Gynaecology - General Flashcards

1
Q

What are the four UKMEC classes?

A

UKMEC 1: a condition for which there is no restriction for the use of the contraceptive method
UKMEC 2: advantages > disadvantages
UKMEC 3: disadvantages > advantages
UKMEC 4: represents an unacceptable health risk

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2
Q

Give examples of UKMEC 3 conditions for the COCP

A

Examples of UKMEC 3 conditions include

more than 35 years old and smoking less than 15 cigarettes/day
BMI > 35 kg/m^2*
family history of thromboembolic disease in first degree relatives < 45 years
controlled hypertension
immobility e.g. wheel chair use
carrier of known gene mutations associated with breast cancer (e.g. BRCA1/BRCA2)
current gallbladder disease

Diabetes mellitus diagnosed > 20 years ago is classified as UKMEC 3 or 4 depending on severity

Changes in 2016 – breast feeding 6 weeks - 6 months postpartum was changed from UKMEC 3 → 2

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3
Q

Give examples of UKMEC 4 conditions for the COCP

A

Examples of UKMEC 4 conditions include

more than 35 years old and smoking more than 15 cigarettes/day
migraine with aura
history of thromboembolic disease or thrombogenic mutation
history of stroke or ischaemic heart disease
breast feeding + < 6 weeks post-partum
uncontrolled hypertension
current breast cancer
major surgery with prolonged immobilisation

Diabetes mellitus diagnosed > 20 years ago is classified as UKMEC 3 or 4 depending on severity

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4
Q

Which are the three systems used to classify POP (pelvic organ prolapse)

A

• POP-Q system [pelvic organ prolapse quantification, NICE recommended, most comprehensive and widely used according to RCOS] (measures different anatomical landmarks in relation to the hymen)
o Positions are recorded as coordinates relative to the physiological position of the pelvic organs as seen in the picture below. The hymen is used as a reference point
o Distal to hymen is a +ve number, proximal is a -ve number
o Stage 0 – no prolapse
o Stage 1 – >1cm above hymen
o Stage 2 – within 1cm proximal or distal to the plane of the hymen
o Stage 3 – >1cm below the plane of the hymen but protrudes no further than 2cm less than the total length of the vagina
o Stage 4 – complete eversion of the vagina

• Shaw’s (most commonly used, looks at extent of descent of prolapse)
o 1st degree – descent to the introitus
o 2nd degree – extends to the introitus but descends past the introitus on straining
o 3rd degree – prolapse descends through the introitus

• Baden-Walker or Beecham classification systems
o 1st degree – cervix is visible when the perineum is depressed – prolapse is contained within the vagina
o 2nd degree – cervix prolapsed through the introitus with the fundus remaining in the pelvis
o 3rd degree – procidentia (complete prolapse) – entire uterus is outside the introitus

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5
Q

Which are the different types of pelvic organ prolapse? POP

A

Anterior compartment prolapse
• Urethrocele
o Prolapse of the urethra into the vagina
o Frequently associated with urinary stress incontinence
• Cystocele
o Prolapse of the bladder into the anterior vaginal wall
o Isolated cystocele  Rarely causes incontinence, usually leads to few or no symptoms
o Large cystocele   urinary frequency, frequent UTI, pressure sensation/mass at the introitus
• Cystourethrocele – prolapse of both urethra and bladder

Middle compartment prolapse
• Uterine prolapse – scent of the uterus into the vagina
• Vaginal vault prolapse
o Descent of the vaginal vault post-hysterectomy
o Often associated with cystocele, rectocele, enterocele
o With complete inversion – the urethra, bladder, distal ureters may be included resulting in varying degrees of retention + distal ureteric obstruction

Posterior compartment prolapse
• Enterocele
o Prolapse of the upper posterior vaginal wall containing loops of small bowel (small intestine and perineum are involved)
o Herniation of the pouch of Douglas (incl. small intestine/omentum) into the vagina
o Small enteroceles are usually asymptomatic
o Can occur following pelvic surgery
o The neck of the hernial sac is usually sufficiently wide to make strangulation very rare
o Can be difficult to differentiate clinically from a rectocele
 A cough impulse can be felt in enterocele on combined rectal + vaginal examination
• Rectocele – prolapse of the anterior wall of the rectum into the lower posterior vaginal wall

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6
Q

RF for POP (pelvic organ prolapse)

A

• Weakening of the support structure
o Direct muscle trauma
o Neuropathic injury
o Disruption or stretching

•	Confirmed RF
o	Increasing age
o	Vaginal delivery 
o	Increasing parity
o	Obesity
o	Previous hysterectomy 
•	Possible RF
o	Prolonged 2nd stage of labour (>2h)– levator ani dysfunction 
o	Increased birth weight
o	Pregnancy
o	Use of forceps
o	Age <25 at first delivery
o	Shape of pelvis
o	FHx of prolapse
o	Constipation
o	Connective tissue disorders – Marfan’s, Ehlers-Danlos syndrome 
o	Occupations involving heavy lifting
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7
Q

Aetiology and RF for USI

A

Aetiology
• Pelvic floor weakness
• Incompetent intrinsic sphincter

RF
•	Age
•	Women
o	Pregnancy
o	Parity
o	Vaginal delivery, forceps use, heavier birth weight
	Can cause anatomical or neuromuscular injury 
	Can damage the pelvic floor muscles 
o	DM
o	Oral oestrogen therapy
o	High BMI
o	UTI
o	Vaginal hysterectomy
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8
Q

RF for OAB (overactive bladder syndrome)

A
  • Prevalence increases with age
  • PD
  • Spinal cord injury
  • Diabetic neuropathy
  • MS
  • Dementia
  • Stroke

Causes
Idiopathic
Neurogenic

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9
Q

Urogynaecology history cribsheet

A

Urogynaecology history cribsheet

Introduction
Name, Age

PC: Can you tell me what’s brought you into hospital today?

HPC:
Timeline: when it started, has it worsened recently?

Urge Urinary incontinence 
Urinary frequency: 8 times normal 
Urinary urgency 
Urinary incontinence
Nocturia: 1 time a night is normal 

How often do you go for a wee in the daytime?
Do you ever feel like you need to rush to the toilet?
If yes, how often does that happen in the day? (50%/100%)
Do you ever have accidents when you can’t get to the toilet in time?
If yes, how often and how much (drops/large amounts)
Do you go to the toilet at nighttime? How often?

Stress Urinary Incontinence
Do you leak urine when you cough or sneeze?
Do you leak urine when you lift heavy objects/grandchildren?
Do you leak urine when you stand?

How much urine comes out?

UTI
Ask about symptoms of UTIs
Ask about diagnosis with urine dipstick or MC+S
Ask about ABx treatment, how often, which ABx

Prolapse
Are you aware of a prolapse/lump/heaviness in the vagina?
Does the lump come to the entrance of the vagina?
Does the lump come out of the vagina?
Do you have to put the lump back in the vagina with your fingers to help empty your bladder or bowels?

  1. Ask if sexually active, if affects UI/UTI’s
  2. Ask about bowel function
  3. Ask about postmenopausal bleeding
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10
Q

What is PID (pelvic inflammatory disease)?

A
  • Infection of the upper female genital tract (uterus, fallopian tubes, ovaries)
  • Usually results from ascending infection from the cervix
  • Serious and common complication of STIs (esp. chlamydia + gonorrhoea)

• Pelvic infections are often polymicrobial
o Genital mycoplasmas, endogenous vaginal flora (actnomycetes), aerobic streptococci
o M. TB + STIs e.g. Chlamydia trachomatis (most common), Neisseria gonorrhoea
• Most common STI – chlamydia
• Incidence of gonorrhoea is increasing – it is becoming a more common cause of PID
• Other organisms – those associated with bacterial vaginosis (Gardnerella vaginalis, mycoplasma hominis, mobiluncus)

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11
Q

RF for PID (pelvic inflammatory disease)?

