Gynaecology

Question 1

Define premenstrual syndrome.

Answer 1

Physiological and emotional disturbances that occur 1-2 wk prior to menses and last until a few days after onset of menses; common symptoms include depression, irritability, tearfulness, and mood swings

Question 2

What are the common symptoms of PMS?

Answer 2

• affective: depression, angry outbursts, irritability, anxiety, confusion, social withdrawal
• somatic: breast tenderness, abdominal bloating, headache, swelling of extremities

Question 3

Describe the aetiology of PMS?

Answer 3

• multifactorial: not completely understood; genetics likely play a role
• CNS-mediated neurotransmitter interactions with sex steroids (progesterone, estrogen, and testosterone)
• serotonergic dysregulation – currently most plausible theory

Question 4

WHat are the treatment options for PMS?

Answer 4

• goal: symptom relief
• psychological support
• diet/supplements
  
  • avoid sodium, simple sugars, caffeine, and alcohol
  • calcium (1,200-1,600 mg/d), magnesium (400-800 mg/d), vitamin E (400 IU/d), vitamin B 6
• medications
  
  • NSAIDs for discomfort, pain
  • spironolactone for fluid retention: used during luteal phase
  • SSRIs: used during luteal phase x 14 d or continuously
  • OCP: primarily beneficial for physical/somatic symptoms
  • danazol: an androgen that inhibits the pituitary-ovarian axis
  • GnRH agonists if PMS is severe and unresponsive to treatment (may use prior to considering definitive treatment with BSO)
• mind/body approaches
  
  • regular aerobic exercise
  • cognitive behavioral therapy
  • relaxation, light therapy biofeedback, and guided imagery
• herbal remedies (variable evidence)
  
  • evening primrose oil, black cohosh, St. John’s wort, kava, ginkgo, agnus castus fruit extract
• Bilateral salphingo-oophorectomy (BSO) if symptoms severe

Question 5

What are the primary and secondary causes of dysmenorrhea?

Answer 5

• primary/idiopathic
• secondary (acquired)
  
  • endometriosis
  • adenomyosis
  • uterine polyps
  • uterine anomalies (e.g. non-communicating uterine horn)
  • leiomyoma
  • intrauterine synechiae
  • ovarian cysts
  • cervical stenosis
  • imperforate hymen, transverse vaginal septum
  • pelvic inflammatory disease
  • IUD (copper)
  • foreign body

Question 6

What Ix should be done for dysmenorrhea?

Answer 6

• ß-HCG
• Urinalysis
• FBC, ESR/CRP - rule out PID
• STI screen: gono and chlamydia PCR
• Pap smear and cervical cytology
• US abdominal and transvaginal: endometriosis, cysts, fibroids
• Colposcopy
• Hysteroscopy +/- biopsy
• Laparoscopy

Question 7

What is the management plan for dysmenorrhea?

Answer 7

• Step 1: Initial Dysmenorrhea Evaluation
  
  • Obtain history (including red flags suggestive of Secondary Dysmenorrhea)
  • Perform pelvic examination
  • Urine Pregnancy Test
• Step 2: Empiric Primary Dysmenorrhea Management
  
  • Treat with NSAIDS
  • Consider Oral Contraceptives
  • Reevaulate every 6 months if symptoms controlled
• Step 3: Secondary Dysmenorrhea evaluation (if refractory Pelvic Pain to above measures)
  
  • Obtain Secondary Dysmenorrhea evaluations as above (Urinalysis, CBC, ESR or CRP, STD testing)
  • Consider pelvic Ultrasound
  • Treat Pelvic Inflammatory Disease if present
• Step 4: Refractory Dysmenorrhea (with negative or nondiagnostic evaluation in step 3)
  
  • Consider additional abdominal imaging (e.g. MRI or CT Abdomen and Pelvis)
    
    • MRI Abdomen and Pelvis may be considered for Adenomyosis or deep pelvic endometriosis evaluation (if pelvic Ultrasound negative)
  • Consider Laparoscopy
  • Consider Hysteroscopy
  • Manage as Chronic Pelvic Pain

Question 8

What informtion do you want to get from the Hx of a pt with dysmenorrhea?

Answer 8

• Pain: SOCRATES
• Menstrual Hx
• Past Obs & gynae
• Screen for GIT symptoms
• Screen for Red flags
• Sexual Hx
• Social Hx

Question 9

What physical examination would you need to perform on a patient with dysmenorrhea?

Answer 9

• Abdominal
• Bimanual
• Speculum exam

Question 10

Describe the aetiology of endometriosis.

Answer 10

• not fully understood
• proposed mechanisms (combination likely involved)
  
  • retrograde menstruation (Sampson’s theory)
    
    • seeding of endometrial cells by transtubal regurgitation during menstruation
    • endometrial cells most often found in dependent sites of the pelvis
  • immunologic theory: altered immunity may limit clearance of transplanted endometrial cells from pelvic cavity (may be due to decreased NK cell activity)
  • metaplasia of coelomic epithelium
    
    • undefined endogenous biochemical factor may induce undifferentiated peritoneal cells to develop into endometrial tissue
  • extrapelvic disease may be due to aberrant vascular or lymphatic dissemination of cells
    
    • e.g. ovarian endometriosis may be due to direct lymphatic flow from uterus to ovaries

Question 11

Describe the epidemiology of endometriosis?

Answer 11

• incidence: 15-30% of pre-menopausal women
• mean age at presentation: 25-30 yr
• regresses after menopause

Question 12

First thought:

Endometriosis.

Answer 12

The presence of endometrial tissue (glands and stroma) outside of the uterine cavity

Question 13

What are the DDx of endometriosis?

Answer 13

• Chronic PID, recurrent acute salpingitis
• Hemorrhagic corpus luteum
• Benign/malignant ovarian neoplasm
• Ectopic pregnancy

Question 14

What are the risk factors for endometriosis?

Answer 14

• family history (7-10x increased risk if affected 1st degree relative)
• obstructive anomalies of the genital tract (earlier onset) – resolve with treatment of anomaly
• nulliparity
• age >25 yr

Question 15

What are the clinical features of endometriosis on Hx and exam?

