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Fertility > Male reproductive physiology > Flashcards

Male reproductive physiology Flashcards

1
Q

What are the two main functions of the male testis?

A
  • Male sex steroid production
  • Spermatogenesis
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2
Q

List the actions of androgen (testosterone and DHT):

A
  • Male fetus embryogenesis
  • Negative feedback/regulation of gonadotrophin secretion by the HPA
  • Spermtaogenesis
  • Male sexual maturation and maintenance
  • Male sexual function and libido
  • Bone and muscle mass increase and maintenance
  • Increasing and maintenance of erythropoiesis and haematocrit
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3
Q

Regarding the hypothalamic-pituitary-testicular axis:

What is the actions of
LH and FSH on the testis?

A

LH:

  • Binds to receptors in Leydig cells.
  • Stimulates steroid hormone production: testosterone, oestradiol and DHT.

FSH:
- Binds to receptors on Sertoli cells and stimulates spermatogenesis.

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4
Q

Regarding the hypothalamic-pituitary-testicular axis:

Describe testicular negative feedback on gonadotrophin secretion:

A

Negative feedback at hypothalamus level:

  • Testosterone is converted to oestradiol through aromatisation (aromatase-enzyme) in the testes (20%).
  • Oestradiol suppresses GnRH secretion and therefore LH secretion.

Negative feedback at pituitary level:

  • Testosterone directly suppresses LH secretion from the pituitary.
  • Inhibin B (Sertoli cell product) and oestradiol inhibit FSH secretion.
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5
Q

Regarding the hypothalamic-pituitary-testicular axis:

What other things may suppress this axis?

A
  • Stress/acute illness
  • Exogenous corticosteroids
  • Hyperprolactinaemia.
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6
Q

What are the two compartments of the testis and what do they contain?

A
  1. Interstitial compartment: consists of Leydig cells, peritubular myoid cells, fibroblasts, neurovascular cells and macrophages, capillaries.
  2. Seminiferous tubule compartment consists of Sertoli cells and germ cells in various stages of spermatogenesis.

They are separated by the blood-testis barrier.

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7
Q

Describe the blood-testis barrier:

A
  • Basal lamina: ECM that forms outer rim of the seminiferous tubules and separates the two compartments (interstitial compartment and inside the seminiferous tubule).
  • BL lined by spermatogonia (undifferentiated germ cells) and Sertoli cells with tight junctions separating the undifferentiated and differentiated germ cells.
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8
Q

Describe the flow of sperm from the seminiferous tubules to ejaculation:

A

The testes are where sperm is manufactured. The epididymis is a long coiled structure topping the testis, and it receives immature sperm from the testis and stores them as they mature.

When ejaculation occurs, sperm are forcefully expelled from the tail of the epididymis into the vas deferens. Sperm then travel through the vas deferens through up the spermatic cord into the pelvic cavity, over the ureter to the prostate behind the bladder. Here, the vas deferens joins with the seminal vesicle to form the ejaculatory duct, which passes through the prostate and empties into the urethra. When ejaculation occurs, rhythmic muscle movements propel the sperm forward.

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9
Q

How many mature sperm are made every day?

A

100 million sperm

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10
Q

How long does sperm formation take?

A

74 days / 2 months

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11
Q

Describe the process of spermatogenesis:

A

Spermatogenesis begins after puberty.

  1. Mitotic / proliferative phase:
    - Dark spermatogonia undergo mitosis to replenish stem cell pool.
    - Some dark spermatogonia differentiate into pale spermatogonia
  2. Meiotic phase:
    - B spermatogonia loses contact with basememnt membrane of seminiferous tubule and passes through blood-testis barrier to become two primary spermatocytes (46 XY)
    - First meiotic division: forms two secondary spermatocytes (23 X or Y).
    - Second meiotic division: forms 4 spermatids (23 X or Y)
  3. Spermiogenesis:
    - Spermatids gain tails and mature into spermatozoa
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12
Q

What are the functions of the leydig and sertoli cells?

A
  • Leydig cells - produce testosterone
  • Sertoli cells - contribute to blood-testis barrier, and secrete nutrients for the developing spermatogonia/spermatocytes
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13
Q

Purpose of the epididymis?

A

Stores sperm until ejaculation.

Collects sperm from the testis and provides the environment for sperm to mature and acquire the ability to move.

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14
Q

Purpose of the vas deferens?

A

transports sperm from the epididymis. Travels from each epididymis to the back of the prostate and joins with one of the two seminal vesicles.

In the scrotum, other structures, such as muscle fibers, blood vessels, and nerves, also travel along with each vas deferens and together form an intertwined structure, the spermatic cord.

