General gynaecology Flashcards

1
Q

What is the frequency of menstrual cycle?
Duration of flow?
Volume of blood loss?
Regularity of cycle?

A

Frequency: 21-35 days
Duration of flow = 8 days
Volume of blood loss = 5-80ml
Regularity of cycle = cycle to cycle variation +2-20 days over 12 months

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2
Q

What is the normal range of menarche and menopause?

A

Menarche = 10-16 years (average = 12)
Menopause = 40-55 years (average = 51)

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3
Q

Define frequent periods, infrequent periods

A

Frequent periods = menses occur more frequently than every 12 days over 6 months
Infrequent periods = menses occur less frequently than every 35 days over 6 months

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4
Q

Define primary and secondary amenorrhea

A

Primary: absence of spontaneous onset of period by age of 16
Secondary: absence of periods for > 6 months when a patient has regular period before and patient has irregular cycles all along >12 months

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5
Q

What is prolonged vs shortened menstrual bleeding?

A

Prolonged menstrual bleeding: menstrual periods > 7 days on a regular basis
Shortened menstrual bleeding: menstrual period <2 days on a regular basis

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6
Q

What is heavy vs light menstrual bleeding?

A

Heavy menstrual bleeding: >80ml of blood loss per cycle. Excessive menstrual blood loss which interferes womens physical, emotional, social and material QoL. Change pads <2 hour on the day of heaviest bleeding.
Light menstrual bleeding: <5ml of blood loss per cycle

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7
Q

What is irregular menstrual bleeding defined as?

A

Variation defined as shortest to longest cycle length: variation >7-9 days

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8
Q

What are the hormonal changes in the follicular phase?

A
  • Hypothalamus secretes GnRH
  • GnRH stimulates the pituitary gland to secrete FSH and LH
  • LH and FSH stimulates the production of estrogen from thecal and granulosa cells
  • FSH stimulates the growth of the follicles
  • Estrogen at low level inhibits hypothalamus to secrete GnRH. Inhibits the pituitary gland to secerete FSH to prevent the ovary from developing another follicle
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9
Q

What are the hormonal changes in the ovulatory phase?

A
  • Estrogen is high which stimulates the hypothalamus to secrete GnRH. Stimulates the pituitary gland to secrete large amounts of FSH and LH
  • Progestoerone low level: potentiates the effect of estrogen on LH surge
  • LH and FSH at high level stimulates ovulation. Detection of high level of LH in blood is evident of occurrence of ovulation
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10
Q

What are the hormonal changes in the luteal phase?

A

LH (high level): stimulate ruptured follicle to develop into corpus luteum. Stimulates corpus luteum to secrete estrogen and progesterone
Estrogen (high level): promote growth of uterine lining preparing for implantation. Inhibit the hypothalamus to secrete GnRH. Inhibit the pituitary gland to secrete FSH and LH.

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11
Q

What are the hormonal changes in menstruation?

A
  • LH (low level): corpus luteum degenerates and stops secreting estrogen and progesteorne
  • Estrogen and progesterone (low level): break down of the thickened uterine lining. Remove inhibition on pituitary gland to secrete FSH
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12
Q

What are the changes in the endometrium over the menstrual cycle?

A
  • Proliferative phase: estrogen effect is predominant. Causes proliferation of endometrial glands
  • Secretory phase: progesterone effect if predominant, inhibit proliferative changes. Stimulates the secretory function of endometrial glands to provide hospitable environment for implantation
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13
Q

How to assess menorrhagia in historuy taking?

A

Defined as excessive cyclic menstrual bleeding defined as >80ml of menstrual loss

  • Number of pads used
  • Frequency of changing pads each day (change every <2 hours suggest heavy menses)
  • Degree of soiling of pads (half soaked/fully soaked)
  • Flooding sensation
  • Presence of large blood clots
  • Activitiy limitation: interferes with daily activities suggests heavy menses (staining clothes or sheets, waking patients from sleep)
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14
Q

What is the most common cause of menorrhagia?
What is its pathophysiology?

A

Dysfunctional uterine bleeding (dx of exclusion and there is no underlying organic cause)

Anovulatory DUB: common at extremes of reproductive age including early puberty when menarche just started and perimenopausal women. Absence of ovulation and therefore corpus luteum is not formed and progesterone cannot be produced.
Unopposed estrogen leads to continuous proliferation of endometrial glands leading to overgrowth of uterine lining. Delayed period leading to irregularity and when menstruation occurs it will be heavy and prolonged.

Ovulatory DUB: unknown mechanism but may be related to inadequate production of progesterone from corpus luteum

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15
Q

What is the PALM-COEIN classification for menorrhagia?

A

PALM (structural causes)
* Polyps
* Adenomyosis: benign invasion of myometrium by ectopic endometrium. Accompanied by hyperplasia of adjacent smooth muscle
* Leiomyoma (fibroids): benign overgrowth of myometrium
* Malignancy

COEIN (non structural causes)
* Coagulopathy
* Ovulatory dysfunction
* Endometrial disorders
* Iatrogenic
* Not classified

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16
Q

How to classify causes of menorrhagia by age group?

A

Premenarche
* Infection
* Sexual abuse
* Foreign body
* Ovarian cancer
* Precocious puberty

Early post menarche
* Infection
* Pregnancy
* Platelet disorders or coagulopathy
* Stress
* Dysfunctional uterine bleeding (DUB)

Reproductive age
* Infection
* Pregnancy
* Platelet disorders or coagulopathy
* Stress (psychogenic or excercise induced)
* Dysfunctional uterine bleeding
* Gential tract disorders: endometrial/cervical/vaginal polyps. Adenomyosis, leiomyoma
* Endocrine dysfunction: PCOS, thyroid disease
* Drug induced: hormonal contraceptives/intrauterine device (IUCD)

Menopausal transition
* Anovulation
* Ovarian/endometrial/cervical/vaginal/vulvar cancer
* Genital tract disorders: endometrial/cervical/vaginal polyops. Adenomyosis, leiomyoma (fibroids)

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17
Q

Classify causes of menorrhagia according to genital tract disorders

A
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18
Q

Classify causes of menorrhagia according to pregnancy

A
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19
Q

Classify causes of menorrhagia according to systemic diseases

A
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20
Q

Classify causes of menorrhagia according to drugs

A
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21
Q

What is the history taking for menorrhagia?

