynaecomastia?

A
  • Make sure to perform a testicular exam
  • Older men >50 exclude breast cancer
  • Reassure teenagers
  • Tamoxifen + surgery may be trialled
102
Q

CERVICAL CANCER
What is the most common histological types of cervical cancer?
What is the strongest factor associated with cervical cancer?

A
  • Squamous cell carcinoma 80%, adenocarcinoma (20%)

- Human papillomavirus (HPV 16, 18 + 33)

103
Q

CERVICAL CANCER

What genes may be implicated in cervical cancer and how does this relate to the pathogenesis?

A
  • P53 + RB are tumour suppressor genes
  • HPV produces two oncoproteins (E6 + E7)
  • E6 inhibits P53, E7 inhibits RB
104
Q

CERVICAL CANCER

What are some risk factors for cervical cancer?

A
  • Smoking
  • HIV
  • High parity
  • Multiple sexual partners
  • Lower socioeconomic status
  • COCP
105
Q

CERVICAL CANCER

How does cervical cancer present?

A
  • Asymptomatic + smear detected
  • Abnormal PV bleeding (POSTCOITAL, intermenstrual)
  • PV discharge, pelvic pain, dyspareunia
106
Q

CERVICAL CANCER
What is the initial thing you would do when suspecting cervical cancer?
What would you do based off this?

A
  • Speculum exam (take swabs to exclude infection)

- Abnormal cervix appearance = urgent colposcopy > ulceration, inflammation, bleeding, visible tumour

107
Q

CERVICAL CANCER

What other investigations would you do in cervical cancer?

A
  • 1st line = colposcopy (punch biopsy to get tissue sample for histology)
  • CT CAP for FIGO staging if confirmed
108
Q

CERVICAL CANCER
Other than cervical cancer, what might colposcopy diagnose and how?
What might colposcopy reveal?

A
  • Dysplasia (premalignant change) in cervical cells using the cervical intra-epithelial neoplasia (CIN) grading system
  • CIN I = mild dysplasia
  • CIN II = moderate dysplasia
  • CIN III/cervical carcinoma in situ = severe dysplasia
109
Q

CERVICAL CANCER

What is the management of CIN I–III?

A
  • Large loop excision of transformation zone (LLETZ) or cone biopsy
  • Cervical screening at 6m as test of cure after
110
Q

CERVICAL CANCER
What is the cervical cancer screening programme?
What are some notable exceptions?

A
  • Sexually active women 25–64 (triennially 25–50, 5y 50–64) smear test
  • Exceptions = HIV +ve screened annually, delayed in pregnancy until 3m post-partum unless missed screening or previous abnormal smears
111
Q

CERVICAL CANCER

What is the process of cervical smears?

A
  • First = tested for high-risk HPV (hrHPV) and if positive then cytological examination to identify precancerous changes (dyskaryosis)
112
Q

CERVICAL CANCER

Explain how you would initially interpret cervical cancer screening results

A
  • Negative hrHPV = return to normal recall
  • Positive hrHPV = examine cytologically
    – Abnormal cytology (borderline, mild, moderate or severe dyskaryosis) > colposcopy
    – Normal cytology = repeat at 12m
113
Q

CERVICAL CANCER
A patient had positive hrHPV but normal cytology on their cervical screening last year. They ask you what happens this time around, specifically what happens if they are hrHPV +ve again next year too?

A
  • Cytology abnormal at any stage = colposcopy
  • Now hrHPV -ve = return to normal recall
  • Still hrHPV +ve but cytology -ve = further repeat at 12m
    – Now hrHPV -ve at 24m = return to normal recall
    – Still hrHPV +ve and cytology -ve at 24m = colposcopy
114
Q

CERVICAL CANCER

How are inadequate samples managed in cervical screening?

A
  • Inadequate sample = repeat in 3m

- Two consecutive inadequate = colposcopy

115
Q

CERVICAL CANCER

What is the prophylaxis for cervical cancer?