A
  • RF for acquiring STIs
  • IUCD inserted in the previous 20 days
  • Termination of pregnancy
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12
Q

Complications of PID pelvic inflammatory disease

A
  • PID can damage the fallopian tubes and tissues in and near the uterus and ovaries
  • Delaying treatment by 2-3 days increases the risk of infertility
  • Untreated PID- infertility, ectopic pregnancy, tubo-ovarian abscess formation, chronic pelvic pain, perihepatitis (Fitz-Hugh Curtis syndrome) – RUQ pain, reactive arthritis

• In pregnancy - in preterm delivery, maternal and fetal morbidity

• Neonatal
o Perinatal transmission of C. trachomatis or N. gonorrhoea can cause ophthalmia neonatorum
o Chlamydial pneumonitis

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13
Q

DDx of PID pelvic inflammatory disease

A
  • Ectopic pregnancy
  • Appendicitis (N+V seen more often than PID),
  • Other causes of dyspareunia – e.g. endometriosis
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14
Q

Bartholin’s cysts definition and aetiology

A
  • Pair of glands, each about the size of a pea, whose secretions maintain the moisture of the vestibular surface of the vagina
  • Damage or infection of the ostium of the duct causes blockage + a cyst occurs that may become infected

Causative organisms
• Aerobic organisms are the usual pathogens – E. coli is the most common
• STIs can also be cultured
• Staphylococcus or GBS

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15
Q

Define endometriosis

A

• Chronic oestrogen-dependent condition
• Characterised by growth of endometrial tissue in sites other than the uterine cavity
o Most commonly the pelvic cavity (incl. the ovaries)
o The uterosacral ligaments
o The pouch of Douglas
o The rectosigmoid colon
o The bladder
o The distal ureter
o Rarer sites – umbilicus, scar sites (following C-section, laparoscopy), pleura, pericardium, CNS

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16
Q

Define adenomyosis

A

• Adenomyosis = invasion of myometrium (muscular outer layer of the uterus) by endometrial tissue
o Age 40-50
o Heavy menstrual bleeding
o Dysmenorrhoea
o Dyspareunia
o Sometimes bowel/bladder change due to bulk effect (pressure symptoms)
o Diffusely large uterus on bimanual examination
o Pelvic USS – enlarge uterus, globular or asymmetrical, myometrial cysts, Venetian blind sign

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17
Q

Endometriosis aetiology and risk factors

A
  • RETROGRADE MENSTRUATION
  • Lymphatic/circulatory dissemination
  • Metaplasia – cells in the pelvic + abdominal area change into endometrial-type cells
  • Genetic predisposition
  • Environmental factors
  • Immune dysfunction

Risk factors (remember endometriosis is a chronic oestrogen dependent condition)
• Obstruction to vaginal outflow – hydrocolpos, female genital mutilation, defects in uterus or fallopian tubes
• Early menarche/late menopause
• Late first sexual encounter
• Delayed childbearing
• Nulliparity
• Genetic factors – first degree relatives
• Other RF – white ethnicity, low BMI, smoking

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18
Q

Complications of endometriosis + differentia diagnosis

A
Complications
•	Increased risk of 
   clear cell of the endometrium
   low grade serous ovarian cancer 
   endometroid invasive carcinoma of the ovary

• Infertility
o Moderate to severe endometriosis can cause tubal damage
o Lesser degrees of endometriosis – subfertility, increased risk of ectopic pregnancy

  • Adhesion formation
  • Increased risk of IBD

Differential diagnosis
• PID, ectopic pregnancy, torsion of an ovarian cyst, primary dysmenorrhoea, uterine fibroids
• UTI
• Appendicitis, IBS

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19
Q

Define fibroids

A
  • Common benign monoclonal tumours of the smooth muscle cells of the uterine myometrium containing a large amount of extracellular matrix with disordered collagen
  • Multiple, single-cell seedlings distributed throughout the uterine wall - These then increase in size very slowly over many years, stimulated by oestrogens and progestogens  As fibroid grows, central areas may not receive adequate blood supply  benign degeneration often followed by calcification

• Hormone dependent
o Contain lots of oestrogen and progesterone receptors
o Enlarge in pregnancy (oestrogen)
o Shrink in menopause

• Classified according to their position within the uterine wall

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20
Q

Types of fibroids

A

https: //laparoscopysurgeries.com/wp-content/uploads/2018/07/Fibroids-Imagae-1200x900.jpg
https: //www.google.com/search?q=wall+of+uterus+histology&sxsrf=APq-WBvJrb3KRZ2w_Lo9cwnSYVjONDovlw:1648037806490&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjZvKCgm9z2AhUXhf0HHQ3eB74Q_AUoAXoECAEQAw&cshid=1648037871293217&biw=1280&bih=577&dpr=1.5#imgrc=qXrJI8OoAKyiXM

Submucosal (endometrum)
Intramural (myometrium) - most common type of fibroid
Subserosal (perimetrium)

The uterus has three layers: mucosa (endometrium), muscularis (myometrium) and serosa/adventitia (perimetrium)

https://www.nhs.uk/conditions/fibroids/

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21
Q

Fibroid risk factors and protective factors

A

• Most common non-cancerous tumours in women of childbearing age

•	Risk – BONE
o	Black women
o	Obesity
o	Nulliparity
o	Expecting (pregnancy), early menarche
•	Protective factors – SECM
o	Smoking
o	Exercise
o	COCP
o	Multiparity

• Usually present between 30-50 years old

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22
Q

Fibroids ddx

A
  • Uterine Sarcoma – abdominal pain, abnormal bleeding
  • Dysfunctional uterine bleeding
  • Endometriosis
  • Endometrial polyps, endometrial cancer
  • Ovarian tumour
  • Tubo-ovarian abscess
  • Chronic PID
  • Pelvic masses
  • Pregnancy
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23
Q

Complications of fibroids

A
  • Iron deficiency anaemia
  • Bladder frequency, constipation ( increased pelvic pressure)
  • Ureteral obstruction – hydronephrosis
  • Hyaline degeneration (asymptomatic)
  • Torsion of pendunculated fibroid

• Infertility
o Narrowing of the isthmic portion of the fallopian tube
o Interference with implantation – submucosal fibroids
o Only caused by submucosal fibroids

•	In pregnancy 
o	Recurrent miscarriage
o	Foetal malpresentation
o	IUGR
o	Premature labour
o	PPH
o	Hydronephrosis
o	Red degeneration – fever, pain, vomiting (Mx – conservative – resolve in 4-7 days)
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24
Q

Cervical polyp definition

A
  • Normal epithelium of the cervix is endocervix (columnar) - transformation zone - ectocervix (squamous)
  • Benign neoplasms of the cervix
  • Smooth, fingerlike growths on the cervix that appear red or purple
  • Most common in women in their 40s and 50s who have had more than one child
  • Also common during pregnancy – may occur due to an increase in the hormone oestrogen

• Can be endocervical or ectocervical
o Endocervical – arise from the cervical glands, most common type of cervical polyp
 Overgrowth of endocervical columnar epithelium
 single/multiple, cherry red lesions, pedunculated lesion on a stalk of varying length
o Ectocervical – arise from the outer surface layer of cells on the cervix

  • Premenopausal women are more likely to have endocervical polyps
  • Postmenopausal women are more likely to have ectocervical polyps

• Formation may be linked to
o Increased levels of oestrogen
o Chronic inflammation of the cervix, vagina or uterus
o Clogged blood vessels

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25
Q

What is a cervical ectropion?

