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YEAR 2 - Applied Physiology & Pharmacology > 57. Reproduction > Flashcards

57. Reproduction Flashcards

1
Q

What is the diameter of a human egg?

A

100 microns -> Just visible to the human eye

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2
Q

Label this diagram of fertilisation.

A
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3
Q

What are the important stages of fertilisation?

A
  • Zona pellucida binding
  • Acrosome reaction
  • Cortical reaction
  • Resumption of egg’s second meiotic division
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4
Q

What are some important structural and functional features that an oocyte must have in order to undergo successful fertilisation?

A
  • Expanded cumulus cell matrix (inner layer = corona radiata) -> To aid passage into fimbria, protect zygote and provide an additional barrier to polyspermy
  • Zona pellucida -> Provide a surface receptor for sperm, prevent polyspermy, protect preimplantation embryo and prevent fusion of embryos
  • Initiated second meiotic division at ovulation
  • Enough proteins, RNA, ribosomes, mitochondria, etc for development of the early embryo (only maternal gene expression until ~8 cell stage)
  • Ability to decondense sperm nucleus
  • Multiple mechanisms to prevent polyspermy (e.g. cortical reaction)
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5
Q

Label this oocyte.

A
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6
Q

What is the corona radiata, how is it formed and what is its function?

A

What it is:

  • The innermost layer of the cells of the cumulus oophorus, directly adjacent to the zona pellucida

Function:

  • Supply vital proteins to the cell
  • Sperm must get through it to reach oocyte

Formation:

  • Formed by follicle cells adhering to the oocyte before it leaves the ovarian follicle
  • Originates from the squamous granulosa cells present at the primordial stage of follicular development
  • The corona radiata is formed when the granulosa cells enlarge and become cuboidal, which occurs during the transition from the primordial to primary stage
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7
Q

What is the zona pellucida and what is its function?

A
  • A glycoprotein layer surrounding the plasma membrane of oocytes.
  • It is secreted by both the oocyte and the ovarian follicles.
  • The zona pellucida is surrounded by the corona radiata
  • Functions:
    • Provides a surface receptor for sperm
    • Prevents polyspermy
    • Protects preimplantation embryo + prevents fusion of embryos
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8
Q

How does an oocyte travel down the oviduct (Fallopian tube)?

A
  • High levels of estradiol at the end of follicular phase and in luteal phase cause muscular activity in the oviduct
  • Its fimbriated end becomes closely apposed to ovulation site
  • Its folded, ciliated epithelium wafts ovulated oocyte & corona into tube
  • Secretions from epithelial cells help nourish the developing embryo
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9
Q

What hormone is responsible for the movement of a oocyte down the oviduct (Fallopian tube) after release? When are the levels of this hormone high?

A
  • Estradiol (a type of oestrogen)
  • High levels are at the end of follicular phase and in the luteal phase
  • They cause muscular activity in the oviduct, so that the fibriated end comes close to where the oocyte is
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10
Q

What cross-section is shown here?

A

Oviduct (Fallopian tube)

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11
Q

How can you monitor for when ovulation is happening?

A
  • Basal body temperature rises within a few hours of ovulation
  • Immunosticks with an anti-LH antibody (since there is a surge of LH)
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12
Q

What happens to body temperature just after ovulation?

A

It rises within a few hours.

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13
Q

Describe the epithelium of the oviduct (Fallopian tube).

A
  • Fimbriae -> Ciliated columnar cells
  • Secretory cells
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14
Q

Describe sexual behaviour in different species.

A
  • Most adult male mammals show sexual behaviour when an attractive and receptive female is present, while most female mammals (not primates) show sexual behaviour only at oestrus when proceptive (‘courting’) behaviour may also be shown
  • Most animals need sex hormones for sexual behaviour, but more complex in primates:
    • Female primates are potentially sexually receptive at all times
    • Rhesus monkeys interact sexually more at the time of ovulation; because the female is then more attractive to the male (vaginal aliphatic acid odour)
    • Ovariectomized women do not all show reduced sex activity or libido
    • Castration of male primates gradually reduces, but often does not eliminate sexual activity. -> Anti-androgens are used to curb ‘unwanted’ activity
    • Non-hormonal stimuli including rearing are very important in all primates
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15
Q

What are the different stages of sexual activity in males and females?

A
  • Arousal (excitement)
  • Plateau
  • Orgasm
  • Resolution
  • Only in males: Refractory period
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16
Q

In males, what occurs during arousal and how is this controlled?

A
  • Erection
    • Due to arteriolar vasodilation + compression of veins
    • Controlled by parasympathetic innervation -> Relaxation due to non-cholinergic NO + cGMP
  • Elevation of scrotum
  • Elevation and swelling of testes
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17
Q

In males, what occurs during the plateau phase of sexual activity and how is this controlled?

A
  • Distension of the penis and testes
  • Mucus bulbourethral gland secretion
    • Controlled by parasympathetic innervation -> Cowper’s glands
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18
Q

In males, what occurs during orgasm and how is this controlled?

A

Emission:

  • Contraction of vas deferens, seminal vesicles and prostate
  • Relaxation of urethral sphincter
  • Controlled by sympathetic innervation

Ejaculation:

  • Rhythmic contraction of bulbospongiosus and anal sphincter
  • Controlled by somatic innervation -> Pudendal nerve
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19
Q

Describe how viagra works. [EXTRA]

A
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20
Q

How exactly do spermatazoa move?

A

Tail flagellates propel the sperm cell by rotating like a propeller, in a circular motion

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21
Q

At what speed do spermatazoa move?

A

At about 1-3 mm/minute in humans

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22
Q

Where does hyperactivation of sperm occur?

A

In the oviduct

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23
Q

Compare male and female spermatazoa.

A

Female sperm (X) have a larger head in comparison to the male sperm (Y) and are therefore slower and weaker swimmers.

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24
Q

Where does fertilisation occur typically?

A

At the isthmus-ampulla junction.

(On the diagram, the oocyte comes in from the top, while the sperm comes from the bottom)

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25
Q

What are some hazards to spermatazoa that may stop them from reaching the oocyte at the isthmus-ampulla junction?

A
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26
Q

What are some structural and functional features that spermatazoa must have in order for successful fertilisation to occur?

A
  • Haploid complement of DNA
  • Potential for strong motility
  • Receptors for the zona pellucida and egg
  • Ability to penetrate cumulus and zona pellucida
  • Ability to fuse with the egg
  • Ability to activate an egg
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27
Q

What is capacitation of spermatazoa?

A

The physiological changes spermatozoa must undergo in order to have the ability to penetrate and fertilize an egg.

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28
Q

Describe how the process of capacitation occurs.

A
  • In the epididymis, the sperm become mature due to changes in glycosylation -> This allows them to be able to swim
  • In the female genital tract, capacitation happens -> It relies on secretions from the prostate and seminal glands -> There are further changes in glycosylation, activates an enzyme released in the acrosome reaction (acrosin), increases in motility, and loss of cholesterol from the sperm head
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29
Q

How does the egg direct sperm to it?

A
  • Atrial natriuretic peptide (ANP) may act as a chemoattractant
  • Progesterone + Atrial natriuretic peptide (ANP) from cumulus cells stimulate motility & acrosome reaction
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30
Q

What is capacitation of spermatazoa dependent on?

A

Secretions of seminal vesicles and prostate

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31
Q

How long is sperm stored for in the female and where?

