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RANZCOG -Gynaecology 2024 Edward > Paediatric gynaecology and pelvic pain > Flashcards

Paediatric gynaecology and pelvic pain Flashcards

1
Q

Discuss ambiguous genitalia
-Incidence
-Causes - 3 groups

A
  1. Incidence: 1:4000. 50% secondary to CAH
  2. Causes
    Virilization of female karyotype (46XX)
    -CAH most common
    -Exposure to maternal androgens
    -Placental aromatase deficiency
    Under masculinisation of male karyotype 46XY
    -Partial gonad dysgenesis - Swyers
    -Complete or partial androgen insensitivity syndrome
    -Defect in testosterone biosynthesis
    -5-alpha reductase deficiency -converts testosterone to DHT (Important for peripheral virilization)
    Mosacism of XX and XY - true hermaphrodism - 20% of DSD
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2
Q

What investigations should be done to investigate disorders of sex development (ambiguous genitalia)
-4 groups

A
  1. FISH and Karyotype
  2. Bloods
    -Serum 17 hydroxyprogesterone levels (CAH)
    -Urea and electrolytes (CAH with salt wasting)
    -Synacthen test
    -Basal GnRH FSH and LH
    -Androgen levels - basal and HCG stimulated (Functioning sertoli cells produce testosterone with HCG stimulation)
    -AMH - low in dysgenic gonads
  3. USS - check for uterus and ovaries
  4. EUA to assess morphology of urogenital sinus
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3
Q

How should disorders of sex development (Ambiguous genitalia) be managed?
-Who should be involved
-What are the most important first steps
-What surgery should be considered

A
  1. Do not guess genitalia at birth
  2. MDM approach should be taken lead by paeds endocrinologist/ urologist/psychologist
  3. 50% of DSD caused by CAH. Needs to assess and correct salt wasting
  4. Do full work up for causes and then discuss with parents
  5. Consider gonadectomy when
    -non-virilized 46XY assigned to female. PAIS - 30% chance of malignancy - do straight away. CAIS 3% chance can wait.
  6. Consider feminising surgery with child input
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4
Q

Discuss Congenital Adrenal Hyperplasia
-Incidence
-Pathophysiology
-Presentation
-Management

A
  1. Incidence
    -Most common DSD 50%
    -1:10,000
  2. Pathophysiology
    -Caused by 21 hydroxylase deficiency in 90% of cases
    -Caused by shunting steroid production towards testosterone resulting in reduced costisol and aldosterone
  3. Presentation
    -Diagnosis is high levels of 17-OH hydroxyprogesterone. If equivocal then synachten test can be done
    -Causes varying degrees on virilisation due to androgen excess
    -May only be picked up at puberty. Hard to distinguish from PCOS
  4. Management
    -Hydrocortisone
    -Manage salt wasting early
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5
Q

Discuss androgen insensitivity
-Types
-Incidence
-Pathophysiology
-Presentation
-Management

A
  1. Incidence - 1:40-60,000 CAIS>PAIS
  2. Complete androgen insensitivity and partial androgen insensitivity
  3. Pathophysiology
    -x-linked inheritance
    -Normal testicular function but abnormal androgen receptors
    -Testes produce AMH causing regression of Mullarian structures so absent fallopian tubes, uterus, and upper 2/3rds of vagina.
  4. Presentation
    CAIS - normal female appearance but short vagina. Picked up with primary amenorrhoea usually
    PAIS - Ambiguous genitalia with varying virilisation
    Dx with rise in testosterone after HCG stimulation test
  5. Management
    -Disclose 46XY karyotype and implications for reproduction and menstruation (can’t)
    -CAIS - 3% chance of gonads causing malignancy - consider removing after puberty.
    -Estrogen replacement, vaginal expansion or dilators
    -PAIS - 30% chance of malignancy - remove immediately
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6
Q

Discuss 5 alpha reductase deficiency
-Incidence
-Pathophysiology
-Presentation
-Management

A
  1. Rare
  2. Caused by lack of enzyme which converts testosterone to DHT (dihydrotestosterone).
    DHT important for peripheral virlisation
  3. Presentation
    Ambiguous or female genitalia. Virlisation seen at puberty
    Dx: Normal testosterone, decreased DHT
  4. Gondectomy at puberty if raised female to avoid virilisation
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7
Q

Discuss the embryology of the genital tract

A
  1. The mullerian ducts for the female genitalia
  2. Production of testosterone + AMH from XY fetus suppresses mullerian duct formation
  3. Where testosterone + AMH is absent the female genitalia develop
  4. The mullerian ducts form the fallopian tubes uterus and upper vagina
  5. The external genitalia develop from the genital tubercule -clitoris, labioscrotal swelling - labia majora and urogenital folds - lower vagina
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8
Q

What are the Fraser Guidelines for competency of minors
-5 guidelines

A
  1. That she understands the advice
  2. That the health care professional cannot persuade her to inform her parents or are not allowed to inform them
  3. That she is already having sex or will start and do so without contraception if not provided
  4. That her physical +/- mental health is likely to suffer without contraception
  5. That it is in the best interests of the girl to have contraception without parental consent
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9
Q

Discuss congenital anomalies of the genital tract
-Incidence (4)
-Pathophysiology
-Classification