A
  • Normal epithelium of the cervix is endocervix (columnar) - transformation zone - ectocervix (squamous)
  • Ectropion = ectocervical migration of columnar epithelium (Speculum – red outer cervix due to shift of transformation zone)

• Linked to oestrogen exposure – pregnancy, COCP

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26
Q

What is an endometrial polyp?

A

• Proliferation of benign endometrial stroma and glandular elements, protruding into endometrial cavity

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27
Q

Difference between fibroids and polyps

A

Fibroids - benign proliferation of the myometrium

Polyps - benign proliferation of the endometrium

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28
Q

Complications of polyps

A

• Occasionally polyps may grow big enough to obstruct the external os – infertility

• Surgery to remove polyps
o Vagally stimulated bradycardia – may need treatment with atropine
o Haemorrhage – may require cautery for haemostasis

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29
Q

Define

Perimenopause
Menopause
Postmenopause
Menopausal women

A

Perimenopause – the time in which a woman has irregular cycles of ovulation + menstruation leading up to menopause and continuing until 12 months after her final period
Also known as menopausal transition or climacteric
Accompanied by an increased risk of new + recurrent depression

Menopause
a biological stage in a woman’s life that occurs when she stops menstruating and reaches the end of her natural reproductive life
defined as having occurred when a woman has not had a period for 12 consecutive months
Can only be defined with certainty after 12 months’ spontaneous amenorrhoea (need to ask about this specifically in history to establish if women are menopausal or not)

Postmenopause – the time after menopause has occurred starting when a woman has not had a period for 12 consecutive months

Menopausal women – includes women in perimenopause and postmenopause

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30
Q

Define

Early menopause
Premature ovarian insufficiency (POI)

A

Early menopause – women who go through menopause between 40-45 years

Premature ovarian insufficiency (POI) – women under 40
Syndrome characterised by amenorrhoea, elevated gonadotrophins and oestrogen deficiency

NICE POI definition – diagnose POI in women aged under 40 years based on
Menopausal symptoms incl. no or infrequent periods (taking into account whether the woman has a uterus)
Elevated FSH levels on 2 blood samples taken 4-6 weeks apart

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31
Q

How can menopause be induced?

A
•	Menopause can also be induced by 
surgical removal of the ovaries 
iatrogenic ablation of ovarian function 
    by chemotherapy, radiotherapy 
    treatment with GnRH analogues
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32
Q

Physiological changes during menopause

A
  • The changes associated with menopause occur when the ovaries stop producing maturing eggs and secreting oestrogen and progesterone
  • Natural phenomenon which occurs in all women when their finite number of ovarian follicles becomes depleted
  • As a result, oestrogen and progesterone hormone levels fall
  • LH + FSH increase in response
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33
Q

Menopause associated diseases

A

• CVD – coronary artery disease, stroke, PAD

• Osteoporosis
o Loss of ovarian oestrogens associated with declines in BMD
o Low oesteogen levels associated with an increased risk of both hip + vertebral fractures in older women – this association is independent of age + body weight

• Urogenital atrophy

• Redistribution of body fat
o Tends to be distributed around the abdomen with age

• AD

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34
Q

Risks in early menopausal women

A

All women with an early menopause have an increased risk of osteoporosis, cardiovascular disease and dementia if they are not given HRT appropriately

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35
Q

RF for atrophic vaginitis

A
  • Natural menopause or oophorectomy
  • Anti-oestrogenic treatments e.g. tamoxifen, aromatase inhibitors
  • Radiotherapy or chemotherapy
  • Can also occur postpartum or with breast feeding due to reduced oestrogen levels
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36
Q

DDx for atrophic vaginitis

A

• Genital infections
o Bacterial vaginosis, trichomonas, candidiasis, endometritis
o May co-exist (atrophic vaginitis predisposes the vagina to bacterial infection)
o Trichomonas + bacterial vaginosis give a more alkaline result on pH testing

  • Uncontrolled DM may cause vaginal or urinary symptoms
  • Local irritation due to soap, panty liners, spermicides, condoms, biological washing powder, tight fitting clothes
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37
Q

What is Asherman’s syndrome?

A
  • Cervical stenosis and cervical or intrauterine adhesions/scarring or synechiae
  • Bonding of scar tissue that lines the walls of the uterus, this decreases the volume of the uterine cavity
  • In many cases the front and back walls of the uterus stick to one another, in other cases adhesions occur in a small portion of the uterus
  • The extent of the adhesions defines whether a case is mild, moderate or severe
  • Adhesions can be thin or thick, spotty in location or confluent

• Synonyms
o Intrauterine synechiae
o Uterine synechiae
o Intrauterine adhesions (IUA)

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38
Q

Asherman’s syndrome complications

A
  • Infertility
  • Recurrent miscarriage
  • Menstrual disturbance
  • Abnormal placentation
  • IUGR
  • Placenta accreta
  • Hematometra

• Endometriosis
o Either due to complete destruction of the uterine lining or by obstruction of the cervix or lower portion of the uterus due to adhesions – menses are either retained in the uterus (hematometra) or flow into the abdominal cavity causing endometriosis

• Endometrial cancer
o Risk is not higher than in the general population
o Patients might miss warning signs (excessive uterine bleeding)
o Therefore pelvic ultrasound is a routine part of their annual gynaecologic visit

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39
Q

Asherman’s syndrome ddx

A

• Primary amenorrhoea
o Absence of menstruation by the age of 15 or 3 years after the first signs of breast development
o Abnormal GnRH level
o Incomplete/underdeveloped external genitalia and breasts, ovarian deficiency, underactive pituitary

• Endometriosis
o Inability to shed the tissue build-up of the uterus before menstruation
o Lower back or thigh pain, excessive pain during menstrual cycle
o Can cause Asherman’s syndrome

• PID
o Infection of the fallopian tubes, cervix, uterus, ovaries
o Transmitted by sexual intercourse, childbirth, abortion

• PCOS
o Absent/abnormal menstruation
o Sterility
o Mild signs of secondary sex characteristics – hirsutism, acne
o Obesity
o 3 diagnostic criteria – hyperandrogenism, ovulatory dysfunction, polycystic ovaries on US

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40
Q

List RF for Asherman’s syndrome

A

• Trauma to the endometrial lining forms adhesions
o D+C - missed/incomplete miscarriage, RPC, elective abortion
o Sometimes also after other pelvic surgeries – C-section, surgery to remove fibroids/polyps

• Factors that trigger inflammation in the uterus
o Endometriosis
o Sporadic inflammation of the uterus

• Infection
o Genital TB
o Schistosomiasis

• Can affect
o 1.5% of women undergoing hysterosalpingogram (HSG)
o 5-39% of women with recurrent miscarriage
o Up to 40% of patients who have undergone D+C for RCT (retained products of conception) of incomplete abortion

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41
Q

Define early vs late miscarriage

How common is it?

A

Loss of pregnancy before 24 weeks of gestation
Early - <12 weeks
Late – 13-24 weeks

Bleeding after 24 weeks is antepartum haemorrhage
Common – 1 in 5 pregnancies
• 85% of spontaneous miscarriages occur in the 1st trimester

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42
Q

What are the 5 different types of miscarriage?

