Endo 11 - Endocrinology of Pregnancy Flashcards Preview

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Flashcards in Endo 11 - Endocrinology of Pregnancy Deck (32)
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1
Q

The seminal vesicles are located behind which organ

A

The prostate

2
Q

What do Leydig cells make?

A

Testosterone

3
Q

In M, where is oestrogen made and give 2 uses for it

A

Made from the conversion of testosterone to oestrogen via aromatase.

  1. Needed for tubular fluid reabsorption for semen concentration
  2. Needed for bone growth - signals closure of the growth plates (epiphyses)
4
Q

What induces secretion of nutrients and glycoprotein into the epididymal fluid?

Why are glycoproteins and nutrients secreted into the epididymal fluid?

A

Androgens

Needed to provide energy for impending journey (sperm) and to coat the surface of spermatozoa

5
Q

What are the constituents of sperm?

A
  1. Spermatozoa - 15-120 million/ml
  2. Seminal fluid - 2-5ml
  3. Leukocytes
  4. Potential viruses (e.g. HIV / Hep B)

Only 1/million reach ovum

6
Q

Seminal fluid comes mainly from the accessory sex glands, which are

A
  1. Seminal vesicles
  2. Prostate
  3. Bulbourethral glands

(small contribution from epididymis and testis)

7
Q

What is capacitation of sperm?

Where does capacitation occur?

A

It is the way in which sperm achieve fertilising capability in the female reproductive tract. 3 things happen:

  1. Loss of glycoprotein coat
  2. Change in surface membrane characteristics
  3. Develop whiplash movements of tail

Capacitation occurs in ionic and proteolytic environment of the Fallopian tube

8
Q

Capacitation of sperm is dependent on which 2 things?

A
  1. Oestrogen

2. Ca

9
Q

Describe the acrosome reaction

A
  1. Capacitated sperm - binds to ZP3 receptor on ovum
  2. Ca influx into sperm (stimulated by progesterone)
  3. Causes acrosome to release hyaluronidase and proteolytic enzymes —-> enables spermatozoon to penetrate the zona pellucida

Zona pellucida = glycoprotein layer that surrounds the oocytes plasma membrane

10
Q

If fertilisation does not occur in the Fallopian tube, what is it called

A

Ectopic pregnancy

11
Q

Where does fertilisation occur?

A

In the fallopian tube

12
Q

What reaction does fertilisation trigger

A

Cortical reaction

Cortical granules release molecules which degrade bona pellucida (e.g. ZP2 and 3) - prevents further sperm binding as no receptors

Haploid —> Diploid

13
Q

How does fertilisation cause expulsion of the 2nd polar body?

A

In oogenesis meiosis, chromosomes evenly divided between daughter cells, but the cytoplasm is divided unevenly.

The ovum retains the cytoplasm, whilst the other cell degenerates as it has no cytoplasm

14
Q

Explain the development of the conceptus

A

Fertilized egg continues to divide as it moves down Fallopian tube.

Conceptus receives nutrients from uterine secretions - this free-living phase lasts for 9-10 days

Conceptus compacts to form a 8-16 cell morula - which then becomes a blastocyst

15
Q

Describe the cellular arrangements in a blastocyst

A

Inner cell mass will become the embryo

Trophoblast cells will form the chorion/placenta

16
Q

Transfer of the conceptus/blastocyst to the uterus is facilitated by?

A

An increasing progesterone:oestrogen ratio - luteal phase

17
Q

Describe the 2 phases of implantation

A
  1. Attachment phase - outer trophoblast cells contact uterine surface epithelium
  2. Decidualisation phase - changes in underlying uterine stroll tissue (within few hours) - requires progesterone domination in the presence of oestrogen (progesterone promotes gestation)
18
Q

Which 2 factors in the attachment phase stimulates adhesion of the blastocyst to endometrial cells?

A
  1. Leukaemia inhibitory factor (LIF) - from endometrial secretory glands
  2. IL-11
19
Q

in the decidualisation phase of implantation, endometrial changes occur due to progesterone. These changes include?

What factors are involved?

A

Endometrial changes:

  1. Glandular epithelial secretion
  2. Glycogen accumulation in stroll cell cytoplasm
  3. Growth capillaries
  4. Increased vascular permeability (causing oedema)

Factors involved:

IL-11, histamine, certain prostaglandins and TGF-B

20
Q

TGF-B promotes what

A

Angiogenesis

21
Q

hCG is produced where?

A

Placenta (by trophoblasts)

22
Q

2 ways to check if an egg is present?

A
  1. Ultrasound

2. Day 21 progesterone should be high

23
Q

In the first 40 days, where is progesterone and oestrogen produced and what stimulates it?

A

Corpus luteum, stimulated by hCG which acts on LH receptors

hCG acts on LH receptors

LH and FSH inhibited (-ve feedback)

24
Q

In the first 40 days, why is progesterone and oestrogen production vital?

A

Important for developing fetoplacental unit

25
Q

From day 40, how is progesterone and oestrogen produced?

A

Placenta starts to take over

26
Q

In a pregnancy test, what should be measured?

A

Foetal hCG levels (takes 2 weeks after conception)

If you want to test earlier, check plasma hCG levels

27
Q

Describe placenta-independent progesterone and oestrogen production

A

Mother and foetus both produce DHEAS —> converted through the placenta into oestradiol

28
Q

What hormones may increase during pregnancy?

A
  1. ACTH
  2. Adrenal steroids
  3. Prolactin - if you wanna detect prolactinoma in pregnancy, use MRI and visual fields
  4. IGF1 - stimulated by placental GH-variant
  5. Iodothyronines - hCG shares an alpha subunit with TSH
  6. PTH related peptides
29
Q

What hormones may decrease during pregnancy?

A
  1. Gonadotrophins
  2. Pituitary GH
  3. TSH
30
Q

Parturition occurs because a rise in Ca causes uterine contraction. How does this happen

A
  1. Oestrogen and oxytocin drive this (progesterone inhibits)
  2. Oestrogen rises constantly in pregnancy –> increases effect of oxytocin by increasing the number of oxytocin receptors on muscles
31
Q

Explain endocrine control of lactation

A
  1. Suckling - stimulates neural pathways to hypothalamus
  2. This stimulates APG (prolactin) and PPG (oxytocin).
  3. Prolactin = milk synthesis
    Oxytocin = milk ejection (as well as cervical dilatation and uterine contraction)
32
Q

How can marathon runners get hypogonadotrophich hypogonadism

A

Nipple stimulation when running –> increased prolactin —> GnRH suppressed

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