Endometrium + abnormalties Flashcards

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1
Q

Why study the endometrium? (2)

A

abnormalities = very common

all women will visit healthcare professions about their period

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2
Q

Layers of the Endometrium (4)

A

Layers 1-3: prolif stage (anchored in basal layer):

1) Compactum (bleed all away)
2) Spongiosum
3) Basalis (all epithelial)

  • Junctional zone = extra layer b/w 3 and myometrium: unique because partly epithelial + myometrial
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3
Q

Menstruation effect of endo. MoA (6)

A
  • Initiated by withdrawal of E and P (directs event but not direct cause)
  • Local mediators PG’s, PAF (molecular cause of menses)
  • # Spiral artery vasoconstriction
  • # Ischaemia and tissue damage (= backache, nauseas discomfort- ischaemic pain)
  • # Spiral artery relaxation
  • Shedding of functional endometrium (majority)
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4
Q

Factors affecting Menstruation explained (7)

A
  • Control E2 + P
  • PGs (E + I vs F2a + Tx) : needs balance 1= vasodil + stop platelets @ endo layer, 2= vasocons. = platelets sticky = clot (F2a = dom.)
  • Interleukins (IL – 8, 13 +16) - endo: brings other inflam cells = balance
  • Tissue Necrosis Factor (TNF) + Platelet Aggregating Factor (PAF)
  • Matrix metallo-proteinases: enzyme group = activation right time + amount
  • Coagulation / fibrinolysis: needs balance - coag cascade - linked to inflam. cascade
  • Junctional zone: intrinsic errors = bleeding probs + vascular properties = pinch vessels
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5
Q

What is needed for normal menstruation?

A

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

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6
Q

What are the Clinical problems regarding the endometrium? (5)

A
  • Anything different from usual pattern
  • Too much bleeding - Menorrhagia (most common)
  • Bleeding too often - Polymenorrhoea (Ovul + vol + reg. problems)
  • IMB / PCB = period bleeding period (directly after, shortly after or during sex
  • Chaotic bleeding ( unsched./ constant)
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7
Q

Nomenclature + classification of uterine bleeding - AUB, factors, Structural + non-Structural (4)

A

1) Abnormal Uterine Bleeding: Acute, Intermittent + chronic

2) Frequency, Regularity, Duration + Volume

Structural:
P olyp
A adenomyosis
L eiomyoma
M alignancy

Non- Structural:
C oagulopathy
O vulatory dysfunction
E ndometrial
I atrogenic
N ot otherwise classified

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8
Q

Causes of Abnormal vaginal bleeding (6)

A

‘Pathological causes’
* Fibroids – (submucous - tumours of smooth muscle (MYO))
* Adenomyosis
* Endometrial pathology – benign adenomas or polyps (ENDO)
- hyperplasia (PCOS)
- carcinoma
* Cervical pathology – polyps (twist it off)
- carcinoma
* Cervical Infection - Chlamydia (teenage/early 20’s - usually asymptom. erractic bleeding)
* Pregnancy!!!

DUB: Dysfun. uterine bleeding - diagnosis of exclusion

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9
Q

Importance of intrauterine
structural abnormalities - fibroids + polyps (3)

A
  • Submucous fibroids (leiomyomas)
    associated w/ 3x increased risk of abnormal bleeding – invariably menorrhagia
  • Endometrial Polyps (adenomas) are more
    frequent in women with menstrual disorders (incidental finding)
  • Causal / casual – diagnostic bias??
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10
Q

Abnormal Bleeding - aims - (5)

A

1) Exclude pregnancy (test)

2) Exclude cervical pathology (look at cervix)

3) Exclude focal benign intracavity pathology
(polyps, submucous fibroids)

4) Consider other endometrial pathology (>
45) - hyperplasia/cancer

5) Use the least invasive method to achieve
this

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11
Q

Endometrial abnormalities (5)

A
  • Dysfunctional uterine bleeding
  • Endometrial polyps
  • Endometrial hyperplasia benign vas atypical
  • Endometrial hyperplasia with atypia (mild–severe)
  • Endometrial adenocarcinoma
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12
Q

Why do you use diagnosis of exclusion?