A
  • Children 12–13 HPV vaccine

- Cervical screening

116
Q

CERVICAL CANCER
What is the management of…

i) CIN or early stage 1A cervical cancer?
ii) Stage 1B-2A
iii) Stage 2B-4A
iv) Stage 4B

A

i) LLETZ or cone biopsy with -ve margins (maintain fertility)
ii) Radical hysterectomy + lymphadenectomy
iii) Chemoradiation
iv) Combination chemotherapy

117
Q

CERVICAL ECTROPION
What is cervical ectropion?
What is the consequence of this?
What is it associated with?

A
  • Columnar epithelium of endocervix extends onto stratified squamous ectocervix
  • Endocervix cells more fragile so prone to trauma + to bleed (post-coital)
  • High oestrogen > young women, COCP, pregnancy
118
Q

CERVICAL ECTROPION

How does cervical ectropion present?

A
  • Increased vaginal discharge
  • Abnormal PV bleeding (IMB + PCB)
  • Speculum = red ring around cervical os (redder endocervix on pinker ectocervix)
119
Q

CERVICAL ECTROPION

What is the management of cervical ectropion?

A
  • Problematic bleeding = cauterisation (silver nitrate or cold coagulation during colposcopy)
120
Q

OVARIAN CANCER

What are the four main types of ovarian cancer?

A
  • Epithelial cell tumours (85–90%)
  • Germ cell tumours (common in women <35)
  • Sex cord-stromal tumours (rare)
  • Metastatic tumours (secondary)
121
Q

OVARIAN CANCER
What is the most common type of epithelial cell tumours and give a secondary example?
What are germ cell tumours and who are they seen in?

A
  • Serous carcinoma #1, endometroid carcinomas

- Often benign teratomas with various tissue types (skin, teeth, hair), common in women <35y

122
Q

OVARIAN CANCER
What are sex cord-stromal tumours?
Give an example of a classic secondary tumour seen in ovarian cancer and a charcteristic feature?

A
  • Arise from connective tissue, rare + aggressive

- Krukenberg tumour commonly GI (stomach) = characteristic “signet-ring” cells on histology

123
Q

OVARIAN CANCER
What are some risk factors for ovarian cancer?
What are some protective factors?

A
  • Unopposed oestrogen = BRCA1/2, early menarche, late menopause
  • COCP, early menopause, breastfeeding, childbearing
124
Q

OVARIAN CANCER

What is the clinical presentation of ovarian cancer?

A
  • Non-specific = abdo pain, bloating, early satiety (IBS picture)
  • Urinary Sx = frequency, urgency
  • Change in bowel habit
125
Q

OVARIAN CANCER
What is the NICE recommended initial investigation for suspected ovarian cancer?
What is a limitation?

A
  • CA125 and if ≥35IU/ml then urgent pelvic + abdo USS

- CA125 falsely raised in endometriosis, menses, fibroids

126
Q

OVARIAN CANCER

What warrants a 2ww gynaecology referral?

A
  • Ascites, unexplained abdominal or pelvic mass

- USS features suggestive of ovarian cancer = ascites, metastases, bilateral lesions, solid areas, multi-locular cysts

127
Q

OVARIAN CANCER

What can be calculated after CA125 and pelvic USS has been done?

A

Risk of malignancy index (multiply together) –

  • Menopausal status = 1 (pre), 3 (post)
  • Pelvic USS findings = 1 (1 feature), 3 (>1 feature)
  • CA125 levels
128
Q

OVARIAN CANCER

What other investigations would be done in ovarian cancer?

A
  • Tumour markers = AFP and beta-hCG for germ cell cancers

- CT CAP for FIGO staging

129
Q

OVARIAN CANCER
What is the prognosis of ovarian cancer?
Where does ovarian cancer commonly spread to?

A
  • Poor as often presents late due to non-specific Sx

- Para-aortic lymph nodes #1 + liver in advanced

130
Q

OVARIAN CANCER

What is the management of ovarian cancer?