A
Threatened
Inevitable
Missed (delayed/late) miscarriage 
Incomplete miscarriage
Complete miscarriage
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43
Q

Define recurrent miscarriage

A
  • > 3 consecutive miscarriages
  • No cause found in 50% (RFs – advancing maternal age, previous miscarriage)
  • Prognosis for future successful pregnancy is 75%
44
Q

What might be some of the reasons for recurrent miscarriage

A

o Structural abnormalities (fibroids, bicornuate or septate uteri (incomplete fusion of paramesonephric ducts))

o Cervical incompetence (late miscarriages - >13 weeks)

o Medical conditions (renal, diabetes, SLE)

o Clotting abnormalities (FV-L, AT-III deficiency, APLS)

45
Q

What might be some of the reasons for miscarriage

A

Fetal
• Abnormal fetal development
• Chromosomal abnormalities in the embryo – trisomy 16
• Genetically balanced parental translocation

Maternal 
•	Uterine abnormality
•	Incompetent cervix (2nd trimester)
•	PCOS
•	APL syndrome
•	Inherited thrombophilias
•	Infections 
•	Poorly controlled DM/thyroid disease 
•	More frequent in women aged >30 years + even more common in those aged >35 years ( risk of chromosomal abnormalities) 

Pregnancy
• Placental failure
• Multiple pregnancy

46
Q

RF for miscarriage

A
  • More frequent in women aged >30 years + even more common in those aged >35 years ( risk of chromosomal abnormalities)
  • Paternal age >45 years
  • Fertility problems, taking longer to conceive, previous miscarriage
  • Cervix/Uterine surgery or abnormalities e.g. incompetent cervix
  • Connective tissue disorders (SLE, APL- lupus anticoagulant/anticardiolipin antibody)
  • Low pre-pregnancy BMI, obsess
  • Uncontrolled DM
  • Smoking, alcohol, illicit drug use (cocaine)s, stressed, anxious, experiencing one or more stressful or traumatic events
47
Q

DDx for miscarriage

A
•	Ectopic pregnancy
o	Ectopic pregnancy – pain is usually great, may be unilateral and usually precedes the bleeding, cervical os is closed, bleeding is less heavy + darker, there is acute pain on manipulating the cervix (cervical excitation) 
•	Implantation bleed
•	Cervical polyp 
•	Cervical ectropion
•	Cervicitis/vaginitis
•	Neoplasia
•	Hydatiform mole
48
Q

Increased risk of further miscarriages after a miscarriage

A

• Increased risk of further miscarriages
o After 3 miscarriages, consider as recurrent spontaneous miscarriage
o 1 miscarriage – 85% chance next will be successful
o 2 miscarriages – 75% chance next will be successful
o 3 miscarriages (RMC) – 60% chance next will be successful

49
Q

What is a hydatidform mole?

A

a benign tumour of the trophoblastic tissue

50
Q

What is gestational trophoblastic disease?

A

• A group of disorders which range from molar pregnancies (also known as hydatidiform moles) to malignant conditions e.g. invasive mole, choriocarcinoma, and the very rare placental site trophoblastic tumour (PSTT) and epithelioid trophoblastic tumour (ETT)

o The diagnosis of complete mole, partial mole, atypical PSN, PSTT, ETT require histological confirmation

51
Q

What is gestational trophoblastic neoplasia?

A

persistence of GTD after primary treatment, mostly commonly defined as a persistent elevation of hCG

o The diagnosis of GTN does not require histological confirmation
o Rapidly metastasising (lung, vagina, brain, liver, kidney)

52
Q

Which are the premalignant gestational trophoblastic diseases?

A

Hydatidiform moles

-Complete hydatidiform mole
 All the genetic material comes from the father
 An empty oocyte lacking maternal genes is fertilised
 Commonly this arises from a single sperm duplicating within an empty ovum
 Less often an empty ovum is fertilised by 2 sperm
 There is no fetal tissue
 46 XY or 46XX

-Partial hydatidiform mole
 The trophoblast cells have three sets of chromosomes (triploid)
 2 sperm are believed to fertilise the ovum at the same time - one maternal set + 2 paternal sets of chromosomes
 There is usually evidence of fetal tissue or fetal blood cells in a partial molar pregnancy – an embryo may be present at the start

53
Q

Which are the malignant gestational trophoblastic diseases?

A

o Hydatidiform mole (complete or partial molar pregnancy) can progress to malignancy
 Complete mole –> invasive mole, choriocarcinoma
 Partial mole –> choriocarcinoma

o Invasive mole
 Develops from a complete mole – hydatidiform mole with invasion of myometrium, necrosis and haemorrhage
 Invades the myometrium

o Choriocarcinoma
 Most often follows a molar pregnancy
 Cytotrophoblast and syncytiotrophoblast without formed chorionic villi invade myometrium
 Can also follow a normal pregnancy, ectopic pregnancy or abortion
 Should always be considered when a patient has continued vaginal bleeding after the end of a pregnancy
 It has the ability to spread locally + metastasise

o Placental site trophoblastic tumour (PSTT)
 Most often follow a normal pregnancy but occasionally arise form molar pregnancies
 Intermediate trophoblasts infiltrate myometrium without causing destruction
 Contains GPL
 May also be metastatic
 Very rare

o Epithelioid trophoblastic tumour (ETT)

54
Q

Which pregnancies confer the biggest RF in the development of choriocarcinoma?

A

o Molar pregnancy > miscarriage > viable pregnancy > ectopic pregnancy

55
Q

Prognosis and complications of gestational trophoblastic disease

cure rate
risk of further molar pregnancy + type 
fertility after therapy for GTD
prognosis for hydatidiform moles
risk of relapse after chemo
menopause + chemo
care of woman in future pregnancies
A

• There is almost 100% cure rate for women with low-risk GTN which is the vast majority of cases
o For high-risk GTN (5% of cases), 5-year survival rates are lower but still up to 90%

  • The risk of a further molar pregnancy is low – >98% of women who become pregnant following a molar pregnancy will not have a further mole or be at increased risk of obstetric complications
  • If further molar pregnancy does occur, it will be of the same histological type in 68-80% of cases

• Fertility is retained in the majority  Further pregnancies are achieved in approximately 80% of women following treatment for GTN with either methotrexate alone or multi-agent chemotherapy

• Hydatidiform mole (complete or partial molar pregnancy) can progress to malignancy
o Complete mole  invasive mole, choriocarcinoma
o Partial mole  choriocarcinoma
• Risk of hydatidiform mole – can invade + damage surrounding tissue

  • Risk of relapse after chemotherapy is around 3% and mostly occurs in the first year
  • Women who receive combination agent chemotherapy for GTN are likely to have an earlier menopause

• Women should notify the screening centre at the end of any future pregnancy and hCG levels are measured 6-8 weeks after the end of the pregnancy to exclude recurrence
o Women who have a pregnancy following a previous molar pregnancy, which has not required treatment for GTN, do not need to send a post-pregnancy hCG sample
o Histological examination of placental tissue from any normal pregnancy, after a molar pregnancy, is not indicated

56
Q

Diagnosis of PCOS – Rotterdam criteria

A

2/3 following criteria are diagnostic of the condition, assuming other causes have been excluded
• Polycystic ovaries (12 or more peripheral follicles in each ovary (measuring 2-9 mm) or increased ovarian volume (>10cm))
• Oligo-ovulation or anovulation (>2 years)
• Clinical and/or biochemical signs of hyperandrogenism

57
Q

PCOS ddx

A

• Hypothyroidism
• Hyperprolactinaemia
• Cushing’s syndrome
• Acromegaly
• SE of medication
• CAH
o 17-hydroxyprogesterone, measured in the follicular phase, will be raised in CAH
• Androgen secreting ovarian or adrenal tumours
• Ovarian hyperthecosis
• If there are signs of virilisation, rapidly progressing hirsutism or high total testosterone level, then suspect one of the latter

58
Q

PCOS complications

A

• Metabolic disorders – T2DM
o Insulin resistance has been shown to worsen metabolic features + T2DM in PCOS
o Insulin resistance is independent of obesity but is further exacerbated by excess weight
o Earlier onset of hyperglycaemia + rapid progression to T2DM

