Pregnancy, Menstrual Cycle and Reproduction Flashcards

1
Q

How is foetal sex determined by the Y chromosome?

A

SRY gene codes for TDF or SRY-protein which switches on testicular development. The Sertoli cells of the testes produce Mullerian-inhibiting substance, which prevents Mullerian duct development.

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2
Q

Where is testosterone produced?

A

Leydig cells

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3
Q

What is the effect of testosterone (Development)

A

Causes Wolffian duct to differentiate into the epididymis, vas deferens, ejaculatory ducts and seminal vesicles.

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4
Q

What is the next step in male sex development (post-W. duct differentiation)?

A

Externally under the influence of dihydrotestosterone (DHT) produced from testosterone in target tissue, the penis forms and the tissue near it fuses to form the scrotum.
The testes descend into the scrotum (stimulated by testosterone)

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5
Q

How is foetal sex determined by the XX chromosomes?

A

Absence of Y chromosome = absence of SRY gene = the female will not have testes and will not secrete MIF or testosterone.

Absence of MIF = Mullerian system does not degenerate and a vagina and female external genitalia develop

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6
Q

Summary of differentiation until 6 weeks

A

Primitive gonads are identical

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7
Q

Summary of differentiation after 6 weeks

A
  • If Y chromosomes are present and thus SRY gene: testes form and Mullerian development is inhibitied
  • If Y chromosome is absent: ovaries form and Mullerian development occurs
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8
Q

Where do both the male and female gonads derive embryologically?

A

the urogenital ridge

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9
Q

Until when are primordial gonads undifferentiated?

A

6 weeks

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10
Q

In the genetic male, the testes begin to develop during the –th week?

A

7th week

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11
Q

What are germ cells? Where do they develop?

A
  • Cells that develop into sperm and ova
  • Originate from the yolk sac of the hind gut
  • Specialised cells which develop into gametes
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12
Q

Anomalies of primary sex development

A
  • Gonadal dysgeneses
  • Intersex - 4XY disorders of sex differentiation
  • Intersex - 4XX disorders of sex differentiation
  • Androgen insensitivity testosterone syndrome
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13
Q

Gonadal dysgeneses CAUSE

A
  • Non-disjunction

- Sex chromosome deletion

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14
Q

Hypothalamic-pituitary-gonadal axis

A
  • Normally, gonadotrophin releasing hormone (GnRH) secreting neuroendocrine cells of the hypothalamus fire a brief burst of action potentials approximately every 90 minutes, secreting GnRH at this time
  • The GnRH travels to the anterior pituitary via the hypothalamal-hypophyseal portal vessels and triggers the release of both LH and FSH
  • FSH primary acts on the Sertoli cells to stimulate the secretion of paracrine agents required to initiate spermatogenesis
  • LH acts primarily on the Leydig cells to stimulate testosterone secretion. Testosterone acts locally by diffusing from the interstitial spaces into the seminiferous tubules and then enters the Sertoli cells where it is able to facilitate spermatogenesis
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15
Q

Hypothalamic-pituitary-gonadal axis - NEGATIVE FEEDBACK

A
  • Testosterone inhibits LH secretion in 2 ways:
    1. Acts on the hypothalamus to decrease the amplitude of GnRH resulting in a decrease in its secretion
    2. Acts directly on the anterior pituitary gland to decrease LH response to GnRH
  • Sertoli cells release INHIBIN which acts on the anterior pituitary to inhibit the release of FSH`
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16
Q

Hormonal control of puberty - before puberty

A
  • Low pulsatility amplitude of GnRH and GHRH (growth hormone releasing hormone) secretion from hypothalamus
  • Low levels of pituitary FSH, LH and gonadal sex steroids
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17
Q

Hormonal control of puberty - at pubertal age

A
  • The trigger is not clearly understood
    • Increased amplitude of GnRH and GHRH
    • Increased levels of FSH, LH and sex steroids
    • Increased levels of growth hormone
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18
Q