A
  • Abdominal hysterectomy + bilateral salpingo-oopherectomy

- Adjuvant chemotherapy

131
Q

OVARIAN CYST

What are the 4 types of ovarian cysts?

A
  • Functional (physiological)
  • Benign epithelial neoplasms
  • Benign germ cell neoplasms/dermoid cysts
  • Benign sex-cord stromal neoplasms
132
Q

OVARIAN CYST
What are functional cysts?
What are the two main types?

A
  • Cysts relating to fluctuating hormones in menstrual cycle

- Follicular #1 and corpus luteum

133
Q

OVARIAN CYST
What is a follicular cyst and its natural course?
What is a corpus luteum cyst and a complication?

A
  • Non-rupture of dominant follicle, regress after few cycles

- Fills with fluid/blood, more likely to cause intraperitoneal bleeding than follicular

134
Q

OVARIAN CYST

Give examples of benign epithelial cysts and any key features

A
  • Serous cystadenoma

- Mucinous cystadenoma > if ruptures = pseudomyxoma peritonei

135
Q

OVARIAN CYST
What are benign germ cell neoplasms/dermoid cysts?
Who are they seen in?
What is a feature of them?

A
  • Various tissue types (skin hair teeth)
  • Common <30y
  • Torsion more likely
136
Q

OVARIAN CYST

Give a key sex cord-stromal neoplasm and what it is associated with

A
  • Fibroma

- Meig’s syndrome = ascites + pleural effusion + fibroma

137
Q

OVARIAN CYST

What are some risk factors for ovarian cysts?

A
  • Obesity
  • Early menarche
  • Infertility
  • FHx for dermoid cysts
138
Q

OVARIAN CYST

What is the clinical presentation of ovarian cysts?

A
  • Abdominal mass
  • Pelvic pain + dyspareunia
  • Pressure effects = urinary frequency, urgency, change in bowel habits
139
Q

OVARIAN CYST

What investigations would you do in ovarian cysts?

A
  • Initial = TV USS to check if simple (benign) or complex (malignant), ?CA125
  • Tumour markers for germ cell tumours = AFP, beta-hCG
140
Q

OVARIAN CYST

What are some complications of ovarian cysts?

A
  • Ovarian torsion
  • Haemorrhage into cyst (follicular + corpus luteal)
  • Cyst rupture
141
Q

OVARIAN CYST
What might cause ovarian cyst rupture?
How would it present?
What can it lead to?

A
  • Physical activity (exercise, sexual intercourse)
  • Acute, sharp abdo/pelvic pain, PV bleed, N+V
  • Peritonitis + shock
142
Q

OVARIAN CYST

What is the management of a ruptured ovarian cyst?

A
  • ABCDE + admission
  • Stable = conservative with analgesia, fluids
  • Unstable/bleeding = surgery ?laparotomy
143
Q

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

A
  • Simple cysts <5cm = repeat USS 8–12w as most resolve, referral if persists
  • By definition, physiological cysts unlikely so all referred to gynaecology
144
Q

OVARIAN TORSION

What is ovarian torsion?

A
  • Partial/complete twisting of ovary on its supporting ligaments that can lead to ischaemia, if fallopian tube involvement = adnexal torsion
145
Q

OVARIAN TORSION

What are some risk factors of ovarian torsion?

A
  • Ovarian mass
  • Pregnancy
  • Reproductive age
  • Ovarian hyperstimulation syndrome
146
Q

OVARIAN TORSION

What is the clinical presentation of ovarian torsion?

A
  • Sudden onset, severe unilateral iliac fossa pain
  • Colicky if twists/untwists
  • N+V
  • Fever may indicate adnexal necrosis
  • Localised tenderness ± palpable pelvic mass
147
Q

OVARIAN TORSION

What are the investigations for ovarian torsion?

A
  • Urinary pregnancy test to exclude ectopic

- Pelvic USS = free fluid or whirlpool sign

148
Q

OVARIAN TORSION

What are some complications of ovarian torsion?

