Gynae Flashcards

1
Q

Summary of premenstrual syndrome?

A

Emotional + physical Sx women experience in luteal phase of normal menstrual cycles

Only in ovulatory cycles, not prior to puberty, in pregnancy, or after menopause.

Emotional: anxiety, stress, fatigue, mood swings.
Physical: bloating, breast pain.

Tx:
Mild: lifestyle, sleep, exercise, smoking, alcohol reg 2-3hrly small balanced meals, complex carbs
Mod: new gen COCP eg Yasmin
Severe: SSRI, continuously or just in luteal phase.

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2
Q

What is primary amenorrhoea?

A

defined as the failure to establish menstruation by 15 years of age in girls with normal secondary sexual characteristics (such as breast development), or by 13 years of age in girls with no secondary sexual characteristics

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3
Q

Causes of primary amenorrhoea?

A

gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes

testicular feminisation

congenital malformations of the genital tract

functional hypothalamic amenorrhoea (e.g. secondary to anorexia)

congenital adrenal hyperplasia

imperforate hymen

Mullerian agenesis (congen absence of part of uterus/ vagina),

5α reductase def (lack enzyme to form DHT, undergo virilisation in puberty),

constitutional delay

Kallman’

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4
Q

What is secondary amenorrhoea?

A

cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea

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5
Q

Causes of secondary amenorrhoea?

A

hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)

polycystic ovarian syndrome (PCOS)

hyperprolactinaemia

premature ovarian failure

thyrotoxicosis* / hypothyroidism

Sheehan’s syndrome

Asherman’s syndrome (intrauterine adhesions)

Cervical stenosis, prev biopsy, curettage, infection. Absence of external OS + bulky uterus on exam

Pit tumours: compressive, ↑PRL

Depo = takes while to recover

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6
Q

Investigations for amenorrhoea?

A

exclude pregnancy with urinary or serum bHCG

full blood count, urea & electrolytes, coeliac screen, thyroid function tests

gonadotrophins

  • low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
  • raised if gonadal dysgenesis (e.g. Turner’s syndrome)

prolactin

androgen levels
- raised levels may be seen in PCOS

USS: outflow obstruction, Mullerian agenesis, androgen insensitivity

oestradiol

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7
Q

Management of primary amenorrhoea?

A

investigate and treat any underlying cause

with primary ovarian insufficiency due to gonadal dysgenesis (e.g. Turner’s syndrome) are likely to benefit from hormone replacement therapy (e.g. to prevent osteoporosis etC)

IVF

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8
Q

Management of secondary amenorrhoea?

A

exclude pregnancy, lactation, and menopause (in women 40 years of age or older)

HPG disorder: exogenous gonadotropins

treat the underlying cause

IVF

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9
Q

What is cervical ectropion?

A

Eversion of endocervix, exposing columnar epithelium. Induced by high levels of oestrogen.

Normal physiological condition, adolescents, pregnancy + oestrogen contraceptives.

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10
Q

Features of cervical ectropion?

A

Vaginal discharge, non-purulent.

Post-coital bleeding, fine BVs in epithelium easily broken intercourse

Asymptomatic

Intermenstrual bleeding

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11
Q

Investigations for cervical ectropion?

A

Speculum: reddish appearance, ring around external OS.

Pregnancy

Triple swabs: any infection.

Cervical swab: rule out IEN.

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12
Q

Treatment of cervical ectropion?

A

Doesn’t require Tx unless symptomatic

1st: stop any oest containing meds, effective in majority.

Can be ablated, sig vaginal discharge until healing completed.

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13
Q

What is lichen sclerosus?

A

Inflammatory condition that usually affects the genitalia and is more common in elderly females.

Lichen sclerosus leads to atrophy of the epidermis with white plaques forming

AI disease

Can be precancerous

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14
Q

Features of lichen sclerosus?

A

white patches that may scar

itch is prominent

may result in pain during intercourse or urination

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15
Q

Diagnosis of lichen sclerosus?

A

usually made on clinical grounds but a biopsy may be performed if atypical features are present (woman fails to respond to treatment or there is clinical suspicion of VIN or cancer or pigmented areas)

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16
Q

Management of lichen sclerosus?

A

topical steroids and emollients

Follow-up: (6m)
increased risk of vulval cancer

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17
Q

What is pelvic organ prolapse?

A

Descent of pelvic organs into vagina due to weakness + lengthening of ligaments + muscles surrounding uterus, rectum, bladder.

It probably affects around 40% of postmenopausal women

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18
Q

Types of pelvic organ prolapse?

A

Uterine

Vault: hysterectomy, vault top of vagina.
Rectocele: post vaginal wall, rectum prolapse into vagina.

Cystocele: ant wall, bladder prolapse into vagina. Urethrocele cytourethrocele.

Enterocele: herniation of pouch of Douglas incl small intestine into vagina

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19
Q

RF’s for pelvic organ prolapse?

A

multiple vaginal deliveries

instrumental, prolonged or traumatic delivery

↑age

postmenopausal

obesity

chronic resp disease (coughing)

chronic constipation (straining)

spina bifida.

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20
Q

Features of pelvic organ prolapse?

A

Feeling of something coming down in vagina

Dragging or heavy sensation in pelvis

Urinary: incontinence, urgency, freq, weak stream, retention.