Answer 15

• may be asymptomatic
• history
  
  • menstrual symptoms
    
    • cyclic symptoms due to growth and bleeding of ectopic endometrium, usually precede menses (24-48 h) and continue throughout and after flow
    • secondary dysmenorrhea
    • sacral backache with menses
    • pain may eventually become chronic, worsening perimenstrually
    • premenstrual and postmenstrual spotting
    • deep dyspareunia
  • infertility
    
    • 30-40% of patients with endometriosis will be infertile
    • 15-30% of those who are infertile will have endometriosis
  • bowel and bladder symptoms
    
    • frequency, dysuria, hematuria
    • diarrhea, constipation, hematochezia, dyschezia
  • physical
    
    • tender nodularity of uterine ligaments and cul-de-sac felt on rectovaginal exam
    • fixed retroversion of uterus
    • firm, fixed adnexal mass (endometrioma)
    • physical findings not present in adolescent population

Question 16

What are the causes of abnormal uterine bleeding?

Answer 16

Question 18

First thought.

Abnormal uterine bleeding in women >40 year old.

Answer 18

Requires an
endometrial biopsy to rule out cancer
even if known to have fibroids

Question 19

What investigations need to be ordered in a patient with abnormal uterine bleeding?

Answer 19

• vitals ± orthostatic vitals
• FBC, and iron studies
• β-hCG to rule out pregnancy
• TSH, free T4
• coagulation profile (especially in adolescents): rule out von Willebrand’s disease
• prolactin if amenorrheic
• FSH, LH
• serum androgens (especially free testosterone)
• day 21 (luteal phase) progesterone to confirm ovulation
• Pap test
• pelvic U/S: detect polyps, fibroids, measure endometrial thickness (postmenopausal)
• endometrial biopsy: consider biopsy in women >40 yr
  
  • must do endometrial biopsy in all women presenting with postmenopausal bleeding to exclude endometrial cancer

Question 20

Name the following anatomy.

Answer 20

Question 21

Name the following anatomy.

Answer 21

Question 22

Name the following anatomy.

Answer 22

Question 23

Describe the events of a normal menstrual cycle

Answer 23

Question 24

What is the treatment for abnormal uterine bleeding?

Answer 24

• resuscitate patient if hemodynamically unstable
• treat underlying disorders
  
  • if anatomic lesions and systemic disease have been ruled out, consider dysfunctional uterine bleeding
• medical
  
  • mild dysfunctional uterine bleeding
    
    • NSAIDs
    • combined OCP
    • progestins:
      
      • Side effects: bloating, mood changes, and weight gain.
    • Mirena® IUD
    • goserelin: GnRH analogues
      
      • Side effects: due to oestrogen deficiency → flushing, vaginal dryness, bone loss.
    • danazol: synthetic steroid, limited use due to side effects
      
      • Side effects: moderate virilisation, liver toxicity, ↑ serum lipid profile, ↑ rissk of ovarian cancer
  • Acute, severe DUB
    
    • replace fluid losses, consider admission
  • Surgical
    
    • endometrial ablation; consider pretreatment with danazol or GnRH agonists
      
      • if finished childbearing
      • repeat procedure may be required if symptom reoccur especially if <40 yr
    • hysterectomy: definitive treatment

Question 27

Describe the pathophysiology of PCOS?

Answer 27

• Chronically elevated LH and insulin resistance cause ovarian growth, androgen production and ovarian cyst formation.
• Obesity (50-65%) may increase the insulin resistance and hyperinsulinaemia.
• Increased Lh and decreased FSH cause anovulation → oligomenorrhea → infertility

Question 30

What are the aetiolgies of intermenstrual bleeding and post-coital bleeding?

Answer 30

• Cervical cancer
• Cervical ectropian
• Cervical polyps
• Cervicitis
• Genital prolapse (including urethral)
• Bengin vascular neoplasms
  
  • Haemangioma
  • Lymphangioma
  • AV malformations
• Lower genital tract infections

Question 31

Define oligomenorrhea.

Answer 31

Mentruation occuring every 35 days to 6 months.

Question 32

DDx for oliogomenorrhea?

Answer 32

• Primary
  
  • genetic or chromosomal abnormalities
  • Abnormalities of the reproductive organs
• Secondary
  
  • PCOS
  • ovarian insufficiency (early menopause)
  • Hypothalamic amenorrhea: hypothalamus slows or stops releasing gonadotropin-releasing hormone (GnRH)
  • Prolactin-secreting tumour
  • Ovarian and adrenal neoplasms
  • Cushing’s syndrome

Question 34

What are the causes of excess androgens?

Answer 34

Question 35

Describe the production of cholesterol hormones.

Answer 35

Question 36

Descibe the hair follicle cycle.

Answer 36

Question 37

What is the diagnostic criteria for PCOS?

Answer 37

• 2 of 3 to make diagnosis:
  
  • oligomenorrhea/irregular menses for 6 mo
  • clinical or lab evidence of hyperandrogenism
  • polycystic ovaries on U/S

Question 38

What are the long term health consequences of PCOS?

Answer 38

• Hyperlipidemia
• Adult-onset DM
• Endometrial hyperplasia
• Infertility
• Obesity
• Sleep apnea

Question 39

What are the clinical features of PCOS?

Answer 39

• average age 15-35 yr at presentation
• in adolescents, wait at least 1-2 yr to make diagnosis
• abnormal/irregular uterine bleeding, hirsutism, infertility, obesity, virilization
• insulin resistance occurs in both lean and obese patients
• acanthosis nigricans: browning of skin folds in intertriginous zones (indicative of insulin resistance)
• family history of DM

Question 40

What Ix need to be ordered for a patient with suspected PCOS?

Answer 40

• goal of investigations is to identify hyperandrogenism or chronic anovulation; and rule out specific pituitary or adrenal disease as the cause
• laboratory
  
  • prolactin, 17-hydroxyprogesterone, free testosterone, DHEA-S, TSH, free T4 , androstenedione, SHBG
  • LH:FSH >2:1; LH is chronically high with FSH mid-range or low (low sensitivity and specificity)
  • increased DHEA-S, androstenedione and free testosterone (most sensitive), decreased SHBG
• transvaginal or transabdominal U/S: polycystic-appearing ovaries (“string of pearls” – 12 or more small follicles 2-9 mm, or increased ovarian volume)
• tests for insulin resistance or glucose tolerance
  
  • fasting glucose:insulin ratio <4.5 is consistent with insulin resistance (U.S. units)
  • 75 g OGTT yearly (particularly if obese)
• laparoscopy
  
  • not required for diagnosis
  • most common to see white, smooth, sclerotic ovaries with a thick capsule; multiple follicular cysts in various stages of atresia; hyperplastic theca and stroma
• rule out other causes of abnormal bleeding

Question 41

Describe the Rx for PCOS?

