Gynaecology Flashcards

(96 cards)

1
Q

Average blood loss in a menstrual cycle

A

37-43ml

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2
Q

Normal menstrual cycle

A

Days 1-4: menses

Days 5-13:

  • Follicular phase ovarian cycle: follicles develop, one follicle becomes dominant
  • Proliferative phase uterine cycle: endometrial proliferation

Day 14: ovulation

Days 15-28:

  • Luteal phase ovarian cycle: formation of corpus luteum
  • Secretory phase uterine cycle: endometrial changes to secretory lining under the influence of progesterone
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3
Q

Hormones involved in the menstrual cycle and at which points

A

Days 5-13: rise in FSH -> development of follicles -> secretion of oestrogen

Day 14: when there is sufficient oestrogen, this causes a surge of LH to be released -> ovulation

Days 15-28: progesterone secreted by corpus luteum. if fertilisation does not occur then the corpus luteum will degenerate and progesterone levels fall. Oestrogen levels rise during this period.

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4
Q

Differential diagnoses for IMB and PCB

A

Cervical bleeding: ectropion, polyps, malignancy, cervicitis

Intra-uterine: polyps, submucous fibroids, endometrial hyperplasia, endometrial malignancy, endometriosis

Hormonal: breakthrough bleeding

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5
Q

Investigations for PCB and IMB

A
High vaginal swab and endocervical swabs (STIs)
Cervical smear (CIN, cancer)
Pelvic USS (polyps, fibroids)
Hysteroscopy and endometrial biopsy
Laparoscopy
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6
Q

How much blood defines menorrhagia?

Signs/symptoms

Causes of menorrhagia

A

> 80ml/cycle
60-70% get anaemia
May have menstrual pain, lethargy, breathlessness, affects QoL

Causes:

  • Systemic: thyroid disease, clotting disorders
  • Iatrogenic: IUD, IUS, POP, implant, depo, anticoag
  • Local pathology: dysfunctional uterine bleeding, fibroids, endometrial polyps, endometrial carcinoma, endometriosis, PID
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7
Q

Dysfunctional uterine bleeding

  • what is it
  • diagnosis
  • management
A

Most common cause of menorrhagia
Diagnosis of exclusion
Managed with OCPs or prostaglandin inhibitors (mefenamic acid)

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8
Q

Investigations for menorrhagia

A

Subjective assessment/ pictorial blood loss chart to assess degree of menorrhagia

  • Blood tests: FBC, TFT, clotting studies
  • Pelvic USS
  • Endometrial biopsy
  • Cervical smears
  • Diagnostic hysteroscopy
  • Diagnostic laparaoscopy
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9
Q

Management of menorrhagia

A

Correct iron deficiency anaemia
Treat systemic disease or focal pathology

First line if needing contraception: mirena IUS
Second line: COCP
Third line: long acting progesterone (eg. depo, implant)

First line if not needing contraception: tranexamic acid (or mefenamic acid, esp if dysmenorrhoea)

Surgical management:

  • Hysteroscopy
  • Open myomectomy
  • Endometrial ablation
  • Hysterectomy
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10
Q

Tranexamic acid

  • MoA
  • Risk
  • At which part of the menstrual cycle are these taken?
A

Antifibrinolytic. Prevents activation of plasminogen into plasmin -> reduces excessive fibrinolysis

Risk of thrombosis

Start taking at the beginning of menses for 4 days

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11
Q

Mefenamic acid

  • MoA
  • At which part of the menstrual cycle are these taken?
A

NSAID.
Prostaglandin inhibitor.
Inhibits COX enzymes -> prevents conversion of arachidonic acid into prostaglandins (prostaglandins are vasodilators and they inhibit platelet aggregation)

Taken during menses

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12
Q

Presentation of endometriosis

A

Growth of ectopic endometrial tissue outside of the uterine cavity
Chronic pelvic pain
Dysmenorrhoea (often starts before menses)
Deep dyspareunia
Subfertility
Urinary symptoms
Dyschezia (painful bowel movements)