Bowel: constipation, incontinence, urgency

Sexual dysfunction: pain, altered sensation ↓enjoyment

Rectocele: constipation, faecal loading, women may use their fingers to press lump back allowing them to open bowels.

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21
Q

Investigation/examination for pelvic organ prolapse?

A

Empty bladder + bowel before exam

Sim’s speculum: U-shaped, single bladed, support ant/post vaginal wall whilst other vaginal walls examined. Woman can be asked to cough or bear down to assess full descent of prolapse

Grades: 0-4 (0 ischial level, 4 past Introitus)

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22
Q

Management of pelvic organ prolapse?

A

Pelvic floor exercises, WL, ↓caffeine

Vaginal oest cream

Ring pessary: give extra support to pelvic organs, clean + changed every 4 mnths. Shelf + Gellhorn (flat disc, stem sits below uterus, can’t have sex), donut/cube shaped. Hodge (rectangular, 1 side hooked around post cervix, other extends into vagina).

Surgery: mesh repairs, plastic mesh to support organs but not recommended.

Cystocele/ cystourethrocele: ant colporrhaphy, colposuspension

Uterine prolapse: hysterectomy, sacrohysteropexy

Rectocele: post colporrhaphy

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23
Q

What is pelvic inflammatory disease?

A

term used to describe infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surrounding peritoneum.

It is usually the result of ascending infection from the endocervix.

RF’s - UPSI, IUD

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24
Q

Causative organisms of PID?

A

Chlamydia trachomatis

+ the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis

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25
Q

Features of PID?

A

lower abdominal pain

fever

deep dyspareunia

dysuria and menstrual irregularities may occur

vaginal or cervical discharge

cervical excitation

Chronic: low grade fever, WL, abdo pain

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26
Q

Investigation for PID?

A

a pregnancy test should be done to exclude an ectopic pregnancy

high vaginal swab - these are often negative

screen for Chlamydia and Gonorrhoea

Abundant WBC on saline microscopy of vaginal secretions, polymorphonuclear cells.

↑ESR, CRP

Transvaginal USS: tubal wall thickness, incomplete septae within tube, fluid in cul-de-sac, cog-wheel appearance on CS of tubal view tubo-ovarian abscess

Pelvic CT: thickened uterosacral ligaments, inflam changes of tubes + ovaries, abnormal fluid collection, reactive inflam.

Pelvic MRI: thickened, fluid-filled tubes, tubo-ovarian abscess, pyosalpinx.

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27
Q

Management of PID?

A

due to the difficulty in making an accurate diagnosis, and the potential complications of untreated PID, consensus guidelines recommend having a low threshold for treatment

oral ofloxacin + oral metronidazole OR intramuscular ceftriaxone + oral doxycycline + oral metronidazole

mild - ntrauterine contraceptive devices may be left in

Removal of the IUD should be considered and may be associated with better short term clinical outcomes’

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28
Q

Complications of PID?

A

perihepatitis (Fitz-Hugh Curtis Syndrome)
> occurs in around 10% of cases
> it is characterised by right upper quadrant pain and may be confused with cholecystitis

infertility - the risk may be as high as 10-20% after a single episode

chronic pelvic pain

ectopic pregnancy

Recurrent PID

Hydrosalpinx: fluid filled fallopian tube

Pyosalpinx: infected fallopian tube filled with purulent matter

Ovarian cancer

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29
Q

What is dyspareunia?

A

Deep or superficial

Deep indicates pathology: scarring, adhesions, endometriosis, masses restricting uterine motility

Acute onset indicates organic cause.

1°: since onset of sexual activity

2°: acquired over pts life

Bartholin’s: non-infectious occlusion of distal Bartholin’s duct, retention of secretions. Mass at inf aspect of labia majora, 5 or 7 o clock position, vulval pressure or fullness, pain during sitting/ walking. Dyspareunia.

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30
Q

Causes of superficial dyspareunia?

A

Abnormalities at introitus

Inadequate lube

Vaginismus

Overwork/depression

Relationship problems

Drug/alcohol problem

Hormonal changes

Vaginitis/vulvovaginitis - burning sensation with coitus, vulvar/ vaginal oedema, discharge, pruritis, dysuria, PV bleed, abdo pain, vaginal dryness.

Herpes simplex - intense vulvar pain, dysuria, burning, pruritis, fever + general malaise.

Vaginal atrophy - vaginal dryness, feeling of tearing during intercourse, post-coital bleeding, vaginal spotting, vaginal mucosa pale, lacks rugae.

Iatrogenic: meds, radiotherapy, COCP, antidepressant, some antihypertensives

Intersititial cystitis, UTI

Bartholin’s cyst.

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31
Q

What is vaginismus?

A

voluntary / involuntary contraction of pelvic floor muscles. Failure of penetration, affects gynae exam, tampon insertion, IUDs.

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32
Q

Management of dyspareunia?

A

Rule out organic cause

Relaxation techniques, self-exploration of genitals, insertion of vaginal trainers

Couple programs, CBT, sexual counselling

Lidocaine

HRT

Botox injections

Bartholin’s cyst: sitz bath, warm compress, marsupialisation, catheter drainage, surgical excision silver nitrate cauterisation alcohol sclerotherapy

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33
Q

What is female genital mutilation?

A

refers to all procedures involving partial or total removal of the external female genitalia or other injury to the female genital organs for non-medical reasons.

