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3a > O&G:Gynae > Flashcards

O&G:Gynae Flashcards

1
Q

What are fibroids also known as?

A

Uterine leiomyoma

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2
Q

What are fibroids?

A

Benign tumours of the myometrium

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3
Q

What are risk factors for fibroids?

A
  • more common near the menopause
  • early puberty
  • afrocarribbean descent
  • family history
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4
Q

What are protective factors for fibroids?

A

Parous women
Late puberty
Previous taking of COCP or injectable progesterone

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5
Q

Histology of fibroids

A

Smooth muscle and fibrous elements present
‘Whorled’ appearance in transverse section
Monoclonal origin

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6
Q

How are fibroids related to hormones?

A

Oestrogen (and probs progesterone) sensitive

  • in pregnancy, equally likely to grow/shrink/stay the same
  • in menopause, regress and calcify due to reduction in circulating oestrogen.
  • HRT may cause growth
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7
Q

What are the possible sites for fibroids?

A

Intramural
Subserosal
Submucosal

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8
Q

Clinical features of fibroids

A
  • asymptomatic 50%
  • menorrhagia 30%
  • intermenstrual bleeding
  • pressure effects: frequency/urgency (bladder), hydronephrosis (ureter), infertility (tubal ostia)
  • sub fertility: blocked tubal ostia, prevention of implantation, dysmenorrhea
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9
Q

Complications of fibroids

A

Painful if:

  • torsion (bedunculated fibroid)
  • degeneration (red, avascular necrosis)
  • malignancy (more likely if pain, rapid growth, growth post menopausal + poor response to GnRH)
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10
Q

What are the pregnancy complications with fibroids?

A
  • premature labour
  • malpresentation
  • PPH
  • transverse lie
  • obstructed labour
  • red degeneration
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11
Q

Investigations of fibroids?

A

Abdo/bimanual pelvic exam

  • solid mass arising from pelvis and continuous with uterus
  • multiple small fibroids give: irregular ‘knobbly’ enlargement of uterus

TVUS/TAUS
MRI/laparoscopy if needed
Hysteroscopy to assess disortion of uterine cavity

FBC

  • decrease if heavy bleeding
  • increase as fibroids can secrete erythropoietin
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12
Q

What is the Mx for fibroids?

A

Asymptomatic + slow growing = none

Fibroids <3cm assoc with heavy bleeding

  • TXA, NSAIDs, progesterone injections
  • IUS or COCP

Fibroids >3cm assoc with heavy bleeding

  • ulipristal acetate (progesterone-receptor modulator)
  • GnRH agonists (induce temporary menopausal state, max 6month use)
  • Mifepristone (anti progesterone - shrinks fibroids)
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13
Q

What are the SE of mifepristone?

A

Vasomotor Sx

Endometrial hyperplasia

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14
Q

What are the SE of GnRH agonists?

A

Bone density loss

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15
Q

What are the surgical Mx options for fibroids?

A 
Hysteroscopic surgery 
Myomectomy
Hysterectomy 
Uterine artery embolisation
Myolysis
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16
Q

What are serous cystadenomas?

A

Papillary growths which may be so prolific the cyst looks solid
Get them aged 40-50yrs old

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17
Q

What are mucinous cystadeonmas?

A

Mucin filled and can become huge

20-40 yrs

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18
Q

What are teratomas?

A

Arising from germ cells
Young, premenstrual women
Can contain hair + teeth

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19
Q

What are benign solid tumours?

A

Fibromas
- can cause Meig’s syndrome: ascites + right pleural effusion

Thecomas
- secrete oestrogen and androgens

Adenofibromas

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20
Q

What are functional cysts?

A

Only in menstruating women (risk factor is early menarche)
Made up of:
- follicular cysts - persistently enlarged cysts
- leutien cysts - persistently enlarged corpora lutea

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21
Q

What are chocolate cysts?

A

Endometriomas caused by endometriosis

Accumulation of blood in the ovary (Dark-brown cyst)

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22
Q

What are symptoms of ovarian cysts?

A
  • asymptomatic
  • ache/pain of abdo + lower back
  • dysparenuina
  • large cysts have pressure effects
    > bladder: urgency
    > veins: oedema and varicostes
  • large cysts can cause abdo distension (dull to percuss)
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23
Q

What are complications of cysts?

A

Rupture
- fever, severe abdo pain, peritonitis, shock
Torsion
- fever, severe abdo pain
Hamorrhage + infarction
Pseudomyxome peritone: in mucinous cyst adenomas, mucinous cells disseminate and clog up pelvic viscera

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24
Q

How do you investigate cysts?

A 
USS
CT/MRI
Laparoscopy + fine needle aspirate 
CA125 (rule out cancer)
Pregnancy test (rule out pregnancy)
Urinalysis (rule out infection)
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25
Q

Why is torsion an emergency?

A

blood supply cut off which leads to ischaemia, infarction and necrosis

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26
Q

What is polycystic ovarian syndrome?

A

Characteristic US appearance of multiple (>12), small (2-8mm) follicles in an enlarged ovary (>10ml volume)

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27
Q

What is the triad of PCOS?

A
  • Polycystic ovaries on US
  • Irregular periods
  • Hirsutism
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28
Q

Pathophys of PCOS?

A

Affected women have raised LH and insulin which leads to raised ovarian androgen (testosterone) production.
Increased insulin causes increased adrenal androgen production + hepatic SHBG production = lots of free floating androgen

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29
Q

What is the effect of free floating androgens in PCOS?

A

Increased intra ovarian androgens lead to

  • PCO
  • Irregular/absent ovulation

Increased peripheral androgens lead to
- Hirsutism

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30
Q

What are clinical features of PCOS?

