Pelvic pain + general gynae Flashcards

1
Q

Causes of acute pelvic pain

A
  • Gynae: adenomyosis, degenerating fibroid, endometriosis, mittelschmerz, ovarian torsion, PID, ruptured ovarian cyst, tuba-ovarian abscess
  • Obstetric: ectopic pregnancy, postpartum endometritis, postpartum ovarian vein thrombosis, placental abruption, uterine impaction, corpus luteum haematoma
  • GI: appendicitis, bowel obstruction, diverticulitis, gastritis, inguinal hernia, IBS, mesenteric venous thrombosis, perirectal abscess
  • Urinary: cystitis, pyelonephritis, ureteric stones
  • Other: dissecting aortic aneurysm, lead poisoning, somatisation disorder, malingering/narcotic seeking, porphyria, sickle cell crisis
  • Adolescent-specific: the above, plus imperforate hymen + transverse vaginal septum
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2
Q

Causes of chronic pelvic pain

A
  • Repro: adenomyosis, adhesions, adnexal tumours, cervical stenosis, cervical/endometrial polyps, endometriosis, fibroids, pelvic varicosities, vulvodynia, pelvic floor relaxation disorders, accessory ovaries
  • Urinary: chronic/recurrent UTIs, urolithiasis, pelvic floor dysfunction, urethral diverticula
  • GI: chronic bowel obstruction, colitis, constipation, diverticular disease, IBD, IBS, peritoneal abscess, herniae
  • Spinal: neoplasia, malformations, postural
  • Other: neuropathies, abdominal migraines, depression/BPAD, chronic fatigue syndrome, chronic visceral pain syndrome, substance abuse
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3
Q

What is endometriosis?

A

Extra-uterine endometrial-like tissue (glands + storm) deposited with an inflammatory response, most commonly diagnosed between 25 and 40y

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4
Q

Pathophysiology of endometriosis

A
  • Repeated inflammatory responses – adherent tissues
  • Deposits of endometrial-like tissue may be in ovary - small or large cysts called endometiromas ‘chocolate cyst’ as whitish capsule w altered blood
  • Deposits also involve the uterosacral ligaments, PoD, pelvic peritoneum, bladder, umbilicus, and can affect the lungs!
  • Endometriomas can rupture causing acute peritoneal irritation

It might be due to retrograde menstruation, but its not fully understood

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5
Q

RF for endometriosis

A

Early menarche, short MC, FH, long duration of menstrual bleeding, HMB, defects of the uterus or tubes

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6
Q

CF of endometriosis and what else could this indicate?

A

CF: often depends on point in MC as oestrogen causes the tissue to react. May bleed from the ectopic tissue during menstruation causing cyclical pelvic pain, dysmenorrhoea, dyspareunia, dyschezia (painful defecation), sub fertility, focal sx of bleeding from distant site e.g. haemothorax, fixed retroverted uterus, nodules on uterosacral ligaments, tenderness

Ddx: PID, ectopic pregnancy, fibroids, IBS

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7
Q

What Ix would you do in a woman suspected of having endometriosis?

A

Urinalysis, STI screen, TV USS (evidence of endometriosis, pelvic mobility, bowel involvement), diagnostic laparoscopy (typical findings are chocolate cysts, adhesions and peritoneal deposits)

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8
Q

How is endometriosis managed?

A
  • Medical: analgesia, ovulation suppression with progestogens/implant/IUS/COCP to encourage atrophy of the lesions, GnRH in the short term
  • Surgical: excision of visible lesions, may need colorectal input
  • Pregnancy and menopause often improve sx
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9
Q

What is adenomyosis and who is at risk?

A

Functional endometrial tissue in the myometrium, hormone-responsive (so sx reduce after menopause). May be focal or diffuse

RF are multiparous women near end of reproductive life, fibroids, uterus surgery

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10
Q

How may adenomyosis present?

A

Menorrhagia, dysmenorrhoea, constant pain, irregular bleeding, deep dyspareunia

O/E - symmetrically enlarged tender uterus ‘boggy’

Ix: TV US shows globular uterus with poor endometrial-myometrial definition, asymmetry, myometrial cysts; MRI should show thickened E-M junctional zone

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11
Q

How do you manage adenomyosis?

A
  • Hormones - COCP/POP/IUS/GnRH agonist/aromatase inhibitors - reduce proliferation so reduce size and less blood loss
  • Uterine artery embolisation to cause shrinkage
  • Hysterectomy - definitive
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12
Q

What are uterine fibroids and who is at risk of them?

A

Benign smooth muscle tumour (leiomyoma), may be single or multiple and vary from tiny to huge

RF: black ethnicities, obesity, nulliparity, PCOS, DM, HTN, FH; in pregnancy they enlarge and in menopause they get smaller

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13
Q

What are the types of fibroids?

A
  • Intramural - commonest, in myometrium
  • Subserosal - go outwards, may distort the normal contours or put pressure on bladder or bowel
  • Submucosa - go inwards, can cause HMB + infertility
  • Cervical - similar to polyps, often pedunculate
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14
Q

How do fibroids present?