Illegal FGM Act 2003

Cultural practice in girls before puberty. Africa: Somalia, Sudan, Eritrea, Yemen, Kurdistan, Indonesia, south + west Asia.

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34
Q

Classification of FGM?

A

Type 1 - Partial or total removal of the clitoris and/or the prepuce (clitoridectomy).

Type 2 - Partial or total removal of the clitoris and the labia minora, with or without excision of the labia majora (excision).

Type 3 - Narrowing of the vaginal orifice with creation of a covering seal by cutting and appositioning the labia minora and/or the labia majora, with or without excision of the clitoris (infibulation).

Type 4 - All other harmful procedures to the female genitalia for non-medical purposes, for example: pricking, piercing, incising, scraping and cauterization.

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35
Q

Features of FGM?

A

Pain, bleeding, urinary retention, urethral damage

Incontinence

UTI, pelvic/ vaginal infections

Dysmenorrhoea

Sexual dysfunction

Dyspareynia

Infertility, pregnancy complications

Psychosocial issues + depression

↓engagement with healthcare + screening

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36
Q

RF’s for FGM?

A

From countries that practise FGM, having relatives affected

Pregnant women with FGM + female child.

Siblings/daughters of women affected by FGM

Women who decline exam or cervical screening

Present with complications of FGM

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37
Q

Management of FGM?

A

Mandatory to report all cases of FGM

Counselling

De-infibulation: T3, correct narrowing of vaginal orifice, improve Sx + try to restore normal function.

Re-infibulation: re-closure of vaginal orifice, requested after childbirth which is illegal.

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38
Q

What is polycystic ovarian syndrome?

A

complex condition of ovarian dysfunction thought to affect between 5-20% of women of reproductive age.

Ovaries contain large no of harmless follicles. Often unable to release egg, no ovulation.
XS androgen production

The aetiology of PCOS is not fully understood.

Both hyperinsulinaemia and high levels of luteinizing hormone are seen in PCOS and there appears to be some overlap with the metabolic syndrome.

Hyperinsulinemia: theca cells express insulin receptors, XS insulin, division of theca cells, ↑LH receptors, hypothalamus ↑GnRH > ↑LH

Theca cells produce XS androstenedione, too much for granulosa cells to convert. Some goes into blood, converted to estrone by aromatase in adipose tissue, neg feedback. Block ant pit from releasing FSH/ LH, no LH surge, no dominant follicle, remains in ovary as cyst, or degen with other follicles, no ovulation.
XS adipose tissue, aromatase, converts androgens to oestrogen.

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39
Q

Features of PCOS?

A

subfertility and infertility

menstrual disturbances: oligomenorrhea and amenorrhoea

hirsutism, acne (due to hyperandrogenism)
obesity

acanthosis nigricans (due to insulin resistance)

oily skin or sweating

depression + anxiety

sexual problems

Rotterdam criteria - oligoovulation or an ovulation, hyperandrogegism, polycystic ovaries on US (or ovarian volume of more than 10cm3)

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40
Q

Investigations for PCOS?

A

pelvic ultrasound: multiple cysts on the ovaries (12+ developing follicles in 1 overt or ovarian volume >10cm)

FSH, LH, prolactin, TSH, and testosterone are useful investigations: raised LH:FSH ratio is a ‘classical’ feature but is no longer thought to be useful in diagnosis. Prolactin may be normal or mildly elevated. Testosterone may be normal or mildly elevated - however, if markedly raised consider other causes

check for impaired glucose tolerance - OGTT

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41
Q

Management of PCOS?

A

weight reduction if appropriate, stop smoking, orlistat > can restore fertility

if a women requires contraception then a combined oral contraceptive (COC) pill may help regulate her cycle and induce a monthly bleed

Hirsutism and acne:
> a COC pill may be used help manage hirsutism. Possible options include a third generation (dianette) COC which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action. Both of these types of COC may carry an increased risk of venous thromboembolism
> if doesn’t respond to COC then topical eflornithine may be tried
> spironolactone, flutamide and finasteride may be used under specialist supervision
> laser hair removal
> topical Tx for acne - retinoid, clindamycin, azelaic acid, tetracyline.

Infertility:
weight reduction if appropriate
supervised by a specialist.
letrozole, clomifene. 2nd line metformin
There is an ongoing debate as to whether metformin, clomifene or a combination should be used to stimulate ovulation
gonadotrophins - follitropin alfa, follitropin beta, menotrophin.
IVF
Laparoscopic ovarian drilling: puncturing cystic ovary, induces ovulation can damage ovary. Doesn’t resolve overall hormonal imbalance.

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42
Q

RFs for PCOS?

A

AD

obesity

lack of PE

gestational DM.

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43
Q

Complications of PCOS?

A

Infertility: ↑testosterone + anovulation

CVD, non-alcoholic fatty liver, hypercholesterolemia, HTN, OSA, endometrial hyperplasia + Ca

Endometrial Ca, unopposed oest causes endometrial hyperplasia.

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44
Q

What is ovarian torsion?

A

the partial or complete torsion of the ovary on it’s supporting ligaments that may in turn compromise the blood supply. If the fallopian tube is also involved then it is referred to as adnexal torsion.

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45
Q

RFs for ovarian torsion?

A

ovarian mass: present in around 90% of cases of torsion

being of a reproductive age

pregnancy

ovarian hyperstimulation syndrome

PCOS

PMHx

46
Q

Features of ovarian torsion?

