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3a. O&G > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

– Cluster 1: Menstrual Cycle –
Describe the hormonal control of the menstrual cycle.

A
  • follicular (days 1-14; variable): rise in FSH, causing growth of endometrium and increased depth of spiral arteries. Primordial follicle matures to a Graafian follicle, then a mature follicle. Receptibility to sperm increases, and mucous becomes abundant and watery
  • ovulation (day 14): LH surge causes mature follicle to break, releasing an oocyte and producing the corpus luteum
  • luteal phase (days 14-28): negative feedback by LH increases progesterone production (by corpus luteum, which also produces oestradiol); mucous thickens (hostile to sperm), and hypothalamic temperature increases
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2
Q

Describe the actions of FSH and LH.

A
  • LH stimulates theca cells to produce progesterone and androstenedione by activating cholesterol desmolase
  • FSH stimulates granulosa cells to convert androstenedione to testosterone, then to 17-beta-oestradiol, by aromatase
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3
Q

Describe the normal blood content of menses.

A
  • Blood volume: ranges from slight spotting to 80ml (average 30ml)
  • Menstrual blood is chiefly arterial (25% is venous)
  • Usual duration of menstrual flow is 3-5 days (normal range 1-8 days)
  • Blood contains prostaglandins, tissue debris, and fibinolysates (lyses clots)
  • Loss >80ml is considered abnormal
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4
Q

– Cluster 2a: Menstrual disorders (PMS) –
Describe the physical, psychological, and behavioural changes observed in PMS.

A
  • physical: headache, mastalgia, weight gain, fluid retention, joint/skin pain
  • psychological: irritability, emotional lability, low mood, tension, mood swings
  • behavioural: sleep disturbance, change in appetite, restlessness, poor conc., confusion, social withdrawal
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5
Q

What is the difference between PMD and PMDD?

A
  • postmenopausal dysphoric disorder: occurs with accompanying mood swings, anxiety, and/or depression
  • SSRIs can benefit
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6
Q

Describe the management options for PMD.

A
  • lifestyle: sleep, exercise, smoking and alcohol, small balanced meals rich in complex carbohydrates
  • 1st line: despiramine-containing COC (Yasmin, Eloine)
  • 2nd line: GnRH agonists [can cause vasomotor symptoms, such as hot flushes, & osteoporosis]
  • SSRIs/SNRIs, CBT
  • hysterectomy with bilateral salpingo-oophorectomy: last resort
  • additional: vitamin B6, oil of evening primrose, oestrogen patches/implants
  • SSRIs / psychotherapy for PMDD
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7
Q

– Cluster 2b: Menstrual disorders (menorrhagia) –
Define heavy menstrual bleeding (HMB).

A

Blood loss that interferes with physical, social, emotional or material aspect of a woman’s life.
* previously defined as total blood loss >80ml/menses, but this is obviously difficult to quantify
* now is shifted to what the woman considers prolonged and increased flow
- accounts for 20% of gynae appts.
- most common cause of iron deficiency anaemia

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8
Q

What are the key causes of menorrhagia?

A
  • gynae: fibroids, adenomyosis, polyps, endometrial hyperplasia, endometriosis, uterine/cervical malignancy
  • obstetric: miscarriage, ectopic, gestational trophoblastic disease, placenta praevia
  • sexual health: copper IUD, PID, surgical TOP, hormones (oestrogen/tamoxifen)
  • endocrine: hormone-producing ovarian tumours, thyroid dysfunction, DM, adrenal disease, prolactin disorders
  • vascular: AVM, coagulation disorders (von Willebrand, ITP, factor deficiencies)
  • systemic: cirrhosis, renal disease
  • drugs: anticoagulants (warfarin, clopidogrel, DOACs)
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9
Q

Define the relationship between dysfunctional uterine bleeding (DUB) and menorrhagia, and describe its investigation.

A
  • DUB: non-organic menorrhagia occuring in the absence of pathology; therefore is a diagnosis of exclusion
  • therefore requires exclusion of other causes of menorrhagia
    – FBC
    – systemic tests (TFTs, coag, renal, LFTs)
    – TVUS (endometrial thickness, fibroids)
    – endo sampling (Pipelle biopsy, D&C etc.)
    – colposcopy (abnormal cervix)
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10
Q

Describe the management options for DUB.

