Gynae disorders Flashcards

1
Q

What is menorrhagia?

A

Heavy menstrual bleeding (HMB)

Excessive menstrual loss over several consecutive cycles which interferes with a woman’s physical, emotional, social & material QoL.

  • In research: objectively measured loss of 60-80mls or more per menstruation (average is 30-40mls and 90% women have losses <80mls).
  • 1/3 women describe periods as heavy, 1/20 age 30-49 consult GP for heavy periods, 12% of all gynaecological consultations.
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2
Q

Causes of menorrhagia?

What to ask in history?

A
  • Dysfunctional uterine bleeding: 40-60% of cases (i.e. no underlying cause)
  • Pelvic pathology (fibroids, endometrial polyps, endometriosis, PID, PCOS)
  • Systemic diseases (coagulation disorders e.g. von Willebrands, hypothyroidism)
  • Iatrogenic (anticoagulant treatment, IUCD)

History
• Age at menarche
• Number of days of menstruation / length of cycle
• How long she considers periods to be heavy
• What they were like previously
• Impact on life
• Inter-menstrual or post-coital bleeding
• Smear status
• Contraceptive use
• ALSO: consider underlying thyroid or coagulation disorder

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3
Q

What are symptoms suggestive of underlying pathology in menorrhagia?

A
  • Persistent post-coital bleeding
  • Persistent inter-menstrual bleeding
  • Dyspareunia
  • Dysmenorrhoea
  • Pelvic pain +/- pressure symptoms
  • Vaginal discharge
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4
Q

Examination and investigations in menorrhagia?

A

Examination:
• Abdominal: fibroids palpable abdominally?
• Pelvic: Speculum (+/- swabs / smear test). Bimanual palpation: (? uterine/adnexal enlargement or tenderness)
• Systemic signs: Anaemia, Endocrine (hirsutism, striae, thyroid enlargement, skin pigmentation)
• Coagulation disorders: bruises or petechiae

Investigations: FBC, thyroid function (if symptoms/signs suggestive), coagulation screen (if history/signs suggestive of bleeding disorder), TVUSS (if uterus palpable abdominally, if pelvic mass of uncertain origin, if has had treatment that has been ineffective).

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5
Q

Tx of menorrhagia? (in primary care)

A

1st line:

  • Levonorgestrel-releasing intrauterine system (LNG-IUS) - provides long-term contraception

2nd line:

  • Tranexamic Acid (anti-fibrinolytic, taken only during menstruation, >50% reduction of menstrual loss- superior to NSAIDs in controlling loss but not pain).
  • Side-effects (few): GIT & CNS disturbances. Avoid if risks of thrombosis.
  • NSAIDs (inhibits PG synthesis): Mefanamic acid, Naproxen, Ibuprofen (only during menstruation or just prior, improves dysmenorrhoea & dyspareunia).
  • Few side effects: GIT & CNS disturbances. Contraindicated in dyspepsia, asthma, renal disorders
  • COCP (Cycle regulation, reduction of flow + dysmenorrhoea - contraceptive but more reversible than LNG-IUS)

3rd line

  • Oral Noristhisterone (Synthetic progestogen, taken during follicular + luteal phase (day 5-26) - may inhibit ovulation but NOT contraception
  • Long-acting progestogens: depot medroxyprogesterone (Depot-Provera), IM injection every 12 weeks

If initial treatment ineffective, switch to an alternative treatment, add on additional drug e.g. tranexamic acid + NSAID / NSAID + COCP. –> Refer to secondary care.

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6
Q

Management of menorrhagia in secondary care (include investigations)?

