12 The Gonads II Flashcards
Q: What type of hormone is aldosterone? Main role?
A: mineralocorticoid
allows retention of salt and therefore water in kidneys-> maintains circulating blood volume
Q: Why do overweight men get moobs?
A: aromatase E is found in fat cells
which means you get more conversion to make oestrogen from testosterone = promotes breast formation
Q: Name 5 hormones in the gonads and explain how they relate to one another.
A: androstendione (weak precursor) can be turned into testosterone and oestrone
testosterone can become dihydrotestosterone (DHT) (more potent testesterone) or oestrone or 17 beta-oestrodiol
testosterone:
- reduced by 5 alpha reductase -> DHT
- aromatisation by aromatase -> oestrogens
Q: Where is DHT made? Examples (7).
A: tissues that have 5 alpha reductase enzyme present
- prostrate
- testes
- (seminiferous tubules)
- seminal vesicles
- skin
- brain
- adenohypophysis
Q: Where are androgens made?
A: BOTH the gonads and the adrenal glands
Q: How does testosterone and DHT differ? What do they do? Where is testosterone produced in females?
A: dihydrotestosterone
is a more potent androgen but will still work on the SAME androgen receptors
gives potent masculising effects
a little in adrenals
Q: Where are oestrogens made? Examples (5). What does oestrogen do?
A: tissue with aromatase present
-adrenals
-testes (sertoli cells)
ovaries
-liver
-skin
-brain
gives feminising effects
Q: How is testosterone (and DHT) transported? (4)
A: not water soluble as are steroid hormones- need a carrier
in blood:
- sex hormone binding globulin (SHBG) which is made in liver=> carrier 60% (reservoir for inactive/bound testosterone)
- albumin=> carries 38%
- FREE= 2% = bioactive
in seminiferous fluid:
-androgen binding globulin ABG
Q: What are the principle actions of androgens in a foetus? (3) Name 2 androgens. Absence results in?
A: Development of male internal and external genitalia
General growth (acting with other hormones)
Behavioural effect (development of sex specific behaviour)
testosterone and DHT
absence of foetal testosterone secretion -> baby may be born with ambiguous genetalia
Q: What are the principle actions of androgens in an adult? (7) How are some androgenic effects mediated?
A: -Spermatogenesis
- Growth and development of Male genitalia (particularly in puberty)
- Growth and development of secondary (accessory) sex glands -> make semen
- Growth and development of secondary sex characteristics -> facial and pubic hair etc
- Stimulation of protein synthesis (increases muscle mass: weight ratio)
- Pubertal growth spurt (with Growth Hormone)
- Behavioural (CNS) effects
by conversion to oestrogen
Q: Define oestrogen. Give 3 examples. Which is the main one during the menstrual cycle? pregnancy? precursor?
A: any substance (natural or synthetic) which induces mitosis in the endometrium (thickens womb)
- 17beta-oestradiol is the MAIN hormone produced in the menstrual cycle
- Oestrone is a precursor
- Oestriol is the main oestrogen produced in pregnancy
Q: How do oestrogens affect the pituitary gland? (2) testosterone?
A: low levels induce negative FB really high (mid cycle) induces positive FB
(when oestrogen levels are high enough for long enough it switches from negative feedback to positive feedback)
negative feedback affect
Q: What are the reproductive effects of oestrogen? (6)
A: -Stimulate proliferation (mitosis) of the endometrium
- Final maturation of the follicle during the follicular phase of the menstrual cycle
- Induction of LH surge resulting in ovulation
- Effects on vagina and cervix secretions
- Stimulates growth of ductile system of breast
- Decreases sebaceous gland secretion (NOTE: androgens stimulate sebaceous gland secretion= opposite)
Q: What are the non-reproductive effects of oestrogen? (7)
A: -Increased salt and water reabsorption
- Increased plasma protein synthesis and therefore drug metabolism (hepatic effect)
- Metabolic actions (e.g. on lipids)-> Tend to increase HDL levels
- Stimulates osteoblasts (androgens also do this)
- Influences the release of other hormones in pituitary gland (e.g. prolactin, thyrotrophin)
- Behavioural effects (responsible for increased sex specific effects/ reproductive behaviour)
- Feedback regulation on GnRH (negative and positive)
Q: Define progesterone. Result? (2) Give 2 examples. Which is the main one?
