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A TO REVISE - PHASE 3A > GYNAE TO DO > Flashcards

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
Q

CERVICAL CANCER
What is used to grade the level of dysplasia, or premalignant change, in the cells of the cervix after colposcopy?

A
  • 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
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26
Q

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

A

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

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27
Q

OVARIAN CANCER
What are the 4 types of ovarian cancer?

A
  • Epithelial cell tumours (85–90%)
  • Germ cell tumours (common in women <35)
  • Sex cord-stromal tumours (rare)
  • Metastatic tumours
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28
Q

OVARIAN CANCER
What are some types of epithelial cell tumours?

A
  • Serous carcinoma (#1)
  • Endometrioid, clear cell, mucinous + undifferentiated tumours too
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29
Q

OVARIAN CANCER
What are sex-cord stromal tumours?

A
  • Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)
  • Sertoli-Leydig + granulosa cell tumours
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30
Q

OVARIAN CANCER
What are some risk factors of ovarian cancer?

A

Unopposed oestrogen + increased # of ovulations –
- Early menarche
- Late menopause
- Increased age
- Endometriosis
- Obesity + smoking
Genetics (BRCA1/2, HNPCC/lynch syndrome)

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31
Q

OVARIAN CANCER
Hence, what are some protective factors of ovarian cancer?

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
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32
Q

OVARIAN CANCER
How is the risk of malignancy index calculated?

A
  • 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
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33
Q

OVARIAN CANCER
What can cause falsely elevated CA-125 levels?

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
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34
Q

OVARIAN CYST
What are the 4 types of ovarian cysts?

A
  • Functional (physiological)
  • Benign epithelial neoplasms
  • Benign germ cell neoplasms
  • Benign sex-cord stromal neoplasms
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35
Q

OVARIAN CYST
What are the three types of functional cysts?

A
  • Follicular (most common)
  • Corpus luteum
  • Theca lutein
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36
Q

OVARIAN CYST
What are corpus luteum cysts?
When are they seen?

A
  • Corpus luteum fails to breakdown, may fill with fluid or blood
  • May burst causing intraperitoneal bleeding
  • Early pregnancy
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37
Q

OVARIAN CYST
What are theca lutein cysts?
Association?

A
  • 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)
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38
Q

OVARIAN CYST
What are some features of neoplastic cysts?

A
  • Often complex
  • > 10cm
  • Irregular borders
  • Internal septations appearing multi-locular
  • Heterogenous fluid
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39
Q

OVARIAN CYST
What are the 2 benign epithelial neoplasms?

A
  • Serous cystadenoma (most common epithelial tumour)
  • Mucinous cystadenoma
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40
Q

OVARIAN CYST
How does serous cystadenoma present?

A
  • May be bilateral, filled with watery fluid, 30–50y
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41
Q

OVARIAN CYST
How does mucinous cystadenoma present?

A
  • Often very large + contain mucus-like fluid
  • Pseudomyxoma peritonei where abdo cavity fills with gelatinous mucin secretions if rupture
  • 30–40y
42
Q

OVARIAN CYST
What are benign germ cell neoplasms?

A
  • 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
Q

OVARIAN CYST
What is an example of sex cord-stromal neoplasms?

A
  • Fibromas (small, solid benign fibrous tissue tumour)
  • Associated with Meig’s syndrome
44
Q

OVARIAN CYST
What are some risk factors of ovarian cysts?

A
  • 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
Q

OVARIAN CYST
What is Meig’s syndrome?
Who is it commonly seen in?
What is the management?

A
  • Triad of fibroma, pleural effusion + ascites
  • Older women
  • Removal of fibroma = complete solution
46
Q

OVARIAN CYST
What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
47
Q

ENDOMETRIAL CANCER
What is the most common histological type of endometrial cancer?
What are some others?

A
  • Adenocarcinoma (80%)
  • Adenosquamous, squamous, papillary serous, clear cell + uterine sarcoma
48
Q

ENDOMETRIAL CANCER
What are some risk factors for endometrial cancer?

A

Unopposed oestrogen –
- Obesity (adipose tissue contains aromatase)
- Nulliparous
- Early menarche
- Late menopause
- Oestrogen-only HRT
- Tamoxifen
- PCOS
- Increased age
- T2DM
- HNPCC (Lynch syndrome)

49
Q

ENDOMETRIAL CANCER
What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
50
Q

ENDOMETRIAL POLYP
What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
51
Q

ENDOMETRIAL POLYP
What is the clinical presentation of endometrial polyps?