• Infertility
o Insulin resistance has been shown to worsen reproductive features

• Endometrial cancer – Oligomenorrhoea + amenorrhoea - predispose to endometrial hyperplasia + endometrial cancer
o Recommend treatment with progestogens to induce a withdrawal bleed at least every 3-4 months using a COCP or cyclical medroxyprogesterone or Mirena coil
o There does not appear to be an association with PCOS + breast or ovarian cancer
o Intervals between menstruation of >3 months (= <4 periods each year) may be associated with endometrial hyperplasia (>7mm) and later cancer

• Increased CVD risk
o Women with PCOS has CV risk factors – Obesity, hyperandrogenism, hyperinsulinemia, hyperlipidaemia, hypertension, metabolic syndrome, diabetes
o Earlier onset of cardiovascular dysfunction (incl. endothelial dysfunction, arterial stiffness, plaques, coronary artery calcification)
o High androgen levels + low SHBG -  CVD risk
o T2DM is a major CVD RF

• Sleep apnoea

• Psychological disorders
o Depression, anxiety, eating disorders, sexual and relationship dysfunction
o Psychosexual problems – hirsutism, obesity, oligomenorrhoea, infertility may lead to feelings of being unattractive and loss of feminine identity
o Negative body image

•	Complications in pregnancy
o	Increased risk of gestational diabetes
o	Women diagnosed as having PCOS before pregnancy (e.g. those requiring ovulation induction for conception) should be screened for GDM at 24-28 weeks of gestation (by OGTT)
o	PTB
o	Pre-eclampsia
59
Q

Define subfertility

A
  • A woman of reproductive age that has not conceived after 12 months of regular, unprotected sexual intercourse or
  • A woman of reproductive age that has not conceived after 6 cycles of treatment of artificial insemination (with either partner or donor sperm)
60
Q

Epidemiology of subfertility

  • 19-26 y/o chance of getting pregnant
  • 80% of couples in the general population will conceive within one year if (3)
  • Of those who do not conceive in the first year…. how many in the second year
  • Sub-fertility affects.. how many couples
  • percentage of IVF treatment resulting in live birth
A

• 19-26 y/o = 98% chance of getting pregnant over 24 months (2/7 unprotected sexual intercourse)

• 80% of couples in the general population will conceive within one year if
o The woman is <40 years
o They do not use contraception
o They have regular sexual intercourse (every 2-3 days)

  • Of those who do not conceive in the first year, about half will do so in the second year
  • Sub-fertility affects 1 in 6 couples
  • Around 25% of IVF treatments result in a live birth
61
Q

Main causes of infertility in the UK

A
o	Male factors – 30%
o	Ovulatory disorders – 25%
o	Unexplained – 25%
o	Tubal damage – 20%
o	Uterine or peritoneal disorders – 10%
62
Q

Disorders of ovulation

List the 3 groups

A

o Group I – hypothalamic pituitary failure (hypothalamic amenorrhoea or hypogonadotropic hypogonadism)
 Hypogonadotropic hypogonadism
 Low gonadotrophins, low oestrogen
 Low weight, excessive exercise, Kallman’s syndrome, Sheehan’s syndrome

o Group II – hypothalamic-pituitary-ovarian dysfunction
 Normogonadotrophic normogonadism
 Normal gonadotrophins, normal oestrogen
 PCOS

o Group III – ovarian failure
 Hypergonadotrophic hypogonadism
 High gonadotrophins, low oestrogen
 Premature ovarian insufficiency (amenorrhoea of 4 months, <40 y/o, FSH high on 2 consecutive tests)

63
Q

List other causes of disorders of ovulation that do not fall into those 3 categories

A

o Other causes
 Pituitary tumours - low LH or FSH, panhypopituitarism = Simmond’s disease

 Sheehan’s disease – pituitary infarction following PPH

 Hyperprolactinaemia – may present with galactorrhoea or amenorrhoea, inhibited by dopamine, stimulated by TSH, therefore there is high prolactin if T4 is low

 Other endocrinological disorders e.g. Cushing’s disease, primary hypothyroidism

 CKD, drugs

 Chromosomal disorders – may result in inadequate ovarian function + usually primary amenorrhoea
• Turner’s syndrome – 45 XO – phenotypic female
• Klinefelter’s syndrome – 47 XXY – phenotypic male

 Premature ovarian failure or premature menopause – secondary amenorrhoea

64
Q

List some problems of the tubes, uterus or cervix that may be causing subfertility

A

• Blocked tubes – infections, adhesions, endometriosis

•	Infection 
Damage to the fallopian tubes
Damage to the uterus 
o	PID
	STIs – chlamydia, gonorrhoea
o	Severe pelvic infection due to infection of RPC following illegal abortion, legal termination or miscarriage 
o	Postpartum infection 
o	Infection may be less direct e.g. spread from appendicitis even without over peritonitis 
o	Asherman’s syndrome 

• Inflammation
o Endometriosis – inflammation, adhesion, distortion in the pelvis - tubal infertility (there is evidence for improvement in conception rates following surgery but not medical treatment of endometriosis)

• Female sterilisation
o Disruption of the tube – results of attempted reversal are poor

• Structural
o Deformity of the uterus – may be more likely to cause recurrent abortion rather than failure to conceive
 Septum
 Bicornuate uterus
o Fibroids
 Might cause significant distortion of the uterine cavity
o Cervix may be shortened + damaged by a cone biopsy
o Salpingectomy

• Barrier
o Problems of cervical mucus, incl. hostility to sperm

65
Q

List some male causes of infertility

A
  • Hypothalamic/pituitary (hypothalamic hypogonadism, hyperprolactinaemia)
  • Functional (erectile dysfunction)
  • Pharmacological (recreational drugs)
  • Infectious (epididymitis, mumps orchitis)
  • Lifestyle (ETOH, smoking, BMI >30)
  • Genetic (Klinefelter’s XXY, Kallman’s, testicular feminisation)
66
Q

What to ask about in an infertility case history

A

• Ask about general health – weight, smoking, drinking, recreational drugs

• Ask about sexual history
o Frequency of coitus (ideally 2-3x/7)
o Any prolonged/recurrent absences of one of the partners
o Potential physical problems – inadequate penetration or dyspareunia

• PMH
o Previous treatment for malignancy – chemo (sterility), radiotherapy and surgery (may be relevant if they involved the pelvic region)
o Systemic disease (may interfere with the HPA axis)
 Autoimmune disease – rheumatoid disease, SLE, APL
 CKD
 Poorly controlled DM
 Anorexia nervosa – can cause anovulation amenorrhoea

• Medication and drug history
o Phenothiazines + older typical antipsychotics + metoclopramide – can increase levels of prolactin
o NSAID use is associate with luteinised unruptured follicles
o Immunosuppressants

67
Q

Criteria for referral for IVF

A

• Full cycle of IVF (+/- ICSI) = 1 episode of ovarian stimulation + the transfer of any resultant fresh/frozen embryo

• In women <40 y/o who have not conceived after 2 years of regular unprotected intercourse or 12 cycles of artificial insemination (where >6 are by intrauterine insemination)
o Offer 3 full cycles of IVF +/- ICSI (intracytoplasmic sperm injection)
o Those women who reach 40 years during treatment should not be offered further cycles
o If the woman reaches the age of 40 during treatment, complete the current full cycle but do not offer further full cycles

• In women 40-42 y/o who have not conceived after 2 years of regular unprotected intercourse or 12 cycles of artificial insemination (where >6 are by intrauterine insemination) – offer 1 full cycle of IVF (+/- ICSI) provided the following 3 criteria are fulfilled
o They have never previously had IVF
o There is no evidence of low ovarian reserve
o There has been a discussion of the additional implication of IVF + pregnancy at this age