A
  • For 5 days after intercourse
  • Most in the isthmus and some in the cervix
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32
Q

What are some changes that occur during capacitation of spermatazoa?

A
  • Acrosin is activated
  • Motility is increased
  • Loss of cholesterol from the sperm head
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33
Q

What is the cumulus oophorus?

A
  • A cluster of cells (cumulus cells) that surround the oocyte.
  • The innermost layer of these cells is the corona radiata.
  • This layer of cells must be penetrated by spermatozoa in order for fertilization to occur
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34
Q

What attracts the spermatazoa to the oocyte and what causes it to penetrate the cumulus oophorus?

A

Cumulus oophorus (which contains the corona radiata) secretes:

  • Progesterone + Atrial natriuretic peptide (ANP) -> Stimulate motility & acrosome reaction
  • ANP may also attract sperm
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35
Q

What does binding of the spermatazoon head to the zona pellucida trigger?

A
  • Acrosome reaction
  • Whiplash-like motility of the sperm
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36
Q

How many zona pellucida proteins are there in humans and which one do spermatazoa bind to first?

A

4 zona pellucida proteins -> Binds to ZP3 first

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37
Q

What is the acrosomal reaction and what occurs during it?

A

It is the reaction when the spermatazoon binds to the zona pellucida:

  • Binds to the ZP3 (zona pellucida protein 3) using the ZP3 receptor on the plasmalemma
  • Lysins are released from the zona pellucida
  • The ZP2 receptor is revealed -> This allows tighter adhesion to the zona pellucida
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38
Q

Draw the general structure of a spermatazoon.

A
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39
Q

Label this sperm.

A
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40
Q

What is the cortical granule reaction and what occurs during it?

A

It is the reaction that occurs after the spermatazoon fuses with the zona pellucida, in order to prevent polyspermy:

  • Cortical granules fuse with the zona pellucida
  • This causes the zona pellucida to harden so that no more sperm can enter
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41
Q

What induces the second meiotic division in the oocyte?

A

Sperm penetration

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42
Q

Draw how the second meiotic division happens after fertilisation.

A
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43
Q

How does fertilisation trigger the sequence of events that follow it?

A

Fertilisation causes Ca2+ transients in zygote:

  • Wave spreads from point of fertilisation
  • Wave initiated by PLCζ (zeta) which is on the internal membranes of sperm equator
  • A few waves stimulate the cortical granule reaction
  • Repeated waves stimulate the start of development, division etc.
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44
Q

How long does it take for a fertilised oocyte to reach the uterus after fertilisation? What happens after this?

A
  • It takes 5 days
  • On the 5th day, hatching from the zona pellucida occurs
  • After this, implantation can occur
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45
Q

Draw the stages of pre-implantation development of a zygote.

A
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46
Q

What must the conceptus implant before?

A
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47
Q

In what part of the Fallopian tube does fertilisation usually occur?

A

Ampulla

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48
Q

What are the different stages of the menstrual cycle and stages of the uterus lining? How do these compare?

A
  • Prior to ovulation, there is the follicular phase -> This corresponds to the proliferative phase of the uterus
  • After ovulation, there is the luteal phase -> This corresponds to the secretory phase of the uterus
  • Finally, there is menstruation
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49
Q

What are the 3 phases of the uterine cycle?

A
  • Proliferative
  • Secretory
  • Menstrual
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50
Q

What hormones control the proliferative and secretory phases of the uterine cycle?

A
  • Proliferative -> Estrogen
  • Secretory -> Progesterone
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51
Q

Describe and explain tbe different phases of the uterine cycle.

A

Proliferative phase:

  • Endometrium is exposed to oestrogen as a result of FSH and LH stimulating its production
  • Oestrogen stimulates repair and growth of the functional endometrial layer allowing recovery from the recent menstruation.

Secretory phase:

  • Occurs after ovulation
  • Driven by progesterone from the corpus luteum.
  • Endometrial glands secrete various substances that will facilitate implantation

Menstrual phase:

  • At the end of the luteal phase, the corpus luteum degenerates (if no implantation occurs), which results in decreased progesterone production.
  • This causes the spiral arteries in the functional endometrium to contract.
  • Endometrium is shed and exits through the vagina as menstruation.
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52
Q

What is an example of the oestrogens involved in the uterine cycle?

A

Estradiol

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53
Q

Which days of the menstrual cycle does each part of the uterine cycle occur in?

A
  • Menstruation -> Days 0 to 7
  • Proliferative -> Days 7 to 14
  • Secretory -> Days 14 to 28
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54
Q

What are the effects of estradiol, progesterone and prostaglandins on the uterine cycle?

A
  • Estradiol -> Promotes proliferation and apiral artery development
  • Progesterone -> Glandular secretion
  • Prostaglandins -> Arterial spasm and uterine muscle spasm
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55
Q

What is another name for menstruation?

A

Menses

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56
Q

What are the two zones of the uterus lining?

A
  • Basal zone -> Not sloughed during menstruation
  • Functional zone -> Sloughed during menstruation and then regenerates
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57
Q

Draw the changes in the uterine vasculature during the uterine cycle.

A
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58
Q

Describe what causes menstruation to occur.

A
  • At the end of the luteal phase, the corpus luteum degenerates (if no implantation occurs).
  • The loss of the corpus luteum results in decreased progesterone production.
  • The decreasing levels of progesterone cause the spiral arteries in the functional endometrium to contract.
  • The loss of blood supply causes the functional endometrium to become ischaemic and necrotic.
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59
Q

In general, how does the uterus control when implantation can occur?

A

Ovulation and receptivity of the uterus are co-ordinated

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60
Q

Following successful implantation, how must degeneration of the uterine lining be stopped?

A

By preventing the degradation of the corpus luteum.

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61
Q

What is the decidual reaction?

A

It is part of the implantation process:

  • The stroma (connective tissue) in the endometrium responds to binding of the blastocyst as well as progesterone from the corpus luteum
  • Stroma cells differentiate into decidual cells (secretory cells) -> These secrete lots of glycogen and mucus for immunological protection
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62
Q

What does the trophoblast do during implantation?

A
  • At one pole of the trophoblast, the syncytiotrophoblast and cytotrophoblast form from trophoblast cells
  • Syncytiotrophoblast cells are the cells that initially invade the endometrium, drawing the blastocyst into the uterine wall -> Ruptures capillaries so creating an interface between maternal blood and embryonic fluid for passive transfer. Also secretes a lot of hCG to maintain corpus luteum
  • Cytotrophoblast cells line the inside of the syncytiotrophoblast and will eventually form the foetal portion of the placenta
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63
Q

What things trigger the decidual reaction?

A
  • Progesterone from the corpus luteum
  • hCG from the synctiotrophoblast assists with this by maintaining the corpus luteum
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64
Q

What are the two states of the uterine epithelium?

A
  • Non-Receptive -> During times when implantation is not favourable, there are mucins that prevent the embryo from implanting
  • Receptive -> During times when implantation is favourable, there are no mucins so the embryo can freely bind

These states are co-ordinated with ovulation, so that ectopic implantation does not occur.

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65
Q

Describe the process of implantation and how it can occur.