A
  1. Incidence
    -5% in unselected population
    -8% in infertile women
    -13% in women with miscarriage
    -25% in women with infertility and miscarriage
  2. Defect in Mullerian duct embryology
  3. Classification
    -ASRM classification system
    I - Hypoplasia/Agenesis
    II-IV - Unification defects
    V-VI - Canalisation defects
    VII - DES defects
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10
Q

Describe the ASRM classification of uterine congenital abnormalities
-7 types
-Definitions

A
  1. Bicorunate - external fundal indentation>1cm
  2. Didelphys - different levels of fusion.
  3. Septate - septum >1.5cm and <90 degrees (T shaped)
  4. Arcuate - septum <1cm and angle of indentation>90 degrees, big scoop
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11
Q

How does congenital genital abnormalities present (7)

A
  1. Primary amenorrhoea
    - +/- cyclical abdo pain
    -Seen with imperforate hymen, transvaginal septum, cervical agenesis, uterine agenesis
  2. Dysmenorrhoea
    -Seen with non-communicating or obstructed horn
  3. Dysparenunia
    -Seen with transverse septum
  4. Infertility
  5. Miscarriage
  6. Obstetric complications
  7. High rates of endometriosis - increased rate of retrograde menstruation
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12
Q

How should congenital genital tract abnormalities be investigated (5)
-Screening
-Dx

A
  1. USS or HSG for screening
  2. 3D TVUSS - diagnosis
  3. MRI - diagnosis
  4. Laparoscopy / hysteroscopy - traditional dx method
  5. Image kidneys as 50% in Type I+II have renal abnormalities
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13
Q

What are the reproductive implications for congenital genital anomalies and mechanisms?
-Antenatal (4)
-Intrapartum (2)
-Postpartum (1)

A
  1. Antenatal
    -Infertility, miscarriage, IUGR, PET/BP
    -Due to abnormal endometrium / placental insertion site / poor/disordered blood supply
  2. Intrapartum
    -Labour dystocia
    -Increased risk for CS
  3. Postpartum
    -PPH - due to incordinate uterine contractions + retained placenta
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14
Q

Discuss reproductive implications for congenital uterine anomalies by type
-Canalisation defects (5)
-Unification defects -Bicornuate and unicornuate (4)
-Unification defects - didelphys (3)

A
  1. Canalisation defects - septate and subseptate
    -Worst reproductive outcomes
    -Reduced conception rate OR 0.86
    -Increased first T miscarriage OR 2.9
    -Preterm birth - OR 2.14
    -Fetal malpresentation - OR 6.14
  2. Unification defects - bicornuate and unicornuate
    -No effect on fertility
    -Increased first T miscarriage OR 3.4
    -Increased preterm birth - OR 2.55
    -Fetal malpresentation - 5.89
  3. Unification defects - didelphys
    -No effect on fertility
    -Increased preterm birth - OR 3.58
    -Fetal malpresentation - OR 3.7
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15
Q

Discuss the management of congenital genital tract anomalies
-Imperforate hymen
-Vaginal septum
-Cervical agenesis
-Non-communicating horn with functional endometrium
-Bicornuate or didelphic uterus
-Septate or subseptate uterus

A
  1. Surgical resection of hymen
  2. Surgical resection of septum
  3. Anastamosis of uterus to vagina laparoscopically
  4. Excision of horn (open or laparoscopically)
  5. Strassman procedure - abdominal metroplasy - doesn’t improve reproductive outcomes
  6. Hysteroscopic resection of septum
    - unclear if improves reproductive outcomes
    -Do in early follicular phase for visualisation
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16
Q

Discuss Mayer-Rokitansky-Kuster-Hauser syndrome
-What it is
-Incidence
-Pathophysiology
-Presentation (4)
-Management (5)

A
  1. Absent or rudimentary uterus or bilateral rudimentary horns on either pelvic side wall, absence of upper 2/3rd of vagina.
  2. Incidence: 1: 4-6,000
  3. Agenesis or hypoplasia or Mullerian ducts. Multifactorial
  4. Presentation
    -Primary amenorrhoea 70%
    -Short vagina
    -Normal other secondary sexual characteristics
    -Associated with renal, auditory, cardiac and skeletal anomalies
  5. Management
    -Pyschological - sterile
    -Surrogacy for fertility
    -Enlarge vagina with dilators alone or post surgery
    -Enlarge vagina with surgery
    -McIndoe-Reed - vagina from buttock grafts
    -Bowel Vaginoplasy - made from sigmoid
    -Davydov - Lined with pelvic peritoneum
    -Vecchitti - synthetic olive placed on tension
    -Investigation and management of associated anomalies
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17
Q

Discuss precocious puberty
-Definition
-Incidence

A
  1. Definition
    -Onset of pubertal development before age 8
    -Onset of menarche before age 9
  2. Incidence
    -0.2-2%
    -Incidence is ethnicity dependent
    -Female to male ration 5:1
    -80% central causes; 20% peripheral causes
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18
Q

Discuss the causes of precocious puberty
1. Central causes
2. Peripheral causes

A
  1. Central causes - true precocious puberty - 80%
    -Gonadotrophic dependant
    -80% idiopathic
    -Brain tumours / cysts / trauma / congenital / hydrocephalus / radiation / Infiltrative
    -Specific gene mutations
  2. Peripheral causes
    -Exposure to exogenous sex steroids
    -Chronic primary hypothyroidism
    -Ovarian tumour - 2-5% (Mostly Granulosa cell tumours)
    -Feminising adrenal tumours
    -McCune Albright syndrome
    -G protein mutation leading to continual activation despite absence of hormonal stimulation.
    -Associated with cafe au lait spots and fibrous dysplasia
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19
Q