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13
Q

Differential diagnoses for endometriosis

A
PID
Pelvic pain syndrome
Submucous fibroids
Ovarian accident
Adhesions
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14
Q

Examination, investigations and management for endometriosis

A

Examination:
Retroverted fixed uterus, tender vaginal fornices, uterine tenderness

Ix:

  • Pelvic USS first as less invasive
  • Diagnostic laparoscopy is gold standard (active endometriosis shows powder-burn spots and chocolate cysts)

Mx:

  • First line analgesia: paracetamol and/or NSAIDs (mefenamic acid, naproxen, ibuprofen)
  • COCP helps symptoms by stopping period
  • POP, depot, implant, IUS

Secondary care:

  • GnRH analogues can induce pseudo-menopause
  • Surgical: laparoscopic diathermy, laser ablation, excision of deposits, total abdominal hysterectomy with bilateral salpingo-oophorectomy
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15
Q

Uterine fibroids presentation

A
Asymptomatic
Menorrhagia (due to increased surface area of endometrium, and production of prostaglandins)
Abdominopelvic mass
Abdominopelvic pain
Subfertility
Urinary frequency, urgency, nocturia
Rectal pressure and abdo bloating
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16
Q

Risk factors for uterine fibroids

Protective factors

A

African-caribbean
Later reproductive years
Nulligravidity
Obesity

Protective factors: smoking, COCP, full term pregnancy, post-menopause

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17
Q

Investigations for uterine fibroids

A

Bimanual examination: fibroids are often palpated, the uterus may feel enlarged firm and irregular

Bloods: FBC, U+E, clotting screen

Pelvic USS is diagnostic to visualise the fibroids

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18
Q

Management of uterine fibroids

A

Leave alone unless symptomatic, rapidly enlarging or concerned about subfertility

Medical:
Fibroids <3cm: IUS, tranexamic acid, mefenamic acid, COCP

Secondary care:

  • GnRH analogues (zoladex) used as surgery adjuncts to reduce fibroid size by reducing oestrogen
  • Mifepristone (antiprogesterone) shrinks fibroids over a 6m period

Surgery:

  • Myomectomy (hysteroscopic approach for submucosal or pedunculated fibroids, abdominal approach for intramural or subserosal fibroids)
  • Uterine artery embolisation (stops blood flow to fibroids)
  • Myolysis (diathermy, laser ablation, high intensity focused US)
  • Hysterectomy
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19
Q

Primary vs secondary amenorrhoea

A

Primary: failure to commence menses (absence of menarche)

  • 16+ in presence of secondary sexual characteristics
  • 14+ in absence of secondary sexual characteristics

Secondary: cessation of periods for more than 6 months after menarche

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20
Q

Causes of amenorrhoea

  • hypothalamic
  • pituitary
  • ovarian
  • adrenal glands
  • genital tract
A

Hypothalamic causes (reduced GnRH):

  • eating disorders, exercise
  • severe chronic conditions (thyroid, sarcoid, psychiatric)
  • Kallmann syndrome (x-linked recessive characterised by failure of migration of GnRH cells)

Pituitary causes:

  • Prolactinoma (prolactin suppresses GnRH)
  • Acromegaly/ cushings syndrome
  • Sheehan’s syndrome (post-partum pituitary necrosis secondary to massive obstetric haemorrhage)
  • Radiation or autoimmune disease destroying pituitary gland
  • Post-contraception amenorrhoea

Ovarian causes:

  • PCOS
  • Turners (45XO)
  • Premature ovarian failure

Adrenal gland causes:
-Late onset/mild congenital adrenal hyperplasia

Genital tract causes:

  • Ashermann’s syndrome
  • Imperforate hymen or transverse vaginal septum
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21
Q

Androgen insensitivity syndrome

  • what is it
  • features
  • diagnosis
  • management
A

X-linked recessive
End-organ resistance to testosterone causing genotypically male children (46XY) with female phenotype

Features:

  • primary amenorrhoea
  • undescended testes causing groin swellings
  • breast development may occur as a result of conversion of tesosterone to oestradiol

Diagnosis:
Buccal smear or chromosomal analysis to reveal 46XY genotype

Management:
Counselling (raise child as female)
Bilateral orchidectomy
Oestrogen therapy

