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Endocrine & Reproductive Systems > L17 18 19 Female > Flashcards

L17 18 19 Female Flashcards

1
Q

What are the main stages for eggs to develop in the ovary?

A
  • oogenesis

- then folliculogenesis

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2
Q

What are the two parts of ovary?

A
  • medulla and cortex.
  • medulla is where blood vessels and nerves are found
  • cortex is where the follicles embedded in the stroma

*we can use ultrasound imaging to visualise the ovary

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3
Q

What are the main stages of folliculogenesis?

A
  • primordial (immature state)
  • primary ( or pre-antral)
  • secondary (or antral)
  • tertiary (or pre-ovulatory)
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4
Q

How are eggs developed from primordial to primary oocytes?

A
  • by spontaneous signals dependent of local growth factors

- these are at the arrested prophase with a very thin flattened layer of granulosa cells

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5
Q

How are primary oocytes transformed into secondary oocytes?

A
  • due to signals of FSH and LH
  • this can only be achieved after onset of puberty
  • Primary oocytes: an increase in size of oocyte and proliferation of granulosa cells
  • secondary oocytes: formation of antrum
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6
Q

How are secondary oocytes transformed into tertiary oocytes?

A
  • due to LH surge and arrives at the pre-ovulatory state
  • tertiary oocyte: the oocyte resumes meiosis and there is an increase in volume of follicular fluid and formation of stigma
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7
Q

What are primordial follicles?

A
  • primary oocytes + layer of flattened, thin granulosa cells
  • they are arrested in prophase
  • primordial follicles are found around the edge of the cortex of ovary
  • primordial follicles can undergo follicular atresia: a programme cell death when the primordial follicles/ primary oocytes do not continue proliferating. Results in loss of follicles
  • atresia can be accelerated by genetic disorders and chemotherapy
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8
Q

What are primary follicles?

A
  • their formation independent on LH and FSH action
  • involves enlargement of oocyte (while still in arrested meiosis)
  • proliferation of granulosa cells (deliver nutrients)
  • formation of theca interna and zona pellucida ( a glycoprotein that is important in fertilisation as prevents multi sperms from binding and early cleavage)
  • Activins and AMH are involved in growth of primary follicles and most primary follicles like primordial follicles undergo atresia
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9
Q

What are secondary follicles?

A
  • They have a fluid-filled antrum (characteristics for secondary follicles)
  • Can only develop with presence of LH and FSH ( involves further proliferation of granulosa cells; formation of antrum; activation of theca interna)
  • roughly 10-12 secondary follicles are developed at the beginning of each menstrual cycle
  • also produce OESTRADIOL
  • most also undergo atresia
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10
Q

How are steroid generated in ovaries?

A
  • by theca cell and granulosa cells
  • LH binds to theca cells, causes cholesterol converting into androstenedione and testosterone
  • Androstenedione and testosterone then diffuse into granulosa cells with the presence of FSH and are converted into oestradiol
  • Presence of FSH is key for granulosa cells to produce oestradiol which is very important for follicle development
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11
Q

How do we decide on which secondary follicle to select to develop into the tertiary follicle?

A
  • there is always one dominant follicle at around day 9 of the cycle
  • in charge of producing 90% of oestradiol and inhibin in ovary
  • high level of oestrogen will suppress FSH level via the negative feedback loop so prevents other secondary follicles from maturing =cant ovulate the other ones!
  • there are also other possibilities, eg favoured blood supply, high aromatase activity…
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12
Q

What are tertiary follicles?

A
  • only one forms in each cycle; formation requires LH surge (LH targets the granulosa cells now, instead of the theca cell so it causes release of high level of oestrogen and stimulate the positive feedback on LH level = create the surge)
  • there is an increase in LH receptor present on granulosa cells so when the LH surge, ovulation could readily occur.