Answer 41

• Lifestyle modifications: conparable to or better than medical treatment.
  
  • Weight loss
  • Increase exercise
  • Diet
• cycle control
  
  • lifestyle modification (decrease BMI, increase exercise) to decrease peripheral estrone formation
  • OCP monthly or cyclic Provera® to prevent endometrial hyperplasia due to unopposed estrogen
  • oral hypoglycemic (e.g. metformin) if type 2 diabetic or if trying to become pregnant
  • tranexamic acid (Cyklokapron®) for menorrhagia only
• infertility
  
  • medical induction of ovulation: clomiphene citrate, human menopausal gonadotropins (HMG [Pergonal®]), LHRH, recombinant FSH, and metformin
    
    • metformin may be used alone or in conjuction with clomiphene citrate for ovulation induction
    • ovarian drilling (perforate the stroma), wedge resection of the ovary
    • bromocriptine (if hyperprolactinemia)
• hirsutism
  
  • any OCP can be used
    
    • Androcur® (cyproterone acetate): antiandrogenic
    • Yasmin® (drospirenone and ethinyl estradiol): spironolactone analogue (inhibits steroid
      receptors)
  • mechanical removal of hair
  • finasteride (5-α reductase inhibitor)
  • flutamide (androgen reuptake inhibitor)
  • spironolactone: androgen receptor inhibitor

Question 42

The effects of hyperandrogenism in women?

Answer 42

• Hirsutism
• Virilisation
• Defeminisation

Question 46

What is the age range for menopause?

Mean age?

Answer 46

48-55 years

51.4 years

Question 47

Describe the signs and symptoms of menopause.

Answer 47

• associated with estrogen deficiency
  
  • vasomotor instability (tends to dissipate with time)
    
    • hot flushes/flashes, night sweats, sleep disturbances, formication, nausea, palpitations
  • urogenital atrophy involving vagina, urethra, bladder
    
    • dyspareunia, pruritus, vaginal dryness, bleeding, urinary frequency, urgency, incontinence
  • skeletal
    
    • osteoporosis, joint and muscle pain, back pain
  • skin and soft tissue
    
    • decreased breast size, skin thinning/loss of elasticity
  • psychological
    
    • mood disturbance, irritability, fatigue, decreased libido, memory loss

Question 48

Describe the risk vs benefit of HRT?

Answer 48

Question 49

Describe the organism, pathophysiology, signs and symptoms, and Rx of candidiasis and bacterial vaginosis.

Answer 49

Question 50

Define menopause.

Answer 50

Lack of menses for 1 yr

Question 51

What are the types of menopause?

Answer 51

• physiological; average age 51 yr (follicular atresia)
• premature ovarian failure; before age 40 (autoimmune disorder, infection, Turner’s syndrome)
• iatrogenic (surgical/radiation/chemotherapy)

Question 52

What Ix should be done in a menopausal women?

Answer 52

• increased levels of FSH (>35 IU/L) on day 3 of cycle (if still cycling) and LH (FSH>LH)
• FSH level not always predictive due to monthly variation; use absence of menses for 1 yr to diagnose
• decreased levels of estradiol (later)

Question 53

Describe the management options for menopause?

Answer 53

• goal is for individual symptom management
  
  • vasomotor instability
    
    • HRT (first line), SSRIs, venlafaxine, gabapentin, propranolol, clonidine
    • acupuncture
  • vaginal atrophy
    
    • local estrogen: cream (Premarin®), vaginal suppository (VagiFem®), ring (Estring®)
    • lubricants
  • urogenital health
    
    • lifestyle changes (weight loss, bladder re-training), local estrogen replacement, surgery
  • osteoporosis
    
    • 1,000-1,500 mg calcium OD, 800-1,000 IU vitamin D, weight-bearing exercise, smoking
      cessation
    • bisphosphonates (e.g. alendronate)
    • selective estrogen receptor modifiers (SERMs): raloxifene (Evista®) – mimics estrogen effects on bone, avoids estrogen-like action on breast and uterine cancer; does not help hot flashes
    • HRT: second-line treatment (unless for vasomotor instability as well)
  • decreased libido
    
    • vaginal lubrication, counseling, androgen replacement (testosterone cream or the oral
      form Android®)
  • cardiovascular disease
    
    • management of cardiovascular risk factors
  • mood and memory
    
    • antidepressants (first line), HRT (augments effect)
  • alternative choices (not evidence-based, safety not established)
    
    • black cohosh, phytoestrogens, St. John’s wort, gingko biloba, valerian, evening primrose
      oil, ginseng, Don Quai

Question 54

Describe the pathophysiology of menopause?

Answer 54

Degenerating theca cells fail to react to endogenous gonadotropins (FSH, LH) → Less estrogen is produced → Decreased negative feedback on hypothalamic-pituitary-adrenal axis → Increased FSH and LH → Stromal cells continue to produce androgens as a result of increased LH stimulation

Question 55

What are the absolute contraindication to HRT?

HINT: ABCD

Answer 55

• Acute liver disease
• Undiagnosed vaginal Bleeding
• Cancer: Breast/uterine, Cardiovascular disease
• DVT (thromboembolic disease)

Question 56

What are the components of HRT?

Answer 56

• Oestrogen
  
  • oral or transdermal (e.g. patch, gel)
  • transdermal preferred for women with hypertriglyceridemia or impaired hepatic function,
    smokers, and women who suffer from headaches associated with oral HRT
  • low-dose (preferred dose: 0.3 mg Premarin®/25 µg Estradot® patch, can increase if necessary)
• Progestin
  
  • given in combination with estrogen for women with an intact uterus to prevent development of endometrial hyperplasia/cancer

Question 57

What are the side effects fo HRT?

Answer 57

• abnormal uterine bleeding
• mastodynia – breast tenderness
• oedema, bloating, heartburn, nausea
• mood changes (progesterone)
• can be worse in progesterone phase of combined therapy

Question 58

What are the absolute and relative contraindication of HRT?

Answer 58

• absolute
  
  • acute liver disease
  • undiagnosed vaginal bleedin
  • known or suspected uterine cancer/breast cancer
  • acute vascular thrombosis or history of severe thrombophlebitis or thromboembolic disease
  • cardiovascular disease
• relative
  
  • pre-existing uncontrolled HTN
  • uterine fibroids and endometriosis
  • familial hyperlipidemias
  • migraine headaches
  • family history of estrogen-dependent cancer
  • chronic thrombophlebitis
  • DM (with vascular disease)
  • gallbladder disease, hypertriglyceridemia, impaired liver function (consider transdermal oestrogen)
  • fibrocystic disease of the breasts

Question 61

Describe the epidemiology/aetiology of HPV?

