Session 7: Conception and Contraception Flashcards

1
Q

What is Coitus? What is Conception?

A

Coitus is the act of sexual intercourse that results in the deposition of sperms in the vagina at the level of the cervix.

[*] From the cervix, a proportion of sperm enters the uterus and reaches the uterine tubes (Fallopian tubes) where they may encounter an ovum (oocyte) released from the ovary.

Fertilization of the ovum by a sperm and the subsequent establishment of pregnancy are collectively referred to as conception.

Sexual Reproduction: formation of a unique individual from the gametes (spermatozoon and oocyte) of two other individuals.

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2
Q

Describe the changes that occur in the excitement phase, plateau phase, orgasmic phase and resolution phase. What are the basic physiological responses of the body?

A

Sexual excitement that leads to the act of coitus involves genital and systemic (e.g. rise In blood pressure) changes in both sexes. These changes constitute the following phases: excitement phase, plateau phase, orgasmic phase and resolution phase. The climax of sexual excitement in the male is accompanied by ejaculation

[*] Sexual arousal/attraction – most individualised phase

[*] The physiological Excitement Phase is stimulated by psychological or physiological stimuli.

[*] This aroused state intensifies in the plateau phase (sustained period, can be variable in length)

[*] If stimulation is sufficient, orgasm or climax occurs. Orgasm is typically experienced as an explosive and pleasant release of sexual tension (ejaculation in the male)

[*] Resolution in the female: sexual arousal dissipates and the physiological changes associated with arousal and orgasm return to baseline.

[*] In men there is a refractory period, which is part of the resolution phase. During this period of time, sexual arousal cannot be restored and orgasm cannot occur in men. In contrast, sufficient stimulation can induce orgasm in women at any point during the resolution phase.

[*] The basic physiological responses of the human body to sexual stimulation are two-fold. The primary reaction is vascular congestion. The secondary response is generalised muscle tension or myotonia. Reflexes activated within the spinal cord are modulated by the higher central nervous system and control each response.

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3
Q

Describe the rates of sperm production

A

[*] Spermatogonia to mature spermatozoa takes up to 74 days (50 in seminiferous, 12-26 in epididymis)

[*] 1000 spermatozoa per second

  • 20 year old: 6.5million/g/day
  • Over 50 year old: 3.8m/g.day
  • Quantity and quality diminishes with age
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4
Q

Describe the female sexual response

A

[*] Blood engorgement and erection: clitoris, vaginal mucosa, breast and nipples

[*] The clitoral response to arousal is less predictable than the penis. Tactile stimulation of the female perineum or the glans clitoris can elicit vasocongestion, engorgement of the body of the clitoris and erection, but only in some women.

[*] Vaginal lubrication begins 10-30s after receipt of arousing stimuli and continues progressively through orgasm (glandular activity allows penis to enter easily).

[*] The more prolonged the excitement and plateau phases, the greater the production of vaginal lubrication. The upper 2/3rds of the vagina also expand and lengthen during the excitement phase which elevates the uterus into the female pelvis, repositions the cervix above the vaginal floor and ‘tents’ the midvaginal plane. These changes result in an increase in the circumference of the vaginal diameter, largely at the level of the cervix.

[*] Finally the labia minora becomes markedly engorged with blood during the excitement phase, displacing the labia majora upward and outwards and increases the functional length of the vagina by at least 1 cm.

[*] Orgasms are not required for fertilisation

[*] No physiological refractory period

[*] Emission and ejaculation do not occur in the female. If sexual stimulation occurs before a woman drops below plateau phase of arousal, the female is capable of rapidly successive orgasms. Finally, the female orgasm may last for relatively long period compared to the male

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5
Q

The normal volume of ejaculate is 2-4ml. What does this contain from the testes?

A
  • 20-200 x106 sperm per ml therefore >40 x106 sperm ejaculate
  • >60% of sperm swimming forward vigorously
  • <30% of sperm have abnormal morphology
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6
Q

The normal volume of ejaculate is 2-4ml. What does this contain from the seminal vesicles?

A
  • 60% of volume
  • Alkaline fluid – neutralises the acid in the male urethra and female reproductive tract
  • Fructose (substrate for ATP production)
  • Prostaglandins
  • Clotting factors
    • Fibrinogen
    • Holds sperm in space after ejaculation, before liquefaction
    • Semenogelin
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7
Q

The normal volume of ejaculate is 2-4ml. What does this contain from the prostate gland?

