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LCRS Year 2 - Endocrinology > The Endocrinology of Pregnancy > Flashcards

The Endocrinology of Pregnancy Flashcards

1
Q

What are the two types of cells found in the testes?

A

Sertoli cells

Leydig cells

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2
Q

What do each cell type in the testes produce?

A

Sertoli cells - sperm

Leydig cells - testosterone

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3
Q

What is fluid reabsorption from the efferent ducts caused by and what does this do to the sperm?

A

Fluid reabsorption is induced by oestrogen

- this concentrates the sperm

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4
Q

How do men get their oestrogen and where does this happen?

A

Aromatisation of testosterone by aromatase in the Leydig cells

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5
Q

What is secreted into the epididymal fluid for the sperm’s benefit and what induces their secretion?

A

Nutrients and glycoproteins are secreted into epididymal fluid
- induced by androgens

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6
Q

How many times its length does the sperm have to travel from testes to Fallopian tube?

A

Travels 100,000x its length

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7
Q

What does the semen contain and how much of each content type does it contain?

A

Spermatozoa - 15-120 million/ml
Seminal fluid - 2-5ml
Leucocytes
- Potentially viruses (hep B, HIV)

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8
Q

How many spermatozoa in ejaculate enter the cervix and how many manage to go from cervix to ovum (egg)?

A

1/100 enter cervix
1/10,000 cervix to ovum
(overall 1/million reach ovum)

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9
Q

Where does seminal fluid come from, both small contributors and main producers?

A

Small contribution from:
- Epididymis/testes

Mainly from accessory sex glands

  • Seminal vesicles
  • Prostate
  • Bulbourethral glands
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10
Q

What is the capacitation of sperm?

A

Process that achieves fertilising capability in the female reproductive tract
(sperm while still in the testes are not in a form capable of fertilisation)

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11
Q

What are the 3 steps of capacitation of sperm?

A

1) Loss of glycoprotein ‘coat’
2) Change in surface membrane characteristics
3) Development of whiplash movements of the tail

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12
Q

Where does capacitation of sperm take place and what is the nature of this environment?

A

Takes place in environment of Fallopian tube

- ionic and proteolytic environment

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13
Q

What are the two things is the capacitation of sperm is dependent on?

A

Ca2+-dependent

Oestrogen-dependent

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14
Q

What is the acrosome reaction?

A

The reaction that occurs when the sperm encounters the egg attempting to penetrate it

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15
Q

Where is the acrosome found?

A

In the head of the sperm cells

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16
Q

What happens in the acrosome reaction?

A

A capacitated sperm encounters the ovum

  • The sperm binds to ZP3 (glycoprotein sperm receptor)
  • Results in Ca2+ influx into the sperm (stimulated by progesterone)
  • Release of hyaluronidase and proteolytic enzyme (from acrosome)
  • These enzymes degrade the zona pellucida (glycoprotein layer covering the ovum) and allow the sperm to penetrate the ovum
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17
Q

If fertilisation does not occur in the Fallopian tube what do we call the resulting pregnancy?

A

An ECTOPIC pregnancy

18
Q

Where does fertilisation occur and what reaction does it trigger?

A

Occurs in the Fallopian tubes

- Triggers the CORTICAL reaction

19
Q

What happens in the cortical reaction?

A

Cortical granules release molecules which degrade the Zona Pellucida, removing ZP2/3 receptors thus preventing further sperm from binding to the same ovum

20
Q

What happens in the egg after the cortical reaction and what does it become?

A

Both egg and sperm head become the female and male pronucleus respectively.
Makes cell go from haploid (one set of chromosomes) to diploid (two sets of chromosomes) and becomes a one-cell zygote

21
Q

How does the development of the conceptus progress after fertilisation in the Fallopian tube has taken place and where does it receive nutrients from?

A
  • Continues to divide as it moves down Fallopian tube to uterus (3-4 days)
  • Receives nutrients from uterine secretions
  • This free-living phase can last for 9-10 days
22
Q

What is the zygote called from fertilised egg to blastocyst?

A 
Fertilised egg
2-cell conceptus
4-cell conceptus
8-cell conceptus
Morula (after compaction)
Blastocyst
23
Q

What does a blastocyst contain? (see presentation for diagram)

A
  • Inner cell mass (soon to be embryo)
  • Trophoblast cells around the outside of the cell (forms chorion, involves placenta)
  • Blastocoelic cavity in the middle
24
Q

What are the phases of implantation and what happens in both phases?

A

Attachment phase
- outer trophoblast cells contact uterine surface epithelium

Decidualisation phase
- changes in underlying uterine stromal tissue (within a few hours)

25
Q

What is the hormone requirement for the decidualisation phase to take place after the attachment phase in the implantation process?

