Uterine Abnormalities Flashcards

1
Q

Define uterine fibroids

A

Benign tumour of the uterine smooth muscle (leiomyoma), i.e of the myometrium

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2
Q

Classify the different types of fibroids based on location

A
Based on location relative to the uterine wall 
•	Submucous  
•	Cervical  
•	Intramural  
•	Subserosal
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3
Q

What is the macroscopic appearance of fibroids?

A

Looks like a well-demarcated, firm, whorled tumour

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4
Q

Outline the aetiology of fibroids

A

Hormone dependent: contain lots of oestrogen and progesterone receptors

  • Enlarge in pregnancy (due to oestrogen), shrink in menopause
  • Cause known
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5
Q

Outline some risk factors and protective factors for developing fibroids

A

RF: nulliparity, family history, obesity, smoking, afro-carib, HRT causing continued fibroid growth following menopause

Protective: smoking, parous women, long term hormonal contraceptive use

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6
Q

Outline 3 different types of fibroid degeneration (occur when the fibroids outgrow their blood supply) that can occur in its natural history

A

Red degeneration:
• Haemorrhage and necrosis occurs within the fibroid typically presenting in the mid-second trimester pregnancy with acute pain

Hyaline degeneration:
• Asymptomatic softening and liquefaction of the fibroid

Cystic:
• Asymptomatic central necrosis leaving cystic spaces at the centre
• Degenerative changes can initiate calcium deposition leading to calcification
• Suspicion is greatest in the postmenopausal period when there is rapidly increasing size of the fibroid

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7
Q

Give some symptoms that can be clinically present due to fibroids

A
  • None (50%)

Symptoms are mainly related to location rather than size

  • Menorrhagia (more likely in submucosal, polypoid)
  • Erratic bleeding (IMB)
  • Pressure effects: pressure sensation, bladder/bowel defects
  • Subfertility (tubal ostia blockage, submucous fibroids blocking implantation)
  • Pain (rarely cause pain, unless torso or red degeneration occurs)
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8
Q

Give some signs of fibroids on physical examination

A

On examination
o Abdo – palpable pelvic mass, continuous with uterus
o Vaginal – enlarged, firm, smooth or irregular non-tender uterus

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9
Q

Outline investigations for fibroids

A
  • Bloods – FBC – anaemia
  • USS – TVUS
  • Other – hysteroscopy if submucosal, MRI if diagnosis is unclear/greater accuracy required
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10
Q

What needs to be considered when deciding treatment strategies for fibroids?

A

?Symptomatic
?Functional impact on QoL
?Desire for fertility
?Desire for preservation of uterus

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11
Q

Outline medical treatment for fibroids

A

Main treatments for HMB
• LNG-IUS (levonorgestrel/progesterone intrauterine system)
• Tranexamic acid/Mefenamic acid
• COCP
These treatments are mainly effective in women with HMB without fibroids, but can be worth trying first-line

Injectable GnRH Agonist
• Only effective medical treatment
• Induces a menopausal state (shuts down ovarian oestradiol production)
• Poorly tolerated because of side effects and bone density loss (can only be used for 6 months)

Ulipristal Acetate (selective progesterone receptor modulator, SPRM)
• As effective as GnRH agonists in reducing fibroid volume and alleviating HMB symptoms
• Not yet widely accepted into clinical practice
• Does NOT induce a menopausal state (therefore no GnRH agonist side effects)
• Can be taken orally
NOTE: neither of the last two options are long-term as fibroids regrow as soon as ovarian function returns

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12
Q

Outline surgical management for fibroids

A

Hysteroscopic surgery (minimally invasive)

  • Fibroid polyps
  • Small (up to 3cm) submucous fibroids

Myomectomy (open or laparoscopic)

  • If medical treatment has failed, but preservation of reproductive function is required
  • Preceded by 2-3 months of GnRH agonists/ulipristal acetate to shrink fibroid
  • Risk of bleeding, which may then require hysterectomy
  • Adhesions can form at site of myomectomy - can affect fertility (C-sections recommended for future pregnancies to prevent uterine rupture)