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22
Q

Causes of oligomenorrhoea

A
PCOS
Contraception/hormonal treatment
Perimenopause
Thyroid disease
DM
Eating disorders
Excessive exercise
Medications (eg. antipsychotics)
Antiepileptics
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23
Q

Investigations for oligomenorrhoea and amenorrhoea

A
  • Pregnancy test
  • Gonadotrophins (LH and FSH) - reduced levels indicate hypothalamic cause, and increased levels indicate ovarian cause
  • Prolactin
  • Androgen levels (raised in PCOS)
  • Oestradiol (converted from testosterone)
  • Thyroid function tests
  • 17 hydroxyprogesterone (CAH)
  • Karyotype
  • Pelvic USS
  • Progesterone challenge test to elicit a withdrawal bleed
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24
Q

PCOS presentation and differentials

A

Presentation:
Subfertility /infertility
Oligo-/Amenorrhoea
Hirsutism and acne (due to hyperandrogenism)
Obesity
Acanthosis nigricans due to insulin resistance

Differentials:
Hypothyroidism
Cushings syndrome
Hyperprolactinaemia
Congenital adrenal hyperplasia
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25
PCOS investigations and management
Ix: - Bloods: FSH, LH, prolactin, TSH, testosterone - Pelvic USS (multiple cysts on ovaries) Raised LH/FSH ratio Raised free androgen index (ratio of testosterone/sex-hormone binding globulin) Prolactin normal or raised Management if normal weight and desiring fertility: 1. Clomifene (+/- metformin, +/- dexamethasone) 2. Gonadotrophins Management if overweight and desiring fertility: 1. Weight loss +/- metformin Management if not desiring fertility: 1. COCP +/- metformin 2. Anti-androgen (spironolactone, finasteride) Weight loss
26
Premature overian failure - what is it - causes - symptoms
Onset of menopause and increased gonadotrophins before the age of 40 Causes: idiopathic, chemo, autoimmune, radiation Symptoms: perimenopause symptoms, infertility, secondary amenorrhoea, raised FSH and LH
27
Diagnosis of menopause
>45 with symptoms = clinical diagnosis 40-45 = FSH and LH blood tests, or clinical diagnosis <40 = FSH and LH tests Menopause = no period + FSH levels >40 on at least 2 occasions (4-6wks apart)
28
Symptoms of perimenopause
Change in period cycle length, dysfunctional uterine bleeding Hot flushes, night sweats Vaginal dryness, atrophy, urinary frequency Anxiety, depression, short-term memory impairment Osteoporosis, increased risk of IHD
29
Combined HRT - Who to give it to - Who to give cyclical combined HRT to - Risks
Give combined HRT to women with a uterus (=oestrogen + progesterone) Give cyclical combined HRT to perimenopausal women who have menopausal symptoms ``` Risks: VTE (risk if given orally) IHD (no risk if started <60y) Breast cancer (risk reduces when stopped) Ovarian cancer ```
30
Unopposed oestrogen HRT - who to give it to - risks
Give to women with no uterus If given to women with a uterus it could cause endometrial proliferation and cancer (they need combined which includes progesterone to prevent overproliferation and cancer) ``` Risks: VTE (risk if given orally) Stroke (if oral) Endometrial cancer (if they have a uterus) Ovarian cancer ```
31
Contraindications to HRT Benefits of HRT
CI: current/past breast cancer, oestrogen-sensitive cancer, undiagnosed vaginal bleeding, untreated endometrial hyperplasia Benefits: prevents osteoporosis, reduces urinary symptoms, reduces risk of UTIs, most effective treatment for menopause
32
Non-hormonal management of menopause
Lifestyle (exercise, good sleep hygiene, weight loss, stress reduction, relaxation) Vasomotor symptoms: fluoxetine, citalopram, venlafaxine Vaginal dryness: lubricants Psychological: self-help groups, CBT, antidepressants Urogenital symptoms: vaginal oestrogen for atrophic vaginitis, lubricants, moisturisers
33
Causes of post-menopausal bleeding - ovary - uterus - cervix - vagina - urethra - vulva