Answer 61

• common viral STD in the United States
• >200 subtypes, of which >30 are genital subtypes
• HPV types 6 and 11 are classically associated with anogenital warts/condylomata acuminata
• HPV types 16 and 18 are the most oncogenic (classically associated with cervical HSIL)
• types 16, 18, 31, 33, 35, 36, 45 (and others) associated with increased incidence of cervical and vulvar intraepithelial hyperplasia and carcinoma

Question 62

What are the clinical features of HPV?

Answer 62

• latent infection
  
  • no visible lesions, asymptomatic
  • only detected by DNA hybridization tests
• subclinical infection
  
  • visible lesion found during colposcopy or on Pap test
• clinical infection
  
  • visible wart-like lesion without magnification
  • hyperkeratotic, verrucous or flat, macular lesions
  • vulvar oedema

Question 63

What Ix can be done for HPV?

Answer 63

• cytology
  
  • koilocytosis: nuclear enlargement and atypia with perinuclear halo
• biopsy of lesions at colposcopy
• detection of HPV DNA subtype using nucleic acid probes (not routinely done but can be done in presence of abnormal Pap test to guide treatment)

Question 64

What is the Rx for HPV?

Answer 64

• patient administered
  
  • imiquimod 5% cream topically (apply to each wart), 3 times weekly on alternate days at bedtime (wash off after 6 to 10 hours) until warts resolve (usually 8 to 16 weeks)
  • podophyllotoxin 0.15% cream or 0.5% paint topically (apply to each wart), twice daily for 3 days followed by a 4-day break; repeat weekly for 4 to 6 cycles until warts resolve.
• provider administered
  
  • cryotherapy with liquid nitrogen: repeat q1-2wk
  • surgical removal/laser

Question 65

What can be done to prevent HPV?

Answer 65

• vaccination: Gardasil®
• condoms may not fully protect (areas not covered, must be used every time throughout entire sexual act)

Question 66

What is the aetiology of HSV?

Answer 66

90% are HSV-2, 10% are HSV-1

Question 67

What are the clincal features of HSV or the vulva?

Answer 67

• may be asymptomatic
• initial symptoms: present 2-21 d following contact
• prodromal symptoms: tingling, burning, pruritus
• multiple, painful, shallow ulcerations with small vesicles appear 7-10 d after initial infection (absent in many infected persons); lesions are infectious
• inguinal lymphadenopathy, malaise, and fever often with first infection
• dysuria and urinary retention if urethral mucosa affected
• recurrent infections: less severe, less frequent and shorter in duration (especially with HSV-1)

Question 68

What Ix can be done for HSV of the vulva?

Answer 68

• viral culture preferred in patients with ulcer present, however decreased sensitivity as lesions heal
• cytologic smear (Tzanck smear)
  
  • multinucleated giant cells, acidophilic intranuclear inclusion bodies
• type specific serologic tests for antibodies to HSV-1 and HSV-2

Question 69

What is the Rx for HSV of the vulva?

Answer 69

• first episode
  
  • acyclovir, famciclovir, or valacyclovir
• recurrent episode
  
  • acyclovir, or acyclovir; famciclovir and valacyclovir may also be used
• daily suppressive therapy
  
  • consider if more than 6 recurrences per yr or one every 2 mo
  • acyclovir or famciclovir or valacyclovir
• severe disease
  
  • IV therapy: acyclovir followed by oral antiviral therapy to complete at least 10 d
• education regarding transmission
• avoid contact from onset of prodrome until lesions have cleared
• use barrier contraception

Question 70

What can be done for women with HSV of the vulva when pregnant?

Answer 70

• Antiviral suppression of women with first episode or history of HSV infections from 36 wk GA onward
• C-section should be performed on women who have active genital lesions at time of delivery
• Treatment: acyclovir 400 mg PO tid

Question 71

How is syphillis classified?

Answer 71

• primary syphilis
  
  • 3-4 wk after exposure
  • painless chancre on vulva, vagina, or cervix
  • painless inguinal lymphadenopathy
  • serological tests usually negative, local infection only
• secondary syphilis (can resolve spontaneously)
  
  • 2-6 mo after initial infection
  • nonspecific symptoms: malaise, anorexia, headache, diffuse lymphadenopathy
  • generalized maculopapular rash: palms, soles, trunk, limbs
  • condylomata lata: anogenital, broad-based fleshy gray lesions
  • serological tests usually positive
• latent syphilis
  
  • no clinical manifestations; detected by serology only
• tertiary syphilis
  
  • may involve any organ system
  • neurological: tabes dorsalis, general paresis
  • cardiovascular: aortic aneurysm, dilated aortic root
  • vulvar gumma: nodules that enlarge, ulcerate and become necrotic (rare)
• congenital syphilis
  
  • may cause fetal anomalies, stillbirths, or neonatal death

Question 72

What anatomical features are associated with vaginal and uterine prolapse?

Answer 72

Question 73

What Ix can be done for syphillis?

Answer 73

• aspiration of ulcer serum or node
• darkfield microscopy (most sensitive and specific diagnostic test for syphilis)
  
  • spirochetes
• non-treponemal screening tests (VDRL, RPR); nonreactive after treatment, can be positive with other conditions
• specific anti-treponemal antibody tests (FTA-ABS, MHA-TP, TP-PA)
  
  • confirmatory tests; remain reactive for life (even after adequate treatment)

Question 74

What is the Rx for syphillis?

Answer 74

• treatment of primary, secondary, latent syphilis of <1 yr duration
  
  • benzathine penicillin G IM single dose
  • treat partners, reportable disease
• treatment of latent syphilis >1 yr duration
  
  • benzathine penicillin G
• treatment of neurosyphilis
  
  • IV aqueous penicillin G
• screening
  
  • high risk groups
  • in pregnancy

Question 75

What is lichen sclerosis of the vulva?

Answer 75

• subepithelial fat becomes diminished; labia become thin, atrophic, with membrane-like epithelium and labial fusion
• pruritus, dyspareunia, burning
• ‘figure of 8’ distribution
• most common in postmenopausal women but can occur at any age
• treatment: ultrapotent topical steroid 0.05% clobetasol x 2-4 wk then taper down

Question 76

What is lichen simplex?

