Gynae problems

Question 1

Describe the phases of the menstrual cycle?

Answer 1

Day 1-4: Menstruation P + E levels have dropped due to the degradation of the corpus luteum causing the shedding of the Endometrium and myometrial contraction to dispel the contents.
Day 5-11: Proliferation/Follicular phase. Pulsatile release of GnRH stim FSH release and induces follicular growth. Multiple follicles develop but one will be most mature and will be released. FSH stim prod aromatase so oocytes can make estradiol. Estrogen inhibits GnRH production so only most mature follicle can survive, the rest regress (bc FSH prod is therefore inhib).
Due to increasing levels E, Endometrial proliferation, thickening of stroma + epithelium.
Day 12-14: Ovulation. Mid-cycle, high Estrogen prod by maturing oocyte has +ve feedback on GnRH causing LH surge.
Day 15-28: Secretory (Luteal) Phase (Progesterone dominant phase). Follow ovulation, follicle remnants form C.L and this secretes P + E. P causes gland enlargement + engorgement, develop spiral a, decidualisation (Glycogen rich glands).
If Fertilisation hasn’t occurred, CL degen and P + E drops off causing menstruation (and allowing GnRH + FSH prod to rise). If it does occur, HCG from develop conceptus maintains CL and P.

Question 2

What are normal ages of menarche + menopause?

Answer 2

menarche <16, menopause >45, median age = 51

Question 3

what are your ddx for abnormal uterine bleeding of any kind?

Answer 3

polyps, ectropic cervix, adenomyosis, leiomyomas (fibroids), malignancy (cervix, ovary, endometrium) + hyperplasia, coagulopathy, PID, ovulatory dysfunction, endometrial haemostasis disorder, iatrogenic, idiopathic.

Question 4

What are the types of abnormal uterine bleeding?

Answer 4

Heavy- Menorrhagia interferes with woman’s emotional, social and physical QoL
Menstrual irregularity : either infreq >38d apart, or freq <24d apart
Amenorrhoea- absent for a 6/12 period or longer
Postcoital (after sex bleeding not assoc menstruation)
Intermenstrual bleeding
Pre- or Post-Menstrual bleeding
Post menopausal bleeding
Dysmenorrhea: painful bleeding.

Question 5

What are the s and s of menopause?

Answer 5

Vasomotor: hot flushes, palpitations, night sweats
Gential Tract (Due to loss of E): dry +thin/ atrophic vagina– atrophic vaginitis (inflamm second to thinning) causing itching, burning, pain, bleeding, increased susceptibility to vaginal infections due to increased pH, dyspareunia, reduced fertility, gradual increase cycle length before amenorrhoea,
UT (E loss thins bladder + urethral mucosa): urinary symptoms- incontinence (due to loss of elasticity of tissues again E dependent), nocturia, freq, urgency, increased UTI.
Mind: headache, fatigue, reduced libido + arousal + orgasm (due to vaginal dysfunction + reduced T second to reduced ovarian function), anxiety, irritability, tearful, cog diff.
General: back ache, stiffness + muscle pain, skin atrophy.

Question 6

what are the complications/ associations (long term) of menopause?

Answer 6

UTIs due to change in pH and structural changes in vagina and UT.
CVD + Stroke risk: E reduces plaque formation by inhib LDL oxidation. LDL levels increase following menopause.
osteoporosis + # risk: E suppresses osteoclast activity + numbers therefore loss of its action allows rapid bone breakdown.

Question 7

what are the tx for menopause?

Answer 7

Vasomotor: HRT (P + E for those w/ uterus, E only if no uterus)
Psychological: Consider HRT/ CBT (no evidence for SSRI/SNRI if NOT depressed)
Alt sexual function: consider add T to HRT if HRT not maintain sexual desire.
Localized Topical Oestrogen for urogenital dysfunction
Tibolone is an option for libido, vasomotor + psychological symptoms for patients who desire amenorrhoea.

Question 8

what is heavy menstrual bleeding and what causes it? What are imp points of hx + exam?