A
  • 1st line: Mirena coil IUS (LNG-IUS)
  • 2nd line: tranexamic acid (anti-fibrinolytic) / COCP
  • 3rd line: DMPA
  • 4th line: surgery
  • unsure in role: mefenamic acid (an NSAID; C/I in PUD, asthma); progestogens, GnRH agonists (goserelin, buserelin), androgen (danazol)
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11
Q

Describe the surgical management of DUB.

A
  • two major options: endometrial resection/ablation, and hysterectomy
  • ablation: day-case procedure, requires combined HRT
  • hysterectomy: major operation, oestrogen-only HRT
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12
Q

– Cluster 2c: Dysmenorrhoea –
Define dysmenorrhoea.

A
  • excessive pain during the menstrual period
  • primary: no underlying pathology, affects 50% of menstrual women
  • secondary: due to underlying pathology
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13
Q

Describe the aetiologies of dysmenorrhoea.

A
  • primary (no underlying pathology): normal examination
  • endometriosis: endometrial tissue in the peritoneum/pelvic cavity; occurs with menorrhagia and dyspareunia
  • adenomyosis: endometrial tissue between muscle layers of the uterus; occurs with prolonged menorrhagia
  • fibroids: menstrual pain with pressure effects on adjacent organs
  • chronic PID: history of STI, pain not limited to menstruation
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14
Q

Define adenomyosis and leiomyoma.

A
  • adenomyosis: presence of endometrial tissue in the myometrium
  • leiomyoma: benign, smooth muscle tumour
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15
Q

Describe the investigations of dysmenorrhoea.

A
  • high vaginal and endocervical swabs (pelvic infection)
  • pelvic USS (endometriosis, adenomyosis, fibroids)
  • diagnostic laparoscopy (other investigations normal but symptoms persist, or when Hx is suggestive of endometriosis)
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16
Q

Describe the management of dysmenorrhoea.

A
  • 1st line: NSAIDs (mefenamic acid, ibuprofen): effective in 80%
  • 2nd line: COCP
  • additional options: LNG-IUS, GnRH analogues
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17
Q

– Cluster 2d: Menstrual disorders (IMB/PCB/PMB) –
Describe the causes of IMB (intermenstrual bleeding).

A
  • cervical ectropion
  • PIDs, STDs
  • endometrial/cervical cancers/polyps
  • undiagnosed pregnancy/complications, hydatidiform molar disease
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18
Q

Define and describe the causes of PCB (postcoital bleeding).

A
  • PCB: bleeding brought on by sexual intercourse
  • most common cause is cervical ectropion
  • cervical carcinoma, trauma, polyps
  • atrophic vaginitis
  • cervicitis secondary to STDs
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19
Q

Describe the pathology, presentation, investigation, and treatment of cervical ectropion.

A
  • cervix develops a red, raw appearance that may bleed on contact, most often occuring due to high oestrogen states in pregnancy, or use of hormonal contraceptives (esp. COCP)
  • commonly presents with PCB (raw area irritated by penis during intercourse) or IMB
  • often diagnosed during smears or colposcopy
  • treatment usually not necessary and ectropion resolves (3-6 months following birth). if Mx necessary: cauterisation
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20
Q

Describe the causes of PMB (postmenopausal bleeding).

A

-PMB in a woman >55 is endometrial cancer until proven otherwise
- atrophic vaginitis (most common)
- endometrial polyps, hyperplasia, carcinoma
- cervical carcinoma
- ovarian carcinoma
- vaginal carcinoma (rare)

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21
Q

Describe the investigation surrounding PMB.

A
  • TVUS is first-line to assess endometrial thickness
    – <3mm: low likelihood of cancer
    – >4mm: further Ix (endometrial biopsy)
    – <5mm: cutoff for patients taking HRT
  • hysteroscopy + endometrial biopsy: indicated for patients on tamoxifen (thickened, cystic, irregular endometrium)
  • CT/MRI of uterus, pelvis, abdomen
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22
Q

Describe the management of PMB.

