physiology of the male and female reproductive tracts

Question 1

where does Spermatogenesis and spermiogenesis

and testosterone production occur

Answer 1

testes

Both of these functions (endocrine and reproductive) are carried out in distinct cells of the testes.

Spermatogenesis and sperimiogenesis take place in the convoluted seminiferous tubules in the testes, while testosterone production proceeds in the interstitial cells of Leydig, in between these seminiferous tubule coils.

Question 2

describe Cryptorchidism

Answer 2

undescended testes

• 3% newborn
• 30% premature
• Overheating, infertility
• treated by Surgery
• increased Cancer risk

Question 3

describe temperature regulation of the testes

Answer 3

• Ideally, testes should be kept at 32oC.
• The reason for the external location of the testes is to facilitate the 2-3oC below core temperature that is necessary for spermatogenesis.
• Cremaster muscle - helps to alter the distance that the scrotal sac hangs from the abdomen, conserving heat in cold conditions and allowing ventilation and cooling in warm conditions.
• Spermatic arteries and Pampiniform plexus
• Counter current heat exchanger - arteries parallel and opposite direction to venous drainage - created temperature gradient

Question 4

describe sperm formation

Answer 4

Four stages:
- Spermatogenesis (production of haploid gametes from diploid precursors)

• Spermiogenesis (The gametes (spermatids) change to become motile
• Spermiation (release of spermatocytes into the lumen of the seminiferous tubules where they swim in seminiferous fluid)
• Capacitation (in epididymis and female genital tract). Final step rendering spermatocytes capable of fertilising the ovum

Question 5

describe spermatogenesis

Answer 5

male reproduction lecture - slide 8

• Spermatozoa develop from progenitor cells next to the basement membrane called spermatogonia.
• These divide by mitosis with one of the resulting cells maturing to become spermatozoa and the other one left behind to form a permanent reserve.
• After this initial differentiation, the daughter cell, undergoes meiosis.
• This involves 2 divisions.
• Initially the genetic material in the cell duplicates, giving a primary spermatocyte with 2 copies of each of the 23 chromosome pairs (essentially giving the primary spermatocyte 2n + 2n genes).
• The gene pairs (homologous chromosomes) line up and exchange genetic material with one another (genetic recombination).
• These then split and cell division occurs (meiosis I) to form the secondary spermatocytes which are haploid cells, each chromosome now being unpaired (n + n in each cell).
• Meiosis II occurs after this, the final division with each cell (spermatid) containing the haploid number of chromosomes unduplicated (n).
• These spermatids must undergo further maturation to become fully motile spermatozoa (spermiogenesis, spermiation and capacitation).

Question 6

describe spermiogeneisi

Answer 6

• Spermatids = correct genetic material but not structural or motile
• Sertoli cell “Nurse cell fxn”:
  > Nourishment
  > Toxins
  > Blood testicle barrier
  > Spermiation & secretion of seminiferous fluid

Question 7

describe a spermatocyte

Answer 7

male reproduction lecture - slide 10

• Head; nuclear material + acrosomal cap

- Mid section:
> Centrioles (cell div)
> Mitochondria
> Microtubular tail - flagellum - rotating corkscrew fashion 
> Corkscrew motility

• Capacitation in epididymis and female genital tract

Question 8

describe hormonal control of sperm production

Answer 8

male reproduction lecture - slide 11

• gonoadotropin releasing hormone is released from the hypothalamus daily, keeping the processes of gametogenesis and testosterone formation “ticking over”.
• It is carried in the hypothalamo-pituitary (hypophyseal) circulation until it reaches the anterior pituitary where it stimulates the release of Follicle Stimulating Hormone (FSH) and Luetenising Hormone (LH).
• These hormones are carried to target cells in the testes.
• Leutenising hormone exerts its effects on the interstitial cells of Leydig and causes them to release testosterone, while Follicle Stimulating Hormone (FSH) promotes spermatogenesis by acting (along with locally produced testosterone) on the Sertoli cells.
• Feedback control is exerted by testosterone directly on LH production in the anterior pituitary and GnRH production in the hypothalamus, and by the hormone Inhibin on FSH production in the anterior pituitary.