Answer 76

• Clinical Presentation
  
  • well-defined plaque(s) of lichenified skin with decreased skin markings ± excoriations
  • common sites: neck, scalp, lower extremeties, urogenital area
  • often seen in patients with atopy
• Pathophysiology
  
  • skin hyperexcitable to itch, continued rubbing/scratching of skin results
  • eventually lichenification occurs
• Investigations
  
  • if patient has generalized pruritus, rule out systemic cause: FBC with differential count, transaminases, renal and thyroid function tests
  • CXR if lymphoma suspected
• Management
  
  • treat pruritus to break the itch-scratch cycle: antipruritics (e. g. antihistamines, topical or intralesional glucocorticoids, Unna boot)

Question 77

What are the 6 Ps of lichen planus of the vulva?

Answer 77

• Purple
• Pruritic
• Polygonal
• Peripheral
• Papules
• Penis (i.e. mucosa)

Question 78

HOw is lichen planus managed?

Answer 78

• topical or intralesional corticosteroids
• short courses of oral prednisone (rarely)
• phototherapy for generalized or resistant cases
• oral retinoids for erosive lichen planus in mouth
• oral metronidazole or systemic immunosuppressants (e.g. azathioprine, methotrexate, cyclosporine)

Question 79

Describe the epidemiology of malignant vulvar lesions?

Answer 79

• 5% of genital tract malignancies
• 90% SCC; remainder melanomas, basal cell carcinoma, Paget’s disease, Bartholin’s gland carcinoma
  
  • Type I disease: HPV-related (50-70%)
    
    • more likely in younger women
    • 90% of VIN contain HPV DNA (usually types 16, 18)
  • Type II disease: not HPV-related, associated with current or previous vulvar dystrophy
    
    • usually postmenopausal women

Question 80

What are the risk factors for malignant vulvar lesion?

Answer 80

• HPV infection
• VIN: precancerous change which presents as multicentric white or pigmented plaques on vulva (may only be visible at colposcopy)
  
  • progression to cancer rarely occurs with appropriate management
  • treatment: local excision (i.e. superficial vulvectomy ± split thickness skin grafting to cover defects if required) vs. ablative therapy (i.e. laser, cauterization) vs. local immunotherapy (imiquimod)

Question 81

What are the clinical features of a malignant vulvar lesion?

Answer 81

• many patients asymptomatic at diagnosis (many also deny or minimize symptoms)
• most lesions occur on the labia majora, followed by the labia minora (less commonly on the clitoris or perineum)
• localized pruritus or lesion most common
• less common: raised red, white or pigmented plaque, ulcer, bleeding, discharge, pain, dysuria
• patterns of spread
  
  • local
  • groin lymph nodes (usually inguinal → pelvic nodes)
  • haematogenous

Question 82

What are the causes of an elevated alpha fetoprotein (AFP) concentration?

Answer 82

• ovarian and testicular malignancy
• hepatoma
• pregnancy
• choriocarcinoma

Question 83

What is the aetiology of pelvic prolapse/relaxation?

Answer 83

• relaxation, weakness, or defect in the cardinal and uterosacral ligaments which normally maintain the uterus in an anteflexed position and prevent it from descending through the urogenital diaphragm (i.e. levator ani muscles)
• related to
  
  • vaginal childbirth
  • aging
  • decreased estrogen (post-menopause)
  • following pelvic surgery
  • increased intra-abdominal pressure (obesity, chronic cough, constipation, ascites, heavy lifting)
  • congenital (rarely)
  • ethnicity (Caucasian women > Asian or African women)
  • collagen disorders

Question 85

What are the clinical features of a uterine prolapse?

Answer 85

• Protrusion of cervix and uterus into vagina
• Clinical features:
  
  • Groin/back pain (stretching of uterosacral ligaments)
  • Feeling of heaviness/pressure in the pelvis
  • Worse with standing, lifting
  • Worse at the end of the day
  • Relieved by lying down
  • Ulceration/bleeding (particularly if hypoestrogenic)
  • ± urinary incontinence

Question 86

What is the treatment for a uterine prolapse?

Answer 86

• General conservative treatment
• Vaginal hysterectomy ± surgical prevention of vault prolapse
• Consider additional surgical procedures if urinarym incontinence, cystocele, rectocele, and/or enterocele are present

Question 87

What are the general conservative treatments for pelvic relaxation/prolpase and urinary incontinence?

Answer 87

• Kegel exercises
• local vaginal estrogen therapy
• vaginal pessary (intravaginal suspension disc)

Question 88

What are the clinical features of a vault prolapse?

Answer 88

• protrusion of apex of vaginal vault into vagina, post-hysterectomy.
• Clinical features:
  
  • Groin/back pain (stretching of uterosacral
    ligaments)
  • Feeling of heaviness/pressure in the pelvis
  • Worse with standing, lifting
  • Worse at the end of the day
  • Relieved by lying down
  • Ulceration/bleeding (particularly if hypoestrogenic)
  • ± urinary incontinence

Question 89

What is the aetiology of overflow incontience?

Answer 89

• is a term sometimes used to describe urinary incontinence as a complication of urinary retention.
• use of the term if used it should be accompanied by the associated pathophysiology (e.g. BPH with overflow incontinence)

Question 90

What is the Rx for a vault prolapse?

Answer 90

• General conservative measures
• Sacralcolpopexy (vaginal vault suspension), sacrospinous fixation, or uterosacral ligament suspension

Question 91

WHat are the different types of incontience and their Rx?

Definition, aetiology, diagnosis, therapy.

Answer 91

Question 92

What are the clinical features of a cystocele?

Answer 92

• protrusion of bladder into the anterior vaginal wall.
• Clinical features:
  
  • Frequency, urgency, nocturia
  • Stress incontinence
  • Incomplete bladder emptying ± associated increased incidence of urinary tract infections – may lead to renal impairment

Question 93

What is the Rx for a cystocele?

Answer 93

• General conservative treatment
• Anterior colporrhaphy (“anterior repair”)
• Consider additional/alternative surgical procedure if documented urinary stress incontinence

Question 94

What are the clinical features of a rectocele?

Answer 94

• protrusion of rectum into posterior vaginal wall.
• Clinical features:
  
  • Straining/digitation to evacuate stool
  • Constipation

Question 95

What are the Rx options for a rectocele?