A
  • Irregular menstrual bleeding (IMB, PMB), menorrhagia
  • Infertility in younger as competing with foetus for space
52
Q

ENDOMETRIAL POLYP
What is the management of endometrial polyps?

A
  • 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
Q

VULVAL CANCER
What are some risk factors for vulval cancer?

A
  • Vulval intraepithelial neoplasia (VIN) due to HPV in younger women
  • Lichen sclerosus in older women
54
Q

VULVAL CANCER
What are 2 types of VIN?

A
  • High grade squamous intraepithelial lesion = type of VIN associated with HPV typically in younger women 35–50
  • Differentiated VIN associated with lichen sclerosus
55
Q

VULVAL CANCER
What is the management of VIN?

A
  • Biopsy to Dx
  • Watch + wait with close follow up
  • Wide local excision to surgically remove lesion
  • Imiquimod cream or laser ablation
56
Q

MENOPAUSE
What are some medium-term presentations of menopause?

A
  • Urogenital atrophy leading to dyspareunia, recurrent UTIs + PMB
57
Q

MENOPAUSE
What contraception is suitable in older women?
How do hormonal contraceptives affect the menopause?

A
  • 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
Q

MENOPAUSE
What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
59
Q

HRT
When would patches be used for HRT?
What is the most common side effect?

A
  • Pt choice
  • GI upset (Crohn’s)
  • VTE risk
  • Co-morbidities like HTN
  • Skin irritation #1
60
Q

HRT
What are the side effects associated with oestrogen?

A
  • Nausea,
  • bloating,
  • headaches,
  • breast swelling or tenderness,
  • leg cramps
61
Q

URINARY INCONTINENCE
What is the physiology of micturition?

A
  • 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
Q

URINARY INCONTINENCE
What are the 6 main types of incontinence?

A
  • Overactive bladder/urge incontinence
  • Stress incontinence
  • Mixed incontinence (of the 2 above)
  • Overflow incontinence
  • Fistula
  • Neurological
63
Q

URINARY INCONTINENCE
What causes urge incontinence/OAB?

A
  • Overactivity + involuntary contractions of the detrusor muscle
64
Q

URINARY INCONTINENCE
What is the purpose of urodynamics?

A

Measures pressure in abdomen + bladder to deduce detrusor pressure

65
Q

URINARY INCONTINENCE
What are last resort options for urge incontinence?

A
  • Augmentation cystoplasty with bowel tissue
  • Bypass (urostomy)
  • Botox can paralyse detrusor + block ACh release
66
Q

CYSTOCELE
What is a cystocele?

A
  • Defect in ant. vaginal wall = bladder prolapses backwards into vagina (can get urethrocele or cystourethrocele)
67
Q

RECTOCELE
What is a rectocele?

A
  • Defect in post. vaginal wall = rectum prolapses forwards into vagina
68
Q

PELVIC ORGAN PROLAPSE
What is an enterocele?

A

Defect in upper posterior wall of vagina > intestine protrusion

69
Q

PELVIC ORGAN PROLAPSE
What are some risk factors of pelvic organ prolapse?

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
70
Q

PREMENSTRUAL SYNDROME
How is PMS diagnosed?

A
  • Sx diary spanning 2 menstrual cycles
  • Definitive Dx with GnRH to temporarily induce menopause = Sx resolve
71
Q

PREMENSTRUAL SYNDROME
What specialist management can be given for PMS?

A
  • 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
Q

AIS
What is androgen insensitivity syndrome (AIS)?

A
  • X-linked recessive condition (androgen receptor gene mutation) with end-organ resistance to testosterone causing male genotype 46XY but female phenotype
73
Q

AIS
Why is their female external genitalia but not internal in AIS?

A
  • Undescended testes in abdo or inguinal canal produce AMH which prevents uterus, upper vagina, tubes + ovaries developing (Mullerian duct structures)
74
Q

ASHERMAN’S SYNDROME
What is the pathophysiology of Asherman’s?

A
  • 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
Q

ASHERMAN’S SYNDROME
What causes Asherman’s syndrome?

A
  • Pregnancy-related dilatation + curettage procedures
  • After uterine surgery
  • Pelvic infection like endometritis
76
Q

ASHERMAN’S SYNDROME
What is the clinical presentation of Asherman’s syndrome?