Discuss puberty
-Definition
-Timing of onset
-Order of anatomical changes
-Pathophysiology

A
  1. Definition
    -Time between childhood and adulthood when sexual and reproductive maturation occurs
  2. Average age of onset ethnicity dependent
    -12.3 Blacks, 12.8 Whites
    -Normal 8-12 yrs
  3. Boobs, pubes, spirt, squirt
    -Thelarche - 8-13
    -Adrenarche - 3 months after Thelarche
    -Growth - 9.5-14.5 yrs
    -Menarche 4th by 2-3 yrs post thelarche
  4. Pathophysiology
    -GnRH, FSH and LH low and HPO axis quiescent
    -Increase in pulsitile GnRH in frequnecy and amplitude.
    -Initially noctunal pulsations only
    -Increase GnRH leads to increase FSH and LH
    -Increase LH and FSH leads to steroidogenesis and folliculogenesis leads to increased estrogen
    -Increased estrogen leads to thelarche
    -GnRH pulsations during the day allow for ovulation and menarche
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21
Q

Discuss the management for precocious puberty
1. Who should manage
2. Central precocious puberty
3. Peripheral precocious puberty

A
  1. Treatment should be by paediatric endocrinologist
  2. Central precocious puberty
    -GnRH analogues - zoladex / Lucrin
    -Stops or reverses puberty
    -Continue until 10 or 11.
    -Give psychological support
    -Monitor yearly, growth, bine maturation
  3. Peripheral causes
    -Surgical tumour resection
    -McCune Albright syndrome
    -block action or biosynthesis of estrogen (Letrozole)
    -Remove exposure to exogenous sex steroids
    -Monitor growth and bone age annually
    -Stop treatment at normal age for puberty
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22
Q

Discuss delayed puberty
-Definition
-Incidence
-Causes - 2 groups

A
  1. Definition
    -Absence of secondary sexual characteristics by 13yrs
    -No menstruation by 16yrs or 3 yrs after breast development
  2. Incidence - 2.5% of population
  3. Causes:
    Hypogonadotrophic hypogonadism - No GnRH to stimulate FSH and LH
    -Constitutional delay (Esp if fam Hx)
    -Chronic illness
    -Functional - excess exercise, anorexia, stress
    -Kallmans Syndrome
    -Hydrocephalus, CNS tumour, infiltrative disease, pituitary adenoma, panhypo
    Hypergonadotrophic hypogonadism - Non functional gonads
    -POI
    -Turners syndrome
    -Swyers syndrome
    -Premature ovarian failure
    -Chemotherapy / radiotherapy
    -Autoimmune / infection / Toxins
    -Gonadal agenesis
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23
Q

Discuss the management of delayed puberty (8)

A
  1. Administer small doses of oestrogen with increasing amount until breast development complete / break through bleeding. Small doses doesn’t imped growth
  2. Add in progesterone (cyclical) - can use COCP
  3. If Hypogonadotrophic hypogonadism can use pulsatile GnRH
  4. In those with gonadal failure need estrogen and progesterone for bone and heart protection
  5. If patient has Y chromosome consider gonadectomy given malignancy risk
  6. Fertility requires oocyte donation
  7. Psychological support
  8. Improve nutritional intake and mineral supplementation
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24
Q

Discuss Kallman’s syndrome
1. Incidence
2. Pathophysiology
3. Presentation

A
  1. 1: 7500 females 7:1 ratio F:M
  2. Pathophysiology
    -Dysgensis of olfactory bulbs and GnRH neurons
    -X - linked
    -Mutation in Kal-1 gene
  3. Presentation
    -Anosmia and delayed puberty
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25
Q

Discuss Turners Syndrome
-Incidence
-Pathophysiology
-Presentation
-Management

A
  1. 1:2500
  2. Pathophysiology
    -45 XO female phenotype
  3. Presentation
    -Antenatal - cystic hygroma, IUGR, non0immune hydrops
    -Short stature, neck fold, low hair line, wide space nipples
    -Aortic coarctation, renal abnormalities, rudimentary ovaries
    -Delayed puberty (Menopausal level at puberty), insulin resistance, hypothyroid
  4. Management
    -Growth hormone for height
    -Induction of puberty with estradiol (Peripheral cause)
    -Long term HRT for heart and bone health
    -Fertility with egg donation
    -Breast implants if concerned
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26
Q

Discuss Swyers syndrome
-Incidence
-Pathophysiology
-Presentation
-Management

A
  1. Rare
  2. Pathophysiology
    -46XY with genetic mutation in SRY gene = no AMH or testosterone = female genitalia but gonadal dysgenesis
    -Uterus and cervix small as no estrogen from gonads
  3. Presentation:
    -Primary amenorrhoea
    -Small undeveloped breasts and sparce pubic hair (some androgens from adrenals)
  4. Management:
    -Induction of puberty
    -Gonadectomy as risk of malignancy 30%
    -Long term HRT
    -Child bearing with egg donation
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27
Q

Discuss genital tract tumours in adolescence
-Presentation (5)
-Risk factor (1)