A
  • Subfertility

- Necrotic ovary can lead to infection, abscess + sepsis

149
Q

OVARIAN TORSION

What is the management of ovarian torsion?

A
  • Laparoscopy both diagnostic + therapeutic = detorsion ±oophorectomy if necrotic
150
Q

ENDOMETRIAL CANCER
What is endometrial cancer?
What is the most common type?

A
  • Cancer of endometrium (lining of uterus) = oestrogen dependent often with good prognosis
  • Adenocarcinoma 80%
151
Q

ENDOMETRIAL CANCER
What is the most common histological type of endometrial cancer?
What are some others?

A
  • Adenocarcinoma (80%)

- Adenosquamous, squamous, papillary serous, clear cell + uterine sarcoma

152
Q

ENDOMETRIAL CANCER

What are some risk factors for endometrial cancer?

A
  • Unopposed oestrogen = obesity, nulliparity, early menarche, late menopause, PCOS
  • Others = DM, tamoxifen, HNPCC
153
Q

ENDOMETRIAL CANCER

What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking
154
Q

ENDOMETRIAL CANCER

What is the clinical presentation of endometrial cancer?

A
  • PMB is endometrial cancer until proven otherwise
  • May have abnormal bleeding (intermenstrual)
  • Abnormal PV discharge, visible haematuria
155
Q

ENDOMETRIAL CANCER
When would you refer someone via the 2ww gynaecology pathway?
What is the first line investigation for endometrial cancer?

A
  • Postmenopausal bleeding in ≥55y

- TVS = endometrial thickness should be <4mm

156
Q

ENDOMETRIAL CANCER

What other investigations is recommended in endometrial cancer?

A
  • Diagnosis = biopsy from Pipelle or hysteroscopy

- CT CAP for FIGO staging

157
Q

ENDOMETRIAL CANCER

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

A
  • Total abdominal hysterectomy with bilateral salpingo-oopherectomy + pelvic LN
158
Q

ENDOMETRIAL POLYP
What is an endometrial polyp?
Key differential?
What is the clinical presentation?

A
  • Benign growths of endometrium, some may be (pre)cancerous
  • DDx = fibroids
  • Menorrhagia, dysmenorrhoea + subfertility
159
Q

ENDOMETRIAL POLYP

What are the investigations and management of endometrial polyps?

A
  • TV USS, hysteroscopy ± endometrial biopsy

- Conservative Mx but if troublesome symptoms = hysteroscopy + polypectomy

160
Q

VULVAL CANCER
What is the most common histological type of vulval cancer?
What are some risk factors?

A
  • Squamous cell carcinoma

- HPV, VIN, lichen sclerosus, immunosuppression

161
Q

VULVAL CANCER

What is the clinical presentation of vulval cancer?

A
  • Vulval itching, soreness + persistent lump on labia majora
  • Non-healing ulceration
  • Inguinal lymphadenopathy
162
Q

VULVAL CANCER

What are the investigations for vulval cancer?

A
  • 2ww urgent gynaecology referral = unexplained vulval lump, ulceration or bleeding
  • Diagnosis = biopsy
  • CT CAP for FIGO staging
163
Q

VULVAL CANCER

What is the management of vulval cancer?

A
  • Simple = radical/wide local surgical excision

- Advanced = radio ± chemotherapy

164
Q

MENOPAUSE
What is menopause?
What is perimenopause?

A
  • Permanent cessation of menstruation for at least 12m due to ovarian failure + subsequent oestrogen deficiency, average age is 51y
  • Period from start of menopausal Sx until 12m after LMP
165
Q

MENOPAUSE

What are the peri-menopausal symptoms?

A
  • Vasomotor (lasts 2–5y) = hot flushes, night sweats
  • Sexual dysfunction = vaginal dryness, decreased libido, dyspareunia
  • General = depression, short-term memory impairment
166
Q

MENOPAUSE

What are the investigations for menopause?

