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Gynaecology Flashcards

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1
Q

Definition of dyspareunia

A

Persistent or recurrent pain with attempted or complete vaginal entry or penile-vaginal intercourse

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2
Q

9 causes of dyspareunia

A
  1. dermatological disease e.g. lichen planus, psoriasis
  2. inadequate lubrication
  3. paravaginal infection e.g. urethritis, vaginitis
  4. vaginal atrophy
  5. vaginismus (sexual pain-penetration disorder)
  6. vulvodynia
  7. endometriosis
  8. pelvic inflammatory disease
  9. interstitial cystitis
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3
Q

What is vaginismus/sexual pain-penetration disorder

A

Involuntary contraction of the pelvic floor muscles that inhibits entry into the vagina

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4
Q

Types of postpartum sexual dysfunction

A

Sexual desire dysfunction
Sexual pain disorders - dyspareunia, SPPD, vulvodynia
Sexual arousal disorder

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5
Q

How is polycystic ovarian syndrome diagnosed

A

Rotterdam criteria - 2 out of 3 of the following:

  1. clinical or biochemical hyperandrogenism
  2. menstrual irregularities (<9 cycles per years or >35 days between cycles)
  3. polycystic ovaries on ultrasound
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6
Q

Symptoms of PCOS

A 
Sub/infertility
Mood changes
Acne
Fatigue
Insulin resistance
High testosterone levels
Excessive body hair growth
Weight changes (gain)
Ovarian cysts
Low sex drive
Irregular or missed periods
Male pattern baldness/thinning hair
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7
Q

Pathophysiology of PCOS

A

Excess androgens produced by theca cells of the ovaries (due to either hyperinsulinaemia or increased LH)

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8
Q

Biochemical results in PCOS

A

Normal or slightly raised testosterone

Increased LH and increased LH:FSH

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9
Q

Biochemical results in premature ovarian insufficiency

A

Raised LH and FSH

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10
Q

Biochemical results in hypogonadotropic hypogonadism

A

Reduced LH and FSH

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11
Q

Complications of PCOS

A

Insulin resistance leading to diabetes, obesity, dyslipidaemia, increased cardiovascular risk

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12
Q

Pharmacological management of PCOS

A

Co-cyprindrol - hirsutism and acne
COCP, progestogen-only pill, IUS - control menstrual irregularity
Metformin
Eflornithine - hirsutism
Orlistat - weight loss, improving insulin sensitivity
Clomifene - induction of ovulation

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13
Q

Mechanism of clomifene

A

Anti-oestrogen which induces gonadotrophin release by occupying oestrogen receptors in the hypothalamus therefore interfering with feedback. Aims to stimulate ovulation.

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14
Q

Regime for clomifene

A

50mg OD for 5 days. If no ovulation by 30 days later, 100mg OD for 5 days. If no ovulation a further 30 days later, 150mg OD for 5 days.

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15
Q

Describe HPV triage system for cervical screening

A

If HPV is positive, sample is examined cytologically. If no abnormal change, repeat HPV test in 12 months. If repeat HPV is negative, return to normal recall. If repeat is still HPV positive, send for cytology again. If still no abnormal change, HPV test repeated again in 12 months. If HPV now negative, return to normal recall. If 2nd repeat HPV (3rd result) is still positive, regardless of cytology, send for colposcopy. If any cytology is abnormal at any point, refer for colposcopy.

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16
Q

What to do with inadequate HPV samples

A

Repeat within 3 months. If second sample is also inadequate, send for colposcopy

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17
Q

What is the most common cause of cervical cancer

A

HPV strains 16, 18, 33

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18
Q

Risk factors for cervical cancer

A 
HPV - frequent UPSI, multiple sexual partners
Smoking
High parity
FHx
Long term use of COCP
HIV
Immunocompromise
STIs
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19
Q

Common presentation of cervical cancer

A 
Abnormal vaginal bleeding
Vaginal discharge
Dyspareunia 
Pelvic pain
Weight loss
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20
Q

Differentials for abnormal vaginal bleeding

A 
Cervical ectropion
Polyp
Fibroids
Pregnancy-related
Cervical cancer
Endometrial cancer
Hormonal contraception
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21
Q

Management approach for early stage cervical cancer

A

Large loop excision of the transformation zone (LLETZ)
Cone biopsy
Simple hysterectomy if fertility not needed