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15
Q

WHO reference values for semen analysis:
Semen volume

A

semen volume: 1.5 ml or more

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16
Q

Guidelines for semen analysis

A

Abstinence for at least 2 days prior

If the result of the first semen analysis is abnormal, a repeat confirmatory test should be offered 3 months after the initial analysis to allow time for the cycle of spermatozoa formation to be completed.

However, if a gross spermatozoa deficiency (azoospermia or severe oligozoospermia) has been detected the repeat test should be undertaken as soon as possible.

Screening for antisperm antibodies should not be offered routinely because there is no evidence of effective treatment to improve fertility.

17
Q

Male factor infertility - Medical options

A
  • If hypogonadotrophic hypogonadism: give gonadotrophins as they are effective in improving fertility.
  • idiopathic semen abnormalities: do not offer antioestrogens, gonadotrophins, androgens, bromocriptine or kinin-enhancing drugs because they have not been shown to be effective.
  • antisperm antibodies: unclear significant and treatment uncertain.
18
Q

Male factor infertility - Surgical options

A
  • Obstructive azoospermia: offered surgical correction of epididymal blockage because it is likely
    to restore patency of the duct and improve fertility. Surgical correction should be considered as an alternative to surgical sperm recovery and IVF.
  • Surgical correction for clinically evident varicoceles improves pregnancy rates.
19
Q

Fertility options for male factor infertility

A
  • Lifestyle changes
    • Donor insemination- is used much less frequently Treatment with donor sperm in an otherwise healthy woman should result in pregnancy rates of 15-20% per cycle.

• Intrauterine insemination – IUI (artificial insemination using partner’s sperm) is used occasionally but is unlikely to be useful if a significant sperm abnormality is present. Randomised controlled trials show that intrauterine insemination is better than timed intercourse for the treatment of male infertility, particularly when used with ovarian hyperstimulation. Nevertheless, success rates of only 5-10% per cycle are reported in most studies when IUI is performed for male fertility.

• ICSI (micro-injection) involves the direct injection of the sperm into an egg as part of in vitro fertilisation (IVF) treatment. It is primarily used when
a major sperm defect has been identified or where there has been poor fertilisation with ordinary IVF. If woman well and <40 then clinical pregnancy rates 30-40% per cycle

After failed ICSI:
There are new methods available which attempt to isolate mature, structurally-intact sperm with high DNA integrity which are then injected into the egg.
• PICSI selects a mature sperm which could bind to the zona.
• IMSI uses high magnification to select a sperm without vacuoles.

20
Q

What is azoospermia?

A

No sperm in the ejaculate

Obstructive or non-obstructive

Potential causes:

  • Genetic conditions such as Klinefelter’s syndrome,
  • Medical treatments such as chemotherapy or radiation,
  • Recreational drugs such as some narcotics,
  • Anatomical abnormalities such as varicoceles or absence of the vas deferens on each side (CVAD in CF).

Investigation:

  • Physical examination
  • Inhibin B and FSH levels

Treatment of non-obstructive:
- microdissection testicular sperm extraction (microTESE) to identify sperm for ART

Obstructive:
- Consider reconstructive surgery

21
Q

Male reproductive endocrinology

A

Testosterone and FSH are needed for optimal testicular development and maximal sperm production

GnRH stimulates production of LH and FSH by the pituitary.

LH stimulates Leydig cells to produce testosterone: this can act as an androgen (via interaction with androgen receptors) but can also be aromatized to produce estrogens.

Negative feedback from testes, via testosterone and inhibin to limit GnRH and gonodotropin production.

Androgens and FSH act on Sertoli cells, to stimulate sperm production.

Optimal spermatogenesis requires the action of both testosterone and FSH.

22
Q

WHO reference values for sperm:
pH

A

• pH: 7.2 or more

23
Q

What features are in the WHO reference values for sperm?

A

Semen volume
pH
Sperm concentration
Total sperm number
Total motility
Total vitality
Sperm morphology

24
Q

WHO reference values for sperm:
Sperm concentration

A

15 million spermatozoa per ml or more

25
Q

WHO reference values for sperm:
Total sperm number:

A

39 million spermatozoa per ejaculate or more

26
Q 
WHO reference values for sperm: 
Total motility (percentage of progressive motility and non-progressive motility):
A

40% or more motile or 32% or more with progressive motility

27
Q

WHO reference values for sperm:
Vitality

A

58% or more live spermatozoa

28
Q 
WHO reference values for sperm: 
Sperm morphology (percentage of normal forms):
A

4% or more.

29
Q

Testicular cause of Azospermia

Semen volume? Normal
Testis volume? Small
Vasa? Palpable
Gonadtrophins? Raised FSH
Testosterone? Normal or low

Management?