Hysterectomy (laparoscopic, vaginally or abdominally)

  • Preceded by 2-3 months of GnRH agonists/ulipristal acetate
  • Not suitable for women wanting to preserve fertility
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13
Q

Outline radiological treatment for fibroids

A

Uterine artery embolisation (UAE)
• Embolisation of both uterine arteries under radiological guidance, to shrink fibroids
• Shorter hospital stay
• Complications: fever, infection, fibroid expulsion, potential ovarian failure
• Adequate counselling is important because the effect on reproductive function are uncertain

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14
Q

Give some complications of fibroids

A
  • Degenerations
  • Malignancy (~0.1% of fibroids are leiomyosarcomas)
  • Anaemia, miscarriage, infertility
  • In pregnancy: premature labour, transverse lie, PPH (should not be removed at C-section as bleeding may be heavy)
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15
Q

Under what conditions are malignant fibroids more likely

A
  • Pain and rapid growth
  • Growth in postmenopausal women not on HRT
  • Poor response to GnRH agonist or ulipristal acetate
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16
Q

Outline the prognosis with fibroids

A
  • 10 year recurrence rate after myomectomy is 20%

- Fibroids regress and calcify after menopause

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17
Q

Define adenomyosis

A

Presence of endometrium and its underlying storm within the myometrium

18
Q

Give some risk factors for developing adenomyosis

A

Most common around 40 yrs

Associated with endometriosis and fibroids

19
Q

Outline the aetiology of adenomyosis

A

Oestrogen dependent
Cause unknown
Effects on fertility are unclear

20
Q

Outline the clinical features of adenomyosis

A

History: asymptomatic, painful, regular HMB may be common
Examination: uterus mildly enlarged and tender

21
Q

What investigations are undertaken for adenomyosis

A
  • Ultrasound

- Clearly diagnosed on MRI

22
Q

Outline the management for adenomyosis

A

Medical treatment (for menorrhagia)

  • Progesterone IUS
  • COCP +/- NSAIDs
  • Trial of GnRH analogue to determine if symptoms attributed to adenomyosis will improve with hysterectomy

Surgical
- Hysterectomy

23
Q

What is endometritis?

A

Inflammation of the endometrial lining

24
Q

Give some risk factors for developing endometritis

A

Occurs secondary to:

  • STIs
  • Complications of surgery (C-section, surgical termination)
  • Foreign tissue (IUDs)
  • Retained products of conception
  • Malignancy (particularly in postmenopausal uterus)
25
Q

What is the treatment for endometritis?

A
  • Antibiotics

- Occasionally ERPC (evacuation of retained products of conception) is required

26
Q

Outline the aetiology of intrauterine polyps

A
  • Benign tumours that grow into uterine cavity (most are endometrial, some are sub mucous fibroids)
  • Common when oestrogen levels are high
  • Post-menopausally: often found in pts on tamoxifen for breast cancer
27
Q

Outline the symptoms of intrauterine polyps, and how it is diagnosed

A
  • Sometimes asymptomatic
  • Menorrhagia, IMB
  • Can prolapse through the cervix

Diagnosis:

  • Ultrasound
  • During hysteroscopy due to abnormal bleeding
28
Q

How are intrauterine polyps treated?

A
  • Resection (cutting diathermy or avulsion)
29
Q

What is haematometra?

A

Menstrual blood accumulating in the uterus due to outflow obstruction

30
Q

Define endometrial cancer

A

Malignancy arising from endometrial tissue

31
Q

Give the two main subtypes of endometrial cancer

A

Type 1: endometrioid adenocarcinomas
• Oestrogen-driven, associated with obesity, less aggressive
• Arise from a background of endometrial hyperplasia

Type 2: high-grade serous and clear cell carcinomas
• Not oestrogen sensitive, not associated with obesity and more aggressive
• Arise from an atrophic endometrium

32
Q

Outline risk factors for the development of endometrial cancer

A

Main risk factor is exposure to oestrogen (endogenous or exogenous)