A

Confirm reproductive status: premenarche/early post menarche/reproductive/menopausal transition/menopause. All post menopausal bleeding is abnormal and requires evaluation
Confirm source of bleeding:
* volume of blooding (size of blood clots –> indicates severity of bleeding)
* color of bleeding (brown staining represents old blood due to light bleeding or spotting from uterus, cervix and upper vagina, red staining can be from any sites in genital tract). Red staining can be any sites in genital tract.
* Timing of bleeding: post coital bleeding typically suggests cervical pathology but can be due to contact during intercourse in lower genital tract such as vagina and vulva
* Haematuria/haematuria/melena: certain from the vagina? Blood in the toilet only or after urination or defacation? Do you see the blood only when you wipe with toilet tissues? Which part of the pad is the bleeding located?

HPI
* Fever, lower abd pain and vaginal discharge: endometritis, PID
* Dysmenorrhea, dyspareunia and infertility: endometriosis, adenomyosis
* Hirsutism, hot flushes, heat or cold intolerance: thyroid disease, PCOS
* Changes in bladder and bowel function: fibroids (mass effect), malignancy (mass effect)

Menstrual history
* Frequency/duration/volume/regularity
* Last menstrual period

Sexual history
* Determine patients risk for pregnancy or STDs
* Contraceptive methods

Medical history
* Thyroid diseases
* Thrombocytopenia or coagulopathy
* Liver failure (decreased synthesis of coagulation factors)
* Renal failure (platelet dysfunction in uremia)

Drug history: anticoagulants

Family history: gynecological malignancy, bleeding disorders, thyroid diseases
Social history: stress (hypothalamic dysfunction), excessive excercise (hypothalamic dysfunction), eating disorders (hypothalamic dysfunction)

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22
Q

What is the PE for menorrhagia?

A

General exam: vital signs (tachycardia), pallor, goiter
Pelvic and speculum examination: presence of adnexal mass, cervical polyp
Size and contour of uterus
* Enlarged uterus: pregnancy/adenomyosis/uterine leiomyoma/uterine malignancy
* Limited uterine motility: pelvic mass or adhesions
* Uterine tenderness: pelvic inflammatory disease (PID)/endometritis

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23
Q

What are the basic and invasive Ix done for menorrhagia?

A
  • CBC D/C: anemia, leukocytosis to look for infection, thrombocytopenia to look for platelet disorders
  • Clotting profile: PT, aPTT to look for coagulopathy
  • Iron profile: look for underlying iron deficiency
  • LFT/RFT: liver and renal failure that leads to platelet dysfunction and coagulopathy
  • TFT: thyroid diseases
  • Pregnancy test: all patients of reproductive age should recieve pregnancy test to rule out possible pregnancy complications
    Endometrial biopsy: pregnancy must be excluded before endometrial sampling. Performed in suspected endometrial hyperplasia or cancer. Indications:
  • All women age >40
  • Women aged <45 with persistent AUB
  • Women aged <45 with history of unopposed estrogen exposure (chronic anovulation)
  • Women aged <45 with high risk of endometrial cancer (e.g. tamoxifen)
  • Pap smear: routine cervical screening
  • High vaginal and endocervical swab: in suspected cervicitis asnd pelvic inflammatory disease
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24
Q

What are the radiological Ix that can be done for menorrhagia and their indications?

A
  • Transabd or transvaginal USG: indicated if structural abnormality is suspected
  • Hysteroscopy: direct visualization of endometrial cavity effective in diagnosing endometrial polyp and leiomyoma. Indications: suspected endometrial polyp or submucosal fibroid Failed endometrial aspiration or results inconclusive. Irregular bleeding while on hormonal therapy >3 months
  • Saline infusion sonohysterography (SIS): better than hysteroscopy as it can assess depth of extension of leiomyoma and identify leiomyoma at other sites to help surgical planning. Can also identify asymmetric or focal endometrial thickeninig in endometrial hyperplasia
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25
Q

What is the medical treatment for menorrhagia?

A
  • Tranexamic acid: anti fibrinolytics which competitively blocks the conversion of plasminogen to plasmin thereby reducing fibrinolysis. Taken only during menses rather than daily usually from day 1 of menstruation to the end of heaviest flow.
  • Mefenamic acid (ponstan): NSAIDs which decreases synthesis of prostaglandings including PGE2 and PGF2a in the endometrium leading to vasoconstriction and reduced bleeding
  • COC pills: helps control mentrual cycle which is beneficial for irregular periods. Additional contraceptive effects
  • Progestogen (norethisterone): indicated in patients with contraindications to combined pills. This is not a form of contraceptive
  • Levonorgestrel releasing intrauterine system (Mirena)
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26
Q

What are the surgical treatment options for menorrhagia?
What are the complications?