A: any substance (natural or synthetic) which induces secretory changes in the endometrium (makes it secretory)
makes it ready to receive implanted embryo but if nothing happens -> womb sheds and you get a period
- Progesterone***
- 17alpha-hydroxyprogesterone
Q: What are the effects of progesterone? (5)
A: Stimulates secretory activity in endometrium and cervix
Stimulates the growth of alveolar system in the BREAST (pregnant women have more progesterone which stimulates breast development -> gets them ready for lactating)
Decrease renal NaCl reabsorption - due to competitive inhibition of aldosterone (doesn’t encourage water retention)
Associated with an increase in body temperature (switches from oestrogen to progesterone dominance)
Negative feedback regulation on hypothalamic GnRH
Q: What is the mechanism of action for steroid hormones? What effects do they have?
A: pass easily through the lipid membrane and binds to intracellular receptors in the nucleus
The receptor-hormone complex acts as a transcription factor which leads to the production of new proteins
important genomic factors
Q: Draw the Hypothalamo-Pituitary-Testicular Axis and describe. (8)
A: REFER
- hypothalamus starts during puberty to release GnRH in pulses every 1/2 hours
- GnRH enters anterior pituitary via portal circulation
- gonadotrophs in the adenohypophysis produce LH and FSH
- travel in blood and reach testes
- LH target leydig cells -> produce androgens (testosterone is the main precursor androgen produced)
=> has virilisation effects (development of male physical characteristics) - FSH target sertoli cells (Seminiferous tubules are essentially made up of Sertoli cells (where the final processing of spermatozoa takes place)) -> produce inhibin
=> supports sperm in development (spermatogenesis) (arrow from testosterone to this as well) - both inhibin (direct and indirect) and testosterone have negative feedback effects on hypothalamus and anterior pituitary
- decreases the amplitude of the pulses of GnRH and LH and FSH production decreases
Q: What stimulates leydig cells? sertoli cells? which one needs more and what?
A: GnRH/LH system
GnRH/FSH system
sertoli cells need GnRh/LH/Testosterone system for complete spermatogenesis
Q: Draw a diagram showing the Hypothalamo-Pituitary-Ovarian Axis. (4)
A: REFER
- hypothalamus releases GnRH in pulses every 1/2 hours
- GnRH enters anterior pituitary via portal circulation
- gonadotrophs in the adenohypophysis produce LH and FSH
- travel in blood and reach ovary
Q: What are the phases of the menstrual cycle? (6)
A: 1. Early Follicular Phase (first 3/4 days)
- Early-Mid Follicular Phase (day 4-8)
- Mid-Follicular Phase (day 8-10)
- Late Follicular Phase (day 10-13)
- ovulation (day 14)
- Luteal Phase (day 15-27)
Q: Draw a graph showing how levels of FSH, LH, oestrogen and progesterone vary during the menstrual cycle. Which oestrogen is the main one?
A: REFER
17beta oestrodiol
Q: Describe stage 1 of the menstrual cycle using a diagram. How do hormone concentrations change?
A: early follicular phase
-refer to hypothalamo-pituitary-ovarian axis
every month around 10-12 follicles will enlarge under LH and FSH influence
-follicles consist of an oocyte (egg) and granulosa cells and theca cells (on outside)
said growing follicles mainly make oestrodiol
oestrodiol has negative feedback effect on hypothalamus and the anterior pituitary gland
but at start not a lot of oestrodiol is made (small follicles) -> not a lot of negative feedback so get lots of GnRH, LH and FSH production
LH and FSH increase and 17beta oestrodiol too
Q: Describe stage 2 of the menstrual cycle using a diagram. How do hormone concentrations change?
A: early-mid follicular phase
-refer to hypothalamo-pituitary-ovarian axis and
There is no further increase in FSH or LH
Oestrogen levels are beginning to rise dramatically (increases in the blood and in the ovaries)
Ovary: Local (autocrine) positive feedback loop in developing follicles enhances oestradiol production
THECAL cell = LH Receptor -> respond to LH by increasing androgen production
GRANULOSA cell = FSH Receptor -> responds to FSH by activating AROMATASE = androgens (from thecal cells) to 17b-oestradiol
Oestrogens produced by the granulosa cells will bind to the oestrogen receptor on the same granulosa cell and stimulate the aromatase enzyme via a second messenger system = AUTO-POSITIVE FEEDBACK
This means that the more oestrogen is produced by androgens, the more oestrogen is produced overall due to the positive feedback
follicles get larger as the Granulosa cells multiply and get bigger-> their growth is a competition between eachother
one will get larger than the rest- due to positive feedback
Q: Describe stage 3 of the menstrual cycle. How do hormone concentrations change?