A

Usually the sudden onset of deep-seated colicky abdominal pain.

Associated with vomiting and distress

fever may be seen in a minority (possibly secondary to adnexal necrosis)

Vaginal examination may reveal adnexial tenderness

Abdo - guarding, RT

47
Q

Investigation for ovarian torsion?

A

Ultrasound may show free fluid or a whirlpool sign. enlarged ovary. Tender on pressure with USS.

FBC: leucocytosis
CRP may be ↑

Laparoscopy is usually both diagnostic and therapeutic.

48
Q

Management of ovarian torsion?

A

Surgical emergency

Laparoscopy with uncoiling

Oophorexy

Salpingo-oopherectomy: if severe vascular compromise, peritonitis or tissue necrosis.

49
Q

What is Nabothian cyst?

A

a lump filled with mucus on the surface of the cervix or cervical canal

Squamous epithelium of ectocervix slightly covers mucus secreting columnar endocervical epithelium. Mucus becomes trapped + forms cyst. Can happen after childbirth, minor trauma to cervix or cervicitis

50
Q

RFs for nabothian cyst?

A

RF: pregnant, child bearing age.

51
Q

Features of nabothian cyst?

A

Asymptomatic

Feeling of fullness if large

Smooth rounded bumps on cervix, usually near OS

Fluid filled cyst.

2mm-30mm

Whitish yellow appearance, if raised + discoloured = concern

Harmless, unrelated to cervical cancer.

Rupture: bleeding, discharge, odour.

52
Q

Investigation for nabothian cyst?

A

Incidentally on speculum

Dr may break a cyst to confirm diagnosis

Uncertain: colposcopy to examine in detail.

Rarely excised or biopsied.

53
Q

Management of nabothian cyst?

A

Reassurance, no Tx needed if diagnosis clear

If discharging may be cauterised.

54
Q

What are ovarian cysts?

A

Benign ovarian cysts are extremely common. They may be divided into physiological cysts, benign germ cell tumours, benign epithelial tumours and benign sex cord stromal tumours.

Complex (i.e. multi-loculated) ovarian cysts should be biopsied to exclude malignancy.

Uncommon in premenarchal + postmenopausal.

Fibroadenoma: small, solid benign fibrous tissue tumours. Meigs syndrome (benign ovarian tumour, ascites, pleural effusion)

Thecoma

Polycystic ovaries

Endometrioma, chocolate cysts.

Brenner’s tumour: rare, benign, borderline or prolif + malig variant. Mostly benign, unilat.

55
Q

Types of physiological cysts?

A

Follicular cysts
> commonest type of ovarian cyst
> due to non-rupture of the dominant follicle or failure of atresia in a non-dominant follicle
commonly regress after several menstrual cycles

Corpus luteum cyst
> during the menstrual cycle if pregnancy doesn’t occur the corpus luteum usually breaks down and disappears. If this doesn’t occur the corpus luteum may fill with blood or fluid and form a corpus luteal cyst
more likely to present with intraperitoneal bleeding than follicular cysts

Theca-lutein: Stim of theca internal cells of ovarian follicles due to XS gonadotrophins eg βhCG. Associated with molar preg + multiple gest

56
Q

What are benign germ cell tumours?

A

Dermoid cyst
> also called mature cystic teratomas. Usually lined with epithelial tissue and hence may contain skin appendages, hair and teeth
> most common benign ovarian tumour in woman under the age of 30 years
> median age of diagnosis is 30 years old
> bilateral in 10-20%
> usually asymptomatic. Torsion is more likely than with other ovarian tumours

57
Q

What are benign epithelial tumours of ovaries?

A

Arise from the ovarian surface epithelium

Serous cystadenoma
> the most common benign epithelial tumour which bears a resemblance to the most common type of ovarian cancer (serous carcinoma)
> bilateral in around 20%

Mucinous cystadenoma
> second most common benign epithelial tumour
> they are typically large and may become massive
> if ruptures may cause pseudomyxoma peritonei

58
Q

RFs for ovarian cysts?

A

obesity

tamoxifen

early menarche

infertility

fertility Tx

FH

PCOS

hypothyroid

hyperandrogenism

smoking (mucinous cysts)

59
Q

Features of ovarian cysts?

A

Asymptomatic

Dull ache or pain in lower abdo (back)

Torsion or rupture: sudden severe sharp abdo pain, fever.

Torsion: intermittent eps of severe pain

Rupture: peritonitis shock, rebound tenderness, guarding, shoulder pain.

Dyspareunia

Swollen abdo, palpable mass

Dull to percussion

Doesn’t appear if bladder emptied

Pressure effects: bladder (freq), venous returns (varicose veins, leg oedema)

Ascites, bloating early satiety

Hormone secreting: virilisation, menstrual irreg, PMB

Affect fertility

Torsion more common in dermoid cysts.

60
Q

Investigation for ovarian cysts?

A

Pelvic USS: transvaginal, enlarged ovary, or portion of ovarian tissue may be cystic, solid or mixed. Hypoechoic or anechoic.

CL: simple ovarian cyst, variable wall thickness, ↑vascularity, ring of fire sign. Small central lucency.

TL: multiple bilat, thin walls, clear content, occasionally solid.

Complex cyst (multi lobulated) should be biopsied to excl malig.