Question 9

describe testosterone function

Answer 9

• Essential in spermiogenesis (local source)
• Devt of male phenotype in utero
• Male reproductive structures in early adulthood, also secondary sexual characteristics
• Adolescent growth spurt in bones and musculature; fusion of epiphyses
• Muscle deposition
• Increased metabolic rate
• Behavioural changes; libido

Question 10

describe how a penis becomes erect

Answer 10

• Turgidity of corpus cavernosa and spongiosum
• Erotic stimuli, mechanical stimuli to glans and anterior penis
• Venous compression - penis enlarges
• Sympathetic withdrawal and Parasympathetic activation
• NO (nitric oxide) vasodilators and cGMP drugs - The NO vasodilator pathway is thought to be essential to erection and drugs that increase production of NO and its related vasodilators (cyclic GMP) are used in the treatment of erectile dysfunction, and, at this stage, have become household names.

Question 11

describe ejaculation

Answer 11

2 phases

Emission; sympathetic reflex stimulating smooth muscle in epididymus, vas deferens, seminal vesicle to mix up secretions forming semen in the urethra

Expulsion; somatic reflex of skeletal muscles around the base of the penis (bulbocavernosus) expelling semen with some force into the vagina

3.5 mls per ejaculation (each ml containing 20 – 100 million sperm)

Question 12

describe the contents of semen

Answer 12

• The semen itself is composed of fluid from the seminal vesicle (60% by volume), a fluid rich in fructose to nourish the sperm, prostaglandins and agents which promote clotting of semen.

Of the remaining volume, 25% comes from the prostate gland containing citrate and proteases which help break down clotted semen.

Prostate specific antigen (PSA) is also secreted, which may be used clinically as a marker for prostate cancer.

The remaining fluid is the mucoid secretion of the bulbourethral gland which helps lubricate the urethra and clear away urine before ejaculation (can also carry sperm from previous expulsions; one of the reasons for failure of withdrawal method of contraception)

Question 13

describe oogenesis

Answer 13

• Female reproduction lecture and slide 6
• or see drawn handout

1 – 2 million oogonia at birth of which 4 – 5 hundred reach maturity

• Maturation of oocytes from their primitive progenitor cells (oogonia) begins even before birth in the female.
• Initially the oogonia undergo a mitotic division to multiply numbers of potential oocytes.
• The oogonia then commence the first meiotic division before birth to form the primary oocytes.
• Thence all division stops until the female reaches puberty.
• At this point the first meiotic division is completed, giving 2 distinct cells.
• One is a haploid cell rich in cytoplasm and nutrient, the secondary (2o) oocyte.
• This, although haploid with unpaired chromosomes still has twice the amount of genetic material of the final gamete.
• The second smaller cell is called the polar body, consisting largely of chromosomal material.
• It may be of interest that all of the female gametes are formed at birth, and they age with the individual. This may explain why older mothers with (older gametes) are more at risk of giving birth to children with some genetic abnormalities (eg. Downs syndrome).

Question 14

describe the ovarian cycle

Answer 14

L = female reproduction
S = 7

Follicular phase (Day 1-14) - very variable time:

• antral follicles and consist of the primary oocyte surrounded by a single layer of cells, the granulosa cells, sitting upon a connective tissue basal lamina.
• The granulosa cells then multiply and create a layer of mucopolysaccharide around the ovum, called the zona pellucida.
• A layer of cells outside the basal lamina differentiates and forms the theca cells.
• At the start of each ovarian cycle, several of these primordial follicles enlarge and a cavity becomes visible filled with follicular fluid produced by the granulosa cells.
• Only one of these follicles develops further, becoming the dominant follicle with the other ones regressing or becoming atretic.
• The remaining follicle, now called the Graafian or antral follicle enlarges and the theca cells differentiate further, becoming the theca interna and theca externa.
• At around 14 days, the follicle is so large that it distorts the surface of the ovary.
• Fluid accumulation within the follicle and proteolytic enzyme activity combine to allow the follicle to rupture, releasing the ovum (secondary oocyte) to the awaiting fimbriae of the fallopian tube (ovulation).

Luteal phase (Day 14-28):

• After rupture the follicle fills with blood, becoming the corpus haemorrhagicum.
• Interestingly, many women get some ovulatory pain (termed “Mittleschmerz”) thought to be due to a little irritation from some of this blood in the peritoneum.
• The granulosa and thecal cells swell up, become rich in yellow fatty deposits, and blood vessels infiltrate the follicle (attracted by vascular endothelium growth factor(VEGF)), by now called the corpus luteum (yellow body), facilitating its important endocrine function.
• If fertilisation doesn’t happen, the corpus luteum degenerates after about 10 days, which precipitates the breakdown of the uterine wall (menses).