Answer 8

Menorrhagia: excessive menstrual bleeding to interefere with woman’s emotional, physical, social + material QoL. Sometimes described as blood loss of >80ml (max amt can lose before become Fe deficient) but rarely measured in practice.
Common causes: Fibroids, polyps, Adenomyosis (endometrial tissue present in myometrium) rarely Thyroid disease, anticoag therapies or coag pathologies implicated. Uncommon- ca and PID (usually cause irreg bleeding)
History: amt + timing of bleeding, flooding + large clots usually imply excessive loss, LMP, previous tx for HMB, contraceptive use, impact on patient, assess for other symptoms- pelvic pain, pressure symptoms, post coital bleed, intermenstrual bleed, smear hx + previous tx, other sites of bleeding (if young- coag problem poss).
Exam: anaemia common, often normal pelvis, but sometimes irreg enlarged uterus- fibroids, tender w/ or w/o enlarge- adenomyosis, ovarian mass may be palpated.

Question 9

what is your ddx for pelvic pain?

Answer 9

endometriosis
PID
adhesions

Question 10

what are pressure symptoms?

Answer 10

for pelvis: urinary retention, constipation, tenesmus- recurrent inclination to poo.
for abdomen: feel fullness, distension, n + v, pain.

Question 11

how should heavy menstrual bleeding be investigated?

Answer 11

1. Examination (not necessary if no indication of pathology)
2. FBC on all women
3. Coagulation screen (if coag is indic in hx)
4. Thyroid test only if indic by hx
5. first line imaging is transvaginal USS if uterus is palpable, pelvic mass noted on vaginal exam, pharma tx fails
6. Endometrial biopsy if persisting intermenstrual bleed, tx failure, woman >45 yrs old
7. Hysteroscopy is only indic if USS inconclusive

Question 12

how should Heavy menstrual bleeding be managed?

Answer 12

If no fibroids/ fibroids of <3cm, options are:
1. IUS progesterone (reduce bleed),
2. COCP, NSAIDS (anti-PG which cause vasodilation of spiral a, encourage prod of PG which cause vasoconstrict), Tranexamic Acid/ Mefanemic Acid (NSAID) (antifibrinolytic stop the breakdown of small clots in spiral arteries which lead to heavy bleeds, during menstruation only),
3. high dose oral P, Depo injections, endometrial ablation (cannot conceive in future, ablate basal layer and tiny layer of myometrium).
If fibroids, ulipristal acetate (P R antagonist), GnRH analogue + endometrial ablation/ uterine artery embolisation, myomectomy (preserve uterus) or hysterectomy

Question 13

What are the causes of inter menstrual bleeding/ menstrual irregularity? how should inter menstrual bleeding / menstrual irregularity be investigated?

Answer 13

anovulatory cycles common at extremes of age (menarche + menopause), ectopic pregnancy, ectropion.
others: fibroids, uterine/ cervical polyps, adenomyosis, ovarian cysts, chronic PID, older women- malignancy ovarian, endometrial, cervical.
Hx: recent change? menorrhagia too, PCB?, timing in relation to cycle, factors increase bleed, assoc fever, abdo pain, dyspareunia, discharge? risk of pregnancy, contraceptive use, smear test, swab tests.
Examination (speculum + bimanual), FBC (anaemia), smear (except v young women), transvaginal USS >35 yrs or young women if tx failed, endometrial biopsy (pipelle) if thickened, polyp suspected, >40yrs
Managed: IUS, COCP, high dose progestogens, HRT if perimenopause, can also use surgery like for Heavy Menstrual bleeding.

Question 14

how is amenorrhoea classified and what are its causes?

Answer 14

primary (if has not started by age 16 with normal secondary sex characterists/ 14 with no 2 sex characteristics), or secondary.
CAUSES: constitutional delay (physiological), prem ovarian failure e.g. Turner’s / chemo/ irradiation, HPO dysfunction- low BMI, excess exercise, systemic illness, HyperPTH, T disease, Cushing’s Syndrome, congenital malf: imperforate hymen, transverse vaginal septum.
Secondary- when previously menstruating but this ceases for more than 3-6 months or 9-12 months in previous oligomenorrhea.
CAUSES: pregnancy, lactation, menopause, PCOS, HPO dysfunction- obesity, low BMI, hyperPTH, Adrenal tumour, T disease, prem ovarian failure- autoimmune, chemo/ radio, Cushing’s.
Location of causes: Hyp (Low BMI/ excess exercise), Pit: HyperPRL - hyperplasia/ benign adenoma, Thyroid- either hypo or hyper/ Adrenals- tumour, Ovary- PCOS, failure- due to irradiation, Congenital- most common is Turner’s, Outflow- congenital e.g. hymen/ stenosed cervix.