A
  • Endometrial biopsy (exclude endometrial cancer or atypical hyperplasia) - If persistent inter-menstrual bleeding, aged 45 years+, treatment ineffective
  • Hysteroscopy (direct visualisation of the uterine cavity. opportunity to take biopsy, when ultrasound inconclusive)
  • GnRH analogues: profound hypogonadal effect through down regulation resulting in no ovulation and no menses- significant adverse effects: perimenopausal (hot flushes, sweating, vaginal dryness)

Surgical treatments

  • Endometrial resection (systematic removal of entire uterine lining including basal endometrium, together with underlying muscle to ensure known depth of tissue & muscle removed (not burned)
  • Endometrial ablation (destroys endometrium and superficial myometrium, pregnancy after contraindicated but is not a contraception)
  • Hysterectomy (Laparoscopic, vaginal, abdominal)
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7
Q

What types of pelvic pain are there?

A

Cyclical
o Gynae: endometriosis, adenomyosis, PID, primary dysmenorrhoea
o GI: IBS

Non-cyclical
o Gynae: PID, adhesions, hydrosalpinges, tumours
o GI: IBS
o Urological: recurrent UTI, interstitial cystitis
o Neurological: nerve injury / entrapment
o Musculoskeletal: myofascial pain

Four Ds: dyspareunia, dysmenorrhoea, dyschesia, dysuria

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8
Q

How to investigate pelvic pain?

A

Most common gynae referral (20% of all gynae consultations).

History: chronicity, dysmenorrhoea, dyspareunia, dyschesia, associated bloating / constipation / diarrhoea / nausea, recent weight change, recent appetite change

Exam: abdominal masses + trigger points, bimanual: size & mobility of uterus, uterosacral ligaments (palpable? nodules?), adnexal masses

Investigations:
• Triple swabs
• MSU
• Pelvic USS (If abnormal findings on examination, if 1st treatment unsuccessful) -NB normal USS does not exclude pathology

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9
Q

What is endometriosis?

How common?

Risk Factors?

A
Eutopic endometrium (glands + stroma) present outside the uterus: induces a chronic, inflammatory reaction.
• Ovaries
• Utero-sacral ligaments
• Pouch of Douglas
• Broad ligament
• Rarely: lung, nasal septum, CNS

Very common: 2-10% in menstruating women (1.5 million), 50% in women with subfertility & 35% in teenagers.

Risk factors: low birth weight, early menarche, short menstrual cycle, late menopause, genetics, red meat, obesity.

Protective factors: fruit + veg, multiple pregnancy, omega 3 & prolonged breastfeeding

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10
Q

What may cause endometriosis?

A

Multiple theories: retrograde menstruation, hereditary, genetic, environmental, coelomic metaplasia of multipotent cells, spread through blood vessels / lymphatics, altered immune function, direct transfer: C-section, or combination. Predominantly oestrogen dependent.

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11
Q

How may endometriosis present (3 main types)

A

Types of presentation:

  • ovarian lesion
  • superficial peritoneal lesion (powder burn or gun shot lesion)
  • deep infiltration endometriosis (solid endometriosis mass situated >5mm deep under the peritoneal surface)

Staged I to IV, mainly for fertility (not helpful for all patients).

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12
Q

Symptoms of endometriosis?

A

May be asymptomatic!

Pain:
o Cyclical (both pain &amp; GIT symptoms)
o Dysmenorrhoea
o Deep dyspareunia
o Chronic pelvic pain
o Dyschesia
o Ovulation pain
  • Infertility / subfertility
  • Urinary: dysuria, urgency, haematuria
  • Chronic fatigue
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13
Q

How is endometriosis assessed / diagnosed?

Include differentials?

A

Pelvic examination: ? reduced organ mobility, tender nodularity in posterior vaginal fornix & visible vaginal endometriotic lesions

Diagnosis

Gold standard: laparoscopy + histological verification: aim to treat at same time. (means earlier Dx + Tx, but still delays as women told symptoms were normal, hormonal drugs provided temporary relief, inadequate tests applied, overlap with IBS, PID + laparoscopy is invasive)

- Laparoscopy for pelvic pain: 
38-45% endometriosis
25-40% normal
5-15% PID
4-13% post-op adhesions
5-8% uterine malformations
2-5% ovarian cyst
  • TVUSS: ovarian endometriosis (endometrioma – ground glass appearance) + rectal endometriosis: little role for this in primary care, should be referred for definitive diagnosis if symptoms are significant.
  • MRI / CT

Differentials: adenomyosis, leiomyomata, PID, uterine myoma / large polyp, ovarian cyst, IBD, interstitial cystitis

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14
Q

Treatment of endometriosis?

