Gynaecology Flashcards
Describe the Hypothalamic-Pituitary-Gonadal axis and the role of each hormone
The hypothalamus releases gonadotrophin-releasing hormone (GnRH). GnRH stimulates the anterior pituitary to produce luteinising hormone (LH) and follicle-stimulating hormone (FSH).
LH and FSH stimulate the development of follicles in the ovaries. The theca granulosa cells around the follicles secrete oestrogen. Oestrogen has a negative feedback effect on the hypothalamus and anterior pituitary to suppress the release of GnRH, LH and FSH.
What is oestrogen and it’s most prevalent and active form? What does is stimulate?
Oestrogen is a steroid sex hormone produced by the ovaries in response to LH and FSH. The most prevalent and active version is 17-beta oestradiol. It acts on tissues with oestrogen receptors to promote female secondary sexual characteristics. It stimulates:
- Breast tissue development
- Growth and development of the female sex organs (vulva, vagina and uterus) at puberty
- Blood vessel development in the uterus
- Development of the endometrium
What is progesterone and what does it do?
Progesterone is a steroid sex hormone produced by the corpus luteum after ovulation. When pregnancy occurs, progesterone is produced mainly by the placenta from 10 weeks gestation onwards. Progesterone acts on tissues that have previously been stimulated by oestrogen. Progesterone acts to:
- Thicken and maintain the endometrium
- Thicken the cervical mucus
- Increase the body temperature
What age does puberty occur and how long does it take?
Puberty starts age 8 – 14 in girls and 9 – 15 in boys. It takes about 4 years from start to finish. Girls have their pubertal growth spurt earlier in puberty than boys.
Why do overweight children go through puberty earlier? Who might have delayed puberty?
Aromatase is an enzyme found in adipose (fat) tissue, that is important in the creation of oestrogen. Therefore, the more adipose tissue present, the higher the quantity of the enzyme responsible for oestrogen creation. There may be delayed puberty in girls with low birth weight, chronic disease or eating disorders, or athletes.
What scale is used to assess the stages of puberty?
Tanner Staging:
- Under 10, no pubic hair, no breast development
- 10-11, light and thin pubic hair, breast buds form behind the areola
- 11-13, course and curly, breast begins to elevate beyond the areola
- 13-14, adult like pubic hair but does not reach the thigh, areolar mound forms and projects from surrounding breast
- 14+, pubic hair extends to medial thigh, areolar mounds reduce, and adult breasts form
What do FSH & LH do in both girls and boys?
The rise in FSH stimulates an increase in oestrogen synthesis and oogenesis in females and the onset of sperm production in males.
The rise in LH stimulates an increase in production of progesterone in females and an increase in testosterone production in males.
Describe the process of thelarche
- born with lobulated glandular tissue embedded in adipose tissue, separated by fibrous connective tissue
- the breasts are in a dormant stage until puberty. In this dormant stage there are only lactiferous ducts with no alveoli.
- puberty- increase in oestrogens causes the development of the lactiferous duct system as the ducts grow in branches with the ends forming the lobular alveoli (small, spheroidal masses).
- mediated by progesterone, these lobules will increase in number through puberty.
Describe pubarche
The second sign of puberty in girls is typically the growth of hair in the pubic area. The hair initially appears sparse, light and straight; however, throughout the course of puberty it becomes coarser, thicker and darker.
Approximately 2 years after pubarche, hair begins to grow in the axillary area as well. In both sexes, hair growth is a secondary sexual characteristic mediated by testosterone.
Describe menarche
It’s the first menstrual period and marks the beginning of the menstrual cycles. It normally occurs around 1.5-3 years after thelarche and is due to the increase in FSH and LH.
The menarche process typically occurs at ~12.8 years (+/- 1.2 years) for Caucasian girls and 4-8 months later for African-American girls
FSH levels plateau about a year before menarche. LH levels continue to rise, and spike just before they induce menarche.
What is the first sign of puberty in boys?
Increased testicular size - increased LH stimulates testosterone synthesis by Leydig cells and the increased FSH stimulates sperm production by Sertoli cells. Spermatogenic tissue (Leydig cells and Sertoli cells) makes up the majority of the increasing testicular tissue.
What other genital changes happen in boys after increase in testicular size?
- scrotal skin grows, becomes thinner, darker in colour and starts to hang down from the body. It also starts to become spotted with hair follicles.
- a year after the testicles begin to grow, first ejaculation happens. The testicles are now producing sperm as well as testosterone. The first ejaculation marks the theoretical capability of procreation. However, on average fertility is reached one year after first ejaculation.
- The penis first grows in length. Then the width of the penis increases as the breadth of the shaft increases. The glans penis and corpus cavernosum also enlarge.
Describe the hormonal changes that result in the pubertal growth spurt
- complex interaction between the gonadal sex steroids (oestradiol/testosterone), GH and insulin-like growth factor 1 (IGF-1).
- GH levels will rise with sex steroids (testosterone which has been converted to oestradiol) and their positive effect on the pulsatile release of GH from the anterior pituitary gland.
- rise in GH causes a rise in the anabolic hormone IGF-1, which causes somatic growth via its metabolic actions (e.g. increases trabecular bone growth.)
In boys, what is a noticeable sign of puberty that happens after the growth spurt?
Following the peak of the growth spurt in males, the larynx and vocal cords (voicebox) enlarge, and the boy’s voice may ‘crack’ occasionally as it deepens in pitch.
What is delayed or absent puberty?
the absence of secondary sexual characteristics by the age of 13 in girls or 16 in boys
Causes:
- Hypogondaotropic hypogonadism
- Hypergonadotropic hypogonadism
- Turner’s Syndrome (45 XO)
- Klinefelter’s Syndrome (47 XXY)
- Androgen Insensitivity Syndrome
- Kallmann Syndrome
What are the phases of the menstrual cycle?
2 phases: the follicular phase and the luteal phase.
- The follicular phase is from the start of menstruation to the moment of ovulation (the first 14 days in a 28-day cycle).
- The luteal phase is from the moment of ovulation to the start of menstruation (the final 14 days of the cycle).
What are follicles and what are their 4 main stages of development in the ovaries?
Granulosa cells surround the oocytes, forming structures called follicles.
- Primordial follicles
- Primary follicles
- Secondary follicles
- Antral follicles (also known as Graafian follicles)
How do primordial follicles become secondary follicles?
- Primordial follicles maturing into primary and secondary follicles is always happening, independent of the menstrual cycle.
- When at secondary follicle stage, FSH receptors develop.