Question 15

what are imp parts of amenorrhoea hx?

Answer 15

contraceptive use- expect to return to normal within 6/12 stop COCP, or 9/12 of Depo
ovarian fail- hot flashes, vaginal dryness
pit tumour- headahe, visual disturb, breast milk (galactorrhoea)
acne, hirsuitism, weight gain- PCOS
weight loss- ED
Exercise levels- Hyp dysf
Stress/ depression- Hyp dysf
symptoms thyroid problems- T disease
obs/ surgical hx- adhesions
chemo/ radio hx
antipsychotics- hyperPRL
illicit drugs- cocaine/ opiates, hypogonadism
fhx early menopause

Question 16

what investigations are imp for amenorrhoea? What findings on hormone testing indicate the location of the pathology?

Answer 16

FSH + LH levels, PRL level, total testosterone, TSH, pelvic US if PCOS suspected.
high FSH + LH= ovarian failure
Normal/ low FSH + normal/ low LH= Hyp dysfunction/ extra-hyp dysfunction e.g. HyperPTH
Normal FSH and normal/ increased LH= PCOS

Question 17

how should primary + secondary amenorrhoea be managed?

Answer 17

primary: refer to Paeds Endocrinologist/ General partic if congenital/ prem ovarian failure of concern. For weight related encourage wt gain + dietician input, for exercise reduce exercise, increase cal intake, for stress- psychiatrist + CBT
secondary: PCOS- healthy lifestyle: wt loss, screen CVD risk, screen T2DM, may use metformin if T2DM/ insulin insensitive, US of Endometrium, COCP/ IUS to reduce chance of endometrial hyperplasia.
HypoT- Thyroxine
Refer to gynae if prem ovarian fail, infertility, PCOS if not manageable in primary care,
Refer to endo for hyperPRL, features Cushings, Low FSH/low LH, increased testosterone.
Offer contraceptives bc slight chance pregnancy with secondary amenorrhoea.

Question 18

what is Postcoital bleeding? What are its causes? How should it be investigated?

Answer 18

Apart from first ever intercourse this is always abnormal.

cervical ectropion common to teens, pregnant women, women on COCP. benign polyps, invasive cervical cancer are the other main causes. cervicitis.
Examination of cervix, Smear test +/ - Colposcopy even if negative smear in past.

Question 19

What is ectropion? How is it managed?

Answer 19

common to teens, pregnant women, women on COCP.
eversion of the transitional zone of the cervix into the vagina so that columnar cells of the cervix are exposed to the vagina. Appearance: Red around the cervical os. PCB, Spotting, clear discharge common PC.
Tx: diathermy/ cryotherapy

Question 20

What is dysmenorrhoea? What are its causes?

Answer 20

painful menstruation due to contraction + uterine ischaemia and associated w/ high levels of PGs
primary- no cause found, common to teens, amenable to NSAIDs (mefenamic acid), or ovulation supp via COCP/ other contraceptive. Normal examination, no other symptoms associated with secondary, instead associated with bloating, n +v, migraine, emotional symptoms.
Secondary- commonly associated dyspareunia, menorrhagia, irreg menstural bleeding. Causes- fibroids, endometriosis, adenomyosis, PID, ovarian tumours. IUD (esp if inserted 3-6/12 earlier).

Question 21

How should dysmenorrhoea be investigated? What are imp Q in history?

Answer 21

primary is a dx once secondary has been excluded.
when did it start in relation to menarche? more likely primary if symptoms from menarche. Other symptoms to ask about: dyspareunia, intermenstrual bleed, PCB, menorrhagia, vaginal discharge.
Abdo exam + bimanual pelvic exam + speculum (unless young and not sexually active)
consider high vaginal + endocervical if young pt, and any associated ab vaginal discharge/ blood.
USS if any masses found on palpation.

