SPR L8 Infertility and Contraception Flashcards Preview

Physiology > SPR L8 Infertility and Contraception > Flashcards

Flashcards in SPR L8 Infertility and Contraception Deck (21)
Loading flashcards...

Infertility and Contraception

Learning Outcomes

For general perusal 

  • To elucidate the importance of Reproduction to the human
  • To define and characterise subfertility
  • To investigate where subfertility may occur in male gametogenesis and sperm transport
  • To outline the processes that may affect subfertility in the female (gametogenesis, egg transport and implantation)
  • To describe how conception may be avoided in couples who wish so to do

Concepts and Learning Outcomes (for general perusal)

  • The processes underlying gamete creation in the male and the female, union of 2 gametes and development of the embryo/fetus can be problematic in some couples, giving rise to infertility (subfertility) which has a clinical definition
  • With the male, subfertility can result from problems with spermatogenesis, sperm transport or sperm delivery to the female.  Poorly motile sperm can also cause subfertility even if they are manufactured in sufficient numbers and delivered to the female genital tract.
  • In the female, subfertility can result from inability to develop follicles or ovulate, from production of anti-sperm antibodies, inability to transport the blastocyst all the way to the uterus or failure in implantation
  • Avoiding conception is possible using barrier or hormonal means, or by using knowledge of the cycle.  Such knowledge can also be used to aid conception where such is desired.


Subfertility: Definition 

  1. Give a definition of Subfertility
  2. In what percentage of couples does the problem lie with the male?
  3. In what percentage of couples if female tubal problems or ovulation problems the difficulty?
  4. In what percentage of couples is inadequate/failing intercourse, or a hostile cervical environment the problem?
  5. For what percentage of subfertile couples can a precipitating cause not be found; idiopathic?

  1. the inability of a couple to conceive after 1 year of unprotected intercourse.  It can be primary,  with no previous pregnancy, or secondary (after a previous pregnancy with the same partner).
  2. 30 – 40% of couples
  3. both 20% each (accounting for a similar proportion of difficulty conceiving in comparison to males)
  4. only 5%  
  5. about 15%


Quick Revision

Summarise the hormonal control of gamete formation in the male and female. (See pictures)

  1. What is common to both?
  2. What feeds back?
  3. In the male, what are the processes required for conception?
  4. In the female, what are the processes required for conception?

  1. a hypothalamo/anterior pituitary/gonad axis controlling gamete formation with androgens created to sustain secondary sexual characteristics in both male and female and endometrial development in the female. 
  2. These androgens and inhibin feedback negatively on the hypothalamus and anterior pituitary to limit the process. 
  3. spermatogenesis, sperm transport through the vas deferens and sperm delivery to the female during coitus. 
  4. oogenesis (in utero), follicular development (after puberty), ovulation, sperm transport, fertilisation, blastocyst migration to the uterus and eventual implantation.


Pathophysiology of Male Subfertility

Subfertility due to spermatogenesis/spermiogenesis: in what ways can this arise?

  • hormonal in origin
    • eg. FSH/LH deficiency, hyperprolactinaemia, or androgen insensitivity. 
  • compromised structures (supporting spermatogenesis and spermiogenesis)
    • 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 of the above affect gametogenesis


Pathophysiology of Male Subfertility

How can transport of sperm be compromised?



How can the act of secual intercourse compromise male fertility?

  • aplasia vas deferens (genetic absence of vas deferens, often occurring concomitantly with CF)
  • obstruction of the vas deferens
  • autoimmune destruction of sperm.  



  • Congenital deformation of the penis (epispadias/hypospadias) can affect sperm delivery
  • 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.
  • poorly motile sperm can have an effect on fertility, affecting ability to reach the ovum.


Pathophysiology of Male Subfertility

Give an overview of the three main ways male fertility can be compromised?

  • difficulties in spermatogenesis/spermiogenesis.
    • hormonal in origin
      • eg. FSH/LH deficiency, hyperprolactinaemia, or androgen insensitivity. 
    • compromised structures supporting spermatogenesis and spermiogenesis
      • 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
    • aplasia vas deferens (genetic absence of vas deferens
    • obstruction of the vas deferens or autoimmune destruction of sperm. 
  • sexual intercourse
    • Congenital deformation of the penis (epispadias/hypospadias)
    • retrograde ejaculation
    • Erectile dysfunction 
    • poorly motile sperm c


Assessment of Male Subfertilty

How can cases be established?

  • clinical examination and history taking, establishing if there is pre existing infection or trauma to the male genital tract, or if there are structural defects
  • Semen may be examined
  • Endocrine investigations (levels of testosterone, prolactin, gonadotrophins) - important for spermatogenesis and spermiogenesis
  • chromosomal analysis - to identify genetic defects that may affect gametogenesis and transport. 

Unfortunately, as outlined above, in some cases, no precipitating cause is found for the infertility

 Nb. Military injuries. Stretching of the pituitary stalk disrupted blood flow, caused panhypopituitism


Can check prostate gland secretions.