A

Hysteroscopic endometrial ablation
* Only indicatesd for menorrhagia due to dysfunctional uterine bleeding
* Absence of large uterine fibroid or coexisting symptomatic adenomyosis or endometriosis in view of potentially worsening of dysmenorrhea after ablation.
* Preop endometrial preparation with GnRH agonist (e.g. IM leuprolide) to thin the endometrium to facilitate tissue destruction
* Preop cervical preparation with vaginal misoprostol which is a cervical riepning agent to dilate the cervix and avoid complications related to difficult passage of hysteroscope through cervical canal

Benefits of procedure
* 40-45/100 have lighter period, 40-45/100 stop menstruation, 4-10/100 have persistent or recurrent abnormal periods

Consequences: pregnancy is contraindicated after endometrail ablation and is recommended only for women with completed family and definitely sure they no longer wish to have more children

Procedure
* GA/RA
* Uterine cavity distended with glycine (conduction agent of monopolar)
* Dilatation of cervix and passage of resectoscope with roller ball electrode (endometrial ablation) or shaved off with a cutting loop (endometrial resection) under hysteroscopic control

Complications
* Frequent complications: bleeding, uterine cramps, mild fluid overload
* Serious complicatuions: hypoNa (absorption of glycine leading to fluid overload and electrolyte disturbances), cervical tear, failure to gain entry into uterine cavity, uterine perforation, pelvic infection, recurrence

Hysterectomy: definitive treatment for uterine bleeding –> no fertility desires–> high patient satisfaction because it is curative and no drug related side effects

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27
Q

How to classify dysmenorrhea?

A

Primary dysmenorrhea: presence of recurrent, crampy, lower abd pain that occurs during menses in the absence of demonstratable disease that could account for these symptoms
Secondary dysmenorrhea: occurs in women with an organic or psychological causes that can account for their symptoms such as adenomyosis, endometriosis or fibroids

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28
Q

What are the causes of secondary dysmenorrhea?

A
  • Adenomyosis: usually occurs in multiparous women, presents with painful vaginal bleeding (i.e. with dysmenorreha), dyspareunia and regularly enlarged uterus
  • Endometriosis
  • Submucosal fibroids: usually happen in primiparous or multiparous women, presents with painless vaginal bleeding and irregularly enlarged, non tender uterus. Fibroids are usually not painful and therefore dysmenorrhea is not typical. Submucosal fibroids can sometimes cause dysmenorrhea during attempted expulsion of submucosal fibroids (when it becomes fibroid polyp and when uterus tries to expel the fibroid polyp)
  • Chronic PID
  • Ovarian cysts
  • Asherman syndrome/intrauterine or pelvic adhesions: intrauterine adhesions (synechiae) caused by endometrial infection or currettage after miscarriage or abortion with partial or complete obliteration of uterine cavity
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29
Q

What is the pathogenesis of dysmenorrhea?

A
  • Prostaglandins released from endometrial sloughing at the beginning of menses causes vasoconstrictions and myometrial contractions
  • Contractions are non rhythmic or incoordinate, occuring in high frequency and result in high intrauterine pressures
  • When intrauterine pressure exceeds arterial pressure, uterine ischemia develops and anaerobic metabolites accumulate which stimulates type C pain neurons resulting in pain
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30
Q

What are features of primary dysmenorrhea?

A
  • Pain over lower abd or suprapubic area radiating down to anterior aspects of thigh
  • Cramping and intermittently intense but may be a continuous dull ache
  • Onset at 1-2 days before menses or on the day of menses
  • Lasts for 2-3 days
  • Usually develops within first 2 years of menarche
  • Associated with nausea, vomiting, diarrhea, headache, dizziness and fatigue
  • Resolution of symptoms with NSAIDs
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31
Q

What are features suggestive of presence of pelvic pathology consistent with secondary dysmenorrhea?

A
  • Age of onset: onset after age 25 as secondary dysmenorrhea usually develops later in reproductive age. Occurs in first few cycles of menarche: congenital uterine outlet obstruction). Late onset without a history of previous dysmenorrhea

Clinical features
* AUB: menorrhagia/oligomenorrhea/intermenstrual bleeding
* Non midline pelvic pain
* Presence of dyspareunia
* Progression in symptom severity
* Absence of nausea, vomiting, diarrhea, headache, dizziness and fatigue

Treatment related: little/no response to NSAIDs or hormonal contraception or both

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32
Q

What is the PE and results pointing towards secondary dysmenorrhea?

A
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33
Q

General treatment principle and medical treatment for dysmenorreha?

A
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34
Q

Define amenorrhea and cryptomenorrhea

A

Amenorrhea: absence of menses and can be transient, intermittent or permanent condition resulting from dysfunction of hypothalamus, pituitary, ovaries, uterus or vagina
Cryptomenorrhea: hidden menstruation –> endometrial shedding occurs but menstrual loss cannot escape due to blockage of parts of lower genital tract usually due to congenital malformations.

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35
Q

What is the classification of amenorrhea?

A
  • Primary amenorreah: absence of menses by age 14 with failure to grow properly or develop secondary sexual characteristics. Absence of menses by age 16 in the presence of normal growth and normal secondary sexual characteristics
  • Secondary amenorrhea: absence of menses for >3 consecutive cycles (total of at least 3 of the previous cycle intervals) in women who have menses before or. Absence of menses for >6 months in women who have menses before
  • Oligomenorrhea: cycle lengths >6 weeks in most of the cycles or number of menses <5 per year
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36
Q

What is the WHO classification of anovulatory disorders?

A
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37
Q

What is the HPO axis?

A
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38
Q

What is the summary of primary and secondary amenorrhea causes?
What are the physiological causes of amenorrhea?

A
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39
Q

What are the causes of primary amenorrhea (organize in HPO axis structure)?

