Lecture 1 – Introduction to RED and HPG Axis Flashcards
What is the main hormone released by the hypothalamus in the HPG axis and what does it act on?
GnRH is released and it acts on the anterior pituitary to stimulate release of LH and FSH.
What triggers gonadal activation in puberty?
Pulsatiles GnRH secretions.
Why can continous rather than pulsatile release of GnRH lead to decreased production of LH and FSH?
It can lead to downregulation of the GnRH receptor on the surface of the gonadotroph cells of the pituitary. This reduces FSH and LH release.
In the female HPG axis what cells do FSH and LH act on and what are the results?
LH acts on the theca cells to cause production of androgens of which oestrogen is the major product. It also causes production of progesterone by the granulosa cells.
FSH acts on the granulosa cells to produce inhibin.
At which levels do Oestrogen and Inhibin feedback in the female HPG axis?
Oestrogen feeds back negatively both to the Hypothalamus and pituitary so causes decreased GnRH, FSH and LH. However in the middle of the cycle it feeds back positively. Inhibin can only feedback to pituitary hence reducing FSH and LH secretion.
How does the hypothalamus communicate with the anterior and posterior pituitary?
It has direct neural connections with the posterior. It uses the vasular network to indirectly communicate with the anterior pituitary, this is via neuropeptides.
What are the three families of sex steriods, where are they produced and what do they do?
- Progestagens - they are produced in the placenta during pregnancy
- Androgens - less than 5% produced in adrenals, mainly produced in testis, cause male characteristics
- Oestrogen - produced in liver, adipose, adrenals and placenta, cause female characteristics.
How do steriods typically travel in the blood\/ give examples.
Bound to proteins e.g. albumin, sex hormone binding globulin, androgen binding protein.
Why do synthetic progestagens in the contraceptive pill have side effects such as acne?
They are andogenic so act on androgen receptors causing acne aswell as their intended progesterone receptor.
What is the difference between primary and secondary hypogonadism?
Primary is the effector gland failing to produce its peptides e.g. testis or ovaries. This means FSH and LH increase but this has no effect on effector gland so no negative feedback.
Secondary is when there is a problem at the regulator gland, there is no increase in FSH and LH in response to low oestrogen.
What are the parts of the mature graffian follicle and what do they produce?
Surrounding the oocyte is the zona pellucida and corona radiata. These are surrounded by an antrum that is then followed by the granulosa cells. These cells produce inhibin. This is then surrounded by the theca interna and externa cells which produce androgens.
What do all sex steriods develop from and where is this produced?
All sex steriods originate from DHEA which is produced mainly in the adrenals and some in the gonads. It is converted to testosterone and then on to oestrodiol in females and a bit in males. Key point is that male hormones are needed to be converted to female hormones.
When does prolactin increase and what are its effects?
Increases in pregnancy and during breast feeding. It causes lactational amenhorrea. It inhibits gonal activity by central depression of GnRH.
What is Oligomennorrhea?
Oligomenorrhea - <9 cycles in last 12 months
What is amenorrhea?
Amenorrhea – no bleed in last 6 months