A
  • Blastocyst hatches from zona pellucida and adheres to endometrium lining if it is in the receptive state (when there are no mucins on it)
  • Trophoblast (trophoectoderm) begins to grow into the uterine wall, forming a syncytiotrophoblast that penetrates epithelium, then basal lamina, and then starts pulling the blastocyst into the uterine wall
  • This triggers decidual reaction: endometrial stroma (connective tissue) responds to blastocyst AND progesterone from the corpus luteum and turns into decidual cells (secretory cells) -> These secrete lots of glycogen and mucus for immunological protection
  • The uterine wall becomes more vascularised and oedematous (swollen)
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66
Q

What is an important gene in the decidual reaction?

A

HOXa10 (9-13) expression in stroma + endometrial glands

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67
Q

What are some common sites for ectopic pregnancy?

A
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68
Q

Which hormone concentration increases after implantation?

A

hCG (human chorionic gonadotrophin)

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69
Q

Label this.

A
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70
Q

What secretes hCG?

A

Syncytiotrophoblast cells

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71
Q

What is the function of hCG?

A

To maintain the corpus luteum so that there is continued production of progesterone.

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72
Q

Describe how hCG blocks the uterine cycle.

A
  • hCG is secreted by syncytiotrophoblast cells upon implantation
  • This hCG maintains the corpus luteum, so that it can keep producing progesterone
  • Progesterone means that glandular secretion in the uterine glands continues and the uterine lining is maintained
  • This is a positive feedback loop
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73
Q

What receptors does hCG act on?

A
  • LH receptors in the corpus luteum
  • These are Gs-coupled (via cAMP)
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74
Q

What is an important variant of hCG?

A

hCG-h

This is hyperglycosylated hCG.

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75
Q

How does the percentage of hCG that is hCG-h change throughout pregnancy?

A

It decreases over pregnancy.

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76
Q

What is the clinical relevance of hCG-H? [EXTRA]

A

It is very high at the very early stages of pregnancy (3-5 weeks), so it is a good diagnostic of preganancy at early stages.

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77
Q

What are hCG and hCG-H produced by?

A
  • hCG -> Syncytiotrophoblast
  • hCG-H -> Cytotrophoblast
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78
Q

In pregancies with Down syndrome, how is hCG affected?

A
  • In general, total hCG levels in the serum are about doubled
  • There are also high levels of hCG-H (heavily glycosylated hCG) may be implicated in high rates of spontaneous abortion
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79
Q

Summarise the production of different hormones in each of the 3 trimesters of pregnancy.

A
  • First trimester
    • Very dominated by hCG
    • This is produced largely by the corpus luteum
  • Second and third trimester
    • All three hormones (hCG, progesterone and estrogen produced)
    • This is because the placenta becomes more dominant
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80
Q

In plain terms, what is the function of the placenta?

A

It is the interface between the mother and the fetus that secretes the hormones and growth factors into the mother.

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81
Q

How long is pregnancy?

A

40 weeks from the last menstrual period

(38 weeks from fertilisation)

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82
Q

What are the 9 months of pregnancy frequently divided into?

A

Trimesters (3 month periods)

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83
Q

What are the main phases of pregnancy and when does each change occur?

A
  • <10 days = Pre-implantation conceptus
  • 3-8 weeks = Embryo
  • >8 weeks = Fetus
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84
Q

What is the earliest that a pre-term baby survive from?

A

From 22 weeks (with high quality care)

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85
Q

What are the different stages of nutrition of the fetus?

[EXTRA?]

A

In order, the fetus obtains nutrition from:

  1. The small amount of yolk proteins in the oocyte
  2. Secretions of the uterus and oviduct (before implantation)
  3. Digestion of the uterine decidua (endometrium that is specialised for implantation)
  4. Maternal blood (via placenta)
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86
Q

What are some requirements of pregnancy?

[EXTRA?]

A
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87
Q

What are some functions of the placenta?

A
  • Attachment of embryo to the uterus
  • Invasion and digestion of endometrial tissue
  • Transfer of:
    • Respiratory gases
    • Nutrients
    • Waste products
  • Synthesis of hormones:
    • To maintain pregnancy
    • To control fetal growth
    • To control maternal metabolism
    • To prepare for partuition
    • To prepare for lactation
  • Immunological protection of the fetus (i.e. barrier to stop the mother attacking the fetus)
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88
Q

How much weight is gained during pregnancy?

[EXTRA?]

A

Around 12.5kg, with most gained during the second trimester. This is due to:

  • Growth of the conceptus and placenta
  • Englargement of maternal organs
  • Maternal storage of fat
  • Increase in maternal blood and interstitial fluid
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89
Q

What are the 4 main fetal membranes and what does each form?

A
  • Chorion (Trophoblast plus extra-embryonic mesoderm) -> This forms the chorionic vesicle, including the placenta
  • Allantois -> Endoderm lining, mesodermal covering, Forms bladder and urachus
  • Yolk sac -> Site of haematopoiesis in early pregnancy; development of gut; primordial germ cells
  • Amnion -> Main source of amniotic fluid in early pregnancy (later from urine, lungs, skin).
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90
Q

Summarise the general structure of the placenta.

[IMPORTANT]

A

The placenta is essentially the interface between the maternal blood and the fetal blood:

  • Fetal vessels pass via the umbilical cord and form branches within villi
  • These villi are surrounded by intervillous spaces, which are supplied by the maternal blood
  • Thus, the fetal blood and maternal blood are completely separated, so the surface of the villi is required for exchange and immunological protection
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91
Q

What are placental villi?

[IMPORTANT]

A

Placental (a.k.a. chorionic) villi are villi that sprout from the chorion to provide maximal contact area with maternal blood.

92
Q

Where on the uterus does the placenta usually form?

A

On the upper posterior aspect of the uterine wall.

93
Q

Give some clinical relevance for placenta development.

[EXTRA]

A

Placenta previa:

  • When the placenta partially or totally covers the mother’s cervix (the outlet for the uterus)
  • Can cause severe bleeding during pregnancy and delivery.
  • If you have placenta previa, you might bleed throughout your pregnancy and during your delivery.
94
Q

Add flashcards from the placenta practical, if necessary.

A

Do it.

95
Q

Describe the development of the placenta.

[IMPORTANT]

A
  • Begins with implantation (see earlier flashcards), including attachment, penetration and decidual reaction
  • The syncytiotrophoblast cells are fused, then maternal blood fills the lacunae in the
  • The cytotrophoblastic cells begin to develop and the layer buldges out, forming primary villi -> These eventually develop into tertiary villi
  • Thus, the syncytiotrophoblast and crytotrophoblast form the outer lining of placental villi, which are surrounded by maternal blood
96
Q

Describe the different stages of placental villi development.

A

This is driven by the buldging of the cytotrophoblast.

97
Q

Draw the cross-section of a primary, secondary and tertiary villus.

A
98
Q

Describe the maturation of a tertiary villus in the placenta.

A
  • The trophoblast attaches to the decidua (maternal) tissue, forming an anchoring villus
  • The villus undergoes branching to increase SA
  • The cytotrophoblast becomes incomplete and the syncytiotrophoblast thins to reduce diffusion distance
  • Capillaries move to edge of the villus, so that they’re essentially apposed to the cytotrophoblast
99
Q

Describe the adaptations of the capillaries in placental villi.

A

The capillaries form a convoluted knot, with a terminal dilation -> This slows down the blood and allows for increased exchange.

100
Q

Draw a summary of the fetal-maternal interface at the placenta.

A
101
Q

In summary, what tissue is the placenta derived from?

[IMPORTANT]

A

Trophoblast

102
Q

How does the fetus avoid immunological rejection by the mother?