A

Hypothalamus
* Functional hypothalamic amenorrhea: stress, anorexia, nervosa, weight loss, excessive excercise, severe illness
* Idiopathic hypogonadotrophic hypogonadism: isolated GnRH deficiency
* Kallmann syndrome: isolated GnRH deficiency + anosmia
* Irradiation of sellar tumors
* Traumatic brain injury

Pituitary
* Hyperprolactinemia: uncommon cause of primary amenorrhea (usually secondary)
* Pituitary tumors: craniopharyngioma, meningioma

Ovary
* Fragile X syndrome
* Turner syndrome: female with classical karyotype 45, XO. Gonadal dysgenesis with oocytes and follicles undergo apoptosis and hence no ovarian estrogen secretion
* Swyer syndrome (46, XY, gonadal dysgenesis): pure gonadal dysgenesis. Male genotype with female phenotype. Fibrous streak gonad cannot secrete anti-Mullerian hormone resulting in persistent mullerian structures. Uterus and fallopian tubes are normally formed but gonads not functional
* Polycystic ovarian syndrome (PCOS): ovulatory dysfunction and hyperandrogenism. Rotterdam criteria: oligo-ovulation or anovulation, hyperandrogenism (clinical/biochemical), polycystic ovaries (sonographic)

Uterus/outflow tract
* Imperforate hymen
* Transverse vaginal septum
* Vaginal agenesis (MRKH syndrome): agenesis or hypoplasia of Mullerian duct system (also known as Mullerian agenesis).
* Androgen insensitivity syndrome (testicular feminization syndrome): X linked recessive disorder with 46, XY karyotypine. Male genotype with female phenotype. External genitilia is female in appearance but tetes may be palpable in the labia or inguinal area. Undescended tests along normal cource of descent. Testes produce Mullerian inhibiting substance which causes regression of all Mullerian structures including fallopian tubes, uterus and upper third of the vagina. Normal breast development occurs (peripheral conversion of androgen to estrogen). Little or no pubic and axillary hair (requires androgen to mature).

Others: constitutional delay of puberty

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40
Q

What are the HPO axis causes of secondary amenorrhea?

A
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41
Q

What are the endocrinopathy causes of secondary amenorrhea?

A
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42
Q

What history taking for amenorrhea?

A
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43
Q

What PE done for amenorrhea?

A
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44
Q

What are the biochemical tests for amenorrhea?

A
  • Pregnancy test: measurement of serum/urine B-hCG level (always rule out pregnancy as 1st step)
  • TFT: TSH to detect hypothyroidism or hyperthyroidism. Hypothyroidism as a cause of hyperprolactinemia should be ruled out
  • Serum prolactin level: stress, sleep, excercise, intercourse and meals can cause serum prolactin transiently and thus prolactin level should be repeated once before pituitary MRI is ordered. Screening for hypothyroidism is necessary since it will lead to hyperprolactinemia
  • Serum FSH and estradiol (E2) level: assessment of estrogen status to interpret with FSH values and guide therapy in hypoestrogenic patients which require estrogen therapy for preventing bone loss.
    Decreased E2 and increased FSH level: dx of ovarian insufficiency can be made if serum FSH >25IU/L on 2 occasions separates by >4 weeks apart. Indicates hypergonadotrophic hypogonadism such as primary and secondary ovarian insufficiency
    Decreased E2 and FSH level: indicates hypogonadotrophic hypogonadism such as hypothalmaic or pituitary disorders
  • Progesterone withdrawal test (MPA): progestational challenge with MPA 10mg/day for 7 days. Assessment of estrogen status to interpret with FSH values and guide therapy in hypoestrogenic patients which requires estrogen therapy for preventing bone loss.
    Presence of withdrawal bleeding = endogenous estrogen production + dx of anovulation can be made.
    Absence of withdrawal bleeding = hypoestrogenism (OR) outflow tract disorder
  • Combined estrogen and progesterone withdrawal test (CEPWT): give COCs to check for withdrawal bleeding. Absence of withdrawal bleeding = outflow tract disorders (or) non functioning endometrium (asherman syndrome)
  • Karyotyping: vaginal (mullerian) agenesis)MRKH) = 46XX (arrange USG urinary tract to look for associated abnormalities). Turner syndrome = 45XO (monosomy X). Swyer sndrome = 46XY (advise gonadectomy due to risk of maignant transformation. Androgen insensitivity syndrome (testicular feminization syndrome): 46XY
  • Serum LH level: increased LH: FSH ratio in PCOS although it is no longer 1 of the diagnostic criteria
  • Serum testosterone, DHEAS and 17-hydroxyprogesterone level: patients with hirsutism should have blood taken for serum testosterone and 17-hydroxyprogesterone. Performed in the presence of clinical hyperandrogenism for biochemical confirmation. Severe biochemical hyperandrogenism followed by checking erum 17-hydroxyprogesterone to rule out 21 hydroxylase deficiency (CAH). Suggests PCOS and androgen secreting tumors.
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45
Q

How to interpret the biochemical test results for amenorrhea and what is the follow up action?

A
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46
Q

What are further Ix after biochemical tests for amenorrhea?

A
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47
Q

What is the diagnostic flowchart for amenorrhea?

A
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48
Q

What is the general treatment principle for amenorrhea?

A
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49
Q

What is the management of amenorrhea according to the type of amenorrhea?

A
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50
Q

Define menopause vs climacteric

A

Menopause is the permanent cessation of menstrual period due to loss of ovarian follicular activity and is defined after 1 year of amenorrhea without any other obvious physiological or pathological cause
Climacteric: critical period around menopause when ovarian function is gradually declining. Extended period that begins years before and lasting yearsr after menopause itself. Menopause transition or peimenopuase begins on average 4 years before the final menstrual period.
* Time of decreasing estrogen level and elevated FSH deu to hypothalamic-pituitary hyperactivity from the lack of negative feedback by follicular hormones.

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51
Q

What are the different types of menopause?

A
  • Natural menopause
  • Premature menopause: defined as menopause that occured before 40 years old. Referred to as primary ovarian insufficiency (premature ovarian failure)
  • Surgical menopause: surgery that involves removal of ovaries (oophorectomy)
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52
Q

What are the beneficial and potential adverse effects of estrogen?