Question 15

describe hormonal control of the ovarian cycle

Answer 15

female reproduction slide 8

• As we’ve already seen there are 2 phases of approximately 2 weeks each in the ovarian cycle, a preovulatory follicular phase and a postovulatory luteal phase, named according to the structure predominantly secreting sex steroids at the time.
• At the start of the cycle Gonadotropin releasing hormone (GnRH) is secreted by the hypothalamus, travels down the hypophyseal portal circulation and causes the release of Follicle Stimulating Hormone (FSH) and Luteinizing hormone (LH) from the anterior pituitary gland.
• These hormones do “exactly as it says on the tin” starting the cycle by stimulating the development of primordial follicles.
• FSH encourages cell division and oestrogen secretion by the granulosa cells, with LH functioning in the formation of the luteal body later in the cycle.
• LH also has a role in the early part of the cycle, stimulating androgen production by the theca cells, androgens which then diffuse into the granulosa cells to be converted into still more oestrogens.
• Normally the gonadotropins are inhibited by the rising concentrations of oestrogens, but after about day 10, oestrogen levels actually stimulate LH secretion, giving rise to a dramatic surge by day 14 which stimulates ovulation.
• The corpus luteum takes over hormone production, producing oestrogen and especially progesterone.
• The levels of these hormones negatively feedback on FSH and LH,keeping them low.
• At around day 22 -24, the corpus luteum undergoes a preprogrammed degeneration or atresia, causing a rapid falling off in hormone levels.
• This removes the negative feedback effect on GnRH, causing its level to rise again, repeating the cycle.

Question 16

describe the uterine cycle

Answer 16

female reproduction lecture - s 10

• At the beginning of the menstrual cyle, about two thirds of the thickness of the endometrial wall sloughs off, leaving just the deep stratum basale layers.
• Under the influence of oestrogens produced in the developing follicles, the uterine lining thickens and proliferates (hence the name of the phase), forming many tube like glands (so called “test tube” glands).
• After ovulation, the predominant hormone is progesterone. This maintains the uterine lining.
• The test tube glands lengthen without a corresponding thickening of the uterine wall and so become tortuous and “saw toothed” in profile.
• They become highly vascularised and fill up with secretions rich in glycogen, ideal for nourishing any potentially implanting embryo.
• If there is no fertilisation and accompanying implantation, then the rapid fall in hormone levels coming from atresia of the corpus luteum at about day 24 causes ischaemia and infarction of the endometrium which subsequently sloughs off and is shed during the menstrual flow.

Question 17

describe secondary sexual characteristics of women

Answer 17

• Fat deposition (breasts and thighs, female specific)
• Breast development
  > Oestrogen – duct
  > Progesterone – secretory lobules
• Wide hips
• Maintenance of voice
• “Flat top” pattern of pubic hair dev’t
• Uterine muscle effects
• Behavioural characteristics

Question 18

describe the process of fertilisation

Answer 18

• Egg must be present (fimbriae, slow wafting and peristalsis)
• The egg is pulled in by the fimbriae of the fallopian tube, and wafted along the tube itself by the action of cilia. This is a very slow process so fertilisation normally takes place in the outer third of the fallopian tube.

Sperm must be present

• Mucous plug only passable when oestrogen/progesterone high
• Only the best sperm get through (5%)
• Uterine contractions (<0.001% arrive at the ovum)

Sperm Capacitation

• Of the approximately 100 to 300 million sperm released in a single ejaculation, only a couple of thousand reach the ovum.
• Theyre guided by chemoattraction of the sperm to substances produced by the ovum.
• They then penetrate the corona radiata of the ovum where they burrow through the granulosa cells to reach the membranous zona pellucida, sticking to it.
• At this point the acrosomal reaction occurs, with the breakdown of the acrosome releasing enzymes (acrosin, related to trypsin) that break down the zona pellucida.
• Once one sperm is through to the ovum, the protein fertilin on the surface of the sperm head permits fusion of the sperm to the ovum membrane.
• This fusion, as well as allowing the sperm access to the ovum, also changes membrane potential in it so as to prevent polyspermy.
• Very rapidly afterwards, the zona pellucida changes structurally to permanently bar access to the ovum.