A
  1. Presentation:
    -Vaginal discharge
    -Vaginal bleeding (esp malignant)
    -Abdominal mass (pelvis not developed)
    -Urinary symptoms
    -Premature sexual development if hormone secreting
  2. Risk factors:
    -DES exposure in utero for clear cell of CX and vagina
28
Q

Discuss the types of genital tract tumours seen in adolescence
1. Ovary
2. Uterus
3. Lower genital tract

A
  1. Ovary - 1% of all childhood tumour. 80% benign
    Germ cell tumours - most common
    -Teratoma benign and immature - malignant
    - Dysgerminoma
    - Endodermal sinus tumour
    - Embryonal carcinoma
    - Choriocarcinoma
    Epithelial
    -Clear cell
  2. Uterus - no tumours recorded
  3. Lower genital tract
    Benign
    -Gartners cyst (mesonephric duct cyst
    -Teratomas
    -Haemangiomas
    -Hymenal cysts
    -Benign granulomas of perineum
    -Condylomata acuminata
    Malignant
    -Botryoid sarcoma - most common if <3yrs
    -Endodermal carcinoma
    -Mesonephric carcinoma
    -Clear cell carcinoma
29
Q

Discuss management of tumours of the genital tract in adolescence
-Benign lower genital tract
-Benign ovarian
-Malignant ovarian
-Malignant vulval

A
  1. Benign lower genital tract
    -If Asx treatment not required
  2. Benign ovarian - aim for fertility sparing
    -cystectomy.
    -Do frozen section if unsure of dx
  3. Malignant ovarian
    -Germ cell - USO +/- Chemo
    -Epithelial - usually need TH + BSO
  4. Malignant vulva
    -Surgical resection if possible
    -Chemo
30
Q

Discuss vulvovaginitis in prepubertal girls
-Incidence
-Causes (4)
-Risk factors (4)
-Presentation (5)
-Management (4)

A
  1. Most common gynae problem in young girls
  2. Causes:
    -Infection - Most common mixed flora then GAS or haemophilis influenza. Thread worm possible. Candidiasis rare.
    -Forgein bodies
    -Dermatological conditions - contact dermatitis, lichen sclerosis, eczema
    -Non-specific irritants - bubble bath etc
  3. Increased risk in prepubesent girls because:
    -Thin vaginal mucosa
    -Alkaline pH
    -Smaller vulval fat pads and no pubic hair
    -Poor hygiene and proximity of vagina to anus
  4. Presentation
    -90% vaginal discharge
    -Itch
    -Discomfort - 80%
    -Dysuria
    -Bleeding = rare - think trauma/ cancer/ precocious puberty
  5. Management
    -Antibiotics if swab +
    -Hygiene advice
    -Avoid irritants
    -Anti-helminths if suspected
31
Q

Discuss labial adhesions
-Definition
-Incidence
-Pathophysiology
-Risk factors (2)
-Presentation (5)
-Management (3)

A
  1. Adhesions between labia minora
  2. Incidence - 1-3% of pre pubertal girls. Peak incidence 1-2yrs
  3. Pathophysiology unknown but likely raw thin labia agglutinate
  4. Risk factors: Nappies, poor hygiene
  5. Presentation
    -ASx if minor
    -If labia fused - dysuria, postmicturition dribble, recurrent UTI, retention
  6. Management
    -If minor and asx no treatment required. Spont resolution at puberty
    -Topical oestrogen cream for max 6/52
    -Surgical separation if recalcitrant to estrogen. Often reform
32
Q

Discuss adolescent sexual assault
-Legal requirements
-How to approach disclosure of sexual assault
-Hx
-Exam
-Ix
-Management
-FU

A
  1. No legal requirement for mandatory reporting
  2. Approach
    -Acknowledge and affirm disclosure
    -Act on any injury that requires immediate attention - PVB/Trauma
    -Maintain confidentiality/ Gain consent to proceed/ Assess competence
    -Offer support person
    -Offer MEDSAC - if unsure they can do forensic exam and decide later
    -If they decide yes for MEDSAC then:
    -NBM, Don’t pee/shower/keep same clothes.
    -If they decide no to MEDSAC then do Hx/Ex/Ix
  3. History:
    -Event info
    -What they have done since, brushed teeth, shower etc
    -Risk of pregnancy (menstrual hx, contraception)
    -STI
    -Social supports and safety
    -General Hx as per usual
  4. Exam:
    -Top to toe
    -Speculum not required unless PVB / pain of if cx specimen required
  5. Investigations
    -STI screen swabs and bloods
    -Blood and urine toxicology
  6. Management
    -Manage physical injuries
    -Treat STI’s
    -Given HIV prophylaxis if high risk
    -ECP if required
    -ACC sensitive claims
  7. FU
    -Call in a week with results +/- treatment
    -3 weeks in person check in, examine injuries, PT, counselling
    -3 months - HIV and Hep B repeat
33
Q

Discuss primary amenorrhoea
-Definition
-When to investigate (3)
-Incidence

A
  1. Def: Absence of menstruation
  2. When to investigate:
    -No secondary sexual characteristics by age 13
    -Secondary sexual characteristics but no menstruation at 15yrs
    -No menstruation 3yrs after breast development
  3. Incidence 0.1-0.3% (Much less common than secondary amenorrhoea)
34
Q

What are the causes of primary amenorrhoea with % makeup (5)

