Uterine Disorders Flashcards

1
Q

What are uterine fibroids? PPx and Ax:

A
  • Benign smooth muscle tumours of the uterus (leiomyomas).
  • Most common benign tumours, risk of becoming malignant is 0.1%.
  • The smooth muscle tumours arise from the myometrium of the uterus.
  • Classified according to their position in the uterine wall.
  • Pathogenesis poorly underwood - growth taught to be stimulated by oestrogen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the different classes of fibroids?

A
  • Intermural (most common) - confined to the myometrium.
  • Submucosal - directly underneath the endometrium of the uterus and can protrude into the uterine cavity.
  • Subserosal - protrudes into and distorts the serosal (outer) surface of the uterus, can be pedunculated (on a stalk).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Risk factors of fibroids?

A

1) Obestiy
2) Early menarche
3) Increasing age
4) Family history (1st degree relative)
5) Ethnicity (afro-carribeans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical features of fibroids?

A

MAJORITY are ASYMPTOMATIC - discovered incidentally on pelvic or abdominal examination.

1) Pressure symptoms +/- abdominal distention - (urinary frequency or retention)
2) Heavy menstrual bleeding
3) Subfertility due to obstructive effect of fibroid
4) Acute pelvic pain (rare) - may occur in pregnancy due to red degeneration where rapidly growing fibroids undergo necrosis and haemorrhage. Torsion may occur in pedunculated fibroids.

Sign: Solid mass or enlarged uterus palpable on abdominal/bimanual examination - uterus usually non-tender.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ddx of fibroids?

A

1) Endometrial polyp
2) Ovarian tumour
3) Leiomyosarcoma - malignancy of mymetrium
4) Adenomyosis - presence of endometrial tissue in myometrium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigation of fibroids?

A

1) Pelvic ultrasound

2) MRI - rarely required only if sarcoma suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Medical Management of fibroids?

A
  • Asymptomatic patients rarely need treatment, medical/surgical options available for symptomatic fibroids.
  • Medical:
    1) Tranexamic acid or mefanamic acid
    2) Hormonal contraceptives - COCP, POP, mirena IUS (controls menorrhagia)
    3) GnRH analogue (Zolidex) - Supresses ovulation, temporary menopausal state, used preoperatively to reduce fibroid size and lower complications. (6 months only due to osteoporosis risk)
    4) Selective progesterone receptor modulator (Ulipristol/Esmya) - Reduce size of fibroid/menorrhagia, pre-op or alternative to surgery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Surgical management of fibrosis?

A

1) Hysteroscopy and Transcervical Resection of Fibroids (TCRF) - useful for submucosal fibroids
2) Myomectomy - for women wanting to preserve uterus
3) Uterine artery embolisation - via femoral artery (pain and fever post-op)
4) Hysterectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is endometriosis? Ax and PPx?

A
  • Chronic condition in which endometrial tissue is located at sites other than the uterine cavity - ovaries, pouch of Douglas, uterosacral ligaments, pelvic peritoneum, bladder, umbilicus and lungs.
  • 25-40yrs
  • PPx unclear - retrograde menstruation? - endometrial cells travel backwards from uterine cavity through Fallopian tubes and deposit onto pelvic organs where they seed and grow - and to distant sites through lymphatics and vasculature.
  • SENSITIVE TO OESTROGEN - Sx dependant on menstrual cycle. Bleeding from ectopic tissue during menstruation - pain, bloating and distention at these sites. Repetitive inflammation and scarring can lead to adhesions - symptoms reduced during pregnancy and menopause.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Risk factors of endometriosis?

A

1) Early menarche
2) Family history
3) Short menstrual cycles
4) Long duration of menstrual bleeding
5) HMB
6) Defects in uterus/Fallopian tubes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical features of endometriosis?

A

1) CYCLICAL PELVIC PAIN - at time of menstruation, can be constant where adhesions have formed.
2) Dysmenorrhoea, dyspareunia, dyschezia, dysuria
3) Subfertility
4) Focal symptoms of bleeding in ectopic sites of endometriosis DURING MENSTRUATION, e.g. haemothorax at lungs.