- Further development after the secondary follicle stage requires stimulation from FSH.
Describe the follicular stage of the menstrual cycle
- At the start of the menstrual cycle, FSH stimulates further development of the secondary follicles.
- As they grow, granulosa cells that surround them secrete increasing amounts of oestradiol (oestrogen).
- oestradiol has a negative feedback effect on the pituitary gland, reducing the quantity of LH and FSH produced.
- The rising oestrogen also causes the cervical mucus to become more permeable, allowing sperm to penetrate the cervix around the time of ovulation.
- One follicle will develop further than the others and become the dominant follicle.
- LH spikes just before ovulation, causing the dominant follicle to release the ovum (an unfertilised egg) from the ovary.
- Ovulation happens 14 days before the end of the menstrual cycle, for example, day 14 of a 28-day cycle, or day 16 of a 30-day cycle.
Describe the luteal phase
- After ovulation, the follicle that released the ovum collapses and becomes the corpus luteum.
- It secretes high levels of progesterone, which maintains the endometrial lining. - This progesterone also causes the cervical mucus to become thick and no longer penetrable.
- The corpus luteum also secretes a small amount of oestrogen.
- When there is no fertilisation of the ovum, and no production of hCG, the corpus luteum degenerates and stops producing oestrogen and progesterone.
- This fall in oestrogen and progesterone causes the endometrium to break down and menstruation to occur.
- Additionally, the stromal cells of the endometrium release prostaglandins.
- Prostaglandins encourage the endometrium to break down and the uterus to contract.
What happens if there is fertilisation?
When fertilisation occurs, the syncytiotrophoblast of the embryo secretes human chorionic gonadotrophin (HCG). HCG maintains the corpus luteum. Without hCG, the corpus luteum degenerates. Pregnancy tests check for hCG to confirm a pregnancy.
What is menstruation?
Menstruation involves the superficial and middle layers of the endometrium separating from the basal layer. The tissue is broken down inside the uterus, and released via the cervix and vagina. The release of fluid containing blood from the vagina lasts 1 – 8 days.
Menstruation starts on day 1 of the menstrual cycle. The negative feedback from oestrogen and progesterone on the hypothalamus and pituitary gland ceases, allowing the levels of LH and FSH to begin to rise, and the cycle to restart.
What is primary amenorrhoea?
Primary amenorrhoea is defined as not starting menstruation:
- By 13 years when there is no other evidence of pubertal development
- By 15 years of age where there are other signs of puberty, such as breast bud development
What are the causes of primary amenorrhoea?
- Hypogonadism (can be hypo or hyper-gonadotropic)
- Kallman Syndrome
- Turner’s Syndrome
- Congenital Adrenal Hyperplasia
- Androgen Insensitivity Syndrome
- Congenital malformations of the genital tract
What is hypogonadotropic hypogonadism?
deficiency of LH and FSH due to hypothalamic or anterior pituitary dysfunction, leading to deficiency of the sex hormone.
This could be due to:
- hypopituitarism
- damage to hypothalamus or pituitary from radiotherpay/surgery/cancer
- significant chronic conditions (e.g. CF/IBD)
- Excessive exercising or dieting
- constitutional delay in growth and development
- endocrine disorders e.g. cushings
- kallman syndrome
What is hypergonadotropic hypogonadism?
the gonads fail to respond to stimulation from LH and FSH. Without negative feedback from the sex hormones (oestrogen), the anterior pituitary produces increasing amounts of LH and FSH. Consequently, you get high gonadotrophins (“hypergonadotropic”) and low sex hormones (“hypogonadism”).
This could be due to:
- Previous damage to the gonads (e.g. torsion, cancer or infections such as mumps)
- Congenital absence of the ovaries
- Turner’s syndrome (XO)
What is Turner’s Syndrome?
A female has a single X chromosome, making them 45 XO. The O referrs to an empty space where the other X chromosome should be.
Presents with:
Short stature
Webbed neck
High arching palate
Downward sloping eyes with ptosis
Broad chest with widely spaced nipples
Cubitus valgus
Underdeveloped ovaries with reduced function
Late or incomplete puberty
Most women are infertile
What are the associated conditions with Turner’s?
Recurrent otitis media
Recurrent urinary tract infections
Coarctation of the aorta
Hypothyroidism
Hypertension
Obesity
Diabetes
Osteoporosis
Various specific learning disabilities
How is Turners managed?
There is no way to treat the underlying genetic cause of Turner syndrome. Treatment aims to help with the symptoms of the condition:
- Growth hormone therapy can be used to prevent short stature
- Oestrogen and progesterone replacement can help establish female secondary sex characteristics, regulate the menstrual cycle and prevent osteoporosis
- Fertility treatment can increase the chances of becoming pregnant
Patients need monitoring for the associated conditions and complications.
What is Kallman Syndrome?
an X-linked recessive disorder characterised by failure of migration of GnRH cells and anosmia
What is congenital adrenal hyperplasia?
congenital deficiency of the 21-hydroxylase enzyme causing underproduction of cortisol and aldosterone, and overproduction of androgens from birth.
It is a genetic condition inherited in an autosomal recessive pattern. In a small number of cases, it involves a deficiency of 11-beta-hydroxylase rather than 21-hydroxylase.
In severe cases, the neonate is unwell shortly after birth, with electrolyte disturbances and hypoglycaemia. In mild cases, female patients can present later in childhood or at puberty with typical features:
Tall for their age
Facial hair
Absent periods (primary amenorrhoea)
Deep voice
Early puberty
High levels of 17- hydroxyprogesterone are present in the blood.
What is androgen insensitivity syndrome?
cells are unable to respond to androgen hormones due to a lack of androgen receptors. It is an X-linked recessive genetic condition, caused by a mutation in the androgen receptor gene on the X chromosome. Extra androgens are converted into oestrogen, resulting in female secondary sexual characteristics. It was previously known as testicular feminisation syndrome.
There is complete and partial. Partial is less severe with more ambiguous signs such as a micropenis or clitoromegaly, bifid scrotum, hypospadias and diminished male characteristics
What sex is someone genetically if they have androgen insensitivity syndrome?
Genetically male with an XY genotype
What anatomy does someone with androgen insensitivity syndrome have?
Typical male sexual characteristics do not develop, and patients have normal female external genitalia and breast tissue.
Patients have testes in the abdomen or inguinal canal, and absence of a uterus, upper vagina, cervix, fallopian tubes and ovaries. The female internal organs do not develop because the testes produce anti-Müllerian hormone, which prevents males from developing an upper vagina, uterus, cervix and fallopian tubes.
