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Year 3- Repro > Endometrium & its Pathology I&II > Flashcards

Endometrium & its Pathology I&II Flashcards

1
Q

Endometrium Layers

A

Compactum
* Spongiosum
* Basalis
* Junctional zone

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2
Q

Menstrual Cycle

A

Bleed away endometrium in first half of the cycle

Secind half of the cycle is always 14days

Spiral arteries get muh more twisted- only supply there is (___)

Increased secretions (big inflammatory cells near day 22 when endometrium increases

Rapid drop in hormones triggers menstruation

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3
Q

How is menstruation initiated?

A

Menstruation initiated by withdrawal of E and P, local mediators = PGs, PAF (platelet aggregating factor)
Spiral artery vasoconstriction -> ischaemia and tissue damage -> spiral artery relaxation -> shedding of functional endometrium
PGs causes vasoconstriction in SMCs
Drop in steroids causes menstruation
Bleed down to the basal layer during menstruation
Endometrium becomes secretory during the follicular phase
Implant 5/max 6 days after ovulation- when endometrium is thickest

some of the spongiosum is also shed along with the compactum

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4
Q

Menstruation mediators

A

Controlled E2 and P
PGs (E and I vs F2alpha and thromboxane Tx)

E and I = SM relaxation/vasodilation and stop platelets working at the endothelial level (therefore you bleed)

F2a and Tx = vasoconstriction and make platelets clot (stop bleeding)
Interleukins (IL8, 13, 16): bring other inflammatory cells and have other effects

TNF and PAF (platelet aggregating factor)

Matrix metallo-proteinases (participate in the membrane shedding)
Involved in remodelling, so when activated they break down collagen

Coagulation/fibrinolysis (aid the clotting- needs to be balanced so antagonistic mechanisms)

Junctional zone
For normal menstruation: correct balance and regulation of inflammation, coagulation and fibrinolysis in the endometrium

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5
Q

Prostaglandins effect

A

ischemic pain- back pain, nausea

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6
Q

For normal menstruation

A

Correct balance and regulation of
inflammation, coagulation and fibrinolysis
in the endometrium is needed

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7
Q

Clinical problems- anything different from ususal pattern

(due to problems in ovulation)

A

Too much bleeding- menorrhagia

Bleeding too often- polymenorrhea

Inter Menstrual Bleeding/Post Coital Bleeding

Chaotic bleeding

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8
Q

Abnormal bleeding can either be

A

Structural (PALM)

polyp
adenomyosis
leiomyoma
malignancy (uncontrolled bleeding: cancer of the cervix or the cancer of the endometrium)

Non-structural (COIN)

coagulopathy
ovulatory dysfunction
endometrial
iatrogenic (relating to illness caused by medical examination or treatment.)
not otherwise classified

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9
Q

Pathological causes of abnormal bleeding

A
  • Fibroids – submucous
  • Adenomyosis
  • Endometrial pathology – benign adenomas or polyps
    - hyperplasia
    - carcinoma
  • Cervical pathology – polyps
    - carcinoma
  • Cervical Infection - Chlamydia (might present with erratic bleeding)
  • Pregnancy!!!

DUB (diagnosis of exclusion)

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10
Q

Endometrial polyps

A

Endometrial polyps are benign endometrial adenomas; rest of endometrium is normal - Endometrial Polyps (adenomas) are more frequent in women with menstrual disorder

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11
Q

Fibroids

A

Fibroids often don’t cause abnormal uterine bleeding; however submucosal fibroids poke into uterine cavity and cause distortion and stretching of the uterine cavity; Submucous fibroids (leiomyomas) are associated with a threefold increased risk of abnormal bleeding – invariably menorrhagia

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12
Q

adenomyosis

A

Adenomyosis is when endometrial tissue is located within the myometrium – usually an artefact of childbirth and causes very heavy/painful periods

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13
Q

Importance of intrauterine structural abnormalities

A

Submucous fibroids (leiomyomas) are
associated with a threefold increased risk of
abnormal bleeding – invariably
menorrhagia
- indent the submucosal cavity (cause heavy bleeding: causal rather than casual)

Endometrial Polyps (adenomas) are more
frequent in women with menstrual disorders

Causal / casual – diagnostic bias??