Answer 95

• General conervative treatment
• Also laxatives and stool softeners
• Posterior colporrhaphy (“posterior repair”), plication of endopelvic fascia and perineal muscles approximated in midline to support rectum and perineum (can result in dyspareunia)

Question 96

What are the Rx options of a enterocele?

Answer 96

• Similar to hernia repair
• Contents reduced, neck of peritoneal sac ligated, uterosacral ligaments, and levator ani muscles approximated

Question 97

How are pelvic organ prolapses gradded?

Answer 97

• 0 = no descent during straining
• 1 = distal portion of prolapse >1 cm above level of hymen
• 2 = distal portion of prolapse ≤1 cm above or below level of hymen
• 3 = distal portion of prolapse >1 cm below level of hymen but without complete vaginal eversion
• 4 = complete eversion of total length of lower genital tract
• Procidentia: failure of genital supports and complete protrusion of uterus through the vagina

Question 98

Define stress incontinence.

Answer 98

Involuntary loss of urine with increased intra-abdominal pressure (coughing, laughing, sneezing, walking, running)

Question 99

Define urinary incontinence.

Answer 99

involuntary leakage of urine

Question 100

What is the aetiology of urgency incontinence?

Answer 100

• detrusor overactivity
  
  • CNS lesion, inflammation/infection (cystitis, stone, tumor), bladder neck obstruction (tumor, stone), BPH, idiopathic.
• decreased compliance of bladder wall (inability to store urine)
  
  • CNS lesion, fibrosis
  • sphincter/urethral problem

Question 101

What is the aetiology of stress incontience?

Answer 101

• common in women; seen in men after prostate cancer treatment or pelvic operations
• urethral hypermobility
  
  • weakened pelvic floor and musculofascial urethral and vaginal supporting mechanisms allows bladder neck and urethra to descend with increased intra-abdominal pressure
  • urethra is pulled open by greater motion of posterior wall of outlet relative to anterior wall
  • associated with childbirth, pelvic surgery, aging, levator muscle weakness, obesity
• intrinsic sphincter deficiency (ISD): weakness of the urethra and associated smooth and striated muscle elements
  
  • pelvic surgery, neurologic problem, aging and hypoestrogen state
• ISD and urethral hypermobility can co-exist

Question 102

What is the aetiology of mixed incontience?

Answer 102

combination of stress and urgency incontinence

Question 104

Describe the epidemiology of urinary incontinence.

Answer 104

• variable prevalence in women: 25-45%
• F:M = 2:1
• more frequent in the elderly, affecting 5-15% of those living in the community and 50% of nursing home residents

Question 106

What are the risk factors for stress incontinence in women?

Answer 106

• pelvic prolapse
• pelvic surgery
• vaginal delivery
• hypoestrogenic state (post-menopause)
• age
• smoking
• neurological/pulmonary disease

Question 107

What are the Rx options of stress incontience?

Answer 107

• General conservative treatment
• surgical
  
  • tension-free vaginal tape (TVT), tension-free obturator tape (TOT), prosthetic/fascial slings or retropubic bladder suspension (Burch or Marshall-Marchetti-Krantz procedures)

Question 108

Define urge incontience.

Answer 108

• urine loss associated with an abrupt, sudden urge to void
• “overactive bladder”
• diagnosed based on symptoms

Question 109

What is the aetiology of urge incontinence?

Answer 109

• idiopathic (90%)
• detrusor muscle overactivity (“detrusor instability”)

Question 110

What are the associated symtpoms of urge incontience?

Answer 110

• frequency, urgency, nocturia, leakage

Question 111

What is the treatment for urge incontinence?

Answer 111

• behavior modification (reduce caffeine/liquid, smoking cessation, regular voiding schedule)
• Kegel exercises
• medications
  
  • anticholinergics: oxybutinin, tolterodine, solifenacin
  • tricyclic antidepressants: imipramine

Question 112

What is the classic triad of endometriosis?

Answer 112

• Dysmennohea: painful periods
• Dyspareunia: painful sex
• Dyschezia: constipation associated with a defective reflex for defecation

Question 113

Describe the physiology of continence, voiding and micturition.

Answer 113

• Neural control of the bladder and urethra
  
  • Voiding reflex
    
    • Controlled at the level of the pons
    • Afferent fibres respond to distention of the bladder wall and pass to the spinal cord
    • Efferent parasympathetic fibres pass back to the detrusor muscle and cause contraction, and also enable opening of the bladder neck
    • Efferent sympathetic fibres to the detrusor muscle are inhibited
  • Continence
    
    • Dependent on the pressure in the urethra being greater than the bladder
    • Urethral pressure influenced by urethral muscle tone, pelvic floor and intra-abdominal pressure
    • Detrusor muscle is expandable, and so as the bladder fills there is no increase in pressure
  • Micturition
    
    • Results when bladder pressure exceeds urethral pressure
    • Achieved voluntarily by simultaneous drop in urethral pressure (partly due to pelvic floor reaction) and an increase in bladder pressure due to detrusor muscle contraction

Question 114

Describe the effectiveness of contraceptions?

Physiological and barrier methods.

Answer 114

Question 115

Describe the effectiveness of contracption?

Hormonal, copper IUD, surgical and emergency contracption.

Answer 115

Question 119

What is the mechanism of action of steroidal (oestrogen and prosterin) contraception?

Answer 119

• Ovulatory suppression through inhibition of LH and FSH
• Decidualization of endometrium
• Thickening of cervical mucus resulting in decreased sperm penetration

Question 120

What are the advantages of steroidal contraception?

Answer 120

• Highly effective
• Reversible
• Cycle regulation
• Decreased dysmenorrhea and menorrhagia (less anemia)
• Decreased benign breast disease and ovarian cyst development
• Decreased risk of ovarian and endometrial cancer
• Increased cervical mucus which may lower risk of STDs
• Decreased PMS symptoms
• Improved acne
• Osteoporosis protection (possibly)

Question 121

What are the side effects of oestrogen contraception?

Answer 121

• Nausea
• Breast changes (tenderness, enlargement)
• Fluid retention/bloating/edema
• Weight gain (rare)
• Migraine, headaches
• Thromboembolic events
• Liver adenoma (rare)
• Breakthrough bleeding (low estradiol levels)

Question 122

What are the side effects pf progesterone contraception?

Answer 122

• Amenorrhea/breakthrough bleeding
• Headaches
• Breast tenderness
• Increased appetite
• Decreased libido
• Mood changes
• HTN
• Acne/oily skin*
• Hirsutism*

Question 123

What are the absolute contraindications of steroidal contraception?