Normal puberty

A
  • Centrally driven
  • Depends on intact Hypothalamus-Pituitary-Gonadal axis
  • Influenced by nutrition, leptin and insulin, socio-cultural, genetic and exercise factors
  • Trigger is not well understood
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19
Q

Causes of precocious puberty

A
  • Gonadotrophin dependent
  • Gonadotrophin independent
  • Other variants
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20
Q

Gonadotrophin dependent (precocious puberty) reasons

A
  • Intracranial lesions
    • Infections
    • Encephalitis
    • Gn secreting tumours
    • Hypothyroidism
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21
Q

Gonadotrophin independent (precocious puberty) reasons

A
  • CAH
    • Sex hormone secreting tumours
    • E2 ingestion
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22
Q

Other variants (precocious puberty) reasons

A

Premature thelarche or adrenarche

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23
Q

Treatment of premature adrenarche

A

androgen receptor blockage

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24
Q

Causes of delayed puberty

A

General

- Constitutional delay (most cases)
- Malabsorption (coeliac disease, inflammatory bowel disease)
- Chronic disease or underweight

Gonadal failure
- Turner’s syndrome autoimmune syndrome

Gonadotrophin deficiency

- Kallman's syndrome
- Hypothalamic/pituitary lesions
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25
Q

What covers the testes anteriorly?

A

Sac-like extension of the peritoneum → tunica vaginalis

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26
Q

Name of white fibrous capsule?

A

Tunica albugenia

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27
Q

Septa divide the testes into compartments containing — — where sperm are produced

A

seminiferous tubules

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28
Q

What do seminiferous tubules drain into?

A
  • A network called RETE TESTIS
  • The sperm then travel through efferent ductules which leave the rete testis and pierce the tunica albuginea and empty into a single duct within the epididymis
  • The epididymis leads to a vas deference (a large thick walled tube lined with smooth muscle)
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29
Q

Which cells promote sperm cell development?

A

Sertoli cells

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30
Q

What forms the blood-testis barrier

A

tight junctions between sertoli cells separating sperm from immune system

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31
Q

Heat exchange of Pampiniform Plexus

A
  • Spermatogenesis cannot take place at 37 degrees but needs to take place at a temperature that is lower (35)
  • A special temperature regulation is done by heat exchange that happens by the pampiform plexus where venous blood carries away heat
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32
Q

Spermatogenesis

A
  • Spermatogonia produce 2 kinds of daughter cells
    - Type A remain outside blood-testis barrier and produce more daughter cells until death
    - Type B differentiate into primary spermatocytes and these cells must pass through the blood-testis barrier to move inward toward lumen. Meiosis I produces 2 secondary spermatocytes and Meiosis II produce 4 spermatids.
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33
Q

What is spermiogenesis?

A

the transformation of spermatids into spermatozoa (where a tail is sprouted and cytoplasm is discarded)

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34
Q

Which two structures secrete most of the fluid in which ejaculated sperm is suspended?

A
  • prostate gland

- seminal vesicles

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35
Q

Chemical substances secrete by main two secretory structures (male)

A
  • The prostate and seminal vesicle secretions contain a large number of different chemical substances
    • Buffers for protecting sperm against the acidic vaginal secretions and residual urine in the male urethra
    • Chemicals (particularly from SV) increase sperm motility e.g. fructose to provide energy
    • Prostaglandins - to stimulate female peristaltic contractions
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36
Q

What percentage of the expelled fluid is from which structure?

A
  • 60% seminal vesicle fluid
  • 30% prostatic
  • 10% sperm and trace of bulbourethral fluid
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37
Q

Normal sperm count

A

50-120 million mL

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38
Q

How do bulbourethral glands contribute?

