REPRO - Menstrual Cycle and Physiology Flashcards

1
Q

Primordial Germ Cells (PGCs) undergo many cycles of mitosis, and migrate to the genital ridge. In females they enter…

A

ovaries to become oogonia which are diploid egg precursors

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2
Q

Oogonia proliferate by mitosis then..enter meiosis and arrest..

A

at anaphase (meiosis I) as primary oocytes

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3
Q

At birth what happens to the number of primary oocytes? Why?

A

Massive decrease as they undergo apoptosis as errors are discarded.

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4
Q

Where are primary oocytes packed

A

the cx of ovary (outer layer)

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5
Q

In the foetal ovary, what are the surrounding cells that condense around the oocyte and differentiate?
These secrete what? All together this is the..

A

Granulosa cells, secrete an acellular layer, the basal lamina
-Together structure is the “primordial follicle”

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6
Q

How do follicles grow initially in follicullogenesis in puberty?

A

follicles grow by multiplication of granulosa cells and synthesising protein, lays down the protective Zona Pellucida layer

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7
Q

Once the cohort start growing in folliculogenesis, what is the second layer of cells that differentiate around the basal lamina?

A

The theca cells

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8
Q

FSH drives most of folliculogenesis. But early growth is.. in this at puberty..

A

FSH independent..at puberty cohort of early follicles leave the resting pool and grow continously = follicle initiation

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9
Q

How do the antrum (follicullar fluid filed spaces) form?

A

-follicle increases rapidly in diametre and granulosa cells divisions increase so gaps form in the GC’s layers (becomes fluid filled)

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10
Q

What are follicles with an antrum (antral follicles) AKA?

A

Secondary follicles

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11
Q

Which layer is higher vascularised and brings the circulatory influences to allow growth of the follicle?

A

Theca cell layer

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12
Q

What are the contents of follicular follicle in the antrum?

A
  • exudate of plasma

- secretatory products of oocytes and GCs

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13
Q

Are pre-antral or secondary follicles visible on US next to dominant follicle?

A

Secondary (although pre-antral is always there, just cant see)

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14
Q

After follicle initiation how are some recruited?

A

those that can respond to FSH reach right size for recruitment into menstrual cycle (MC) when FSH is at peak

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15
Q

What happens to those not recruited for MC?

A

They are growing at a different rate/stage so die.

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16
Q

How many cycles does it take for a follicle to go from resting stage to ovulation?

A

3 cycles

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17
Q

In the dominant follicle the steroids produced –> “ 2 cell, 2 Gonadotrophin Theory” which means..

A
  • LH stimulates theca cells to make androgens and progesterone
  • FSH stimulates granulosa cells to make oestrogens from androgens
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18
Q

LH receptors are only on..

Except will appear on… just before… to enable them to make…

A

Theca cells

appear on…GCs just before Ovulation. to enable them to make…Progesterone

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19
Q

FSH receptors are only on

A

Granulosa cells

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20
Q

What effect does oestrogen have on granulosa cells and on follicles?

A

Multiplication and more follicle growth

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21
Q

What happens to the meiosis just before ovulation?

A

They finiish meiosis I and arrest again in metaphase II until fertilisation/death

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22
Q

Menstrual cycle is about 28days, when is day one?

What are the phases?

A

Day 1 = 1st day of bleeding

-follicullar phase and luteal phase

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23
Q

What happens in the follicular phase of MC? Hormone?

A
  • growth of recruited early antral follicles
  • one selected to be the dominant follicle
  • oestrogen
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24
Q

What happens in the Luteal phase of MC? Hormone?

A

corpus luteum remnant of dominant follicle secretes progesterone, if no fertilisation this dies after exactly 14 days

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25
Q

What causes the intercycle rise in FSH?

A

CL dies, progesterone falls, releasing the neg. feedback

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26
Q

The antral follicle growth with lots of neg. feedback causes LH/FSH to decrease, what makes them rise again?

A

-As dominant follicle matures and oestrogen increases sooo much there is a switch to positive feedback

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27
Q

What does the interphase rise in FSH allow for?

A

Recruitment of a cohort of large enough early antral follicles to grow

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28
Q

What happens in the midfollicular phase of the MC, leading to one dominant follicle?

