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LCRS Endocrinology > 11. Endocrinology of Pregnancy > Flashcards

11. Endocrinology of Pregnancy Flashcards

1
Q

LOOK AT YEAR 1 GONADS LECTURE

A

LOOK AT YEAR 1 GONADS LECTURE

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2
Q

Role of oestrogen in the rete testis and early epididimus

A

Used to control tubular fluid reabsorption there

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3
Q

Where is oestrogen in tubular fluid produced

A

Produced by sertoli cells

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4
Q

Where is a vasectomy perforemed

A

A the vas deferens towards the bottom end

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5
Q

Components of semen

A
  1. Spermatozoa- 15-120 x106/ ml
  2. Seminal fluid- 2-5ml
  3. leucocytes
  4. Potentially viruses

A lot of fluid will be added to the spermatozoa between the vas deferens and the urethra so the concentration further down the reproductive tract is lower than in the vas deferens

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6
Q

Role of seminal fluid

A

Important in providing energy so that the spermatazoa can function properly

Also consists of fibrinogen and fibrinolytic enzymes- after ejaculation the semen initially clots and must be broken down

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7
Q

Activation of spermatozoon

A

In the seminiferous tubule: quiescent and incapable of fertilising an ovum

In the vas deferens: capable of limited movement and have limited capability for fertilisation

Within the female reproductive tract: full activity and fertilising capability

This is CAPACITATION

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8
Q

Capacitation of the spermatazoa

A

Changes are OESTROGEN DEPENDANT (all changes are also calcium dependant)

Glycoprotein coat has a protective function in the vagina but is no longer necessary in the ovum- lost

Changes in the surface membrane lead to the acromosome reaction

Tail begins to move in a whiplash fashion

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9
Q

Acromosome Raction

A

AS the sperm enters the uterus, changes in its surface membrane occur as part of capacitation

This allows the spermatazoon to bind to the ZP3 glycoprotein on the zona pellucida of the ovum.

One bound, progesterone stimulates Ca2+ influx into the sperm

This stimulates the spem to bind to a secondary receptor, ZP2 and causes release of enzymes from the acromosome (cap at anterior end of sperm)

Allows penetration of the zona pellucida

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10
Q

Immediate result of fertilisation in fallopian tube

A

Expulsion of the second polar body

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11
Q

Zonal reaction following fertilisation

A
  • Cotical granules release molecules which degrade the zona pellucida
  • This prevents further binding of sperm to ZP2/3 domains
  • Calcium dependant
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12
Q

Development of the conceptus

A
  • The 2-cell conceptus develops once diploidy is established
  • Continues to divide as it moves down the fallopian tube towards the uterus
  • Recieves nutrients from uterine secretions
  • Continues until there is an imbalance between the nutrients the outer and inner cells of the conceptus recieve
  • Free living phase= 9-10 days (during luteal phase)
  • 8-16 cell morula is now developed
  • Becomes a BLASTOCYST with: inner cell mass (embryo), trophectoderm (placenta)
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13
Q

How is blastocyst transfer to the uterus fascilitated

A

By increasing progesterone, oestrogen ratio

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14
Q

Implantation Process

A

INVASIVE in humans

  • Involves an initial attachment phase- trophoblast cells must make contat with the uterine surface
  • Now get decidualisation of the underlying uterine stromal tissue
  • DECIDUA= modified mucous membrane shed with afterbirth
  • This process requires PROGESTERONE DOMINATION in the prescence of oestrogen
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15
Q

Process of attachment and molecules involved

A

TWO molecules are of particular importance:

  • Leukemia Inhibitory Factor (LIF)
  • Interleukin (IL-11)

LIF:

Produced from endometrial secretory glands and blastocyst. Stimulates adhesion of blastocyst to the endometrial cells

IL-11:

Also released from endometrial cells. Released into the uterine fluid. Involved in trophoblast migration and decidualisation

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16
Q

Decidualisation reaction

A

Invasion of underlying uterine stromal tissue by the trophoblast cells of the blastocyst

Leads to:

  • Increased vascular permeability associated with oedema
  • Localised changes in intracellular composition
  • DECIDUALISATION

Factors involved:

  • IL-11
  • Jistamine
  • prostoglandins
  • TGFb- angiogenesis
17
Q

Main Hormone changes during pregnancy

A
  • Human chorionic gonadotrophin (HCG) reaches a peak around 8 weeks- important in this period as a replacement for LH

Normally negative feedback of E and P cause falling LH levels, case falling E/P. But in pregnancy high levels of E and P are required so HCG is produced by trophoblast cells. It binds to receptors on the corpus luteum.

  • After 5 weeks the placenta takes over production of the hormones
  • E and P levels increase throughout, Progesterone remains dominant
  • Human Placental Lactogen- is also produced by the placenta and has prolactin like effects- growth and development
18
Q

Production of oestrogens in pregnancy

A

Steroid production is achieved by action of the mother, foetus AND placenta:

  1. Mother- provides precursors (tends to be pregenalone) leading to the production of progesterone, produces DHEAS (dehydroepiandrosterone sulfate) along with the foetus
  2. Foetus- Produces DHEAS and uses progesterone in steroid production. Produces the main oestrogen of pregnancy OESTRIOL (weak but lots of it) by conjugation of DHEAS to 16a hydroxy DHEAS in liver
  3. Placenta- takes up DHEAS to produce oestrone. Deconjugates 16a-hydroxyDHEAS
19
Q

Implications of oestradiol and oestrone deficiency in pregnancy

A

Does not tell you much about the health of the baby since oestradiol and oestrone come from the mother as well as the baby- need to look at the ratio of Oestriol: oestradiol and oestrone

20
Q

Changes in maternal hormones during pregnancy

A

Most hormone production will increase

  • Apart from hGH (Human growth hormone)- this decreases as placental hGH variant increases- inhibits normal hGH

Pituitary gland increases

21
Q

Endocrine control of parturition

A

Parturition is about contraction of actin and myosin filaments- requires CALCIUM

  • You need to increase the intracellular [Ca2+]
  • oestrogen stimulates production of prostoglandins in endometrium
  • Prostoglandins stimulate production and release of calcium into the cytoplasm from intracellular stores
  • Oestrogens therefore increase chance of contraction
  • Progesterone has exactly the opposite effect by inhibiting prostoglandins
  • During parturition OXYTOCIN is released which causes contraction by opening ca2+ channels
  • once the baby reaches a certain size production of oestrogen is also switched so IT IS DOMINANT
22
Q

Endocrine Control of Lactation

A
  • Prolactin - promotes milk synthesis
  • Oxytocin - promotes milk ejection

LCRS Endocrinology (18 decks)

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