Question 19

describe the initial cell division after fertilisation

Answer 19

fertilisation L - slide 9

Once the male pronucleus enters the ovum, the 2^o oocyte completes the second meiotic division to form the ovum and the second polar body.

• The genetic material from the male and female coalesce to form a diploid zygote.
• This then immediately starts mitotic cell division to eventually become a solid ball of cells, the morula.
• The morula gets transported to the uterus via cilia and persistaltic movements of the fallopian tube.
• Once in the uterus, the ball of cell develops into the blastocyst.
• The blastocyst consist of an outer layer of trophoblast cells, surrounding a fluid cavity, the blastocoele and a small mass of cells the inner cell mass, with the trophoblast forming the foetal placenta, the blastocoele the yolk sac and the inner cell mass becoming the embryo itself.

Question 20

describe implantation

Answer 20

fertilisation L - s 11

• Initially, (7-10 days), the morula and blastocyst are nourished by the glycogen from mucous secreted by the uterine sawtooth glands.
• However, after this period, the embryo must associate itself more with the uterus.
• The trophoblast cells start to digest the wall of the uterus, sending finger like projections into it, releasing nutrients for the embryo.
• As well as this, the process causes the release of prostaglandins that make the endometrial lining more vascular, forming the decidua, into which the embryo embeds itself fully after about 12 days.
• Placental trophoblast no MHC I and II genes - instead HLA-G gene (non polymorphic) - so No rejection

Question 21

describe the formation of the placenta

Answer 21

fertilisation L - slide 12

• Eventually a more permanent metabolic attachment between mother and foetus must develop, as cannibalising endometrial tissues provides only a finite source of nutrients and gases.
• The chorion, a double cell layer derived from the foetal trophoblast erodes the capillaries of the decidua forming large blood filled spaces into which chorionic fingers project.
• Each of these chorionic fingers has foetal capillaries at its core.
• The maternal blood is kept from coagulating by substances secreted by the chorion, and blood vessels start to develop in the endometrium connecting the chorionic fingers with the uterine vasculature.
• By week 5 the placenta is well developed with its maternal (Decidual) and foetal (chorionic) components.
• In this way, maternal and foetal blood are closely associated, allowing gas and nutrient exchange, but still separated by a barrier formed by chorionic tissue and capillary walls.

Question 22

what are the functions of the placenta

Answer 22

The functions of the placenta are as follows.

1) Nutrient and gas exchange (especially favoured by increased O2 affinity of foetal haemoglobin).
2) Removal of foetal waste products and transfer to maternal blood.
3) Partial protection of foetus from teratogens and pathogens in the maternal circulation
4) Endocrine functions

Question 23

describe the levels of hormones in pregnancy

Answer 23

fertilisation l - s 14

• To sustain a pregnancy, high levels of oestrogen and progesterone are required.
• Initially the corpus luteum provides these.
• If no fertilisation occurs, the corpus luteum regresses after about 10 days, but if implantation occurs, the developing chorion secretes a hormone human chorionic gonadotropin (hCG) which prevents regression and maintains the corpus luteum of pregnancy that secretes oestrogen, progesterone and relaxin.
• hCG is detectable in the urine within about 14 days of conception (and in the blood by sensitive radioimmunoassay within 6 days of conception), and is thus used in pregnancy testing kits.
• hCG levels increase up until about 6 weeks after fertilisation as the placenta enlarges.
• At this time, levels fall to a lower plateau.
• Notwithstanding this, oestrogen and progesterone continue to rise, since the placenta itself becomes the primary source of sex hormones from about 3 months on.

Question 24

briefly describe some of the increased demands/physiological changes of the mother in pregnancy

Answer 24

morning sickness

increased CO and Blood volume

Increased oxygen consumption and CO2 production

increased ventilation

increased BMR

increased GFR/Na&H2O reabsorption (net fluid retention)

increased nutritional demands

Weight gain

Question 25

describe parturition pre birth

Answer 25

due to relaxin - cervix softens and dilates - pubic symphysis more flexible

• smooth muscle of the uterus becomes more excitable and more connected by gap junctions
• due to increased oestrogen
• prostaglandin production goes up and the number of oxytocin receptors also rises
• prepares the myometrium for its impending task. These changes may underlie the irregular uterine contractions that occur in the last trimester.
• In the foetus itself, CRH production is increased during this time
• having a positive feedback effect on placental feedback production, increasing foetal ACTH and cortisol.
• cortisol is thought to be vital to the final maturity of the foetal respiratory system, preparing it for its drastic change in environment.
• In effect the foetus picks the time to be born my increasing its own CRH production.