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14
Q

Aims- abnormal bleeding

A
  • Exclude pregnancy
  • Exclude cervical pathology
  • Exclude focal benign intracavity pathology
    (polyps, submucous fibroids)
  • Consider other endometrial pathology (>
    45)
  • Use the least invasive method to achieve
    this
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15
Q

Endometrial abnormalities examples

A
  • Dysfunctional uterine bleeding (MOST LIKELY)
  • Endometrial polyps
  • Endometrial hyperplasia
  • Endometrial hyperplasia with atypia (mild –
    severe)
  • Endometrial adenocarcinoma
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16
Q

Causes of endometrial abnormalities

A

Of women presenting with menorrhagia 50-
60% will have NO structural or obvious
pathological cause identifiable – it is a
problem at the molecular level i.e. cellular
dysfunction
* It is a diagnosis of exclusion

17
Q

DUB (Where is the dysfunction)?

A

PGs (E + I vs F2a + Tx)
* Interleukins (IL – 8, 13 +16)
* Tissue Necrosis Factor (TNF) + Platelet
Aggregating Factor (PAF)
* Matrix metallo-proteinases
* Coagulation / fibrinolysis
* Junctional zone

2 areas above all else:
- PG’s (>E+I compared to F2a+Tx)
- Coagulation /(fibrinolysis in particular)

Heavy bleeding tend to be caused by increased fibrinolysis

18
Q

Polyps

A

Benign endometrial adenomas
* Focal problem
* Rest of endometrium is normal

19
Q

History and Examination (points in history)

A

-LMP – was it normal?

Regular or irregular periods
- cycle control (ovulation vs anovulation)
- heavy- clots, flooding?
- with bleeding between (IMB)?
* post coital bleeding (PCB)?
* Pain

Medication, smoker, smear, operations

Contraception - hormonal vs non-hormonal

20
Q

Points in examination

A
  • BMI (overweight- testosterone to oestrogen (in men and women) )
    – Abdomen
  • Distension, scars, pain, masses
    – Bimanual
  • Uterine size, adnexal masses, pain
    – Cervix
  • polyps, suspect lesions
21
Q

Investigation

A
  • Pregnancy test where appropriate
  • Hb if heavy bleeding
  • Swabs – endocervical (Chlamydia)
  • Cervical smear – only if due
  • Transvaginal ultrasound
    +/- Endometrial sampling
    +/- Hysteroscopy - in-patient or OPD
22
Q

Transvaginal sonography TVS

A
  • Can assess the relationship of fibroids to the cavity
  • Has a high detection rate for polyps
  • Assess function – anovulatory cycles
  • Can reliably assess structures outside the uterus
    (tubal and ovarian pathology)
  • Well accepted by patients
  • Relatively cheap with few complications
23
Q

TVS values

A

Periovulatory endometrium is hard to hide
pathology in – or immediately post menstrual to
assess ET
* Cut-off values for ET are arbitrary in
premenopausal women - @ 6 mm post menstrual
or 12 mm anytime in cycle
* Ultrasound is ideal for focal pathology but not
good for predicting endometrial pathology – a
biopsy is still needed in many cases

24
Q

Hysteroscopy

A

If TVS abnormal
* Non-response to medical therapy
* Multiple risk factors for endometrial
pathology

25
Q

Difference between polyp and fibroid characterisation

A

Polyp- epithelial lighter in colour
Fibroid- muscular darker in colour

26
Q

Risk factors for significant endometrial abnormality

A

Obesity
* Nullipartity
* Early menarche / late menopause – length
of E2 exposure – weak factor
* HT / DM
* Anovulation e.g. PCOS
* Genetics - FH breast / endometrial / colonic
cancer – Lynch syndrome (HNPCC)

27
Q

Endometrial Hyperplasia

A

Simple Hyperplasia; Very thick and glandular such that glandular:stromal ratio is very high; present with terrible bleeding between cycles and even post meno-pausal
Atypical hyperplasia; Cells start to de-differentiate and look abnormal
Eventually will become carcinoma and because it is glandular it becomes endometrioid adenocarcinoma driven by unopposed oestrogen

28
Q

Causes of unopposed oestrogen

A

Obesity – peripheral conversion of
androgen to oestrogen (aromatase)
* BMI most vital factor
* The more adipose tissue the more
conversion