Question 22

what are the red flags for cervical ca?

Answer 22

persistent intermenstrual bleeding, PCB, abnormal cervical appearance. ADD TO

Question 23

what are the risks of HRT?

Answer 23

• VTE risk is increased in oral HRT
• Stroke small increased risk if oral E
• If E + P increased risk of Breast ca but related to length of tx and risk reduces post stopping.
• Endometrial ca (unopposed E therapy therefore no longer recommended in women who have a uterus)

Question 24

what is postmenopausal bleeding? what are the causes? How is it investigated?

Answer 24

vaginal bleeding occurring at least 12 months after LMP.
endometrial ca, endometrial hyperplasia +/- polyps + atypia, cervical carcinoma, atrophic vaginitis (dx exclusion) / cervicitis, ovarian carcinoma, cervical polyps. if regular bleeding as increasing HRT, it is due to this therapy and does not need investigation.
Bimanual + speculum + smear
Transvaginal USS: endometrial thickness, fibroids, ovarian cysts. If multiple episodes bleeding/ endometrial thickened, endometrial biopsy (pipelle) +/- hysteroscopy,

Question 25

how is suspected menopause confirmed?

Answer 25

History
FSH levels- higher levels suggest reduced ovarian reserve (ie number of oocytes) bc trying to stimulate oocytes and there is not adequate E to suppress its prod. But in perimenopause FSH levels fluctuate within cycle and during day so not partic reliable.
Only in women 40-45 with menopause symptoms
or women <40 suspected of premature menopause

Question 26

How is menopause managed? What are the benefits of HRT?

Answer 26

HRT: Can be delivered orally, subcut, transdermal
Women w/ uterus: E + P. P given to reduce risk of Endometrial hyperplasia + ca which occurs in unopposed E use.
Women w/o uterus: E only
Tx BENEFITS: Vaginal symptoms, hot flushes, reduce risk of osteoporosis of hip + spine, reduces risk colon ca.
RISKS: Endometrial ca for unopposed E therefore P is added in all women with uterus, Breast Ca slight increase if combined, E only has no effect.
Non-HRT:
1. Vasomotor: Fluoxetine 20mg OD / Citalopram 20mg OD
2. Vaginal dryness: Vaginal lubricant/ moisturiser
3. sexual dysfunction: T supplementation
4. Psych symptoms: CBT, self help

Question 27

What are the complications of fibroids? How is it investigated?

Answer 27

malignancy (.1% are leoisarcomata) suspect if grow rapidly, if grow in postmenopausal or sudden onset pain
Torsion of pedunculated fibroid- pain
degeneration - most common being red degen during pregnancy where blood supply cannot meet demands of enlarged fibroid and it infarcts causing severe pain + uterine tenderness.
Pregnancy- premature birth, transverse lie, obstructed labour, PPH.
USS number, size + position.
Hysterosalpingogram can be used to see how distorted uterus is if subfertile.

Question 28

what are fibroids? Where can they be located? What are the RF for developing?
What are the common symptoms of fibroids?

Answer 28

benign growths of myometrium that are v common - 70% women have at least one by age 50. RF: asian, obese, increasing age in reproductive years, fhx, early menarche.
Subserosal
Intramural
Submucosal
Growth is under the influence of E + P therefore during pregnancy anything may happen they may grow / shrink/ stay same. Regress post menopause due to reduction of sex H.
- HMB is most common complaint.
- IMB if submucosal. Pain unlikely unless red degeneration in pregnancy/ torsion.
- Subfertility if submucosal/ intramural
- Pressure effects: press on ureters- hydronephrosis, press on bladder- increased freq or retention.

Question 29

What are the med and surgical tx for fibroids?