O/E: Fixed + retroverted uterus, uterosacral ligament nodules, general tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ddx of endometriosis?

A

1) Fibroids
2) PID
3) Adenomosis
4) Ectopic pregnancy
5) IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Investigations of endometriosis?

A

1) LAPROSCOPY - chocolate cysts, adhesions, peritoneal deposits (differentiate with chronic infection).
2) Pelvic Ultrasound - determine severity and needs to be undertaken before surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Management of endometriosis?

A

Dependant on individual requirement, if asymptomatic no treatment is needed.

1) Pain - Analgesia, NSAIDs (follow analgesic ladder)
2) Ovulation - suppressing ovulation for 6-12 months can cause atrophy of endometriosis lesions + reduce symptoms. (LOW DOSE COCP or norethisterone, or injected hormones/intrauterine devices (mirena coil).
3) Surgery - if endometriosis is severe - excision, fulguration, and laser ablation to completely remove endometrial tissue in peritoneum, uterine muscle, pouch of Douglas. Relapses can occur and surgery may have to be repeated.
4) Ultimate management - hysterectomy with removal of ovaries - hormone replacement until menopausal age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Adenomyosis? Ax and PPx:

A
  • Presence of functional endometrial tissue within the myometrium - benign invasion of the middle layer of uterine wall.
  • Main Sx - menorrhagia and dysmenorrhoea (frequently occurs with fibroids)
  • Occurs in multiparous women at the end of reproductive life. Symptoms reside post menopause as ectopic tissue is hormone responsive.

When endometrial storm is allowed to communicate with myometrium after uterine damage: Pregnancy and childbirth, caesarian section, uterine surgery, surgical management of miscarriage/termination of pregnancy. Commonly in posterior wall of uterus.
Adenomyoma - collection of endometrial glands forming grossly visibly nodules in myometrium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Risk factors of Adenomyosis?

A

1) High parity
2) Previous Caesarian
3) Uterine surgery (endometrial curettage, ablation)
4) Hereditary
5) Surgical management of miscarriage/termination of pregnancy

17
Q

Clinical features and Ddx of adenomyosis?

A

1) Menorrhagia
2) Dysmenorrhoea (progressive - cyclical to chronic daily)
3) Deep dyspareunia
4) Irregular bleeding
On abdominal and bimanual palpation - symmetrically enlarged tender uterus.

Ddx:

1) Endometriosis
2) Fibroids
3) PID (pelvic pain > cyclical/dysmenorrhoea)
4) Endometrial hyperplasia/carcinoma
5) Endometrial polyps

18
Q

Investigations of adenomyosis?

A

1) Transvaginal Ultrasound - observer-dependant - globular uterine configuration, poor definition of endometrial-myometrial interface, myometrial anterior-posterior asymmetry, intrayometrial cysts and a heterogenous myometrial echo texture.
2) MRI - endo-myometrial junctional zone - can be distinguished from endometrium and outer myometrium due to irregular thickening of this zone.

HISTOLOGICAL (after hysterectomy) is definitive diagnosis.

19
Q

Management of adenomyosis?

A

Main aim to control dysmenorrhoea and menorrhagia. Only curative therapy is hysterectomy. Symptomatic - same as endometriosis - NSAIDs for analgesia, and hormonal therapy for reduction of bleeding and cycle control.

Hormonal therapy: COCP, POP/IUS, GnRH agonists, Aromotase inhibitors. (continuous COCP and high dose progestins temporarily regress adenomyosis).
Hormones reduce proliferation of ectopic endometrial cells - reducing mass and hence uterine size.

Non-hormonal therapy: Only hysterectomy curative. Uterine artery embolisation can be used as an alternative treatment option in the short and medium term - for women who want to avoid hysterectomy and preserve fertility (block blood supply to adenomyosis causing them to shrink). Endometrial ablation + resection, laparoscopic excision and magnetic resonance-guided focused ultrasound.

20
Q

Endometrial cancer - Ex, Ax and PPx?