A

small volume of lubricating mucoid secretions

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39
Q

Summary of path of sperm to outside:

8

A
  1. Seminiferous tubules
  2. Rete testis
  3. Efferent ducts
  4. Epididymis
  5. Vas Deferens
  6. Ejaculatory ducts
  7. Urethra
  8. Penile urethra
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40
Q

Spermatic ducts

A

Efferent ductules
Epididymis
Ductus vas deferens
Ejaculatory duct

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41
Q

Efferent ductules

A

12 small ciliated ducts collecting sperm from the rete testes and transporting it to the epididymis

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42
Q

Epididymis

A
  • 6 m long coiled duct adhering to the posterior of testis
  • Site of sperm maturation and storage
  • fertile for 40-60 days
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43
Q

Ductus vas deferens

A

muscular tube 45cm long passing up from scrotum through the inguinal canal to posterior surface of bladder

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44
Q

Ejaculatory duct

A

2cm duct formed from ductus deferens and seminal vesicle and passing through prostate to empty into urethra

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45
Q

2 main phases of menstrual cycle

A

Follicular phase: Day 1-13

Luteal phase: Day 14-28

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46
Q

Different types of follicles

A
Primordial
Primary
Preantral
Early antral
Mature
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47
Q

Primordial follicles

A

Consist of one primary oocyte surrounded by a single layer of granulosa cells which secrete oestrogen, small amounts of progesterone (just before ovulation) and inhibin.

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48
Q

Primary follicles

A
  • The oocyte increases in size and become separated from the inner granulosa cells but the zona pellucida (secreted by the surrounding follicular cells).
  • The zona pellucida contains glycoproteins that play an important role in the binding of a sperm cell to the surface of the egg after ovulation.
  • The inner layer of granulosa cells stay in contact with the oocyte via cytoplasmic processes that transverse the zona pellucida and form gap junctions through which nutrients and chemical messengers are passed to it.
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49
Q

Preantral follicle

A
  • Through the mitosis of the granulosa cells the follicle grows larger
  • Connective-tissue cells surrounding the granulosa cells differentiate and from layers of cells known as the THECA which function together with the granulosa cells in the synthesis of oestrogen.
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50
Q

Early antral follicle

A
  • The primary oocyte reaches full size
  • The ANTRUM (fluid filled space) begins to form in the midst of the granulosa cells as a result of the fluid they secrete)
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51
Q

Mature follicle

A
  • At the beginning of each menstrual cycle around 10-25 of these preantral and early antral follicles being to develop into larger antral follicles
  • Around 1 week into the cycle, a further selection process occurs whereby only one of the larger antral follicles - the dominant follicle - continues to develop
  • The non-dominant follicles undergo atresia (a degenerative process)
  • The dominant follicle enlarges as a result of the increase in fluid
  • As the time for ovulation approaches the primary oocyte emerges from its meiotic arrest due to the surge in LH and completes its first meiotic division to become a secondary oocyte
  • The mature follicle (graafian follicle) becomes so large that it balloons out on the surface of the ovary
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52
Q

When does ovulation occur?

A

When the thin walls of the follicle and ovary rupture at the site where they are joined because of enzymatic digestion the secondary oocyte is carried out of the ovary and onto the ovarian surface by the antral fluid - this occurs on DAY 14

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53
Q

Luteal phase - Day 14-28

A
  • After the mature/graafian follicle discharges its antral fluid and egg, it collapses and undergoes rapid transformation
  • The granulosa cells enlarge greatly and a gland-like structure called the CORPUS LUTEUM is formed, and secretes oestrogen, progesterone and inhibin
  • If the discharged egg in the fallopian tube does not get fertilised by fusing with a sperm cell, the corpus luteum reaches its maximum development with in 10 days and then rapidly degenerates via apoptosis which triggers MENSTRUATION and the beginning of a new cycle.
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54
Q

Site of synthesis of ovarian hormones

A

Oestrogen

- Oestrogen is synthesised and released into the blood during the follicular phase mainly by GRANULOSA cells
- After ovulation, oestrogen is synthesised and released by the CORPUS LUTEUM

Progesterone

- Progesterone is synthesised and released in very small amounts by the GRANULOSA and THECA cells just before ovulation
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55
Q

Major hormones in menstrual cycle

A
GnRH
FSH
LH
Oestrogen
Progesterone
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56
Q

Sequence of menstrual cycle depends on the levels of

A

GnRH

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57
Q

When does FSH increase, and then decrease?