The insensitivity to androgens also results in a lack of pubic hair, facial hair and male type muscle development. Patients tend to be slightly taller than the female average. Patients are infertile, and there is an increased risk of testicular cancer unless the testes are removed.
How does androgen insufficiency syndrome present?
Androgen insensitivity syndrome often presents in infancy with inguinal hernias containing testes. Alternatively, it presents at puberty with primary amenorrhoea.
What hormone blood test results would you expect in someone with androgen insufficiency syndrome?
Raised LH
Normal or raised FSH
Normal or raised testosterone levels (for a male)
Raised oestrogen levels (for a male)
How is androgen insensitivity syndrome managed?
Specialist MDT
- Bilateral orchidectomy (removal of the testes) to avoid testicular tumours
- Oestrogen therapy
- Vaginal dilators or vaginal surgery can be used to create an adequate vaginal length
Generally, patients are raised as female, but this is sensitive and tailored to the individual. They are offered support and counselling to help them understand the condition and promote their psychological, social and sexual wellbeing.
What structural abnormalities can cause primary amenorrhoea?
If the ovaries are unaffected, there will be typical secondary sexual characteristics, but no menstrual periods. There may be cyclical abdominal pain as menses build up but are unable to escape through the vagina. Structural pathology that can cause primary amenorrhoea include:
Imperforate hymen
Transverse vaginal septae
Vaginal agenesis
Absent uterus
Female genital mutilation
When do you investigate primary amenorrhoea?
The threshold for initiating investigations is no evidence of pubertal changes in a girl aged 13. Investigation can also be considered when there is some evidence of puberty but no progression after two years.
What investigations would you undertake in suspected primary amenorrhoea?
- Initial investigations assess for underlying medical conditions:
Full blood count and ferritin for anaemia
U&E for chronic kidney disease
Anti-TTG or anti-EMA antibodies for coeliac disease - Hormonal blood tests assess for hormonal abnormalities:
FSH and LH will be low in hypogonadotropic hypogonadism and high in hypergonadotropic hypogonadism
Thyroid function tests
Insulin-like growth factor I is used as a screening test for GH deficiency
Prolactin is raised in hyperprolactinaemia
Testosterone is raised in polycystic ovarian syndrome, androgen insensitivity syndrome and congenital adrenal hyperplasia - Genetic testing with a microarray test to assess for underlying genetic conditions:
Turner’s syndrome (XO) - Imaging can be useful:
Xray of the wrist to assess bone age and inform a diagnosis of constitutional delay
Pelvic ultrasound to assess the ovaries and other pelvic organs
MRI of the brain to look for pituitary pathology and assess the olfactory bulbs in possible Kallman syndrome
How do you manage primary amenorrhoea?
Depends on the cause…
- if necessary, replacement hormones can induce menstruation and puberty
- constitutional delay may just need observation
- if it is due to stress/ED then they need CBT, stress reduction and healthy weight gain
- if it’s an underlying condition then treatment of that cause needs optimisation
- in hypogonadotropic hypogonadism, pulsatile GnRH can induce ovulation and menstruation. If pregnancy is not wanted then COCP can induce menstruation and prevent symptoms of oestrogen deficiency
- COCP can also be used with ovarian causes
What is secondary amenorrhoea?
no menstruation for more than three months after previous regular menstrual periods. Consider assessment and investigation after three to six months. In women with previously infrequent irregular periods, consider investigating after six to twelve months.
What are the causes of secondary amenorrhoea?
- Pregnancy is the most common cause
- Menopause and premature ovarian failure
- Hormonal contraception (e.g. IUS or POP)
- Hypothalamic or pituitary pathology
- Ovarian causes such as polycystic ovarian syndrome
- Uterine pathology such as Asherman’s syndrome
- Thyroid pathology
- Hyperprolactinaemia
How does hyperprolactinaemia cause secondary amenorrhoea?
- High prolactin levels act on the hypothalamus to prevent the release of GnRH.
- Without GnRH, there is no release of LH and FSH.
- This causes hypogonadotropic hypogonadism.
NB only 30% of women with a high prolactin level will have galactorrhea (breast milk production and secretion).
The most common cause is a pituitary adenoma secreting prolactin. A CT or MRI scan of the brain is used to assess for a pituitary tumour. Often there is a microadenoma that will not appear on the initial scan, and follow up scans are required to identify tumours that may develop later.
Often no treatment is required for hyperprolactinaemia. Dopamine agonists such as bromocriptine or cabergoline can be used to reduce prolactin production. These medications treat hyperprolactinaemia, Parkinson’s disease and acromegaly.
How do you investigate secondary amenorrhoea?
- Pregnancy test
- LH and FSH
- Prolactin
- TSH + T3+4
- Testosterone
Which hormone levels indicate:
1. Primary Ovarian Failure
2. PCOS
High FSH suggests primary ovarian failure
High LH, or LH:FSH ratio, suggests polycystic ovarian syndrome
Which condition does high testosterone indicate?
polycystic ovarian syndrome, androgen insensitivity syndrome or congenital adrenal hyperplasia.
How is secondary amenorrhoea managed?
Management of secondary amenorrhoea involves establishing and treating the underlying cause. Where necessary, replacement hormones can induce menstruation and improve symptoms.
Patients with amenorrhoea associated with low oestrogen levels are at risk increased risk of osteoporosis. Where the amenorrhoea lasts more than 12 months, treatment is indicated to reduce the risk of osteoporosis:
Ensure adequate vitamin D and calcium intake
Hormone replacement therapy or the combined oral contraceptive pill
What is an ectopic pregnancy and its risk factors?
Ectopic pregnancy is when a pregnancy is implanted outside the uterus. The most common site is a fallopian tube. An ectopic pregnancy can also implant in the entrance to the fallopian tube (cornual region), ovary, cervix or abdomen.
RFs:
- Previous ectopic pregnancy
- Previous pelvic inflammatory disease
- Previous surgery to the fallopian tubes
- Intrauterine devices (coils)
- Assisted conception
- Older age
- Smoking
How common are ectopic prgenancies?
1 in 90 pregnancies are ectopic
How does ectopic pregnancy present?
It typically presents around 6-8 weeks gestation
Missed period
Constant lower abdominal pain in the right or left iliac fossa
Vaginal bleeding/Prune juice coloured discharge Lower abdominal or pelvic tenderness
Cervical motion tenderness (pain when moving the cervix during a bimanual examination)
Dizziness/Syncope (blood loss)
Shoulder tip pain (peritonitis)
On examination - cervical excitation and/or adnexal tenderness
What signs should you look out for when suspicious of a ruptured ectopic pregnancy?
the patient may also be haemodynamically unstable (pallor, increased capillary refill time, tachycardia, hypotension), with signs of peritonitis (abdominal rebound tenderness and guarding). Vaginal examination may reveal fullness in the pouch of Douglas.