[EXTRA]

A
  • Class 1 MHC antigens of paternal origin are not expressed on the membrane of trophoblast cells in contact with the maternal blood. Instead, the trophoblast expresses a specific HLA-G which interacts with maternal cells including uterine natural killer (uNK) cells to prevent rejection.
  • Trophoblast secretes molecules which exert some inhibition of the immune response (hCG and progesterone)
  • ITrophoblast produces an enzyme (IDO indoleamine 2,3-dioxygenase) that degrades tryptophan that is necessary for T-cell activation. If IDO is inhibited, allogeneic pregnancies are rejected rapidly by a T-cell mechanism
  • The uterine T cell population is shifted from Th1 (cell-mediated immunity) type to Th2 (antibody-mediated).
103
Q

Describe placental blood flow.

A

Fetal circulation:

  • Umbilical arteries (from the internal iliac) take blood to the placenta, where it picks up oxygen
  • Oxygenated blood returns to the fetus’ liver via the umbilical vein and from there to the right atrium

Mother’s circulation:

  • Uterine arteries (branches of the internal iliac) take blood to the uterus
  • Spiral arteries supply the intervillous spaces
  • Uterine veins drain the uterus

Uterine contractions allow blood to spurt in from the arteries, but close venous outflow, causing the low pressure in the intervillous space to rise. When the myometrium relaxes, veins reopen and intervillous pressure falls.

104
Q

The placenta grows throughout pregnancy (to around 1kg at term). However, the fetus grows relatively faster and so placental efficiency must increase to supply the fetus. What are some processes that allow this to happen?

A
  • Branching of villi and formation of a brush border on the syncytiotrophoblast
  • Decrease in diameter of villi from 140-200µm in early pregnancy to 40µm in late pregnancy
  • Thinning of the placental ‘barrier’ which consists of :
    • Endothelium and basal lamina of fetal capillary
    • Stroma of villus (not present in some areas of the late placenta)
    • Basal lamina of the cytotrophoblast
    • Syncytiotrophoblast
105
Q

What are some important hormones produced by the placenta?

[IMPORTANT]

A

Peptide and protein hormones:

  • hCG (human chorionic gonadotrophin)
  • hPL (h placental lactogen)
  • Relaxin

Steroid hormones:

  • Estrogens -> Esterone, Esteriol, Estradiol
  • Progesterone
106
Q

What part of the placenta produces peptide and protein hormones?

A

Syncytiotrophoblast cells

107
Q

What is the importance of hCG and where is it produced?

A
  • Produced in the syncytiotrophoblast
  • It signals the presence of a fertilised egg, maintaining the corpus luteum and stimulating its production of progesterone
  • Progesterone is important in stopping the shedding of the endometrium and preventing contractions of the myometrium
  • This progesterone from the corpus luteum is important for the first 6-8 weeks of pregnancy, until the placenta is established and becomes the main source of progesterone

(Thus, hCG levels drop around 10 weeks, but continue to be produced)

108
Q

What is the importance of hPL and where is it produced?

A
  • Produced in the syncytiotrophoblast of the placenta
  • It rises in concentration in the maternal circulation between 8 and 35 weeks
  • Has weak GH and PRL activity -> Therefore, increases somatic growth in the mother (e.g. breast growth) and increases milk secretion
  • Also has metabolic effects -> Increases nutrient concentrations in the blood, for better supply to the fetus (e.g. increases maternal lipid breakdown)
109
Q

What does hPL stand for?

[IMPORTANT]

A

Human placental lactogen

110
Q

What is the importance of relaxin and where is it produced?

A
  • Produced in the syncytiotrophoblast
  • Relaxes pelvic joints and ligaments and softens the cervix in preparation for partuition
111
Q

Summarise the effects of hPL.

A
  • hPL essentially has diabetogenic effects, increasing concentrations of sugar and fatty acids in the blood for the fetus.
  • This can lead to gestational diabetes
112
Q

Describe the changes in concentration of the different steroids involved in pregnancy and where they are produced.

A
  • At first, after implantation happens, hCG from the placenta (syncytiotrophoblast) maintains the corpus luteum -> Thus, the ovaries produce most of the progesterone at first
  • By the second trimester, the corpus luteum has degraded and the placenta has developed -> More progesterone and estrogen are produced from the placenta, as hCG decreases
  • In the third trimester, there is very little hCG, while progesterone and estrogen peak
113
Q

Describe the concept of the maternal-placental-fetal unit.

[IMPORTANT]

A
  • The mother requires progesterone and estrogens for maintaining pregnancy
  • The mother provides the LDL cholesterol required for synthesis of these, but she lacks the enzymes to produce them, so she cannot synthesise them along
  • Therefore, a maternal-placental-fetal unit is required for synthesis -> The placenta and fetal adrenal/liver provide the enzymes for progesterone and estrogen synthesis

(Details of enzymes are not core)

114
Q

Describe the changes in the fetal adrenal glands with age.

A

The fetal zone of the adrenal gland develops to a large size unit birth, then it regresses again. It is involved in the production of weak androgens, which can then be converted to weak estrogens.

115
Q

What are some changes in the maternal hormones (apart from progesterone and estrogens) during pregnancy?

A
  • Pituitary, thyroid and adrenal glands increase in size:
    • Increased cortisol production
    • Increased T3 and T4
  • Parathyroid glands increase in size to control calcium homeostasis
116
Q

Summarise the functions of estrogens during pregnancy.

[IMPORTANT]

A
  • Growth of uterus and preparation of the uterus for partuition
  • Growth of breasts (along with progesterone)
  • Increase in blood volume -> Via sodium retention, reduced water excretion, and vasodilation
  • Connective tissue effects -> Makes the body more pliable
117
Q

Summarise the functions of progesterone during pregnancy.

[IMPORTANT]

A
  • Nausea + Constipation
  • Reduces bladder and ureter tone (increased micturition)
  • Reduces distolic pressure and causes vasodilation
  • Maintains the uterus in a quiescent state (so that the fetus is not lost)
  • Relaxes cardiac sphincter -> Leads to heart burn
  • Alters taste and appetite
118
Q

Summarise the different functions of placental hormones.

A
  • Signalling pregnancy (e.g. hCG preserves the corpus luteum)
  • Maintaining pregnancy: (e.g. Progesterone to maintain uterine quiescence, Estradiol for uterine growth)
  • Converting maternal metabolism to the pregnant state (e.g. hPL increases maternal lipid breakdown to provide the fetus with energy
  • Preparing for & initiation of parturition (e.g. Estradiol induces production of contraction-associated proteins by the myometrium, stimulates production of oxytocin receptors; and increases the excitability of the myometrium
  • Stimulating myometrial contractions and modifying the cervix for parturition (e.g. Placental prostaglandins)
  • Preparing for lactation (e.g. Estradiol stimulates development of the duct system of the mammary gland; Progesterone causes development of the alveoli, hPL has a lactogenic action, developing the secretory potential of the breast alveoli -> However, during pregnancy, production of milk is suppressed by the high levels of progesterone and estradiol)
119
Q

Describe the different transport methods across the placenta.