29
Q

Effects of unopposed oestrogen

A

Chronic anovulation e.g. PCOS
* Follicular ovarian oestrogen production
continues
* Progesterone only produced after ovulation
* Unopposed oestrogen
* Over years leads to hyperplasia and
sometimes cancer

30
Q

Treatments

A

For focal stuff like polyps, can be identified with hysterectomy and removed via surgey using transcervical resection
For small fibroids, can use progesterone implant (Mirena) which induces thinning of the endometrium
Removal of uterus itself – myomectomy
For DUB…
Need to ask:
Does she need or want treatment?
Does she need contraception/desire pregnancy?
How much is the problem affecting her quality of life? Often become anemic

31
Q

Options for treating DUB (medical)

A
  • Nothing
  • Medical
    – Non Hormonal (what is the dysfunction????)
  • Tranexamic acid - anti fibrinolytics 40-50%
    reduction in blood loss
  • Corrects excessive fibrin breakdown in
    endometrium (affects plasminogen action)
  • Mefanamic acid 30% reduction in blood loss
  • NSAID – corrects PG imbalance to allow normal
    vasoconstriction and platelet aggregation
  • Good for pain also!
32
Q

Options for treating DUB (hormonal)

A

Hormonal
* Mirena IUS – 90% reduction blood loss
* 30% amenorrheic
* Local high dose progestagen - thin endometrium
* Kyleena new 4 year option
* COCP – 20 - 30% reduction in blood loss
* Removes cyclical events – thin endometrium
* Progestagens less beneficial for volume loss
* Use to control cycle length in anovulatory DUB

33
Q

Options for treating DUB (SURGERY)

A

Surgery – for failed medical treatment
–Endometrial resection/ablation
–Hysterectomy - Vaginal/abdominal
–Remove ovaries?

34
Q

What factors need to be considered for real cases?

A

How old is patient (< or >45)
* Is the cycle regular?
* Is there erratic bleeding?
* Do you need to investigate the
endometrium?
* If so, how?
* Treatment?

35
Q
  • 41 year old – heavy periods for 9 months
  • Bleeds for 9 days every 28 reg (K= 9/28)
  • Affecting ability to go to work
  • NO IMB or PCB
  • Smear 2 years ago – normal
  • Contraception – condoms
  • No other relevant medical or family history
A

DUB

DUB (ovulatory)
* Treatment – volume control
* Tranexamic acid
* Mefanamic acid
* Mirena IUS

36
Q

CASE 2:

43 year old
* Heavy periods K = 7-8 / 35 – 65days
* No IMB / PCB
* Contraception- condoms
* Smear 18/12 ago - normal
* No other relevant medical or family history

TVS – normal – no polyps or fibroids
* Endometrial biopsy – proliferative (doesn’t ovulate so not secretory but proliferative)
endometrium, no atypia or hyperplasia seen

DIAGNOSIS?

A

Diagnosis (volume problem and cycle length problem)

DUB (anovulatory)
* Treatment – volume and cycle control?
* Tranexamic acid
* Mefanamic acid
* Mirena IUS
* COCP

37
Q

45 year old
* IMB for last 6 months
* K = 5 / 29 regular
* Contraception condoms
* Smear 1 year ago – normal
* No other medical history of note

A

Polyp found using TVS/

NOT FIBROIDS (shouldn’t cause inter cycle bleeding)

Treatment:
hysteroscopy (remove the polyp)

38
Q

51 year old
* Heavy bleeding most days last 3 months
* Cycles used to be irregular (every 2-6
months)
* Gynae history of PCOS
* Nulliparous
* Contraception - condoms
* Medical – obesity / NIDDM / High BP

A

More likely to have a significant endometrial abnormality

HYPERPLASIA/CANCER

Diagnosis:
TVS – thickened endometrium – no discrete
polyp seen

Endometrial biopsy

39
Q

Endometrial abnormalities

A

Most menorrhagia is DUB and treatments
reflect the dysfunction
* Exclude focal pathology – needs focal
removal
* Beware erratic bleeding – pathology much
more likely
* TVS and biopsy +/- hysterosocpy diagnosis
in nearly all

Year 3- Repro (34 decks)

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