• When IVF is used and a top-quality blastocyst is available, a single embryo transfer is recommended to minimise the numbers and associated risks of a multiple pregnancy

68
Q

prediction of IVF success

A

Prediction of IVF success

  • Female age – chance of a live birth following IVF treatment falls with rising female age
  • Number of previous treatment cycles – overall chance of live birth falls as the number of unsuccessful cycles increases
  • Previous pregnancy history - IVF is more effective in women who have previously been pregnant and/or had a live birth
  • BMI – should be in the range 19-30
  • Lifestyle factors – smoking, alcohol, coffee
69
Q

Risk of malignancy with

  • Ovulation induction/ ovarian stimulation
  • IVF +/- ICSI
A

• Ovulation induction/ ovarian stimulation
o No direct association bn these treatments and invasive cancer

• IVF +/- ICSI – small increased risk of borderline ovarian tumours

70
Q

Causes of azoospermia

A

o Most commonly due to varicocele

o Non-obstructive azoospermia – many cases - in some cases testicular biopsy and testicular sperm extraction may be indicated

o Obstructive lesions of the seminal tract should be suspected in azoospermic or severely oligo-azoospermic patients with normal sized testes and normal endocrine results

71
Q

Define endometrial hyperplasia

A

Irregular proliferation of the endometrial glands with an increase in the gland: stroma ratio when compared with proliferative endometrium

Endometrial hyperplasia can be split into 2 groups
• Hyperplasia without atypia
• Atypical hyperplasia

72
Q

RF for endometrial hyperplasia

A

• Tamoxifen
o Women taking tamoxifen for the treatment of breast cancer should be encouraged to report any abnormal vaginal bleeding or discharge promptly – increased risk of developing endometrial hyperplasia and cancer

• Aromatase inhibitors (e.g. anastrozole, exemestane, letrozole) – these medications are not known to increase the risk of endometrial hyperplasia + cancer

73
Q

Define endometrial cancer

A
  • Mainly an adenocarcinoma (80%)
  • Arises from the lining of the uterus
  • Is an oestrogen-dependent tumour
74
Q

Describe the 2 types of endometrial cancers

A

Type 1 - 85%
 SEM – secretory, endometrioid, mucinous carcinoma
 Oestrogen-dependent non-endometrioid carcinoma
 Younger patients
 Invade superficially
 Low grade
 Deeper invasion
 Higher grade
 >4 mutations must accumulate to cause this
• PTEN, PI3KCA, K-Ras, CTNNB1, FGFR2, P53

Type 2 - 15%
 SC – uterine papillary serous carcinoma (UPSC), clear cell carcinoma
 Oestrogen-independent non-endometrioid carcinoma
 Older patients
 Deeper invasion
 Higher grade
 Mutations associated
• Serous carcinoma – p53 (90%), PI3KCA (15%), Her-2 amplification
• Clear cell carcinoma PTEN, CTNNB1, Her-2 amplification

75
Q

List the RF for endometrial cancer

A

• Prolonged periods of unopposed oestrogen
o Medication
o Anovulatory cycles – where the corpus luteum does not mature and secrete progesterone

•	Endometrial hyperplasia 
•	Nulliparous 
•	Early menarche
•	Late menopause
•	Obesity – raises oestrogen levels ( adiposity   aromatase activity  leads to the conversion of androgens to oestrogens)
•	DM
•	PCOS
o	Primary infertility due to PCOS – RF for pre-menopausal endometrial caner
•	Tamoxifen 
•	Endometrial hyperplasia 
•	Radiotherapy 
•	Hx of HNPCC (Lynch syndrome) 
•	FHx of endometrial/breast/ovarian cancer/PTEN syndromes
76
Q

List protective factors for endometrial cancer

A

COCP

77
Q

endometrial cancer prognosis

A
  • Patients with stage IA disease without myometrial invasion – low risk of recurrence following surgical staging
  • Majority of women will be diagnosed with early-stage disease + are cured with surgery
  • Most recurrences occur within the first 3 years after treatment
  • Patients without metastatic disease – 5 year overall survival ranges from 74% to 91%
78
Q

Prognosis of

endometrial hyperplasia without atypia
atypical hyperplasia

A

• Risk of endometrial hyperplasia without atypia progressing to endometrial cancer is less than 5% over 20 years

• One third of women with atypical hyperplasia had concurrent endometrial cancer
o Complex hyperplasia with atypia – premalignant condition that often co-exists with low-grade endometrioid tumours of the endometrium – 25-50% risk of progression to endometrial cancer

79
Q

List the 3 types of ovarian tumours

A
  • Epithelial ovarian tumours
    • Most common type (90%)
    • Arises from the epithelial surface of the ovary
    • Post-menopausal Women >50
    • 95% malignant
    • Present late with bad prognosis
    • Endometriosis associated with clear cell > endometroid ovarian cancer
    • Endometroid ovarian carcinoma often found alongside endometroid endometrial carcinoma
  • Germ cell tumours
  • 5-10%
  • 95% benign
  • Derived from primitive germ cells of embryonic gonad
  • Bimodal <35 y/o > 65-70 y/o
  • Rapidly enlarging abdominal mass which causes considerable pain
  • Often undergo torsion
  • Often curable with high survival rates
  • Mature teratomas = benign, immature = malignant
  • Sex cord-stromal tumours
    • <5% of all ovarian tumours
    • All ages, most common in post-menopausal
    • Derive from connective tissue cells
80
Q

List the benign, malignant and variable subtypes of epithelial ovarian tumours

A

Benign
• Serous cystadenoma – most common benign epithelial tumour which bears a resemblance to the most common type of ovarian cancer (serous carcinoma) // cystic // bilateral in around 20% // 40-60 y/o // cyst lined by ciliate cells (similar to fallopian tube) // develop papillary growths which may be so prolific that the cyst appears solid
• Mucinous cystadenoma – second most common // 30-50 y/o (10%) // cystic // bilateral in around 5% // cyst lined by mucous-secreting epithelium (similar to endocervix) // filled with mucinous material // if it ruptures may cause pseudomyxoma peritonei // may be multilocular + may become enormous
• Clear cell – 40-80 y/o. Around 50% associated with endometriosis (6%) // solid or cystic **
• Endometroid – 50-70y/o. Around 5% associated with endometriosis (20%) // solid or cystic **
• Brenner (transitional cell) – solid // contain Walthard cell rests (benign cluster of epithelial cells), similar to transitional cell epithelium – typically have “coffee bean” nuclei // can display benign, borderline or proliferative and malignant variants // usually benign and mostly unilateral // may be associated with mucinous cystadenoma and cystic teratoma
• Undifferentiated (15%)

  • BRCA = serous tumours
  • *HNPCC = mucinous tumours, endometroid tumours

Malignant tumours
• Serous cystadenocarcinoma – often bilateral, psammoma bodies seen (collection of calcium)
• Mucinous cystadenocarcinoma – may be associated with pseudomyxoma peritonei

81
Q

List the benign, malignant and variable subtypes of germ cell tumours

A

Benign
• Dermoid/Teratoma – cystic // majority // most common benign growth <30 y/o // arise form primitive germ cells // usually lined with epithelial tissue and hence may contain skin appendages, hair, teeth // bilateral in 10-20% // asymptomatic // most likely to tort // Rokitansky protuberances = multiple or single white shiny masses that protrude out