A
  • Simple diffusion -> Small molecules, ions, unconjugated non-polar molecules
  • Facilitated diffusion -> Glucose, Some fatty acids
  • Secondary active transport -> Amino acids
  • Carrier mechanisms involving specific receptors on the syncytiotrophoblast brush border:
    • For large molecules: e.g. immunoglobulins (may involve receptor-mediated endocytosis)
    • To concentrate substances in the fetal circulation: e.g. Fe, Ca, Cu, glucose, vitamin B12, folate, riboflavin, vitamin C, amino acids, some hormones

(Note: Most proteins are not transported but are synthesized from amino acids by the placenta or fetus)

120
Q

Describe how estradiol is produced in the placenta.

A
  • Although the placenta can produce progesterone from cholesterol, it does not have the key enzymes necessary to produce estradiol from cholesterol
  • Instead it uses the weak androgen dehydroepiandrosterone (DHEA) which is synthesized in the fetal adrenal gland.
  • This is converted by the placenta in part to estradiol.
  • However, it is also 1,6-hydroxylated by the liver, to yield a steroid which is converted by the placenta to estriol, a weak oestrogen which is the main oestrogen secreted in the urine. Some estrone is also formed.
121
Q

Describe how placental function changes throughout pregnancy.

A
  • It increases throughout pregnancy, then falls near term.
  • This means that pregnancies that go over term are at much higher risk of placental insufficiency
122
Q

What is toxaemia of pregnancy?

[EXTRA?]

A
  • Some mothers, in late pregnancy, develop very high ABP which causes renal damage (albumin appears in the urine) and oedema.
  • It is most common in first pregnancies in lower socio-economic groups. It is also most likely if there is a large placental mass as with multiple fetuses or a ‘hydatidiform mole’ (a tumour of trophoblast with no fetus present).
  • The blood pressure can rise so high and so fast that, on occasion, the mother may suffer convulsions or even death.
  • The cause is still unclear, but an abnormality of placental spiral arteries, which fail to dilate normally, is thought to restrict uteroplacental blood flow and causes placental ischaemia.
123
Q

Give some important examples of prenatal diagnosis.

[IMPORTANT]

A
  • Ultrasound and MRI -> Used to examine the fetus morphologically
  • Amniocentesis -> Sampling of amniotic fluid at 16-20 weeks pregnancy, followed by culture of fetal cells are cultured and karyotyped to check for chromosomal abnormalities, single gene disorders, and signs of spina bifida.
  • Chorionic villus sampling -> Used for diagnosis of:
    • Chromosomal abnormalities
    • Single gene disorders
    • Transplacental virus infection (eg. Rubella)
    • Fetal blood grouping (eg. Rh).
124
Q

What are some examples of placental abnormalities?

[EXTRA]

A
  • Abnormal implantation site -> ‘Placenta praevia’ is where the placenta covers cervical outlet (risk of fatal haemorrhage)
  • Abnormal shape: peripheral attachment of cord
  • Hydatidiform mole: non-invasive tumour of trophoblast
  • Choriocarcinoma: invasive malignant tumour of trophoblast 4
  • Placental insufficiency: functional insufficiency leading to fetal malnutrition; smoking causing uterine vasoconstriction.
125
Q

Explain the concept of fetal programming.

[IMPORTANT]

A
  • The concept is that a person’s health can be largely affected by the conditions they face when they are still a fetus
  • For example, risk of Type 2 diabetes and hypertension is affected by fetal conditions.
  • Those born underweight have a reduced life expectancy. This is in part due to long-term programming of the glucocorticoid stress axis, which becomes chronically overactive.
126
Q

Describe how the uterus remains relatively quiescent until the time of partuition.

A
  • The uterus grows at the same rate as the conceptus, so there is little stretching until the very end of pregnancy.
  • Progesterone is essential for uterine quiescence:
    • Acts on the muscle cells directly
    • Acts on chorionic enzymes (which prevent the accumulation of activating prostaglandins from reaching the myometrium)
    • Reduces the numbers of oxytocin receptors within the uterine muscle.
  • The prostaglandin produced before term is largely prostaglandin I which relaxes smooth muscle

On the other hand, estrogen (estradiol) is the main hormone causing growth of the uterine muscle. It also stimulates development of contraction-associated proteins and oxytocin receptors to prepare the smooth muscle for parturition.

127
Q

Remember to add flashcards on the morphology of the placenta, uterus and umbilical cord.

A

Do it -> Use practical in week 4 of Michaelmas.

128
Q

Summarise the function of the cytotrophoblast and syncytiotrophoblast.

A
  • Syncytiotrophoblast cells:
    • Initially invade the endometrium, drawing the blastocyst into the uterine wall and rupturing capillaries so that there is an interface between maternal blood and embryonic fluid for passive transfer.
    • Also secretes a lot of hCG to maintain corpus luteum.
  • Cytotrophoblast cells:
    • Line the inside of the syncytiotrophoblast and buldge out to form placental villi for transfer
129
Q

Summarise the function of the intervillous spaces in the placenta.

A

They are the spaces between the chorionic (placental) villi, which fill with maternal blood and allow for exchange.

130
Q

Summarise the function of the endometrium.

A

It is the inner lining of the uterus, where the blastocyst implants.

131
Q

Summarise the function of the amnion and chorion.

A
  • Amnion -> A membrane that covers the embryo when it is first formed. It contains the amniotic fluid, used for protection.
  • Chorion -> The outermost fetal membrane. It contains chorionic fluid, usd for protection. Chorionic villi (a.k.a. placental villi) are used for exchange with the mother.
132
Q

What is the decidua basalis? Summarise the function.

A
  • The term given to the uterine endometrium at the site of implantation where signaling transforms the uterine stromal cells (fibroblast-like) into decidual cells.
  • Functions:
    • Exchanges of nutrition, gas, and waste with the gestation
    • Protects the pregnancy from the maternal immune system
    • Hormone production
133
Q

What are cotyledons?

A
  • They are divisions of the placenta, separated by septa, only visible from the maternal side.
  • Each cotyledon consists of a main stem of a chorionic villus as well as its branches and subbranches.
134
Q

Summarise the function of uterine glands.

A
  • Uterine glands tubular glands of the endometrium
  • They secrete [INSERT HORMONES]
135
Q

Draw a cross-section of the umbilical cord.

A
136
Q

Summarise the function of Wharton’s jelly.

A
  • A gelatinous substance within the umbilical cord, largely made up of mucopolysaccharides (hyaluronic acid and chondroitin sulfate).
  • It acts as a mucous connective tissue, important in the protection of the vessels in the umbilical cord.
137
Q

Name the different hormones involved in partuition.

A
  • Progesterone + Relaxin -> Decrease contractility
  • Estrogens -> Increase contractility
  • Corticotrophin-releasing hormone (CRH)
  • Adrenocorticotropic hormone (ACTH)
  • Prostaglandins -> Increase contractility
  • Oxytocin -> Used to induce labour
  • Prolactin (PRL)
138
Q

Summarise how the main steroid hormones involved in partuition are synthesised.

A
  • They are all derived from cholesterol, which is provided by the mother
  • The placenta converts the cholesterol to progesterone (via pregnenolone) -> Decreases contractility
  • The fetus converts cholesterol to DHEA-S and 16-OH DHEA-S, which are used to synthesis weak estrogens -> Increase contractility

This makes sense because as the fetus grows, the uterus needs to increase contractility for childbirth.

139
Q

What are some requirements for partuition to occur?