Question 26

describe partition birth stage

Answer 26

pregnancy L s 7

Labour has 3 stages.

Dilation (8-24 hr):

• canal through the cervix is dilated by the action of the babies head pushing down on it by myometrial contractions.
• stretch causes a reflex release of oxytocin from the posterior pituitary which acts on an myometrium already very sensitive to oxytocin (see above) to further increase contraction, increasing cervical stretch, thus positively feeding back and amplifying the contractions.
• Prostaglandins also stimulate myometrial contraction, and, as described above, relaxin is important in increasing flexibility of the cervix and pubic symphysis.

Expulsion (30 – 90 min):

• begins when the cervix is fully dilated to 10 cm
• The head exiting the cervix triggers reflexes which contract abdominal muscles to help expel the baby through the vagina
• can be reinforced voluntarily by consciously pushing with them

Delivery of placenta (15 – 30 min)

• shears off the wall of the contracted uterus.
• Low blood loss (300 – 400 ml) because uterus is already contracted
• Following delivery there is a dramatic drop in maternal oestrogen and progesterone due to the loss of the placenta which had been manufacturing them and the corpus luteum of pregnancy
• leads to a regression of the decidual endometrium giving a discharge post birth termed lochia.
• Pre pregnancy state in 4-6 wk

Question 27

describe lactation

Answer 27

• breasts develop to become milk secreting organs
• under the inflence of the increased amounts of oestrogen and progesterone from the placenta.
• Prolactin from the mothers anterior pituitary gland and human chorionic somatomammotropin (a general anabolic hormone, sometimes termed “the maternal growth hormone of pregnancy) from the placenta act to develop the enzymes necessary for successful milk production.
• About 20 weeks into pregnancy, a female is fully capable of producing milk.
• This is prevented by the high levels of oestrogen and progesterone before birth.
• As described above, however, these drop with birth.

Question 28

describe suckling

Answer 28

• Mechanical stimulation of the nipple causes secretion of prolactin by decreasing the secretion of prolactin inhibitory hormone (PIH)
• This initiates and maintains milk production
• Nipple stimulation also increases oxytocin output from the hypothalamus (released in the posterior pituitary; a genuine neuroendocrine reflex),
• causes contraction in the smooth muscle surrounding the secretory alveoli
• expels milk into the mouth of the expectant infant

Question 29

describe the components of breast milk

Answer 29

• Triglycerides, carbs (lactose), protein, vitamins, calcium and phosphate
• For the first few days after birth, however, humans secrete colostrum which has more protein and less fat and lactose.
• contains lactoferrin, an antibacterial, and maternal antibodies of the IgA type, providing passive immunity.

Question 30

describe/define subfertility

Answer 30

• Subfertility or “infertility” is defined as the inability of a couple to conceive after 1 year of unprotected intercourse.
• It can be 1o (primary) with no previous pregnancy, or 2o (secondary) (after a previous pregnancy with the same partner).
• male is the reason (30 – 40% of couples),
• female:
  > tubal problems (20%)
  > ovulation problems (20%)
• For some couples inadequate or failing intercourse, or even a hostile cervical environment can reduce fertility (only 5% of couples).
• 15% of subfertile couples a precipitating cause cannot be found and the difficulty is said to be idiopathic.

Question 31

describe the pathophysiology of male sub fertility

Answer 31

• Males may be subfertile due to difficulties in spermatogenesis/spermiogenesis. - These can be hormonal in origin, eg. FSH/LH deficiency, hyperprolactinaemia, or androgen insensitivity.
• The structures supporting spermatogenesis and spermiogenesis themselves may be compromised, with infections of the testes (bacterial or viral orchitis), a varicocele (varicosity of the pampinform plexus veins) cryptorchidism/anorchidism, tumours, radiation, chemotherapy, drugs or toxins all affecting gametogenesis.
• transport of sperm can be compromised by aplasia vas deferens (genetic absence of vas deferens, often occurring concomitantly with CF), obstruction of the vas deferens or autoimmune destruction of sperm.
• The act of sexual intercourse
• Congenital deformation of the penis (epispadias/hypospadias) can affect sperm delivery, as can retrograde ejaculation, where sperm are forced into the bladder rather than out into the female genital tract.
• Erectile dysfunction, although technically not a failure in fertility, can have significant negative effects on couples trying to concieve.
• Also poorly motile sperm can have an effect on fertility, affecting ability to reach the ovum.