A
  1. Simple analgesia: NSAIDs + paracetamol
  2. Hormonal (empirical therapy is acceptable for short duration): Progestogens, COCP, Mirena: LNG-IUS reduces blood flow + dysmenorrhoea, supports retrograde theory

GnRH agonists +/- add back HRT (if given continuously, acts like a GnRH antagonist causing ↓GnRH receptors on pituitary and ↓FSH/LH/oestrogen > inhibition of endometrial cell proliferation, if given in pulsatile manner will increase these hormones – used in infertility)

Cochrane: all hormonal treatments of equal efficacy for symptom control + all usually cause disease regression but all are contraceptive therefore no role if desiring pregnancy + recurs after treatment is stopped in majority of cases

  1. Conservative surgical (aim to destroy all visible endometriosis)
    o Diathermy / ablation
    o Excision
    o Laser (e.g. lasering cysts may improve fertility)
  2. Radical surgical
    o Remove uterus, ovaries & nodules

Surgery improves fertility in minimal-mild endometriosis & improves pain in women with endometriosis. Excision preferred to ablation as disease deep.

Involve other specialities (e.g. colorectal, pain team, support groups). Severe disease refer to tertiary level service unless locally available.

Complications: infertility, adhesions (inflammation or post-surgery), post-surgical ovarian failure, increased risk of autoimmune diseases and mental health conditions

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15
Q

What is Asherman Syndrome?

Tx?

A

Irreversible damage of single layer thick basal endometrium does not allow normal regeneration of endometrium. Endometrial cavity undergoes fibrosis & adhesion formation. Results in reduced or absent menstrual shedding: can occur with curettage of uterine cavity during evacuation of RPOC (miscarriage / secondary PPH). In this ‘soft’ uterine state myometrium (including basal layer) can be inadvertently excavated. The same principle is deliberate in endometrial destruction (surgical treatment for menorrhagia where diathermy loop or ball (1st generation) and ablative methods (2nd generation – hot water balloon, bipolar diathermy, laser, microwave) are used to destroy the basal layer. TB & schistosomiasis can also cause Asherman syndrome.

Mainstay of treatment is preventative but hysteroscopic techniques may be used to manually break down or lyse the adhesions.

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16
Q

What is a fibroid? How common / risk factors?

A

Benign tumour of uterine smooth muscle: leiomyoma.

Common (20-30% of women >30).
Occur in ~20% white and ~50% black women in later reproductive years.
Rare before puberty (develop in response to oestrogen) + rarely progress after menopause.

Vast majority asymptomatic but may be identified coincidentally (abdominal examination may indicate firm mass arising from pelvis).

17
Q

What are types of fibroid?

A

Gross appearance: firm, whorled tumour located adjacent to & bulging into:

  • Endometrial cavity (SUBMUCOUS fibroid)
  • Centrally within myometrium (INTRAMURAL fibroid)
  • Outer border of myometrium (SUBSEROSAL fibroid)
  • Attached to uterus by narrow pedicle containing blood vessels (PEDUNCULATED fibroid)
  • Arising from cervix = cervical fibroid

Fibroids can also arise separately from the uterus (especially broad ligament): most likely from embryological remnants > typical whorled appearance may be altered following degeneration:

18
Q

What are the types of degeneration of fibroids?