A

Beneficial effects
* Improvement in lipid profiles (decreased LDL and increased HDL)
* Enhanced endothelial dysfunction
* Improved insulin sensitivity

Potential AE of estrogen
* Increase in serum triglyerides level
* Prothrombotic effect including reduction in serum fibrinogen, factor 7 and antithrombin 3
* Proinflammatory effect including increase in hepatic synthesis of vascular inflammatory markers such as CRP

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53
Q

What are the causes of menopause?

A
  • Natural
  • Iatrogenic menopause: oophorectomy, hysterectomy, post chemo, post radio
  • Infection: TB, post mumps infection
  • Autoimmune disease
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54
Q

What are the climacteric symptoms of menopause?

A
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55
Q

How to make a dx of menopause?

A

Normally retrospective dx

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56
Q

What are the indications for starting HRT In menopause?
What are the benefits?
What are the contraindications?

A
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57
Q

What are the side effects of HRT in menopause?

A
  • Breast bloating and tenderness
  • Weight gain
  • Mood symptoms
  • Breakthrough bleeding
58
Q

What is the evaluation before HRT prescription for menopause?

A
59
Q

What HRT preparations are there for menopause?
What different kinds of regimen?

A
60
Q

What are the routes of admin for HRT in menopausal women?

A
61
Q

What is duration of treatment of HRT for menopausal women?
Discontinuation of treatment?
Counselling and advise?
Follow up?

A
62
Q

What is the use of local vaginal estrogen in HRT for menopausal women?

A
63
Q

What is the most common pelvic tumor in women?

A

Uterine fibroid (leiomyoma)

64
Q

What is the FIGO classification for uterine fibroids?
Which types most commonly cause symptoms?
Which types are the most common site of fibroids?

A
65
Q

What is the classical clinical manifestations for uterine fibroid (leiomyioma)?

A
66
Q

What is history taking and PE for uterine fibroid?

A
67
Q

What further Ix after biochemical Ix done for suspected uterine fibroid (leiomyoma)?

A
68
Q

What are the non surgical treatment approach for uterine fibroids?

A
69
Q

What interventional radiologist treatment approach for uterine fibroid?
What are the indications?
What are the contraindications?

A

Uterine artery embolization (general features)
* Both uterine arteries blocked
* Relieve adverse symptoms due to uterine fibroids which include menorrhagia and pressure symptoms: fibroid will shrink by 40-70% by volume. Menorrhagia and dysmenorrhea will improve in 80% of patients

Indications
* Symptomatic fibroids who might otherwise be advised to have surgical treatment
* Symptomatic fibroids where multiple or difficult myomectomy will be encountered
* Symptomatic fibroids but wish to avoid surgery or unwilling to receive blood transfusion
* Women indicating desire for future fertility

70
Q

What are the contraindications for uterine artery embolization for uterine fibroid?

A
  • Asymptomatic uterine fibroids
  • Evidence of pregnancy
  • Evidence of uterine malignancy
  • Evidence of current genitourinary infection or malignancy
  • Evidence of pedunculated submucosal fibroids, dominant pedunculated serosal fibroids
    (attachment point < 50%)
  • Concurrent use of GnRH agonist (GnRHa)
  • History of allergic reaction to contrast medium and renal impairment
  • Refusal to undergo hysterectomy following peri- or post-UAE complications
71
Q

Describe the procedure of uterine artery embolization for uterine fibroids
When is FU?

A
  • Patients should be fasted 6 hours prior to the procedure
  • Performed under LA and conscious sedation
  • Small catheter is inserted into femoral artery under the groin area and is directed deeply to each uterine artery in turn
  • Another smaller catheter (coaxial catheter) may be inserted through the original catheter
  • Small particles will be injected to block uterine arteries and their branches
  • Continuous monitoring of vital signs such as BP and pulse after procedures
  • Diet as tolerated (DAT) after the procedure and IV fluid can be stopped once diet waswell-tolerated
  • Allow mobilization after 6 hours

1st FU 2 weeks after the procedure. Second FU 3 months after MRI appointment. FU MRI will be arranged at 3 months after the procedure

72
Q

What are frequent complications of uterine artery embolization for uterine fibroid?
What are serious complications?

A
73
Q

Describe HIFU for uterine fibroid
What are the frequent/serios complications that can arise?

A

Procedures
* Under consious sedation
* IV set and catheter inserted into urinary bladder
* USG beam burns the uterine fibroid from outside the body
* IV fluids and analgesics continued after procedure
* Discharged from hospital when pain is under control and can eat adequately

74
Q

What are the surgical treatment options for uterine fibroids?

A
  • Hysteroscopic endometrial ablation
    Only indicated for menorrhagie due to dysfunctional uterine bleeding. Pregnancy contraindicated after endometrial ablation and is recommened only for women with completed family.
  • Myomectomy
  • Hysterectomy
    Total abd hysterectomy: cutoff uterine size >12 weeks
    Vaginal hysterectomy + laparoscopic assistance: cutoff uterine size <12 weeks
    Laparoscopic assisted vaginal hysterectomy (LAVH): upper part of uterus is freed laparoscopically, lower part of uterus is freed vaginally. QMH favors LAVH due to presence of expertise for VH. Adv: smaller bad wounds/less painful/fast post op recovery.
    Total laparoscopic hysterectomy (TLH): same as LAVH except lower part of the uterus is freed laparoscopically.