Answer 123

• Known/suspected pregnancy
• Undiagnosed abnormal vaginal bleeding
• Prior thromboembolic events, thromboembolic disorders (Factor V Leiden mutation; protein C or S, or antithrombin III deficiency), active thrombophlebitis
• Cerebrovascular or coronary artery disease
• Oestrogen-dependent tumors (breast, uterus)
• Impaired liver function associated with acute liver disease
• Congenital hypertriglyceridemia
• Smoker age >35 yr
• Migraines with focal neurological symptoms (excluding aura)
• Uncontrolled HTN

Question 124

What are the relative contraindications of steroidal contraception?

Answer 124

• Migraines (non-focal with aura <1 h)
• DM complicated by vascular disease
• SLE
• Controlled HTN
• Hyperlipidemia
• Sickle cell anemia
• Gallbladder disease

Question 125

Describe the mechanism of action of progesterone only contraception?

Answer 125

• Progestin prevents LH surge
• Thickening of cervical mucus
• Decrease tubal motility
• Endometrial decidualization
• Ovulation suppression – oral progestins (not IM) do not consistently suppress compared to combined OCPs

Question 126

What are the indications for progestin only contraceptive?

Answer 126

• Suitable for postpartum women (does not affect breast milk supply)
• Women with contraindications to combined OCP (e.g. thromboembolic
  or myocardial disease)
• Women intolerant of estrogenic side effects of combined OCPs

Question 127

What are the contraindications of progestin only contraception?

Answer 127

None

Question 128

What are the mechanisms of action for IUD contraception?

Answer 128

• Copper-containing IUD: mild foreign body reaction in endometrium toxic to sperm and alters sperm motility
• Progesterone-releasing IUD (Mirena®): decidualization of endometrium and thickening of cervical mucus; minimal effecton ovulation
• Highly effective (95-99%); failurerate 0-1.2%
• Contraceptive effects last 5 yr
• Reversible, private, convenient
• May be used in women with contraindications to OCPs or wanting long-term contraception

Question 129

What are the side effects of IUDs?

Answer 129

• Both Copper and Progesterone IUD
  
  • Breakthrough bleeding
  • Expulsion (5% in the 1st yr, greatest in 1st mo and in nulliparous women)
  • Uterine wall perforation (1/1,000) on insertion
  • If pregnancy occurs with an IUD, increased risk of ectopic
  • Increased risk of PID (within first 10 d of insertion only)
• Copper IUD: increased blood loss and duration of menses, dysmenorrhea
• Progesterone IUD: bloating, headache

Question 130

What are the absolute contraindications of IUD?

Answer 130

• Both Copper and Progesterone IUD
  
  • Known or suspected pregnancy
  • Undiagnosed genital tract bleeding
  • Acute or chronic PID
  • Lifestyle risk for STDs*
• Copper IUD:
  
  • Known allergy to copper
  • Wilson’s disease

Question 131

What are the relative contraindication to IUDs?

Answer 131

• Both Copper and Progesterone IUD
  
  • Valvular heart disease
  • Past history of PID or ectopic pregnancy
  • Presence of prosthesis
  • Abnormalities of uterine cavity, intracavitary fibroids
  • Cervical stenosis
  • Immunnosuppressed individuals (e.g. HIV)
• Copper IUD: severe dysmenorrhea or menorrhagia

Question 132

Describe the normal histology of the cervix.

Answer 132

• Endocervix: lined by columnar epithelium that secretes mucus; epithelium has complex infoldings that resemble glands or clefts on cross section; mucosa rests on inconspicuous layer of reserve cells
• Ectocervix (exocervix): covered by nonkeratinizing, stratified squamous epithelium, either native or metaplastic; has basal, midzone and superficial layers; after menopause is atrophic with mainly basal and parabasal cells with high N/C ratio that resembles dysplasia; prepubertal girls have similar appearing epithelium
• Squamocolumnar (SC) junction: where squamous and columnar epithelium meets; lined by krt7+ non-stratified cuboidal cells; can migrate proximately as columnar epithelium is replaced by metaplastic squamous epithelium, due to increased estrogen production and growth of vaginal bacterial flora (new SC junction); recent studies support SC junction as site of “embryonic cell population”, involved in cervical remodeling (metaplasia and microglandular hyperplasia), and as cell of origin for cervical cancer and its precursors.
• Transformation zone: also called ectropion, area between original SC junction and new SC junction due to regenerative metaplastic response; site of > 90% of squamous cell carcinomas and dysplasia

Question 133

What are the requirements for conception?

Answer 133

• Ovary
• Tube
• Cervix
• Endometrium
• Sperm

Question 134

Define infertility.

Answer 134

Inability to conceive or
carry to term a pregnancy after 1 yr of
regular, unprotected intercourse

Question 135

Define primary and secondary infertility.

Answer 135

• Primary infertility: infertility in the context of no prior pregnancies
• Secondary infertility: infertility in the context of a prior conception

Question 137

Describe the pathogenesis of type I endometrial carcinoma?

Answer 137

• Most are well differentiated and mimic proliferative endometrial glands.
• Typically arise in the setting of endometrial hyperplasia, and like endometrial hyperplasia they are associated with:
  
  • Obesity
  • DM (found in more than 60%)
  • HTN
  • infertility
  • Unopposed oestrogen stimulation
• Needs to develop alterations in tumour suppressor genes and oncogenes.
  
  • PTEN mutation develops forming hyperplasia of the endometrium.
  • Further development of mutations in PI3K/AKT pathway which is a hallmark of this particular tumour → this augments expression of oestrogen receptor-dependent target genes in endometrial cells. Individual tumours may harnour multiple mutations that increase PI3K/AKT signalling which include:
    
    • PIK3CA
    • ARID1A
    • KRAS

Question 138

Describe the pathogenesis of Type II endometrial carcinoma?

Answer 138

• Arise in the setting of endometrial atrophy, 10 years later than those with type I.
• Poorly differentiated
• Serous carcinoma is the most common subtype, others include clear cell and malignant mixed mullerian.
• Mutations in the tumour suppressor TP53 are present in at least 90% of serous endometrial carcinoma. The majority are missense mutations that result in an accumulation of the altered protein.
• Poorer prognosis than type I.

Question 139

What are some causes of postmenopausal bleeding?

