GYNAE TO DO Flashcards

1
Q

CONGENITAL STRUCTURES
In vaginal hypoplasia and agenesis what structure is not affected?
What is the management?

A
  • Ovaries – leading to normal female sex hormones
  • Prolonged period with vaginal dilatation for adequate size or surgery
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2
Q

FIBROIDS
What are the different types of fibroids?

A
  • Intramural (most common) = within the myometrium
  • Subserosal = >50% fibroid mass extends outside uterine contours
  • Submucosal = >50% projection into the endometrial cavity
  • Subserosal + submucosal can be pedunculated (on stalk = risk of torsion)
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3
Q

FIBROIDS
What is the first line hormonal management of fibroids <3cm?

A
  • Mirena coil is 1st line (fibroids <3cm with no uterus distortion)
  • 2nd = COCP triphasing (back-to-back for 3m then break)
  • Cyclical oral progestogens
  • Norethisterone 5mg TDS can be used short-term to rapidly stop menorrhagia from 3d before period until bleeding acceptable
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4
Q

FIBROIDS
What are the 5 main surgical options of managing fibroids?

A
  • Trans-cervical resection of fibroid via hysteroscopy
  • 2nd gen endometrial ablation
  • Uterine artery embolisation
  • Myomectomy
  • Hysterectomy
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5
Q

ADENOMYOSIS
What is the initial management of adenomyosis?

A
  • Same as fibroids or menorrhagia in general
  • TXA or mefenamic acid
  • Mirena coil 1st line if no uterus distortion
  • COCP triphasing
  • Cyclical progesterone
  • Norethisterone 5mg TDS short-term
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6
Q

ENDOMETRIOSIS
What are 3 theories about the cause of endometriosis?

A
  • Sampson’s = retrograde menstruation (endometrial lining flows backwards through fallopian tubes + into pelvis/peritoneum where endometrial tissue seeds itself
  • Meyer’s = metaplasia of mesothelial cells
  • Halban’s = via blood or lymphatics
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7
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?

A
  • Early menarche,
  • late menopause,
  • obstruction to vaginal outflow (imperforate hymen)
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8
Q

ENDOMETRIOSIS
What is the initial management of endometriosis?

A
  • NSAIDs ± paracetamol first line for Sx relief
  • COCP triphasing (can’t take for longer as if not irregular bleeding
  • POP like medroxyprogesterone acetate
  • GnRH analogues to “induce” menopause, reversible, quicker than triphasing but need HRT + only short-term as risk of osteoporosis
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9
Q

PCOS
How does insulin resistance contribute to PCOS?

A
  • Insulin resistance = pancreas produces more insulin
  • Insulin mimics action of insulin-like growth factor 1 which augments androgen production by theca cells in response to LH
  • Higher insulin = higher androgens (testosterone)
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10
Q

PCOS
How does high insulin levels contribute to PCOS?

A
  • Insulin suppresses sex hormone-binding globulin (SHBG) produced by liver which normally binds to androgens + suppresses their function further promoting hyperandrogenism
  • Also contribute to halting development of follicles in ovaries > anovulation + multiple partially developed follicles (polycystic ovaries)
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11
Q

PCOS
What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
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12
Q

PCOS
What are some differentials of hirustism?

A
  • Ovarian or adrenal tumours that secrete androgens
  • Cushing’s syndrome
  • CAH
  • Iatrogenic (steroids, phenytoin)
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13
Q

PCOS
What diagnostic criteria is used in PCOS?

A

Rotterdam criteria (≥2) –
- Oligo- or anovulation (may present as oligo- or amenorrhoea)
- Hyperandrogenism (biochemical or clinical)
- Polycystic ovaries (≥12) or ovarian volume >10cm^3 on USS

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14
Q

PCOS
What hormone tests may be used in PCOS?

A
  • Testosterone (raised)
  • SHBG (low)
  • LH (raised) + raised LH:FSH ratio (LH>FSH)
  • Prolactin (normal), TFTs (exclude causes)
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15
Q

PCOS
What other investigation may be useful at indicating PCOS?

A

2h 75g OTT for DM –
- IFG = 6.1–6.9mmol/L
- IGT (at 2h) = 7.8–11.1
- Diabetes (at 2h) = >11.1

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16
Q

PCOS
What are some associations and complications of PCOS?