In tertiary follicles,

  • the oocytes are suspended by the granulosa cells
  • there is lutenisation of granulosa cells
  • formation of stigma ( site of rupture)
  • resumption of meiosis
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13
Q

When do tertiary follicles rupture? (ie ovulate)

A
  • when 24 hours after onset of LH surge, empty follicle forms corpus luteum
  • poor LH surge may result in lutenisation without ovulation
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14
Q

After the primary oocyte undergo meiosis 1, what are the products formed?

A
  • a secondary oocyte and polar body formed
  • polar body= contains lots of cytoplasm and half of the chromosome
  • meiosis does not carry on until fertilsation
  • a fertilised egg is called ootid
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15
Q

Where does fertilisation take place in the female reproductive tract?

A
  • ampulla of fallopian tube
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16
Q

Were does the fertilised embryo being embedded?

A
  • at the uterus
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17
Q

What are the three uterine layers?

A
  • perimetrium = on the outside
  • myometrium= the smooth muscle layer
  • endometrium= the lining of uterus
  • pre-menopause women’s endometrium= 4-5 mm; post-menopause women’s endometrium= <1mm
  • uterus usually flexes towards the surface of abdomen when visualised by images
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18
Q

What are the reasons in having menstrual cycles?

A
  • controlled development of follicles at correct time
  • provide full preparation for implantation of conceptus in uterine endometrium
  • allows next cycle to start as soon as possible in absence of fertilsation
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19
Q

What are the different phases of menstrual cycle?

A
  • menses -> pre-ovulatory phase (follicular phase where oestrogen is dominant) -> ovulation -> post ovulatory phase (lunteal phase where progesterone in dominant) -> mense
  • menses= shredding of lining
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20
Q

What are the 2 layers of endometrium?

A
  • stratum functionalis (where changes occur here) and stratum basalis (where it remains relatively constant)
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21
Q

What is the name of first ever period and the last period?

A
  • menarche= first period -> first year doesn’t produce functional secondary follicles
  • menopause= last period
  • period can be less regular after puberty and approaching menopause ( could have anovulatory)

*period can last between 25-35days; mean=28days

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22
Q

What does inhibin acts on in hypothalamo-pituitary-ovarian axis?

A
  • inhibin provides a negative feedback on LH/FSH at anterior pituitary level
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23
Q

How does progesterone act on in hypothalamo-pituitary-ovarian axis?

A
  • progesterone provides -ve feedback on GnRH at hypothalamus level
24
Q

How does oestrogen act on in hypothalamo-pituitary-ovarian axis?

A
  • At a LOW level: provides +ve feedback on FSH/LH at anterior pituitary and hypothalamus
  • At a HIGH level: provides -ve feedback on FSH/LH at anterior pituitary and hypothalamus
25
Q

What are the peak serum hormone level within the menstrual cycle?

A
  • LH: 100 mlU/ml
  • FSH: 30 mlU/ml
  • oestrogen: 300pg/ml
  • progesterone: 10ng/ml
26
Q

What events occur at the early follicular phase? (DAY 1-5)

A
  • Both oestrogen and progesterone level is low due to follicles are still small
  • lack of oestrogen means no -ve feedback on FSH= high FSH level is seen
  • this is when 10-20 secondary follicles grow
  • shredding of lining of endometrium occurs
27
Q

What events occur at late follicular phase? (DAY 6-13)

A
  • secondary follicles start to develop
  • FSH level falls due to developing follicles start to produce oestrogen = -ve feedback on FSH level
  • oestrogen and inhibin level rises as they are produced by the secondary follicles
  • endometrium is repairing
28
Q

What events occur in ovulatory phase? (DAY 14)

A
  • LH surge due to +ve feedback of oestrogen
  • level of progesterone rises
  • while level of oestrogen and inhibin fall
  • ovulation of tertiary follicle occurs, empty follicle forms corpus luteum
  • basal temp increases when ovulate
29
Q

What events occur at the luteal phase? (DAY 15-28)