How do you investigate a possible ectopic pregnancy?
- pregnancy test
- transabdominal USS, if no intrauterine pregnancy seen then offer transvaginal
- if positive preganancy test but no uterine pregnancy then this is a pregnancy of unknown location meaning it is a very early intrauterine pregnancy, a miscarriage or an ectopic pregnancy
- in this scenario a serum beta HCG should be taken
What would you see on USS in a patient with an ectopic pregnancy?
- non-specific mass may be seen in the tube. When a mass containing an empty gestational sac is seen, this may be referred to as the “blob sign”, “bagel sign” or “tubal ring sign”
- adnexal mass that moves separatelyto the ovary. Sensitivity of 87-99%. Do not confuse with corpus luteum which moves with the ovary
- In 20% of cases apseudosacmay be seen as fluid within the uterine cavity
- Free fluid may be seen but is not diagnostic of an ectopicpregnancy
- If there’s been a miscarriage then a gestational sac containing a yolk sac or fetal pole may be seen in a fallopian tube.
In a suspected ectopic pregnancy, what would you do if serum beta hcg was more than 1500iU?
If there is no intrauterine pregnancy on transvaginal ultrasound, then this should be considered an ectopic pregnancy until proven otherwise, and a diagnostic laparoscopy should be offered.
In a suspected ectopic pregnancy, what would you do if serum beta hcg was less than 1500iU?
if the patient is stable, a further blood test can be taken 48 hours later:
- In a viable pregnancy, HCG level would be expected to double every 48 hours.
- In a miscarriage, HCG level would be expected to halve every 48 hours
- Where the increase or drop in the rate of change is outside these limits, an ectopic pregnancy cannot be excluded and the patient should be managed accordingly.
If a beta HCG test is done after 48 hours of the initial test, what does a rise of more than 63% indicate?
an intrauterine pregnancy. A repeat ultrasound scan is required after 1 – 2 weeks to confirm an intrauterine pregnancy. A pregnancy should be visible on an ultrasound scan once the hCG level is above 1500 IU / l.
If a beta HCG test is done after 48 hours of the initial test, what does a rise of less than 63% indicate?
ectopic pregnancy. When this happens the patient needs close monitoring and review.
If a beta HCG test is done after 48 hours of the initial test, what does a fall of more than 50% indicate?
a miscarriage. A urine pregnancy test should be performed after 2 weeks to confirm the miscarriage is complete.
How is an ectopic pregnancy managed?
It must be terminated as it is not a viable pregnancy.
Options:
1. Expectant management (awaiting natural termination)
2. Medical management (methotrexate)
3. Surgical management (salpingectomy or salpingotomy)
What is the criteria for conservative/expectant management in ectopic pregnancy?
Follow up needs to be possible to ensure successful termination
The ectopic needs to be unruptured
Adnexal mass < 35mm
No visible heartbeat
No significant pain
HCG level < 1500 IU / l
What is the criteria for medical management of ectopic pregnancy?
Follow up needs to be possible to ensure successful termination
The ectopic needs to be unruptured
Adnexal mass < 35mm
No visible heartbeat
No significant pain
HCG level < 5000 IU / l
Confirmed absence of uterine pregnancy on ultrasound
If a woman fits the criteria she will receive an IM dose of methrotrexate
What are the contraindications for medical management of ectopic pregnancy?
Contraindications include thrombocytopaenia, hepatic or renaldysfunction, immunocompromised, breastfeeding and pepticulcer disease
What follow up is done after medical management of an ectopic pregnancy?
The serum β-HCG level is monitored regularly to ensure the level is declining (by >15% in day 4-5). If there isn’t such a decline, a repeat dose is administered.
What advice must you give to someone having methotrexate for management of ectopic pregnancy and what side effects do you need to warn them of?
Women treated with methotrexate are advised not to get pregnant for 3 months following treatment. This is because the harmful effects of methotrexate on pregnancy can last this long.
Common side effects of methotrexate include:
Vaginal bleeding
Nausea and vomiting
Abdominal pain
Stomatitis (inflammation of the mouth)
Which patients with ectopic pregnancy would be managed surgically?
Anyone that does not meet the criteria for expectant or medical management requires surgical management. Most patients with an ectopic pregnancy will require surgical management. This include those with:
Pain
Adnexal mass > 35mm
Visible heartbeat
HCG levels > 5000 IU / l
What are the surgical management options for ectopic pregnancy?
Laparoscopic salpingectomy is the first-line treatment for ectopic pregnancy. This involves a general anaesthetic and key-hole surgery with removal of the affected fallopian tube, along with the ectopic pregnancy inside the tube.
Laparoscopic salpingotomy may be used in women at increased risk of infertility due to damage to the other tube. The aim is to avoid removing the affected fallopian tube. A cut is made in the fallopian tube, the ectopic pregnancy is removed, and the tube is closed.
There is an increased risk of failure to remove the ectopic pregnancy with salpingotomy compared with salpingectomy. NICE state up to 1 in 5 women having salpingotomy may need further treatment with methotrexate or salpingectomy.
What must you give to a rhesus negative woman having surgical management of ectopic pregnancy?
Anti-rhesus D prophylaxis is given to rhesus negative women having surgical management of ectopic pregnancy.
What are the complications of an untreated ectopic pregnancy?
An untreated ectopic pregnancy can lead to fallopian tube rupture. The resulting blood loss can cause hypovolaemic shock, resulting in organ failure and death.
What are the causes of heavy menstrual/abnormal uterine bleeding?
Structural = PALM = Polyp, Adenomyosis, Leiomyoma (Fibroid) and Malignancy & hyperplasia
Non-structural = COEIN = Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified
Dysfunctional uterine bleeding (no identifiable cause)
Extremes of reproductive age
Fibroids
Endometriosis and adenomyosis
Pelvic inflammatory disease (infection)
Contraceptives, particularly the copper coil
Anticoagulant medications
Bleeding disorders (e.g. Von Willebrand disease)
Endocrine disorders (diabetes and hypothyroidism)
Connective tissue disorders
Endometrial hyperplasia or cancer
Polycystic ovarian syndrome
What are the main RFs for heavy menstrual bleeding?