Answer 29

MED
Transexamic Acid / Mefanemic Acid (NSAIDS) often ineffective but worth trying
IUS Progesterone may not help
GnRH analogues (max use 6/12), due to amenorrhoea + simulate menopause (increase risk of bone density loss, + menopause like SE) – fibroids return when tx stopped. Shrinks fibroids, reduces vascularity + thins endometrium.
Ulipristal Acetate - Progesterone R modulators which shrink fibroids + cause transient amenorrhoea but not SE of GnRH . another good pretx for surgery.
SURGERY
hysteroscopy removal if small, post GnRH analogue
Myomectomy if med tx has failed + woman still wants to conceive
Hysterectomy radical but good outcomes, good if woman completed family.
Uterine a embolisation, good success rate but lower than hysterectomy/ myomectomy.

Question 30

What is adenomyosis? How does it present? How is it dx? What is the management?

Answer 30

Endometrial tissue within the myometrium of the uterus. Symptoms stop after menopause. PC: painful, regular, heavy periods. Uterus may be mildly enlarged + tender OE. MRI is best at dx and often incidental finding on hysterectomy. Oestrogen dependent condition therefore IUS or COCP + NSAIDS may control symptoms of bleeding + pain but often hysterectomy is opted for.

Question 31

What are the causes of a pruritic vulva?

Answer 31

infections:
candidiasis (May get accompanying discharge)
HSV
vulval warts (condylomata acuminata)
pubic lice
scabies 
Derm disease:
Irritant contact dermatitis (e.g. due to moisture, faeces, excess washing, lack of oestrogen), Eczema, psoriasis, lichen simplex, lichen planus, lichen sclerosus
Malignancy:
carcinoma (SCC)
premalignant (VIN)
extramammary paget's disease

Question 32

what is lichen simplex? How is it managed?

Answer 32

aka vulval dermatitis, chronic inflammation of the vulva (often associated with eczema) causing intractable pruritis that is often worse at night. Labia majora become thickened + inflamed, and hypo/ hyperpigmentation occurs, broken off hairs. Localized lichenification! (Leathery) in response to excessive itching. Site is imp diff from sclerosus but these may coexist.
Chemical/ contact dermatitis + stress may worsen symptoms + irritants should be avoided. Emollients, moderate potency steroids + antihistamines used to break cycle if itching + scratching.
Biopsy if diagnosis uncertain.

Question 33

what is lichen planus?

Answer 33

Affects mucus memb e.g. mouth + genital region, flat papular purplish lesions. Usually painful rather than pruritic.
Thought to be autoimmune. high potency steroids used.
It can cause erosions/ ulcers.

Question 34

What is lichen sclerosus?

Answer 34

Autoimmune mediated. Epithelium is thin with loss of collagen. Severe pruritis + worse at night. Uncontrolled itching may cause bleeding + skin splitting + pain, dyspareunia (superficial). Pink-white papules, which coalesce to form parchmentlike skin with fissures. may coexist with other lichen simplex/ planus, vitilgo + thyroid disease. primarily involves the non-hair bearing, inner areas of the vulva but may spread to perianal skin + inguinal fold.
white crinkled or thickened patches of skin that have a tendency to scar. Adhesions can form, potentially fusion of the labia and narrowing of the introitus. Vulval
carcinoma can develop in 5% of cases. (SCC) therefore Biopsy. Tx ultra-potent steroids.

Question 35

What are the RF for candida? How does it present?

Answer 35

obesity, pregnancy, antibiotic use, immunosuppression, diabetes.
Itching and soreness of vulva + anus

Question 36

What is the relative strength of different forms of natural estrogens?

Answer 36

Oestrodiol strongest
Oestrone 12x less potent than oestrodiol
Oestriol 80x less potent than oestrodiol.

Question 37

what is tibolone?

Answer 37

inert steroid compound converted to metabolites with oestrogenic, progestognenic + androgenic properties. Used to tx vasomotor, psychological + libido issues and achieve amenorrhoea. It conserves bone mass.

Question 38

What is the difference between combined + sequential HRT and who should they be used in?

Answer 38

Continuous: causes amenorrhea
Sequential: pt has monthly/ 3 monthly bleed
Continuous causes endometrial atrophy and may reduce risk of endometrial cancer comp to sequential.
Continuous are used in those with LMP > 1year ago
Sequential for those who’s LMP<1 year ago.