A
  • Retrospective diagnosis after 12m of amenorrhoea in women >45y
  • NICE recommends FSH (high) blood test in women <40 with suspected premature menopause or women 40–45 with menopausal Sx or change in menstrual cycle
167
Q

MENOPAUSE

What are the long-term complications of menopause?

A
  • Osteoporosis
  • CVD
  • Stroke
168
Q

MENOPAUSE

What is the lifestyle advice given in menopause?

A
  • Regular exercise = improves hot flushes, sleep issues, mood + cognition
  • Good sleep hygiene
  • Relaxation
  • Weight loss
169
Q

MENOPAUSE

What is the medical management of menopause?

A
  • 1st line vaso-motor = HRT
  • 2nd line vaso-motor = clonidine (alpha-adrenergic receptor agonist) or SSRI like fluoxetine
  • Vaginal dryness = topical oestrogen creams
170
Q

MENOPAUSE

What is the management of contraception in the context of menopause?

A
  • 12m after LMP in women >50y

- 24m after LMP in women <50y

171
Q

HRT

What is Hormone Replacement Therapy (HRT) and how does it differ to contraceptives?

A
  • Treatment to alleviate Sx associated with menopause by giving a physiological dose of hormones compared to contraceptives which provide supraphysiological doses
172
Q

HRT

What are some contraindications to HRT?

A
  • Current or past breast cancer
  • Any oestrogen sensitive cancer (endometrial)
  • Undiagnosed PV bleeding
  • Untreated endometrial hyperplasia
173
Q

HRT

How do you decide which HRT regime to prescribe?

A
  • No uterus = oestrogen-only HRT
  • Uterus = add progesterone (combined HRT)
  • Period within last 12m = cyclical HRT
  • Period >12m = continuous HRT
174
Q

HRT

What is the management of contraception in the context of HRT?

A
  • Period within last 12m then contraception for 12m after LMP if >50y or 24m if <50y
  • Progesterone only is safe to use alongside cyclical HRT
175
Q

HRT

What are some benefits of HRT?

A
  • Relief of vaso-motor symptoms
  • Reduced risk of osteoporosis
  • Relief of urogenital symptoms
  • Improved QOL
176
Q

HRT

What are some risks with HRT?

A
  • Increased risk of breast cancer (combined HRT), reduces after stopping
  • Increased risk of VTE (unless patch used)
  • Increased risk of CVD + stroke
  • Increased risk of endometrial (if oestrogen only)
177
Q

HRT
What are the various preparations that HRT comes in?
How might you be guided for which preparation to use?

A
  • Oestrogens = PO, transdermal, topical (urogenital Sx)
  • Progestogens = PO, transdermal, IUS
  • E.g., patches = patient choice, GI disorders (Crohn’s), at risk of VTE
178
Q

ATROPHIC VAGINITIS

What is atrophic vaginitis and what causes it?

A
  • Dryness + atrophy of vaginal mucosa related to lack of oestrogen e.g., menopause, oophorectomy, anti-oestrogens (tamoxifen, anastrozole)
179
Q

ATROPHIC VAGINITIS

What is the clinical presentation of atrophic vaginitis?

A
  • Postmenopausal with PV dryness, dyspareunia + occasional spotting
  • Exam = sparse pubic hair, vagina may be pale + dry, painful exam
180
Q

ATROPHIC VAGINITIS

What is the management of atrophic vaginitis?

A
  • Vaginal lubricants + moisturisers like Sylk + Replens

- Topical oestrogen like estriol cream, HRT if severe

181
Q

POI

What is premature ovarian insufficiency (POI)?

A
  • Onset of menopausal Sx and elevated gonadotropin levels before age 40
182
Q

POI

What are some causes of POI?

A
  • Majority idiopathic or FHx
  • Iatrogenic = bilateral oophorectomy, radio/chemotherapy
  • Infection = mumps
  • Autoimmune
183
Q

POI

What are the clinical features of POI?