A 
Obese
Acne
Excess body hair
Oligo/amenorrhea
Miscarriage
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31
Q

What is diagnostic criteria for PCOS?

A

2 or more of:

  • PCO
  • Irregular periods (>5 weeks apart)
  • Hirsutism (clinical or biochemical)
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32
Q

Investigations for PCOS?

A

Bloods

  • FSH: raised in ovarian failure, decreased in hypothalamic disease, normal in PCOS
  • Prolactin: normal in PCOS, used to exclude prolactinaemia
  • TSH: normal in PCOS
  • Serum tesosterone: raised
  • LH: raised but not diagnostic

TVUS
- shows PCO

Fasting lipids + glucose
- screen for complications (T2DM, Gestational diabetes + endometrial cancer)

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33
Q

What is the Mx for PCOS?

A
  • Obese patients: lose weight
  • COCP: regulates menstruation and treats hirsutism
  • Clomifene or tamoxifen: oestrogen receptor modulators to regulate hormones and lead to ovulation
  • Metformin: treats hirsutism
  • Ovarian diathermy: regulates ovulation for years
  • Ovulation induction with gonadotrophins
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34
Q

What is adenomyosis?

A

The presence of ectopic endometrial tissue and underlying stromatolites within the myometrium

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35
Q

What is the hormone relationship with adenomyosis?

A

Oestrogen dependent. Endometrium grows into the myometrium, pockets of menstrual blood can be seen n the myometrium if severe.

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36
Q

What are the symptoms of adenomyosis?

A
  • Asymptomatic

- Painful, regular, heavy menstruation

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37
Q

What are the signs of adenomyosis?

A

Mildly enlarged, tender uterus

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38
Q

How do you diagnose adenomyosis?

A

MRI

Histology on hysterectomy

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39
Q

Treatment of adenomyosis?

A

Medical: Progesterone IUS, COCP +/- NSAIDs or a GNRH agonist trial.
Surgical: Hysterectomy.

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40
Q

What is a intrauterine polyp?

A

Small benign tumours that grow into uterine cavities, usually endometrial in origin, sometimes submucosal fibroid origin.

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41
Q

Pathophysiology of polyps?

A

They arise a result of disordered cycles of apoptosis and regrowth of the endometrium. The fibrous tissue core is covered by columnar epithelium.

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42
Q

What is the clinical presentation of polyps?

A
  • Asymptomatic
  • Menorrhagia
  • IMB
  • Occasional prolapses through cervix
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43
Q

Diagnosis of polyps?

A
  • Ultrasound

- Hysteroscopy

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44
Q

Management of polyps?

A
  • Resection w/ cutting diathermy

- Avulsion

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45
Q

What are congenital uterine abnormalities?

A

Result from differing degrees of failure of fusion of mullerian ducts at about 9 weeks. Increased risk of renal abnormalities.

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46
Q

What are the pregnancy complications of congenital uterine abnormalities?

A
  • Malpresentaion
  • Transverse lie
  • Preterm labour
  • Retained placenta
  • Recurrent miscarriage
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47
Q

Management of congenital uterine abnormalities?

A
  • Surgical
  • Hysteroscopy for simple septa
  • Redimentary horns removed
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48
Q

What is endometriosis?

A

Presence of endometrium like tissue found outside the uterus, usually within the peritoneal cavity.

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49
Q

What is the hormonal affect in endometriosis?

A

Oestrogen dependent
Regresses during pregnancy and after menopasue
Bleeds at menstruation

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50
Q

Common sites for endometriosis?

A
  • Pouch of douglas (uterosacral ligament)

- On/behind ovaries

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51
Q

What are the causes of endometriosis?

A

Most common:
- Retrograde menstruation (sampsons theory)
Other:
- Extra-peritoneal endometriosis (eg. umbilical scar) Halbans theory. + embolisation
- Metaplasia

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52
Q

What are the clinical features of endometriosis?

A
  • Asymptomatic
  • Chronic pelvic pain –> constant or cyclic
  • Severe dysmenorrhoea
  • Dysparaeunia
  • Dysuria
  • Infertility
  • Dyschezia –> during menses
  • Acute pain, when there is rupture of choco cyst
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53
Q

Who does endometriosis normally affect?

A

Young, low parity women

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54
Q

Why is pouch of douglas affected in endometriosis?

A

Has endometrium tissue, is damaged on sex, causing dyspareunia.

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55
Q

Signs of severe disease in endometriosis?

A
  • Cyclical haematuria
  • Rectal bleeding
  • Umbilicus bleeding
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56
Q

What do you see on scan for endometrioma?

A
  • Blue cyst
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57
Q

What is frozen pelvis?

A

When all pelvic organs are immoblised by adhesions, due to pelvic inflammation and progressive fibrosis due to endometriosis.

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58
Q

What are the investigations of endometriosis?

A 
Gold standard: Laparoscopy and biopsy
Vaginal exam:
 - tenderness
 - thickening behind uterus or in adnexa
 - nodules in posterior vaginal fornix or uterosacral ligament
 - rectovaginal nodules
 - fixed retroverted uterus (2dary to adhesions)
USS:
 - to visualise chocolate cysts
 MRI:
 - if adenomyosis suspected
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59
Q

When is laparoscopy indicated in endometriosis?

A

When there is NSAID resistant lower abdo pain
Pain is causing days off work ad hospitalisation.
Pain and infertility

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60
Q

Treatment of endometriosis?

A 
Medical:
- COCP 
- Medroxyprogesterone acetate
- GnRH analogues
- Levenorgesterone releasing IUD
- Donazol
- Aromatase inhibitors
Surgery:
- Lesions are destroyed on laparoscopy if consented
- Disection of adhesions
- Hysterectomy
- Salpingoopherectomy
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61
Q

What treatment aboloshises cyclicity?