A
  • 25% of volume
  • Milky, slightly acidic fluid
  • Proteolytic enzymes – break down clotting factors, re-liquefying sperm in 10-20 minutes (liquefaction typically occurs within 1 hour) – in order to move in to the female tract
  • Citric acid
  • Phosphotase
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8
Q

The normal volume of ejaculate is 2-4ml. What does this contain from the bulbourethral glands?

A

[*] (Cowper’s glands):

  • Very small volume
  • Alkaline fluid
  • Mucous – lubrication of the end of the penis and urethral lining

NB: Sperm is only 2.5% of seminal fluid.

Abnormal Oligozoospermia: <20 x106 sperm per ml

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9
Q

Describe the physiological processes involved in emission

A

Emission is the movement of ejaculate into the prostatic urethra before ejaculation. This occurs due to peristalsis of the vas deferens and secretions from accessory glands including seminal vesicles and Bulbourethral.

[*] During emission, muscular contractions are induced within the prostate gland, vas deferens and seminal vesicles => seminal plasma and spermatozoa are secreted into the prostatic urethra (into the base of the urethra)

[*] This process is mediated by sympathetic output travelling through the hypogastric plexus and can be abolished by alpha-adrenergic blockade.

[*] Leakage of penis occurs before ejaculation and there is current debate whether the leakage contains sperm or not.

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10
Q

What types of stimuli can lead to erection of the penis?

A
  • Psychogenic stimuli can include imagined sensory cues or direct visual cues including explicitly erotic images. These signals are integrated within the limbic system of the brain and translated via descending projections to the spinal cord. They then travel via autonomic and visceral efferent nerves to the penis. Stimuli can be very rapid (5-10 seconds).
  • Somatogenic stimuli include touching the penis or adjacent perineum and will reflexly activate the same efferents as the spinal cord pathway. This tactile reflex is typically preserved following spinal cord transection.
  • Somatic efferents innervate the skeletal muscles around the penis which autonomic efferents include both SNS and PNS.
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11
Q

Describe the haemodynamic changes that occur following stimuli

A

[*] Inhibition of sympathetic arterial vasoconstrictor nerves

[*] Activation of parasympathetic nervous system

  • Pelvic nerve
  • Normally vasoconstriction/dilation is governed by more/less sympathetic stimulation. This is one of the few examples where an increase in parasympathetic stimulation causes vasodilation.
  • Release of Ach => M3 receptors on epithelial cells
  • Rise in [Ca2+] => activation of Nitric Oxide Synthase (NOS) => Formation of Nitric Oxide (NO)

[*] Activation of non-adrenergic, non-cholinergic nerves to arteries releasing NO (so NO is also directly released from nerves)

[*] NO diffuses into and causes relaxation of vascular smooth muscle (vasodilation)

  • Increased NO => formation of cyclic GMP => Ca2+ taken up into intracellular stores
  • Decreased [Ca2+] => less actin-myosin cross-bridges are formed and smooth muscle relaxes.

[*] The central arteries in the Corpa Cavernosa (helicine arteries) straighten, enlarging their lumen and allowing blood to flow into and dilate the cavernous spaces in the corpora of the penis (VASODILATION)

NB: a corpus cavernosum (singular) is one of a pair of sponge-like fibrous regions of erectile tissue. The corpora cavernosa (pleural) contain most of the blood in the penis during an erection.

[*] The Corpus Spongiosum also dilates, but not very much as it would compress and close off the urethra.

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12
Q

What do the Bulbospongiosus and Ischiocavernosus muscles do?

A

The Bulbospongiosus and Ischiocavernosus muscles compress veins egressing from the corpora cavernosa, impeding the return of venous blood. This combined with the dilation of the helicine arteries causes the Corpora Cavernosa to become engorged with blood near arterial pressure, causing erectile bodies to become turgid (enlarged and rigid) and erection occurs.