A

-antral follicles make lots of E2 from GCs, neg feedback causes massive FSH decrease so all follicles bar 1, die.

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29
Q

What 3 things does the sustained high E2 level swtich to + feedback, LH surge result in?

A
  • final oocyte maturation
  • completion of meiosis I
  • ovulation and empty follicle –> CL
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30
Q

How does the 1 dominant follicle survive the fall in FSH? (NB: -as FSH decreases LH increases)

A
  • dominant follicle aquires LH receptors (as the gene for this is switched on by FSH) on GCells
  • DF has more FSH receptors better coupled with their downstream signalling
  • can sustain growth in low levels
  • has more GCs
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31
Q

Name 4 processes in ovulation?

A
  • blood flow to follicle increases lots
  • appearance of apex/stigma on ovary wall
  • local release of proteases and inflamm. mediators
  • enzymatic breakdown of protien of ovary wall
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32
Q

What is released in ovulation? How is it collected?

A

Cumulus-oocyte complex, collected by fibriae of tubes and progress down by peristalsis + cilia

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33
Q

When meoisis I completes with the LH surge, what happens to half the chromosomes in this division? The egg is then the..?

A

There is unequal division as half the chromosomes are put in a small package in the egg, “1st polar body”. Making the egg now the “secondary oocyte”

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34
Q

What receptors does the CL have? which 2 hormones support it?

A
  • has LH receptors

- LH and hCG support it

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35
Q

Name 3 functions of the progesterone secreted by the CL?

A
  • maintains itself
  • supports oocytes journey
  • prepares the endometruim
  • controls u.tubes cells and alters cervix secretions
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36
Q

What does the CL secrete oestrodiol for?

A

The endometrium

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37
Q

7/28 or 5-6/27-32 in notes is how MC is shown. What is normal variation month to month in MC?

A

Should be less than 4 day variation to be normal

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38
Q

Rough guide to time of ovulation is..

A

1st day of bleeding + 14
..rise in temp
…tender breasts, abdo bloating, spotting, thin mucus

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39
Q

The fertile period spans how many days?

Affected by?

A

6days, depends on lifespan of egg (up to 24hrs) and lifespan of sperm (av. 1.5days, up to 5)

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40
Q

What 3 layers of the uterus’s myometrium make it a dynamic organ?

A
  • inner circular layer
  • middle spiral fibre layer
  • outer longitudinal layer
41
Q

What layer of the uterus do uterine fibroids develop?

A

Myometruim

42
Q

How is the endometriums vasculature specialised?

A
  • arteries are spiralled to increase SA

- dense capillary network

43
Q

What develops in the endometrium at full receptivity (1wk post ovulation)?

A

-uterine glands that secrete GFs, adhesion…onto the luminal surface

44
Q

In the first half of the MC, oestrogen leads to proliferation of what?

A

Stromal layer proliferation

45
Q

In the second half of the MC, progesterone leads to what?

A
  • maturation of endometrium
  • coiling of arteries
  • development of glands
46
Q

What is the stromal matrix?

A

Small collumnar cells with glandular extensions. 2-3cm thick.

47
Q

Follicular phase of MC in uterus is AKA..

-stimulated by E2 from dominant follicle..result is

A
  • Proliferative phase

- endometrium proliferation, stromal cell division, development of ciliated surface, glands expand, neoangiogenesis.

48
Q

Around day 12-14 when endometrium is >4mm, there is induction of…

A

progesterone receptors on the endothelium

and small muscular contractions of the mypmetrium

49
Q

The luteal phase of MC is AKA..

2-3days post-ovulation is a gradual rise in.. causing

A

Secretatory Phase

  • progesterone rise causes reduced cell division
  • glands become more tortuous and distend
  • glycoprotein and lipids are secreted
50
Q

Why does oedema occur in the secretory phase of MC? 3 reasons

A
  • increased vascular permeability
  • arterioles coil and contract
  • myometrial cells enlarge and movement is supressed
51
Q

What rescues the CL?

A

hCG from blastocyst binding to LH receptors

52
Q

What causes menstruation?