Proteases break up the clumps that might form, when there are clumps the sperm can’t swim through the semen 


Treatment of Male Subfertility

  1. What may be undertaken in cases of structural defect?
  2. Give examples of hormonal treatments that may be given
  3. When may assisted reproduction be appropriate?
    1. In what form may this be?

  1. surgery to repair
  2.  eg replacement of gonadotropins or treatment of prolactin secreting tumour may be appropriate. 
  3. In some cases where sperm are present but in small numbers, or poorly motile.


  • artificial insemination with concentrated sperm
  • in vitro fertilisation (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) where the sperm (with tail removed)  is injected directly into the cytoplasm of the ovum. 
    • concern has been expressed about the increased likelihood of birth defects with ICSI, given that the practitioner selects the sperm rather than the ovum itself. (Usually, only the best sperm would get through)



Pathophysiology of Female Subfertility

  1. Outline the potentially multifactorial problems with conception.
  2. What can be compromised by endocrine defects?
    1. Give examples of these defects
  3. What defects can arise in the ovaries themselves?
  4. What can give rise to failure of sperm transport in the female?
  5. What can prevent travel of the blastocyst to the uterus where it would implant? 
    1. What is this caused by?
  6. What can implantation failure be due to?


  1. from gametogenesis to problems with sperm, egg or blastocyst transport, or failure to implant the blastocyst. 
  2. Follicular development and ovulation
    1. FSH/LH deficiency, hyperprolactinaemia, inadequate oestrogen/progesterone, hypothyroidism and weight loss (leptin permissive to progesterone action). 
    2. 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 idopathic premature menopause. 
    3. some women producing anti-sperm antibodies.   
    4. Tubal obstruction
      1. 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.
      2.  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.



Pathophysiology of Female Subfertility

Give an overview

  • Follicular development/ovulation failure
  • Endocrine Problems
    •             FSH/LH deficiency
    •             Hyperprolactinaemia
    •             Oestrogen/progesterone
    •             Weight loss (leptin permissive to progesterone action) (less than 17% body fat, women are less fertile)
  • Ovarian Defects
    •             Polycystic ovaries/tumour
    •             Endometriosis
    •             Drugs/radiotherapy/toxins
    •             Chromosomal abnormalities
    •             Idiopathic premature menopause\Sperm Transport Failure (antibodies)
  • Tubal Obstruction
    •             PID (potential +- STIs)
    •             Endometriosis
    •             Adhesions
    •             Fibroids in the fallopian tube/uterus interface
    •             Congenital
  • Implantation Failure
    •             Fibroids
    •             Menstrual Problems (secretory phase inadequacy)


Assessment of Female Subfertility

What does this involve?




Picture:  a longitudinal transvaginal ultrasound of the ovary, revealing multiple ovarian cysts (Polycystic ovary syndrome (PCOS). 

  • clinical history taking and examination to establish potential menstrual problems, infections, sexual history for potential STI’s and the presence of ovarian swelling. 
  • Ovulation tests
    • observing temp change (rising by 0.5oC) on ovulation, or noting a decrease in “stretchability or spinnbarkeit” and reduced “ferning” of cervical mucous once progesterone rises with ovulation. 
  • Endocrine evaluations: relative levels of gonadotropins and oestrogen/progesterone indicating several potential pathologies of reproduction (see picture for patterns)
  • 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 (appropriate if no other cause can be found).

As with the male, often no definitive cause of female infertility is found.



Assessment of Female Subfertility

Endocrine evaluations: relative levels of gonadotropins and oestrogen/progesterone indicating several potential pathologies of reproduction are tested 

What would the findings in the following be?

  1. Ovarian Failure
  2. Gonadotrophin Failure
  3. Hyperprolactinaemia
  4. PCS
  5. Androgen Excess
  6. Uterine/Vaginal Abnormality
  7. Pregnancy


  1. Increased LH and FSH, Decreased Oestrogen
  2. Decreased LH, FSH and Oestrogen
  3. Decreased LH, FSH and Oestrogen, Increased Prolactin
  4. Possiblity of increased LH, Prolactin and Androgens
  5. Decreased or Normal LH, FSH and Oestrogen, Large increase in androgens
  6. All levels normal
  7. Decreased LH and FSH, Increased Oestrogen and Prolactin



Treatment of Female Subfertility

  1. What can surgical interventions involve?
  2. How can endocrine problems be treated?
  3. How can ovulation be 'kick-started'?
    1. Why are these used?
  4. What risk do the treatment of endocrine issues carry?
  5. Give examples of assisted reproduction

  1.  removal of adhesions or endometriosis tissue over ovary. 
  2. by supplementing gonadoptropins, removing the prolactin secreting tumour if it is present or correcting hypothyroidism or weight loss. 
  3. by administering anti oestrogens (clomiphene which binds to hypothalamic oestregen receptors without activating them and tamoxifen (less effective, mainly used in breast cancer))
    1. to reduce negative feedback and give a burst of GnRH. 
  4. the risk of release of more than one follicle and therefore of multiple pregnancies.
  5. (IVF, ICSI and surrogacy


Contraception - Males

  1. How may spermatogenesis and spermiogenesis be inhibited?
  2. How does a vasectomy work?
  3. What injection into the vas deferens has been proposed as a method of contraception?
  4. How is of sperm entry into the vagina prevented?