Malignant
• Dysgerminoma – most common type // excellent prognosis for stage I // hisological appearance similar to that of testicular seminoma // associated with Turner’s syndrome // typically secrete hCG and LDH
• Endodermal sinus tumours
• Embryonal carcinoma
• Choriocarcinoma – part of the spectrum of gestational trophoblastic disease // increased hcg levels // early haematogenous spread to the lungs
• Yolk sac tumour – typically secrete AFP, Schiller-Duval bodies on histology are pathognomonic
• Sarcomas

82
Q

List the benign, malignant and variable subtypes of sex cord stromal tumours

A

Benignn
• Fibroma – no endocrine function // solid// associated with Meigs’ syndrome (triad of a) benign ovarian tumour, b) ascites, c) R sided pleural effusion that resolves after resection of tumour) // solid tumour consisting of bundles of spindle-shaped fibroblasts // typically occur around the menopause // classically causing a pulling sensation in the pelvis
• Fibrosarcoma
• Thecoma – solid// oestrogen

Variable
• Sertoli-Leydig tumours – androgens, variable // musicalizing effects // associated with Peutz-Jegher syndrome
• Granulosa cell tumour – oestrogen // precocious puberty in children, endometrial hyperplasia in adults // contains call-Exner bodies (small eosinophilic fluid-filled spaces between granulosa cells)

83
Q

Describe

metastatic ovarian tumours
endometriomas
Krukenberg tumours

A
  • Metastatic - Secondary tumours may arise from breast, GIT, haematopoietic system, uterus or cervix
  • Endometrioma (chocolate cyst, from endometriosis) – benign – if ruptures – can cause acute pain (rule out ectopic from LMP)
  • Krukenberg tumour – malignant – bilateral, metastases from breast/GIT – mucin-secreting signet-ring cell adenocarcinoma
84
Q

RF for ovarian cancer

A

• Increasing age
• Lifestyle – smoking, obesity, lack of exercise, talcum powder use, occupational exposure to asbestos
• Hormonal factors – anything that increases the number of ovulations
o Hx of infertility or use of fertility drugs e.g. clomifene
o Nullips more likely than >P3
o Early menarche + late menopause
o HRT
 4% of ovarian cancer cases in the UK are caused by postmenopausal hormones
 Ovarian cancer risk is 37% higher in current or recent users of HRT
 This association may be limited to serous and endometrioid ovarian tumours
• Genetic factors
o FHx of ovarian cancer
o BRCA1 or BRCA 2 genes
o MLH1, MSH2
o Other genetic associations – p53 (serous), BRAF, K-ras
o Dermoid cysts can run in families
• PMH
o PMH of ovarian/breast/bowel cancer
o Hx of endometriosis – link between ovarian endometriosis and clear-cell ovarian cancer (?linked mutation of the ARID1A gene)

85
Q

Protective factors for ovarian cancer

A
•	Protective factors
o	Childbearing
o	Breastfeeding
o	Early menopause
o	COCP
86
Q

Which women are considered high risk for ovarian cancer

A

o Known carrier of BRCA1, BRCA2 or any other known relevant cancer gene mutations
o 1st or 2nd degree relative who carries a known relevant gene mutation
o 2 x 1st degree relatives have ovarian cancer
o One family member with both breast and ovarian cancer
o A family member who has ovarian cancer at any age + is a 1st degree relative of someone who developed breast cancer <50 y/o or 2 who developed it <60 y/o
o >3 family members with colon cancer
o 2 family members with colon cancer + 1 with stomach/ovarian/endometrial/small bowel/urinary tract cancer in 2 generations (must be diagnosed <50 y/o + should be first-degree relatives of each other)

87
Q

Most important prognostic factor of ovarian cancer

A
  • Most important prognostic factor – no residual disease following laparotomy
  • Complete clearance of all visible disease at the time of surgery is associated with better prognosis
88
Q

Ddx of ovarian cancer

A

• Other causes for a mass
o Non-neoplastic functional cysts – follicle cyst, corpus luteum cyst, theca lutein cyst
o Benign ovarian tumour or cyst
o Fibroids
o Primary peritoneal carcinoma
o Other pelvic malignancy (uterus, cervix, bladder, rectum)
o Secondary carcinoma – breast, GIT, lymphoma, pelvic organ tumours – all metastasize to the ovary
• Endometriosis
• Other causes of ascites e.g. cirrhosis
• Other causes of altered bowel habit/abdominal pain/bloating
o IBS
o Constipation
o Coeliac disease
o IBD – Crohn’s or UC
o Gastroenteritis
o Diverticular disease
o PID

89
Q

What is a functional cyst?

A

benign

o A sac that forms on the surface of a woman’s ovary during ovulation
o It holds a maturing egg
o It usually goes away after the eff is released
o If the egg is not released/or if the sac closes up after the egg is released – the sac can swell up with fluid
o To be classified as a functional cyst, the mass must reach a diameter of at least 3 cm

90
Q

Which are the 3 functional cysts?

A

• Follicular cyst
o Commonest type of ovarian cyst
o Due to non-rupture of the dominant Graafian follicle or failure of atresia in a non-dominant follicle
o Lined by Granulosa cells
o May occasionally continue to produce oestrogen and lead to endometrial hyperplasia
o Commonly regress after several menstrual cycles

• Corpus luteum cyst
o During menstrual cycle if pregnancy doesn’t occur the corpus luteum breaks down and disappears
o If this doesn’t occur the corpus luteum may fill with blood or fluid and form a corpus luteal cyst
o Lined by luteal cells
o More likely to present with intraperitoneal bleeding than follicular cysts

• Theca lutein cyst
o Bilateral functional ovarian cyst
o Filled with clear, straw-coloured fluid
o Results from exaggerated physiological stimulation
o Associated with markedly elevated levels of bHCG
o Associated with gestational trophoblastic disease, DM, alloimmunisation to Rh-D, multiple gestations
o Resolve after pregnancy

91
Q

Ovarian cyst complication

of the cyst
of the surgery

A

• Of the cyst
o Torsion
 >5cm
 Most common in dermoid
o Rupture
 Most common with functional cysts
 Conservative (pain relief) + watchful waiting
 Laparoscopy +/- cautery (if evidence of active bleeding)
o Infarction
o Haemorrhage
 More common for tumours of the R ovary
o Malignant change
• Infertility
o Can occur as a result of ovarian tumours or their treatment
o Surgery does not seem to improve pregnancy rates
• Surgery
o Chemical peritonitis due to spillage of dermoid cyst contents – 0.2%
 Peritoneal lavage of the peritoneal cavity using large amounts of warmed fluid
o Oophorectomy
 Can be either an expected or unexpected part of the procedure

92
Q

Prognosis for
ovarian cysts
ovarian torsion
ovarian malignancy

A

• Most small ovarian cysts in premenopausal women will resolve spontaneously
• Ovarian torsion
o If operated within 6 hours of onset of symptoms – tissue will remain viable
• Mean survival time for women with ovarian malignancy is significantly improved when managed within a specialised gynaecological oncology service – early dx + referral is important

93
Q

Define lichen sclerosus

Incidence

A

• Chronic inflammatory dermatosis
• Usually affect the skin of the
o Anogenital region in women
• Occurs less commonly in extragenital areas
• Does not cause any systemic disease outside the skin

Two peaks of incidence
o Prepubertal girls <10 y/o
o Postmenopausal women >60 y/o

94
Q

Lichen sclerosus prognosis

A
  • Chronic condition in most females
  • Symptom control is often successful
  • Scarring is not reversible with pharmacological treatment
  • Symptom remission with potent steroids – 98% in compliant vs 75% of non-compliant women
  • 75% of girls who develop LS prepubertally will continue to need maintenance treatment after menarche
  • Lifetime risk of SCC is 4-5%
  • In some cases LS recurs
  • Women with uncomplicated lichen sclerosus do not require routine hospital-based follow-up but should be informed of the risks of invasion
95
Q