A

Increases in the early part of the follicular phase and then steadily decreases throughout the remainder of the cycle except for a small mid-cycle peak.

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58
Q

Why does FSH secretion increase as one cycle ends and another begins?

A

This is due to decreased progesterone, oestrogen and inhibin and thus no negative feedback on the hypothalamus and anterior pituitary.
Elevated FSH secretion means that the enlargement of preantral and early antral follicles is stimulated.

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59
Q

FSH acts on – cells in the first week to …

A

FSH acts on the granulosa cells in the first week (because they have FSH receptors but no LH receptors at this point in the cycle) to stimulate their multiplication, and production of oestrogen. Oestrogen works with FSH (and growth factors) to stimulate the proliferation of granulosa cells

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60
Q

FSH is involved with the degradation of …

A

FSH is also involved with the degradation of non-dominant follicles; since there is not enough FSH to prevent size decrease and thus atresia

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61
Q

FSH induces – receptors on …

A

FSH induces LH receptors on dominant maturing follicles

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62
Q

When the dominant follicle starts to secrete more oestrogen, what is the effect on FSH?

A

When the dominant follicle starts to secrete more oestrogen it causes levels of FSH to decrease because oestrogen exerts a negative feedback mechanism on the secretion of gonadotrophins from AP + hypothalamus.

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63
Q

Levels of LH during menstrual cycle

A

Constant for most of the follicular phase but then shows a very large mid cycle increase (LH surge) peaking around 18 hours before ovulation, which is followed by a rapid decrease and then a further slow decline during the luteal phase

64
Q

LH acts on – cells in the first week. Why?

A

LH acts on theca cells in the first week since at this point in the cycle, the theca cells have LH receptors but NO FSH receptors

65
Q

LH stimulate – cells to …

A

stimulate theca cells to proliferate and synthesis androgens which then diffuse into the granulosa cells and are converted to oestrogen

66
Q

Which enzyme converts androgens to oestrogen

A

aromatase

67
Q

Oestrogen action (5 steps)

A
  1. Oestrogen remains fairly low and stable for the first week
  2. Increases rapidly during the second week as the dominant ovarian follicle grows and secretes more oestrogen
  3. It then begins decreasing shortly before LH has peaked
  4. This is then followed by a SECOND increase due to secretion by the CORPUS LUTEUM
  5. Ends with a rapid decrease during the last days of the cycle
68
Q

– amounts of progesterone are released by the – during the – phase until just before –

A

Very small amounts of progesterone are released by the ovaries during the follicular phase until just before ovulation

69
Q

Soon after –, the developing – – begins to produce – amounts of progesterone

A

Soon after ovulation, the developing corpus luteum begins to release LARGE amounts of progesterone

70
Q

When do progesterone levels rapidly decrease?

A

the last days of the cycle

71
Q

When does inhibin increase, stabilise and decrease?

A
  • Increases during the late follicular phase
  • Remains high during the luteal phase
  • Decreases as the corpus luteum degenerates
72
Q

How does oestrogen cause an LH surge to induce ovulation?

A
  • Increasing oestrogen secretion for 1-2 days during the oestrogen peak of the late follicular phase results in the secretion of large amounts of oestrogen, which acts on the anterior pituitary gland and hypothalamus in a different way to what low conc. did.
    Large concentrations act to INCREASE SENSITIVITY of LH-RELEASING CELLS to GnRH = a positive feedback mechanism
  • Net result = rapidly rising oestrogen leads to LH surge and the high plasma [LH] acts upon the granulosa cells which induces ovulation
73
Q

When does the LH surge decline?

A

Just as ovulation is occurring due to the small increase in progesterone from corpus luteum which induces a negative feedback on the AP + H.

74
Q

What does the LH surge do other than induce ovulation?

A

Stimulate the reactions that transform the remaining granulosa and theca cells of that follicle into a corpus luteum

75
Q

In order for pregnancy to occur, the introduction of sperm must occur between — days before and — day after ovulation - why?