A
  • atrophic vaginitis: topical oestrogen, vaginal lubricants, HRT
  • endometrial hyperplasia: D&C, progestogen (Mirena IUS first-line)
  • cancer: refer to oncology
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23
Q

– Cluster 2e: Menstrual disorders (PCOS) –
Describe the pathology of PCOS.

A
  • increased frequency of the GnRH pulse generator, causing an increase in LH pulses and androgen secretions
  • hyperinsulinaemia and insulin resistance, hypertension etc.: mechanism not completely understood
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24
Q

Describe the clinical features of PCOS.

A
  • subfertility, infertility
  • oligo/amenorrhoea (increased risk of endometrial hyperplasia and carcinoma)
  • hyperandrogenism (hirsutism, acne, acanthosis nigricans, virilisation)
  • metabolic (obesity, insulin resistance, diabetes, lipid abnormalities, increased cardiovascular risk)
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25
Q

Describe the diagnostic criteria for PCOS.

A

These are the Rotterdam criteria.
- oligo/amenorrhoea
- hyperandrogenism (e.g. acne, hirsutism, raised testosterone)
- USS: polycystic ovaries (12+ follicles 2-9mm; or increased ovarian volume >10cm^3)
2/3 criteria are diagnostic.

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26
Q

Describe the investigations of PCOS.

A
  • serum testosterone, free androgen index (testosterone/SHBG x 1000)
  • other androgens
  • LH:FSH (>2); classically used, current utility is doubtful
  • exclusion of other disorders (17a-hydroxyprogesterone for CAH, TFTs, prolactin, 24hr urinary cortisol for Cushing’s)
  • ovarian/pelvic ultrasound
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27
Q

Describe the management of PCOS.

A
  • health promotion is appropriate for all; this includes weight loss and exercise
  • metformin is beneficial for restoring menstrual regularity, hirsutism, acne, and fertility
  • otherwise, management depends largely on what the patient presents with and what their main concerns are.

Hirsutism and acne
- first line: co-cyprindol (Dianette)
- other options: COCP, elfornithine (antiprotozoal), specialist guided (spironolactone, flutamide, finasteride)

Infertility
- first line: weight loss if BMI >30 indicated before ovulation treatment
- medical first line: clomiphene citrate
- additional treatments: metformin, gonadotrophins, ovarian drilling, IVF as a last resort

Amenorrhoea
- COCP, cyclical medroxyprogesterone, or Mirena IUS (for endometrial risk)
- refer for TVUS to assess endometrial thickness

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28
Q

– Cluster 2f: Amenorrhoea –
Define primary and secondary amenorrhoea.

A
  • primary: failure to establish menstruation by 15 years in girls with normal 2ndry sexual characteristics, or 13 in girls with no 2ndry sexual characteristics
  • secondary: cessation of menstruation in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea
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29
Q

Name the causes of primary amenorrhoea.

A
  • anatomical/congenital
    – congenital malformation of the genital tract
    – Mullerian agenesis
    – imperforate hymen
    – genetic (Turner’s, androgen insensitivity, 5-alpha reductase deficiency)
  • premature ovarian failure/insufficiency
  • endocrine
    – hypothalamic (Kallmann’s, anorexia)
    – pituitary (adenoma, sarcoidosis)
    – testicular feminisation
    – congenital adrenal hyperplasia
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30
Q

Name the causes of secondary amenorrhoea.

A
  • hypothalamic (e.g. secondary stress, excessive exercise)
  • hyperprolactinaemia
  • Sheehan’s syndrome, Asherman syndrome
  • thyrotoxicosis, hypothyroidism
  • premature ovarian failure
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31
Q

Describe the investigation and management of amenorrhoea.

A
  • Ix: exclude pregnancy, FBC, U&Es, TFTs, gonadotrophins (?hypothalamic or ovarian dysfunction), prolactin, androgens (PCOS), oestradiol
  • primary: investigate and treat any underlying cause
  • gonadal dysgenesis: HRT to prevent osteoporosis etc.
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32
Q

Describe the broad differential diagnosis of infertility based on sex hormone analysis.