A
  1. Pituitary driven (Hypogonadotrophic hypogonadism) - 35%
    -Constitutional delay, chronic disease, Kallmans, Infection, Infiltration, Rad/Chemo, Tumour, Functional
  2. Ovarian driven (Hypergonadotrophic hypogonadism) - 40%
    -POI, Turners, Swyers, Pure gonadal dysgenesis, Galactosaemia, Fragile X premutation, CAH, Aromatase deficiency, Autoimmune, Chemo/Rad/Surg, Infection
  3. Reproductive tract - 20%
    -Absent uterus - MRKH, CAIS
    -Obstructive - imperforate hymen, vaginal septum, cervical agenesis
  4. Thyroid
    -Hyper / hypo thyroid
  5. Hyperandrogenism
    -PCOS
    -HAIR-AN (Hyperandrogenism, insulin resistance, acanthosis niagracans)
    -Ovarian tumour
35
Q

Discuss dysfunctional uterine bleeding in adolescence
-Definition
-Aetiology
-Management

A
  1. Definition: Heavy and irregular bleeding
  2. Aetiology
    -85% DUB is due to anovulation cycles from an immature HPO axis
    -Infection
    -Endocrine abnormalities - Thyroid, prolactin
    -Stress
    -Bleeding disorders
    -Rarely structural abnormalities - polyps, fibroids etc
  3. Management
    -Correct anaemia
    -NSAIDs, TXA, COCP
36
Q

Discuss primary dysmenorrhoea
1. Definition
2. Incidence
3. Presentation
4. Pathophysiology
5. Management

A
  1. Definition: Pain during menstruation
  2. Incidence: Up to 60%
  3. Presentation
    -Pain typically begins 6-12 months post menarche when ovulatory cycles begin
    -Pain typically starts before or during menstruation and lasts up to 72hrs.
  4. Pathophysiology: Decrease in progesterone ->Increased prostaglandins -> Increased uterine contractility ->Myometrial ischemia and pain.
  5. Management
    -NSAIDS to interrupt COX mediated prostaglandin production
    -Start 2 days prior to menses and for 2-3 days during. Decreases blood flow by 30%
    -COCP to inhibit ovulation
    -If no response to therapy consider secondary dysmenorrhoea work up
37
Q

Discuss endometriosis in adolescents
-When to suspect
-Incidence
-Diagnosis / imaging
-When to treat surgically
-Treatment - medically
-Appearance

A
  1. Suspect if chronic pelvic pain not responsive to medical management, Family Hx, Hx of congenital genital tract abnormalities, cyclical absenteeism
  2. 66% of adolescence undergoing laparoscopy for chronic pelvic pain will have endometriosis
  3. Diagnosis
    -TVUSS if appropriate and if not TAUSS or MRI
  4. Consider risk and benefits of surgery as a shared decision
    Consider surgery if no improvement with medical treatment
  5. Treatment medically
    -NSAIDS
    -Hormones - consider bone density effect
    -GnRH agonists up to 1 yr with add back if Lap confirmed endo
  6. Adolescent endometriosis = clear or red not powder lesions. Tend to be more metabolically active with increased prostaglandins and inflammation.
38
Q

Discuss adenomyosis
-Histology
-Definition
-Subtypes
-Pathophysiology of symptoms
-Co-existing pathology
-Incidence

A
  1. Endometrial glands and stroma surrounded by hypertrophic and hyperplastic myometrium. lack of submucosa endometrial/myometrial interface
    -Estrogen dependant. Not seen in PM
  2. > 2.5mm of glandular extension below the endometrial/myometrial interface
  3. Subtypes:
    -Focal - adenomyoma
    -Diffuse - more common
  4. Pathophysiology of symptoms
    -HMB (60%) from increased vascularity of uterus, increased endometrial surface area and impaired myometrial contractility
    -Pain (25%) from trapped endometrial cells in myometrium during menstruation leading to myometrial hypertrophy
  5. Fibroids, Endometriosis 30%
  6. Incidence
    -20-35% of women
39
Q

What imaging should be used for adenomyosis and what are the USS findings (7)

A
  1. Imagine
    -USS or MRI - Similar specificity / sensitivity (USS 87% and 81%)
    -MRI not first line.
  2. USS findings
    -No set definitions
    -Asymetrical wall thickening
    -Venitian blinds
    -Myometrial cysts
    -Disrupted myometrial/endometrial junction
    -Subendometrial lines or thickening
    -Focal hyperechoic lesions
    -Increased vascularity on doppler
40
Q

How should adenomyosis be managed
-Medical (3)
-Surgical (4)

A
  1. Medical management
    -Limited evidence. Hormonal seem to work (None superior)
    -GnRH decreases uterine size
    -Mirena effective for HMB
  2. Surgical intervention
    -Surgical resection if focal lesion - fertility sparing (needs CS)
    -Endometrial ablation if disease is superficial - No evidence
    -Hysterectomy - no evidence that it will improve pain but will impact HMB
    -High intensity focused USS. Non-invasive and fertility sparing
    -Image guided thermal ablation - targeted ablation of adenomyosis tissue
41
Q

Discus ovarian torsion
1. Epidemiology
2. Pathophysiology
3. Risk factors(5)
4. USS findings (6)
5. Management principles