A

Causes: (approx 60% of cases)

  • Undescended testis
    • Torsion
    • Injury
    • Orchitis (mumps, chlamydia, gonnorhea, TB)
    • Post chemotherapy
    • Klinefelter syndrome 47XXY
    • Micro Y deletions
  • Smoking/recreational drugs - alcohol, marujana, heroin and cocaine
  • Prescribed drugs - SSRIs, calcium channel blockers, anti-epileptics (phenytoin, valproate, carbamazepine), anabolic steroids, HAART, chemotherapy)
  • anti-sperm antibodies
    • Unknown

Semen volume? Normal
Testis volume? Small
Vasa? Palpable
Gonadtrophins? Raised FSH
Testosterone? Normal or low

Management:

  • Micro TESE and ICSI
30
Q

Obstructive cause of Azospermia

Causes:

Semen volume?
Testis volume?
Vasa?
Gonadtrophins?
Testosterone?

Treatment?

A

Causes:
• Post vasectomy
• CBAVD in CF
• Ejaculatory duct obstruction
• Retrograde ejaculation
• Anejaculation e.g. spinal injury

Semen volume? Normal or low (depending on site of obstruction)
Testis volume? Normal
Vasa? Absent in CBVAD (congenital bilateral absence Vas Deferens)
Gonadtrophins? Normal
Testosterone? Normal

Treatment? Needle extraction and use for ICSI

  • TESE = testicular sperm extraction
  • PESA = percutaneous epididymis sperm aspiration
31
Q

Pretesticular cause of Azospermia

Causes:

Semen volume?
Testis volume?
Vasa?
Gonadtrophins?
Testosterone?

Treatment?

A

Causes:

  • Pituitary tumours (craniopharyngioma)
  • Head trauma, surgery, irradiation
  • Kallmann syndrome (KAL1 mutation)
  • Prader willi / Laurence moon biedel
  • Raised prolactin
  • Thyroid dysfunction
  • chronic illness/malnutrition

Semen volume? Normal or reduced
Testis volume? Normal or reduced
Vasa? Palpable
Gonadtrophins? Reduced FSH and LH
Testosterone? Reduced

Treatment? Treatment of cause and gonadotrophin replacement with FSH and HCG; usually requires 12-18 before adequate sperm in ejaculate to perform ICSI

32
Q

What cut-off defines oligozoospermia /azoospermia?
What should your next test be?
How will you interpret the results of this test?

A
  • <15 million spermatozoa per ml
  • Hormone profile: FSH, LH, testosterone, oestrogen, prolactin

Interpretation helps classify cause:

  • Low FSH, low testosterone = pretesticular (hypogonadotrophic hypogonadism)
  • High FSH, low testosterone = testicular
  • Normal FSH and testosterone = obstructive/post testicular
  • Low FSH, high testosterone = anabolic steroid use
33
Q

Apart from infertility, what are the other adverse outcome associated with abnormal semen analysis?

(O&G magazine 2021)

A

Evidence points to increased incidence of co-morbidities such as:

  • cardiovascular disease,
  • type 2 diabetes,
  • increased incidence of testicular cancer,
  • increased mortality

There is increasing evidence that both genetic and non-genetic factors in sperm, for example microRNA’s, have an influence on the health of children.3

34
Q

After semen analysis is there evidence for more advanced testing, e.g. DNA fragmentation?

A

No.

More advanced testing of samples, such as DNA fragmentation has reported effects on conception and miscarriage risk.

35
Q

Why is testicular examination warranted in all cases of Oligo-/azoospermia?

A

A surprising number of previously undiagnosed conditions such as undescended testes are detected by the physical examination.

It may be helpful to use orchidometer beads to assess testicular volumes.

Particularly important is palpation of the vasa deferentia, because congenital absence of the vas deferens (CBAVD) is relatively common.

Examination of the scrotum is best performed in the standing position, as this will make detection of varicoceles easier.

36
Q

What is the classification of azoospermia?

A
  • Pre-testicular (hypogonadotropic) (rare)
  • Testicular (60%)
  • Obstruction (40%)
  • Retrograde and anejaculation
37
Q

Patients with CBAVD should also be screened for what?

A

Also check for unilateral renal agenesis (URA) and cystic fibrosis gene mutations in these patients.

38
Q

Epidemiological and lifestyle factors that can affect male fertility.

A
  • Aging male
  • Obesity
  • Poor diet
  • Unhealthy lifestyle, including smoking, excessive alcohol and recreational drugs
  • Medical disorders such as diabetes and hypertension
  • Varicocele
  • Infections
  • Exposure to environmental chemicals and toxins
  • Excessive heat
39
Q

What can be given to improve sperm quality?

A
  • Antioxidant supplements
  • HCG

Fertility (10 decks)

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