A
  • Red degeneration: follows acute disruption of blood supply during active growth, classically during mid 2nd trimester of pregnancy (may present as sudden onset pain with localised tenderness to area of the uterus), associated with mild pyrexia + leucocytosis. Symptoms typically resolve over few days + surgery rarely required.
  • Hyaline degeneration: gradually outgrows blood supply and may progress to central necrosis, leaving central cystic spaces (cystic degeneration). Calcification of a fibroid may be detected incidentally on abdominal X-ray in a post-menopausal woman (final stage in the natural history of fibroid).
  • Malignant or sarcomatous degeneration: occurs very rarely (incidence <1 in 2000) – suspicion greatest in post-menopausal period when fibroid size is rapidly increasing
19
Q

What are risk factors for clinically significant fibroids?

Common presenting symptoms?

A

Clinically significant fibroids: risk factors
• Obesity
• Positive family history
• African origin

Common presenting symptoms
• Menstrual disturbance (menorrhagia, cramps)
• Pressure symptoms (urinary frequency with larger fibroids)
• Pain unusual unless acute degeneration occurs
• Bloating
• Subfertility

Menorrhagia usually indicates fibroid is of submucous origin which is distorting the endometrial cavity by increasing the endometrial surface area (removal of the submucous component in presence of other types of fibroids can resolve the menorrhagia symptoms).

Subfertility may result from mechanical distortion / occlusion of tubes or endometrial cavity grossly distorted by submucous fibroids may prevent implantation of fertilised ovum (fibroids do not require removal until proven infertility).

20
Q

How do fibroids affect pregnancy?

A

Once pregnancy established, risk of miscarriage NOT increased.

  • In late pregnancy, fibroids located in cervix or lower uterine segment may cause an abnormal lie
  • After delivery, postpartum haemorrhage may occur due to inefficient uterine contractions
21
Q

Investigations for fibroids?

A

Clinical features alone may be sufficient, Hb to assess anaemia if menorrhagia.

TVUSS mainstay: to distinguish between fibroid + ovarian mass. In the presence of large fibroids, USS helpful to exclude hydronephrosis from pressure on ureters.

22
Q

Treatment of fibroids?

A

If asymptomatic / incidental detection – manage conservatively.

USS / repeat clinical examinations may monitor growth rate (6-12 months).

Menorrhagia: GnRH AGONISTS main treatment - shrinks fibroid but regrow to previous dimensions when ovarian function returns (so usually just used in preparation for surgery)

  • (tranexamic acid, mefenamic acid, COCP generally ineffective)
  • Mifepristone (antiprogestogen) shrinks fibroids at low dose but not available for use because it causes endometrial hyperplasia.

Surgical treatment: hysteroscopic removal (if menorrhagia associated with submucous fibroid or fibroid polyp).
• Myomectomy
• Hysteroscopic endometrial ablation
• Hysterectomy

23
Q

What is adenomyosis? Common? Symptoms?

A

Endometrial tissue within the myometrium

~1 in 10 women, can occur in any menstruating woman but most common if age 40-50 and multiparous.

Cause unknown. Does not affect fertility but may increase miscarriage risk & preterm birth.

Symptoms dysmenorrhoea, menorrhagia + pre-menstrual pelvic pain (less common dyspareunia and dyschesia).
~1/3 asymptomatic. Symptoms stop after menopause.

Enlarged, boggy uterus.

24
Q

How is adenomyosis diagnosed? Management?

A

~1/2 detected on TVUSS, but MRI may be necessary

Management: conservative (wait), medications for menorrhagia, hormones (COCP/POP/IUS), GnRH injections (temporary menopause but not for long term use), hysterectomy or uterine artery embolization (less invasive, may preserve fertility, stops symptoms for ~2 years).

25
Q

What are endometrial polyps?

Risk factors?

A

May be referred to as ‘uterine polyps’, originate from endometrium therefore not the same as fibroids (myometrium).