Question 32

describe how you may assess male subfertility

Answer 32

infertility and contraception L - slide 11

Clinical examination and history taking

• Infection or trauma
• Defects

Sperm “counts”

Hormone levels

• Gonadotropins
• Prolactin
• Testosterone

Chromosomal analysis

Question 33

describe treatment of male subfertility

Answer 33

Surgery:
- repair any structural abnormalities in the genital tract.

Hormone treatments:
- eg replacement of gonadotropins or treatment of prolactin secreting tumour may be appropriate.

Assisted reproduction:

• In some cases where sperm are present but in small numbers, or poorly motile
• artificial insemination with concentrated sperm
• in vitro fertilisation where sperm and ovum are brought together in a petri dish and the resulting zygote is re implanted in the mother,
• intra cytoplasmic sperm injection (ICSI) (right) where the sperm (with tail removed) is injected directly into the cytoplasm of the ovum.

Question 34

describe the pathophysiology of female subfertility

Answer 34

• Follicular development and ovulation can be compromised by endocrine defects, (FSH/LH deficiency, hyperprolactinaemia, inadequate oestrogen/progesterone, hypothyroidism and weight loss).
• There can be defects in the ovaries themselves
• Examples of these defects include polycystic ovaries, endometriosis (endometrial tissue outside the uterus which can potentially physically compromise the ovaries), damage due to radiation/chemotherapy/drugs/toxins, chromosomal defects and finally, idopathic premature menopause.
• Failure of sperm transport in female can happen, with some women producing anti-sperm antibodies.
• Tubal obstruction can prevent travel of the blastocyst to the uterus where it would implant. This can be due to pelvic inflammatory disease (scarring of female genital tract by infection (often STI’s), endometriosis, pelvic adhesions due to infection or trauma, uterine fibroids (benign tumours of smooth muscle often found at the junction of the fallopian tube and the uterus) or congenital defects of the genital tract.
• Implantation failure can also be due to uterine fibroids (this time elsewhere in the uterus), or inadequate secretory or luteal phase of the menstrual cycle not preparing an appropriate medium for implantation.

Question 35

describe the assessment of female subfertility

Answer 35

infertility and contraception L - slide 16

History taking, examination:
- Menstrual problems, infections, sexual history, recent weight loss

Ovulation tests can be carried out:
- such as observing the change in temperature (rising by 0.5o C) on ovulation, or noting a decrease in “stretchability or spinnbarkeit” and reduced “ferning” of cervical mucous once progesterone rises with ovulation.

Endocrine evaluations:

• Gonadotropin levels
• Prolactin levels
• Oestrogen/progesterone levels
• LH surge for ovulation
• Thyroid hormone levels - hypothyroidism causes subfertility

Chromosomal analysis

taking a pre menstrual endometrial biopsy to assess the secretory endometrium while the uterine lining is at its thickest

imaging the female genital tract for ovarian follicles/cysts/ or uterine fibroids is appropriate if no other precipitating causes can be found.

Question 36

describe treatment of female subfertility

Answer 36

sugery:
- to remove adhesions or endometriosis tissue over ovary.

Endocrine:

• supplementing gonadoptropins
• removing the prolactin secreting tumour if its present
• correcting hypothyroidism or weight loss.

Ovulation can be “kick started” by administering anti oestrogens (clomiphene which binds to hypothalamic oestregen receptors without activating them and tamoxifen (less effective, mainly used in breast cancer)) to reduce negative feedback and give a burst of GnRH.

All of these treatments do carry with them the risk of release of more than one follicle and therefore of multiple pregnancies.

Finally, as with the male, assisted reproduction (IVF, ICSI and surrogacy) may also be attempted to treat problems with fertility in the female.

Question 37

describe contraception methods in males

Answer 37

Spermatogenesis and Spermiogenesis may be inhibited by using female sex hormones (eg Progesterone analogues)
Exogenous androgens may inhibit gonadotropin production and local testosterone action, hence reducing fertility. This is thought to be one of the reasons why steroid abuse in sportspeople leads to infertility.

Sperm transport though the vas deferens may be prevented by vasectomy. Injection of spermicidal gel into the vas deferens has also been proposed as a means of contraception.