Ovary: ovarian carcinoma, oestrogen-secreting tumour Uterine body: submucous fibroid, atrophic changes, polyp, hyperplasia Cervix: atrophy, squamous cell carcinoma, adenocarcinoma Vagina: atrophy Urethra; Urethral caruncle, haematuria Vulva: vulvitis, dystrophies, malignancy
34
Investigations for PMB
``` Pelvic USS (endometrial thickness should be <5mm) Hysteroscopy Endometrial biopsy ```
35
Atrophic vaginitis features and management
Post-menopausal Vaginal dryness, dyspareunia, occasional spotting O/E: vagina is pale and dry Mx: vaginal lubricants and moisturisers, or topical oestrogen cream
36
Risk factors for urinary incontinence
``` Advancing age Previous pregnancy and child birth High BMI Hysterectomy/ previous pelvic surgery Family history Smoking -> chronic cough -> worsens incontinence Neurological history ```
37
Different types of pelvic organ prolapses
Cystocele= bladder bulges into the anterior vaginal wall Rectocele= rectum bulges into the posterior vaginal wall Uterine prolapse- uterus hangs down into vagina, and may protrude outside of the body if severe Enterocele= pouch of douglas bulges into posterior vaginal wall
38
Risk factor for prolapse
``` Increasing age Multiparity Obesity Spina bifida Constipation Persistent chronic cough Prolonged heavy lifting Hysterectomy/ pelvic surgery ```
39
Management of prolapse
Conservative: weight loss, pelvic floor exercises, stop smoking, avoid constipation, avoid heavy lifting, avoid high-impact exercise Vaginal oestrogen Pessary: more beneficial for anterior and uterine prolapse Surgery: - Pelvic floor repair - Sacrocolpopexy or supraspinous fixation - Vaginal hysterectomy - Colpocleisis (close the vagina)
40
Causes of chronic pelvic pain
Adenomyosis, endometriosis, adhesions (gynae operations, PID, appendicitis), gynae malignancy, GI pathology (diverticulosis, IBD)
41
Causes of acute pelvic pain
``` Ectopic pregnancy Miscarriage Ovarian torsion PID Ovarian cysts UTI Appendicitis ```
42
Presentation and investigations for ovarian cysts
Presentation: asymptomatic, or chronic pain, acute pain, PV bleed, bloating, change in bowel habit, change in urinary frequency, weight loss, IBS Ix: transvaginal pelvic USS
43
Non-neoplastic ovarian cysts
Functional: - Follicular cysts: most common, <3cm. Developing follicle. - Corpus luteal cysts: <5mm. Luteal phase. Pathological: - Endometrioma (chocolate cyst) - Polycystic ovaries (ring of pearls on US) - Theca lutein cyst (raised hCG, eg. molar pregnancy)
44
Benign neoplastic cysts
Epithelial tumours: - Serous cystadenoma: most common. 30% bilateral - Mucinous cystadenoma: unilateral - Brenner tumour: unilateral. grey/yellow Benign germ cell tumours: -Dermoid cyst: hair, skin, teeth, bone Sex cord stromal tumours: -Fibroma: most common
45
Management of ovarian cysts
Premenopause: - Measure LDH, AFP, hCG - Simple cyst <5cm -> rescan in 8-12wks. If persistent -> monitor with USS and CA-125 3-6monthly - If >5cm -> laparoscopic cystectomy or oophorectomy Postmenopause: - Low malignant risk: monitor with USS and CA-125 for 1 yr - Moderate risk: bilateral oophorectomy, if malignancy is found then stage it - High risk: staging and laparotomy
46
Pelvic inflammatory disease risk factors and causes
``` History of STIs Young age of onset of first sexual activity Unprotected sex Multiple sexual partners IUD History of PID ``` Causes: chlamydia trachomatis (most common), Neisseria gonorrhoea, Mycoplasma genitalium, Mycoplasma hominia
47
Presentation of PID
``` Lower abdo pain Fever Deep dyspareunia Dysuria and menstrual irregularities Vaginal or cervical discharge Cervical excitation ``` Chandelier sign: patient reaches out to the ceiling during vaginal examination due to pain Perihepatitis: Fitz-Hugh-Curtis syndrome. RUQ pain, often confused with cholecystitis
48
Investigations for PID
``` Pregnancy test High vaginal swab Endocervical swabs Blood tests (FBC, CRP, ESR, blood cultures) MSU Transvaginal USS ```
49
Complications of PID