A 
COCP (triphasic, fixed dose)
GnRH analogues (60-90min pulses)
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62
Q

What treatment causes glandular atrophy?

A

Oral progesterone
Depot provera
Mirena

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63
Q

Risks of GnRh?

A

Prolonged treatment necessary

HRT add-back therapy to prevent BMD decrease and prevent menpause sx.

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64
Q

What is the most common genital tract cancer?

A

Endometrial cancer

  • prevalence highest at age 60yrs
  • only 15% occurs pre-menopausal
  • <1% in women <35 yrs
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65
Q

What are the different types of endometrial cancer?

A

1) Adenocarcinoma of columnar endometrial gland cells (>90%)
2) Adenosquamous CA (poorer prognosis, most common of the rest)
3) Endometrial hyperplasia (pre-malignant condition)

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66
Q

What are the risk factors for endometrial cancer?

A

Exogenous oestrogen

  • unopposed oestrogen therapy
  • tamoxifen (oestrogen antagonistic breast, but agonist in pros-menopausal uterus)

Endogenous oestrogen excess

  • PCOS with prolonged amenorrhea
  • obesity
  • nulliparity
  • late menopause
  • ovarian granuloma cell tumours (secrete oestrogen)

Other:

  • T2DM
  • Lynch type II syndrome
  • HNPCC
  • Pelvic irradiation
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67
Q

What is a protective factor for endometrial cancer?

A

COCP

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68
Q

What are the symptoms for endometrial cancer?

A
  • Postmenopausal bleeding ***

- If premenopausal: irregular bleeding/IMB, sometimes recent onset menorrhagia

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69
Q

What are the signs of endometrial cancer?

A
  • Atrophic vaginitis
  • Abnormal columnar cells on cervical smear
  • Pelvis: often normal
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70
Q

How do you investigate endometrial cancer?

A 
TVUS
Endometrial biopsy
Pipelle/hysteroscopic biopsy + histology
MRI (if spread suspected or high risk biopsy)
CXR (exclude rare pulmonary spread)
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71
Q

What are the indications for endometrial biopsy if suspecting endometrial cancer?

A

Endometrium >4mm thick on TVUS if postmenopausal

Endometrium >10mm thick on TVUS if premenopausal

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72
Q

What are some causes of PMB?

A 
Endometrial cancer
Endometrial hyperplasia
Cervical carcinoma
Atrophic vaginitis
Cervical polyps
Ovarian carcinoma
Cervicitis
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73
Q

What is the Mx for endometrial cancer?

A

Stage 1: hysterectomy + bilateralsalpingoopherectomy

Stage 2:

  • radical hysterectomy with system pelvic node clearance
  • alternative: hysterectomy + adjuvant therapy

Stage 3/4: maximum bulking surgery, combo chemo, radio + surgery

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74
Q

What are the indications for radiotherapy in endometrial cancer?

A
  • High risk for extrauterine disease (poor grade, deep myocetrial/cervical stroll spread)
  • Proven extrauterine disease
  • Inoperable/recurrent disease
  • Palliation for Sx (e.g bleeding)
  • Surgery not poss (e.g. meds CI)
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75
Q

Describe the stages of endometrial cancer

A

Stage 1: lesions confined to uterus

1a: <1/2 of myometrial invasion
1b: >1/2 of myocetrial invasion

Stage 2: as above but in cervix swell
(Cevrical stromal invasion, but not beyond uterus)

Stage 3: tumour invades through uterus

3a: invades serosa or adnexa
3b: vaginal and/or parametrial involvement
3ci: pelvic node involvement
3cii: para-aortic involvement

Stage 4: further spread

4a: in bowel or bladder
4b: distant mets

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76
Q

Where is the most common site for endometrial cancer recurrence?

A

At the vaginal vault (in first 3 years)

- treated with vaginal vault radiotherapy

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77
Q

What is haematometra?

A

Menstrual blood accumulating in the uterus because of the outflow obstruction.

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78
Q

What causes haematometra?

A
  • Cervical canal usually occluded by fibrosis after endometrial resection, cone biopsy or carcinoma
  • Congenital abnormalities (e.g. imperforate hymen or blind rudimentary uterine horn) present in adolescence as primary amenorrhoea
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79
Q

What is endometritis?

A

Infection of the uterus but commonly spreads to the pelvis if left untreated

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80
Q

What causes endometritis?

A
  • instrumentation of the uterus
  • complication of pregnancy
    Therefore is common after c-section and miscarriage.
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81
Q

What organisms can cause endometritis?

A

Chlamydia, gonococcus, e.coli, staphylococci, clostridia

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82
Q

What are the clinical features of endometritis?

A

persistent, heavy vaginal bleeding + pain
(+maybe fever initially)

> tender uterus
cervical os = open

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83
Q

What are the Ix for endometritis?

A

Vaginal + cervical swabs
FBC
Pelvic US

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84
Q

What is the Tx of endometritis?

A

Broad-spec Abx

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85
Q

What are the different uterine sarcomas?

A

1) Leiomyosarcomas
2) Endometrial stromal tumours
3) Mixed mullein tumours

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86
Q

What are leiomyosarcomas?

A

Malignant fibroids (rapid painful enlargement of a fibroid)

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87
Q

What are endometrial stromal tumours?

A

Tumours of the storm beneath the endometrium
- vary histologically from benign nodules to malignant sarcoma
Most common in perimenopausal women

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88
Q

What are mixed mullein tumours?

A

Derived from embryological elements of the uterus
More common in older age
Present with: irregular/IMB or rapid painful enlargement of a fibroid
Tx: hysterectomy

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89
Q

What can cause carcinoma of the vulva?