- age (more likely at menarche and approaching the menopause)
- obesity
There are also other risk factors that relate to the specific causes of HMB. One example would be previous caesarean section – as a risk factor for adenomyosis.
What are the main clinical features of HMB? What things do you need to ascertain from the history?
- Bleeding during menstruation deemed to be excessive for the individual woman.
- Fatigue
- SOB (if associated anaemia)
- A menstrual cycle history should be taken
- Date of LMP
- Intermenstrual bleeding and post coital bleeding
- Smear history
- Contraception, medical history and medications
- Sexual history
- Possibility of pregnancy
- Plans for future pregnancies
- Cervical screening history
- Migraines with or without aura (for the pill)
What should be included on a physical exam investigating HMB?
Examination of the patient should include a general observation, abdominal palpation, speculum and bimanual examination.
- Pallor (anaemia)
- Palpable uterus or pelvic mass
- Try to ascertain if the uterus is smooth or irregular (fibroids)
- A tender uterus or cervical excitation point toward adenomyosis/endometriosis
- Inflamed cervix/cervical polyp/cervical tumour
- Vaginal tumour
How would you investigate HMB?
- Urine pregnancy test
- FBC
- Other bloods to consider = TFT, hormones for pcos, coag + vWF
- Pelvic US - transvaginal
- Cervical smear - don’t need to if up to date
- High vaginal and endocervical swabs
- Pipelle endometrial biopsy:
Indications for biopsy include persistent intermenstrual bleeding, >45 years old, and/or failure of pharmacological treatment. - Hysteroscopy and endometrial biopsy:
Typically performed when ultrasound identifies pathology, or is inconclusive.
How do you manage HMB/AUB medically?
- Exclude underlying pathology
- Treatment depends on whether woman wants contraception:
If she does not want contraception:
- Tranexamic Acid and Mefanamic Acid during menstruation
If she does:
- Mirena IUS
- COCP
- Cyclical oral progestogens - POP, Depo, Implant
What are management options for HMB in secondary care?
- Pharmacological: gonadotrophin-releasing hormone (GnRH) analogues (induce hypogonadal state). Use of GnRH analogues is reserved for specialists and may be a bridge to other therapies.
- Surgical: endometrial ablation, hysterectomy. Uterine artery embolization and myomectomy can be used for fibroids.
Why would someone be referred to secondary care for HMB?
- Failure of medical therapy
- Need for surgery
- Iron-deficiency anaemia not responding to medical therapy
- Cancer red flags:
- Persistent intermenstrual or post-coital bleeding
- Unexplained vulval lump or vulval ulceration and bleeding
- Palpable abdominal mass that is not obviously a fibroid
- Clinical features of cervical cancer
What are fibroids? What is their epidemiology?
Uterine fibroids (leiomyomas) are benign smooth muscle tumours of the uterus.
They are the most common benign tumours in women, with an estimated incidence of 20-40%. The risk of a fibroid becoming malignant is 0.1%.
What is the pathophysiology of fibroids and how are they classified?
Benign smooth muscle tumours coming from the myometrium. Poor understanding but growth is thought to be stimulated by oestrogen.
- Intramural (most common) – confined to the myometrium of the uterus.
- Submucosal – develops immediately underneath the endometrium of the uterus, and protrudes into the uterine cavity.
- Subserosal – protrudes into and distort the serosal (outer) surface of the uterus. They may be pedunculated (on a stalk).
What are the risk factors for fibroids?
Obesity
Early menarche
Increasing age
Family history- Women with a 1st degree relative affected carry a 2.5x increased risk.
Ethnicity- African-Americans are 3x more likely to develop fibroid than Caucasians.
Pregnancy and Progestogen only contraception seem to reduce risk
How do fibroids present?
- Often asymptomatic
- Heavy menstrual bleeding (menorrhagia) is the most frequent presenting symptom
- Prolonged menstruation, lasting more than 7 days
- Abdominal pain, worse during menstruation
- Bloating or feeling full in the abdomen
- Urinary or bowel symptoms due to pelvic pressure or fullness (frequency or retention)
- Deep dyspareunia (pain during intercourse)
- Reduced fertility
A pregnant woman with a history of fibroids presents with severe abdominal pain and a low-grade fever. What is the diagnosis?
Red degeneration refers to ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply. Red degeneration is more likely to occur in larger fibroids (above 5 cm) during the second and third trimester of pregnancy. Red degeneration may occur as the fibroid rapidly enlarges during pregnancy, outgrowing its blood supply and becoming ischaemic. It may also occur due to kinking in the blood vessels as the uterus changes shape and expands during pregnancy.
Red degeneration presents with severe abdominal pain, low-grade fever, tachycardia and often vomiting. Management is supportive, with rest, fluids and analgesia.
Rarely, pedunculated fibroids can undergo torsion.
What would you expect from examination of a patient with fibroids?
A solid mass or enlarged uterus may be palpable on abdominal or bimanual examination. The uterus is usually non-tender.
What are possible differential diagnoses for fibroids?
Endometrial polyp
Ovarian tumours
Leiomyosarcoma – malignancy of the myometrium.
Adenomyosis – presence of functional endometrial tissue within the myometrium.
What investigations would you undertake to diagnose fibroids?
- Transvaginal Pelvic ultrasound - the main reason for requesting a pelvic ultrasound is identification of a pelvic mass or menorrhagia that is not responsive to conventional treatment.
Gold - Pelvic MRI +/- hysteroscopy. MRI is usually reserved for operative planning or complicated cases to differentiate from other diagnoses
Can also do bloods for FBC - anaemia
What is the medical management of fibroids?
Depends on HPC which is usually HMB so you would do:
- Mirena coil (1st line) – fibroids must be less than 3cm with no distortion of the uterus
- Symptomatic management with NSAIDs and tranexamic acid
- Combined oral contraceptive
- Cyclical oral progestogens
What are more complex pharmacological management options for fibroids which need to be started by a specialist?
- GnRH analogues (goserelin (Zoladex) or leuprorelin (Prostap)) suppress ovulation, inducing a temporary menopausal state. They are useful pre-operatively to reduce fibroid size and lower complications. Can be used for 6 months only, due to the risk of osteoporosis
- Selective Progesterone Receptor Modulators (Ulipristal / Esmya) reduce size of fibroid and menorrhagia so they are useful pre-operatively or as an alternative to surgery. Use of Ulipristal is restricted due to risk of severe liver injury.
What is the surgical management for fibroids?