A

Progesterone domination in the presence of oestrogen

26
Q

What are the two key molecules in the attachment phase of implantation that are produced by the endometrial lining, what do they do and what type of cell releases them?

A

Leukaemia inhibitory factor (LIF)

  • stimulates adhesion of blastocyst to endometrial cells
  • released from endometrial secretory glands

Interleukin-11 (IL11)

  • may be involved, specifics unclear
  • released from endometrial cells into uterine fluid
27
Q

In the decidualisation phase, what endometrial changes are caused by progesterone?

A
  • Glandular epithelial secretion
  • Glycogen accumulation in stromal cell cytoplasm
  • Growth of capillaries (more blood supply needed for growing zygote)
  • Increased vascular permeability (again more blood supply, can lead to oedema)
28
Q

What chemical factors (molecules) are involved in decidualisation?

A

Interleukin-11 (IL11)
Histamine
Certain prostaglandins
TGFbeta (promotes angiogenesis)

29
Q

What is hCG?

A

Human Chorionic Gonadotrophin

30
Q

How are the levels of hCG, progesterone, oestrogens, and human placental lactogen expected to change over the course of a 40 week pregnancy? (see graph in presentation, maybe try to draw general trends)

A
  • hCG rises fast (up within 2 weeks) and then falls again in the first 10 weeks
  • progesterone rises increasingly quickly to a peak at roughly 35 weeks where it then sharply falls
  • oestrogen rises similarly to progesterone but only reaches around half the peak at the same time before sharply falling
  • human placental lactogen is very similar to oestrogen but slightly below it
31
Q

Which cells produce hCG?

A

Trophoblasts in conceptus/blastocyst (depending on time)

32
Q

How and where is progesterone and oestrogen production stimulated in the first 40 days, what is this essential for and how does this affect LH/FSH levels?

A

hCG acts on LH receptors, stimulating production in corpus luteum

  • Essential for developing fetaplacental unit
  • Inhibits maternal LH/FSH by negative feedback on pituitary gland
33
Q

After the first 40 days, where does the foetus get its oestrogen?

A

The placenta makes oestrogen after day 40

uses de-conjugation and its own enzymes to make oestriol which is the placental equivalent of oestrogen

34
Q

Which maternal hormones will increase during pregnancy?

A
  • ACTH (provides false high free cortisol urine results)
  • Adrenal steroids
  • Prolactin (a prolactinoma can no longer be checked by serum levels but can scan it for size)
  • IGF1 (stimulated by placental growth hormone variant)
  • Iodothyronines (T3/T4, thyroid hormones)
  • PTH-related peptides (calcium balance maintenance during pregnancy)
  • Kisspeptin
35
Q

Which maternal hormones will decrease during pregnancy?

A
  • Gonadotrophins (LH/FSH)
  • Pituitary GH
  • TSH
36
Q

Why does T3/T4 rise during pregnancy including when TSH is being decreased?

A

hCG shares an alpha subunit with TSH, thus will stimulate T3/T4 production as more thyroid hormone needed

37
Q

How is contraction (parturition) stimulated endocrinologically?

A

Oxytocin, produced by the neurohypophysis, binds to oxytocin receptors which stimulates influx of Ca2+ ions which begin the chain of reactions resulting in contraction

  • Oestrogen and cortisol both also influence this but oxytocin is the main hormone at work
38
Q

What is the process milk synthesis and ejection starting with the stimulus and ending in the desired effects? (draw out on paper)

A

Suckling (or a stimulus) stimulates neural pathways leading to the hypothalamus

  • the hypothalamus stimulates the both anterior and posterior pituitary glands
  • adenohypophysis produces PROLACTIN
  • neurohypophysis produces OXYTOCIN

Prolactin promotes milk synthesis
Oxytocin stimulates milk ejection

39
Q

What is the common effect of oxytocin between parturition and milk ejection, and what can be extrapolated from this about the general effect of oxytocin?

A

Oxytocin is a contraction stimulant

  • contraction is required in both milk ejection and parturition
  • the way to remember which hormone controls parturition and milk ejection is to remember that both involve contraction and when oxytocin binds to its receptors, at least in the uterus, it causes Ca2+ influx, causing the contraction. It’s probably very similar in the breast
40
Q

Thinking logically along the lines of what nipple stimulation causes hormone-wise, what happens if there is overstimulation of the nipples in a setting outside of pregnancy and what signs and symptoms would be seen?

A

Excessive prolactin and oxytocin production

  • symptoms of hyperprolactinaemia
  • galactorrhoea, amenorrhoea in females, low libido in males
41
Q

What are the 3 main effects of oxytocin?

A
  • Milk ejection
  • Cervical dilatation
  • Uterine contraction (parturition)

LCRS Year 2 - Endocrinology (21 decks)

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