A
  • Lichen sclerosis

- Vulval intraepithelial neoplasia (VIN)

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90
Q

What is vulval intraepithelial neoplasia?

A

Premalignant disease assoc with HPV.

  • pruitus + pain
  • benefits from emollients + topical steroids
  • Gold standard: local surgical excision + histology to exclude cancer
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91
Q

What are the types of vuval cancer?

A

Squamous cell carcinoma (95%)
Malignant melanoma
Bartholin’s gland
Paget’s disease

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3
4
5
Perfectly
92
Q

What are the Sx of vuval cancer?

A
  • vulval itching + soreness
  • ulcer/mass on labia major/clitoris
  • dysuria
  • bleeding
  • discharge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

How is vulval cancer diagnosed?

A

Biopsy

94
Q

What is the Tx for vulval cancer?

A

Stage 1a: wide, local excision
Other stages: wide local excision + groin lymphadenectomy
Radiotherapy Neo-adjuvantely

95
Q

What cancer is usually secondary to malignancy of cervix, endometrium or vulva?

A

Carcinoma of the vagina

96
Q

Describe primary vaginal carcinomas?

A

Affect older women
Squamous cell carcinoma
Bleeding, discharge + mass/ulcer
Intravaginal radiotherapy

97
Q

Describe clear cell adenocarcinomas?

A

Secondary to DES exposure in utero
Presents in late teenage years
Good prognosis post surgery + radio

98
Q

Describe the epidemiology of ovarian cancer?

A
  • Presents late due to vague Sx (5yr survival <35%)
  • Lifetime risk: 1 in 48
  • 80% in >50yrs old
  • Highest incidence: 80-84 years old
99
Q

What are the risk factors for ovarian cancer?

A

Increased risk with no. of ovulations:

  • early menarche + late menopause
  • nullparity
  • HRT

Gene mutation: BRCA 1 + 2, HNPCC
- benign cysts can undergo malignant change

100
Q

What are the various types of epithelial tumours in ovarian cancer?

A

Epithelial tumours account for 90% of ovarian cancer

  • Serous cystadenocarcinomas (40-60years)
  • Endometrial carcinoma (50-60years)
  • Mucinous cystadenocarcinomas (30-50 years)
  • Clear cell carcinoma (40-80years)
101
Q

What are the various types of germ cell tumours in ovarian cancer?

A
  • Dysgerminomas
  • Teratomas

These arise from primitive germ cells of the embryonic gland
Women <35yrs
No Sx, more curable

102
Q

What are protective factors for ovarian cancer?

A
  • Pregnancy
  • Lactation
  • COCP
103
Q

What are the Sx of ovarian cancer?

A
  • Asymptomatic/vague initial Sx
  • Abdo distension/bloating
  • Early satiety
  • Loss of appetite
  • Pelvic/abdo pain
  • Urgency/frequency
104
Q

What are the signs of ovarian cancer?

A

Ascites
Abdo/pelvic mass
Cachexia (weakness + wasting of body due to severe illness)

105
Q

What are the Ix for ovarian cancer?

A

CA125: test this in any older woman with IBS-like Sx
- if it is raised then do an USS

Detected mass? > urgent referral

106
Q

Describe the staging of ovarian cancer

A

Stage 1: confined to the ovary
Stage 2: confined to the pelvis
Stage 3: confined to the abdomen
Stage 4: extra-abdominal disease

107
Q

How do you work out the risk of malignancy index (RMI) in ovarian cancer?

A

USS findings (1 or 3)x menopausal status(1or3) x CA 125

USS findings get

  • 1 point for 1 finding
  • 3 points for 3-5 findings
    findings: multi ocular cysts, solid areas, mets, ascites, bilateral lesions

Menopausal status:
Premenopausal: 1 point
Postmenopausal: 3 points

RMI of 250 or more needs MDT + CT for staging

108
Q

If a 70 year old woman with a solid cystic adnexal mass of 8cm with ascites and a CA125 of 400 came into the clinic, what would her RMI be?

A

Postmenopausal: 3
>1 abnormal feature of cyst on USS: 3

3x3x400 (CA125 score) = 3600
= needs referral to gynaecologist oncologist

109
Q

What is the surgical treatment for ovarian cancer?

A
  • Midline laparotomy for full view of pelvis then remove everything cancerous
  • Total hysterectomy, sapling-oopherectomy, partial omentectomy + peritoneal + lymph node samples
110
Q

What treatment is there for ovarian cancer patients who cannot have surgery?

A

Chemo

111
Q

How do you manage ovarian cancer patients following tx?

A

Repeat CA125s + repeat Its

Prognosis is improving but is not great so palliative care is important

112
Q

When are the peaks of incidence in cervical carcinoma?

A

30s and 80s

Majority: 25-49 yrs

113
Q

What is the cause of cervical carcinoma?

A

HPV

114
Q

What are the types of cervical carcinoma?

A

Squamous cell carcinoma (70%)
Mixed pattern (15%)
Adenocarcinoma (15%) –> from columnar epithelium + worse prognosis

115
Q

What are the risk factor for cervical carcinoma?

A
  • early age intercourse (<16yrs)
  • multiple sexual partners
  • STDs
  • cigarette smoking
  • previous CIN
  • multiparty
  • OCP usage
  • other genital tract neoplasia
116
Q

How can cervical carcinoma spread?

A

Lymph
- pelvic nodes = early feature

Direct invasion
- parametric, vagina, pelvic side wall, uterus, bladder, rectum, ovary (rare)

Blood
- occurs late

117
Q

What are the symptoms of cervical carcinoma?