A
  • Secondary amenorrhoea + typical peri-menopause Sx before age 40
  • FSH level = >40IU/L on 2 samples >4w apart, low oestradiol
184
Q

POI

What are the complications of POI?

A
  • Higher risk of conditions due to lack of oestrogen > CVD, stroke, osteoporosis
185
Q

POI

What is the management of POI?

A
  • HRT or COCP required at least until average age of menopause (51) to reduce risks
186
Q

URINARY INCONTINENCE
What is urinary incontinence?
What are some risk factors?

A
  • Involuntary leakage of urine at socially unacceptable times
  • Age, multiparity, previous pelvic surgery, high BMI
187
Q

URINARY INCONTINENCE

What are the 5 main types of incontinence?

A
  • Overactive bladder/urge incontinence
  • Stress incontinence
  • Mixed incontinence (of the 2 above)
  • Overflow incontinence
  • Functional
188
Q

URINARY INCONTINENCE
What causes urge incontinence/OAB?
What causes stress incontinence?

A
  • Detrusor overactivity

- Weakness of pelvic floor + sphincter muscles

189
Q

URINARY INCONTINENCE

What is overflow incontinence?

A
  • Bladder outlet obstruction leads to overflow + incontinence, more common in men (e.g., BPH, MS, anticholinergics)
190
Q

URINARY INCONTINENCE

What is functional incontinence?

A
  • Comorbidities impair patient’s ability to reach bathroom e.g., dementia
191
Q

URINARY INCONTINENCE

What is the clinical presentation of urge incontinence/OAB?

A
  • Urgency, frequency, nocturia
  • ‘Key in door’ + ‘handwash’ trigger bladder contractions
  • Intercourse
192
Q

URINARY INCONTINENCE

What is the clinical presentation of stress incontinence?

A
  • Involuntary leakage when increased pressure (cough, laugh, lifting, exercise)
193
Q

URINARY INCONTINENCE
What is the first line investigation in urinary incontinence?
What are some other initial investigations?

A
  • Bladder diary (frequency volume chart) first line
  • Urine dipstick + MC&S
  • Post void bladder USS scan
  • Electronic Personal Assessment Questionnaire = determines impact of urinary, vaginal, bowel + sexual Sx on QOL
194
Q

URINARY INCONTINENCE

What are you looking for in urine dipstick + MC&S?

A
  • Nitrites + leukocytes = infection
  • Microscopic haematuria = glomerulonephritis
  • Proteinuria = renal disease
  • Glycosuria = DM, nephropathy
195
Q

URINARY INCONTINENCE

What more advanced investigations might you consider?

A
  • Urodynamics = measures abdo + bladder pressure to deduce detrusor pressure
  • Cystogram with contrast = visualise the bladder
196
Q

URINARY INCONTINENCE

What is some lifestyle advice for urinary incontinence?

A
  • Weight loss
  • Stop smoking
  • Reduce caffeine + alcohol
197
Q

URINARY INCONTINENCE

What are some conservative treatments for urinary incontinence?

A
  • Barrier bads

- PV oestrogen if related to menopause

198
Q

URINARY INCONTINENCE

What is the stepwise management of urge incontinence/OAB?

A
  • 1st line = bladder retraining (6w gradually increasing time between voiding)
  • 1st line drugs = anti-muscarinics (oxybutynin, tolterodine, darifenacin)
  • Mirabegron (beta-3-adrenergic agonist) if anti-muscarinics not tolerated
199
Q

URINARY INCONTINENCE
What is the mechanism of action of anti-muscarinics?
What are some side effects?

A
  • Parasympathetic so Pissing = decreases need to urinate + spasms
  • “Can’t see, spit, pee or shit” > caution in elderly as falls esp oxybutynin immediate release in frail
200
Q

URINARY INCONTINENCE
What is the mechanism of action of beta-3-adrenergic agonists?
What is a caution of these?

A
  • Sympathetic so Storage = relaxes detrusor + increases bladder capacity
  • C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP
201
Q

URINARY INCONTINENCE

What are last resort options for urge incontinence?