A
  • 5 days before - 1 day after
  • This is due to the fact that sperm, following ejaculation into the vagina, remain capable of fertilising an egg for up to 4-6 days and the ovulated egg remains viable for only 24-48 hours
76
Q

Egg transport (4 steps)

A
  1. At ovulation, the egg is extruded onto the surface of the ovary
  2. The smooth muscles of the fimbrae (located on the end of the fallopian tube) cause the fimbrae to pass over the ovary while the cilia of the fimbriae beat in waves towards the interior of the fallopian tube
  3. These ciliary motions sweep the egg into the fallopian tube
  4. Once inside the fallopian tube, the eggs move by the fallopian tube cilia, the cilia are slow and it takes around 4 days for the egg to be beaten into the uterus
77
Q

What is passage of the sperm through the cervical mucus dependent on?

A

The release of oestrogen causing the mucus to be water to enable to sperm to easily travel through it

78
Q

Why is sperm mortality high during the trip to the vagina?

A

The vaginal environment is acidic to provide protection against yeast and bacterial infections

79
Q

Capacitation of sperm; what is it?

A

CAPACITATION = the final maturation stage of spermatozoa that takes place in the female genital tract before the spermatozoa gain the ability to fertilise the oocyte

80
Q

Capacitation of sperm; why does it happen?

A

Once the sperm have reached the fallopian tube they are unable to fertilise the egg since they are not mature enough so must reside in the female tract for several hours and then be acted upon by secretions of the tract

81
Q

What does capacitation cause?

A
  • The previous wavelike beats of the sperms tail to be replaced by more whip like action that will propel the sperm forward in stronger surges
  • The sperms plasma membrane to become altered to that it will be capable of fusing with the surface membrane of the egg
82
Q

Pre-implantation stages

Days 1 to ~6

A
Fertilisation
Cleavage
Compaction
Cavitation and differentiation
Expansion
Hatching
83
Q

Fertilisation (7)

A

Day 1

  • Begins with the fusion of egg and sperm within a few hours of ovulation (occurs at the AMPULLA of the fallopian tube)
  • Many sperm bind to the glycoprotein receptors on the zona pellucida
  • Acrosomal enzymes digest a path through the zona pellucida
  • The first sperm to penetrate the entire zona pellucida fuses with the egg
  • The head of the sperm passes into the cytosol of the egg and the egg is now known as the ZYGOTE
  • 4-7 hours after gamete fusion the zygote completes meiosis 2; the 2 sets of haploid chromosomes (23 egg 23 sperm) are known as PRONUCLEI, and the pronuclei migrate to the centre of the cell where DNA replication occurs in preparation for the first mitotic division.
  • 46 chromosomes organise at the spindle equator.
84
Q

Mechanism to block polyspermy

A
  • egg membrane potential changes
  • cortical reaction initiated resulting in exocytosis of secretory vesicles into the space between the ZP and egg plasma membrane → enzymes which inactivate sperm binding receptors
85
Q

Cleavage

A

Day 2-3

  • The zygote remains in the fallopian tube for 3-4 days because oestrogen maintains the contraction of the smooth muscle near where the fallopian tube enters
  • Around 24 hours after fertilisation occurs, a number of mitotic cell divisions occur (CLEAVAGE).
  • There is no cell growth but successive cleavages result in an increase in cell numbers - essential to provide sufficient cells for differentiation
  • Each cell is TOTIPOTENT stem cell
86
Q

Compaction

A

Day 4
The cells flatten and maximise intracellular contacts resulting in the formation of tight junctions and the polarisation of outer cells - ESSENTIAL to be able to differentiate QUICKLY

87
Q

Cavitation and differentiation

A

Day 5

  • Fluid filled cavity expands to form BLASTOCYST consisting of an outer layer of cells known as the trophoblast, an inner cell mass & a central fluid filled cavity
  • BLASTOCYST is defined as having greater than 80 cells - these cells have lost their totipotentiality and have begun to differentiate
88
Q

