Endocrinology of pregnancy Flashcards

1
Q

hCG

function + structure

A
  • α & β subunits
  • α subunit identical to LH, FSH and TSH

Function
- Acts on LH receptors on corpus luteum
- Maintains corpus luteum
- Stimulates DHEA production in fetal adrenal

In males – stimulates testosterone → masculinisation

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2
Q

When can hCG be dected and when does it stop

A

in early pregnancy doubles every 48 hrs

detected days 8-12 + stops around 12 weeks

  • clinically used to measure if there’s problem
  • if it doesn’t rise by 60% in 48 hours their can be problems
    • progesterone may be given early pregnancy
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3
Q

What synthesises hCG

A

synctitrophoblast

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4
Q

What happens if you block hCG via antibodies

A

block pregnancy

how?
hormone keeps progesterone levels good, no progesterone no endometrium to implant into

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5
Q

Progestrone

function, where produced

A

Initially produced from corpus luteum
Produced from cholesterol by syncytiotrophoblast – the placenta takes over from corpus luteum ~6-8 weeks

Function
-maintains pregnancy
-affects myometrium: how -> decreses syntheise of contractile protiens, via progestrone b recpetor
-inhibits expression of oxytoxin receptors on myometrium during pregnancy
-Decidual transformation/maintenance (you know viilli, spiral arteries, Immune suppressive effect)

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6
Q

How can oestrogen be made

A
  • cholesterol taken and converted in placenta to from pregnalalone to progesterone
  • progesterone can be processed by fetal adrenal or liver, to make 17, OH then converted to DHEA
  • DHEA can go back to the mother that is a conjugated sulfate
    • so mum can take in DHEA, and convert it into oestrogen which makes de conjugated
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7
Q

What are the three oestrogens and their roles

A
  • Oestrone, E1: Predominates after menopause
  • Oestradiol, E2: Regulates menstruation
  • Oestriol, E3: Pregnancy-specific
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8
Q

What happens to oestrogen during pregnancy

A

rises throughout pregnancy
Oestriol production predominates (oestriol&raquo_space; oestrone & oestradiol)
Produced co-operatively by the placenta and fetus

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9
Q

What form is oestrogen in

A
  • hormones bound to carrier proteins
  • and are sulfated means they are inactive
  • and then they are deconjugated in placenta
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10
Q

What is the role of oestrogen after implanation

A

**Vascular changes
**
- Vasodilation – increase uterine blood flow
- Increase in prothrombotic mechanisms
- Activated Protein C resistance increases
- Antithrombin III and Protein S decrease
- slight increase in risk of thrombosis in pregnancy

**Increase contractile-associated proteins
**– Gap junctions (e.g. Connexin 43), Oxytocin & its receptors, Myometrial glycogen stores, Breast development (for lactation)

**Metabolism
**
- reduces peripheral glucose uptake
- increases cholesterol & triglycerides – decreases HDL

Breast development

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11
Q

When does placental growth hormone (PGH) secretion start

A

Secretion starts from 15-20 weeks from syncytiotrophoblast & EVTs

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12
Q

What is PGH role

A
  • Stimulates maternal gluconeogenesis & lipolysis
    • aids nutrition across placenta
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13
Q

What do PGH levels correlate with

A

Non pulsatile
So Levels correlate with placental size
- big fetus big placneta
- levels correlate with placenta size

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14
Q

What hormones are related to human placental lactogen

A

GH & PRL

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15
Q

Where is human placental lactogen produced and what is its function

A

-Produced by the syncytiotrophoblast
Stimulates gluconeogenis and lipolysis

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16
Q

What happens to HPL levels

A

Rises as hCG falls

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17
Q

What is the role of HPL

A

-Development of acinar cells in mammary glands
- ready for milk production
- Aids fetal nutrition

Suppresses action of insulin in mother – “acts as metabolic screwdriver”
- increases blood glucose levels – more available to the fetus
- glucose goes across on a gradient
- hormone allows gradient to be maintained
- stops peripheral uptake of glucose
- which can lead to insulin sensitivity
- mobilises maternal FAs to meet fetal demand
Increases risk of GD

Large amounts in maternal blood – little reaches fetus

  • IGF -1 produced by the liver which leads to insulin resistance and break down of fats
  • so you get an increase of glucose to the fetus, and steroids synthesis happens on placenta
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17
Q

What is the structure of relaxin and where is it produced

A

Structure
Peptide hormone ~6 kDa related to insulin

Proudced by
produced by corpus luteum
-can be made during menustration

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18
Q

What is the function of relaxin

A

Function
- Increases cardiac output and arterial compliance
- Increases renal blood flow
- Relaxes pelvic ligaments and is believed to soften pubicsymphysis, also promotes cervical ripening

19
Q

What happens to relaxin levels

A

Levels rise in 1st trimester – peaks at ~14 weeks and again at delivery

20
Q

What is the role of prolactin

A
  • important for milk production
  • stimulated by growth hormone
21
Q

where is prolactin made

A

synthesised by lactotrophs in anterior pituitary gland

22
Q

what happens to prolactin levels during pregnancy

A

rises linearly through pregnancy

23
Q

How do you keep prolactin levels up

A

breastfeeding needed to maintain levels

23
Q

What stimulates prolactin release

A

oestrogen

24
Q

What are the stages of delievry

A
  1. Contractions begin, dilation & shortening/effacement of cervix
  2. Full dilation of cervix – delivery of baby
  3. Delivery of placenta
25
Q