Discrete outgrowths attached by a pedicle (move with the flow of the distention medium). Pedunculated (have elongated pedicle) or sessile (large flat base).

o Pedunculated more common, and can protrude though cervix into vagina.

  • Single or multiple
  • Variable size (0.5-4cm).

No cause known but appear to grow in response to circulating oestrogen

Risk factors: obesity, hypertension, Hx of cervical polyps, tamoxifen, HRT.

Use of IUS containing levonorgestrel in women taking tamoxifen may reduce incidence of polyps.

26
Q

Symptoms of endometrial polyps?

Management?

A

Often asymptomatic, but may cause irregular bleeding, IMB, menorrhagia, and PMB (bleeding from vessels of the polyps). If protrudes into vagina, may have dysmenorrhoea (pain).

<40: Unlikely to be significant (may cause IMB but only removed if symptoms persist for >3 months).

> 40 + premenopausal: if diagnosed by USS or hysteroscopy, consider removal (endometrial hyperplasia most common abnormality, increases with age – can be present in the polyp tissue + removal of polyp usually resolves symptoms).

Post-menopausal: removal mandatory (can be due to hyperplasia or malignancy) – can also be caused by tamoxifen treatment (~30% of those treated). They are benign in most cases but removal is necessary to exclude the remote possibility of malignancy.

27
Q

What are cervical polyps?

How common?

A

On surface of cervical canal, almost all benign. Usually <1cm diameter. May be pedunculated + occasionally prolapse into vagina (may be mistaken for endometrial polyps or submucosal fibroids).

Most common if menstruating women / previous pregnancy. Cause unknown, often associated with cervical inflammation, ?raised oestrogen or clogged cervical blood vessels. ~1% will show neoplastic change which may lead to cancer.

28
Q

Symptoms, diagnosis and Tx of cervical polyps?

A

Symptoms: usually asymptomatic, can cause IMB, menorrhagia, PMB, leukorrhoea.

Dx: may be found incidentally during routine smear - red / purple projections from cervical canal during pelvic exam, (usually bright red, spongy texture). Dx can be confirmed by biopsy.

Tx: removal with forceps and cauterise base with silver nitrate sticks. Send polyp for histology – if endometrial origin will need TVUSS and referral for further Ix of endometrium (to ensure complete removal).

99% remain benign. After removal, they are unlikely to regrow.

29
Q

What is a nabothian cyst?

A

Mucus filled cyst on surface of cervix, most often caused when stratified squamous epithelium of ectocervix grows over simple columnar epithelium of endocervix > tissue growth can block cervical crypts (subdermal pockets 2-10mm diameter) trapping cervical mucus inside crypts.

Typically appear as firm bumps on surface of cervix – woman may notice (e.g. cap / diaphragm / fertility assessment) or may notice during pelvic exam. If unusual appearance, colposcopy will rule out other diagnoses.

If blood vessels short, comma-like or corkscrew-shaped (and bleed on contact), cyst may be a rare mucin-producing carcinoma of cervix (MRI distinguishes cancer from Nabothian cyst).

Tx not required, resolve on their own (cryotherapy possible but very rarely necessary).

30
Q

What is cervical ectropion?

A

Benign condition (sometimes incorrectly termed ‘erosion’): ‘raw’ area on cervix due to presence of columnar epithelium (glandular) on vaginal aspect of cervix.

Can present with excessive clear odourless mucus-type discharge.

Commonly develops under 3Ps: puberty, pill, pregnancy.

If troublesome, predisposing factor can be stopped or cervix ablated if cytology is normal. Screen to exclude chlamydia + other STIs prior to Tx.

If persistent ectropion, columnar epithelium undergoes metaplasia to a ‘stronger’ squamous epithelium. This transformation zone undergoes dyskaryosis + possible malignant change due to HPV infection (subject to screening by cytology).

Sometimes the columnar glands in the transformation zone become sealed over forming small (2-10mm) mucus-filled cysts visible on ectocervix > ‘Nabothian follicles’ with no pathological significance. No treatment usually required.