Lichen sclerosus ddx

A

• Children
o Sexual abuse

  • Vitiligo
  • Candida infection
  • Localised scleroderma (morphoea)
  • Lichen planus
  • Leucoplakia
  • Vulval intraepithelial neoplasia
  • Bowen’s disease (SCC)
  • GvH disease
96
Q

WHO FGM classification

A

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

Type 2 - partial or total removal of the clitoris and the labia minora, +/- labial majora excision (excision)

Type 3 - Narrowing of the vaginal orifice with creation of a covering seal by cutting and appositioning the labia minora and/or labia majora +/- excision of the citoris (infibulation)

Type 4 - all other harmful procedures to the female genitalia for non-medical purposes e.g. pricking, piercing, incising, scraping, cauterization

97
Q

Safeguarding in FGM for girls <18

A
  • It is an offense for those with parental responsibility to fail to protect a girl from the risk of FGM
  • If FGM is confirmed in a girl <18 y/o (either on examination or bc the patient/parent says it has been done) reporting to the police is mandatory + this must be within 1 month of confirmation

• (a person found guilty of an offence under the Act is liable for a prison sentence of up to 14 years)

98
Q

FGM complications

A

• Women with type 3 FGM – introitus may be too narrow for childbirth and the tissues that have sealed together need to be separated (deinfibulation)

• Short term complications
o Haemorrhage
o Urinary retention
o Genital swelling

• Long term complications
o Urinary tract complications – poor urinary flow, urinary obstruction, stasis, recurrent UTI, urinary or vaginal calculi
o Menstrual difficulties – haematocolpos
o Dyspareunia, pareunia, impaired sexual function
o Genital infection + PID - increased risk of BV, HSV2
o Infertility
o HIV HBV
o Obstetric complications – increased risk of prolonged labour, PPH, perineal trauma, CS, neonatal resuscitation, risk of stillbirth, early neonatal death, fear of childbirth, difficulty in IP monitoring (incl. application of fetal scalp electrodes and fetal blood sampling), difficulty in catheterisation during labour, wound infection, retention of lochia

99
Q

Interaction between lamotrigine and oestrogen

A

• Oestrogen-based contraceptive
o Can result in a sig. reduction of lamotrigine levels
o Can lead to loss of seizure control
o Women taking lamotrigine monotherapy and oestrogen-containing contraceptives should be informed of the potential  in seizures due to fall in the levels of lamotrigine

100
Q

• Enzyme-inducing AEDs

A
•	Enzyme-inducing AEDs
o	Carbamazepine
o	Phenytoin
o	Phenobarbital
o	Primidone
o	Oxcarbazepine
o	Topiramate
o	Eliscarbazepine
101
Q

• Non-enzyme inducing AEDs

A
•	Non-enzyme inducing AEDs SLGVTP
o	Sodium valproate
o	Levetiracetam
o	Gabapentin
o	Vigabatrin
o	Tiagabine
o	Pregabalin
102
Q

Things to discuss with women with epilepsy during adolescence/childbearing potential

A

confirm dx
take menstrual hx
possible effect of monthly cycle on seizures
effect of AEDs on monthly cycle (possibility of developing PCOS)
sexual activity + contraception
enzyme inducing AEDs interaction with COCP + depot injection
seizure risks (alcohol/sleep/recreational drugs)
cosmetic SE
cognitive SE
return for pre-pregnancy counselling

103
Q

When can women self-refer to the early pregnancy unit for assessment?

A
  • Recurrent miscarriage (>3)
  • Previous ectopic
  • Previous molar
  • All other women with pain and/or bleeding should be assessed by a HCP (GP, A+E dr, midwife, nurse) before referral to an EPAU
104
Q

List some other PSE – potential sensitising events

A

• Invasive fetal procedures
o Intrauterine transfusion/surgery/insertion of shunts/laser
o Intra-operative cell salvage
• Medical intervention
o Chorionic villus sampling
o Amniocentesis
o ECV
• Gynae
o Ectopic pregnancy
o TOP (any method, any GA), IUD, stillbirth, molar pregnancy
o Miscarriage, Threatened miscarriage
o Evacuation of molar pregnancy
• APH/PV bleed in pregnancy (>12w, prolonged and <12w)
• Abdominal trauma (sharp/blunt, open/closed)
• Placental trauma
• Previous blood transfusion (rare if in UK)
• Delivery
o Traumatic deliveries
o Sickle cell disease
o CS
o Instrumental
o Normal delivery of a Rh+Ve baby
• Over 99% have an FMH of <4ml at deliver – Large FMH RF
o Traumatic deliveries incl. C-section
o Manual removal of the placenta
o Stillbirths + IUD
o Abdominal trauma during the 3rd trimester (26-37w)

105
Q

the abortion act 1967

A

• pregnancy should not exceed its 24th week + the continuance of the pregnancy would involve risk, greater than if the pregnancy was terminated, of injury to the physical or mental health of the pregnant woman or any existing children of her family or
o the limit of 24th week does not apply in cases where it is necessary to save the life of the woman, there is evidence of extreme feral abnormality or there is risk of serious physical or mental injury to the woman
• that the termination is necessary to prevent grace permanent injury to the physical or mental health of the pregnant woman or
• that the continuance of the pregnancy would involve risk to the life of the pregnant woman, greater than if the pregnancy was terminated or
• that there is substantial risk that if the child were born it would suffer from such physical or mental abnormalities as to be seriously handicapped

  • two registered medical practitioners must sign a legal document (in an emergency only one is needed) (they don’t both need to see the patient)
  • only a registered medical practitioner can perform an abortion, which must be in an NHS hospital or licensed premise
106
Q

Information + referral to women requesting an abortion

A

Woman requesting TOP
• SENIOR INPUT
• Refer to Marie Stopes UK (<10wks) or EPAU
• Women should be able to self-refer to abortion services, without having to talk to the GP or another HCP
• Ensure minimal delay in the abortion process, ideally
o Provide assessment within 1 week of the requires
o Provide TOP within 1 week of the assessment
• If woman wants to wait longer for an abortion, inform her of
o The legal limit for abortions, as stated in the Abortion Act
o That delaying the abortion will increase the risk of complications, although the overall risk is low
• Provide or refer women for support to make a decision if they want counselling

Providing information
• Provide patient leaflets + signpost to NHS choices
• Having an abortion is not associated with increased risk of infertility, breast cancer or mental health issues
• What it involves + what happens afterwards
• How much pain + bleeding to expect
• Ask if they want information on contraception
• Inform women who choose medical abortion
o That they might see the products of pregnancy as they are passed
o What the products of pregnancy will look like and whether there may be any movement
o Explain how to be sure that the pregnancy has ended
• Safety net
• Provide women with information about the different options for management and disposal of pregnancy remains
• If a woman is having an abortion because of fetal anomaly – explain to women that there might not be any physical signs of fetal anomaly

107
Q

Complications of TOP

A

o Complications of TOP:
 N, V, D due to PGs – occasional but transient
 Significant bleeding (1:1000)
 Genital tract infection (5-10%)
 Surgical TOP
• Uterine perforation (1-4:1000)
• Cervical trauma (1:1000)
• Failed TOP (2.3:1000)
• Haemorrhage
• Infection
 Medical TOP
• Uterine rupture – mid-trimester medical TOP (<1:1000)
• Failed TOP (1-14:1000)
 RPC
 Psychological sequelae – short-term anxiety, depressed mood
 Long-term regret + concern about future fertility
o Safety net: heavy bleeding (RPC), severe pain, smelly vaginal discharge, fever; ongoing signs of pregnancy (nausea or sore breasts), damage to cervix/ uterus/ etc. shoulder tip pain, mental health