A
  • FSH and LH level are low due to high level of progesterone (-ve feedback on GnRH)
  • corpus luteum present so release progesterone and oestrogen (but mainly progesterone)
  • oestrogen, progesterone and inhibin level are high
  • endometrium is in secretory state and at its thickest
  • luteolysis after 14 days unless conception occurs
30
Q

How are the pre-eggs developed? (oogenesis)

A
  • Primordial germ cells are developed between 4-8 weeks in ovary
  • mitosis takes place and forms oogonia at 6-30 weeks (max numbers in ovary in the entire life)
  • further mitosis takes place to form primary oocytes from oogonia at 10 weeks to 45 years
  • These primary oocytes are pre-eggs that arrest at prophase= storage form of eggs.
  • primary oocytes + later of granulosa cells= primordial follicle (where most eggs are at this stage)
  • primordial germ cell -> oogonia -> primary oocytes -> (combining with granulosa cells) primordial follicle
31
Q

How is LH surge achieved?

A
  • gradual onset that lasts 48 hours due to the high level of oestrogen causes a positive feedback
  • (meanwhile, FSH rises too)
  • LH acts quickly to luteinise dominant follicle = increases level of progesterone while a decrease in oestrogen level
  • Ovulation occurs 12-24 hours after LH peak
32
Q

Feedback effects: OESTROGEN

A
  • low threshold levels exerts negative feedback on pituitary and hypothalamus. (stronger effect on FSH than LH) So there is a FSH rise at the start of the cycle and a FSH and LH rise after ovariectomy and at menopause due to oestrogen is not present
  • high threshold levels exerts positive feedback on LH to provide the LH surge (stronger effect on LH than FSH)
  • medication which stimulates ovulation can has a reduction of oestrogen -ve feedback
33
Q

Feedback effects: INHIBIN

A
  • principal source of -ve feedback on FSH
  • inhibin release in the cyclic and follows the pattern of oestrogen
  • acts at pituitary to suppress FSH synthesis and release
34
Q

Feedback effects: PROGESTERONE

A
  • high level exert -ve effect on GnRH in hypothalamus so causes a low FSH/ LH level (in luteal phase) = no further ovulation
  • high level also blocks oestrogen and positive feedback so prevent further LH surge and ovulation occurs out of the menstrual cycle
35
Q

What is primary amenorrhea?

A
  • menstrual cycles never started, usually due to failure to develop reproductive tracts
36
Q

What is secondary amenorrhea?

A
  • cycles suddenly stop.

- most common is due to prgenancy

37
Q

What are the causes for primary/ secondary amenorrhea?

A

1) hypothalamic defects: Kallman’s syndrome (failure to start puberty of complete puberty, associated with loss of smell) ; craniopharyngioma ( tumours in Rathke’s pouche)
2) pituitary defects: empty sella syndrome (where pituitary gland is being highly compressed); sheehan’s syndrome (hypopituitarism due to ischaemic necrosis of tissues)
3) ovarian defects: gonadal dysgenesis; chemo/radiotherapy damage; resistant ovary syndrome

  • other more complex endocrine disturbances: Hyperprolactinaemia, polycystic ovary syndrome, obesity, chronic stress, pregnancy
38
Q

What are the distinctive features of polycystic ovary syndrome?

A
  • high LH to FSH ratio: usually more than 3 times of LH are released
  • theca cells produce excessive androgens and low level of SHBG
  • androgens are converted into oestrogen in adipose tissues
    excess androgens mean that there is a -ve feedback on FSH so follicles fail to mature and excess androgens can cause hirsuitism
  • oligo or anovulation
  • 12> follicles in at least 1 ovary or ovarian volume >10 cm3
39
Q

What is the structure of endometrium?

A
  • it is the mucosal lining of uterus
  • simple columnar epithelium and stroma
  • contains a basal layer and a functional layer
  • contains simple tubular glands; straight + spiral arteries
40
Q

What are the functions of endometrium?

A
  • sperm transport

- surface implantation of blastocyst and provide nutrients (by blood vessels)

41
Q

What are the changes in the endometrium at PROLIFERATIVE phase (day 6-14)?