Answer 139

• Cancer:
  
  • Uterus, endometrial, uterine sarcoma
  • cervix or vagina
• Endometrial atropgy or vaginal atrophy
• uterine fibroids or polyps
• INfection
• Medictions: HRT, tamoxifen
• Pelvic trauma
• Bleeding from rectum or urinary tract
• Endometrial hyperplasia

Question 140

What are the risk factors for endometrial cancer?

Answer 140

• Type I: excess estrogen (estrogen unopposed by progesterone)
  
  • obesity
  • PCOS
  • unbalanced HRT (balanced HRT is protective)
  • nulliparity
  • late menopause
  • oestrogen-producing ovarian tumors (e.g. granulosa cell tumors)
  • HNPCC (hereditary non-polyposis colorectal cancer)/Lynch II syndrome
  • tamoxifen
• Type II: not estrogen-related
  
  • possibly tamoxifen

Question 141

Describe the classification and clinical features of endometrial cancer?

Answer 141

• Type I (well-differentiated endometrioid adenocarcinoma) ~80% of cases:
  
  • postmenopausal bleeding in majority, abnormal uterine bleeding in majority of affected pre-menopausal women (menorrhagia, intermenstrual bleeding)
• Type II (serous, clear cell carcinoma, grade 3 endometrioid, undifferentiated, carcinosarcoma) _~15% of cases:
  
  • may not present with bleeding in early stage, more likely to present with advanced stage disease with symptoms like ovarian cancer (i.e. bloating, bowel dysfunction, pelvic pressure).

Question 142

What Ix need to be done with a women who has postmenopausal bleeding?

Thinking it cancer?

Answer 142

• Physical exam:
  
  • Vaginal including bimanual
  • Cardio
  • Lymph nodes
• Blood tests: Rule out other causes of bleeding
  
  • FBC, UEC, LFTs,
• endometrial sampling
  
  • office endometrial biopsy
  • D&C ± hysteroscopy
• ± pelvic ultrasound (in women where adequate endometrial sampling not feasible without invasive methods)
  
  • not acceptable as alternative to pelvic exam or endometrial sampling to rule out cancer

Question 143

Describe the principle macroscopic and microscopic features of a mature teratoma.

Answer 143

• Macroscopic:
  
  • These tumors are often called “dermoid cysts” because they are mostly cystic and mostly contain ectodermal elements, typically resulting in the abundant hair.
• Microscopic:
  
  • this teratoma is seen to have cartilage as well as adipose tissue and even intestinal glands at the right, while at the left are a lot of thyroid follicles. The presence of abundant thyroid tissue within a mature teratoma can be termed struma ovarii. Rarely, a struma ovarii can even be a cause for hyperthyroidism.

Question 146

Describe the histological features of type I and type II endometrial carcinoma?

Answer 146

• Type I:
  
  • Endometrioid microscopic pattern with glandular, cribriform, and papillary features.
• Type II:
  
  • Serous microscopic pattern with papillary features with glands having irregular luminal borders; high mitotic rate.

Question 147

Discuss an approach to the DDx of pelvic pain?

Answer 147

Question 148

What Ix should be performed on a patient with an ovarian mass?

Answer 148

• Exam:
  
  • Pelvic
  • Vaginal + spectulum: PAP smear + high vaginal swab
• Laboratory:
  
  • FBC, UEC, LFT
  • ß-HCG
  • CA-125
  • Urinalysis: MCS
• Imaging:
  
  • US: pelvic, transvaginal ± Biopsy or FNA
  • CT/MRI (if pregnant)

Question 149

DDx for ovarian mass?

Answer 149

• Functional tumours (all benign)
  
  • Follicular cyst
  • Lutein cyst
  • Theca-Lutein cyst
  • Endometrioma
  • PCOS
• Benign germ-cell tumours
  
  • Benign cystic teratoma (dermoid)
• Malignant germ cell tumours
  
  • Dysgerminoma
  • Immature teratoma
  • Gonadoblastoma
• Epithelial ovarian tumours (malignant or borderline)
  
  • Serous

Question 150

Describe the histogenesis of teratomas?

Answer 150

• Elements of all 3 cell lines: ectoderm, mesoderm, endoderm.
• Contains dermal appendages (sweat and sebaceous glands, hair follicles, teeth)

Question 152

What are the risk factors for ovarian cancer?

(epithelial ovarian cancer)

Answer 152

• excess oestrogen
  
  • nulliparity
  • early menarche/late menopause
• age
• family history of breast, colon, endometrial, ovarian cancer
• race: Caucasian

Question 153

What are the protective factors for ovarian cancer?

Answer 153

• OCP: likely due to ovulation suppression (significant reduction in risk even after 1 yr of use)
• pregnancy/breastfeeding
• tubal ligation (recently questioned)
• hysterectomy (without removal of ovaries)
• BSO (prophylactic surgery performed for this reason in high risk women – i.e. BRCA mutation carriers)

Question 154

What is the management principles of cancer of the ovary?

Answer 154

• Do nothing
• Do something:
  
  • Medical:
    
    • Chemotherapy
    • Monitor with CA-125
  • Surgical:
    
    • Tumour resection

Question 156

What are the management options for endometriosis?

Answer 156

• depends on certainty of the diagnosis, severity of symptoms, extent of disease, desire for future
  fertility, and impact to GI/GU systems (e.g. intestinal obstruction)
• medical
  
  • NSAIDs
  • pseudopregnancy
    
    • cyclic/continuous oestrogen-progestin (OCP)
    • medroxyprogesterone (Depo-Provera®)
    • dienogest (Natazia®)
  • pseudomenopause
    
    • 2nd line: only short-term (<6 mo) due to osteoporotic potential with prolonged use, unless combined with add-back therapy (e.g. oestrogen/progesterone or SERM); if
      long-term use required, add-back estrogen+progesterone
    • danazol (Danocrine®): weak androgen
      – side effects: weight gain, fluid retention, acne, hirsutism, voice change
    • leuprolide (Lupron®): GnRH agonist (suppresses pituitary) – side effects: hot flashes, vaginal dryness, reduced libido – can use ≥12 mo with add-back progestin or oestrogen
• surgical
  
  • conservative laparoscopy using laser, electrocautery ± laparotomy
    
    • ablation/resection of implants, lysis of adhesions, ovarian cystectomy of endometriomas
  • definitive: bilateral salpingo-oophorectomy ± hysterectomy
  • ± follow-up with medical treatment for pain control not shown to impact on preservation of fertility
  • best time to become pregnant is immediately after conservative surgery