A
  • Fetus must be fullyt mature, with developed lungs, gut and liver -> This is dependent on cortisol
  • Uterus must begin synchronised contraction -> Dependent on intracellular calcium increases, mediated via prostaglandin and oxytocin action. Synchronicity is due to gap junctions and estrogens.
  • Relaxant effects of progesterone must be stopped -> Dependent on change in the progesterone receptors
  • Cervix must allow passage -> Prostaglandins cause collagen breakdown
140
Q

What prepares for and signals parturition in humans?

[IMPORTANT]

A
  • Fetal hypothalamus produces corticotrophin-releasing hormone (CRH):
    • This leads to increased ACTH secretion from the fetal pituitary
    • This in turn leads to increased fetal adrenal production of cortisol and DHEA-S
    • The cortisol leads to maturation of the lungs, liver and gut, as well as stimulating release of CRH from the placenta -> This acts on the fetal pituitary again, completing the feedback loop
    • Maternal cortisol also stimulates CRH production in the placenta
    • The DHEA-S is converted to estrogens in the placenta, ready for action in the uterus
  • There is remodelling of the uterus, driven by irritation of the cervix, which leads to increased contractility:
    • Although estrogens and progesterone in plasma changes little at term, their intracellular receptors on the uterus change. This inhibits progesterone action and favours estrogen action, which has 2 effects:
      1. Leads to increased prostaglandin action via:
        • Increased synthesis in the uterus
        • Decreased breakdown
        • Prostaglandin receptor activation
          • Prostaglandins stimulate contraction by favouring a rise of calcium levels in the uterine smooth muscle cells. They also soften the uterine cervix.
      2. Leads to an increase in oxytocin receptors in the uterus
        • Oxytocin leads to formation of gap junctions within the uterus, for synchronised contractions.

It is worth noting that the ultimate kickstart for labour to begin is irritation of the cervix and stretch of the uterus (leading to the Ferguson reflex).

141
Q

How do maternal cortisol levels change throughout pregnancy?

A

They spike just before parturition.

142
Q

What are the roles of cortisol in parturition?

A

It is important in the fetus:

  • Stimulates maturation of the lungs, liver and gut
  • Stimulates the release of CRH from the placenta -> CRH is important as an initiator of many downstream effects involved in parturition
143
Q

What hormone levels can be used to predict when parturition will happen?

A
  • Placental CRH levels rise toward term and CRH levels at 16-20 weeks roughly predict when a woman will give birth.
  • High CRH levels are associated with premature labour; low levels usually indicated delayed parturition.
144
Q

Describe the physical changes in the uterus that occur prior to parturition.

A
145
Q

What is the name for the process that enables continued parturition?

[IMPORTANT]

A

Ferguson reflex

146
Q

Describe how parturition is maintained.

A
  • Parturition is properly initiated by irritation of the cervix and stretch of the uterus
  • Sensory fibres convey information about stretch via the spinal cord to the hypothalamus
  • This stimulates the production (in the hypothalamus) and release (in the posterior pituitary) of oxytocin
  • Oxytocin binds to oxytocin receptors on the uterus that have been induced by estrogen in preparation for pregnancy
  • This leads to uterine contraction and increased prostaglandin secretion
  • Prostaglandins also increase uterine contraction, but also stimulate changes in progesterone receptor ratios, decreasing the inhibitory effect of progesterone
  • Decreased activity of progesterone leads to reciprocal increases in prostaglandins and increase uterine contractions
  • This completes the positive feedback loop and also stimulates increased stretch of the uterine wall (which reciprocally induces contractions)
147
Q

Summarise the Ferguson reflex.

[IMPORTANT]

A

It is worth noting that the oxytocin induces uterine contraction in a variety of ways, as shown in the previous slide.

148
Q

Summarise the concepts of preparation and initiation of parturition.

[IMPORTANT]

A
  • Estrogens (and decreased progesterone action) prepare the uterus for contraction by increasing contractility and inducing oxytocin receptors on the uterus, as well as increasing prostaglandins that loosen the cervix
  • CRH appears to be the signal of readiness for parturition
  • Stretch of the cervix and uterus appear to be what ultimately triggers parturition
  • Parturition itself is sustained by the Ferguson reflex, involving oxytocin and prostaglandins that stimulate uterine contraction
149
Q

Summarise the action of prostaglandins in parturition.

A
  • Early in pregnancy, prostaglandins that cause smooth muscle relaxation predominate
  • During parturition, prostaglandins that stimulate contraction are induced by oxytocin acting on the uterus
  • It leads to uterine contraction and changes in the progesterone receptor ratios (so that progesterone action is decreased)
150
Q

Summarise the action of oxytocin in parturition.

A
  • Its action is induced by:
    • Increased production triggered by uterine contraction
    • Increased receptor expression on the uterus
  • It leads to uterine contraction and prostaglandin secretion by the uterus
151
Q

Summarise the synthesis and breakdown of prostaglandins.

A
152
Q

Which prostaglandins are important in inducing uterine contractions?

A

PGF and PGE

153
Q

Give some clinical relevance of prostaglandins.

[EXTRA]

A

PGF and PGE induce uterine contractions, and are therefore used in terminations of pregnancy.

154
Q

Draw the cascade of events caused by estrogen in uterine cells.

A
  1. Estrogen binds to its receptor intracellularly
  2. This leads to changes in transcription and increased production of oxytocin receptors and PLA2
  3. Oxytocin receptors are inserted into the cell membrane
  4. Oxytocin receptors and PLA2 lead to increased prostaglandin synthesis
  5. Prostaglandins and oxytocin receptors lead to an increase in intracellular calcium
  6. This stimulates muscle contraction
155
Q

Describe how inflammation changes during labour.

A

It goes from an anti-inflammatory to a pro-inflammatory state.

156
Q

Summarise the stages of labour.

A
157
Q

What drug can be used to induce the delivery of the placenta after the fetus is delivered?

[EXTRA]

A

Ergometrine -> A smooth muscle stimulant

158
Q

What are some important preparations for post-natal life that must occur in the fetus before birth?

A

Most of these are induced by the secretion of glucocorticoids which increase markedly towards term. They include:

  • Production of surfactant in the lungs -> To allow lung expansion when air is first breathed
  • Changes to gut and liver enzymes to allow the fetus to metabolise its post-natal milk diet
159
Q

What are the dangers of a pre-term and post-term birth?

A
  • Preterm -> The fetus is not yet prepared for extrauterine life
  • Post-term -> Continued fetal growth and placental insufficiency pose problems for both delivery and fetal nutrition
160
Q

Describe the location and circulation of the mammary glands.

A
  • Found in the subcutaneous fat
  • Develops along axillary-to-groin line, but only remains in the breast area. Tail of Spence is part of the breat tissue that extends into the armpit.
  • Blood supplied/drained by axillary and internal thoracic vessels
  • Lymphatics drain to axillary nodes (mostly) and internal thoracic nodes (more minor)
161
Q

What are some requirements for lactation?

A
162
Q

Describe the development of the breasts during pregnancy.

A
  • Before pregnancy, there are few ducts and alveoli
  • Estrogen causes the duct system to develop
  • Progesterone causes the alveoli to develop
  • Human placental lactogen (hPL) has lactogenic action, developing the secretory potential of the mammary glands
  • Estrogen and progesterone suppress milk production during pregnancy
  • After birth, prolactin stimulates lactation and further breast growth
  • After weaning, the breast regresses
163
Q

Describe the structure of the mammary gland system.

A

There is a tubulo-alveolar with 12-20 galactopoetic (milk-producing) lobules each emptying into a common lactiferous duct which opens onto the nipple.