Low threshold for empirical treatment due to the risk of infertility and long-term morbidity Complications if untreated: pelvic abscess, sepsis, infertility, ectopic, chronic pelvic pain, dyspareunia, menstrual disturbance, psychological effects
50
Management of PID
6months contact tracing and management Empirical IM ceftriaxone 500mg stat + oral doxycycline 100mg BD + oral metronidazole 400mg BD for 14 days Pain relief with paracetamol and ibuprofen Consider removing IUS or IUD Avoid sexual intercourse until treatment is complete
51
Ovarian torsion - risk factors - presentation - investigations - management
Risk factors: ovarian cysts, ovarian enlargement, pregnancy, fertility treatment, prior tubal ligation Presentation: sudden onset deep seated colicky lower abdo pain, unilateral, vomiting, distress, fever Vaginal examination may reveal adnexal tenderness Exclude pregnancy Investigations: pelvic USS may show free fluid, laparoscopy is diagnostic and therapeutic Mx: pain relief, laparoscopy (untwist ovary)
52
Ectopic pregnancy risk factors
``` Damage to tubes (salpingitis, PID, previous surgery) Previous ectopic Endometriosis IUD POP IVF ```
53
Ectopic pregnancy presentation and differential diagnoses
Presentation: - Constant unilateral lower abdo pain (tubal spasm) - Vaginal bleeding - History of recent amenorrhoea (6-8wks) - Shoulder tip pain and pain on defaecation/urination if peritoneal bleeding DDx: Ovarian cyst, ovarian torsion, PID, appendicitis, bowel obstruction, IBS, UTI, cervical ectropion/cervicitis, miscarriage, molar pregnancy
54
Examination, investigations and management of ectopic pregnancy
O/E: abdo tenderness, cervical excitation. Do not palpate for adnexal mass due to risk of rupture Ix: Pregnancy test positive Pelvic USS is diagnostic MRI is secondline Repeat transvaginal scans and serial hCG levels to monitor Management: - Size <30mm, no pain, not ruptured, no heartbeat, bhCG <200 and reducing: monitor for 48 hours - Size <35mm, not ruptured, no significant pain, no heartbeat, bhCG<1500: methotrexate injection (surgery if bhCG 1500-5000) - Size >35mm, ruptured, severe pain, heartbeat, bhCG>1500: salpingectomy or salpingotomy
55
Causes of sporadic miscarriage
``` Foetal abnormality Infection (ToRCH, TB, malaria, salmonella, listeria) BV Materan age Abnormal uterine cavity Maternal illness Interventions ```
56
Causes of recurrent miscarriages
``` Antiphospholipid syndrome Endocrine (poorly controlled DM, thyroid disorders, PCOS) Uterine abnormalities Cervical weakness Parental chromocomal abnormalities Smoking ```
57
Types of miscarriages and their presenting features
Threatened miscarriage: closed cervical os, painless PV bleeding <24wks gestation (typically 6-9wks), complication of pregnancy not an actual miscarriage Missed miscarriage: closed cervical os, gestational sac contains dead foetus <20wks gestation without symptoms of expulsion, there may be light PV bleeding, usually painless, normal pregnancy symptoms may disappear Inevitable miscarriage: open cervical os, heavy PV bleeding, clots, pain Incomplete miscarriage: open cervical os, pain and PV bleeding, not all products of conception have been expelled
58
Investigations for miscarriage
Serial pelvic ultrasounds Serum b-hCG measurements Laparoscopy if ectopic likely
59
Management of miscarriage
Uterus usually expels the products on its own (may take weeks) Expectant Mx: first line. Wait 7-14 days for miscarriage to complete spontaneously. Take pregnancy test at 3 weeks, return if positive. Medical Mx: done if expectant hasnt worked or not appropriate. Vaginal or oral misoprostol (synthetic prostglandin analogue) stimulates uterine expulsion Take pregnancy test 3 weeks later and return if positive Surgical Mx: done if products still remain despite medical management or if patient still has symptoms 14 days after expectant, or patient unstable. Manual vacuum aspiration under LA, or surgical intervention under GA. Rh-ve women need anti-D. Syntocinon may be given to encourage uterine contraction and reduce blood loss Send products of conception for histology.
60
