Drugs you can stimulate 
your ovaries with
(if you’ve got ovaries, that is)

My group has decided this week that everybody should learn about everything in the case, but I didn’t really think it was realistic to make a handout about everything. Before you start moaning, here’s some info on what they may have used to stimulate Nusrat’s ovaries with.

To try and get ovulation going, we have four main groups of treatments:
1.	Hypothalamic hormone: gonadorelin
2.	Anterior pituitary hormones: follicle stimulating hormone (FSH) and human chorionic gonadotrophin (hCG) 
3.	Antioestrogens: clomiphene 
4.	Bromocriptine for hyperprolactinaemia

Gonadorelin
Huh? Gonadorelin? This is actually gonadotrophin releasing hormone (GnRH) which causes the anterior pituitary to release luteinising hormone (LH) and follicle stimulating hormone (FSH). This stuff has to be administered in pulses because continuous use causes the receptors to downregulate and actually reduce gonadotrophin release. It’s given by a parenteral route, by intramuscular injection or intranasally. (I’ve always wondered what parenteral meant and finally bothered to look it up: it means by a route other than by mouth). 

Follicle Stimulating Hormone (FSH)
Good old FSH will stimulate the development of ova (as described in any friendly physiology textbook). It’s prepared from the urine of postmenopausal women. There are also preparations which also contain luteinising hormone (LH).

Human Chorionic Gonadotrophin (hCG) 
This horrible sounding hormone is secreted by the placenta – and you’ll never guess where they get it from! Yeah, that’s right – from the urine of pregnant women! What does it do? It has the same actions as LH, which makes the corpus luteum secrete progesterone. It’s used when the ovary doesn’t work because LH is low, so Nusrat wouldn’t get this because her LH levels are quite high already.

Clomiphene
This is a weak oestrogen agonist with less activity than natural oestrogens. It sits in the oestrogen receptors and doesn’t do all that much. When the real oestrogens come along, they can’t get at the receptors i.e. it’s a partial agonist. By blocking oestrogen receptors, there’s no negative feedback and so the pituitary secretes more gonadotrophins and ovulation may be induced. Its main adverse effect is multiple ovulation with multiple pregnancy. Also because if you use it too much, there’s an increased incidence of ovarian carcinoma, the limit that it can be used is six times.

Bromocriptine
Prolactin antagonises the effect of gonadotrophins, and its secretion is inhibited by dopamine at the anterioir pituitary. Bromocriptine is a dopamine receptor agonist and therefore decreases the amount of prolactin released. It has a t½ of 6 hours.

Right, I reckon that’s enough for the first week of a brand new semester. If you want to investigate further, feel free to look up the reference below or some other pharmacology book. Enjoy this semester, I’ve got a feeling that this is going to be a fun, exciting and very interesting time!

“All generalisations are dangerous, even this one!”

Reference:
Clinical Pharmacology (8th Edition) by Laurence, Bennett and Brown (p653).