A

Progesterone drop -> endometrium released PGs

  • PGs cause constriction of spiral arterioles
  • hypoxia and necrosis
  • vessels dilate, bleeding starts
53
Q

What remains after menstruation? What is this covered by?

A

The basal lamina remains and is then covered by extension of glandular epithelium

54
Q

What 3 cell types do the uterine tubes have?

A
  • secretory cells for nutrients to embryo
  • columnar ciliated epithelium to waft oocyte
  • non-cilliated peg cells
55
Q

At the start of MC, high oestrogen causes what in the epithelial cells lining uterine tubes?

A

-differentiation so secretory cells secrete/ciliated cells start wafting

56
Q

What happens to mucosa around ovulation/mid MC?

A

-mucosa increases in height for cilila to recieve the egg

57
Q

If no fertilisation, what does progesterone exposure from CL cause to the uterine tubes?

A
  • undifferentiation of the epithelium

- decrease in height of mucosa

58
Q

Name 3 examples of ways the uterine tubes can be damaged.

A
  • infection e.g. chlamydia
  • endometriosis
  • surgery
  • adhesions
59
Q

What 3 symptoms may uterine tube obstruction/damage to epithelium cause?

A
  • pain
  • infertility
  • ectopic pregnancy
60
Q

What are the 2 processes to assess tubal patency?

A
  • Laporoscopy and Dye (dye via uterine cannula through cervix, see if dye emerges from fimbria)
  • Hystero Salpingo Contrast Sonography (HyCoSy) dye via vagina into uterus. US see dye progress through tube
61
Q

What is the 3mm thick endocervical mucosa lined with?

A
  • single layer of colummnar mucous cells

- many tubular mucus glands emptying viscous, alkaline mucus into lumen

62
Q

How does the cervical mucus viscosity change with MC in?

A

-thick and sticky so sperm cant get though except when ovulating, mucus becomes thin and runny

63
Q

What is the ectocervix covered with?

A

-nonkeratinised stratified squamous epithelium (lkke vagina)

64
Q

What/how makes the mucus watery in the follicular phase of MC?

A

-oestrogen, causes increased vascularity of cervix, oedema, transudate moves out -> watery mucus

65
Q

-Midcycle what makes the mucus runny/how?

A

-oestrogen increase. Mucus has glycoproteins that allign and form microscopic channels that sperm can swim up

66
Q

In the luteal phase what makes the mucus viscous/how?

A

-progesterone –> less water content, reduced secretion, more viscousm glycoproteins now form a mesh-like barrier

67
Q

Vagina is 10cm tube lined by

A

specialised squamous epithelium

68
Q

How is vagina protected from infections?

A
  • constantly shed and flown down layers of epithelium cells
  • secretions from cervix. Transudation from vaginal epithelium as plasma leaks out capillaries in the wall
  • secretions change with cycle usually acidic (anti-microbial)
69
Q

What lubricates the vagina?

A

Bartholins glands

70
Q

Before planning pregnancy: weigh, smoking, alcohol, immunisations, Hb-opathy, STI screen, manage chronic disease.. Then when want to concieve focus on:

A
  • HIV, Hep B, STI, Hb-opathy testing
  • folic acid 400mcg
  • mange chronic disease and alcohol and drugs
71
Q

Name 3 risks with contraception.

A
  • pills/hormones affect CNS
  • neoplastic
  • coil/implants can introduce infection or allergic reaction
72
Q

What is the combined OCP?

A

Progestogen and oestrogen aka “ethinyloestradiol” approx 30mcg. Type of progestogen used varys.

73
Q

How does the high oestrogen in OCP prevent ovulation?

A
  • neg. feedback so low LH/FSH
  • low FSH so follicles dont mature
  • low LH so no ovulation
74
Q

How do oestrogen and progesterones action on endometrium differ e.g. in OCP?

A
  • oestrogen causes proliferation

- progestogens cause thinning

75
Q

What effect do progestogens have on mucus?

A

-thicker cervical mucus and less contractility of uterine tubes

76
Q

What are 3 disadv of OCP?