A
  • raised LH/FSH, low E2: normogonadotropic hypogonadism, e.g. the problem is with the gonads. can include ovarian failure, POI, steroid defect, chemotherapy etc.
  • low LH/FSH/E2: hypogonadotropic hypogonadism, e.g. the problem is with the hypothalamus. can include Kallmann syndrome, weight, exercise, anorexia etc.
  • low LH/FSH/E2, raised PRL: prolactin-related. can include prolactinoma, PCOS, lactation, or dopamine antagonists
  • raised LH/PRL/T: PCOS, or rarely Cushing’s
  • low LH/FSH/E2, raised T: androgen excess: can include gonadal or adrenal tumour, CAH etc.
  • raised E2/PRL: pregnancy
  • normal: anatomical disorder, e.g. uterine/vaginal disorder, imperforate hymen, absent uterus, lack of endometrium
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33
Q

Define premature ovarian insufficiency (POI), and describe its causes, investigation findings, and management.

A
  • the ovaries stop functioning fully before age 40
  • aetiologies: autoimmune (fragile X, Turner’s), radio/chemotherapy, infectious (e.g. mumps), autoimmune
  • elevated LH/FSH (akin to menopause), reduced E2. FSH should be sampled twice 4-6 weeks apart
  • primary disease is rarely treatable, but HRT/COCP is usually given for oestrogen deficiency until the average age of menopause (51) to protect against osteoporosis
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34
Q

– Cluster 3: Menopause –
Define and describe the menopause.

A
  • occurs in all menstruating females due to a non-pathologic oestrogen deficiency
  • granulosa cells (oestrogen production) diminish with age, increasing FSH and LH
  • average age 51, premature menopause defined as <45
  • surgical menopause: hysterectomy with bilateral oophorectomy
  • chemical menopause: antioestrogens, chemotherapy
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35
Q

Describe the symptoms associated with menopause.

A
  • vasomotor: hot flashes, night sweats, palpitation, migraine without aura
  • urogenital: vaginal atrophy, urethral atrophy (incontinence etc.), sexual dysfunction
  • joint aches and pains, dry and itchy skin
  • psychogenic: anger/irritability, anxiety, depression, sleep disturbance, loss of self-esteem
  • hypertension, weight gain
  • decreased height, associated with osteoporosis
36
Q

Describe the lifestyle management of menopause.

A
  • hot flashes: regular exercise, weight loss, reduction of stress
  • sleep disturbance: avoiding exercise in the late evening, good sleep hygiene
  • mood: improving sleep, regular exercise, relaxation
  • cognitive: regular exercise, good sleep hygiene
37
Q

What is HRT? What are its indications?

A
  • HRT consists of an oestrogenic compound (replaces reduced levels experienced through menopause), normally combined with a progestogen (if the woman has a uterus, to reduce risk of endometrial cancer)
  • main indication is vasomotor symptoms
  • HRT is also used in premature menopause to prevent osteoporosis
38
Q

Describe the side effects and complications of HRT.

A
  • oestrogen: breast enlargement, cramps, dyspepsia, fluid retention, nausea, headaches
  • progestogen (similar to PMS): fluid retention, mastalgia, headaches, acne, psychogenic, constipation, increased appetite
  • risk of breast cancer, VTE, stroke, ischaemic heart disease, and ovarian cancer is increased related to duration taken
  • oestrogen alone increases risk of endometrial cancer; progestogen mitigates this risk
39
Q

Name the absolute contraindications of HRT.

A
  • suspected pregnancy
  • gynae: breast, endometrial cancers
  • active liver disease
  • cardiovascular: uncontrolled hypertension, known VTE
  • known thrombophilia
  • otosclerosis
40
Q

Describe the non-HRT medical management of menopause symptoms.

A
  • vasomotor: SSRIs (fluoxetine, citalopram, venlafaxine)
  • vaginal dryness: lubricants, moisturisers (second line: oestrogen cream)
  • psychogenic: self-help groups, CBT, SSRIs
41
Q

Name the causes of vulval pruritis.