- Hysteroscopy and Transcervical Resection of Fibroid (TCRF) is useful for submucosal fibroids
- Myomectomy is an option in women wanting to preserve their uterus and can potentially improve fertility
- Uterine Artery Embolization (UAE)
Performed by a radiologist via the femoral artery - Commonly causes pain and fever post-operatively - Hysterectomy
Endometrial ablation can be used for small fibroids
What are the possible complications from fibroids?
Pregnancy-related complications:
- Infertility (distortion of uterine cavity)
- Miscarriage
- Malpresentation
- Placental abruption
- Intrauterine growth restriction
- Preterm or obstructed labour
- Red degeneration
Non-pregnancy-related complications:
- Prolapsed fibroid
- Constipation, urinary obstruction or UTIs
- Anaemia from HMB
- Endocrine effects (polycythaemia, hypercalcaemia, hyperprolactinaemia)
- Torsion
- Malignant change
What is endometriosis? What is the epidemiology?
a chronic condition in which endometrial tissue is located at sites other than the uterine cavity. It can occur in the ovaries, pouch of Douglas, uterosacral ligaments, pelvic peritoneum, bladder, umbilicus and lungs.
Around 2 million women in the UK are affected, with most diagnoses made between the ages 25 and 40.
What is the pathophysiology of endometriosis?
This is not fully understood but there are some theories:
- Retrograde menstruation: endometrial cells travel backwards from the uterine cavity, through the Fallopian tubes, and deposit on pelvic organs – where they can seed and grow. It has also been suggested that these cells may also be able to travel to distant sites through the lymphatic system and vasculature.
Other theories:
- Embryonic cells destined to become endometrial tissue may remain in areas outside the uterus during the development of the fetus, and later develop into ectopic endometrial tissue.
- Spread through lymphatic system, in a similar way to the spread of cancer.
- Metaplasia, from typical cells of that organ into endometrial cells.
What are the risk factors for endometriosis?
Early menarche
Late menopause
Nulliparity
Delayed childbearing
Short menstrual cycle
Family history
White ethnicity
What are features of a history of endometriosis?
Main Sx is cyclical pelvic pain (but may be constant if adhesions have formed) Other Sx = dysmenorrhoea, dyspareunia, dysuria, dyschezia (difficult, painful defecating), bleeding from other sites e.g. haematuria and subfertility.
What would be expected from a bimanual examination on a patient with endometriosis?
A fixed, retroverted uterus
Uterosacral ligament nodules
General tenderness
Endometrial tissue visible in the vagina on speculum examination, particularly in the posterior fornix
What are the main DDx to exclude when you are concerned about endometriosis?
- Pelvic Inflammatory Disease: This can present with dyspareunia, pelvic pain and abnormal and/or heavy bleeding.
- Ectopic pregnancy: This can present with dyspareunia, pelvic pain and abnormal and/or heavy bleeding, and sometimes collapse.
- Fibroids: This can present with pelvic pain, long duration of menstrual bleedings, heavy menstrual bleeding, a feeling of a mass or bloating.
- Irritable Bowel Syndrome: abdominal pain, dyspareunia and bloating.
How do you investigate endometriosis?
- Ultrasound scans are often unremarkable in patients with endometriosis. Patients with suspected endometriosis need referral to a gynaecologist for laparoscopy.
Laparoscopic surgery is the gold standard way to diagnose abdominal and pelvic endometriosis. A definitive diagnosis can be established with a biopsy of the lesions during laparoscopy. Laparoscopy has the added benefit of allowing the surgeon to remove deposits of endometriosis and potentially improve symptoms.
What might you see on USS of endometriosis?
Chocolate cysts
Adhesions
Peritoneal deposits
A skilled operator can demonstrate “kissing ovaries” – where bilateral endometrioma are adherent together. Pelvic mobility can be demonstrated, including any involvement of bowel.
How is endometriosis staged?
American Society of Reproductive Medicine:
Stage 1: Small superficial lesions
Stage 2: Mild, but deeper lesions than stage 1
Stage 3: Deeper lesions, with lesions on the ovaries and mild adhesions
Stage 4: Deep and large lesions affecting the ovaries with extensive adhesions
NICE guidelines do not use this, just recommend detailed documentation
How is endometriosis managed?
- manage pain using the analgesic ladder
- Hormonal management -COCP which can be used back to back without a pill-free period if helpful, POP, Medroxyprogesterone acetate injection (e.g. Depo-Provera), Nexplanon implant, Mirena coil, GnRH agonists
- Surgical - Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis) or Hysterectomy. It will almost always relapse after surgery.
When do the symptoms of endometriosis tend to stop and why does this happen?
The cyclical pain tends to improve after the menopause when the female sex hormones are reduced. Therefore, treatment options are based on stopping ovulation.
How do GnRH agonists work in the management of endometriosis?
GnRH agonists induce a menopause-like state. e.g. goserelin (Zoladex) or leuprorelin (Prostap). They shut down the ovaries temporarily and can be useful in treating pain in many women. However, inducing the menopause has several side effects, such as hot flushes, night sweats and a risk of osteoporosis.
How do contraceptives improve cyclical pain in endometriosis?
Cyclical pain can be treated with hormonal medications that stop ovulation and reduce endometrial thickening. This can be achieved using the combined oral contraceptive pill, oral progesterone-only pill, the progestin depot injection, the progestin implant (Nexplanon) and the Mirena coil.
What is adenomyosis?
Adenomyosis is the presence of functional endometrial tissue within the myometrium of the uterus.
What is the incidence of adenomyosis? And what are the risk factors?
10% - It may occur alone, or alongside endometriosis or fibroids.
High parity
Uterine surgery e.g. any endometrial curettage, endometrial ablation
Previous caesarean section
Hereditary occurrence has been reported, suggesting a potential genetic predisposition
What is the pathophysiology and aetiology of adenomyosis?
Occurs when the endometrial stroma (connective/supporting tissue) is allowed to communicate with the underlying myometrium after uterine damage. Such interaction may occur in association with Pregnancy and childbirth & Uterine surgery (e.g dilation+ curettage).
Where is endometrial invasion normally seen in adenomyosis?
It can be focal or diffuse and is more commonly found in the posterior wall of the uterus. The extent of invasion is variable, but in severe cases pockets of menstrual blood can be seen in the myometrium of hysterectomy specimens.
What is an adenomyoma?
When a collection of endometrial glands form grossly visible nodules, they are described as an adenomyoma. Oestrogen, progesterone and androgen receptors are found in the ectopic endometrial tissue, making it responsive to hormones.
What are the features seen in a history of adenomyosis?
- Painful periods (dysmenorrhoea)
- Heavy periods (menorrhagia)
- Irregular bleeding
- Pain during intercourse (dyspareunia)
- It may also present with infertility or pregnancy-related complications.