164
Q

Summarise the different hormones involved in mammary gland development during pregnancy.

A

Adrenal steroids are also important in the development of the mammary glands.

165
Q

What does the maintenance of lactation depend on?

A

Suckling

166
Q

What hormones are involved in milk secretion and ejection after birth?

A
  • Prolactin -> Milk secretion
  • Oxytocin -> Milk ejection
167
Q

Describe how milk production and ejection occurs in the mammary glands.

A

Milk production:

  • Produced by mammary epithelial cells that are on top of myo-epithelial cells and a capillary -> Stimulated by prolactin
  • Amino acids, glucose and galactose are taken up into the epithelial cells from the capillary, while water, leukocytes and ions pass via the paracellular route (and also transcellular route for water and ions)
  • Within the epithelial cells, proteins (e.g. casein and lactalbumin) are synthesised in the RER, then secreted in vesicles
  • Fats are produced in the SER, then secreted in vesicles
  • Immunoglobulins are secreted into the milk via transcytosis (vesicular transport through the cell)

Milk ejection:

  • Due to contraction of myo-epithelial cells
  • Stimulated by oxytocin
168
Q

Where is prolactin produced, what does it act on and how are its effects modulated?

A
  • It is produced by the anterior pituitary
  • It acts on the PRL receptors on the mammary glands, stimulating lactation
  • PRL levels rise up to 20-fold during pregnancy, but its action is inhibited by the high levels of estrogen and progesterone
  • It secretion is also inhibited by dopamine
169
Q

Give some clincal relevance relating to the control of lactation.

[EXTRA]

A

Dopamine inhibits PRL release, so dopamine agonists can be uesd to inhibit lactation.

170
Q

What is colostrum?

A
  • It is the initial secretion from the mammary glands after birth, later giving way to milk.
  • It is dense in carbohydrates, proteins and immunoglobulins for passive immunity
171
Q

Summarise the milk ejection reflex.

[IMPORTANT]

A
172
Q

Summarise the control of lactation.

A
173
Q

What are some important hormones for the mother during lactation?

A
  • Prolactin -> Natural contraceptive that decreases fertility
  • Parathyroid hormone -> Mobilises maternal calcium for the baby
  • Calcitonin -> Protects against excessive calcium loss
174
Q

How does prolactin reduce fertility?

[IMPORTANT]

A
  • Prolactin alters GnRH output from the hypothalamus, reducing GnRH pulses.
  • In this way, lactation suppresses ovulation and so prevents a further pregnancy which would create excessive metabolic demand on the mother.
175
Q

How is prolactin release controlled?

A
  • Suckling causes reflex neural input to the hypothalamus
  • Aside from increasing oxytocin release, this leads to decreased dopamine secretion
  • Decreased dopamine secretion leads to decreased inhibition of prolactin release from the anterior pituitary gland
176
Q

What is galactorrhea?

[IMPORTANT]

A
  • The production of milk that is unrelated to childbirth
  • This can be caused by:
    • Tumours of the PRL-releasing cells in the anterior pituitary
    • Antipsychotic drugs (e.g. haloperidol) used to treat schizophrenia -> These may suppress dopamine-mediated inhibition of PRL release
  • It can be treated using radiation therapy for cancers or dopamine receptor agonists
177
Q

Why is fertility/infertility an important topic?

A
  • Infertility is an issue that affects many men and women
  • Controlling fertility is also important due to the rapidly growing population
178
Q

What are some sites in men and women that can be targeted in changing fertility and infertility?

A
179
Q

Give a summary of the way we contraceptives can target different sites in the female.

A
180
Q

What are some routes for delivery of female hormonal contraception?

A
  • Implantation
  • Injection
  • Oral
  • Patches
  • Uterus/vagina
181
Q

How effective are hormonal contraceptive methods in females?

A

Over 99%

182
Q

Describe how hormonal contraceptive methods work in females.

A
  • Include injected or oral steroids that inhibit FSH & LH by enhancing negative feedback on the brain and pituitary
  • There are a few varieties of oral contraceptive pill.
  • These tend to include synthetic estrogens and progestagens
183
Q

Compare the different types of hormonal contraceptive for females.

A
184
Q

Is light bleeding when taking the pill normal menstruation?

A

No, it is the response to withdrawal of the pill.

185
Q

How does emergency contraception work? (i.e. the morning after pill)

A

Prevent implantation by giving a high dose of a synthetic progesterone receptor modulator (levonorgestrel) (or previously, a synthetic estrogen) within 72 hours of unprotected intercourse:

  • High dose estrogen -> Thought to act by speeding movement of the conceptus through the fallopian tube to reach an unprepared uterus – it has now been superceded.
  • Progesterone receptor modulator levonorgestrel -> Thought to act either (a) by preventing ovulation and/or (b) by thickening cervical mucus to reduce/prevent sperm entry. Doesn’t seem to act on the endometrium to prevent implantation.
186
Q

How effective is emergency contraception?

A

Around 95%

187
Q

What are some examples of contraception that target the uterus?

A
  • Intrauterine devices (IUDs) -> Typically copper, which affects the uterine environment and prevents implantation
  • Intrauterine systems (IUSs) -> Carries a progesterone receptor modulator

Can use IUSs as a ‘morning-after’ device containing progesterone receptor modulator. Can also use progesterone receptor antagonist (RU486) to block implantation, and prostaglandin to evacuate uterus.

188
Q

What are some examples of contraception that target the Fallopian tubes?

A
189
Q

What are some examples of contraception that target the vagina?

A
190
Q

What are some unwanted side effects of hormonal contraception and how can they be overcome?

A
191
Q

Give a summary of the way different contraceptives can target different sites in the male.

A
192
Q

Why are there no hormonal cotnraceptive methods in men?

A

All possible methods decrease testosterone, which has too many side effects to be viable.

193
Q

Describe attempts to make a male contraceptive pill.

A
  • A male “pill” is in development
  • It involves desogestrel (synthetic progestagen) + monthly testosterone injections
  • This stops testis making androgens and blocks sperm production
194
Q

How does vasectomy work?

A

It involves cutting the vas deferens -> So the patient can still ejaculate, but there is no sperm in the semen.

195
Q

What is an example of a theoretical male contraceptive?

A

Anti-sperm antibodies

196
Q

What are some factors that can induce infertility in males?

A
  • Plant extracts -> Cannabis (hemp seeds), Gossypol (cotton)
  • Heatt
  • Blocking neural control of vas, emission, ejaculation
197
Q

Give the failure rates of various contraceptives.

A
198
Q

What percentage of infertility cases in couples are due to males, females and both?

A
  • 35% male
  • 35% female
  • 20% both
  • 10% idiopathic
199
Q

What axis control fertility?

A

HPG (Hypothalamo-pituitary-gonadal)

200
Q

What must be done before treating a patient with infertility?

A

You have to determine where in the HPG (hypothalamo-piuitary-gonadal) axis there is a problem, so it can be corrected.

201
Q

How can we diagnose and treat infertility caused by GnRH defects?

[IMPORTANT]

A

Diagnosis:

  • Use GnRH itself for defects
  • Use kisspeptin to test its receptors on the anterior pituitary

Treatment:

  • Supply GnRH -> Pulsatile (in cases of delayed puberty, as in Kallmann syndrome) or long-acting (to synchronise cycles for IVF
202
Q

How can we treat infertility caused by FSH/LH defects?