What mediates parturition

A
  • Increase in oestrogen compared to progesterone which must be suppressed
  • release prostaglandins (PGF2α, PGE2)
    • important in contraction and modifying the cervix
  • Oxytocin
    • drives contraction
26
Q

What happens to oxytocin receptors in pregnancy

A
  • increase towards the end
  • oxytocin promotes spontaneous depolarisation of myometrium muscle
    • secreted by posterior pituitary and decidual tissue
27
Q

What is CRH a precursor for

A

ACTH

28
Q

when do we release CRH

A

when we are stressed

29
Q

What is the function of CRH

A
  • Stimulates corticosteroid production from adrenals
  • CRH & CRH receptor in the placenta/decidua increase at term – CRH binding protein decreases.

Glucocorticoids/cortisol levels increase
- fpr lung maturation – synthesis of surfactants
- promote oestrogen & prostaglandin production

30
Q

How does the fetus contribute to labour

A
  • Placental CRH increases during gestation
  • causes DHEAS increases via fetal adrenal gland
  • this is Converted to oestradiol in the placenta → this has procontactile myometrial effects
31
Q

What is the role of prostoglandins

A

cervical ripening
- stimulation of the cervix due to the production of prostaglandins
- sex can also stimulate prostaglandins
- any irritation of cervical tissue will release prostaglandins

32
Q

What happens to cervical remodelling

A

-loosening of collagen fib res
-cervix moves posterior and gets thinner and smoother
-increased glycosaminoglycans e.g hyaluron
-increased matrix metalloproteinase production e.g collagenase
-increased inflammatory cells and cytokines

33
Q

Oxytocin

where is it made, function,

A
  • Nonapeptide produced by neurohypophysis
  • released by the posterior pituitary
    -promotes love and stuff
    -stimulates post birth contractions so uterus goes to right place
  • Oestrogens main stimulators of oxytocin synthesis
  • Lowers the excitation threshold of the myometrial muscle cell at which spiking occurs
    • allows for contraction
  • Released in response to tactile stimulation of the uterine cervix
  • Operates through a neuroendocrine pathway – Ferguson Reflex
34
Q

Describe the neuroendocrine reflex

A

1.Intramyometrial PGF2 increases uterine contractions + cervical distension
2.this is sensed by neurones
3.causes release of oxytocin
4.oxytocin promotes further uterine contractions and release of prostoglandins

35
Q

Describe anatomy of breast

A
  • 15-20 lobes of glandular tissue interspaced with fibrous/adipose tissue
  • Lobes – lobules of alveoli, blood vessels & lactiferous ducts
  • Alveoli – epithelial “Acinar” cells – synthesise milk
    • myoepithelial cells – contract to move milk to lactiferous ducts for ejection
36
Q

What is the difference in lactiforius ducts at birth and puberty

A
  • At birth – mostly lactiferous ducts, few alveoli
  • Puberty – oestrogen stimulates lactiferous ducts sprout and branch, alveoli start to develop, deposition of fat & connective tissue
37
Q

What hormones are involved in breastfeeding

A

Oestrogen – increases size & number of ducts in the breast
-also causes PRL secretion -which suppresses dopamine

Progesterone – increases the number of alveolar cells - but inhibits lactogenic effects of prolactin

hPL – stimulates the development of acinar glands

Prolactin – levels increase with gestation & promote milk production

oxytocin: promotes let down or milk ejection reflex

38
Q

In summary what does prolactin and oxytocin do in breastfeeding

A

-prolactin causes milk production
-prolcatin maintains milk production
-oxytocin release causes smooth milk contaction -> ejection of milk

39
Q

Quick pathway of lactation

A

sucking (stimulas)
goes to hypothalamus
hypothalamus causes release of prolactin and oxytocin from pituritaty
oxytocin-> milk release
prolactin -> milk production

40
Q

How to maintain milk production

what can inhibit production, increase etc

A

-prolactin release is positive feedback
-Tuberoinfundibulardopamine (TIDA) is a neurone -> its actovity id modulated by reducing dophamine secretition

-dophamine agonists (e.g bromocriptine) inhibit prolactin

-vasointestinal peptide (VIP) + the release causes prolactin secretion

41
Q

Describe the milk ejection reflex

A

1.Nipple stimulated by suckling
2.causes release oxytoxin
3.oxytocin stimulates breast myoepithelial cell contraction
4.causes milk release from alveoli + increase ductal flow of milk to nipples
5.can promote uterine contraction

42
Q

What are the advantages of breast-feeding for the baby

A
  1. Enhances development and intelligence
  2. Protects against infection, illnesses and allergies
  3. Has long term health benefits
43
Q

What are the advantages of breast feeding for the mother

A
  1. Can delay fertility
  2. reduce risk of gynacological cancer
  3. improve emotional health
  4. cause weight loss
  5. protec against oestoprorosis
44
Q

Latent v active phase of labour

A

Latent
-contractions
-last for about a few weeks
Relaxin acts on pubic symphysis

Active
Short regular contractions

45
Q

What is the role of progesterone 3 and 4

A

Prog3trone 3; contraction
Progesterone 4: relaxation produced after labour