A
  1. Epidemiology
    -Mostly occurs in women of reproductive age
    -25% occurs in children
    -Dermoids most common type of cyst (10% tort)
  2. Pathophysiology
    -Rotation around the IP and utero-ovarian ligament
    -Initially impacts venous drainage
    -Ovary becomes oedematous increasing vascular compression
    -Follicles are pushed to periphery secondary to oedema
  3. Risk factors
    -High risk of R ovary torsion
    -Pelvic mass (85% of torsions have a mass)
    -Mass >5cm
    -Pregnancy
    -PCOS or ovulation induction
  4. USS findings
    -Enlarged ovary
    -Adnexal mass
    -Peripheral multiple follicles - string of pearls
    -Ovary anterior to uterus
    -Decreased or absent blood flow (not always)
    -Whirl pool sign (twisting of thickened vascular pedicle
  5. Management principles
    -Leave ovary even if dusky unless
    -Obviously necrotic tissue
    -Concern for malignancy
    - Post menopausal - stop recurrency
    -Prompt surgical intervention in pre-menopausal
    -Prevention of recurrence - ovulation suppression, oopherpexy (no high qual evidence)
42
Q

Discuss the complications of ovarian cysts (4)

A
  1. Torsion
  2. Rupture
    -usually functional
    -Occurs day 20-26 of cycle usually
  3. Haemorrhage
    -Usually CL or theca interna as vascular
    -Usually occurs day 20-26 of cycle
  4. Infection
    -1% of dermoids can become infected - coliforms mostly
43
Q

Discuss the management of benign cysts in premenopausal women
-Asymptomatic simple cysts
-Symptomatic or large cysts

A
  1. Simple asx cysts
    - <5cm no follow up
    - 5-7cm annual FU with USS, If persistent or increasing in size consider surgical management
    - >7cm consider surgical intervention or further imaging - MRI
  2. Symptomatic cysts, ?dermoid / borderline / malignancy, >7cm cysts should be considered for surgery
    -Laparoscopic approach gold standard
    -Avoid aspiration - spillage and high recurrence rates - 54-84%
44
Q

Discuss ovarian cysts in pregnancy
1. Epidemiology
2. Complications
3. Tumour markers
4. Surgical principles (7)
5. FU

A
  1. Epidemiology
    - 1:6 masses in pregnancy malignant
    -0.05 - 2.5%
    - <5% of ovarian cysts in pregnancy require intervention
    -50% dermoid
    -Functional cysts - typically resolve by 16 weeks
  2. Complications
    -Torsion esp in first trimester. Occurs in 5%
  3. Ca125, AFP and HCG all raised in pregnancy so not helpful
  4. Surgical principles
    -Ideally between 16-20 weeks
    -Laparoscopy with Hassan entry (Avoid veres)
    -Left lateral if >20 weeks
    -Max pressure 13mmHg
    -Fetal heart monitoring
    -Consider steroids
    -VTE prophylaxis
  5. If cyst >5cm or complex components FU with USS 1/12 PP
45
Q

Discuss the different O-RADS scores in terms of findings and risk of malignancy

A

O-RADS 1 = Simple cyst or CL.
= Normal and benign
O-RADS 2 = Haemorrhagic cysts, dermoids, endometriomas (<10cm) = Risk of malignancy <1%
O-RADS 3 = Risk of malignancy 1-10%
O-RADS 4 = Risk of malignancy - 10-50%
O-RADS 5 = Risk of malignancy >50%

46
Q

When an ovarian mass is identified in premenopausal women when should tumour markers be done?

A
  1. If cyst looks simple then no need to do a Ca125
  2. If women less than 40 and cyst looks complex then tumour markers should be done and include: LDH, AFP, HCG
  3. If serum Ca125 is done and less than 200 then consider other causes (Increased in fibroids, endo/adeno, chronic illness, Infection)
  4. If Ca125 >200 discuss with GONC
47
Q

How should ovarian cysts be worked up in post menopausal women

A
  1. Ca125 should be done in all women. No other tumour markers are necessary
  2. TVUSS is first line for investigating suspected ovarian cysts
  3. RMI should be calculated and if >200:
    -Refer to GONC
    -CT abdo pelvis.
48
Q

How should ovarian cysts be managed in post menopausal women

A

Ovarian cyst >1cm for post menopausal women
1. Ca125 + TVUSS (MRI if USS inconclusive)
2. Calculate RMI
3. RMI <200 and cyst = aSx, unilocular, unilateral, <5cm
->Conservative management. Repeat evaluation at 6 and 12 months. If no change discharge
4. RMI <200 and cyst has any of the following features: Sx, >5cm, multilocular or bilateral
->Offer surgery -laparoscopy BSO
5. If RMI >200 then CT abdo pelvis and ref to GONC MDM

49
Q

What is the definition of the following:
-Allodynia
-Hyperalgesia
-Persistent pelvic pain

A
  1. The experience of pain triggered by a stimuli which is not normally painful
  2. Increased pain response to stimuli which are normally painful
  3. Non-cyclical pelvic pain lasting 6 months or more, can be intermittent or constant. Sufficient to cause functional disability
50
Q

Discuss persistent pelvic pain
-Epidemiology (2)
-Risk factors (5)
-Pathophysiology (4)

A
  1. Epidemiology
    -1 in 6 women
    -Prevalence 15-27%
  2. Risk factors
    -Previous abuse
    -PTSD
    -Unclear if depression and anxiety has role
    -Female
    -Poor sleep
  3. Pathophysiology
    -Prolonged noxious stimulation
    -Local factors like alpha tumour necrosis factor and chemokines may change peripheral nerve function
    -Altered excitability of dorsal horn neutrons leading to pain from stimulation of injured area and surrounding uninjured area
    -This enhancement of response is called sensitisation
    Descending information from the CNS (previous experiences, emotion, fear) may modify pain perception
51
Q