A

Early:

  • post-coital bleeding
  • offensive vaginal discharge
  • IMP or PMB

Late:
Involvement of ureters, bladder, rectum + nerves
- uraemia, haematuria, rectal bleeding + pain
- Leg oedema, pain, hydronephrosis (leads to CKD + pelvic wall involvement)

118
Q

How do you investigate cervical carcinoma?

A 
Colposcopy to biopsy tumour
Staging:
- vaginal/rectal exam
- cystoscopy
- MRI (size, spread, lymph node involvement)
- CT with contrast
119
Q

What is the staging of cervical carcinoma?

A

Stage 1: lesions confined to the cervix

1ai: diagnosed only by microscope, invasion <3mm in depth and lateral spread <7mm
1aii: diagnosed with microscope, invasion >3m and <5mm with lateral spread <7mm
1bi: clinical visible lesion or greater than 1aii, <4cm in greatest dimension
1bii: clinically visible lesion, >4cm in greatest dimension

Stage 2: invasion into vagina, but not the pelvic side wall

2ai: involvement of upper 2/3rds vagina, without parametrial invasion, <4cm in greatest dimension
2aii: >4cm in greatest dimension
2b: invasion of parametrium

Stage 3: invasion of lower vagina or pelvic wall, or causing ureteric obstruction

Stage 4: invasion of bladder or rectal mucosa, or beyond the true pelvis

120
Q

What factors suggest a poor prognosis with cervical carcinoma?

A 
LN involvement
Advanced clinical stage
Large primary tumour
Poorly differentiated tumour
Early recurrence
121
Q

What is the management for cervical carcinoma?

A

Stage 1ai: cone biopsy, hysterectomy (older women)
Stage 1aii - 2a: surgery, chemo or radio
- pelvic LN dissected + tested laparoscopically
If neg = surgery
If pos = chemo/radio

122
Q

What is Wetheim’s hysterectomy?

A

The surgery for cervical carcinoma which involves pelvic node clearance, hysterectomy tommy, removal of parametric/upper 1/3rd of vagina. Ovaries are left only in young women with squamous carcinoma.

123
Q

What is radical trachelectomy?

A

Alternative surgery for cervical carcinoma. Remove 80% of cervix and upper vagina, insertion of cervical suture to prevent preterm. Women want to conserve fertility.

124
Q

What is the Tx for stage 2b> cervical carcinoma?

A

Chemo/radio (platinum agents e.g. cisplatin)
Combo of internal beam radio + brachytherapy
Palliative radio for bone pain/haemorrhage

125
Q

What is menstruation?

A

Monthly bleeding from reproductive tract induced by hormonal changes of the menstrual cycle.

126
Q

What is the menstrual cycle?

A

The time from the start of a period to the start of the next.

127
Q

What is normal amount of blood loss during menstruation?

A

60-80ml

128
Q

How long is an average menstrual cycle?

A

21-35 days (28 days)

129
Q

How many days do you usually lose blood during menstruation?

A

2-8 days (5 days)

130
Q

What is abnormal uterine bleeding?

A

Any menstrual bleeding from the uterus that is either abnormal in volume, regularity, timing or is non-menstrual.

131
Q

What is menorrhagia?

A

Excessive menstrual blood loss that is subjectively considered to be excessive by the woman and interferes with her physical, emotional, social and material QoL.
Blood loss> 80ml
- ask about flooding and large clots as measurement

132
Q

Why is it 80ml of blood that is classified as excessive menstrual loss?

A

Max amount women on a normal diet can lose per cycle without becoming iron deficient.

133
Q

What are the causes of menorrhagia?

A

Systemic:

  • hypothyroidism
  • coagulopathy
  • diabetes
  • obesity

Local:

  • polys
  • carcinoma
  • fibroids
  • adenomyosis

Treatment-related:

  • IUD
  • Anti-coags
134
Q

How do you investigate menorrhagia?

A
  • Examination: pelvis + bianual
  • Menstrual charting
  • FBC (assess effect of blood loss)
  • Exclude systemic causes: coag + thyroid function
  • Exclude organic causes: TVUS, Endometrial biopsy
  • TVUS (endometrial thickness, exclude uterine fibroid/ovarian mass, detects larger intrauterine polyp)
135
Q

What are indications for biopsy in menorrhagia?

A
  • endometrial thickness
  • abnormal bleeding resulting in acute …?
  • suspected polyps- prior to endometrial ablation/diathermy
  • before insertion of IUS if cycle irregular
  • IMB
  • > 40 with recent onset menorrhagia
136
Q

What is the medical treatment for menorrhagia?

A 
1st line: IUS (not copper coil)
2nd line: 
- antifibrinolytics (tranexamic acid)
- NSAIDs (mefenamic acid)
- COCP
3rd line: progesterones + GnRH analogues
137
Q

What is the surgical treatment for menorrhagia?

A

Endometrial ablation (remove endometrium(
Hysterectomy (last resort)
Uterine artery embolisation

138
Q

What is amenorrhoea?

A

The absence of menstruation

139
Q

Difference between primary and secondary amenorrhoea?

A

Primary: menstruation has not started by the age of 16 years
Secondary: previously normal menstruation that stops for >6months

140
Q

What is oligomenorrhoea?

A

Infrequent periods (>every 35 days for 6 months)

141
Q

What are the causes of amenorrhoea?

A

Physiological

  • constitutional delay
  • drugs

Pathological

  • anorexia nervosa
  • psychological
  • athleticism
  • PCOS
  • hyperprolactinaemia
  • thyroid issues
  • adrenal tumours
  • adrenal hyperplasia
  • turner’s syndrome
  • premature ovarian failure
  • imperforate hymen/transverse vaginal septum
142
Q

Investigations for amenorrhoea

A
  • pregnancy test
  • FSH/LH levels
  • prolactin levels
  • thyroid function
  • total testosterone + sex-hormone binding globulin level
  • pelvic US (if PCOS)
143
Q

Why should prolactin levels be measured at least twice in amenorrhoea?

