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Y3 Patient Sem 1 > hormones and reproduction > Flashcards

hormones and reproduction Flashcards

1
Q

what causes the endometrium to recover?

A

oestrogen

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2
Q

when does menarche occur in most women?

A

12 years

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3
Q

when does menopause occur in most women?

A

51 years

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4
Q

when does the end of the follicular phase occur?

A

Around day 14 - this is when ovulation occurs

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5
Q

what day do you have the menstrual bleed?

A

day 28

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6
Q

what is the process of the endometrium regenerating?

A

proliferation

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7
Q

what are gonadotropins?

A

polypeptide hormones

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8
Q

what do gonadotropins do/

A

regulate steroid production - they are water soluble and need to meet receptors at cell surfaces

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9
Q

what are steroids?

A

fat soluble chemical

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10
Q

what is structure of the female sex steriods?

A

all contain 4 fused carbon rings, all related biosynthetically.

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11
Q

what is something to note about structure of oestrogen?

A

unusual

have an aromatic ring, no other steroid hormones have this

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12
Q

what is the precursor of the steroid hormones?

A

cholesterol

acetate -> pregnenolone -> progesterone

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13
Q

what are the majority of steroid receptors?

A

intracellular

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14
Q

what is gene expression?

A

production of mRNA (transcription) which usually leads to translation of protein,

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15
Q

where does transcription occur?

A

nucleus

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16
Q

where does translation occur?

A

cytoplasm

17
Q

what is specific about the steroid hormone receptors?

A

they have two binding sites
- one for the steroid
- one for the DNA
the binding causes a conformational change

18
Q

what happens when binding occurs?

A

binding of the steroidal ligands produces a complex that acts as DNA
binding of the complex to sites on DNA alters the genes expressed by target
- this is known as transcription factors

19
Q

how are the hypothalamus and pituitary linked?

A

close by to eachother and are connected. the hypothalmus signals to the pituitary and this is what causes the release of hormones

20
Q

what is the HPO axis chain of events?

A

hypothalmus –> release gonadotropins releasing hormones in a pulsatile release–> this goes to anterior pituitary –> this release LH and FSH –> this goes to the ovary and produce follicle or sex steroids

21
Q

what do gonadotropins control?

A

sex steroid production
follicle maturation
ovulation

22
Q

what are gonadotrophin releasing hormone (GnRH)?

A
  • 10 amino acids: Glu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly
  • acts at GnRH receptor
  • a G protein-coupled receptor (GPCR)
  • GnRH release is pulsatile - frequency important - regulated by sex steroids (- / +) sex steroids can feed back
  • stimulates release of FSH & LH
23
Q

which hormone is stimulated by the slow release?

A

FSH stimulated by slow GnRH

24
Q

which hormone is stimulated by fast release?

A

LH is stimulated by fast GnRH pulse frequencies

25
Q

what is an example of synthetic agonist or antagonist of GnRH?

A

both shut down the ovary – sometimes this is used in IVF to stimulate and collect eggs, this stops the production of FSH and LH.
If you use an agonist is down regulates itself, either way production of GnRH is stalled.
The antagonist would block the receptor of LH and FSH snd this would stop production of GnRH.

26
Q

what is buserelin?

A 
is an agonist at the GnRH receptor.
It can stimulate FSH and LH production. You can use this to create an artificial cycle, 
but 	
long term constant levels cause:
- GnRHR down-regulation
- resulting insensitivity to GnRH
- loss of production of FSH and LH
H-Pyr-His-Trp-Ser-Tyr-D-Ser(tBu)-Leu-Arg-Pro-NHEt
27
Q

what is puberty in girls controlled by?

A

leptin (fat muscles), as they age there is an increased in fat levels and this affects GnRH neurone in turn leading to production of gonadotropin

28
Q

what are people at risk of with early puberty?

A
  • Early puberty is associated with higher risks of type 2 diabetes (T2D) and cardiovascular disease in women and men.
  • Increasing age at menarche is associated with higher risks for osteoporosis but lower risks for breast cancer.
  • Higher levels of fat usually do come with an increased risk of T2D so this could just be coincidence.
29
Q

what are the cells that grow in follicle called?

A

granulosa cells - these contain full chromosomal complement

30
Q

what is the process called twhere the follicles that dont make it die?

A

atresia

31
Q

what is the ovarian cycle/

A
  • ovulation stimulated by LH
  • FSH stimulates the growth of follicle from primary to secondary to tertiary
  • corpus leutum is stimulated by LH
32
Q

what happens if there isnt a pregnancy?

A

corpus leutum regresses and the hormones will decline

33
Q

what happens at the early follicular phase?

A

We have production of oestrogen at low levels, you get slow GnRH pulses and FSH is starting to respond to this and increase but not too much and encourage promotion cohort of follicles

34
Q

what happens in the mid follicular phase?

A

FSH production is now starting to decline this coincides with an increase of oestrogen. This is an example of oestrogen exerting negative feedback on the hypothalamic production of GnRH.
As oestrogen begins to rise there is a negative feedback down regulation action, which stops increase of FSH production.
As you get closer to ovulation it hits the transient phase, during which the oestrogen is acting positively feeding back to the hypolathmic and pituitary axis. This is the only time that positive feedback occurs.\this is what gives you the spike of LH just before ovulation. This only occurs when the level is at the highest. Then oestrogen levels decline and it goes back to negative feedback

35
Q

what is the late luteal phase?

A

you get negative feedback from progesterone aswell as the oestrogen. This causes a decrease in GnRH and LH. Post ovulation LH and FSH are both declining.
The spike of gluttonising enzyme in the green occurs 36 hours before ovulation, as an increase in FSH stimulates ovulation.
In fertility centres people either look for early rise of LH or the spike of LH, but the plot is not very resolved as the dotted line at 14 hours should be more to the right.

It is at the negative feedback where you can inhibit the enzymes and stop the cyclical production of the ovaries. You can do the same in the male testes.
Combined E2 and P (prostergone like compounds) inhibit GnRH. Prolonged high E2 (this isn’t usually used as it is more dangerous effects) alone also has this effect.  contraceptive options.

36
Q

what is the mechanism of steroid hormone action/

A

Steroids binds receptors in the cell (semi circle) this complex goes to the nucleus and binds to subset of genes which has a specific sequence. And the effect of this is to recruit co-activators and this stimulates the rate of mRNA. This allows the gene to respsond in response to a steroid.

37
Q

what are anti-oestrogens?

A

binds the estrogen receptor and blocks its ability to activate target genes. This doesn’t create a complex which can activate in that way.
whole range of compounds that have a range of activities which postion them between a full agonist and a full antagonist so they are partial of both

Y3 Patient Sem 1 (20 decks)

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