CA125: doesn’t need to be done in premenopausal who have had USS of simple ovarian cyst as it is unreliable due to large number of false pos.

Risk of malig index: menopausal status, USS findings, CA125

Rule out germ cell tumours: LDH, AFP, hCG.
All women <40 with complex ovarian mass.

61
Q

Management of ovarian cysts?

A

Functional cysts usually resolve on their own.

<50mm diameter: simple doesn’t require follow up.

50-70mm: simple, yearly follow up.

If persistent, unchanged <10cm, normal CA125, likelihood of invasive cancer low. Observation

NSAIDs if painful

Surgery: suspicion of malig, solid ovarian cyst, ↑size, complex ovarian cyst in post-menopausal, pregnant women (symptomatic, non-suspicious cyst, or if >8cm), cystectomy (children + women wishing to be pregnant). Immediate surgical intervention indicated for haemorrhagic cyst.

Solid ovarian cyst: laparotomy + gynaecological oncology review.

62
Q

What is infertility?

A

Infertility affects around 1 in 7 couples. Around 84% of couples who have regular sex will conceive within 1 year, and 92% within 2 years

Causes
male factor 30%
unexplained 20%
ovulation failure 20%
tubal damage 15%
other causes 15%
63
Q

Investigations for infertility?

A

Investigations initiated when couple trying for 12mnths w/o success, 6mnths if F>35

semen analysis

Serum FSH + LH: day 2-5. ↑FSH (poor ovarian reserve, little eggs, pit tried to compensate by producing more FSH), ↑LH (PCOS), ↑FSH:LH (PCOS)

Serum progesterone day 21. 7 days before end of cycle/expected period. Rise indicates ovulation. <16 repeat, if consistently low refer, 16-30 repeat, >30 indicates ovulation.

TFTs, PRL, AMH (any time of cycle, most reliable measure of ovarian reserves but not readily available, high is good, released by granulosa cells)

Transvaginal USS: structural abnormalities, PCOS

Hysterosalpingogram: patency of tubes, tubal obstruction, spillage of dye with XR. Dilation of cervix via cannula for contrast can lead to ↑ conception rates.

Laparoscopy + dye test: same idea, done with laparoscopy. Adhesions + endometriosis. Dye injected to see if there is any spillage.

64
Q

Counselling points for infertility?

A

folic acid
aim for BMI 20-25
advise regular sexual intercourse every 2 to 3 days
smoking/drinking advice

65
Q

Male RFs for infertility?

A

varicocele

CF

cryptorchidism

prior chemo or radiotherapy

congen bilat absence of vas deferens

Klinefelter’s

epididymitis

prostatitis

mumps

orchitis

STD

testicular torsion or trauma

smoking

alcohol consumption

obesity

> 55 (can affect sperm motility)

66
Q

Female RF for infertility?

A

> 35

STI
very high/ low body fat

Cannabis, alcohol, caffeine

stress

smoking.

67
Q

Features of infertility?

A

BMI: low (anovulation), high (PCOS)

STI: chlamydia, PID

Semen analysis: quality + quantity. Mumps in males. <15 million sperm/mL, <40% motile spermatozoa, <4% normal morphology, >42% sperm necrosis.

Seminal fluid parameters: low volume, ↓pH, presence of fructose, ↑leukocyte count

Rubella immunity in mother

68
Q

Management of infertility?

A

General advice: 400mcg folic acid daily, healthy BMI, no smoking or XS alcohol, ↓stress, intercourse 2-3 X a wk, avoid timing intercourse

Anovulation: WL, gonadotrophins (stim ovulation, menotrophin, follitropin alda, lutropin alfa). Clomiphene: SERM, stop neg feedback of oest on hypothalamus. ↑FH + LH secretion, growth of follicle + ovulation. Letrozole: stim ovulation. Ovarian drilling: PCOS.

Tubal + uterine: laparoscopy to remove adhesions, endometriosis or polyps.

IVF: 2 eggs (young women) 5 (women >40)

Sperm: surgical sperm retrieval, surgical correction of obstruction, IU insemination, intracytoplasmic sperm injection, donor insemination

Men: hormonal (chorionic gonadotrophin, follitropin alfa, pulsatile GnRH, clomifene, tamoxifen), ↑PRL due to pit adenoma (bromocriptine, cabergoline), antisperm Ig (IVF), varicocele (percut embolization, microsurgical dissection + ligation).

69
Q

What is ovarian hyperstimulation syndrome?

A

complication seen in some forms of infertility treatment. It is postulated that the presence of multiple luteinized cysts within the ovaries results in high levels of not only oestrogens and progesterone but also vasoactive substances such as vascular endothelial growth factor (VEGF). This results in increased membrane permeability and loss of fluid from the intravascular compartment

Whilst it is rarely seen with clomifene therapy is more likely to be seen following gonadotropin or hCG treatment. Provoked by trigger injection hCG 36 hrs before oocyte collection that matures follicles in IVF. RAAS, ↑renin

Up to one third of women who are having IVF may experience a mild form of OHSS

70
Q

Classification of OHSS?

A

Mild - Abdominal pain,• Abdominal bloating

Moderate - As for mild, Nausea and vomiting,• Ultrasound evidence of ascites

Severe - As for moderate, Clinical evidence of ascites, Oliguria, Haematocrit > 45%, Hypoproteinaemia

Critical - As for severe, Thromboembolism, Acute respiratory distress syndrome, Anuria, Tense ascites

71
Q

RFs for OHSS?