Describe the causes of persistent pelvic pain by system
-Gynaecological
-Gastrointestinal
-Urological
-Neurological
-MSK
-Psychological

A
  1. Gynaecological
    -Endo/adenomyosis
    -Pelvic congestion
    -Adhesions (only if dense vascular adhesion does adhesiolysis have an impact)
    -Residual ovarian syndrome or trapped ovarian syndrome
    -Infection
    -Fibroids
  2. GIT
    -IBS (present in 50% of those with PPP)
    -Assess with Rome III criteria
  3. Urological
    -Interstitial cystitis - (Present in 34-84% of those with PPP)
  4. Neurological
    -Nerve entrapment. (Present in 3.7% post pfannestiel)
  5. MSK
    -Referred lower back pain
    -Pelvic floor spasm
  6. Psychological
    -Increased in women who have experienced abuse
52
Q

How should chronic pelvic pain be managed
-Assessment (3 points relevant to Hx)
-Therapy (5 points)

A
  1. Assessment
    -Time to listen to their story
    -Consider woman’s theory of pain
    -Explore multifactorial approach to pain
  2. Therapy
    -Multifactorial approach done simultaneously best approach
    -If pain cyclical trial hormonal treatment as first line. Dx lap as second line (50% of women with PPP have a neg lap)
    -If IBS trial FODMAP and antispamodics
    -Consider analgesia but avoid opiates. If no improvement involve pain team
    -If interstitial cystitis - amytriptyline first line
    -If MSK component consider PT
    -For centralised pain
    -CBT
    -Pain education and health literacy
    -Hyperanalgesia retraining
    -Physical therapy - exercise
    -Improve sleep
    -Manage mental health
53
Q

Discuss endometriosis
-Incidence (4)
-Definition
-Frequency of symptoms (5)

A
  1. Incidence
    -2-10% of women of reproductive age (11%)
    -40% of women with genital tract anomalies
    -50% of women with infertility
    -70% of women with pelvic pain
  2. Definition
    -Presence of endometrial like tissue outside uterine cavity inducing a chronic inflammatory reaction.
  3. Symptoms
    -Chronic pelvic pain - 70%
    - Dysmenorrhoea - 62%
    -Dyspareunia - 55%
    - Cyclical Dyschezia - 48%
    -Subfertility - 40%
    -Cyclical dysuria
54
Q

Describe the theories of endometriosis pathogenesis (6)

A
  1. Samson theory - retrograde menstruation
  2. Haematological / Lymphatic dissemination of cells
  3. Coelomic metaplasia - prolonged irritation and oestrogen exposure may induce metaplasia in these cells.
  4. Genetics
  5. Altered immunity - not recognising abnormal cells leading to implantation
  6. Iatrogenic dissemination with Lap surgery, hysteroscopy, CS
55
Q

Describe the ASRM staging for endometriosis
-Basis
-Stages
-Advantages (3), Disadvantages (3)

A
  1. Based on a points system depending on size, depth, location and associated adhesions
  2. Stages
    Stage 1 = minimal (1-5 points)
    Stage 2 = mild (6-15 points)
    Stage 3 = moderate (16-40 points)
    Stage 4 = Severe (>40 points)
    - Complete obliteration of POD - 40 points
    - >3cm bilateral infiltration of ovary (20 points each side)
    - Dense adhesions around tube or ovary (16 points each)
  3. Advantages:
    -Accepted globally
    -Useful for research
    -Can be helpful for patients
    Disadvantages:
    -Poor correlation with patient symptom severity and fertility
    -Lots of inter-observer bias
    -Doesn’t classify DIE in retroperitoneal structures
56
Q

Discuss endometrial classification system
-ENZIAN (3)
-EFI (4)

A
  1. ENZIAN
    -Designed to completement ASRM for DIE
    -Designed according to location and depth
    -Better correlation with symptom severity
  2. EFI (Endometriosis fertility Index)
    -Designed to predict fertility
    -Does not correlate with pain
    -Reflects pregnancy rates better then ASRM
    -Reflects IVF success rates better than ASRM
57
Q

Discuss management of endometriosis
-Conservative
-Medical (6)
-Types (3)
-Points (4)

A

Treat symptoms not the disease stage
1. Conservative management
-Simple analgesia (NSAIDS +/- Paracetamol)
-Neuromodulators (pregabalin/gabapentin - no evidence for or against)
-Psychological support
-No evidence for alternative therapy
-Refer to pain specialist
-Encourage sleep hygiene and exercise
2. Medical
Hormonal therapy
-Doesn’t decrease lesion size. Will not result in remission. Pain returns once stopped
-No hormonal treatment has been found to be superior
-Good post surgery for delaying recurrence
-Don’t use if seeking fertility
-COCP - continuous better than cyclical
-Progesterone only
-GnRH agonists - second line. Give add back
-GnRH anatogonists - second line Give add back
-Aromatase inhibitors - third line
-Danazol, anti-progesterones, uterosacral nerve ablation presacral neurectomy no longer recommended
3. Points
-Medical same as surgical
-All medicines equivalent
-3/12 GnRH pre-op for DIE recommended to reduce operative complications
-Don’t treat asx endometriosis