Investigations for recurrent miscarriages
Karyotype both partners and the products of conception Pelvic USS High vaginal swab Antiphospholipid antibodies assay on two occasions at least 6 weeks apart
61
Molar pregnancy - what are they - risk factors - presentation - Ix - Mx
Hydatidiform moles are chromosomally abnormal pregnancies that have the potential to become malignant Risk factors: extremes of maternal age, previous gestational trophoblastic disease Presentation: usually presents in first trimester, PV bleeding, unusually large uterus for gestational age, hyperemesis gravidarum Ix: Serum bhCG >100,000 USS shows snow storm appearance in uterine cavity Histological examination of products of conception Mx: Dilation and evacuation Hysterectomy if no intention on becoming pregnant again
62
Adenomyosis - what is it - at risk group - investigations - management
Growth of endometrial tissue in the myometrium Multiparous women towards the menopause TVUS or MRI ``` Tranexamic acid or mefenamic acid COCP, POP or IUS GnRH analogues Uterine artery embolisation Hysterectomy ```
63
Criteria for PCOS
Rotterdam criteria: at least 2 of the 3 for diagnosis 1. Oligomenorrhoea/ anovulation 2. Clinical/ biochemical hyperandrogenism 3. Multiple cysts on USS (>= 12 follicles on 1 ovary)
64
What is infertility and what is primary vs secondary infertility
Infertility = failure to conceive after regular unprotected sexual intercourse for at least 1 year Primary: never been able to conceive. Secondary: has conceived before but now unable to
65
Causes of female infertility
Ovulatory dysfunction: chronic systemic illness, eating disorders, PCOS, hyperprolactinaemia, hypo/hyperthyroidism, cannabis, NSAIDs, congenital adrenal hyperplasia Tubal damage: PID, previous tubal surgery, previous ectopic, endometriosis Uterine dysfunction: fibroids, uterine septae, congenital anomaly, ashermann's syndrome (Adhesions following curettage or TOP) Coital dysfunction: vaginismus, dyspareunia
66
Causes of male infertility
Semen: lack of semen, sperm that arent moving properly, abnormal sperm Testicles: infection, testicular cancer, testicular surgery, congenital defect, undescended testes, trauma Sterilisation Ejaculation disorders Hypogonadism Drugs; Sulfasalazine, anabolic steroids, chemo, marijuana, cocaine
67
Investigations for female infertility
- Mid-luteal phase progesterone levels (7 days before the end of a cycle, eg. day 21 of a 28 day cycle) - STI screen - FSH and LH levels - TFTs - Prolactin levels - Test for tubal patency: diagnostic laparoscopy and dye, or hysterosalpingography - Consider: Pelvic USS, hysteroscopy, testosterone levels/ sex hormone binding globulin
68
Investigations for male infertility
``` Semen analysis Chlamydia screen (/STI screen) ```
69
Semen analysis (what is normal?) - sperm count - motility - vitality - morphology - volume - fructose - pH
``` Sperm count (conc): >15million/ml Motility: 50% Vitality (healthy living sperm): 60% Morphology: >4% should have normal morphology Vol: 1.5-5.0ml Fructose: >13micromoles/sample pH: 7.2-7.8 ```
70
Management of infertility
Conservative: stress management, stop smoking, aim for BMI 19-25, occupational risks, reduce alcohol consumption, medication review Medical treatment: - Clomifene citrate (anti-oestrogen): raises FSH and LH levels - Gonadotrophins: offerend to clomifene-resistant women - Pulsatile GnRH and dopamine agonists can induce ovulation Surgical treatment: - Tubal microsurgery - Surgical ablation or resection of endometriosis Assisted conception: - Intrauterine insemination (sperm is placed into the utuerus during ovulation) - In-vitro fertilisation: fertilisation in a petri dish and then implant - Intracytoplasmic sperm injection: inject sperms into the egg - Donor insemination of sperm - Oocyte donation - Embry donation
71
Side effects of clomifene citrate
``` Multiple pregnancy Reversible ovarian enlargement Double vision Headache Hot flushes Abnormal uterine bleeding Breast tenderness ```