[IMPORTANT]

A
  • Supply FSH/LH, although this can be problematic because no human recombinant of these and therefore the animal FSH/LH supplied can elicit antibody production
  • Cannot use testosterone since the dose required is too high
203
Q

How can we diagnose and treat infertility caused by sperm defects?

[IMPORTANT]

A
  • Sperm donation -> Although sperm donors have reduced since new laws reducing anonymity have been introduced
  • Cryoprotection of semen, spermatozoa, spermatids -> This is done in cancer patients who know that their
  • Spermatagonia transplant (experimental!)
  • Intra-Cytoplasmic Sperm Injection (ICSI) -> Insertion of a single spermatozoon into an oocyte in vitro
  • Round Spermatid Injection (ROSI) -> Insertion of a spermatid into an oocyte in vitro (less successful)
204
Q

Give some experimental evidence relating to gender selection of spermatazoa.

[EXTRA]

A

(Johnson, 1993):

  • The principle behind sorting sperm into male and female is the fact that the X chromosome is larger than the Y, so that there is 2.8% more DNA in female sperm
  • “Microsort” uses a modified fluorescence-activated cell sorter to separate male and female sperm stained with the non-damaging fluorochrome bisbenzimide based on DNA content (not colour as in diagram)
205
Q

How can the cause of female infertility be detected?

A
  • FSH & LH assays -> If normal, may suggest poor corpus luteum formation in conjunction with effects on progesterone levels
  • Measure circulating anti-Mullerian hormone -> Secreted by primary follicles and therefore indicates how many follicles remaining (when they run out, it marks infertility)
  • Ultrasound of ovaries
206
Q

How can some problems causing infertility relating to the uterus be treated?

A

Surgery can be used to treat:

  • Endometriosis (growth of the endometrium outside the uterus)
  • Incompetent cervix (which has a risk of spontaneous abortion)
  • Congenital uterine abnormalities
207
Q

How can some problems causing infertility relating to the Fallopian tube be treated?

A

If there are problems with the sperm getting through the Fallopian tube, semen can be introduced into the vagina or uterus by GIFT (Gamete Intra-Fallopian Tube injection) or ZIFT (Zygote Intra-Fallopian Tube injection).

However, this has been largely superceded by IVF.

208
Q

Describe how oocytes are collected for use in IVF.

[IMPORTANT]

A
  • GnRH analogues are used to block LH surge (GnRH is usually an agonist, but here the analogue is an antagonist), which synchronises the cycle
  • FSH & LH and/or clomiphene (oestrogen receptor modulator) are used to stimulate follicle formation/ripening
  • Oocytes are collected under ultrasound guidance
  • Follicle are stored and culture

Note that the oocytes can also be collected earlier in their maturation without using all of these complex hormones, which is known as in vitro maturation. This is less effective but has fewer side effects.

209
Q

Describe the standard IVF method.

[IMPORTANT]

A
210
Q

What are some strategies for improving IVF?

A
  • Improving collection methods for collecting oocytes
  • Improving culture conditions
  • Screening individual blastocyst cells for aneuploidy, etc.
  • Selecting only appropriate blastocysts for transfer
211
Q

How is prenatal diagnosis done in IVF?

A

A cell is obtained from the early blastocyst or a polar body is taken from the fertilised oocyte. It is then checked for genetic abnormalities.

212
Q

When is it best to cryopreserve female gametes?

A

All of the early stages can be preserved, up to the early embryo.

213
Q

Explain three-parent IVF.

A
  • Used to prevent mitochondrial diseases
  • If the mother has a mitochondrial disease, her fertilised egg can be taken and both the paternal and maternal pronuclei can be removed.
  • These can then be inserted to an enucleated zygote.
  • It was approved for use in the UK in December 2016.
214
Q

What are two hormones that have an important effect on sexual behaviour and reproduction?

[IMPORTANT]

A
  • Oxytocin
  • Vasopressin
215
Q

What is the chemical class of oxytocin and vasopressin?

A

They are peptide hormones.

216
Q

Compare the peripheral and central roles of oxytocin and vasopressin.

[IMPORTANT]

A
217
Q

What are the receptors for oxytocin and vasopressin? Where are they found and what are their downstream effects?

A
218
Q

Summarise the central roles of oxytocin.

[IMPORTANT]

A

Maternal behaviour

219
Q

Summarise the central roles of vasopressin.

[IMPORTANT]

A
  • Courtship
  • Aggression
  • Territorial defense
  • Paternal care of young
  • Pair bonding

(Mostly in males)

220
Q

Explain the animal models that can be used for investigating the central roles of oxytocin and vasopressin.

[EXTRA]

A
221
Q

Give some experimental evidence for the central roles of oxytocin and vasopressin.

[EXTRA]

A
  • Oxytocin antagonists (e.g. atosiban) block oestrogen-controlled maternal behaviour such grooming (Fahrbach, 1985)
  • Radioactive oxytocin administration shows that oxytocin receptors are denser in monogamous vole brains
  • Oxytocin KO mice show a lack of maternal behaviour, including percentage of scattered pups, effects on the latency to retrieve scattered pups and latency of crouching over the pups. Oxytocin receptor KO mice also have impaired social recognition (Takayanagi, 2005)
  • Oxytocin KO male mice have social amnesia, which involves the mice being unable to recognise mice that they have encountered 10 minutes earlier (Ferguson, 2000)
  • Mating of male priarie vole mice leads to increased oxytocin and vasopressin levels, which leads to pair bonding, parental care and aggression to male (Wang, 1994)
  • Vasopressin antagonist blocks mating-induced aggression (Winslow, 1993)
  • Vasopressin increases aggression in prairie but not meadow voles (Young, 1997)
  • Vasopressin induces pair bonding in prairie voles but not meadow voles (Young, 1999)
  • In situ hybridisation can be used to find the location of vasopressin receptors -> Vasopressin receptor is denser in the ventral pallidum of monogamous voles (Young, 1997)
  • Viral expression of V1a receptor in meadow vole gives it “prairie” characteristics (Lim, 2004)
  • Homozygosity in the 334 RS3 allele upstream of the vasopressin receptor transcription start site is associated with marital problems (Walum, 2008)
  • Intranasal administration of oxytocin increases trust in humans (Kosfeld, 2005)
  • Oxytocin may be a potential treatment for autism (Andari, 2010)
222
Q

Describe an experiment to investigate pair bonding in mice.

[EXTRA]

A
223
Q

What are some situations in which ovulation may be suppressed?

A
  • Starvation
  • Severe exercise
  • Emotional stress
224
Q

What are some causes of precocious (early) puberty?

A
  • Central:
    • Damage to the inhibitory system of the brain (due to infection, trauma, or irradiation)
    • Hypothalamic cancers producing pulsatile gonadotropin-releasing hormone (GnRH)
  • Peripheral:
    • Endogenous and exogenous sources of sex steroids
225
Q

What are some causes of delayed puberty?

A
  • Malnutrition
  • Various systemic diseases
  • Defects of the reproductive system (hypogonadism)
  • Lack of responsiveness to sex hormones
226
Q

What are the hormonal changes seen at menopause?

A
  • The depletion of the ovarian reserve causes an increase in circulating follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels because there are fewer oocytes and follicles responding to these hormones and producing estrogen.
  • The ovaries produce less oestrogen and progesterone.
227
Q
A

YEAR 2 - Applied Physiology & Pharmacology (11 decks)

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