58
Q

Discuss surgical management of endometriosis
-Recurrence post op
-Treatment recommendations pre/post op
-Management of peritoneal disease
-Management of DIE
-Management of endometrioma
-Evidence for hysterectomy
-Prognostic markers to aid in selection of patients

A
  1. Recurrence post-op
    -20% undergo repeat surgery in 2 yrs. 30% within 5 years
  2. Post op hormonal management can prolong time to recurrence and improve pain
    Pre-op hormonal not recommended
    ->stops dysmenorrhoea but not pelvic pain or dyspareunia
  3. Management of peritoneal disease
    ->Ablation or excision. Excision allows for histology confirmation
    ->Excision has better outcomes for pain
  4. Management of DIE
    ->Surgical removal for stages 3-4 doesn’t improve fertility
    ->Surgical removal effective for pain and QoL
    ->Consider MDT input
  5. Management of endometrioma
    ->Aim for cystectomy not drainage. reduces recurrence.
    ->Post op use hormonal meds to stop recurrence (GnRH or COC)
    ->No evidence that surgical removal before ART improves outcome but does drop AMH
    ->Excision increases the rate of spont pregnancy
  6. There is no evidence for effectiveness of hysterectomy for management of endometriosis
    All endometriotic lesions should be excised at the time of hysterectomy
    Total hyst is recommended if undertaken
  7. Prognostic markers
    -There are no factors which help to indicate which patients will benefit from surgery
59
Q

What are the risk factors for endometriosis

A
  1. Risk factors
    -Low BMI
    -Family hx
    -Congeital genital tract anomalies
    -Nulliparity
    -Prolonged estrogen exposure
    -HMB
60
Q

Discuss endometriosis
-Histological findings
-Pathophysiology of pelvic distortion
-Cancer risk

A
  1. Histological findings:
    -endometrial glands and stroma, histocyctes and hemosiderin laden macrophages. Tissue is like but no the same as endometrium
  2. Pathophysiology
    -Increased fibrosis in lesions cause nodularity
    -Inflammation and fibroisis cause shortening and thickening of uterosacral ligaments and ovarian ligaments
    -Ovaries pulled medially (Kissing ovaries)
    -Inflammation and fibrosis causes obliteration of POD
  3. Endometriomas ass with increased risk of endometroid and clear cells ovarian cancer.
    -Risk 2 extra cases per 10,000
    -Risk of malignancy 1% in premenopausal and 2.5% in post menopausal
    -No role for surveillance
61
Q

Discuss consent
-Code of rights
-Requirements for informed consent (4)
-If unable to given informed consent

A
  1. Consent is outlined in right 7 of code of rights
  2. Infomred consent requires
    -Information that can be understood by the patient
    -Information needs to be specific to the intervention
    -Consent needs to be voluntarily given
    -Patient needs to have capacity
  3. If patient unconscious or life threatening situation
    -Seek next of kin to assess patient’s preference
    -If no next of kin act in patient’s best interest (Duty of care)
62
Q

Discuss the diagnosis of endometriosis (6)

A
  1. Examination is important
  2. Normal examination or imagining doesn’t rule out endometriosis
  3. USS should be considered
  4. MRI and CT are not first line investigations.
    -Consider MRI for DIE if USS negative but symptoms suggestive
  5. Don’t do ca125
  6. In Laparoscopy Bx for diagnosis is recommended (Gold standard and highly specific)
63
Q

Discuss endometriosis in postmenopausal women
-Occurrence (1)
-Treatment (2)
-Management of menopausal sx in women with Hx of endo

A
  1. Occurrence
    -Can still be active in post menopausal women
  2. Treatment
    -Consider surgical management
    -Aromatase inhibitors
  3. Menopausal sx
    -Avoid estrogen only treatment - leads to malignant transformation
    -Treat surgical menopause with combined MHT until natural menopause
64
Q

How does adenomyosis impact pregnancy
-Pathophysiology of subfertility (5)
-Impact to pregnancy (7)

A
  1. Pathophysiology of subfertility
    -Uterine dysperistalsis
    -Impaired sperm transport
    -Impaired endometrial receptivity for implantation
    -Increased endometrial inflammatory factors
    -Impaired endometrial / myometrial interface
  2. Impact to pregnancy - poor implantation
    -Miscarriage esp in IVF
    -PET
    -IUGR
    -APH and PPH
    -PTB
    -Increased CS rate
    -Increased malpresentation
65
Q

What are the investigations for precocious puberty
-Bloods (5)
-Imaging (3)
-Stimulation (2)

A
  1. Bloods:
    -LH and FSH - high in central, low in peripheral
    -Oestradiol (E2)
    -DHEAs, 17-OH progesterone (High androgens), testosterone
    -TFT
    -IGF-1
    -Prolactin
  2. Imaging
    -Pelvic, abdo USS - ovarian, adrenal tumour
    -MRI brain - central tumour
    -Wrist XR - bone maturation (good measure for PP)
  3. Stimulation test
    -GnRH stimulation test - gold standard for central precocious puberty.
    Give GnRH and measure LH. If LH is high then suggests prematurely mature HPO axis
    -ACTH stimulation test to unmask mild CAH with increased levels of 17-OH progester

RANZCOG -Gynaecology 2024 Edward (11 decks)

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