A: mid follicular phase
- LH and FSH levels decrease
- oestrogen increases
eventually the growing follicles make so my 17beta oestrodiol that the pituitary is suppressed (negative feeback)= much less FSH and LH produced
(inhibin produced by ovaries also has role in negative feedback)
A lot of these follicles are FSH dependent so by removing FSH, you kill the cells which are still FSH dependent (ATRESIA)
usually ONE OVUM which can grow under its own production of local oestrogens and this is the GRAAFIAN FOLLICLE (dominant follicle)
Q: What is the graafian follicle? What does it produce? What does it eventually cause?
A: The LARGEST follicle - it no longer needs FSH to develop and proliferate
It continues to grow and produce large amount of 17b-oestradiol
rising concentration of 17b-oestradiol in the absence of progesterone, for a minimum of 36 hours and at a sufficient level, results in the negative feedback switching to positive feedback on GnRH/LH secretion = which causes the LH SURGE
Q: What occurs during phase 4 of the menstrual cycle? Hormone concentrations?
A: late follicular phase
had high oestrogen in the absence of progesterone for long enough to induce an LH surge (graafian follicle) (just before ovulation)
The LH surge at this point is sufficiently high to overcome the FSH negative feedback and so you get a lesser FSH surge (just before ovulation)
little rise in 17a-hydroxyprogesterone just before ovulation
Q: What occurs during phase 5 of the menstrual cycle?
A: ovulation
little rise in 17a-hydroxyprogesterone
large LH surge
smaller FSH surge
egg is released
-graafian follicle breaks open and egg starts travelling down Fallopian tubes -> remnants of the graafian follicle form the corpus luteum (which makes progesterone)
Q: What occurs during phase 6 of the menstrual cycle? Include diagram. How do hormone concentrations change?
A: luteal phase
corpus luteum makes mainly progesterone (inhibin and oestrodiol too) (stimulated by FSH and LH as still has receptors for them)
get rising progesterone and oestrogen levels and eventually exerts negative feedback effect on the hypothalamo-pituitary axis - direct effect on ant pituitary to decrease FSH and LH levels and indirect effect on hypothalamus to decrease GnRH levels
Unless something happens to produce FSH and LH, as the levels fall away, the corpus luteum will no longer be stimulated to produce OESTROGEN and PROGESTERONE = levels begin to fall
As these levels fall, the negative feedback on the hypothalamo-pituitary axis is reduced so LH and FSH levels start to RISE again so they can reach a critical level at the start of the cycle again
Q: How does the final stage of the menstrual cycle vary depending on whether fertilisation occurs or not?
A: If fertilisation occurs, you will need a lot of oestrogen and progesterone so the placenta, at an early stage, will start producing a molecule which mimics the effects of LH - Human Chorionic Gonadotrophin (hCG)
If fertilisation does NOT occur - PROGESTERONE, OESTRADIOL and INHIBIN exert a negative feedback on LH and FSH release - leading to LUTEOLYSIS and MENSTRUATION
Q: Define amenorrhoea. Primary? Secondary?
A: absence of menstrual cycles
PRIMARY = menstrual cycles NEVER happened
SECONDARY = menstrual cycles did happen but then stopped (can be physiological e.g. pregnancy)
Q: Define oligomenorrhoea. Cause?
A: infrequent menstrual cycles - less than every 6-8 weeks
Causes: various, but can be due to absence of LH surge (e.g. due to insufficient oestrogenic effect at the end of the follicular phase)
Q: How is infertility defined? Causes? (5)
A: inability to get pregnant (women) or the inability to impregnate (men) following 12 months of regular unprotected sex (2/3 times a week)
- pituitary failure (if you develop adenoma- small pit. tumour//born with it= congential pituitary failure)
- prolactinoma (high levels of prolactin- weak effect)
- testicular failure eg mumps, klinefelters (XXY)-lose sperm making abilities in 20s
- ovarian failure eg turners (XO)
- polycystic ovarian syndrome (PCOS)- going through menopause early/before 40years
Q: What’s the criteria for PCOS?
A: polycystic ovarian syndrome
need 2/3 at least:
- infrequent periods
- hyper-androgenaemia eg increased male pattern hair/acne
- polycystic ovaries- increased number of enlarging ovarian follicles)