Discussion for bilateral salpingectomy or bilateral salpingooopherectomy (BSO): considered if there is concomitant ovarian pathology.
* Removal in premenopausal women requires hormonal therapy which has risks including CA breast, DVT and gallstones
* Prophylactic BSO should be discussed with post menopausal women: 5 in100 chance of future operation for ovarian pathology. Removal of tubes reduces risk of CA ovary
* Prophylactic bilateral salpingectomy should be discussed with premenopausal women

75
Q

What is the consequences after a bilateral salpingooopherectomy (BSO)?

What are the frequent and serious complications?

A
  • Unable to get pregnant
  • No menstruation
  • Does not affect coitus
  • Does not affect hormonal status if ovaries are not removed but ovarian failure may occur 2-4 years earlier than natural menopause by unknown mechanism possibly due to impairment in ovarian blood supply.
76
Q

What are the complications of uterine fibroids?
What are the specuific complications during pregnancy?

A
77
Q

What is adenomyosis?

A
  • Presence of tissue resembling endometrial glands and stroma within the myometrium of the uterus
  • Ectopic endometrial tissues appear to induce hypertrophy and hyperplasia of surrounding myometrium resulting in diffusely enlarged uterus
78
Q

Compare endometriosis and adenomyosis by RF, symptoms, PE and treatment

A
79
Q

What is the pathological features of adenomyosis?

A

Macroscopic appearance: grossly global enlargement of uterus. Spongy appearance with no cleavage plane
Microscopic appearance: pathognomonic feature of adenomyosis is the presence of endometrial tissue within the myometrium at a distance of at least 1 power field

80
Q

What is the SS for adenomyosis?
What is the PE?
What basic tests done?

A
  • Menorrhagia
  • Dysmenorrhea: pain due to bleeding and swelling of endometrial islands confined by myometrium
  • Chronic pelvic pain
  • Dyspareunia

PE: uterine tenderness, uniformly diffusely enlarged uterus (often termed globular enlargement analogous to the concentric enlargement of the pregnant uterus)

Biochemical tests: endometrial biopsy (indicated to rule out other causes of menorrhagia)

81
Q

What imaging is done for adenomyosis?

A

Transvaginal ultrasound (TVUS)
MRI scan
* Especially T2Wi
Findings suggestive of adenomyosis
* Asymmetric thickening of the myometrium (posterior myometrial typically thicker)
* Increased myometrial heterogeneity
* Loss of a clear endomyometrial border
* Linear striations radiating out from the endometrium
* Presnece of myometrial cysts

Thickening of junctional zone of the myometrium
* Junctional zone is a structurally distinct region (appearing as a dark band on T2W MRI) that separates the subendometrial myometrium from the outer myometrium
* >12mm generally dx of hte disease and <8mm excluding adenomyosis

82
Q

What is treatment for adenomyosis?

A
83
Q

What is the classical triad of endometriosis?

A

Dysmenorrhea +dyspareunia + infertility (+ chronic pelvic pain)

Endometrial glands and stroma that occurs outside the uterine cavity
Estrogen dependent, benign, inflammatory disease

84
Q

What are the anatomical sites of endometriosis in decreasing order of frequency?

A
85
Q

How can endometriosis lesions in pelvis be categories?

A
86
Q

What is the pathogenesis of endometriosis?

A
87
Q

What is histological features of endometriosis?

A
88
Q

What is the RF for endometriosis?

A

 Nulliparity
 Prolonged exposure to endogenous estrogen
* Early menarche < 12 (Normal = 10 – 16)
* Late menopause > 55 (Normal = 40 – 55)
* Shorter menstrual cycles

89
Q

What are the SS and complications of endometriosis caused by>

A
  • Proliferation and bleeding at different sites
  • Ectopic endometriotic tissues that induce inflammation, fibrosis and adhesions
    o Endometrial deposits and also leakage from chocolate cysts induce pelvic inflammation and adhesion formation between posterior uterus, ovaries, fallopian tubes and sometimes bowel and bladder
    o Adhesions are sometimes dense and obliterates POD causing bowel or ureteric obstruction
90
Q

What are the SS of endometriosis?

A
91
Q

What is the manifestation for different types of endometriosis?

A
92
Q

What is PE and Ix done for suspected endometriosis?

A
93
Q

What is the medical treatment for endometriosis?

A
  • NSAIDs: mefenamic acid (ponstan) is 1st line treatment of pelvic pain including endometriosis related pain. Avoid selective COX2 inhibitor in women who desire conception (can delay ovulation)
  • COC pills: 1st line treatment for endometriosis related pain –> microgynon 30 (ethinyl estradiol +levonorgestrel) –> suppress ovarian fuunction and hence endogenous estrogen production that supports the growth of endometriosis.
  • Progestin only treatment: indicated in patients who are unable to take or prefer to avoid COCs. Oral dienogest. IM medroxyprogesterone acetate (MPA) every 3 months
  • Gonadotrophin releasing hormone (GnRH) agonist + add back therapy (estrogen/progestogens –> reduces AE such as decreased BMD and menopausal symptoms). GnRH agonist binds to GnRH receptors which paradoxically decreases pituitary secretion of LH and FSH due to down regulation of GnRH receptors and pituitary desensitization. Suppress ovarian follicular growth and ovulation resulting in low levels of circulating estradiol and progesterone. e.g. leuprolide/goserelin/buserelin/nafarelin
  • Danazol: androgens that suppres HPO axis and decrease endogenous production
94
Q

What is the surgical treatment options for endometriosis?

A
95
Q

What is the classification of ovarian cyst?
What is the cutoff size for pathological cyst?

A

Physiological cyst: follicular cyst, corpus luteal cyst
Pathological cysts: endometrioma, cystic component of benign or malignant neoplasm

Cutoff size is 7cm for physiological cyst and any cysts >7cm are unlikely to be physiological.
USG repeated in physiological cyst in around 4 months to allow cyst to resolve

96
Q

What is the IOTA (international ovarian tumor analysis) criteria for ovarian tumor features?