- Around a third of patients are asymptomatic.
NB. The dysmenorrhoea is commonly progressive; beginning as cyclical pain, but can worsen to daily pain.
What would be seen in an examination of someone with adenomyosis?
On examination (abdominal and bimanual palpation), a symmetrically enlarged tender uterus may be palpable. It will feel more soft than a uterus containing fibroids. “Boggy uterus”
How do you investigate adenomyosis?
- Transvaginal ultrasound of the pelvis
- MRI and transabdominal ultrasound are alternative investigations where transvaginal ultrasound is not suitable.
The gold standard is to perform a histological examination of the uterus after a hysterectomy. However, this is not usually a suitable way of establishing the diagnosis. Potential for hysteroscopic biopsy.
What would you see on the ultrasound of someone with adenomyosis?
- a globular uterine configuration
- poor definition of the endometrial-myometrial interface
- myometrial anterior-posterior asymmetry
- intramyometrial cysts
- heterogeneous myometrial echo texture
What would you expect to see on the MRI of someone with adenomysosis?
‘endo–myometrial junctional zone’ that can be distinguished from the endometrium and outer myometrium. An irregular thickening of this zone is now recognised as the hallmark of adenomyosis
What is the definitive cure for adenomyosis?
The only curative therapy is hysterectomy
What is the medical management of adenomyosis?
Same as for endometriosis
- Tranexamic and Mefenamic acid
- Hormonal = COCP, Progestogens (oral or Intrauterine system e.g. Mirena), GnRH agonists, aromatase inhibitors
What are other options for invasive management of adenomyosis except hysterectomy?
In the UK, uterine artery embolisation can be used as an alternative treatment option in the short and medium term for women who wish to avoid hysterectomy and or preserve their fertility. The aim is to block the blood supply to the adenomyosis, causing it to shrink.
Other treatment options include endometrial ablation and resection, laparoscopic excision and magnetic resonance–guided focused ultrasound.
What problems can adenomyosis cause in pregnancy?
Infertility
Miscarriage
Preterm birth
Small for gestational age
Preterm premature rupture of membranes
Malpresentation
Need for caesarean section
Postpartum haemorrhage
What are cervical polyps and how common are they?
benign growths protruding from the inner surface of the cervix. They are typically asymptomatic, but a very small minority can undergo malignant change.
2-5% of women
What is the histological pathophysiology of cervical polyps?
Cervical polyps develop as a result of focal hyperplasia of the columnar epithelium of the endocervix.
The aetiology is unclear, but suggested causes are:
Chronic inflammation
Abnormal response to oestrogen (cervical polyps are associated with endometrial hyperplasia)
Localised congestion of the cervical vasculature
What group has a higher incidence of cervical polyps?
They are more common in multigravidae, with a peak in incidence between 50 and 60 years of age.
What are the features of a history of cervical polyps?
- often asymptomatic, identified only via routine cervical screening.
- most common clinical feature is abnormal vaginal bleeding. This can be in the form of menorrhagia, or intermenstrual, post-coital, or post-menopausal bleeding.
- can also cause increased vaginal discharge.
- Rarely, they grow large enough to block the cervical canal, causing infertility.
What would you expect to see on examination of a patient with cervical polyps?
On speculum examination, cervical polyps are usually visible as polypoid growths projecting through the external os.
It can be confused with endometrial polyp – which could be projecting through cervical canal.
What investigations do you do if you suspect cervical polyps?
- Triple swabs – endocervical and high vaginal swabs should be taken
- Cervical smear – to rule out cervical intraepithelial neoplasia (CIN)
- Definitive = histology after removal of the polyp
What should you investigate if someone has cervical polyps?
Approximately 27% of women with cervical polyps have associated endometrial polyps. Especially the post-menopausal age group. If symptoms of bleeding persist after removal of the polyp, an ultrasound scan should be arranged to assess the endometrial cavity.
What is the management of cervical polyps?
Cervical polyps have a small (less than 0.5%) risk of malignant transformation – and so it is common practice to remove them whenever they are identified (even if asymptomatic).
How do you remove polyps?
- GP - polypectomy forceps+ twist so it is avulsed as the pedicle becomes twisted. The polyp should not be pulled off as it will result in more bleeding. Any resulting bleeding can be cauterised with silver nitrite.
- 2nd care - Larger polyps, or those that are more difficult to access can be removed by diathermy loop excision in the colposcopy clinic, or under general anaesthesia if the base of the polyp is broad.
Any excised polyps should be sent for histological examination to exclude malignancy. They have a recurrence rate of 6-12%.
What are the complications of polypectomy?
Infection, haemorrhage and uterine perforation (rare) - in outpatients setting only remove the ones you can actually see
What is a cervical ectropion?
there is eversion of the endocervix, exposing the columnar epithelium to the vaginal milieu. It is also known as a cervical erosion, although no “erosion” of cells actually occurs.
Who do you see cervical ectropions in physiologically?
commonly seen on examination of the cervix in adolescents, in pregnancy, and in women taking oestrogen containing contraceptives.
What is the histological make up of the endocervical canal?
the more proximal, and ‘inner’ part of the cervix. It is lined by a mucus-secreting simple columnar epithelium.
What is the histological make up of the ectocervix?
the part of cervix that projects into the vagina. It is normally lined by stratified squamous non-keratinised epithelium.
What is the histological definition of a cervical ectropion?
the presence of everted endocervical columnar epithelium on the ectocervix
Why do some people with an ectropion have more discharge or post-coital bleeding?
The columnar epithelium contains mucus-secreting glands, and thus some individuals with cervical ectropion experience increased vaginal discharge.
It may also give rise to post-coital bleeding, as the fine blood vessels present within the epithelium are easily broken during intercourse.
What are the RF/causes for cervical ectropion?
Oestrogen:
COCP
Pregnancy
Adolescence
Menstruating age (it is uncommon in post-menopausal women)
What are the signs of ectropion in a history?
Asymptomatic, post-coital bleeding, intermenstrual bleeding, dyspareunia or excessive discharge (non-purulent).
What would you see on a speculum examination of someone with an ectropion?
On speculum examination, there will be a well-demarcated border between the redder, velvety everted columnar epithelium extending from the external os, and the pale pink squamous epithelium of the ectocervix. This border is the transformation zone.
What differentials would you consider in someone with an ectropion?
cervical cancer, cervical intraepithelial neoplasia, cervicitis (inflammation of the cervix, typically caused by infection), and pregnancy
What is the transformation zone?
