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BIOL30001 reproductive biology > W11 L1 Mon uterine disorder > Flashcards

W11 L1 Mon uterine disorder Flashcards

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1
Q

What is menstrual cycle

A

The regular renewal of the lining of the uterus (the endometrium) to prepare for potential embryo implantation.

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2
Q

Step in the menstrual cycle

A
  1. Menses – Thickened endometrium is eliminated
  2. Proliferative – Endometrium re-grows
  3. Secretory – Post-ovulation, the endometrium decidualises and prepares for implantation
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3
Q

Period pain is considered normal if

A
  • Pain is present on the first 1 or 2 days of menses
  • Pain is relieved by heat packs or mild medications
  • Pain does not prevent you from doing day-to-day activities
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4
Q

Period pain is considered abnormal if

A
  • Pain is severe enough to disrupt normal activities
  • Pain persists beyond the menses period
  • Pain is chronic and last more than 6 months
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5
Q

Primary Dysmenorrhea

A
  • High prevalence (43-93%)
  • Severe pain experienced (30%)
  • Lasts 1-3 days
  • Unknown cause – speculated hyperproduction of prostaglandins (induce uterine contractions)
  • Treated with Non-steroidal anti-inflammatory drugs NSAID (aspirin, ibuprofen), COX inhibitors (naproxen)
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6
Q

Secondary Dysmenorrhea

A
  • Pain due to an underlying pathology
  • Common causes are endometriosis and adenomyosis
  • Treatment is OCP (progestin) and/or surgery (removal of underlying cause)
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7
Q

Abnormal Uterine Bleeding (AUB)

A

occurs when menstrual bleeding falls outside normal parameters 25-80ml(for a period >6 months)
§ Causes: PALM-COEIN to investigate structural changes to uterus + non-structural issues
Ø PALM: Polyps, Adenomyosis, Leiomyoma (fibroids), Malignancy + hyperplasia
Ø COEIN: Coagulopathy (clotting disorders), Ovarian dysfunction, Endometrial dysfunction, Iatrogenic (nonmenstrual bleeding/spotting due to hormonal therapies), Not otherwise classified

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8
Q

Heavy Menstrual Bleeding (HMB)

A

§ HMB: excessive menstrual blood loss which interferes with physical, emotional, social + quality of life
Ø Normal 5-80mL blood loss (35mL average)
Ø >80mL causes anaemia + severe fatigue (27-54% of menstruating women)

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9
Q

pathology of HMB

A

uterine fibroids (30%) + polyps (10%) but most histologically normal

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10
Q

impact of HMB in QoL

A

bloodstains, pain, anxiety/depression, moodiness, interference w/ life

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11
Q

Treatment for HMB

A
  • hormonal (OCP or progestagens to stop cycle)
  • prostaglandin inhibitors (block prostaglandin production),
  • anti-fibrinolytic agents (blocks fibrinolysis = removal of small clots),
  • manage iron deficiency,
    -surgery (ablation – removal of uterine lining but regrows under E; hysterectomy – remove uterus)
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12
Q

What is Uterine fibroids and the incident rate

A

“benign tumours of smooth muscle cells of the myometrium”
* Most common being tumour (77% of reproductive-aged women)
* Incidence and severity is higher in women of African descent
* Main indication for hysterectomy

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13
Q

Possible symptom for fibroids

A
  • None
  • Heavy menstrual bleeding
  • Chronic pain, dysmenorrhoea and pressure symptoms
  • Fertility and pregnancy problems
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14
Q

Characteristic of fibroids

A
  • Firm, round, well separated from surrounding myometrium, non-invasive
  • Occur as single or multiple tumours
  • Vary in size and growth rates
  • Vary in location:
    – Submucosal
    – Intramural
    – Sub-serosal
    – Pedunculated
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15
Q

Clonal origion of fibroids

A

derived from a single smooth muscle cell
* Although clonal, multiple cell types exist within the fibroid (SMC, fibroblasts, endothelial cells, immune cells)
* Fibroid cell sub-populations may be clonally expanded from a multipotent progenitor cell that undergoes differentiation.
* Fibroids are vascularized often with an avascular core (which stimulates more vascularization).

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16
Q

Treatment of Uterine Fibroids

A

§ Treatment:
-GnRH analogues (hypoestrogenism to shrink tumour before surgery; short term use only),
-hormone modulators (selecive oestrogen receptor modulators SERM + progesterone (SPRMs) to slow growth),
-progestins (reduce HMB by stopping cycle)
§ Surgical treatment:
-hysterectomy (remove uterus), myomectomy (remove uterine fibroid),
- uterine artery embolisation (block blood supply feeding fibroid),
-magnetic resonance-guided focused-ultrasound MRgFUS (untrasound energy heats + destroy fibroid)

17
Q

Adenomyosis

A

presence of endometrial tissue wtihin myometrium
Ø Demarcation line b/w endometrium + myometrium destroyed
Ø 5-70%: mean frequency at hysterectomy 20-30%, coexists with other pathologies

18
Q

Cause and symptom of adenomyosis

A

§ Causes: invasive endometrial tissue; unknown mechanism (may be overproduction of protein breakdown enzymes)
§ Symptoms: asymptomatic or pelvic pain, abnormal uterine bleeding, infertility

19
Q

diagnosis of adenomyosis

A

-hysterectomy + histopathology,
-imaging (ultrasound, MRI)