A
  • Secondary amenorrhoea
  • Infertility
  • Significantly lighter periods
  • Dysmenorrhoea
77
Q

ASHERMAN’S SYNDROME
What is the management of Asherman’s syndrome?

A
  • Hysterosalpingography = contrast injected into uterus + XR
  • Sonohysterography = uterus filled with fluid + pelvic USS
  • Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
78
Q

ENDOMETRIOSIS
What are some protective factors?

A

Multiparity + COCP

79
Q

VAGINAL CANCER
What causes it?

A

HPV or metastatic spread from cervix or vulva

80
Q

MENOPAUSE
What can urogenital atrophy lead to?

A

Urinary incontinence + pelvic organ prolapse

81
Q

HRT
What are the side effects associated with progesterone?

A

Mood swings,
fluid retention,
weight gain,
acne
greasy skin

82
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for uterine prolapse?

A

Hysterectomy or sacrohysteropexy

83
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for rectocele?

A

Posterior colporrhaphy

84
Q

HYDATIDIFORM MOLE
What are the 3 types of hydatidiform mole?

A
  • Complete
  • Partial
  • Invasive
85
Q

HYDATIDIFORM MOLE
What is a complete mole?

A
  • Diploid trophoblast cells
  • Empty egg + sperm that duplicates DNA (all genetic material comes from father)
  • No foetal tissue
86
Q

HYDATIDIFORM MOLE
What is a partial mole?

A
  • Triploid (69XXX, 69XXY) trophoblast cells
  • 2 sperm fertilise 1 egg
  • Some recognisable foetal tissue
87
Q

HYDATIDIFORM MOLE
What is an invasive mole?
What is the significance of this?

A
  • When a complete mole invades the myometrium
  • Metaplastic potential to evolve into a choriocarcinoma
88
Q

HYDATIDIFORM MOLE
What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
89
Q

HYDATIDIFORM MOLE
What is the management of hydatidiform mole after evacuation?

A
  • Check urinary pregnancy test in 3w – if high or mets may need chemo (cisplatin)
  • Effective contraception as advised to avoid pregnancy for 12m
90
Q

PELVIC INFLAMMATORY DISEASE
What are some risk factors for PID?

A
  • Not using barrier contraception
  • Multiple sexual partners
  • Intrauterine device
  • Younger age
  • Existing STIs
  • Previous PID
91
Q

PID
What might you look for on microscopy in PID?
What is the relevance?

A
  • Pus cells on swabs from vagina or endocervix
  • Absence is useful to exclude PID
92
Q

PELVIC INFLAMMATORY DISEASE
What are the non-infective causes of PID?

A
  • Post-partum (retained tissue),
  • uterine instrumentation (hysteroscopy, IUCD),
  • descended from other organs (appendicitis)
93
Q

PELVIC INFLAMMATORY DISEASE
What are the non-STI infective causes of PID?

A

Gardnerella vaginalis,
H. influenzae,
E. coli.

94
Q

GENITAL TRACT FISTULA
what are the causes of genital tract fistulas?

A

injury (primarily in childbirth),
surgery,
infection
radiation.

95
Q

GENITAL TRACT FISTULA
what are the different types?

A

➢ Vesicovaginal fistula
➢ Ureterovaginal fistula
➢ Urethrovaginal fistula
➢ Rectovaginal fistula
➢ Enterovaginal fistula
➢ Colovaginal fistula

96
Q

GENITAL TRACT FISTULA
what are the risk factors for genital tract fistulas?

A

➢ Childbirth
➢ Surgery
➢ Infection
➢ IBD
➢ Radiation

97
Q

GENITAL TRACT FISTULAS
what are the investigations for genital tract fistulas?

A

➢ 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
Q

OVERACTIVE BLADDER
what are the risk factors for overactive bladder?

A

➢ Old age
➢ Pregnancy/childbirth
➢ Hysterectomy
➢ Obesity
➢ Family history

99
Q

URINARY INCONTINENCE
What are some side effects of anti-muscarinics?

A
  • “Can’t see, spit, pee or shit” > caution in elderly as falls esp oxybutynin immediate release in frail
100
Q

URINARY INCONTINENCE
What is a caution of beta-3-adrenergic agonists?

A
  • C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP

A TO REVISE - PHASE 3A (16 decks)

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