A
  • Most common gynaecological cancer in the developed world.
  • Linked with obesity - peak incidence between 65 to 75 years.
  • Most common form - adenocarcinoma - neoplasia of epithelial tissue (glandular in origin and/or glandular characteristics).
  • Most cases caused by stimulation of the endometrium, by oestrogen (without the protective effects of progesterone - unopposed oestrogen).
  • Progesterone is produced by the corpus luteum after ovulation (longer period of an ovulation - predisposed to malignancy).
  • Unopposed oestrogen can also cause endometrial hyperplaysis (precancerous state).
21
Q

Risk factors of endometrial cancer?

A

1) Anovulation - early menarche or late menopause, low parity, polycystic ovarian syndrome, hormone replacement therapy (with oestrogen alone), Tamoxifen use.
2) Age
3) Obesity - greater than subcutaneous fat faster the rate of peripheral aromatisation of androgens to oestrogen - increases unopposed oestrogen levels in post-menopausal women.
4) Hereditary factors - genetic conditions that predispose to cancer (hereditary non-polyposis colorectal cancer/Lynch syndrome)

22
Q

Clinical features of Endometrial cancer?

A

1) Main feature - post-menopausal bleeding (PMB) as bleeding one year after periods have stopped. This is non-specific.
2) Clear/white vaginal discharge
3) Abnormal cervical smears
4) Abdominal pain/Weight loss
(Rarely develop in premenopausal women - irregular bleeding/intermenstrual bleeding)

O/E:
Abdominal/pelvic masses, speculum examination (cervical lesions or vulval/vaginal atrophy), bimanual examination (assess size and axis of uterus prior to endometrial sampling).

23
Q

Ddx of endometrial cancer?

A

Main symptom PMB:

1) Vulval causes - atrophy, premalignant/malignant causes
2) Cervical causes - polyps or malignancy
3) Endometrial causes - hyperplasia without malignancy, benign polyps, endometrial atrophy.

24
Q

Investigations for Endometrial cancer?

A

1) Transvaginal ultrasound (1st line) - usually patients with endometrial cancer will have >5mm thickness on ultrasound
2) Endometrial biopsy - IF >4mm thickness on ultrasound - Pipelle biopsy: histology should be diagnostic.
3) If HIGH RISK - due to heavy bleeding or very thick endometrium, on ultrasound - hysteroscopy with biopsy.
4) If endometrium <4mm and appears normal on ultrasound - defer sampling unless abnormal bleeding persist.
5) If malignancy confirmed - MRI/CT for staging - take baseline bloods before operational intervention (FBC, LFT, U+Es and a GROUP and SAVE)

25
Q

FIGO staging?

A

Stage I - within uterine body (1A - endometrium, 1B - myometrium).
Stage II - may extend to cervix but not beyond uterus.
Stage III - carcinoma extends beyond uterus but confined to pelvis (3A - ovary, 3B - vagina, 3C - lymph nodes)
Stage IV - involved bladder/bowel or has metastasised to distant sites.

26
Q

Management of endometrial hyperplasia?

A

Hyperplasia - Non-malignant ‘simple’ or ‘complex’ hyperplasia without atypic can be treated with progestogens (Mirena coil IUS). Surveillance biopsies - identify progression to atypic/malignancy.
- Atypical hyperplasia - highest rate of progression to malignancy - treat with abdominal hysterectomy and bilateral salpingo-oopherectomy, if surgery contraindicated - regular biopsies for surveillance.

27
Q

Management of endometrial cancer?

A

Stage I - Total hysterectomy and bilateral salpingo-oopherectomy. Peritoneal washings additionally taken. Open or laparoscopic.

Stage II - Radical hysterectomy - vaginal tissue around cervix also removed and supporting ligaments of uterus), assessment and removal of pelvic lymph nodes (lymphadenopathy).

Stage III - Maximal de-bulking surgery - if possible, additional chemotherapy is usually given prior to radiotherapy.

Stage IV - Maximal de-bulking surgery if possible, in many stage IV patients - palliative approach preferred - low dose radio, or high dose oral progestogens.