A
  • spiral arteries uncoil and glands increase in length
  • stroma proliferates and thickens to 3-4mm
  • mostly under influence of oestrogen
42
Q

What are the changes in the endometrium at SECRETORY phase (day 14-28)?

A
  • mainly under influence of progesterone ( with some oestrogen)
  • glands lengthen and become distended
  • stroma becomes oedamatous and expands to 6-7mm
43
Q

What are the changes in endometrium at MENSTRUAL phase ( Day 1-5)?

A
  • caused by fall of oestrogen and progesterone
  • endometrium loses water and shrinks
  • spiral arteries coil up and constrict
  • upper functional layer becomes ischaemic and die
  • spiral arteries then dilate and causes bleeding + increases contraction of the uterus
44
Q

What is breakthrough bleeding?

A
  • ‘spotting’
  • caused by continuous steroid use (either progesterone or oestrogen) so endometrium becomes over-developed and fragile -> the level of oestrogen can no longer sustain the lining so bleeding occurs
45
Q

What is withdrawal bleeding?

A
  • due to loss of steroidal support, ie withdrawal of pills
46
Q

What are the main disorders of menstruation? (4)

A

1) amenorrhea = no periods
2) oligomenorrhea = infrequent periods
3) menorrhagia = heavy periods
4) Dysmenorrhea = pain with periods

47
Q

What causes primary amenorrhea?

A
  • define as failure of menses to occur by age of 16
  • failure to develop a reproductive tract/ hypogonadism
  • hypogonadism can be caused by hypothalamic / pituitary defects; eating disorders; systemic diseases
  • can also occurs when endometrium does not respond to androgens (eugonadism)
  • Turner syndrome: 45XO = infertility ; androgen insensitivity syndrome: 46XY
48
Q

What causes secondary amenorrhea?

A
  • pregnancy
  • hypothalamic/ pituitary/ ovarian disorders
  • functional shut down of hypothalmic-pituitary ovarian axis -> due to stress/ anxiety
49
Q

What is menorrhagia and what causes it?

A
  • excess blood loss which interferes with the woman’s quality of life
  • number of days of bleeding and cycle length decreases with age; blood loss increases with age
  • structural risk factors for menorrhagia: uterine fibroids, endometrial polyps, endometrial hyperplasia/ carcinoma
50
Q

What are the treatment options for menorrhagia?

A

1) medical
- first line treatments: contraceptive pills
- Levonorgestrel-releasing intrauterine system (small plastic device that is inserted into your womb and slowly releases progesterone) ; tranexamic acid (helps blood in your womb clot) ; mefenamic acid (NSAID that targets prostaglandin which is likely to linked to heavy periods)

2) surgical
- endometrial ablation (destroy the lining of uterus): microwave, thermal balloon
- myometomy (removal of fibriods)
- polypectomy (removal of polyps)
- hysterectomy (removal of uterus)

51
Q

What defines as oligomenorrhea and polymenorrhea?

A
  • oligomenorrhea= infrequent periods, cycle >35 days

- polymenorrhea= cycle <21 days

52
Q

What is dysmenorrhoea?

A
  • primary dysmenorrhea= caused by prostaglandins

- secondary dysmenorrhea= copper coil; endometriosis

53
Q

What is endometriosis?

A
  • chronic condition that can cause painful/ heavy periods
  • due to ectopic endometrial tissues
  • can associate with pelvic pain and causes infertility
54
Q

Structure of cervix

A
  • connective tissues lined by endocervix = secretory epithelium
  • tubular glands mostly opens into crypts
  • filled with mucus made of mucopolysaccharide
  • forms barrier to infection and sperm
  • the secretion in cervix is driven by oestrogen and reversed by progesterone ( secretion can increase from 40-700mg/day)
55
Q

What is premenstrual syndrome?

A
  • a condition manifests with distressing symptoms in the absence of causes which regular occurs during the luteal phase of each menstrual cycle

Endocrine & Reproductive Systems (11 decks)

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