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22
Q

Management approach for middle stage cervical cancer

A

Radical hysterectomy with lymphadenectomy

Chemoradiation

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23
Q

Management approach for end stage cervical cancer

A

Chemotherapy and palliative radiotherapy

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24
Q

Downsides of cone biopsy

A

Weakens the cervix therefore patient is at higher risk of miscarriage or preterm labour

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25
What is a trachelectomy
Removal of cervix, surrounding tissue and upper part of vagina (uterus left in place)
26
Cervical screening programme
Women (and transgender men with retained cervix) aged 25-64 25-49 = every 3 years 50-64 = every 5 years
27
3 types of ovarian tumour
Epithelial ovarian tumour Germ cell tumour Sex cord-stromal tumour
28
Examples of germ cell tumour and demographic
Dysgerminoma Teratoma Women under 35 most commonly
29
Risk factors for ovarian cancer
``` Smoking Obesity Asbestos High number of ovulations: use of clomifene, nulliparous, early menarche and late menopause BRCA1 and 2 FHx Endometriosis ```
30
Protective factors for ovarian cancer
Childbearing Breastfeeding Early menopause OCP
31
Common presentation of ovarian cancer
Vague symptoms: weight loss, fatigue, anorexia, IBS-like symptoms (abdo pain, distension, bloating), urinary frequency Late stage associated with ascites and pleural effusion
32
What is the risk malignancy index
Calculated by ultrasound findings, menopausal status and CA 125 level (cancer antigen) to determine the risk that an adnexal mass is malignant Refer to specialist MDT if >250
33
What is the surgical approach for treatment of ovarian cancer
Optimal debulking + chemotherapy
34
What stage is ovarian cancer commonly found
Late stage - 60% of cases
35
What is CIN
Cervical intraepithelial neoplasia - pre-cancerous state when abnormal tissue is found on the cervix, commonly caused by HPV
36
What is endometrial hyperplasia
Abnormal proliferation of the endometrium - risk factor for developing endometrial cancer (greater number of cells)
37
Classification of endometrial hyperplasia
Hyperplasia without atypia - risk of developing into cancer <5%, cells appear normal Atypical hyperplasia - risk of developing into cancer ~28%, cells appear abnormal/irregular
38
What causes endometrial hyperplasia
Unopposed oestrogen (oestrogen without progesterone)
39
Risk factors for endometrial hyperplasia
``` Obesity Exogenous oestrogen use Oestrogen-secreting ovarian tumour Tamoxifen PCOS Nulliparity Hereditary non-polyposis colorectal carcinoma Diabetes ```
40
Presentation of endometrial hyperplasia
Abnormal vaginal bleeding - IMB, PMB, PCB, menorrhagia, oligomenorrhoea
41
How to investigate for endometrial hyperplasia
``` Pipelle biopsy (+/- hysteroscopy) Transvaginal ultrasound in post-menopausal women to determine whether biopsy is needed ```
42
Management of typical endometrial hyperplasia
Address risk factors e.g. obesity Progestogen treatment e.g. Mirena, oral progestogen Endometrial biopsy every 6 months Consider hysterectomy
43
Management of atypical endometrial hyperplasia
Total hysterectomy and bilateral salpingo-oophorectomy is gold standard Progestogen treatment and 3-monthly biopsy if fertility needing to be preserved
44
Most common type of endometrial cancer
Endometrioid adenocarcinoma (oestrogen-dependent)
45
Risk factors for endometrial cancer
``` Unopposed oestrogen: Nulliparous Late menopause Obesity Endometrial hyperplasia Hereditary non-polyposis colorectal carcinoma PCOS T2DM Tamoxifen ```
46
Common presentation of endometrial cancer
Post-menopausal bleeding
47
Investigations for endometrial cancer
Transvaginal ultrasound (if post-menopausal) to determine thickness of endometrium and assess need for hysteroscopy and biopsy
48
Staging system for gynaecological cancers
FIGO (international federation for gynaecology and obstetrics)
49
Management of early stage endometrial cancer
Total abdominal/radical hysterectomy and bilateral salpingo-oophorectomy +/- lymphadenectomy
50
Management of late stage endometrial cancer