The border between the columnar epithelium of the endocervix (the canal), and the stratified squamous epithelium of the ectocervix (the outer area of the cervix visible on speculum examination). When the transformation zone is located on the ectocervix, it is visible during speculum examination as a border between the two epithelial types.
How do you diagnose a cervical ectropion?
Usually a clinical diagnosis based on examination. You can do the following to rule out other things:
- Pregnancy test
- Triple swabs – suggestion of infection (such as purulent discharge), endocervical and high vaginal swabs should be taken
- Cervical smear – to rule out cervical intraepithelial neoplasia. If a frank lesion is observed, a biopsy should be taken (note that biopsies are not performed as routine).
How are cervical ectropians managed? Should someone with an ectropion have the COCP?
Asymptomatic ectropion require no treatment. Ectropion will typically resolve as the patient gets older, stops the pill or is no longer pregnant. Having a cervical ectropion is not a contraindication to the combined contraceptive pill.
How can you manage problematic bleeding caused by a cervical ectropion?
cauterisation of the ectropion using silver nitrate or cold coagulation during colposcopy. This will result in significant vaginal discharge until healing is completed.
Medication to acidify the vaginal pH has been suggested, such as boric acid pessaries.
What are ovarian cysts? Are they cause for concern?
A cyst is a fluid-filled sac. Functional ovarian cysts related to the fluctuating hormones of the menstrual cycle, and are very common in premenopausal women. The vast majority of ovarian cysts in premenopausal women are benign. Cysts in postmenopausal women are more concerning for malignancy and need further investigation.
What are the risk factors for ovarian cancer?
Nulliparity
Early menarche
Late menopause
Hormone replacement therapy containing oestrogen only
Smoking
Obesity
Asbestos
IVF
Positive FHx
BRCA1&2
Lynch II Syndrome
What are protective factors for ovarian cancer?
Multiparity
Combined contraceptive methods
Breastfeeding
Why are more ovulations considered a risk factor for ovarian cancer?
Ovarian cancers are believed to derive from surface epithelial irritation during ovulation. Therefore, the more ovulations that take place, the increased risk of developing malignancy
Which genetic factors can increase risk of ovarian cancer?
BRCA 1&2 and Hereditary nonpolyposis colorectal cancer (Lynch II Syndrome)
What is BRCA 1&2?
these mutations increase the risk of breast and ovarian cancers. Ovarian cancer risk is as much as 46% at age 70 in BRCA1 positive families and 12% in BRCA2. Prophylactic bilateral salpingo-oophorectomy can be performed in these patients however this does not completely eradicate the risk of developing malignancy.
BRCA 1 is chromosome 17, 2 is chromosome 13
What equation is used for Risk of Malignancy Index?
RMI = U x M x CA125
U is ultrasound features and M is menopausal status
RMI >250 should be referred to gynae specialist
How do ovarian cysts present?
Most asymptomatic
Pelvic pain
Bladder and bowel (freq+constipation)
Bloating
Fullness in the abdomen
PV bleeding
A palpable pelvic mass (particularly with very large cysts such as mucinous cystadenomas)
Ovarian cysts may present with acute pelvic pain if there is ovarian torsion, haemorrhage or rupture of the cyst
Look out for red flags like weight loss
Describe a follicular cyst
Follicular cysts represent the developing follicle. When these fail to rupture and release the egg, the cyst can persist. Follicular cysts are the most common ovarian cyst, they are harmless and tend to disappear after a few menstrual cycles. Typically they have thin walls and no internal structures, giving a reassuring appearance on the ultrasound.
Describe a corpus luteum cyst
Corpus luteum cysts occur when the corpus luteum fails to break down and instead fills with fluid. They may cause pelvic discomfort, pain or delayed menstruation. They are often seen in early pregnancy.
What types of ovarian cysts are non-neoplastic?
Follicular and non-neoplastic cysts
What are the 3 types of pathological ovarian cysts?
Endometriomas, Polycystic Ovaries and Theca Lutein Cysts
What is an endometrioma on the ovary?
These are also called chocolate cysts and are present in those with endometriosis. There has been bleeding into the cyst resulting in the appearance.
What are polycystic ovaries?
An ultrasound diagnosis.
The ovaries contrain more than 12 antral follicles, or ovarian volume greater than 10ml. The classic ‘ring of pearls’ sign is seen on ultrasound scanning.
PCO is present as one of the features of polycystic ovarian syndrome (Rotterdam criteria criteria). Isolated PCO does not equate to PCOS.
What is a Theca Lutein Cyst?
These result as a consequence of markedly raised hCG e.g. molar pregnancy. They regress upon resolution of the raised hCG.
What are the 3 types of benign neoplastic ovarian cysts?
Epithelial, Benign Germ Cell tumours and sex cord stromal tumours
What are epithelial ovarian cysts?
Serous cystadenoma – reflects the most common type of malignant ? ovarian tumour and is usually unilocular with up to 30% being bilateral.
Mucinous cystadenoma – these are often multiloculated and usually unilateral.
Brenner tumour – unilateral with a solid grey or yellow appearance.
What are benign germ cell tumours?
Mature cystic teratoma (Dermoid cysts) – 10% are bilateral, usually occur in young women and occur frequently in pregnancy. As germ cell in origin they can contain teeth, hair, skin and bone.
What are sex cord stromal cell tumours on the ovary?
These are rare tumours, that can be benign or malignant. They arise from the stroma (connective tissue) or sex cords (embryonic structures associated with the follicles). There are several types, including Sertoli–Leydig cell tumours and granulosa cell tumours.
Fibroma is the most common stromal tumour. Important to know about as up to 40% present with Meig’s syndrome which is the association between these tumours and ascites/pleural effusion.
What investigation is used for diagnosing ovarian cysts?
Ultrasound - TV or Abdo
What is the general management approach you should take with ovarian cysts?
Premenopausal
<5cm watch and wait
5-7 cm gynae referral and yearly scan
>7cm surgery
Postmenopausal
CA125 tumour marker and gynae referral
If a premenopausal woman has had an ultrasound which shows a simple ovarian cyst which measures less than 5cm, how would you proceed?
No further investigations
If a woman under 40 years old has a complex ovarian mass, how would you proceed?
Need to investigate incase there is a germ cell tumour:
Lactate dehydrogenase (LDH)
Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)
What is CA125?
glycoprotein and tumour marker for epithelial cell ovarian cancer. Not very specific and can be raised by various things. Non-malignant causes include endometriosis, fibroids, adenomyosis, pelvic infection, liver disease and pregnancy.