A
  • Asymptomatic - 50%
  • Menorrhagia (SM, IM), irregular (SM)
  • Lower abdominal cramping pain, often during menstruation, or acute pain from torsion
  • Palpable from abdomen, bloating
  • Urinary sx from pressure
  • Constipation/tenesmus
  • Subfertility - esp IM+SM
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15
Q

How are fibroids managed?

A
  • Asymptomatic - no management needed
  • Levornogestrel-releasing IUS first line
  • Other medical - COCP, mefenamic acid/tranexamic acid (to regulate + reduce menorrhagia + pain)
  • Short term use of GnRH agonists to reduce size
  • Uterine artery embolisation - shrink fibroids by ischaemia, fertility can be impaired
  • Surgical: myomectomy, hysteroscopic ablation, hysterectomy
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16
Q

Endometrial polyps

A

Outgrowths of endometrium - usually asymptomatic but sometimes affect fertility or cause IMB/HMB/PMB or protrude through cervix causing PCB

US - best seen during secretory phase, occasionally develops into hyperplasia

M: if symptomatic via hysteroscopic removal

17
Q

Cervical polyps

A

Focal hyperplasia of columnar epithelia, common + usually asymptomatic but increases cancer risk, peak in 50-60y age group + multiparous women

CF: abnormal bleeding, increase in discharge, infertility (if big, uncommon)

Ix: tripe swabs (infection), smear (CIN/Ca), US to check for endometrial polyps

M: remove all polyps using polypectomy forceps or diathermy loop excision

18
Q

Cervical ectropion

A

This is a benign eversion of the endocervix (the inner mucus secreting bit) so it is exposed to the vaginal ectocervix so there is stratified squamous to columnar metaplasia of the ectocervix

A normal variant, common in adolescence pregnancy + oestrogen contraceptives, rare post-menopause

CF: asymptomatic, abnormal bleeding, PCV, increased non-purulent discharge, red everted epithelium seen with ring around external Os

M: smear to exclude CIN, triple swabs for infection, stop oestrogen meds if causing sx, if persists can ablate the columnar bit

19
Q

What is a Bartholin’s cyst and who is most at risk?

A

A fluid filled sac in the greater vestibular glands, which are mucinous glands positioned at the sides of the vestibule in 4 o’clock and 8 o’clock positions. Secretions build up forming a cyst - if infected becomes an abscess (commonly E coli, STIs and MRSA)

RF: nulliparous, reproductive age, previous Bartholin’s cyst, sexually active, vulval surgery

20
Q

How do Bartholin’s cysts present?

A

Can be asymptomatic if small, vulval pain (esp walking/sitting), superficial dyspareunia, spontaneous rupture causing relief; abscesses - acute pain + dysuria; O/E cysts are soft fluctuant + non-tender whereas abscesses are hard + tense + often surrounded by cellulitis

DDx: Bartholin’s gland cancer, benign tumour, sebaceous/Skene’s/mucus cysts

21
Q

Management of Bartholin’s cysts

A
  • Ix: endocervical + HVS, biopsy if >40 (to exclude Ca vulva)
  • Warm bath may stimulate rupture of a small one
  • Abx if systemically unwell
  • Definitive management is incision + drainage with marsupialisation (eversion of cyst wall) or putting a catheter in it for a few weeks to allow epithelialisation
22
Q

What is lichen sclerosus?

A

A chronic inflammatory skin disorder causing thinning of the epidermis which usually occurs in pre-pubescent girls or post-menopausal women (the latter group have a 5% risk of it becoming SCC)

It is likely autoimmune in aetiology

23
Q

How does lichen sclerosus present?

A
  • White atrophic patches in the anogenital region (occasionally also in the axillae/buttocks/thighs)
  • Pruritic (usually)
  • Erosions/fissures - pain, dysparenuina
  • May get adhesions e.g. clitoral head fusion so lose vaginal opening

Ddx: lichen simplex (lichenification from chronic scratching), vitiligo, vulva Ca, VIN, candidiasis, post-inflammatory hypo pigmentation

Usually clinical diagnosis but may do biopsy if uncertain or suspecting neoplasia

24
Q

How is lichen sclerosus managed?

A

Topical steroids + emollients
F/U due to risk of SCC
Avoid irritants, inc minimising urinary contact

25
Q

What may complicate fibroids?

A
  • Torsion - acute pelvic pain
  • Red degeneration - haemorrhage into the fibroid, usually during pregnancy as they enlarge at this time, causes acute pain
  • In pregnancy the risks of recurrent miscarriage, PPH and preterm labour are increased
  • Recommend CS
  • Haemorrhage - rare, if submucosal fibroid prolapses through the cervix
26
Q

What is the management for fibroids causing fertility issues?

A

Myomectomy

This is cos GnRH treatment stops ovulation + when stop the drug the fibroids re-grow, UA embolisation impairs ability to implant + grow and endometrial ablation means conceptus wouldn’t be able to implant

27
Q

What is the difference between gravidity and parity?

A

Gravidity - number of pregnancies, regardless of outcome. Twin pregnancy is counted as 1.

Parity - number of pregnancies reaching a viable gestational age, which includes live births + twin births. Twin pregnancies carried to viable gestational age is 1.

  • Given birth once before-primiparous (never=nulliparous), given birth 2+-multiparous
  • Plus added when there has been miscarriage or TOP - e.g. G2P1+1 is pregnant twice, 1 to viable, 1 miscarriage