12 The Gonads II Flashcards
(34 cards)
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