A
  • Progestogen –> HT
  • E2 –> increased risk DVT, PE and migrane
  • neoplastic
  • insulin resistance, Chrons, gall stones
77
Q

What type of drugs can affect metabolism or E2/progestogens in OCP..? Clue rifampicin is an e.g

A
  • liver enzyme inducing drugs

- anti-epileptics

78
Q

Progesterone only contraception includes implants, injections, IUCD, POPs e.g. Desogestrel, why is this pill so popular?

A
  • POP so can breastfeed on this, better SE profiles than OCP
  • predictable bleeding
  • 12hr window if you forget to take one to work
79
Q

Name 3 ways the IUCD works other than hormonal?

A
  • spermicidal
  • causes inflammatory reaction–prostoglandin secretion
  • mechanical effect
80
Q

If pregnancy occurs with an IUCD what are the 2 risks?

A
  • miscarrigae

- ectopic pregnancy

81
Q

Name 3 contraindications for IUCD.

A
  • pelvic infammatory disease
  • suspected pregnancy
  • unexplained vag. bleeding
  • uterine cavity abnormalites
82
Q

Diaphragm latex caps fit across vag. must be used with spermacide, name 1 adv and 1 disadv.

A
  • can be put in advance

- must be left in 6hrs+ after

83
Q

Suction cervical plastic caps also need spermacide and 6hrs+ in, what are the adv. compared to diaphragm?

A

-suitable for those with poor pelvic floor muscles
-no rubber allergies
-unobtrusive..
but higher faliure rate and need a suitable cervix

84
Q

Fertility awareness, most fertile period is week after ovulation, so abstain around then (most accurate is 2/3rd cycle spent abstaing), name 3 adv of this method.

A
  • non medical, can be used in developing areas
  • allowed by catholic church
  • can lead to closeness between partners
85
Q

What are 3 disAdvs of fertility awareness method of contraception?

A
  • faliure rate is user dependent
  • need skilled teaching
  • need cooperation between partners
  • limited sex can cause relationship strain
86
Q

When can post-coital pills be taken after UPSI?

A

up to 72hrs or 120hrs (copper coil)

87
Q

In what post-coital scenario is a copper coil acceptable for emergency contraception?

A
  • up to 120hrs after

- ONEx UPSI

88
Q

1.5mg Levonelle - Levonorgestral - 1.7% failure rate can be used when?

A
  • best in first 24hrs
  • not with anti TB meds, or BMI over 26
  • can use many times in same cycle
89
Q

EllaOne - Ulipristal Acetate - 1.2% - SPeRM - Selective Progestogen Receptor Modulator. How does it work?

A
  • delays ovulation by 5 days

- less effective if progesterone taken in 7 days before or after use

90
Q

In the luteal phase, oestrogen maintains the endometrium, what does progesterone do?

A
  • makes endometrium become secretatory and receptive to implantation
  • makes cervical mucus viscous at end of L.Phase so no more sperm enter
91
Q

After 14days when the CL dies by shrinking and vasculature breakdown what is left?

A

Corpus Albicans

92
Q

Fall in which hormone means the endometrium is no longer maintained so is shed in menses?

A

Progesterone when CL dies

93
Q

The outer layer of the oocyte at ovulation is the Cumulus Oophorus, what is it made of? What is its function?

A
  • made of Granulosa cell remnants

- protects egg and secretes mucus

94
Q

The corona radiata around the oocyte at ovulation is a secretion of what?

A

Extra-Cellular Matrix esp. Hyaluronic Acid

-CR is made of 2 layers of GCells just covering egg

95
Q

What is the Zona Pellucida a layer of? What is its function in relation to sperm?

A
  • a glycoprotein layer secreted by oocyte via cytoplasmic projections at LH surge, projections withdraw
  • bind sperm e.g. ZP3 adheres to proteins on sperm head
96
Q

What is the Perivitelline space under the ZP?

A
  • layer to help block multiple sperm entering (prevents polyspermy)
  • by undergoing changes at fertilisation
97
Q

After 3 days, a 6-8 cell embryo is known as…

A

a morula

98
Q

After 5 days, a 100 cell embryo that has begun to differentiate is known as…

A

a blastocyst

99
Q

What three layers does a blastocyst have?

A
  • an inner cell mass
  • a fluid filled blastocoele
  • the trophoblast (will be placenta)