Expansion

A

Day 6

Cavity expands further and the diameter of the blastocyst increases and the zona pellucida THINS

89
Q

Hatching

A

Day 6+
Blastocyst expansion and enzymes result in the hatching of the embryo from the zona pellucida; this is necessary for implantation

90
Q

Implantation stages after the embryo reaches the uterus at day 5/6

A
Apposition
Attachment
Differentiation of trophoblast
Invasion
Decidual reaction
Maternal recognition
91
Q

Apposition - Day X after fertilisation

A

9
The hatched blastocyst orientates via embryonic pole and synchronises with the receptive endometrium on day 19-22 of menstrual cycle

92
Q

Attachment

A

Endometrial epithelial cells and trophoblastic cells express integrins which connect with one another

93
Q

Differentiation of trophoblast

A

The trophoblast differentiates into

  • Cytotrophoblast
  • Syncitiotrophoblast (erodes endometrial blood vessels - using proteolytic enzymes)
94
Q

Invasion

A

Enzymatic degradation of the basal lamina

95
Q

Decidual reaction

A

Differentiation of the stromal cells adjacent to the blastocyst

96
Q

Maternal recognition

A

Secretion of interleukin-2 prevents antigenic rejection of embryo

97
Q

When does the placenta begin to develop?

A

begins to develop at blastocyst implantation

98
Q

What is the placenta?

A

A combination of interlocking foetal and maternal tissues which serves as an organ of exchange

99
Q

Development of the placenta (4 stages)

A
  1. 8 cell morula arrives at the uterus and develops into blastocyst
  2. The outer cell layer from the primary trophoblastic cell mass (TCM) then invades the endometrium which degenerates and the trophoblast contacts stroma
  3. Implantation is complete by the 11th day post ovulation
  4. Implantation is the first stage of placental development
100
Q

What is the embryonic portion of the placenta supplied by?

A
  • the outermost layers of trophoblast cells, the CHORION
  • Chorionic villi extend from the chorion into the endometrium which is altered by enzymes secreting from villi so that each villus becomes completely surrounded by a pool or placental sinus of maternal blood
101
Q

How does maternal blood enter the placenta? (entry + which artery)

A
  • placental sinuses

- umbilical artery

102
Q

What simultaneously takes place in terms of blood flow?

A

Blood flows from the foetus into the capillaries of the chorionic villi via the umbilical arteries and out of the capillaries back to the foetus via the umbilical vein

103
Q

What is the maternal portion of the placenta supplied by?

A
  • decidua
  • uterine lining forming the maternal part of the placenta
  • underlying chorion
104
Q

main functions of the placenta:

A
  • metabolism
  • transport
  • endocrine
  • provides nutrition, gas exchange, waste removal and endocrine + immune support
105
Q

Placental metabolism; what does it synthesise?

A
  • glycogen
  • cholesterol
  • fatty acids
106
Q

Placental transport; what does it transport? (11)

A
  • gases and nutrition (O2 + CO2)
  • Water
  • Glucose (faciltiated diffusion via hexose transporters)
  • Vitamins
  • Amino acids (active transport)
  • Hormones, mainly steroid NOT protein
  • Electrolytes
  • Maternal antibodies IgG and NOT IgM
  • Waster products (urea, uric acid, bilirubin)
  • Drugs and their metabolites - can result in foetal drug addiction
  • Infectious agents
107
Q

What are placental barriers to transport from maternal to foetus?

A
  • Maternal endothelial cells
  • Maternal connective tissue
  • Endometrial epithelial cells
  • Chorionic epithelial cells
  • Fetal connective tissue
  • Fetal endothelial cells
108
Q

When does the placenta become well-established?

A

5 weeks after implantation (the foetal heart has begun to pump blood, the entire mechanism for nutrient of the embryo is in operation)

109
Q

What forms between the inner cell mass and the chorion while the placenta develops? What is the name for the epithelial layer lining this?

A
  • amniotic cavity

- amnion or amniotic sac

110
Q

Throughout pregnancy, plasma concentrations of which hormones continuously increase?