72
Cervical screening programme
Offered every 3 years for women aged 25-49, and every 5 years to women aged 50-64 Women >65 only need a smear if they have recently had abnormal tests
73
Cervical screening results interpretation
Inadequate: insufficient/ unsuitable sample. Repeat after 3 months. If 3 consecutive inadequate sample -> colposcopy within 6 weeks. Negative (normal) Borderline: abnormal nuclei but cant say for certain that it is dyskaryosis. Test HPV, if positive then colposcopy <6wks, if negative then return to normal screening programme Mild dyskaryosis: usually cervical intraepithelial neoplasia grade 1 (CIN1) on biopsy. Test HPV, if positive colposcopy within 6 weeks, if negative return to normal screening programme. Moderate dyskaryosis: CIN grade II. considered pre-cancerous with intermediate risk of developing into cancer. Colposcopy within 2 weeks. Severe dyskaryosis: CIN grad III, high risk developing into cancer. Colposcopy within 2 weeks.
74
What happens during colposcopy?
Examines the cervix to look for any abnormalities suggesting precancerous/cancerous changes. If acetic acid is applied to the cervix, abnormal areas (such as CIN) tend to turn white (sometimes referred to as acetowhite). If an iodine solution is applied, normal tissue (on the outside of the cervix) stains dark brown. Pre-cancerous abnormalities may not stain with iodine. The cells on the inner part of the cervix do not stain brown. May take a biopsy to confirm the diagnosis. Loop excision Needle excision Cone biopsy
75
Risk factors for cervical cancer
``` HPV 16 and 18 Early age of first intercourse High number of sexual partners Low socioeconomic group Smoking Partner with prostatic or penile cancer Premenopausal age ```
76
Presentation and types of cervical cancer
90% are squamous cell carcinomas and 10% are adenocarcinomas Presentation: may be asymptomatic. PCB, discharge, IMB, ulcer/ mass
77
Investigations for cervical cancer
Borderline or mild dyskaryosis at smear: HPV test -> if positive then colposcopy clinic in 6 weeks, if negative then return to normal screening programme Moderate or severe dyskaryosis: colposcopy within 2 weeks Colposcopy investigations: staining with acetic acid or iodine, and a biopsy (loop, needle, cone biopsy) Following diagnosis -> MRI/CT examination to check for mets and staging Blood tests and CXR may also be done
78
Management and staging of cervical cancer
Staging: 0 - carcinoma in situ 1 - confined to cervix 2 - beyond the cervix 3 - spread to the pelvic side wall, or affecting ureter or lower third of vagina 4 - involves rectal or bladder mucosa, or beyond true pelvis Management: - If a large loop excision has been done and the lesion has been completely removed then no further Mx is necessary - Surgery, chemo, radiotherapy are all options depending on patient circumstances
79
Endometrial cancer risk factors | Endometrial cancer protective factors
``` Postmenopausal Unopposed oestrogen (exogenous, obesity, PCOS, nulliparity, late menopause, tamoxifen) ``` Protective factors: COCP, combined HRT
80
Features and presentation of endometrial cancer
Most are adenocarcinomas | Presentation: PMB, irregular bleeding, IMB, normal examination
81
Endometrial hyperplasia
Premalignant condition Simple hyperplasia and complex hyperplasia - treated with progesterone to encourage regression Atypical hyperplasia has a high chance of developing into cancer so hysterectomy is advised
82
Investigations for endometrial cancer
Gold standard: hysteroscopy and biopsy Pelvic USS (measure endometrial thickness) Endometrial sampling (pipelle biopsy) MRI/CT for staging Post menopausal women should have an endometrial thickness of <5mm due to their low oestrogen levels, endometrial cancer causes increased oestrogen which thickens the endometrium
83
Staging and prognosis of endometrial cancer
Stage 1: body of the uterus (85% 5yr) Stage 2: extends to cervix (60% 5yr) Stage 3: adnexae, or +ve peritoneal cytology (40% 5yr) Stage 4: involves bladder or bowel mucosa (10% 5yr)