A

Can be temporarily high due to stress, eating, recent breast exams.

144
Q

What is primary dysmenorrhoea?

A

Cramping/pain in lower abdo just before or during period.

  • usually coincides with start of menstruation and improves as menses progresses
  • due to contraction and uterine ischaemia
145
Q

What are some non-gynae Sx of dysmenorrhoea?

A

N+V
Migraine
Bloating
Emotional

146
Q

What are clinical features of primary dysmenorrhoea?

A

Normal pelvic examination

Assoc with high prostaglandin levels in endometrium

147
Q

What is the Mx of primary dysmenorrhoea?

A

NSAIDs or COCP
Local application of heat (e.g. hot water bottle)
TENS (set to high freq)
Reassurance

148
Q

What is secondary dysmenorrhoea?

A

painful periods often preceding (and relived by) onset of menstruation

149
Q

What are some assoc features of secondary dysmenorrhoea?

A

Deep dyspareunia
Menorrhagia
Irregular menstruation

150
Q

What Ix are done for secondary dysmenorrhea?

A

Examination
Swabs (if STI risk)
Pelvic US
Pelvic laparoscopy

151
Q

Causes of secondary dysmenorrhoea?

A 
Fibroids
Adenomyosis
Endometriosis
PID
Ovarian tumours
152
Q

What are the causes of irregular menstruation + intermenstrual bleeding?

A

Anovulatory cycles
- early/late reproductive years

Pelvic pathology

  • fibroids
  • polyps
  • adenomyosis
  • ovarian cysts
  • chronic pelvic infection
  • malignant: ovarian, cervical, endometrial
153
Q

What Ix are there for irregular menstruation + intermenstrual bleeding?

A 
FBC (blood loss)
Cervical smear
TFT/clotting
FSH/LH
USS of uterine cavity (>35yrs)
Endometrial biopsy
154
Q

What is the Tx for irregular menstruation + intermenstrual bleeding?

A

1st line: IUS or COCP
2nd line: Progesterone, HRT

Surgical

  • treat underlying cause (e.g. polyp)
  • menorrhagia tx
155
Q

What is post-coital bleeding?

A

Vaginal bleeding following intercourse that is not menstrual loss.
- except for 1st intercourse this is always abnormal and cervical carcinoma must be excluded.

156
Q

What are causes of PCB?

A 
Cervical carcinoma
Cervical ectropion
Cervical polyps
Cervicitis
Vaginitis
157
Q

When is cervix most likely to bleed?

A

When it is not covered by healthy squamous epithelium?

158
Q

What is the Mx for PCB?

A

Smear

Colposcopy

159
Q

What is the menopause?

A

The permanent cessation of menstruation resulting from loss of ovarian follicular activity.

  • diagnosed after 12 consecutive months of amenorrhoea (or onset of Sx if hysterectomy)
  • average age: 51 years
160
Q

What is perimenopause?

A

Time beginning with first features of approaching menopause (e.g. vasomotor sx + menstrual irregularity) and ends 12 months after the last period.

161
Q

What is premature menopause?

A

Menopause <40 years old. Usually no cause but may be:

  • post bilateral oophorectomy
  • infection
  • autoimmune disordes
  • chemo
  • ovarian dysgeneis
  • metabolic diseases
162
Q

What are the short term vasomotor symptoms of the menopause?

A

Hot flushes
Night sweats > sleep disturbance (tired + irritable)
Usually lasts <5yrs

Is sue to fluctuations in oestrogen levels

163
Q

What are the medium term urogenital problems of menopause?

A
  • urethral mucosal/vaginal atrophy
  • urinary problems: frequency, nocturne, incontience, recurrent infection, increase in vaginal pH
  • dyspareunia, itching, burning, dryness, cessation of sexual activity
164
Q

What are some general symptoms of menopause?

A
  • mood change/irritability
  • loss of memory/concentration
  • headaches, dry+itchy skin, joint pain
  • loss of confidence, lack of energy
165
Q

What are some long term symptoms of menopause?

A

Osteoporosis
- decreased risk if you take oestrogen

CVD
- adverse changes in lipid

Dementia
- increased prevalence with early menopause

166
Q

When should you investigate for the menopause?

A
  • <40 years (premature menopause0
  • consider in ages 40-45years
  • > 45 years with atypical symptoms
167
Q

How to investigate menopause?

A

FSH: gives estimate of ovarian reserve

  • high levels = low oocytes
  • measure between days 2-5

AMH (anti-mullerian hormone) is produced in granuloma cells of natural/pre-natural follies: gives direct measurement of ovarian reserve
- can measure any day as it is stable throughout cycle

TFTs
Catecholamine 
- increased in phaeochromocytoma/carcinoid syndrome
LH
Oestradiol
Progesterone
DEXA
168
Q

What is the aim of menopausal treatment?

A

To relieve Sx

169
Q

What is the tx for menopause?

A

HRT

  • Oestrogen: if hysterectomy
  • Oestrogen + progesterone: if no hysterectomy as this decreases risk of endometrial cancer
170
Q

How does a combine oestrogen + progesterone treatment help reduce risk of endometrial cancer in menopausal tx?

A

Progesterone counteracts the proliferative effect of oestrogen. If you didn’t have it then the uterus would hyperplase and lead to neoplasia.

171
Q

What are the routes to give oestrogen?

A

Oral
Transdermal (best)
Subcutaneous

172
Q

What are the routes to give progesterone?

A

Oral
Transdermal
IUS

173
Q

How long should you have menopause treatment for?