20
Q

Treatment of adenomyosis

A

-GnRH analogues (hypoestrogenism + antiproliferative effects)
- progestins (endometrial atrophy + hypoestrogenism),
- OCP (endometrial atrophy),
-NSAIDs (block prostaglandins, reduce pain)

21
Q

what is endometriosis

A

Presence of estrogen-dependent endometrial- like lesions containing glands and stroma outside of the uterus

22
Q

incidence of endometriosis

A
  • 11.4% of reproductive-aged women
  • 50-60% of women with pelvic pain
  • 30-50% of women with infertility
23
Q

Cost of endometriosis

A

High personal (quality of life) and healthcare costs (7 billion AUD annually)
-burden of disease
-direct healthcare cost
-productivity loss
-taxation

24
Q

lesion of endometriosis

A

contains glands + stroma (similar to normal endometrium);
-hormonally responsive + bleed/wound repair like endometrium,
- scarring/adhesion formation

25
Q

possible location of lesion for endometriosis

A

-uterus,
-fallopian tubes (can cause blockage),
-ovaries,
-ovarian fossa,
-uterosacral ligaments,
-rectovaginal septum,
-pouch of Douglas + uterovesical fold

26
Q

stage of endometriosis

A
  • Stage I & II (minimal to mild)
    – More common
    – Superficial
  • Stage III & IV (moderate to severe)
    – Deep infiltrating / ovarian
    – Adhesions
27
Q

Symptoms of endometriosis

A
  • Pain symptoms include (but not limited to):
    – Dysmenorrhea (menstrual period pain)
    – Dyspareunia (pain during sexual intercourse)
    – Chronic non-menstrual pelvic pain
    – Lower back pain
    – Ovulation pain
  • Bowel and Bladder symptoms
  • Infertility issues
  • Increased risk of adenomyosis, autoimmune disease, ovarian cancer
28
Q

theory of endometriosois

A

There are several different theories about the aetiology of endometriosis, but no one theory can explain all aspects of the pathology

29
Q

Genetics of Endometriosis

A
  • Endometriosis is a complex disease caused by interactions of many genetic and environmental factors
  • Environmental factors (eg. pesticides and toxins), that affect estrogen metabolism play a part in endometriosis – Also consider smoking and diet
  • Aggregation of endometriosis cases within families & increased prevalence of endometriosis among related vs unrelated women strongly suggest the presence of predisposing genetic (heritable) factors
30
Q

Diagnosis of endometriosis

A
  • Delay in diagnosis - from symptom onset to diagnosis - mean delay of 6.7 years
  • Definitive diagnosis requires surgery (laparoscopy)
31
Q

Treatment of endometriosis

A
  • Multi-disciplinary: Surgical, medical and management approaches
  • Surgery
    – Removal of lesions and adhesions (by laparoscopy)
    – Sometimes hysterectomy
  • Medical
    – Manipulation of hormones to produce a pseudo-pregnant or pseudo-menopausal state (amenorrhea)
  • Androgens (eg. Danazol), GnRH antagonists (eg. Zoladex),
    Progestogens (eg. Mirena), OCP
  • Pain relief
  • analgesics, non-steroidal anti-inflammatory drugs
  • Side effects have to be considered
  • Desire for pregnancy
  • Symptoms often recur after treatment
32
Q

Problem with endometriosis

A
  • “It is evident that endometriosis can have a profound impact on women, girls, their families, partners and carers, and society as a whole”
  • “There is significant frustration with the under-recognition and misdiagnosis of endometriosis, and the subsequent delays from onset to diagnosis and treatment”
33
Q

Clinical database for endometriosis

A

1100s Women undergoing laparoscopy for pelvic pain and treatment for endometriosis and infertility are recruited
-have follow up questionnaire and look at genetic and molecular data for identification of possible bio marker

34
Q

Endometriosis Research result VEZT in endometriosis

A
  • VEZT encodes the adherens junction protein VEZATIN
  • Vezatin is essential to life (knockout is embryo lethal)
    Ø Expressed on endometriosis lesions, leucocytes + endothelial cells
    Ø Hormonally regulated in endometrium (high in secretory phase)
    Ø Essential for blastocyst integrity + sperm maturation; binds to Myosin VII (essential for listeria infection)
35
Q

The Functional Role of
VEZT in Endometriosis

A

Over expression of VEZT in HESC significantly altered the expression of 6,594 genes
Ø Significantly upregulated: role of pattern recognition receptions, neuroinflammation signalling pathway,
dendritic cell maturation, interferon signalling
§ RSAD2 gene x8 encodes viperin that inhibits viral infections as part of interferon gamma pathway + innate immune system; elevated in secretory phase
Ø Significantly downregulated: LXR/RXR activation, leucocyte extravasation pathway
§ PTGES3L-AARSD1 gene x7

36
Q

Conditional Overexpression
of VEZT in a murine model

A
  • CRISPR-CAS9 technology was used to generate a conditional knock-in VEZT mouse
  • CTV-VEZT mice were then crossed with a Tamoxifen inducible Cre mouse (UBC-Cre-ERT2) to produce the conditionally overexpressed VEZT mouse (TgCre)
  • VEZT overexpression at 12 weeks significantly dysregulates hormone receptor expression and increase cytokine gene expression
  • increases lesion formation in WT and TgCre mice
37
Q
A

BIOL30001 reproductive biology (33 decks)

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