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Reproductive Biology 3 > L3: Reproductive Endocrinology > Flashcards

L3: Reproductive Endocrinology Flashcards

1
Q

Which are the water soluble reproductive hormones?

A

Peptides and proteins:
- Gonadotrophin releasing hormone (GnRH)
- Follicle stimulating hormone (FSH)
- Luteinising hormone (LH)
- Prolactin
- Oxytocin
- Anti-Mullerian hormone
- inhibins/activins

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2
Q

What is the site of secretion of GnRH?

A

Hypothalamus

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3
Q

What is the site of secretion of FSH?

A

Anterior pituitary

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4
Q

What is the site of secretion of LH?

A

Anterior pituitary

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5
Q

What is the site of secretion of prolactin?

A

Anterior pituitary

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6
Q

What is the site of secretion of oxytocin?

A

Posterior pituitary

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7
Q

What is the site of secretion of anti-Mullerian hormone?

A

Ovary

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8
Q

Which are the lipid soluble reproductive hormones?

A

Steroid hormones:
- androgens (testosterone, 5alphaDHT)
- Oestrogens (oestradiol, oestriol, oestrone)
- progestagens (progesterone)

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9
Q

What is 5alphaDHT?

A

Converted from testosterone, much more potent

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10
Q

What are the different oestrogens and when are they expressed?

A
  • oestradiol during reproductive age
  • oestriol and oestrone is post-menopausal
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11
Q

What is the site of secretion of androgens?

A

testes

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12
Q

What is the site of secretion of oestrogens?

A

ovary

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13
Q

What is the site of secretion of progestagens?

A

ovary

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14
Q

What is the mechanism of action of water soluble hormone transport?

A
  1. Binding of hormone (first messenger) to its receptors activates G proteins, which activate adenylate cyclase
  2. activated adenylate cyclase converts ATP to cAMP
  3. cAMP serves as a second messenger to activate protein kinases
  4. activated protein kinases phosphorylate other enzymes
  5. millions of phosphorylated enzymes catalyze reactions that produce physiological reactions that produce physiological responses
  6. phosphodiesterase inactivates cAMP

water soluble hormones travel freely around the blood; they cannot diffuse through the membrane so they work through GPCRs

SEE L3, SLIDE 5 for diagram

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15
Q

What is the mechanism of action of lipid soluble hormone transport?

A
  1. lipid-soluble hormone diffuses into cell
  2. activated receptor-hormone complex alters gene expression in the nucleus
  3. newly formed mRNA directs synthesis of specific proteins on ribosomes
  4. new proteins alter cell’s activity

hydrophobic, so diffuse through the membrane, don’t travel in blood freely, need transport proteins; acts as transcription factors
SEE L3, SLIDE 5 for diagram

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16
Q

What is the action of gonadotropins in males?

A
  • LH and FSH travels down from pituitary.
  • FSH mainly acts on Sertoli cells (support maturation of sperm), within seminiferous tubules.
  • Leydig cells are found in the interstitial space between the seminiferous tubules and they are hormonal cells. Produces testosterone under the influence of LH.

SEE L3, SLIDE 6 for diagram

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17
Q

What is the action of gonadotropins in females?

A
  • FSH primary works on granulosa cells, stimulates production of oestradiol.
  • Androstenedione (essential enzyme for production of oestradiol) comes from theca cells, and it’s made under the influence of LH.
  • Two-cell – two-gonadotropin hypothesis.

OR

  • LH acts on theca, produces androstenedione
  • FSH acts on granulosa, which converts androstenedione to oestradiol
    SEE L3, SLIDE 7 for diagram
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18
Q

What are the examples of steroid hormones?

A

Testosterone, 5-alpha-dihydrotestosterone, oestradiol, progesterone

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19
Q

What do testosterone and 5alpha-dihydrotestosterone regulate?

A
  • Male reproductive function (e.g. spermatogenesis, prostate secretions)
  • Secondary male characteristics (e.g. anabolic (muscle build), facial and body hair, deep voice, libido, aggression) (in females with higher levels of testosterone, similar characteristics can be seen)
  • Male sex determination and genital development
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20
Q

What does oestradiol regulate?

A
  • Endometrial proliferation during menstrual cycle (thickens the endometrium)
  • Female genital development
  • Secondary female sex characteristics (e.g. breast development, body fat distribution, bone (epiphyseal closure; that’s why women stop growing in height))
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21
Q

What does progesterone regulate?

A
  • progesterone prepares for pregnancy
  • Endometrial secretion and vascularization during menstrual cycle (prepare uterus for pregnancy)
  • Maintain pregnancy and support embryo
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22
Q

What is hormonal contraception?

A

Manipulation of steroid gonadal hormones

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23
Q

How does hormonal contraception work in females?

A
  • suppress ovulation via negative feedback of progesterone
  • oestrogen in combined pill provides additional feedback and promotes progesterone receptor expression (supports effects of progesterone)
  • secondary effects on female genital tract (e.g. maintain endometrium in thin state; progesterone is able to thicken cervical mucus, acts as a plug, so sperm cannot enter; can make uterine environment not hospitable for sperm)
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24
Q

How does hormonal contraception work in males?