A

up to 5 years

or up to age 51 in premature menopause

174
Q

Talk about the breast cancer risk with menopause treatment?

A

Only an increased risk of breast caner with oestrogen and progesterone therapy
STOP HRT if develop breast cancer
- do not offer HRT routinely if they have Hx of breast cancer
- can still give to people with family Hx of breast cancer

175
Q

Talk about the VTE risk with menopause treatment?

A

Only increase risk if using oral HRT because it does 1st pass metabolism= increased clotting factor production in liver.
Transdermal is better as it gives a constant level (esp good for migraines, epilepsy + crohns)

176
Q

Talk about the CVD risk with menopause treatment?

A

No solid evidence
HRT can reduce plaques if started before they have formed however it can destabilise already formed plaques
- do not give to >60 years without careful consideration

177
Q

Talk about the stroke risk with menopause treatment?

A

Risk increased on oral HRT

178
Q

Talk about the T2DM risk with menopause treatment?

A

No assoc risk

179
Q

How often is mirena replaced if used in HRT?

A

Every 4 years

180
Q

Who should have transdermal HRT tx?

A

Everyone but esp:

  • gastric upset (e.g. crohns)
  • need for steady absorption (migraine, epilepsy)
  • perceived increased risk of VTE
  • older women
  • HTN
  • patient choice
181
Q

What is premature ovarian insufficiency (POI) aka?

A

Premature menopause (<40yrs)

182
Q

What are some causes of POI?

A
  • mostly idiopathic
  • chromosomal abnormalities
  • FSH receptor gene polymorphisms
  • inhibin B mutations
  • iatrogenic: surgery, chemo/radio
  • enzyme deficiencies
  • autoimmune disease
  • infections: mumps, TB, malaria
183
Q

How do you diagnose POI?

A

FSH 25iu/l on 2 samples >4weeks apart
AND
4months of amenorrhoea

184
Q

How do you treat POI?

A 
Oestrogen replaement
- HRT preferred
- COCP (increased risk of VTE)
Fertility 
- donor egg
- surrogacy
Androgen replacement
- testosterone gel
185
Q

Why is it recommended to give HRT until menopause in POI patients?

A

To try and rebalance the deficiency to protect from stuff like decreased BMD which is likely to happen earlier on

186
Q

Do you still need contraception during (premature) menopause?

A

Contraception required as fertile for:

  • 2 years if menopause <50
  • 1 year if menopause >50
187
Q

What are some non-hormonal treatments for POI?

A

Alpha-adrenergic receptor agonists
- clonidine (for hot flushes)

SSRI
- fluoxetine, paroxetine, citalopram, sertraline

SNRI
- venlafaxine

Anti-epileptics
- gabapentin

188
Q

What does sertraline CI with?

A

Tamoxifen

189
Q

Why should you gradually stop clonidine?

A

It is an anti-hypertensive so needs to be gradually topped to avoid rebound HTN.

190
Q

What are some causes of irregular menstrual bleeding?

A

Benign: idiopathic, anovulatory cycles, fibroids, PID, polyps, endometriosis, adenomyosis
Malignant: Endometrial carcinoma, cervical carcinoma
Systemic: Thyroid or clotting abnormalities

191
Q

Investigations in irregular menstrual bleeding?

A
  • FBC, TFTs,
  • Pregnancy test
  • Cervical smear
  • USS (biopsy if abnormal)
192
Q

Management of irregular menstrual bleeding?

A

If <35: IUS, COCP or NSAIDS/TXA if wanting to conceive
If >35: Pelvic USS +/- biopsy first. IUS/COCP or NSAIDS/TXA. HRT if perimenopausal
If postmenopausal bleeding: urgent pelvic uss, biopsy if endometrium >4mm or bleeding
If PCB: Cervical smear + colposcopy. consider cryotherapy

193
Q

What is androgen insensitivity syndrome?

A

AIS occurs when a male has cell receptor insensitivity to androgens, which are converted peripherally to oestrogens. The indiviudal appears to be female: the diagnosis is only uncovered when ‘she’ presents with amenorrhoea. The uterus is absent and rudimentary testes are present. These are removed because of risk of malignant change and oestrogen replacement therapy is started.

194
Q

What is Lichen Sclerosis?

A

Lichen Sclerosis is thought to be an autoimmune disorder. Elastic tissue turns to collagen (usually after middle age or before puberty).

195
Q

What are the signs of Lichen Sclerosis?

A
  • Bruised, red, purpuric areas
  • Bullae, erosions, ulcerations
  • Vulva gradually becomes white, flat and shiny.
  • May be an hourglass shape around vulva and anus.
  • intensely itchy
196
Q

Treatment of lichen sclerosis?

A
  • Clobetasol propionate cream

- If steroid resistant use Tacrolimus.

197
Q

What are hydatidiform moles?

A

Type of gestational trophoblastic disease in womb. Tumours consisting of proliferating chorionic villi which have swollen and degenerated. Derived from chorion, it makes lots of hCG, giving rise to exaggerated pregnancy symptoms and strongly positive pregnancy tests.

198
Q

What makes hydatidiform moles more likely to occur?

A
  • Extremes of childbearing age
  • After previous mole
  • Asian women
199
Q

Signs of hydatidiform moles?

A
  • Early pregnancy failure eg. failed miscarriage or signs on USS
  • Bleeding may be heavy
  • Molar tissue may look like frogspawn
  • Rarer: Severe morning sickness or 1st trimester pre-eclampsiai.
200
Q

What would USS scan show for hydatidiform moles?

A

‘Snowstorm effect’.

201
Q

Treatment of hydatitiform moles?