Exogenous
- Oestrogen-only HRT, tamoxifen (oestrogen agonist in postmenopausal women)

Endogenous

  • Nulliparity or infertility (due to increase number of anovulatory cycles)
  • Early menarche/late menopause (also related to number of anovulatory cycles)
  • PCOS, oestrogen producing ovarian tumours (granulosa/theca)
  • Obesity (aromatisation of fat-derived peripheral androgens)
  • Diabetes (?due to raised BMI)
33
Q

Outline the main epidemiology of endometrial cancer

A
  • Prevalence highest at 60 years of age

- Only 15% of cases occur premenopausally, with <1% occurring before the age of 35

34
Q

Describe the premalignant stages of disease in endometrial cancer

A
  • Oestrogen acting unopposed –> hyperplasia of endometrium
  • -> Abnormalities of cellular/glandular architecture –> atypical hyperplasia

If diagnosis of endometrial hyperplasia with atypic is made, hysterectomy should be considered.

If fertility is a concern, try P-IUS with 6 monthly hysteroscopy and endometrial biopsy

35
Q

Outline the clinical features of endometrial cancer

A

History:

  • PMB (10% RISK OF CARCINOMA) - perform speculum to rule out vulval, vaginal, cervical carcinoma
  • Premenopausal: IMB, recent onset menorrhagia
  • Other symptoms: abdominal pain, urinary dysfunction, bowel disturbance

Examination:

  • May be normal
  • Bimanual: bulky uterus probable
36
Q

Describe the FIGO staging system for endometrial cancer (1-4b)

A

Stage 1 (confined to uterus)

  • 1a: <1/2 myometrial invasion
  • 1b: >1/2 myometrial invasion

Stage 2
- Cervical stromal invasion, but not beyond uterus

Stage 3 (invades through the uterus)

  • 3a: serosa or adnexae
  • 3b: vaginal and/or parametrium
  • 3ci: pelvic node
  • 3cii: para-aortic node

Stage 4 (further spread)

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

In addition, grades 1-3 are classified (grade 1 is well-differentiated)

37
Q

Outline investigations for endometrial cancer

A
  • Bloods: FBC, U&E, LFT, glucose testing (to assess baseline fitness of patient)
  • Imaging: pelvic USS, TVUS (depth of myometrial invasion, if <4mm very unlikely to be EC), MRI (staging), CXR (pulmonary spread)
  • Tissue diagnosis: pipelle biopsy, hysteroscopy and biopsy
38
Q

Outline the stages of management for endometrial cancer

A

Surgery (abdominal or laparoscopic)

  • Stage 1 – total abdominal hysterectomy (TAH) with bilateral salpingo oophorectomy (BSO) with peritoneal washings
  • Stage 2/3 – modified radical or radical hysterectomy
  • Pelvic/para-aortic lymphadenectomy may be required

Adjuvant therapy (following surgery)

  • External beam radiotherapy (in patients considered high risk for LN involvement)
  • Vaginal vault radiotherapy (reduces local recurrent rate, but does not improve survival)
  • Chemotherapy

Hormone Treatment
• High-dose oral or intrauterine progestins
• Useful for women with complex atypical hyperplasia and low-grade stage 1A endometrial tumours
• May be suitable for women who are not fit for surgery or want to avoid surgery for fertility reasons

39
Q

What is the management approach for pre-menopausal women with endometrial cancer who want to preserve their fertility?

A

Mainly in PCOS causing endometrial cancer pts

  • Alternatives to hysterectomy: only possible for pre-cancer or early-stage low-grade endometrial cancers
  • Hormone therapy (oral progestogens or LNG-IUS): but associated with high relapse rates

Referral to a specialist to discuss ovarian conservation and/or stimulation for egg retrieval and surrogacy

40
Q

Outline the prognosis for endometrial cancer

A
5-year survival rates
Stage 1: 90
Stage 2: 75
Stage 3: 60
Stage 4: 25
Overall: 75

Recurrence is most common with vaginal vault radiotherapy

Poor prognostic factors: older age, advanced stage, deep myometrial invasion, high grade