A
  • dermatological: eczema, atopic dermatitis, psoriasis, candida
  • lichen sclerosus
  • lichen planus
  • infection: candida, trichomonas
  • Extramammary Paget’s disease of the vulva
42
Q

Describe the appearance, presentation, and management of lichen sclerosus and lichen planus.

A
  • both are chronic inflammatory conditions of unknown aetiology; they are, however, thought to be autoimmune and often co-present with thryoid issues or pernicious anaemia
  • pruritis, skin irritation, atrophy (‘parchment paper’ appearance), plaques, fusion of labia, dyspareunia
  • as they are similar conditions they are difficult to differentiate; Wickham’s striae are specific for lichen planus
  • both are premalignant lesions and may lead to vulvar intraepithelial neoplasia (VIN), meaning biopsy is often used to exclude malignancy
  • first-line: topical high-dose steroids and emollients
  • second-line: TCIs (e.g. tacrolimus), imiquimod
43
Q

– Cluster 4: Abdominopelvic pain –
Name the differential for unilateral pelvic pain in the female.

A
  • ectopic pregnancy
  • appendicitis
  • ovarian torsion, cyst accident, fibroid degeneration
  • renal calculi
44
Q

Name the differential for diffuse pelvic pain in the female.

A
  • miscarriage
  • PID, UTI, diverticulitis
  • endometriosis
  • constipation, IBS, urinary retention
45
Q

What is the likely diagnosis for a female who experiences sudden unilateral pelvic pain after sexual intercourse or contact sport?

A

Cyst rupture/accident

46
Q

– Cluster 4a: Abdominopelvic pain (ectopic pregnancy) –
Define ectopic pregnancy.

A
  • the implantation of a fertilised ovum outside the uterus
  • 97% are tubal, with most in the ampulla; isthmus is more dangerous
47
Q

Name the risk factors associated with ectopic pregnancy.

A
  • damage to the tubes (PID, surgery)
  • previous ectopic pregnancy
  • endometriosis
  • IUCD
  • progesterone-only pill
  • IVF (3% of IVF pregnancies)
48
Q

What are the symptoms and signs of ectopic pregnancy?

A

Symptoms
- pain (constant and unilateral tubal spasm) > bleeding (less than a normal period, may be dark brown)
- dizziness, eclampsia, shoulder tip pain (peritoneal bleeding), dyspnoea
- pallor, haemodynamic instability, peritonism
- red flag: abdominal/pelvic pain requiring opiates

Signs
- abdominal tenderness
- pelvic examination: cervical excitation (cervical motion tenderness)
- vaginal examination: not recommended, as there is an increased risk of rupturing the pregnancy; if performed, however, may demonstrate an adnexal mass

49
Q

What is pregnancy of unknown location (PUL), and how is it managed?

A
  • a halfway diagnosis of ectopic pregnancy (i.e., not found on any scans)
  • M6 model: measurement of progesterone guides follow-up management
  • theoretically reveal IU/ectopic pregnancy
  • can be managed with methotrexate
50
Q

Describe the management of ectopic pregnancy.

A
  • acutely unwell: laparoscopic salpingectomy (98% of ectopic pregnancies are in Fallopian tubes)
  • stable: manage with methotrexate
  • GEM II: adds gefitinib to MTX; may reduce surgery
51
Q

Describe the types of management of ectopic pregnancy, their associated findings, and the management itself.

A
  • expectant: HCG <1000 and <35mm; no symptoms; manage with close observation and monitor beta-HCG
  • medical: HCG <1500 and <35mm; no significant symptoms; manage with methotrexate and follow-up
  • intermediate: HCG 1500-5000; offer patient choice of methotrexate and surgery
  • surgical: HCG >5000 and/or >35mm; pain and visible foetal heartbeat; managed with either salpingectomy (no risk factors for infertility) or salpingotomy (risk factors for infertility)
52
Q

– Cluster 4b: Abdominopelvic pain (acute abdomen, gynae)
Describe the clinical features, investigation, and management of Mittelschmerz.