31
Q

What is cervical stenosis?

A

Usually iatrogenic: Tx of pre-malignant disease using cone biopsy or loop diathermy. Recent increase in endometrial ablation has seen higher incidence, especially where internal os (isthmus) has been ablated  hematometra (blood collected within uterus, unable to be released through cervix) causes cyclical dysmenorrhoea with no associated menstrual bleeding. Treatment: surgical dilatation of cervix with hysteroscopic guidance (under LA). anaesthesia. Re-stenosis can occur and sometimes hysterectomy required to relieve pain.

32
Q

What is PID? Causes?

A

Term used to describe infection and inflammation of the female pelvic organs (any part of higher reproductive system) including the uterus, fallopian tubes, ovaries and the surrounding peritoneum. It is usually the result of ascending infection from the endocervix. Salpingitis sometimes used interchangeably but this is inflammation of fallopian tubes.

  1. Chlamydia trachomatis – (most common cause)
  2. Neisseria gonorrhoeae
  3. Mycoplasma genitalium
  4. Mycoplasma hominis
33
Q

Risk factors for PID?

A
Young (16-24)
Multiple partners
Chlamydia / gonorrhoea (90% PID acquired sexually, and mostly due to chlamydia – 10% cases occur after childbirth particularly if forceps used)
IUD insertion
Previous PID
Bacterial vaginosis

Note: everyone having IUD inserted should be screened for infection before insertion to reduce the risk of PID – IUD can introduce infection from lower tract > upper tract.

34
Q

Features of PID?

A

Often asymptomatic: lower abdominal pain (unilateral or bilateral), fever, deep dyspareunia, dysuria and menstrual irregularities may occur, vaginal or cervical discharge, cervical excitation.

  • Heavy blood loss suggests endometritis
  • Cervicitis: cervix appears red and will bleed easily
  • Nausea & vomiting suggests peritonitis!

Perihepatitis (Fitz-Hugh Curtis Syndrome) in ~10% of cases – inflammation of liver capsule, secondary to PID. Characterised by RUQ pain and may be confused with cholecystitis.

35
Q

Examination / diagnosis of PID?

A

Examination: cervical excitation, tenderness / peritonism and tenderness at fornices

Diagnosis: suspect in any woman with lower abdo pain, consider in any women with unexplained irregular bleeding

Investigations:
• Screen for Chlamydia and Gonorrhoea (endocervical swab), most women have negative swabs – does not rule out PID.
• Bloods / urine test
• Pregnancy test
• TVUSS
• Laparoscopy e.g. to rule out appendicitis / suspected complication that can

36
Q

Management of PID?

A

Due to difficulty in making an accurate diagnosis, and potential complications of untreated PID, consensus guidelines recommend having a low threshold for Tx.
If very unwell may have to admit for IV ceftriazone.

  1. IV Ceftriaxone 1g + PO doxycycline 12 hourly + PO metronidazole 8 hourly (14 days)
  2. PO ofloxacin 12 hourly + PO metronidazole 8 hourly
  3. Cannot tolerate oral: IV Ceftriaxone 1g + IV clarithromycin 12 hourly + IV metronidazole 8 hourly

o RCOG guidelines: in mild cases, IUDs may be left in. More recent BASHH guidelines suggest that the evidence is limited but that ‘Removal of the IUD should be considered and may be associated with better short term clinical outcomes’

o Avoid intercourse until patient and partner treated (also contact tracing as per STI)

37
Q

Complications of PID?

A
  • Infertility - the risk may be as high as 10-20% after a single episode
  • Abscess formation: (up to 15%), may cause severe pain and peritonitis, may rupture
  • Chronic pelvic pain
  • Ectopic pregnancy
  • Fitz-Hugh-Curtis syndrome
  • Chronic salpingitis > can cause fibrosis and adhesions (may occur if PID not treated promptly).