A

oestrogen

progesterone

111
Q

Why does oestrogen plasma conc continuously increase during pregnancy?

A
  • stimulates growth of uterine muscle mass
  • regulates progesterone levels
  • prepares breasts for feeding
  • induces the synthesis of receptors for the posterior pituitary hormone OXYTOCIN
112
Q

Why does progesterone plasma conc. continuously increase during pregnancy?

A
  • Inhibits uterine contractility so that the foetus is not expelled prematurely
  • Increases thickness of uterine lining to prevent miscarriage
113
Q

What is the full name of hCG?

A

human chorionic gonadotrophin

114
Q

What is hCG produced by? When?

A

trophoblast cells around the time they begin their endometrial invasion at day 7-8 (onset of implantation)

115
Q

What does hCG do?

A

prevents degradation of the corpus luteum, strongly stimulates CL secretion of oestrogen and progesterone

116
Q

When does hCG peak and then decrease?

A

60-80 days after last menstruation, then rapidly decreases so by the end of the 3rd month it has reached a low conc. that remains constant until the end of pregnancy

117
Q

What happens as hCG levels decrease?

A

placenta begins to secrete large quantities of O + P

118
Q

What are the precursors of oestrogen? What is supplied by these via which structures? What happens to them there?

A
  • androgens
  • The placenta is supplied with androgens by maternal ovaries, maternal adrenal medulla and foetal adrenal medulla
  • The placenta then converts the androgens into oestrogen by expressing the enzyme called AROTOMASE
119
Q

Prolactin function

A

has roles in milk production and the prevention of ovulation

120
Q

What is prolactin produced by?

A

antetior pituitary gland

121
Q

When do prolactin levels increase and decrease?

A

increase @ end of pregnancy when O and P decrease

After birth, O and P levels drop drastically which allows prolactin to stimulate production of milk

122
Q

What controls prolactin release?

A

suckling

123
Q

What is the function of relaxin?

A

limit uterine activity
soften the cervix
involved in cervical ripening

124
Q

What is relaxin produced by?

A

ovary

placenta

125
Q

When are relaxin levels high?

A

early pregnancy

126
Q

What does oxytocin stimulate?

A

uterine contractions during pregnancy and labour

triggers caring reproductive behaviours

127
Q

Where is oxytocin produced?

A

posterior pituitary gland

128
Q

When does oxytocin secretion increase?

A

secreted throughout pregnancy but increases at the end

129
Q

What is oxytocin function during labour?

A

drug used to induce labour

130
Q

What is the main prostaglandin?

A

PGF2a

131
Q

What is the most powerful prostaglandin?

A

PGE2

132
Q

What is the function of the main and most powerful prostaglandin?

A

initiate labour

133
Q

What are the prostaglandins produced by?

A

uterine tissues

134
Q

Cardiovascular changes during pregnancy

A
  • Increased Cardiac Output
  • Reduced Systemic Blood Pressure
  • Reduced Total Peripheral Resistance
  • Increased Uterine Blood Flow
  • Increased Blood Volume
  • Increased Plasma & Blood cell mass
135
Q

Respiratory changes during pregnancy

A

Increased alveolar ventilation

136
Q

GI changes during pregnancy

A

Increased acid reflux and gastroparesis (Delayed emptying)

137
Q

Skin changes during pregnancy

A
  • Linea nigra - dark central line on abdomen
  • Striae gravidarum - stretch marks in lumbar/lower
    abdominal regions
  • Darkened areolar of breasts
138
Q

Biochemical changes during pregnancy

A

Weight gain - maternal & fetoplacental:
• Obese women do not put on much weight during pregnancy since they
have fat stores which can be mobilised to supply the energy for
pregnancy
• Skinny women do not have these fat stores so must put on weight thus
they put on more extra weight during pregnancy

  • Increased protein and lipid synthesis
  • Insulin RESISTANCE
139
Q

How long does a normal pregnancy last?

A

40 weeks

140
Q

What is parturition?