A
97
Q

How is the risk of malignancy index calculated for ovarian cysts?

A

RMI = U x M x CA125

Ultrasound status: scored 1 point for each of the following characteristics (multilocular cyst, solid areas, metastasis, ascites, bilateral lesion)
U=0 (ultrasound score of 0 point), U = 1 (ultrasound score of 1 point), U=3 (ultrasound score of 2-5 points)

Menopausal status. M= 1 (premenopaussal), M = 3 (post menopausal). Post menopausal is defined as no period for more than 1 year or a woman over 50 yearrs of age who has had a hysterectomy

Interpretation: RMI >200 suggest the risk of ovarian malignancy and should be referred to a speciaist or gynaecological oncology team.

98
Q

What imaging done for ovarian cyst?
What findings are indicative of benign causes?

A
99
Q

What is medical treatment of ovarian cyst?

A

Oral contraceptives: suppression of HPO axis so new cyst will not form. However it does not help with regression of current cyst

100
Q

What is the 4 aims of sugery for ovarian cyst?

A

Symptomatic relief
Delineate nature of cyst
Prevent complications such as bleeding, torsion and rupture
Prevent malignancy

101
Q

What are the cyst size cutoffs for different surgical approach?

A

Laparotomy cutoff: cyst >10cm
Laparoscopy cutoff: cyt <10cm

102
Q

What is the followup approach to ovarian cyst?

A

Premenopausal women: repeat USG scan in 4 months and discuss surgery
Post menopausal women: repeat USG scan and CA125 in 4 months to look for interval change anf close case if the cyst size is static for 3 consecutive times

103
Q

What surgery is indicated for ovarian cyst in premenopausal vs postmenopausal women?

A
104
Q

What are the frequent and serious complications with surgical approach for ovarian cyst removal?

A
105
Q

What are the complications of different ovarian cysts?
How are the 2 major complications managed?

A
  • Corpus luteal cysts are very vascularized and can bleed causing haemoperitoenum
  • Dermoid cysts (benign mature cystic teratoma) tend to have torsion since the cysts are heavy in weight and very mobile
  • Endometriotic cysts tends not to have torsion since there are dense adhesions
  • Endometriotic cysts tends to recur and may require post operative OC pills

Ovarian torsion
* Salvage of the torsed ovary by untwisting the vascular pedicle should be considered
* Bivalve technique: opening of ovarian cortex with a linear incision to salvage a torsed ovary. Decreases intraovarian pressure caused by venous occlusion
* Oophorectomy: indicated with ovaries with severe necrosis and non viable appearance

Rupture of ovarian cyst: release of cystic fluid/blood that may irritate the peritoneal cavity. Dermoid cyst contains sebaceous fluid, hair, fat, bone or cartilage and rupture of these cysts results in severe peritoneal irritation.
Must exclude ruptured ectopic pregnancy which has similar clinical presentation

Management: expectant management in uncomplicated rupture of cyst in the absence of haemodynamic instability, blood loss, fever and leukocytosis.
Laparoscopic surgery for ongoing hemorrhage that needs to be controlled or haemodynamic instability.

106
Q

What are the 4 typical features of PCOS?

A

Oligo-amenorrhea + infertility +hirsutism + obesity

107
Q

What is the pathogenesis of PCOS?

A

Gonadotrophin stimulation is required for ovarian steroidogenesis
GnRH pulse generator in hypothalmaus is resistant to the negative feedback from progesterone in patietns with PCOS
* High GnRH pulse frequency increases LH and decreases FSH
* Promotes androgen production by theca cells by LH stimulation: LH action at ovarian level is enhanced in PCOS. LH receptors are overexpressed in theca and granulosa cells from polycystic ovaries

Insulin resistance and compensatory hyperinsulinemia
* Hyperinsulinemia contributes to excess androgens in several ways: facilitates LH stimulates androgen synthesis by ovarian theca cells.
* Inhibits hepatic synthesis of sex hormone binding globulin (SHBG) leading to an increase in free testosterone level
* Hyperandrogenemia favors excess abd fat deposition exacerbating insulin resistance and hyperinsulinemia. Further enhances the secretion of ovarian androgens

108
Q

What are the biochemical consequences of PCOS?

A
  • Increased androgen levels due to stimulation by LH
  • Increased adrenal androgen levels including androstenedione, DHEA and testosterone
  • Increased estrogen levels due to conversion from androgens in fatty tissues and ovaries: high estrogen environment feedback on pituitary gland gonadotrophin secretion leading to relative excess of LH secretion compared to FSH (increased LH:FSH ratio>3)
  • Failure of ovulation since deveoping Graafian follicle depends upon stimulation of FSH
  • Decreased conversion of androgen to estrogen by ovarian aromatase by FSH stimulation
109
Q

What is the microscopic and macroscopic appearane of PCOS?

A
  • Macroscopic appearance: bilateral adrenal and lobular ovaries
  • Microscopic appearance: multiple atretic follicles representing the polycystic features, thecal cell hyperplasia, generalized increased in stroma
110
Q

What are RF of PCOS?

A

 Obesity
 Type I/II/ Gestational DM
 Family history of PCOS in 1st degree relative
 History of premature adrenarche
 Oligo-ovulatory infertility

111
Q

What are SS of PCOS?
What are long term complications?

A
112
Q

What is the diagnostic criteria for PCOS?

A

Rotterdam consensus
*20 or more follicles (has been changed)

113
Q

What is history taking and PE for PCOS?

A
114
Q

What are the basic Ix and imaging Ix done for suspected PCOS?

A
115
Q

What are the general treatment principles for PCOS?

A
116
Q

What is the PCOS treatment of menstrual disturbances + prevention of endometrial hyperplasia/carcinoma?