A
  • suppress spermatogenesis via negative feedback of testosterone
  • progesterone used in combination with testosterone
  • development has been slow due to lack long-lasting testosterone preparations
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25
Q

What is the mechanism of action of negative feedback in HPG axis?

A
  • hypothalamus releases GnRH which acts on pituitary gland
  • pituitary gland releases FSH and LH which acts on ovaries and testes
  • ovaries release oestrogens and progesterones which inhibit the action of hypothalamus and pituitary gland
  • testes release androgens which inhibit the action of hypothalamus and pituitary gland

SEE L3, SLIDE 10 for diagram

26
Q

What is the function of activins in positive feedback in HPG axis?

A

Hormone produced by Sertoli cells and granulosa cells which encourages FSH secretion from anterior pituitary (semi-positive feedback loop)

27
Q

What are the examples of positive feedback in HPG axis?

A
  • Main point where it’s seen is ovulation: as follicle grows it produces more oestrogen (negative –> positive). At a certain threshold, its effect reverses. It now has a positive effect on FSH secretion and causes LH surge, it’s still not fully known why)
  • Another example (where it’s not really sure if it’s positive feedback or not: when females get potential blastocyst made. If fertilization occurs, blastocyst is made, it implants, then starts to make hCG (LH analogue). hCG has ability to bind on LH receptors, mainly on corpus luteum, thus CL does not regress. As CL is maintained then progesterone levels are also maintained. Progesterone then keeps the blastocyst healthy, until placenta takes over.
28
Q

What is the general function of prolactin and oxytocin?

A

lactation

29
Q

How are prolactin and oxytocin released?

A

suckling sends nerve impulses to brain –> release of prolactin (anterior pituitary) and oxytocin (posterior pituitary)

30
Q

How does prolactin act?

A

alveoli swell and secrete milk

31
Q

What prevents milk secretion prior to birth?

A

steroid block at placenta; because of the high levels of steroid hormones from the placenta during pregnancy –> it’s hard for a pregnant woman to breastfeed

32
Q

What are the effects of oxytocin?

A

Oxytocin has major effects on smooth muscle contraction:
- myoepithelial cell contraction around alveoli causing milk expulsion (milk ejection reflex)
- also used to induce labour (effects on uterine smooth muscle)
- also known as love/cuddle hormone, released during orgasm  peer bonding

33
Q

What is the function of anti-Mullerian hormone?

A
  • critical for sex determination in male embryos
  • and for female primordial follicles pause
34
Q

How is anti-Mullerian hormone activated in males?

A

activated by SOX9 in Sertoli cells

35
Q

How does anti-Mullerian hormone act in males?

A

Inhibits development of Mullerian ducts (fallopian tubes, upper vagina, uterus)

36
Q

How does anti-Mullerian hormone act in females?

A
  • Made by granulosa cells from primary stage onwards
  • Inhibitory effect on follicle development (as the ovary has more and more follicles produced, it produces more AMH, then AMH can act on primordial follicle pool and can pause primordial follicle growth; no AMH receptors on follicles seen, so may be not a direct effect)
  • Unaffected by gonadotropins/steroid hormones – used clinically for a reliable reflection of growing follicles (standalone hormone, not involved in feedback loops; doesn’t tell about quality, just the number of follicles)
37
Q

Where is GnRH synthesised?

A

Synthesised by hypothalamic GnRH neurons. Cell bodies in medial preoptic area and arcuate nucleus with projections to median eminence.

38
Q

Why is pulsatile release of GnRH into hypophyseal portal system important?

A
  • prevents receptor desensitisation and downregulation
  • surge prior to ovulation
  • important for timing of puberty and menstrual cycle
39
Q

What are the effects of GnRH on FSH and LH?

A

FSH secretion more irregular than LH:
- The way it’s released means that GnRH has different effects on FSH and LH secretion – FSH secretion more irregular than LH.
- If GnRH is released really quickly it affects LH secretion, needed ovulation
- if it’s released slowly it affects FSH secretion. - When GnRH is removed from the system, LH levels drop really quickly, whereas FSH levels drop much more slowly.

40
Q

What is the importance of kisspeptin signalling pathway?

A
  • essential for puberty, gonadotropin secretion and regulation of reproduction
  • regulation of sexual and social behaviour, emotional brain processing, mood, audition, olfaction, metabolism, body composition and cardiac function
41
Q

What is the kisspeptin receptor? Where is it located?

A

KiSS1 receptor is a G-protein-coupled receptor located on KiSS neurons found in hypothalamus

42
Q

What is the key experimental evidence for kisspeptin signalling pathway?

A
  • Cannot measure GnRH in circulation so LH is measured as a proxy (hard to measure, changes quickly)
  • One experiment showed: Kisspeptin causes depolarization and increases firing rate of GnRH neurons, which shows that kisspeptin stimulates secretion of GnRH in hypothalamic explant cultures
  • Then it’s observed that GnRH mRNA is up-regulated in GnRH neurons following kisspeptin exposure
  • Some evidence suggests kisspeptin can directly stimulate pituitary gonadotropes to release LH/FSH but this is probably secondary
  • Pubertal disorders in humans with KiSSR mutations
    i) Inactivating mutations – cause delayed puberty
    ii) Activating/missense mutations – precocious puberty (less common)
43
Q

What is the mechanism of action of kisspeptin signalling pathway?