A
  • DM, CVD + hypercholesterolaemia
  • Obstructive sleep apnoea, MH issues, sexual problems
  • Endometrial hyperplasia or cancer
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17
Q

PCOS
Why does PCOS increase risk of endometrial hyperplasia + cancer?

A
  • Oligo/anovulation means endometrial lining continues proliferating with unopposed oestrogen as no corpus luteum releasing progesterone
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18
Q

PCOS
What is the most crucial part of PCOS management?

A
  • Weight loss as can improve overall condition
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19
Q

PCOS
What are the PCOS risk factors for endometrial cancer?
How is the risk of endometrial cancer managed in PCOS?

A
  • Obesity, DM, insulin resistance, amenorrhoea
  • Mirena coil for continuous endometrial protection
  • Induce withdrawal bleed AT LEAST every 3m with COCP or cyclical progesterones medroxyprogesterone 10mg 14d)
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20
Q

PCOS
How is infertility managed in PCOS?

A
  • Weight loss initial step to restore regular ovulation
  • Clomiphene to induce ovulation
  • Metformin may help (+ helps insulin resistance)
  • Laparoscopic ovarian drilling or IVF last resort
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21
Q

PCOS
How is hirsutism + acne managed?

A
  • Hair removal cream, topical eflornithine to treat facial hirsutism
  • Co-cyprindiol is COCP licensed for hirsutism + acne as anti-androgen effect but only used for 3m as increased VTE risk
  • Spironolactone by specialist (mineralocorticoid antagonist with anti-androgen effects)
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22
Q

CERVICAL CANCER
What genes may be implicated in cervical cancer?

A
  • P53 + pRb are tumour suppressor genes
  • HPV produces two oncoproteins (E6 + E7)
  • E6 inhibits P53, E7 inhibits pRB
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23
Q

CERVICAL CANCER
What are some risk factors for cervical cancer?

A
  • Increased risk of catching HPV = early (unsafe) sex, lots of sexual partners
  • Smoking (limits availability to clear HPV)
  • HIV
  • COCP
  • High parity
  • Previous CIN/abnormal smear or FHx
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24
Q

CERVICAL CANCER
How is cervical cancer staged?

A

FIGO staging –
- 1 = confined to cervix
- 2 = invades uterus or upper 2/3 vagina
- 3 = invades pelvic wall (e.g. ureter) or lower 1/3 vagina
- 4 = invades beyond pelvis