A

birth process (intra- to extra-uterine life)

141
Q

What changes are there to smooth muscle cells of myometrium in the last few weeks of pregnancy?

A

Throughout most of pregnancy the smooth muscle cells of the myometrium are relatively disconnected from each other:

  • This feature is maintained mainly by progesterone
  • During the last few weeks of pregnancy, as a result of the increasing
    concentrations of oestrogen, the smooth muscle cells synthesis CONNEXINS
  • proteins that form gap junctions between the cells, which allow the
    myometrium to undergo coordinated contractions
142
Q

What is cervical ripening?

A

growth and remodelling of the cervix prior to labour

143
Q

During pregnancy, the uterus is …

This feature is maintained mainly by what hormone?

A
  • sealed at its outlet by the firm, inflexible collagen fibres that constitute the cervix;
    • progesterone
144
Q

What changes to the cervix in the last few weeks of pregnancy?

A

becomes soft and flexible due to an enzymatically mediated breakdown of its collagen fibres

145
Q

What mediates the synthesis of the enzymes which change the cervix in the last few weeks of pregnancy ?

A
  • oestrogen
  • placental prostaglandins - PGE
  • Relaxin
    • softens cartilaginous joins in the pelvis in preparation for labour
146
Q

Summary of the events of prelabour (7)

A
  • Enhanced prostaglandin production
  • Initiation of labour
  • Maternal signal: oxytocin
  • Foetal signal: oxytocin, vasopressin and cytokines
  • PGF2a enhances the action of oxytocin
  • Increased pressure on the cervix stimulates the release of prostaglandins
  • Contraction of the actomyosin in the myometrium
147
Q

Action of the two hormones involved in initiating and promoting labour

A

Labour is initiated by increased PGFa which in turn enhances the action of oxytocin which results in myometrial contraction which in turn exerts pressure on the cervix and promotes further contraction

148
Q

What happens during onset of labour and initial contractions?

A
  • At the onset of labour, the amniotic sac RUPTURES and the amniotic fluid flows through the vagina
    • When labour begins in earnest the uterine contractions become stronger and occur at 10-15 minute intervals - the contractions begin in the upper portion of the uterus and sweep downward
    • Cervix gradually forced open (dilation) to max. diameter of 10cm
149
Q

Phases of labour

A

Latent phase
Active phase
Post-partum phase

150
Q

Latent phase

A

little cervical dilation: 8 hours

151
Q

Active phase

A
  • Stronger higher freq contractions
  • Full dilation resulting in foetal expulsion (birth)
  • Placental expulsion
152
Q

What are oral contraceptives based on?

A

the fact that oestrogen and progesterone can inhibit anterior pituitary gland gonadatrophin release thereby preventing ovulation

153
Q

Mechanism of menopause (8)

A
  1. Depletion of primordial follicles - occurs around 40 years
  2. Decrease in follicular oestrogen production
  3. Gradual increase in FSH and LH due to lack of negative feedback
  4. Decline of inhibin → further increase in FSH and LH
  5. Increase in FSH results in the rapid increase in oestrogen secretion from existing follicles
  6. Short menstrual cycle
  7. As fewer follicles remain, increase in FSH no longer stimulates the increase in oestrogen (6-12 months pre-menopause)
  8. Decrease in oestrogen and lack of ova = menopause
154
Q

Signs of menopause - short term

A
  • Hot flushes, sweats, palpitation, headaches
  • Irritability, lethargy, panic attack & depression
  • Shorter menstrual cycle
  • Altered blood loss
  • Skin dryness
155
Q

Signs of menopause - long term

A
  • Vaginal dryness - resulting in painful intercourse
  • Decrease in libido
  • Hair loss/thinning
  • Diminished urethral seal and loss in compliance
  • General aches and pains
156
Q

Osteoporosis

A

Women are more at risk of developing osteoporosis than men because of the hormone changes that occur in menopause directly affect bone density – oestrogen is essential for healthy bones, after menopause, oestrogen levels drop resulting in a rapid decrease in bone density