A

young age
↓BMI
↑AMH, antral follicle count + oestrogen levels during ovarian stim.
PCOS

72
Q

Features of OHSS?

A

7 days after injection

Late OHSS: >10days

Peritonitis from rupturing follicles releasing blood

Rapid weight gain

Abdo pain, bloating, ascites, VTE/PE, ARDS

73
Q

Investigations for OHSS?

A

During simulation with gonadotropins (FSH), monitoring: ↑oestrogen ↑ risk, USS (follicles, ↑ + larger ↑ risk).

USS: ovaries bigger, large fluid filled follicles

Bloods: U+E, leukocytosis, LFTs

Monitor hematocrit: assess volume of fluid in intravascular space, conc of RBCs in blood, if high, less fluid in intravascular space, indicate dehydration

74
Q

Management of OHSS?

A

Prevention: GnRH antagonist instead of agonist, ↓dose of gonadotropins, + hCG injection, alternative to hCG > GnRh agonist or LH

Supportive

Oral fluids

Monitor UO

LMWH: prevent VTE

Paracentesis

IV colloids: human albumin solution.

Don’t give diuretics

Analgesia: paracetamol +/or opioids, NSAIDs avoided.

75
Q

What is menopause?

A

The average women in the UK goes through the menopause when she is 51 years old. The climacteric is the period prior to the menopause where women may experience symptoms, as ovarian function starts to fail

Premenopausal: vasomotor Sx + irregular periods. >45. 4 yrs before FMP.

Perimenopause: transition, from onset of Sx until 1 yr after menopause. 45-55.

Menopause: no periods for 12 mnths. Average age 52

Premature: <40

Lack of ovarian follicular function, oocytes lost due to aging, ↓oestrogen + progesterone ↓hypothalamic inhibition > ↑bursts of GnRH > ↑FSH + LH. But still no oestrogen, endometrium doesn’t develop, anovulation, irregular menstrual cycle + amenorrhea

76
Q

Sx of menopause?

A

Hot flushes, night sweats. Diaphoresis, palpitations.
Emotional liability or mood. Anxiety + depression, diff concentrating.
Premenstrual synd
Joint pains, muscle pain
Heavier/lighter periods, change in length of periods
Vaginal dryness + atrophy.
STM impairment
↓libido
UT dysfunction: dysuria, urinary urgency, freq.

77
Q

Complications of menopause?

A

Atrophic vaginitis: post-menopausal, vaginal dryness, dyspareunia, occasional spotting. Vagina may appear pale + dry

CVD + stroke

Osteoporosis #

Pelvic organ prolapse

UI: GU atrophy

↓risk of breast cancer

Late menopause ↑ risk of endometrial cancer

Unopposed oestrogen ↑risk of endometrial Ca if woman still has uterus.

78
Q

Investigations of menopause?

A

FSH: <40 suspected prem menopause, 40-45 menopausal Sx or change in cycle. Cessation of menses <45. Perimenopause Sx <45, + iatrogenic amenorrhoea (hysterectomy, POC, endometrial ablation). Women on POC>50 + wishes to stop

No need for bloods: >45yrs menopausal Sx + irregular periods. No period for 12 mnths, not on contraception, hysterectomised with Sx, difficult in women on hormonal Tx for HMB, can’t use FSH if on CHC or high dose progestogen.

Transdermal preferred in women at risk of VTE.

Unscheduled vaginal bleeding common in 1st 3/12.

79
Q

Management of menopause?

A

Contraception in: <50 2yrs after LMP, >50 1yr after

Reg exercise, WL, ↓stress, smoking, alcohol, caffeine

Sleep hygiene: avoid late evening exercise

Vasomotor: resolve in 2-5 yrs w/o Tx. Avoid triggers eg hot drinks, spicy food, maintain cool ambient temp, lighter clothing. HRT, fluoxetine, citalopram, venlafaxine

HRT: ↑endometrial + breast ca, VTE, small ↑ CVD/stroke. ↓CRC + osteoporosis. Oestrogen HRT may ↓risk of CVD

HRT CI: current/past breast ca, oest-sensitive ca, undiagnosed vaginal bleeding, untreated endometrial hyperplasia, VTE/DVT unless on anticoag, active/recent arterial disease eg anginal/MI, uncontrolled BP, acute liver disease/ abnormal LFTs, porphyria, pregnancy, Dubin-Johnson/ Rotor (close monitoring)

Clonidine: agonist of α adrenergic receptors.

Psychological Sx: self help groups, CBT, antidepressants

Urogenital atrophy: vaginal oest. Moisturisers + lubricants.

Altered sexual function: HRT, testosterone. Gel eg testogel. Patch > intrinsa, tibolone.

80
Q

What is premature ovarian failure?

A

defined as the onset of menopausal symptoms and elevated gonadotrophin levels before the age of 40 years.

Follicles stop responding to LH + FSH, disrupted ovulation, ↓oest, progest, androstenedione > amenorrhoea, hypogonad, hypoestrogenism

It occurs in around 1 in 100 women.

81
Q

Causes of premature ovarian failure?