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25
CERVICAL CANCER What is used to grade the level of dysplasia, or premalignant change, in the cells of the cervix after colposcopy?
- Cervical intra-epithelial neoplasia (CIN) - CIN I = mild, affects 1/3 thickness of epithelial layer, likely to return to normal without Tx - CIN II = mod, affects 2/3 thickness of epithelial layer, likely to progress to cancer without Tx - CIN III or cervical carcinoma in situ = severe, v likely to progress to cancer without Tx
26
CERVICAL CANCER What is the management of... i) CIN or early stage 1A cervical cancer? ii) Stage 1B-2A iii) Stage 2B-4A iv) Stage 4B
i) LLETZ or cone biopsy with -ve margins (maintain fertility) ii) Radical hysterectomy + removal of pelvic LN with chemo (cisplatin) + radiotherapy iii) Chemo + radiotherapy iv) Combination of surgery, chemo/radio + palliative care
27
OVARIAN CANCER What are the 4 types of ovarian cancer?
- Epithelial cell tumours (85–90%) - Germ cell tumours (common in women <35) - Sex cord-stromal tumours (rare) - Metastatic tumours
28
OVARIAN CANCER What are some types of epithelial cell tumours?
- Serous carcinoma (#1) - Endometrioid, clear cell, mucinous + undifferentiated tumours too
29
OVARIAN CANCER What are sex-cord stromal tumours?
- Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles) - Sertoli-Leydig + granulosa cell tumours
30
OVARIAN CANCER What are some risk factors of ovarian cancer?
Unopposed oestrogen + increased # of ovulations – - Early menarche - Late menopause - Increased age - Endometriosis - Obesity + smoking Genetics (BRCA1/2, HNPCC/lynch syndrome)
31
OVARIAN CANCER Hence, what are some protective factors of ovarian cancer?
- COCP - Early menopause - Breast feeding - Childbearing
32
OVARIAN CANCER How is the risk of malignancy index calculated?
- Menopausal status = 1 (pre) or 3 (post) - Pelvic USS findings = 1 (1 feature) or 3 (>1 feature) - CA-125 levels IU/mL as marker for epithelial cell ovarian cancer
33
OVARIAN CANCER What can cause falsely elevated CA-125 levels?
- Endometriosis - Fibroids + adenomyosis - Pelvic infection - Pregnancy - Benign cysts
34
OVARIAN CYST What are the 4 types of ovarian cysts?
- Functional (physiological) - Benign epithelial neoplasms - Benign germ cell neoplasms - Benign sex-cord stromal neoplasms
35
OVARIAN CYST What are the three types of functional cysts?
- Follicular (most common) - Corpus luteum - Theca lutein
36
OVARIAN CYST What are corpus luteum cysts? When are they seen?
- Corpus luteum fails to breakdown, may fill with fluid or blood - May burst causing intraperitoneal bleeding - Early pregnancy
37
OVARIAN CYST What are theca lutein cysts? Association?
- Stimulates growth of follicular theca cells so usually bilateral as resting follicles on both sides - Overstimulation of hCG (multiple + molar pregnancy as hCG v high)
38
OVARIAN CYST What are some features of neoplastic cysts?
- Often complex - >10cm - Irregular borders - Internal septations appearing multi-locular - Heterogenous fluid
39
OVARIAN CYST What are the 2 benign epithelial neoplasms?
- Serous cystadenoma (most common epithelial tumour) - Mucinous cystadenoma
40
OVARIAN CYST How does serous cystadenoma present?
- May be bilateral, filled with watery fluid, 30–50y
41
OVARIAN CYST How does mucinous cystadenoma present?
- Often very large + contain mucus-like fluid - Pseudomyxoma peritonei where abdo cavity fills with gelatinous mucin secretions if rupture - 30–40y
42
OVARIAN CYST What are benign germ cell neoplasms?
- Dermoid cysts or teratomas - Common in women <35 - May contain various tissue types (skin, teeth, hair + bone) - Can be bilateral, associated with ovarian torsion as heavy
43
OVARIAN CYST What is an example of sex cord-stromal neoplasms?
- Fibromas (small, solid benign fibrous tissue tumour) - Associated with Meig's syndrome
44
OVARIAN CYST What are some risk factors of ovarian cysts?
- Obesity, tamoxifen, early menarche, infertility - Dermoid cysts = most common in young women, can run in families - Epithelial cysts = most common in post-menopausal (?malignant)
45
OVARIAN CYST What is Meig's syndrome? Who is it commonly seen in? What is the management?
- Triad of fibroma, pleural effusion + ascites - Older women - Removal of fibroma = complete solution
46
OVARIAN CYST What are the germ cell tumour markers?
- Lactate dehydrogenase - Alpha-fetoprotein - Human chorionic gonadotropin
47
ENDOMETRIAL CANCER What is the most common histological type of endometrial cancer? What are some others?
- Adenocarcinoma (80%) - Adenosquamous, squamous, papillary serous, clear cell + uterine sarcoma
48