A
  • Augmentation cystoplasty
  • Bypass (urostomy)
  • Botox can paralyse detrusor + block ACh release
202
Q

URINARY INCONTINENCE

What is the stepwise management of stress incontinence?

A
  • Pelvic floor exercises with physio for 3m
  • Surgery
  • SNRI duloxetine if surgery not preferred
203
Q

URINARY INCONTINENCE

What surgical options are there for stress incontinence?

A
  • Colposuspension
  • Tension free vaginal tape
  • Mid urethral sling
204
Q

PELVIC ORGAN PROLAPSE
What is pelvic organ prolapse?
What are some risk factors?

A
  • Descent of ≥1 pelvic organs resulting in protrusion on the vaginal walls
  • Increasing age, obese, multiparity, pelvic surgery, menopause
205
Q

PELVIC ORGAN PROLAPSE

What are the three broad locations where prolapses can occur?

A
  • Anterior vaginal wall
  • Posterior vaginal wall
  • Apical vaginal wall
206
Q

PELVIC ORGAN PROLAPSE

What prolapses might you get from the anterior vaginal wall?

A
  • Cystocele (bladder > stress incontinence)
  • Urethrocele (urethra)
  • Cystourethrocele
207
Q

PELVIC ORGAN PROLAPSE

What prolapses might you get from the posterior vaginal wall?

A
  • Enterocele (small intestine)

- Rectocele (rectum)

208
Q

PELVIC ORGAN PROLAPSE

What prolapses might you get from the apical vaginal wall?

A
  • Uterine prolapse

- Vaginal vault prolapse (common after hysterectomy)

209
Q

PELVIC ORGAN PROLAPSE

What is the clinical presentation of pelvic organ prolapse?

A
  • “Something coming down” = dragging/heavy sensation in pelvis
  • Urinary Sx = incontinence, urgency, frequency
  • Bowel Sx = constipation, incontinence + urgency
  • Sexual dysfunction = pain, altered sensation + reduced enjoyment
210
Q

PELVIC ORGAN PROLAPSE

What are the investigations for pelvic organ prolapse?

A
  • Sim’s speculum (U-shaped) to show if something is there

- May have urodynamics, USS or MRI

211
Q

PELVIC ORGAN PROLAPSE

What is the management for pelvic organ prolapse?

A
  • Conservative = pelvic floor exercises, weight loss
  • Vaginal pessary = ring (preferred + can have sex), shelf or Gellhorn
  • Surgery
212
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for…

i) cystocele/cystourethrocele?
ii) uterine prolapse?
iii) rectocele?

A

i) Anterior colporrhaphy or colposuspension
ii) Hysterectomy or sacrohysteropexy
iii) Posterior colporrhaphy

213
Q

PREMENSTRUAL SYNDROME

What is premenstrual syndrome (PMS)?

A
  • Emotional + physical symptoms a woman may experience in the luteal phase of the normal menstrual cycle
214
Q

PREMENSTRUAL SYNDROME

How may PMS present?

A
  • Mood = anxiety, mood swings, stress, fatigue
  • Physical = bloating, headaches, breast pain
  • Resolves on menstruation
215
Q

PREMENSTRUAL SYNDROME

What is the management of mild PMS?

A
  • Lifestyle advice = exercise, alcohol + smoking cessation, good sleep
  • Regular + frequent small balanced meals with complex carbs
216
Q

PREMENSTRUAL SYNDROME
What is the management of moderate PMS?
What is the management of severe PMS?

A
  • New-generation COCP

- SSRI taken continuously or just during luteal phase (days 15–28)

217
Q

FGM

What is female genital mutilation (FGM)?

A
  • All procedures involving partial or total removal of female external genitalia or injury to female organs for non-medical reasons, often pre-pubertal
218
Q

FGM

Is FGM illegal?

A
  • Yes as stated in FGM Act 2003 – legal requirement for HCPs to report cases of FGM to the police
219
Q

FGM

What is the epidemiology in FGM?