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

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13
Q

DUB - explained (2)

A

all factors: but mostly:

1) PGs: E+I imbalance
2) Fibrinolysis - excessive clot breaking not lack of making

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14
Q

Polyps (3)

A
  • Benign endometrial adenomas
  • Focal problem
  • Rest of endometrium is normal
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15
Q

Abnormal Bleeding
History and Examination (8)

A

Points in history
– 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

– BMI ( < = no period, > PCOS)

– Abdomen
* Distension, scars, pain, masses

– Bimanual
* Uterine size, adnexal masses, pain

– Cervix
* polyps, suspect lesions

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16
Q

Abnormal Bleeding
Investigation (5)

A
  • Pregnancy test where appropriate
  • Hb if heavy bleeding
  • Swabs – endocervical (Chlamydia)
  • Cervical smear – only if due
  • Transvaginal ultrasound : main thing to do - but if sexual
    +/- Endometrial sampling
    +/- Hysteroscopy - in-patient or OPD
17
Q

Transvaginal sonography
TVS- benefits (6)

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
18
Q

1) TVS + endo. (3) - not or global but focal (hyperplasia)

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
19
Q

2) Hysteroscopy

A
  • If TVS abnormal
  • Non-response to medical therapy
  • Multiple risk factors for endometrial
    pathology
20
Q

Risk factors for significant
endometrial abnormality (6)

A
  • Obesity!!!!!
  • Nulliparity - no preg./contraception = protective - inc. turnover
  • Early menarche / late menopause – length
    of E2 exposure – weak factor
  • HT / DM - hypertension/diabetes
  • Anovulation e.g. PCOS
  • Genetics (5-10%) - FH breast / endometrial (30/40yrs) / colonic
    cancer – Lynch syndrome (HNPCC - faulty mismatch repair function)
21
Q

Endometrial hyperplasia causes/types (3)

A
  • Simple - benign overgrowth (big women - adipose)
  • Atypical - Unopposed E2
  • Carcinoma - post-menopausal
22
Q

Unopposed oestrogen risk explained- obesity(6)

A
  • Obesity – peripheral conversion of androgen to oestrogen (aromatase) - abundant aromatase = T -> E2
  • BMI most vital factor
  • The more adipose tissue the more conversion
  • Chronic anovulation e.g. PCOS (resist. to LH/FSH = no df)
  • Follicular ovarian oestrogen production
    continues
  • Progesterone only produced after ovulation
    = Unopposed oestrogen =
    Over years leads to hyperplasia/ sometimes cancer
23
Q

Polyp treatment

A

only surgery - TCRP

24
Q

Fibroid treatment (2)

A

medical: medical Mirena IUS/ Kyleena (coil) = stops bleeding (releas. P in cavity = switch off)

surgery: TCRF/myomectomy (if too big), hysterectomy (total/subtotal, vaginal)

25
Q

Treatments q’s for DUB (3)

A
  • Does she need or want treatment?
  • Does she need contraception/desire
    pregnancy?
  • How much is the problem affecting her
    quality of life?
26
Q

Non-hormonal treatments of DUB (6)

A

Fixing PG’s or Fibrinolysis!!

  • 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 (inhib. COX or PG’s - wrong PG’s produced E/I) = restores ratio via vasodil. + cons.)
  • Good for pain also!
27
Q

hormonal treatments of DUB (3)

A
  • Mirena IUS – 90% reduction blood loss
  • 30% amenorrheic
  • Local high dose progestagen - thin endometrium (red. side effects because delivered in uterus)
  • Kyleena new 4 year option
  • COCP – 20 - 30% reduction in blood loss
  • Removes cyclical events – thin endometrium
  • Progestagens less beneficial for volume loss (higher than n levels to red. bleeding = inc. bloating, appetite + constipation)
  • Use to control cycle length in anovulatory DUB
28
Q

Options for treating DUB

A

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

29
Q

How to approach real cases - (6)

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?
30
Q

Summary (4)

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