A

Principle = periodic induction of withdrawal bleeding to protect the endometrium against endometrial hyperplasia and carcinoma secondary to chronic unopposed estrogen stimulation

COC pills: 1st line treatment if fertility is unwanted (good cycle control + provide contraception + protect endometrium + ameliorarte hyperandrogenic symptoms due to androgen lowering effect (by increasing SHBG)
Newer generation pills with lower androgenicity (e.g. Yasmin, Marvelon, Mercilon) may be more beneficial since greater androgenicitiy may impair glucose tolerance

Periodic progestogen pills: protects endometrium + avoid metabolic AE of estrogen which is useful in women manifesting metabolic disturbances such as glucose intolerance
No therapeutic effect on hyperandrogenic symptoms and contraception
Provera 10mg daily x 10-14 days once every 2-3 months

117
Q

What is the PCOS treatment of hyperandrogenism?

A
118
Q

What is the PCOS treatment of anovulatory infertility?

A

Clomiphene citrate CC (clomid). Alternative: letrozole (aromatase inhibitor)
1st line treatment if pregnancy is wished. Start on day 2-6 following a spontaneous or progestogen induced bleeding and continue for 5 days

Dosage. Starting dose: CC 50mg daily or letrozole 2.5mg daily
Step up to CC100mg daily or letrozole 5mg daily if no ovulatoary response
Maximum dose is CC 150mg daily or letrozole 7.5mg daily

Effectiveness: ovulation rate = 80%, conception rate = 22% per ovulatory cycle
MoA: SERM with both estrogen aagonist and anatagonist effect that increases gonadotrophin release. Primarily acts on the levl o of hypothalmus which interferes with receptor cycling and effectively depletes hypothalamic ERs. Inhibits the normal estrogen negative feedback mechanism which results in increased pulsatile GnRH secretion from hypothalamus and subsequently pituitary gonadotrophins including LH and FSH release

Side effects: vasomotor flushes, abd pain anda bloating, multiple pregnancy is rare

Metformin (not as 1st line treatment)

Gonadotropins: 2nd line treatment of CC resistant patients

Laparoscopic ovarian drilling (LOD): alternative to gonadotropin treatment in patients with CC resistance.

In vitro fertilization: 3rd line treatment for those failing ovulation induction treatment or those with other concurrent indications for IVF

119
Q

What areas are involved in pelvic inflammatory disease?

A

involves any or all of the uterus, fallopian tubes and ovaries due to ascending spread of microorganisms. Does not specify the exact location of infection. Does not involve vaginal and vulva infection (anything above cervix)

Accompanied by involvement of neighbouring pelvic organs resulting in endometritis, salpingitis, oophoritis, peritonitis, perihepatitis and tuboovarian abscess –> preferred terms.

120
Q

What are the RF of PID?

A
121
Q

What is the micbio of PID?

A
122
Q

What is the ddx of PID?

A
123
Q

What are the SS of PID?
What are SS of complications?

A
124
Q

What history taking and PE for PID?

A
125
Q

What basic Ix done for PID

A
126
Q

What non basic Ix may be indicated for PID?

A
127
Q

What are the indications for PID in patient management?

What must broad spectrum antibiotics cover?

A
  • Surgical emergency cannot be excluded
  • Clinically severe disease
  • Tubo-ovarian abscess (TOA)
  • PID in pregnancy
  • Irresponsive or intolerance to oral medications

Must cover neisseria gonorrhoea, chlamydia trachomatis, anaerobes, gram negative facultative bacteria and streptococci

128
Q

If patient doesnt respond to broad spectrum antibiotics within what number of days what should be considered?

A

Clinical improvement within 3 days

Things to be considered:
o Tubo-ovarian abscess (TOA)
o Retained products of gestation
o Other causes of abdominal pain
o Drug fever
o Drug adherence
o Removal of IUCD (IUCD can left-in-situ in women with clinically mild PID but shall be removed in severe PID after commencement of antibiotics)
o Septic pelvic thrombophlebitis

129
Q

What is outpatient and in patient treatment regimen for PID?

A
130
Q

What is surgical treatment regimen for PID?

A
131
Q

What are early and late complications of PID?

A
132
Q

What are the causes of vaginitis?

A
133
Q

What is SS of vaginitis?
What are the ddx?

A
134
Q

What is the diagnostic criteria for vaginitis?

A
135
Q

What is the history taking for vaginitis?

A
136
Q

What is the PE and possible findings for vaginitis?

A
137
Q

What biochemical tests for vaginitis?

A
138
Q

What are the summary of biochemical test results for vaginitis?

A
139
Q

What is the treatment of vaginitis?

A
140
Q

What are the complications of vaginitis?

A
141
Q

What are the indications of using GnRH analogue?

A
  • Endometriosis (effective in relieving endometriosis associated): GnRH agonist + add back therapy (estrogen or/and progestogen reduces side effects such as decreased BMG and menopausal symptoms without negative effect on the efficacy of treatment of GnRHa
  • Uterine fibroids
  • Thinning agent for hysteroscopic procedures such as endometrial polyp/dysfunctional uterine bleeding (must exclude adenomyosis and uterine fibroid before doing hysteroscopic endometrial ablation) –> IM leuprolide to visualize/destroy endothelium easier

Not certain
* Pituitary down regulation (in long protocal of IVF and induction of ovulation)
* Before and during chemotherapy for breast cancer to preserve ovarian function

142
Q

Can myomectomy be done during Caesarean section?
In what situation may myomectomy be done during C-section?

A

No, the uterus and fibroid is alrady highly vascularized during pregnancy.
If operate on during C-section there will be increased post partum hemorrhage.

Myomectomy only indicated if it is accidentally ligated, hence will need to operate on and suture the wound.