Finally prevention of ejaculation into the vagina is a well used contraceptive, using a condom and spermicidal gel for extra security.

Question 38

describe contraception in females

Answer 38

Inhibiting follicular development with female sex hormones (the “pill”) is among the most commonly used means of preventing conception:

• The combined oestrogen/progesterone pill does this by interfering with gonadotropin production and by making mucous impassable by sperm with high progesterone levels.
• The progesterone only pill is also available, and exerts its effects by thickening cervical mucous in low doses, or in higher doses by both inhibiting follicular development and thickening cervical mucous. It can also be used as an “emergency” contraceptive in very high doses, preventing ovulation and compromising implantation if unprotected sex has occurred.

Sperm transport can be compromised in the female using the cap or diaphragm or female condom, along with vaginal spermicide. As mentioned above, blocking sperm transport through thickened mucous is one of the mechanisms of action of the pill.

Blocking migration of ovum through the fallopian tubes is a less important action of the contraceptive pill and is the means of action of female surgical sterilisation (tubal ligation).

Implantation can be inhibited by action of an intra-uterine device (which can also be used as an “emergency” contraceptive, or as one of the (less important) actions of the hormonal contraceptives (they inhibit the secretory phase of the menstrual cycle).

Finally, medical abortion can be induced by progesterone receptor antagonists such as mifepristone, (used with prostaglandins usually) inducing decidual degeneration and disinhibiting uterine contraction.

Question 39

explain fatal circulation

Answer 39

neonatal physiology lecture slides 5 and 6 - see notes for explanation

Question 40

describe the respiratory adjustments at birth

Answer 40

Because the lungs take over gas exchange from the placenta at birth, it is vital that they begin function immediately if brain anoxia and damage is to be avoided.

The initial breath requires a huge inspiratory intrapleural pressure to be developed to overcome the surface tension of the fluid that fills the alveoli.

However, this rapidly reduces (above).

However, neonatal compliance remains less than that of an adult.

As well as this, expiration is active rather than passive in the newborn to overcome increased resistance from fluid in the airways.

With a respiratory rate of 40 breaths per minute and a minute volume of 650ml.min-1 (contrasting with 12 per min and 6 litres.min-1 in the adult), the neonate has about twice the adult ventilation when differences is body size are taken into account.

Respiratory distress syndrome (esp seen in preterm infants) is due to surfactant deficiency increasing the work of breathing

Question 41

describe the weight change just after birth

Answer 41

Over the first few days of life, the neonate often drops in weight (by as much as 10%, mostly due to fluid loss) due to difficulties in breastfeeding both from the mother initiating the supply and the infant mastering the art of suckling.

This rapidly resolves, thankfully by day 10 with weight tripling in the first year of life.

Vitamin D, calcium and Iron are much in demand during this period, so supplementation for breastfeeding mothers is often indicated.

Question 42

describe thermoregulation in newborns

Answer 42

The infant has about twice the metabolic rate of the adult, so generates more heat.

Despite this, there is an initial drop in temperature in the newborn infant of about 1 – 2 degrees celcius which only resolves after about 12 hours.

Fluctuations in core temperature still occur for the first few weeks of life due to immaturity of thermoregulatory mechanisms.

To add to this problem, the neonate has a lot of surface area to body volume and so loses heat quicker. This may be countered by brown fat in the infant which uncouples ADP phosphorylation from mitochondrial function, with all of the energy going to heat. This extra heat generated may be vital to infants

Question 43

describe the liver function of infants

Answer 43

The liver is poorly formed at birth, leading to a rise in plasma bilirubin which reaches a maximum about 5 times greater than normal after 1 – 2 weeks (neonatal jaundice).

As the liver matures, however, levels fall back to normal over the next few months.

Glycogen storage and manufacture are also compromised (glucose can drop to 2mmol.l-1 in the first day after birth, and this necessitates frequent feeding.

Plasma protein levels are also low (including clotting factors, increasing the risk of bleeding).

Question 44

describe immune function of infants

Answer 44

Active acquired immunity is poorly devloped in the newborn so it must rely on the mothers immunoglobulins (IgG’s) absorbed from the placenta. More may be absorbed (IgA’s) in the colostrum.

This passive immunity does decline over the first few months of life, being slowly taken over by immunity acquired by infant exposure to pathogens

Generally infant immunisation programmes only start after 2 - 3 months, when the infant has a capable acquired immunity.