Lecture 13 & 14: Male and Female Sex Homones Flashcards
1
Q
How is the male reproductive system produced from birth?
A
- Wks 1-6: Females and males arent different
- 7th week: SRY gene on Y chromosome produces testis determining factor
- Triggers gonads (precursor) to become testis (gonad cortex regresses and medulla forms testis)
- They then produce leydig cells and sertoli cells which secrete hormones
2
Q
What do the leydig cells produce and what are their function in males?
A
- Leydig cells: produces testosterone allows development of Wolffian duct to form epididymis (sperm storage and maturation), vans deferens (sperm transport), Seminal vesicles (semen production) + external genitalia
3
Q
What do the sertoli cells produce and what are their function in males?
A
- Secrete anti-mullerian hormone which causes the regression of the mullerian duct which causes female structures to regress
4
Q
What is testosterone?
A
- Potent androgen synthesised from leydig cells in testes.
- Also some produced in adrenal cortex in both sex
- Derived from cholesterol
- Responsible for maintenance of male characteristics
- DHEA & androstenedione are adrenal androgens secreted by the adrenal cortex and precursors to the production of testosterone. weak.
5
Q
What are the products that can be produced from testosterone?
A
- DHT by 5-a reductase type 1 and 2: more potent than testosterone and stimulates external genitalia + male characteristics
- Estradiol by aromatase (most potent oestrogen and produces female organs)
6
Q
What are the functions of testosterone?
A
- Stimulates enlargement of testes and male accessory organs
- Increases body hair
- Thickening of vocal cords
- Thickening of skin
- Muscle and bone growth + wide shoulders
7
Q
Where is the sperm produced?
A
- In the testis (coiled structure) in the seminiferous tubule
- Sertoli and Leydig cells are present
- Has spermatogonium which differentiate into sperm and needs presence of sperm
8
Q
What are the target organs for testosterone?
A
- Male sexual organs
- Kidney
- Skin
- Muscle and bones
- Brain: aggression & cognition
9
Q
What is the mechanism of action of steroids and how they regulate male development?
A
- DHT binds to androgen receptor
- Binding to the receptor promotes the release of the heat shock protein (that kept it inactive)
- Steroid receptor complex migrates to the nucleus
- Binds to specific regions of DNA that contain androgen response elements
- Drives expression of genes that determine male phenotype
10
Q
What are the levels of testosterone like in males in their lives?
A
- Mini puberty at 6 months and they then stay low until puberty
- High at puberty and remain high in adult life
- Starts to decline at old age
11
Q
Describe the hormonal regulation of spermatogenesis
A
- Stimuli (low levels of testosterone)
- Causes release of gonadotrophin releasing hormone from the hypothalamus
- Stimulates the anterior pituitary gland to release LH and FSH
- LH activates leydig cells to secrete testosterone
- FSH acts on sertoli cells and secretes androgen binding protein into lumen which binds to T or DHT and concentrates them in semineferous tubules which provide high conc for spermatogenesis. Also produces inhibin
- Inhibin and high T (negative feedback)
12
Q
What happens when you inject anabolic steroids for male?
A
- Are exogenous androgens
- Repeat injections = high level of androgen
- FSH and LH is supressed
- FSH cant stimulate ABP -> spermatogenesis is inhibited
- High T is metabolised to oestrogen = enlarged breast tissue
13
Q
What is the process of gametogenesis in males?
A
- Germ cell (spermatogonium) = 2n diploid w/ 23 pairs of chromosomes (limited mitosis to incr spermatogonia in early)
At puberty: mitosis to produce another spermatogonium (remains in stem cell pool) and a primary spermatocyte. - Primary spermatocyte (2n) = meiosis 1 and produces 2 secondary spermatocytes (n)
- Undergo meiosis 2 and produces 4 spermatids
- Each undergo structural changes to produce mature sperm
14
Q
What is primary and secondary hypogonadism?
A
- Primary hypogonadism: Issues w/ testes not producing enough testosterone even with proper signals
- Secondary hypogonadism: Issues w/ pituitary/hypothalamus (not sufficient GnRH/LH/FSH)
15
Q
How is the female reproductive system produced from birth?
A
- 1-6 weeks undifferentiated
- 7th week: No SRY gene, no TDF, no AMH, no testosterone, no DHT
- Wolffian duct regresses and mullerian duct becomes fallopian tube, uterus, cervix
- Gonad cortex becomes ovary and medulla regresses
16
Q
What is the gametogenesis like in femals?
A
- Germ cell: oogonium (2n) in fetal mitosis. Fixed number in birth and undergo mitosis to produce primary oocytes (2n)
- Primary oocytes undergo meiosis 1 in puberty and produce a secondary oocyte (n) and first polar body (small + eventually degenerates)
- Secondary oocyte released from ovary and only undergoes meioisis 2 if fertilisation occurs also a secondary polar body is produced and degenerates
17
Q
What are the follicular and luteal phases of a secondary oocyte and how its released?
A
- Follicular phase: Primordial follicle -> primary follicle -> Secondary follicle -> Graafian follicle
- In ovulation Graafian follicle releases secondary oocyte into fallopian tube
- Luteal phase: If fertilisation: Graafian follicle becomes corpus luteum and secretes oestrogen and progesterone for pregnancy and remains active for 10-12 weeks until placenta takes over hormonal control. No fertilisation: Graafian follicle becomes corpus luteum, which degenerates after 10-14 days = corpus albicans. Low P and O = shedding
18
Q
How does oestrogen regulate gene expression
A
- Mediated by oestrogen receptor
- The oestrogen-oestrogen receptor complex binds to specific DNA sequences which are called hormone response elements which activates transcription for target genes and controls gene expression
19
Q
What are the functions of oestrogen?
A
- Stimulates Uterine Growth: allow implanatation of blastocyst
- Breast Growth:
- Menstrual Cycle:
- Secondary characteristics
20
Q
What are the stages of the menstrual cycle?
A
- Late Luteal Phase (Pre-Menstrual Phase): 5–7 days, All hormones (progesterone and oestrogen) are low, triggering the shedding of the uterine lining (menstruation), stimulates GnRH from the hypothalamus, which prompts the pituitary to release FSH and LH, starting the next cycle.
- Early to Mid Follicular Phase: FSH stimulates follicular growth in the ovaries, dominant follicle releases oestrogen This inhibits FSH (preventing multiple follicles from developing) and causes the uterine lining to thicken in preparation for a potential pregnancy.
- Ovulation: A surge in LH triggered by peak oestrogen levels causes the egg to be released into the fallopian tube, Inhibin produced by the dominant follicle suppresses FSH secretion.
- Early to Mid Luteal Phase: If no fertilization occurs, the corpus luteum degenerates, drop in P & O, causing the endometrial lining to shed. This drop in hormones triggers menstruation, and the cycle begins again.
21
Q
What do the Theca cells (outer) do and produce? - found on graafian follicle
A
- Contain LH receptors
- Produce androgens (androstenedione & testosterone) in response to LH which are then converted to oestrogen by Granulosa cells
22
Q
What do the Granulosa cells (inner) do and produce? - found on graafian follicle surrounds oocyte
A
- Contains FSH receptors and respond to FSH stimulation
- Using aromatase they convert androgens produced from theca cells into oestrogen
- Secretes inhibin
- Produces anti mullerian hormone in early stage follicles which is important for follicular development (make follicles less sensitive to FSH, preventing excessive depletion of ovarian reserves
23
Q
What are the 3 forms of oestrogen?
A
- 17 B estradiol (E2)
- Estone (E1): in post menopause produced by fat cells (weak form of E2)
- Estriol (E3): pregnancy -> stronger than E1
24
Q
What are the 3 forms of progestegans?
A
- Pregnenolone -> metabolic intermediate
- Progesterone -> naturally occuring
- 17 OH progesterone -> cortisol
25
Q
Name some examples of androgens (typically thought as male hormones)
A
- DHT
- Testosterone
- Androstendione
- DHEA
26
Q
What happens to the sperm and egg after fertilisation?
A
- Sperm fertilises egg = zygote and divides rapidly = morula.
- After 5-6 days = blastocyst
- Male + fem genetic material combines 24-30 hrs after fertilisation
- Blastocyst attaches to uterine wall on day 6-7 and implants on 11/12 day
- Embryo = 4 weeks
27
Q
How does HCG support early pregnancy?
A
- After fertilization, the placenta releases human chorionic gonadotropin (HCG), which keeps the corpus luteum from degenerating.
- This enables the corpus luteum to continue producing progesterone and oestrogen, which maintain the uterine lining and prevent the release of more eggs (no ovulation).
- As the placenta begins to produce sufficient progesterone and oestrogen, HCG levels decrease. By this time, the placenta has taken over hormone production, and the corpus luteum is no longer needed.
28
Q
What are some names of placental hormones?
A
- Oestrogen - E3
- HcG
- Progestins
- Placental lactogen (hPl): placental growth hormone which breaks fats down from mum to feed baby. Can cause insulin resistance (diabetes and carbohydrate intolerance)
29
Q
How are the mammary glands developed?
A
- Modified sweat glands in both genders but only functional in females in response to prolactin (produce milk)
- E2 causes ductal growth and progesterone causes alveolar proliferation and inhibits milk production and secretion in late pregnancy
30
Q
What are the functions of prolactin and oxytocin in breastfeeding?
A
- Prolactin: Released from pituitary gland. Helps alveoli (milk producing cells) to make milk
- Oxytocin: Its production is stimulated by oestrogen and inhibited by preogesterone. In response to infant suckling and allows milk to flow out of nipple
31
Q
Name examples of labour related drugs?
A
- Oxytocin: Enhances contractile activity of uterine smooth muscle
- Selective B2 adrenergic receptor antagonist: Prevents smooth muscle contractions, and slow contractions, prevents premature labout and use in over 20 week gestation. Adverse effects: palpitation, tachycardia, hypotension