ENDOMETRIAL CANCER What are some risk factors for endometrial cancer?
Unopposed oestrogen – - Obesity (adipose tissue contains aromatase) - Nulliparous - Early menarche - Late menopause - Oestrogen-only HRT - Tamoxifen - PCOS - Increased age - T2DM - HNPCC (Lynch syndrome)
49
ENDOMETRIAL CANCER What are some protective factors for endometrial cancer?
- COCP - Mirena coil - Multiparity - Cigarette smoking (Seem to have anti-oestrogenic effect)
50
ENDOMETRIAL POLYP What are some risk factors of endometrial polyps?
- Being peri or post-menopausal - HTN - Obesity - Tamoxifen
51
ENDOMETRIAL POLYP What is the clinical presentation of endometrial polyps?
- Irregular menstrual bleeding (IMB, PMB), menorrhagia - Infertility in younger as competing with foetus for space
52
ENDOMETRIAL POLYP What is the management of endometrial polyps?
- Conservative but monitor or biopsy if concerns - GnRH analogues as oestrogen sensitive - If post-menopause or pre but symptomatic = hysteroscopic resection or morcellation of polyps - Hysterectomy if severe
53
VULVAL CANCER What are some risk factors for vulval cancer?
- Vulval intraepithelial neoplasia (VIN) due to HPV in younger women - Lichen sclerosus in older women
54
VULVAL CANCER What are 2 types of VIN?
- High grade squamous intraepithelial lesion = type of VIN associated with HPV typically in younger women 35–50 - Differentiated VIN associated with lichen sclerosus
55
VULVAL CANCER What is the management of VIN?
- Biopsy to Dx - Watch + wait with close follow up - Wide local excision to surgically remove lesion - Imiquimod cream or laser ablation
56
MENOPAUSE What are some medium-term presentations of menopause?
- Urogenital atrophy leading to dyspareunia, recurrent UTIs + PMB
57
MENOPAUSE What contraception is suitable in older women? How do hormonal contraceptives affect the menopause?
- UKMEC1 = barrier, IUS/IUD, POP, long-acting progesterone (<45), sterilisation - UKMEC2 = COCP after 40 used until 50, try ones with levonorgestrel or norethisterone as lower VTE risk - They don't but may mask Sx
58
MENOPAUSE What is the mechanism of action of clonidine?
- Alpha-adrenergic receptor agonist
59
HRT When would patches be used for HRT? What is the most common side effect?
- Pt choice - GI upset (Crohn's) - VTE risk - Co-morbidities like HTN - Skin irritation #1
60
HRT What are the side effects associated with oestrogen?
- Nausea, - bloating, - headaches, - breast swelling or tenderness, - leg cramps
61
URINARY INCONTINENCE What is the physiology of micturition?
- Detrusor = smooth muscle, transitional epithelium normally only contracts during micturition = sacral parasympathetic innervation from S2-4 - M2+3 muscarinic receptors with ACh - Sympathetic nerve fibres from T11-L2 maintain relaxation of bladder for storage
62
URINARY INCONTINENCE What are the 6 main types of incontinence?
- Overactive bladder/urge incontinence - Stress incontinence - Mixed incontinence (of the 2 above) - Overflow incontinence - Fistula - Neurological
63
URINARY INCONTINENCE What causes urge incontinence/OAB?
- Overactivity + involuntary contractions of the detrusor muscle
64
URINARY INCONTINENCE What is the purpose of urodynamics?
Measures pressure in abdomen + bladder to deduce detrusor pressure
65
URINARY INCONTINENCE What are last resort options for urge incontinence?
- Augmentation cystoplasty with bowel tissue - Bypass (urostomy) - Botox can paralyse detrusor + block ACh release
66
CYSTOCELE What is a cystocele?
- Defect in ant. vaginal wall = bladder prolapses backwards into vagina (can get urethrocele or cystourethrocele)
67
RECTOCELE What is a rectocele?
- Defect in post. vaginal wall = rectum prolapses forwards into vagina
68
PELVIC ORGAN PROLAPSE What is an enterocele?
Defect in upper posterior wall of vagina > intestine protrusion
69
PELVIC ORGAN PROLAPSE What are some risk factors of pelvic organ prolapse?
- Age - BMI - Multiparity (vaginal) - Spina bifida - Pelvic surgery - Menopause
70
PREMENSTRUAL SYNDROME How is PMS diagnosed?
- Sx diary spanning 2 menstrual cycles - Definitive Dx with GnRH to temporarily induce menopause = Sx resolve
71
PREMENSTRUAL SYNDROME What specialist management can be given for PMS?
- Continuous transdermal oestrogen with progestogens - GnRH analogues if severe (add HRT to mitigate osteoporosis risk) - Hysterectomy + bilateral oophorectomy to induce menopause if severe - Danazol + tamoxifen for cyclical breast pain - Spironolactone for breast swelling + bloating
72
AIS What is androgen insensitivity syndrome (AIS)?
- X-linked recessive condition (androgen receptor gene mutation) with end-organ resistance to testosterone causing male genotype 46XY but female phenotype