A
  • mid-cycle pain, often sharp pain, little systemic disturbance
  • may be recurrent, settles over 24-48hrs
  • FBC normal, USS may show
  • Mx is conservative: simple analgesics and reassurance
53
Q

Describe the clinical features, investigation, and management of endometriosis.

A
  • asymptomatic (25%), other pelvic pathology (25%), menstrual irregularity, infertility, pain, deep dyspareunia, subfertility (50%)
  • USS shows free fluid; laparoscopy shows lesions; vaginal examination shows tender nodularity in the posterior fornix
  • medical management: NSAIDs, paracetamol, COCP, progestogens
  • surgical management: removal of lesions, possible colonic/rectal resection
54
Q

Describe the clinical features, investigation, and management of ovarian torsion.

A
  • sudden onset of deep colicky abdominal pain with vomiting and distress; vaginal examination may reveal adnexal tenderness
  • USS: free fluid/classic whirlpool sign
  • laparoscopy is both diagnostic and therapeutic. necrotic ovaries need to be removed.
55
Q

Describe the clinical features, investigation, and management of pelvic inflammatory disease (PID), briefly.

A
  • bilateral lower abdominal pain with vaginal discharge +/- dysuria; fever >38; Fitz-Hugh-Curtis may develop
  • pregnancy test usually negative; FBC (leucocytosis), amylase (normal); take high vaginal and urethral swabs
  • antibiotics and surgical drainage in the case of pelvic abscess
56
Q

Describe the presentation of ovarian cyst rupture/haemorrhage.

A
  • unilateral dull ache which may be intermittent, or present only during intercourse (dyspareunia)
  • torsion or rupture may lead to severe abdominal pain
  • large cysts may cause abdominal swelling or pressure effects on the bladder
57
Q

Describe the clinical features, investigation, and management of fibroids.

A
  • may be asymptomatic, present with menorrhagia, dysmenorrhoea, intramenstrual pain, subfertility, and/or pressure symptoms (urinary symptoms)
  • Ix is with TVUS
  • first-line management is Mirena IUS
  • additional options include myomectomy, hysterectomy, short-term GnRH agonist (goserelin), or uterine artery embolization
58
Q

What are the main causes of abnormal uterine bleeding (AUB, aka DUB)?

A
  • uterine: anovulatory cycles, pregnancy, miscarriage, endometritis, polyp, leiomyoma, adenomyosis
  • endocrine: PCOS, thyroid disorders, hyper PRL, hormone changes
  • bleeding disorders
  • hyperplasia, neoplasia
59
Q

– Cluster 4c: Abdominopelvic pain (ovarian cysts) –
Describe ovarian cysts.

A
  • follicular, luteal, endometriotic, epithelial, mesothelial
  • follicular cysts are very common, occurring when menstruation doesn’t
  • rarely >5cm, formed of thin-walled granulosa cells
  • may cause menstrual disturbance, may bleed/rupture, may cause acute abdomen, may be incidental
60
Q

Describe the pathology and clinical features of dermoid cysts.

A
  • formed from pluripotent stem cells (germ cells), material can include teeth, sebaceous tissue, thyroid tissue etc.
  • may be asymptomatic, pelvic pain, dyspareunia etc.
61
Q

Regarding a pelvic mass, the pelvis can be split into 4 main compartments. What are these, and what are the main pathologies that can affect each?

A
  • anterior (bladder): bladder tumour, distension
  • middle (uterus): fibroids, adenomyosis, carcinoma, sarcoma
  • posterior (bowel): bowel tumours, appendiceal mass, hernia, diverticular abscess
  • lateral (adnexae): ovarian, tubal mass, hydrosalpinx, ectopic pregnancy
62
Q

– Cluster 5: Ovarian cancer –
Name the five main categories of ovarian malignancy.

A
  • epithelial (90%): serous (70-80% of these), mucinous, endometrioid, clear cell, Brenner, undifferentiated
  • germ cell: mature cystic teratoma (‘dermoid cyst’), immature teratoma (embryonal), dysgerminoma, yolk sac, choriocarcinoma
  • stromal: fibroma, thecoma, granulosa, Sertoli, Sertoli-Leydig, steroid
  • metastatic
  • miscellaneous
63
Q

Describe the risk and protective factors associated with ovarian cancers.