A

idiopathic
> the most common cause
> there may be a family history

bilateral oophorectomy
> having a hysterectomy with preservation of the ovaries has also been shown to advance the age of menopause

radiotherapy

chemotherapy

infection: e.g. mumps

autoimmune disorders

resistant ovary syndrome: due to FSH receptor abnormalities

genetic - Turner’s, fragile X synd, BRCA1 mutation > gonadal dysgenesis.

82
Q

Features of premature ovarian insufficiency?

A

climacteric symptoms: hot flushes, night sweats

infertility

secondary amenorrhoea

raised FSH, LH levels
> e.g. FSH > 40 iu/l
> elevated FSH levels should be demonstrated on 2 blood samples taken 4–6 weeks apart

low oestradiol
> e.g. < 100 pmol/l

83
Q

Management of premature ovarian insufficiency?

A

hormone replacement therapy (HRT) or a combined oral contraceptive pill should be offered to women until the age of the average menopause (51 years)

it should be noted that HRT does not provide contraception, in case spontaneous ovarian activity resumes

IVF Tx

84
Q

Investigations for premature ovarian insufficiency?

A

USS: shrunken ovaries

↓oestrogen, ↑LH, FSH (2 blood samples 4-6 wks apart)

If AI: test for steroid cell antibodies/ STCAs

Genetic testing: karyotype, chr abnormalities, evaluate for genetic disease.

85
Q

What is menorrhagia?

A

what the woman considers to be excessive and aims to improve quality of life measures.

86
Q

Causes of menorrhagia?

A

dysfunctional uterine bleeding: this describes menorrhagia in the absence of underlying pathology. This accounts for approximately half of patients

anovulatory cycles: these are more common at the extremes of a women’s reproductive life

uterine fibroids

hypothyroidism

intrauterine devices* (copper coil)

pelvic inflammatory disease

bleeding disorders, e.g. von Willebrand disease

Fibroids, endometriosis, adenomyosis, polyps,

malig (endometrium, cervical, ovarian)

endometrial hyperplasia

87
Q

Sx of menorrhagia?

A

Dx on Sx not vol: changing pads every 1-2 hrs, >7 days, passing large clots.

Normal 40ml, XS >80ml

Speculum + bimanual palp

Swabs: infection

88
Q

Investigations of menorrhagia?

A

FBC: iron studies, ferritin.

Pelvic + transvaginal USS: palpable pelvic mass (large fibroids) pelvic pain + tenderness on exam (adenomyosis), obesity (exam difff) if Sx suggest structural or histological abnormality.

Outpt hysteroscopy: submucosal fibroids, endometrial pathology (Ca or hyperplasia).

89
Q

Management of menorrhagia?

A

1st: mirena coil

COCP

Tranexamic acid 1g or mefenamic acid.

Long-acting progestogens eg Depo Provera

Endometrial ablation

Hysterectomy

90
Q

What are fibroids?

A

Benign tumours of smooth muscle of uterus

Common in black women

Oest sensitive: grow

Intramural: in myometrium.

Subserosa: just below outside layer of uterus. Grow out + become very large, filling abdo cavity

Submucosal: just below lining of uterus (endometrium)

Pedunculated: on stalk

91
Q

Sx of fibroids?

A

Asymptomatic.

Rare before puberty

Heavy menstrual/ prolonged bleeding

Abdo pain, lower, cramping, worse on menstruation

Dyspareunia

Bloating or feeling full in abdo

Abdo + biman may reveal palpable mass or enlarged, firm, non-tender uterus

92
Q

Complications of fibroids?

A

Generally regress after menopause

Iron def anaemia

Urinary/ bowel Sx due to pressure or fullness, constipation

↓fertility

Polycythaemia 2° to production EPO

Miscarriages, prem labour, obstructive labour

Urinary outflow obstruction

UTIs

Torsion of fibroids

Malig changes: rare, leiomyosarcoma

93
Q

Investigations of fibroids?

A

TVUS

Hysteroscopy: visualise fibroids

Pelvic USS: larger fibroids.

MRI: before surgery, info needed about size, shape, blood supply.

94
Q

Management of fibroids?

A

Asymptomatic: no Tx, periodic review

GnRH agonists: goserelin or leuprorelin. ↓size of fibroid before surgery. Induce menopause like state, used in ST.

Mifepristone

Menorrhagia: mirena coil, NSAIDs (mefenamic acid), tranexamic acid, COCP, progestogen.

Myomectomy - abdominally, laparoscopically or hysteroscopically

Endometrial ablation

Uterine a embolism

Hysterectomy

95
Q

What is red degeneration of fibroid?

A

haemorrhage into tumour - commonly occurs during pregnancy

Fibroid rapidly enlarges in preg outgrow blood supply, or kinking in BVs as uterus changes shape + expands in preg. ischaemia, infarction, necrosis of fibroid.

96
Q

Sx of red degeneration of fibroid?

A

Preg woman with Hx of fibroids

Severe abdo pain + low grade fever

↑HR. vomiting.

Large fibroids >5cm

2nd/3rd trim of preg

97
Q

Management of red degeneration of fibroid?

A

Supportive

Fluids

Rest

Analgesia

Should resolve within 4-7 days

98
Q

What is dysmenorrhoea?

A

characterised by excessive pain during the menstrual period. It is traditionally divided into primary and secondary dysmenorrhoea.

99
Q

Summary of primary dysmenorrhoea?