84
Management of endometrial cancer
Total abdominal hysterectomy and bilateral salpingo-oophorectomy = mainstay of treatment Stage 3 requires surgical debulking before radiotherapy Stage 4 requires a mixture of surgery, radiation and palliation
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Risk factors for ovarian cancer | Protective factors for ovarian cancer
``` Age (60-64 peak incidence) FHx BRCA 1/2 Lynch II syndrome Nulliparity Early menache and late menopause Smoking Obesity ``` Protective: pregnancy, breast feeding, exercise (due to less ovulation)
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Features and presentation of ovarian cancer
Epithelial, germ cell, sex-cord stromal, secondary malignant Presentation: often a silent killer. Abdo distension, bloating, abdo pain, abdo mass, urinary frequency, PMB, loss of appetite
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Investigations for ovarian cancer
Pelvic USS CA125 tumour marker CT abdo pelvis (+/- chest) Suspected patients under 40 should have AFP, b-hCG and CA125 levels
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Staging and prognosis for ovarian cancer
Stage 1: localised to ovary/ovaries (80% 5yr) Stage 2: peritoneal deposits in pelvis (60% 5yr) Stage 3: peritoneal deposits outside of pelvis (25% 5yr) Stage 4: distant mets (5-10% 5yr)
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Management of ovarian cancer
Surgery: total abdominal hysterectomy and bilateral salpingo-oophorectomy and omentectomy (plus peritoneal washings) Chemotherapy may be required post-op in stage 2 and 3 Surgery is usually for palliation in stage 4
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Risk factors for vulval cancer
``` Age >60 History of CIN, VIN or HPV HIV/ SLE/ immunosuppression Iatrogenic immunosuppression Smoking ```
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Features and presentation of vulval cancer
Most are squamous cell Presentation is often late. Pruritis, bleeding, discharge, ulcer, mass, inguinal nodes
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Staging for vulval cancer
1 - confined to vulva, <2cm diameter, no inguinal nodes 2 - confined to vulva, >2cm diameter, no inguinal nodes 3 - confined to vulva and suspicious nodes, or beyond vulva and no suspicious nodes 4 - obvious inguinal nodes, or involving rectum, bladder, urethra, or bone, or pelvic or distant mets
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Investigations and management of vulval cancer
Biopsy, thorough examination, CT/MRI, staging Management: Wide local excision Radical vulvectomy, Bilateral groin lymphadenectomy +/- radiotherapy
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Types of female genital mutilation
1: partial/total removal of clitoris and/or prepuce 2: partial/total removal of clitoris and labia minora +/- excision of labia majora 3: narrowing of vaginal orifice with creation of a covering seal (apositioning of labia) 4: all other harmful procedures for non-medical reasons
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Cervical ectropion - what is it - presentation - investigations - management
High oestrogen causes the stratified squamous epithelium of the ectocervix to undergo metaplastic change into columnar epithelium with releases mucus Presentation: asymptomatic, discharge, IMB, PCB Ix: clinical diagnosis, pregnancy test, triple swabs, cervical smear Mx: leave alone if asymptomatic, stop oestrogen medications, ablation (cryotherapy, or electrocautery)
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Cervical polyps - what are they - presentaiton - ix - mx
Benign growths protruding form inner surface of cervix Asymptomatic, abnormal vaginal bleeding (menorrhagia, IMB, PCB, PMB), vaginal discahrge Histological exam after removal, triple swabs, cervical smear Mx: Small polyps -> grab and twist with forceps -> falls off Large polyps -> remove with diathermy Send polyps for histology