A

Risk factors
- genetic: BRCA1/2, TTN, TP53, HNPCC (Lynch syndrome)
- many ovulations (early menarche, late menopause, nulliparity)
- endometriosis
- smoking and obesity
- it was traditionally thought infertility treatments increased risk; recent evidence, however, does not suggest a significant link

Protective factors
- reduced number of ovulations (COCP, pregnancies)
- breastfeeding
- sterilisation

64
Q

Describe the symptoms associated with ovarian malignancy.

A

Presentation is notoriously vague. Some symptoms can be remembered by BEAT:
- bloating and distension
– may be associated with ascites +/- pleural effusion
– women >50 with ‘IBS’
- early satiety (eating less, feeling fuller)
- abdominal and pelvic pain
- tell your GP

Others include
- urinary symptoms (e.g. urgency)
- PV bleeding
- diarrhoea

65
Q

Name the tumour markers that are associated with ovarian cancers.

A
  • CA-125 (produced by mesothelium, increased in mucinous cancers)
  • CEA (most useful with CA-125/CEA ratio, suspicious when <25)
  • AFP, HCG, LDH
66
Q

— RESUME EDITING FROM HERE —
Describe the risk of malignancy index (RMI) score used for ovarian cancer risk.

A
  • premenopausal, postmenopausal [1, 3]
  • USS findings (multiloculated, solid areas, bilateral, ascites, metastases) [none 0, 1 = 1, >1 = 3]
  • serum CA-125 [absolute level]
  • RMI = above 3 parameters multiplied
67
Q

Describe the management options for ovarian cancer.

A
  • staging laparotomy and debulking first used, where abdomen and pelvis are assessed for deposits and allow staging
  • early: open hysterectomy, BSO, infracolic omentectomy
  • late: radical debulking with aggressive cytoreduction
  • neoadjuvant chemo
68
Q

What is a Kruckenberg tumour?

A

Has a characteristic signet ring histology which metastasise from the GI tract (usually the stomach).

69
Q

– Cluster 6: Endometrial cancer –
Describe the classification of endometrial hyperplasia.

A
  • simple: general distribution, dilated glands, normal cytology
  • complex: foetal, crowded glands, normal cytology
  • atypical: atypical cytology, cancer precursor
70
Q

Describe the classification of uterine adenocarcinoma.

A
  • type 1: endometrioid, mucinous - unopposed oestrogen, atypical hyperplasia, PTEN, KRAS, PK3CA
  • type 2: serous, clear cell - elderly postmenopausal women, more aggressive
71
Q

How does obesity increase the risk of uterine adenocarcinoma?

A
  • endocrine and inflammatory changes to adipocytes, which express aromatase
  • dec. SHBG (inc. free biologically active hormone)
  • altered insulin (IGF can then exert effects of the endometrium)
72
Q

Describe the management options for uterine malignancy, including the complications.

A
  • surgical removal of uterus and cervix, traditionally by open approach
  • other options: BSO and/or PLND
  • complications: haemorrhage, infection, bladder/bowel problems, DVT/PE, hernias etc.
73
Q

– Cluster 7: Cervical cancer –
Name and describe the main histological areas of the cervix.

A
  • endocervix (inner): mainly glandular
  • ectocervix (outer): squamous epithelium
  • transitional zone (squamocolumnar junction): between ecto- and endo-, most likely to be infected by HPV
74
Q

Describe the categories of pathology affecting the cervix.

A
  • inflammation (cervicitis, follicular, chlamydia, HSV)
  • CIN (HPV 16/18, many sexual partners, young at first intercourse etc.)
  • condylomata acuminatum (HPV 6/11; thickened papillomatous squamous epithelium with cytoplasmic vacuolisation ‘koilocytosis’)
  • cervical cancers (SCC 75-95%, adenocarcinoma 5-25%)
75
Q

Describe the histological findings and classification of cervical intraepithelial neoplasia (CIN).