Maximal/optimal debulking surgery with adjuvant chemotherapy/radiotherapy
51
What is the medical name for uterine fibroids
Leiomyomas
52
Definition of fibroids
Benign smooth muscle tumours of the uterus arising from the myometrium
53
Risk factors for fibroids
``` Early menarche Increasing age Obesity Ethnicity (black females) FHx in first degree relative ```
54
Differentials for fibroids
Endometrial polyps Ovarian tumour Leiomyosarcoma (myometrial malignancy) Adenomyosis
55
What is adenomyosis
Presence of functional endometrial tissue within the myometrium
56
Protective factors for fibroids
Pregnancy
57
Pathophysiology of fibroids
Benign growth beginning in a single myometrial cell and causes upregulation of hormone receptors. High levels of oestrogen and progesterone maintain growth of fibroids.
58
In what time of life do fibroids tend to develop
Child-bearing age Don't occur before puberty due to low levels of oestrogen/progesterone Tend to shrink after menopause due to decreasing hormone levels
59
3 types of fibroid related to location
Intramural - confined to myometrium Submucosal - protrudes into uterine cavity Subserosal - protrudes and distorts perimetrium, may be pedunculated
60
Most common presentation of fibroids
Asymptomatic, picked up incidentally on pelvic imaging or abdominal examination
61
Possible symptoms of fibroids
``` Menorrhagia Dysmenorrhoea Abdominal swelling Pelvic pain Dyspareunia Urinary/bowel symptoms Subfertility ```
62
Signs on examination for fibroids
Solid mass or enlarged uterus palpated on bimanual or abdo exam
63
Pregnancy-related complications of fibroids
``` Infertility Malpresentation Placental abruption IUGR Preterm labour Red degeneration ```
64
Non-pregnancy related complications of fibroids
Prolapsed fibroid Hyaline degeneration, cystic degeneration Anaemia Endocrine effects - polycythaemia, hypercalcaemia, hyperprolactinaemia
65
Investigations for fibroids
Transvaginal USS (1st line) FBC Pelvic MRI +/- hysteroscopy
66
Medical management of fibroids
Tranexamic acid, mefenamic acid COCP, POP, IUS GnRH analogues (used pre-operatively to reduce size, can only be used for 6 months)
67
Surgical management of fibroids
Hysteroscopy and transcervical resection of fibroid (TCRF) Myomectomy - preserves fertility (uterus) Hysterectomy Uterine artery embolization (UAE)
68
Adenomyosis after menopause
Symptoms subside as ectopic endometrial tissue is hormone responsive
69
Difference between endometriosis and adenomyosis
``` Endometriosis = when endometrial tissue is found outside of the uterus Adenomyosis = when endometrial tissue invades into myometrium ```
70
Risk factors for adenomyosis
High parity Uterine surgery e.g. curettage or ablation Previous c-section Genetic predisposition
71
Causes of menorrhagia and dysmenorrhoea
``` Endometriosis Adenomyosis Fibroids Endometrial hyperplasia/ carcinoma PID (not cyclical) Hypothyroidism Coagulation disorders ```
72
Pathophysiology of adenomyosis
Endometrial tissue (stroma) is allowed to communicate with underlying myometrium after uterine damage (e.g. pregnancy, childbirth, c-section, uterine surgery, surgical MOM or TOP)
73
Most common location of adenomyosis
Posterior uterine wall
74
What hormone receptors are found in endometrial tissue in adenomyosis
Oestrogen, progesterone, androgen
75
What is an adenomyoma
Collection of endometrial glands in the myometrium forms a visible nodule
76
Symptoms of adenomyosis
Menorrhagia Dysmenorrhoea - starts as cyclical pain but may worsen to daily pain Deep dyspareunia Irregular bleeding
77
Investigations for adenomyosis
Transvaginal USS MRI Definitive dx made from histology after hysterectomy
78
MRI findings in adenomyosis
Endo-myometrial junctional zone shows irregular thickening
79
Management principles for adenomyosis
Control of dysmenorrhoea and menorrhagia | Only curative therapy is hysterectomy
80
Medical management of adenomyosis
``` Conservative - analgesia (NSAIDs) Reduce menorrhagia: - COCP - POP - IUS - GnRH - aromatase inhibitors ```
81
Surgical management of adenomyosis
Uterine artery embolization Endometrial ablation and resection Hysterectomy (curative)

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