73
AIS Why is their female external genitalia but not internal in AIS?
- Undescended testes in abdo or inguinal canal produce AMH which prevents uterus, upper vagina, tubes + ovaries developing (Mullerian duct structures)
74
ASHERMAN'S SYNDROME What is the pathophysiology of Asherman's?
- Damage to basal layer of endometrium, damaged tissue may heal abnormally, creating scar tissue (adhesions) - Adhesions can bind uterine walls together or endocervix, sealing it shut causing obstruction > infertility, 2* amenorrhoea
75
ASHERMAN'S SYNDROME What causes Asherman's syndrome?
- Pregnancy-related dilatation + curettage procedures - After uterine surgery - Pelvic infection like endometritis
76
ASHERMAN'S SYNDROME What is the clinical presentation of Asherman's syndrome?
- Secondary amenorrhoea - Infertility - Significantly lighter periods - Dysmenorrhoea
77
ASHERMAN'S SYNDROME What is the management of Asherman's syndrome?
- Hysterosalpingography = contrast injected into uterus + XR - Sonohysterography = uterus filled with fluid + pelvic USS - Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
78
ENDOMETRIOSIS What are some protective factors?
Multiparity + COCP
79
VAGINAL CANCER What causes it?
HPV or metastatic spread from cervix or vulva
80
MENOPAUSE What can urogenital atrophy lead to?
Urinary incontinence + pelvic organ prolapse
81
HRT What are the side effects associated with progesterone?
Mood swings, fluid retention, weight gain, acne greasy skin
82
PELVIC ORGAN PROLAPSE What surgical intervention is provided for uterine prolapse?
Hysterectomy or sacrohysteropexy
83
PELVIC ORGAN PROLAPSE What surgical intervention is provided for rectocele?
Posterior colporrhaphy
84
HYDATIDIFORM MOLE What are the 3 types of hydatidiform mole?
- Complete - Partial - Invasive
85
HYDATIDIFORM MOLE What is a complete mole?
- Diploid trophoblast cells - Empty egg + sperm that duplicates DNA (all genetic material comes from father) - No foetal tissue
86
HYDATIDIFORM MOLE What is a partial mole?
- Triploid (69XXX, 69XXY) trophoblast cells - 2 sperm fertilise 1 egg - Some recognisable foetal tissue
87
HYDATIDIFORM MOLE What is an invasive mole? What is the significance of this?
- When a complete mole invades the myometrium - Metaplastic potential to evolve into a choriocarcinoma
88
HYDATIDIFORM MOLE What are some risk factors for hydatidiform mole?
- Extremes of reproductive age - Previous molar pregnancy - Multiple pregnancies - Asian women - OCP
89
HYDATIDIFORM MOLE What is the management of hydatidiform mole after evacuation?
- Check urinary pregnancy test in 3w – if high or mets may need chemo (cisplatin) - Effective contraception as advised to avoid pregnancy for 12m
90
PELVIC INFLAMMATORY DISEASE What are some risk factors for PID?
- Not using barrier contraception - Multiple sexual partners - Intrauterine device - Younger age - Existing STIs - Previous PID
91
PID What might you look for on microscopy in PID? What is the relevance?
- Pus cells on swabs from vagina or endocervix - Absence is useful to exclude PID
92
PELVIC INFLAMMATORY DISEASE What are the non-infective causes of PID?
- Post-partum (retained tissue), - uterine instrumentation (hysteroscopy, IUCD), - descended from other organs (appendicitis)
93
PELVIC INFLAMMATORY DISEASE What are the non-STI infective causes of PID?
Gardnerella vaginalis, H. influenzae, E. coli.
94
GENITAL TRACT FISTULA what are the causes of genital tract fistulas?
injury (primarily in childbirth), surgery, infection radiation.
95
GENITAL TRACT FISTULA what are the different types?
➢ Vesicovaginal fistula ➢ Ureterovaginal fistula ➢ Urethrovaginal fistula ➢ Rectovaginal fistula ➢ Enterovaginal fistula ➢ Colovaginal fistula
96
GENITAL TRACT FISTULA what are the risk factors for genital tract fistulas?
➢ Childbirth ➢ Surgery ➢ Infection ➢ IBD ➢ Radiation
97
GENITAL TRACT FISTULAS what are the investigations for genital tract fistulas?
➢ Vaginal/anal examination (could use proctoscope or speculum) ➢ Contrast tests (barium enema) ➢ Blue dye test ➔ put a tampon in the vagina then blue dye in rectum. If tampon is stained = test positive ➢ CT, MRI, Ultrasound, Manometry
98
OVERACTIVE BLADDER what are the risk factors for overactive bladder?
➢ Old age ➢ Pregnancy/childbirth ➢ Hysterectomy ➢ Obesity ➢ Family history
99
URINARY INCONTINENCE What are some side effects of anti-muscarinics?
- "Can't see, spit, pee or shit" > caution in elderly as falls esp oxybutynin immediate release in frail
100
URINARY INCONTINENCE What is a caution of beta-3-adrenergic agonists?
- C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP