Please enable JavaScript.

Coggle requires JavaScript to display documents.

Reproduction - Coggle Diagram

- - - - resemble estrogen (eg: soya products), these soya products in combo with low fibre and high fat western diet increase plasma oestrogen and also inhibit testicular maturation and function
    - - nandrolone (anabolic steroids), a testosterone analogue causes increased negative feedback and decrease pituitary LF and FSH levels
      - convert to oestrogen like molecule and cause negative feedback (turns off GnRH production, LH/FSH production and testosterone production) and the excess oestrogen can lead to feminisation (breast formation)
      - testicular atrophy (sertoli cells die off), altered spermatogenesis, infertility, prostrate hypertrophy and gynecomastia (breast tissue growing)
      - Alcohol consumption
        
        release b-endorphins (pleasure chemical) and turn off GnRH secretion. The alcohol is membrane permeable and can affect cell function of signalling pathways (such as: LH, leydig cells etc..) and cause low sperm sounds and infertility
- - - - follicular phase: characterised by presence of maturing follicles. Follicles operate to produce mature egg for ovulation
      - luteal phase: corpus lutein is present and prepare reproductive tract for pregnancy if fertilisation takes place
    - - follicular phase
        
        start with primary follicles with primary oocytes (egg - purple in middle) and single layer of granulose cells that provide mechanical and nutritional cell . These follicles pofilerate and growth at start of cycle
        
        Granulosa cells layer greatly proliferate and zone pellucida between oocyte and rest of follicle
        
        then outer thecal cell layer generated (come from surrounding ovarian tissue)
        
        developing secondary follicle: antrum formation (contains follicular fluid and mucopolysaccharides) support oocyte
        
        one follicle chosen and it is the Graafian follicle, the one grows fatstest will be chosen because it produces oestrogen and inhibits growth of others
        
        1 more item...
      - luteal phase (collapse) and become corpus luteum (remains of follicle) and turns into hormone factory will produce progesterone and estrogen
        
        yellow colour due to cholesterol: building block of steroid hormones, so can convert to progesterone and estrogen
        
        It gets larger and blood supply for these metabolic processes. If no fertilisation, it will go into degeneration phase that lasts for 14 days and then returns as a primary follicle to begin the cycle again
    - - LH and FSH promote maturation of ova and stimulate secretion from ovaries of oestrogens and progesterone
        
        hormonal changes during follicular phase (FSH AND OESTROGEN)
        
        The relatively high levels of FSH at the start of cycle (low at end) stimulates growth of follicles and promotes antrum formation and starts cycle
        
        FSH and LH (relatively high) stimulations estrogen secretion by selected grafian cell. The estrogen in green is from follicle and will stop others from growing
        
        Cholesterol is a building block, so thecal stimulated by LH will take the cholesterol and convert to androgens. The FSH stimulated by granulose cells to convert androgen to estrogen , increase oestrogen nd larger follicle cells we have more thecal cells. and granulose cells and therefore estrogen. The rise in estrogen is due to enlargement of follicle. FSH will slowly decrease due to increased negative feedback. Rising estrogen have negative feedback on GnRH and FSH, the LH keeps rising --> tonic secretion and not sensitive to negative feedback by secretion. We hit peek of estrogen and triggers LH/ FSH surge.
        
        Moderate level of estrogen is moderate negative feedback. Two sets of neutrons that are sensitive (negative feedback ones) and the neurons with low affinity for neurons are stimulated when there's a high level of estrogen and undergo positive feedback and enhance LH secretion . The GnRh will go up. Meiosis occurs before ovulation and happens due to LH surge and get gamete, halts estrogen secretion and induces prostaglandins production (activates myoepithelial cells in uterus and that ruptures upper part of ovary) LH surge induces ovulation
        
        LH surge desensitisation of anterior pituitary to GnRH and effects of estrogen and no more LH/ FSH left even if stimulated, so FSH and LH start to plummet.
        
        Hormonal changes during the luteal phase (progesterone and estrogen)
        
        Basically the hypothalamus release of GnRH and consequently LHmaintains the corpus lute and stimulates progesterone and estrogen secretion. Therefore progesterone and inhibin A increase
        
        Inhibin A acts as negative feedback for hypothalamus and anterior pituitary resulting in low LH levels. As a result of no fertilisation and deceased LH, the corpus lutem (need Lh to stay functional or else apotosis) degenerates . Therefore progesterone and estrangen levels fall, no negative feedback and therefore jump in FSH and LH rise again and starts the cycle again
- - - - First six weeks: tissues of body turning to gonads can go either depending on kind of signals received
      - why do males have nipples? : nipples form around fifth week
      - 7th week of gestation: changes occur and get either male or female lines
        
        Male: Y chromosome (SRY region that codes for certain protein called H-Y antigen). The H-Y antigen is a signal that causes gonadal tissue to form testes. The testes secrete androgen (male hormones) and activate other tissues to form anatomy
        
        No Y chromosome --> no H-Y antigen and so ovaries form that do not secrete any hormones. In the absence of no hormones will result in female anatomy
  - - - systems initially undifferentiated
        
        No H-Y antigen--> Sertoli cells in testes secrete antimullarian hormone that attacks mullarian ducts and causes regression (rid of female system), since it doesn't produce AMH or testosterone
        
        H-Y antigen --> Leydig cells secrete testosterone which stimulates/ support and induce growth and differentiation of wolfian ducts system and produce AMH and testosterone and induce male system to grow
        
        AMH: rids female system by attacking mullarian ducts
      - External genitalia
        
        embryonic testes produce testosterone and that's converted by 5a reductase to convert to dihydrotestosterone and together induce growth and differentiation of the male external genitalia
        
        No embryonic testes >> no testosterone or dihydrotestosterone and no female external genitalia
        
        Genetic defects/ mutation
        
        Androgen insensitivity syndrome: male (not sensitive to testosterone and no test receptors for it, so testes will produce testosterone with no effect) so have female external genitalia
        
        5a reductase deficiency: won't make this reductase and won't make dihydrotestosterone (main player). The mutation will result in testosterone but look much more like female than male. During puberty testosterone takes over and gives final growth spurt and turns to penis 'penis at 12 syndrome'
        
        Genitalia tubercule develops into: clitoris(female) or glans (male)
        
        Urethral fold and labioscrotal swelling into: labia minor and labia major (female) or urethra (fusion of folds) and scrotum (male)
        
        urogenital slit developer in vaginal opening and urethra (female)
- - - - pituitary gland plays a role, so neutrons releasing GnRH that travels down to portal system to anterior pituitary and binds to receptors on certain endocrine cells that going to produce reproductive hormones
      - The hypothalamus will produce gonadotropin releasing hormone that binds to receptors on endocrine cells which produce LH (luteinzing hormone that induces hormone secretion) and FSH (follicle stimulating hormone that induces germ cell development) and go on to govern reproductive function in male and female
    - - released at puberty and results from the synchronous firing of many hypothalamic neurons
      - release is essential is a code and therefore released in accordance to time
      - appropriate control and maintenance of reproductive axis under different conditions occurs via modulations of the frequency and amplitude of GnRH release
      - Pattern of GnRH secretion changes during development
        
        high levels during neonatal period
        
        periods of quiescence in mid-childhood
        
        sleep-entrained reactivation of GnRH secretion at onset of puberty
        
        adult pattern of pulsatile secretion: Male approx every 2 hours and female varies with stage of menustral cycle
  - - - production of sperm (spermatogenesis)
        
        Commences after puberty
        
        takes place within seminiferous tubules (tiny convoluted hollow tubules)
        
        each tubule bounded by basement membrane and smooth muscle layer to provide peristalsis (muscle push them out of testes and ready for ejaculation)
        
        semineforous tubules contain
        
        spermatogenic cells: divide and differentiate into mature sperm
        
        Sertoli cells: provide mechanical and nutritional support for spermatogenic cells
        
        line seminiferous tubules
        
        connected by tight junctions, which seperate basal and central compartments (Sertoli cell barrier), which prevents chemicals and hormones in the blood from entering lumen of the seminiferous tubules and also prevents anything within from escaping
        
        synthesise and secrete seminiferous tubular fluid which contains androgen-binding protein (keeping testosterone levels at a regulated level to drive spermatogenesis) (testosterone- binding protein). These are cholesterol based and can pass through lipid membrane, so tight junctions don't stop testosterone being made in seminiferous tubules or from leaving cause it can move down concentration gradient. Testosterone anabolic and need to develop growth
        
        secrete stimulatory and inhibitory hormones
        
        phagocytise defective sperm: 12% defective
        
        drain out into epidermis and then drains into vas deferns. They have arterial blood and venous blood and spermatogenesis is better in heat 32 - 33 degrees C (hence external away from body)
        
        How does it keep it in right temperature for optimal spermatogenesis? the arm blood in arteries coming in is 7degree and need 32 degree, the blood from scortum (due to large SA) is cool and heat transferred from arteries to venous blood. So the blood coming into the testes is cooler than normal
        
        spermatogenesis
        
        spermatogenic cells move away from basement membrane (outer part of tubular system) of seminiferous tubules toward tubule lumen
        
        mature spell expelled into lumen of the tubule, takes about 70-80 days
        
        originate from reproductive germ cells called spermatogonia
        
        relationship between sertoli and germ cells
        
        Initially the spermatogonia starts off with splitting into two, where one stays behind (not loose supplies) and other goes on to become sperm. The tight junctions that doesn't allow any substances go either way, but developing spermatogonia that dissolves tight junction and creates one behind and eventually leading to lumen. The growth of spermatogonia into primary spermatocytes and then first meiosis to make secondary spermatocytes and then form spermatids (joined after second meiosis) and then become sperm released into lumen
        
        sperm morphology
        
        head
        
        nucleus (genetic material used to fertilise egg) and acrosome (an enzyme hilled body for penetration of ovum
        
        mid piece
        
        lots of mitochondria that provide fuel for tail
        
        tail: flagella like motion for mobility
        
        sperm maturation
        
        swept along lumen by peristaltic movement, swept into epididymis (undergo development and gain ability to move and fertilise) and then into vas deferent which is storage facility for sperm awaiting ejaculation
        
        cytoplasmic bridges in spermatogenesis
        
        until sperm maturation is complete, spermatocytes hare cytoplasm by cytoplasmic bridges (visible in secondary spermatocytes and spermatids
        
        this permits exchange of cytoplasmic constituents
        
        allows spermatocytes with Y chromosome (15 genes) to receive cellular products essential for sperm development coded for on the X chromosome (1000s genes)
      - secretion of sex hormones
      - transport of sperm from male to the female