A
  • delayed maturation and differentiation (immature basal cells)
  • nucleolar hyperchromasia, increased N:C ratio, pleomorphism)
  • excess mitotic activity
  • CIN I, II, III (basal 1/3, extends to middle 1/3, then full thickness)
76
Q

Cervical SCC is commonly asymptomatic and is highly preventable by screening. What are the possible presentations?

A
  • AUB (PCB/PMB)
  • brownish/blood staining
  • contact bleeding due to friable epithelium
  • pelvic pain
  • haematuria, UTI
  • ureteric obstruction, renal failure etc.
77
Q

Describe the different types of vulvar pathology.

A
  • VIN: usual-type (HPV-driven), dVIN (differentiated, independent of HPV)
  • vulvar invasive SCC
  • vulvar Paget’s (crusting rash with sharp demarcation, pruritis, and pain). may be primary (intraepithelial glandular) or secondary (colorectal, urothelial)
  • candida
  • Bartholin gland abscess
  • dermatoses (lichen sclerosis, planus, psoriasis)
  • vulvovaginal atrophy
78
Q

Describe the surgical management of cervical cancer.

A
  • stage 1a, 2: LLTEZ, coneloscopy (fertility desired); hysterectomy (family completed)
  • stage Ib: trachelectomy (fertility), radical hysterectomy (family completed)
  • > stage Ib: chemotherapy
79
Q

Describe the surgical management of vulvar cancer.

A
  • wide local incision of vulval lesions with 1cm free margin

- if depth >1mm, surgery should involve groin node removal (unilateral / bilateral depending on site)

80
Q

Regarding public health and cervical pathology:

  • who is eligible for screening?
  • who is now vaccinated against HPV?
  • why are both vaccination and screening required?
A
  • all women or those with a cervix aged 25-64
  • girls and boys of school age (12-13); two doses separated by 6 months
  • the vaccination (HPV16/18) only offers protection against 70% of cancers, as 30% are not caused by these subtypes
81
Q

Describe the screening pathway associated with cervical screening.

A

speculum exam, brush sample of transformation zone, testing for HPV 16/18

  • negative: repeat 5y
  • positive: perform cytology test
    • positive: colposcopy
    • negative: repeat screen 12m
82
Q

Describe the risk factors for prolapse.

A

female sex, childbirth, forceps delivery, obesity

  • stressors (smokers cough, COPD, heavy lifting, constipation)
  • Marfan’s, Ehlers-Danlos
83
Q

Describe the symptoms and classification of uterine prolapse.

A
  • heaviness/pressure, bulging, tissue protrusion, urinary incontinence / retention, splinting, vaginal wall, trouble with bowel movements, dyspareunia
  • 1st degree: within the vagina
  • 2nd: at the introitus
  • 3rd: outside the vagina
  • 4th / proincidenta: entirely outside without the vagina
84
Q

Describe the management options for gynaecological prolapse [3+3].

A
  • lifestyle: weight loss, smoking cessation, avoiding heavy lifting, caffeine reduction etc.
  • physiotherapy, pessaries etc.
  • surgeries:
    • cystocele: anterior colporrhaphy
    • rectocele: posterior colporrhaphy
    • uterine: sacrospinous fixation, mesh treatment etc.
85
Q

Regarding ultrasound:
- describe the benefits and difficulties
- describe the two O&G approaches and their differences
[4]

A
  • benefits: cheap and safe (no ionising radiation), very good definition of different pelvic organs and can be used as an adjunct to clinical examination
  • difficulties: obesity, gaseous distension, operator dependant
  • TA (transabdominal): requires full bladder, good initial view
  • TV (transvaginal): requires empty bladder, higher frequency and spatial resolution, can be used to evaluate ovarian volume
86
Q

Describe the key indications for CT [4], MRI [3], and HSG [1] in O&G disease.

A
  • CT: acute abdomen (after USS), post-surgical complications, staging malignancy, assessing response to cancer treatment
  • MRI: cervical cancer staging, evaluation of adnexal masses, subfertility (in conjunction with pituitary MRI)
  • HSG (hysterosalpingogram): infertility by tubal patency

3a. O&G (6 decks)

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