A
  • Very common in Africa (Somalia, Egypt, Ethiopia, Sudan)

- UK hotspots = Sheff, London, Manc, Oxford

220
Q

FGM

What is the WHO classification for the types of FGM?

A
  • 1 = partial or total clitoridectomy
  • 2 = excision
  • 3 = infibulation
  • 4 = all other non-medical harmful procedures incl. pricking, piercing, incising
221
Q

FGM
What is…

i) excision?
ii) infibulation?

A

i) Partial or total removal of clitoris + labia minora ± excision of labia majora
ii) Narrowing/closing of vaginal orifice with creation of a covering seal (stitch labia together)

222
Q

FGM

Is female labia reduction illegal?

A
  • <18 = FGM

- >18 = legal but only performed privately

223
Q

FGM

What are some potential reasons for FGM?

A

Based on customs –

  • It will bring status + respect to family (social norm)
  • Rite of passage + being part of woman
  • Preserves girls’ virginity so acceptable for marriage
  • Cleanses + purifies girl with perceived religious requirement
224
Q

FGM

What are some acute complications of FGM?

A
  • Pain
  • Bleeding
  • Infection (BBV)
  • Sepsis
  • Swelling
225
Q

FGM

What are some chronic complications of FGM?

A
  • Dyspareunia
  • Dysmenorrhoea
  • Infertility + pregnancy issues
  • PTSD
226
Q

FGM

What is the initial management of suspected or confirmed FGM?

A
  • Report ANY FGM in <18 to police + record in notes (consider in >18 after risk assessment e.g. others at risk like unborn children)
  • Educate pts + relatives that FGM is illegal + health consequences
  • Services = social, safeguarding, child protection
227
Q

FGM

What is the overall management of FGM?

A
  • De-infibulation by specialist in FGM in some type 3 to try restore function
228
Q

AIS

What is androgen insensitivity syndrome (AIS)?

A
  • X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children 46XY to have female phenotype
229
Q

AIS

What is the clinical presentation of AIS?

A
  • Complete = primary amenorrhoea, female external genitalia, lack of body hair
  • Partial = ambiguous genitalia
  • Breast development may occur due to conversion of testosterone to oestradiol
230
Q

AIS

What is an important potential complication of AIS?

A
  • Undescended testes cause groin swellings with increased testicular cancer risk
231
Q

AIS

What are the investigations for AIS?

A
  • Pelvic USS = absence of internal female organs

- Karyotyping (46XY)

232
Q

AIS

What is the management of AIS?

A
  • In general, raised as female but MDT input for support
  • Bilateral orchidectomy to avoid testicular cancer
  • Oestrogen therapy + vaginal dilators or vaginoplasty
233
Q

ASHERMAN’S SYNDROME
What is Asherman’s syndrome?
How may it present?

A
  • Adhesion formation within uterus often following pregnancy related dilatation + curettage, uterine surgery or pelvic infection (endometritis)
  • Secondary amenorrhoea + infertility
234
Q

ASHERMAN’S SYNDROME
How would you investigate Asherman’s syndrome?
What is the management?

A
  • Hysterosalpingography = filling defects

- Hysteroscopy gold standard to break down adhesions

235
Q

BARTHOLIN CYST
What are the bartholin glands?
What causes a bartholin cyst?
What causes a bartholin abscess? Presentation?

A
  • 2 glands behind labia minora which secrete lubricating mucus for coitus
  • Blockage of duct
  • Infection (Staph or E.coli) = acutely painful (can’t sit), swollen + tender red swelling of labia
236
Q

BARTHOLIN CYST

How is a bartholin abscess managed?

A
  • Incision + drainage
  • Abx
  • Marsupialisation
237
Q

NABOTHIAN CYST
What is a nabothian cyst?
What is the management?

A
  • Mucus retention cyst found on cervix (white swelling)

- Cryocautery if discharging

FINALS (20 decks)

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