  1.  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.)  
  2. Sperm transport though the vas deferens is prevented
  3.  Injection of spermicidal gel
  4. a condom and spermicidal gel for extra security.


Contraception - Females

  1. What is the most commonly used means of preventing conception?
    1. How does the combined/osterogen/progesterone pill work?
    2. How does the progesterone only pill work?
  2. Which can be used as an 'emergency contraceptive' in very high doses?
    1. What does it prevent?
  3. What is the main mechanism of action of the pill?
  4. How can sperm transport in the female be compromised?
  5. What does tubal ligation involve?
  6. How can implanation be inhibited?
  7. What can medical abortion be induced by?
    1. When can it be used?

  1. Inhibiting follicular development with female sex hormones (the “pill”)
    1. by interfering with gonadotropin production and by making mucous impassable by sperm with high progesterone levels. 
    2. exerts its effects by thickening cervical mucous in low doses, or in higher doses by both inhibiting follicular development and thickening cervical mucous. 
  2. Progesterone only pill
    1. preventing ovulation and compromising implantation if unprotected sex has occurred. 
  3. As mentioned above, blocking sperm transport through thickened mucous is one of the mechanisms of action of the pill. 
  4. the cap or diaphragm or female condom, along with vaginal spermicide.
  5. Blocking migration of ovum through the fallopian tubes (female surgical sterilisation (tubal ligation)) 
  6. 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). 
  7. by progesterone receptor antagonists such as mifepristone, (used with prostaglandins usually) inducing decidual degeneration and disinhibiting uterine contraction. 
    1. It is used up to 49 days gestation in the US and up to 63 days gestation in Britain and Sweden         


Outline Contraception in Males

  • Spermatogenesis/spermiogenesis
    • Progesterone analogues
    • Exogenous androgens affecting GnRH and local testosterone (bodybuilders)
  • Sperm transport
    • Vasectomy
    • Spermicide injection into Vas
  • Barrier method
    • Condom (± spermicyde)


Outline Contraception in Females

  • Follicular development as a target
    • The pill
    • Oestrogen and progesterone
      • GnRH¯, FSH/LH¯ and mucous impassable
    • Progesterone only
      • Depending on the dose
      • Emergency contraceptive
  • Sperm transport
    • Cap or female condom (± spermicyde)
    • FX of pill (thick mucous)
  • Ovum transport
    • Pill and tubal ligation
  • Implantation
    • Intra Uterine Device (IUD) (emergency)
  • Hormonal contraception
    • “Medical” abortion
  • Mifepristone (± prostaglandins)
    • Antagonist of progesterone receptors
    • Decidual degeneration
    • Disinhibits contraction
    • <49 days (US) <63 days Britain and Sweden


Natural Family Planning

  1. What does this involve? 
  2. How is it useful?
  3. What are the basic facts when considering the 'safe period'
  4. What methods can be used to determine when ovulation occurs?

  1. Knowledge of the female cycle
  2. can be used by people trying to avoid conception by restricting intercourse to “safe” periods in the menstrual cycle. In reverse, this knowledge may be employed  by people who want to conceive children. 
  3. 1) Sperm survive for up to 7 days in the female reproductive tract.                                                   2) The lifespan of the ovum is 2 days.  If one can detect when ovulation occurs, and use other contraceptive methods 7 days before and 2 days after this, then a couple may avoid pregnancy. 
  4. The rise in body temperature by a half a degree on ovulation can be charted using a sensitive thermometer.                                                      Cervical mucous becomes thin, clear and elastic around the time of ovulation (for around 24-48 hours) and then becomes thick and cloudy again.  In the last few years Urine tests that detect the surge in LH that stimulates ovulation, or the rise in oestrogen during the follicular phase have been used by couples trying to maximise chances of conception.


Natural Family Planning

What facts should be bourne in mind?


To be sure, when is the safe period, given these facts?

  • While the secretory phase is reasonably constant in women, generally lasting 2 weeks, the follicular phase is quite variable from individual to individual, and sometimes even within the same individual from cycle to cycle. 


For this reason “to be sure” the safe period is from signs of ovulation (plus 2 days; egg life span) until menstruation, because the follicular phase can be a good deal shorter than the usual 2 weeks.  It should also be noted that there are documented (but very rare) cases in the literature of pregnancy resulting from intercourse on every day of the cycle.



Summing Up

(for general perusal)

  • Subfertility in both the male and the female can be caused at every stage of the reproductive process from gamete formation through union to implantation.  Sometimes no cause can be identified.
  • Assessment through examination and history taking are essential when deciding upon a treatment strategy
  • Conception may be avoided using barrier, hormonal and natural means where this is desirable.

Decks in Physiology Class (46):