A
  • Molar tissue is removed from the soft, easily perforated uterus by gentle suction.
  • Send to histo to confirm dx
  • Give anti D if rhesus -ve
  • Avoid pregnancy for 6months until hCg normal
202
Q

Possible complications of hydatidiform moles?

A
  • Choriocarcinoma.

- Or metastisization to lung, vagina, brain, liver and skin

203
Q

Describe characteristics of atrophic vaginitis?

A
  • Clear/blood stained discharge
  • Watery consistency
  • No odour
  • No itch
  • TReatment is with topical oestrogen
204
Q

What is pelvic inflammatory disease?

A

Sexually transmitted upper genital tract infection due to:

  • Ascending endocervical infection
    • Sexual factors
    • No barrier contraception
    • Multiple partners
  • Descending abdominal infection
    • eg appendicitis
205
Q

Common causes of PID?

A
  • Chlamydia (often asymptomatic)
  • Gonorrhoea
  • Anaerobes
206
Q

Clinical presentation of PID?

A
  • Constant or intermittent pelvic pain
  • Deep dyspareunia
  • Bleeding: irregular periods, intermenstrual beeding, post-coital bleeding
  • Discharge (due to concurrent vaginal infection)
  • Uncommonly fever
207
Q

On examination of PID?

A
  • Cervical motion pain

- Adnexal tenderness

208
Q

Investigations for PID?

A
  • Endocervical swabs - for chlamydia and gonorrhoea testing
  • Increased WCC and CRP
  • USS to exclude abcesses and cysts
  • Laparoscopy with fimbrial biopsy and culture
209
Q

Treatment of PID?

A

IM Ceftriaxone followed by Doxycycline or Metronidazole.

210
Q

Complications of PID?

A 
Early: Abcess or pyosalpinx
Late: 
- Tubal obstruction
- Subfertility
- Chronic PID
- Chronic pelvic pain
- Ectopic pregnancy
211
Q

What is chronic PID?

A

Persisting infection as a result of non/inadequate treatment of acute PID, leading to:

  • Dense pelvic adhesions
  • Fallopian tube obstruction
212
Q

Symptoms of chronic PID?

A
  • Chronic pelvic pain
  • Dysmenorrhoea
  • Deep dyspareunia
  • Heavy and irregular menstruation
  • Chronic vaginal discharge
  • Subfertility
213
Q

On exam of chronic PID?

A

Abdominal and adnexal tenderness

Fixed retroverted uterus

214
Q

Investigations for chronic PID?

A
  • TVUS - fluid collection in fallopian tube, surrounding adhesions
  • Laparoscopy would reveal adhesions
215
Q

Treatment of chronic PID?

A
  • Analgesia and abx (only if active infection)
  • Adhesiolysis
  • Salpingectomy
216
Q

Where are the vagina and uterus derived from?

A

Mullerian duct system and urogenital sinus.

217
Q

What are some genital abnormalities?

A
  • Vaginal septae: common, easily missed
  • Duplication of cervix and/or uterus: May only present when woman has coil in but becomes pregnant in the other uterus

-Bicornuate uterus: partially divided uterus
-Unicornuate uterus: one side has dailed to develop.
Bicornuate and unicornuate uterus presents with recurrent miscarriage, difficulties in labour.

-Imperforate hymen

218
Q

What is imperforate hymen?

A

When the membrane at the mouth of the vagina where the mullerian and urogenital systems fuse is imperforate.

219
Q

Signs of imperforate hymen?

A

There is primary amenorrhoea, with history of monthly lower abdo pain and swelling, adn the membrane bulging under the pressure of dammed up menstrual blood (haematocolpos)

220
Q

Treatment of imperforate hymen?

A

Cruciate incision in the membrane.

221
Q

What is turners syndrome?

A

45 X0 monosymy in 40-60%

222
Q

Signs of turners:

A

Newborn: Lymphoedema of hands and feet, cardiac and renal abnormalities (coarc of aorta, absent kidney)
Infancy: Short stature, webbed neck, behavioural difficulties, recurrent otitis media, hearing loss
Adolescence: gonadal dysgenesis (streak ovary) results in absent or incomplete puberty, amenorrhoea, impaired growth.

223
Q

Treatment of turners?

A

Recombinant human growth hormone used to treat short stature.
Supplemental oestrogen initiates puberty and stops osteoporosis.

224
Q

What is Ashermans syndrome?

A

an acquired uterine condition that occurs when scar tissue (adhesions) form inside the uterus and/or the cervix

225
Q

What are the commonest pituitary tumours seen in pregnancy?

A

Prolactinomas

226
Q

Clinical features of prolactinoma?

A
  • Amenorrhoea
  • Galactorrhoea
  • Headache
  • Visual field defects (bitemporal hemianopia)
  • Diabetes Insipidues
227
Q

What is the effect of pregnancy on the prolactinoma?

A

They could increase in size in pregnancy and cause symptoms. Highest risk is in 3rd trimester with macroprolactinomas. Pregnancy should be delayed until tumour shrinkage has occurred wtih drug therapy.

228
Q

What is the effect of the prolactinoma on pregnancy?

A

High prolactin levels lead to infertility. Most cases have no complications in pregnancy.

229
Q

Management of prolactinoma?

A
  • Outside pregnancy: Dopamine receptor agonists eg Cabergoline and Bromocriptine reduce prolactin levels, these should be stopped upon confirmation of pregnancy
  • If sx of tumour expansion do CT or MRI
230
Q

Causes of hyperprolactinaemia?

A
  • Normal pregnancy and breastfeeding
  • Pituitary adenomas
  • Hypothalamus or pituitary stalk lesions
  • Empty sella syndrome
  • Hypothyroidism
  • Chronic renal failure
  • Drugs; phhenothiazine, metoclopramide, methyldopa.

3a (25 decks)

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