A

primary dysmenorrhoea there is no underlying pelvic pathology. It affects up to 50% of menstruating women and usually appears within 1-2 years of the menarche. Excessive endometrial prostaglandin production is thought to be partially responsible. Begins due to onset of ovulatory cycles

Features

  • pain typically starts just before or within a few hours of the period starting
  • suprapubic cramping pains which may radiate to the back or down the thigh
  • V/N/D
  • fatigue
  • headache
  • 1st 2 yrs of menarche

Investigations
- Transabdo USS to rule out pathology.

Management

  • NSAIDs such as mefenamic acid and ibuprofen are effective in up to 80% of women. They work by inhibiting prostaglandin production
  • combined oral contraceptive pills are used second line
100
Q

Summary of secondary dysmenorrhoea?

A

Secondary dysmenorrhoea typically develops many years after the menarche and is the result of an underlying pathology. In contrast to primary dysmenorrhoea the pain usually starts 3-4 days before the onset of the period.

Features:

  • May worsen as progresses.
  • Heavy/ irreg bleeding, discharge, dyspareunia

Causes include:

  • endometriosis
  • adenomyosis
  • pelvic inflammatory disease
  • intrauterine devices* - copper coils
  • fibroids
  • congenital uterine abnormalities
  • cervical stenosis
  • ovarian pathology

Clinical Knowledge Summaries recommend referring all patients with secondary dysmenorrhoea to gynaecology for investigation.

101
Q

What is endometriosis?

A

a common condition characterised by the growth of ectopic endometrial tissue outside of the uterine cavity. Around 10% of women of a reproductive age have a degree of endometriosis.

Cause unknown

Retrograde menstruation: endometrial lining flow back through fallopian tubes + seed around pelvis + peritoneum.

Embryonic cells destined to become endometrial tissue remain in areas outside uterus in development.

Spread of endometrial cells through lymphatic system

Metaplasia: cells outside uterus change to endometrial cells.

Iatrogenic implantation

102
Q

Features of endometriosis?

A

chronic pelvic pain - localised bleeding + inflam > adhesions. Sharp, stabbing, pulling, nausea.

asymptomatic in some cases

secondary dysmenorrhoea
> pain often starts days before bleeding. dull, heavy, burning pain

deep dyspareunia

subfertility

non-gynaecological: due to deposits in bladder/bowel > urinary symptoms e.g. dysuria, urgency, haematuria. Dyschezia (painful bowel movements), PR bleed

on pelvic examination reduced organ mobility, tender nodularity in the posterior vaginal fornix and visible vaginal endometriotic lesions may be seen

103
Q

Investigation for endometriosis?

A

laparoscopy is the gold-standard investigation

there is little role for investigation in primary care (e.g. ultrasound)- if the symptoms are significant the patient should be referred for a definitive diagnosis

Pelvic/transvaginal USS: large endometriomas (endometrial tissue) + chocolate cysts (ovary).

Often unremarkable. Uterus generally not enlarged. Nodules in bladder or rectovaginal septum.

104
Q

Management of endometriosis?

A

Depends on clinical features

1st - NSAIDs and/or paracetamol are the recommended first-line treatments for symptomatic relief

2nd - if analgesia doesn’t help then hormonal treatments such as the combined oral contraceptive pill or progestogens e.g. medroxyprogesterone acetate should be tried

3rd - If analgesia/hormonal treatment does not improve symptoms or if fertility is a priority the patient should be referred to secondary care. Secondary treatments include:
> GnRH analogues - leuproelin, goserelin - said to induce a ‘pseudomenopause’ due to the low oestrogen levels
> drug therapy unfortunately does not seem to have a significant impact on fertility rates
> Immediate fertility desired: clomifene (oestrogen receptor modulator), letrozole (aromatase inhib), menotrophin (highly purified gonadotropins), follitropin alfa. IVF.
> surgery: some treatments such as laparoscopic excision and laser treatment of endometriotic ovarian cysts may improve fertility, hysterectomy

105
Q

Complications of endometriosis?

A

↓fertility: adhesions, block release of eggs, kinking fallopian tubes, damage eggs if deposits in ovaries.

Anaemia

Ectopic preg

Fibrous adhesions, strictures, entrapment of organs. Intestines (C/D, obstruction, ileus, intussusception) ureter (urine retention)

↑risk ovarian Ca

106
Q

What is adenomyosis?

A

Endometrial tissue in myometrium.

More common in later reproductive yrs + in multiparous women.

Can occur alone or alongside endometriosis + fibroids.

Hormone dependent

107
Q

Features of adenomyosis?

A

Dysmenorrhoea

Menorrhagia

Infertility

Dyspareunia

Pregnancy related complications

Asymptomatic

Exam: enlarged, boggy tender uterus. Feel softer than uterus containing fibroids.

108
Q

Complications of adenomyosis?

A

Pregnancy: poor outcomes, infertility, miscarriage, preterm birth, SGA, preterm PROM, malpresentation, C-section, PPH.

109
Q

Investigations for adenomyosis?

A

Transvaginal USS

MRI + transabdo USS if transvaginal USS not suitable

Gold standard: histological exam of uterus after hysterectomy

110
Q

Management for adenomyosis?

A

Contraception: mirena, COP, POP/implant/depot

If not wanting contraception: tranexamic acid if no pain, mefenamic acid when pain.

GnRH agonists

Endometrial ablation. Uterine artery embolization.

Hysterectomy