A

A lot that is known about kisspeptin signalling comes from rodents, human studies slightly limited.
- There is differences of kisspeptin neuron locations in the brain between humans and rodents.
- There are two different types of kisspeptin neurons:
i) Kisspeptin neurons – just release kisspeptin
ii) KNDy neurone: not only releases kisspeptin, but also neurokinin B (NKB) and dynorphin (Dyn). Dynorphin and neurokinin can act on KNDy neurone to monitor kisspeptin output from those neurons
iii) It is believed that majority of the neurons in the brain are KNDy neurons.
- Essentially there is a pathway that ends up in sex steroids being produced, which then have the ability to act on KNDy neurons, as they have ERalpha and PR receptors

SEE L3, SLIDE 19

44
Q

What are the two types of kisspeptin neurons? What is the difference between them?

A

i) Kisspeptin neurons – just release kisspeptin
ii) KNDy neurone: not only releases kisspeptin, but also neurokinin B (NKB) and dynorphin (Dyn). Dynorphin and neurokinin can act on KNDy neurone to monitor kisspeptin output from those neurons
iii) It is believed that majority of the neurons in the brain are KNDy neurons.

45
Q

How are KISS neurons special?

A

KiSS neurons are special as they have ability to integrate signals from multiple hormonal paths from the body, take information through:
i) Adrenal gland – through secretion of cortisol, thus for example stress affects menstrual cycle
ii) Body fat – leptin – weight changes affect fertility
iii) Immune cell
iv) Environmental cues – shift work, airline industry

46
Q

What is the function of kisspeptin signalling in males?

A
  • Kisspeptin drives LH secretion and testosterone production
  • Testosterone is aromatized before binding to ERalpha on KiSS neurons
    i) Only female AVPV neurons can cause LH surge
    ii) Exposure to sex steroids in utero important in establishing neuron ‘gender’
  • Physiological importance of kisspeptin effects on steroidogenesis and sperm function, and whether these are paracrine or endocrine manifestations, remain unclear – no pathways known
47
Q

In what disorders do high LH pulsatility states appear?

A

PCOS, precocious puberty, menopause

48
Q

In what disorders do low LH pulsatility states appear?

A

pubertal delay, hypothalamic ammenorrhoea, obesity/type 2 diabetes

49
Q

In what disorders do normal LH pulsatility states appear?

A

prostatic hypertrophy, endometriosis

50
Q

What is Hypogonadotropic hypogonadism?

A

Hypogonadism - gonads producing too little hormones
Hypogonadotropic - problem with pituitary or hypothalamus

51
Q

What is the indication of hypogonadotropic hypogonadism in newborn males?

A

Micropenis, cryptochidism

52
Q

What is the indication of hypogonadotropic hypogonadism in females?

A

delayed puberty

53
Q

What is hypogonadotropic hypogonadism caused by?

A

i) Structural lesion in pituitary/hypothalamus area (HPG axis off)
ii) Congenital (e.g. mutations in genes that affect GnRH (Calvin syndrome) neuron migration, effect GnRH and gonadotropin secretion)
iii) Acquired infections, trauma, drugs, tumours
iv) Functional (usually reversible; e.g. diet, over-exercise, stress)

54
Q

What is the treatment for hypogonadotropic hypogonadism?

A

HRT (need additional therapy to achieve pregnancy)

55
Q

What is the Polycystic ovarian syndrome?

A

Heterogenous condition, no equivalent in men; quite common 1/5 women

56
Q

How is PCOS diagnosed?

A

(need 2 out of 3 to diagnose); oligo/anovulation, evidence of hyperandrogenism, polycystic ovaries (when scanned – paused development of follicles seen, not actual cysts)

57
Q

What happens during PCOS?

A
  • high LH/low FSH - imbalance
  • increases androgen production from follicle
  • excess androgens causes cystic ovaries (inhibits growth of larger follicles and encourages growth of smaller follicles)
  • increased weight –> decreased SHBG (sex hormone-binding globulin)
  • insulin augments theca cell androgen production
  • vicious cycle between insulin and weight gain
58
Q

What is the management/treatment of PCOS?

A
  • lifestyle changes
  • metformin
  • HRT
59
Q

What is Premature ovarian insufficiency?

A

characterised by depletion of follicles before age of 40 years - amenorrhea, hypoestrogenism and loss of fertility

60
Q

How is Premature ovarian insufficiency diagnosed?

A
  • High LH,
  • High FSH,
  • low oestrogen
61
Q

What are the causes of Premature ovarian insufficiency?

A
  • genetic
  • iatrogenic
  • autoimmune
  • idiopathic (unknown)
62
Q

What is the treatment for Premature ovarian insufficiency?

A

HRT, however no treatment will allow pregnancy, only option is donor eggs/adoption

Reproductive Biology 3 (21 decks)

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