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13
Q

Describe the causes of erectile dysfunction and what could be used to treat it

A

Erectile Dysfunction

[*] Psychological

  • Descending inhibition of spinal reflexes

[*] Tears in fibrous tissue of corpora cavernosa

[*] Vascular

  • Arterial and venous
  • Most common cause

[*] Factors blocking NO

  • Alcohol
  • Anti-hypertensives
  • Diaebetes

Viagra can be used to treat erectile dysfunction. It inhibits the breakdown of cGMP, maintaining erection (as NO can sequester calcium, therefore maintaining the erection)

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14
Q

Describe the physiological changes in the female which facilitate coitus

A
  • Vaginal lubrication
  • Swelling and engorgement of the external genitalia
  • Internal enlargement of the vagina
  • Cervical mucus

[*] Oestrogen – abundant, clear, non-viscous mucous (very easy for sperm to travel through)

[*] Progesterone + oestrogen – thick, sticky mucous plug

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15
Q

Describe the mechanism of ejaculation

A
  • Spinal Reflex
    • Sympathetic Nervous System Control (L1, L2)
  • Simultaneous Contraction of glands and ducts
  • Smooth muscle
  • Bladder internal sphincter contracts.
    • Prevents entry of semen into the bladder. If this doesn’t happen, a dry orgasm (without ejaculate) may occur
  • Rhythmic striatal muscle contractions
    • Pelvic floor
    • Ischiocavernosus – Pudendal (S2-S4)
    • Bulbospongiosus – Pudendal (S2-S4)
    • Hip and anal muscles

[*] PNS may also be involved

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16
Q

Describe the process involved in sperm transport through the cervix and uterus

A
  • Immediately after ejaculation, the semen first coagulates due to the action of clotting factors, namely fibrinogen and vesiculae (this is considered to prevent the sperms from being physically lost from the vagina) and then liquefies by the action of enzymes derived from prostatic secretions (fibrinolysis) 10 to 20 minutes later.
  • The vast majority of the sperm does not enter the cervix of the uterus and are lost by leakage from the vagina.
  • Those that enter the uterus have to travel a distance of some 15 to 20 centimetres to reach the uterine a tube, a journey that may last a few hours.
  • Transport of sperms to the uterine tube is probably the result of their own propulsive capacity and the fluid currents caused by the action of ciliated cells in the uterine tract.
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17
Q

What does capacitation and acrosomal reaction result in?

A

During their passage through the uterus to the uterine tube, the sperm undergo a further series of maturational changes, capacitation and acrosomal reaction, that results in their acquiring a full capacity to fertilise the ovum; these changes first begin during their transport from the testis to the epididymis and continuing during their storage there until ejaculation

Newly ejaculated spermatozoa cannot fertilize an oocyte until capacitation has occurred (usually within the female genital tract, but it can be induced in vitro).

18
Q

What does capacitation mean?

A

[*] Further maturation of sperm in female reproductive tract (6-8 hours)

[*] Removal of a glycoprotein coat promotes change in the sperm-cell membrane, allowing fusion with oocyte cell surface.

[*] Tail movements change from waves/beats to whip-like thrashing movement, propelling the sperm along. (3mm/hour)

[*] The spermatozoa also become **responsive to signals from the oocyte. **

19
Q

Describe the acrosome reaction

A

200-300 million sperm ejaculation

[*] 300 reach fertilisation site

[*] 1 sperm required for fertilization but

[*] 299+ needed to disperse the zona pellucida

Acrosomal Reaction

[*] When a capacitated sperm comes in contact with the oocyte zona pellucida, the membranes fuse and this marks the commencement of the acrosomal reaction.

  • Sperm pushes through granulosa cells
  • Proteins on sperm head bind to ZP3 proteins of zona pellucida.
  • Binding trigger acrosome reaction

[*] The acrosome swells and liberates its contents by exocytosis.

[*] Proteolytic enzymes and further binding facilitate penetration of the zona pellucida by the sperm, which takes around 15 minutes.

  • Acrosomal enzymes exposed to zona pellucida
  • Hydrolysing enzymes digest path through ZP
  • One sperm penetrates: fusion of plasma membranes (egg and sperm)
  • Sperm moves into cytoplasm: zygote
  • Polyspermy blocked.
20
Q

How is polyspermy blocked?

A
  • First the egg cell membrane depolarizes, preventing membrane fusion with additional spermatozoa (primary block to polyspermy)
  • Second event is the cortical reaction. Cortical granules lie just beneath the egg cell membrane and with the cortical reaction, they fuse with the membrane and release their contents into the zona pellucida. This hardens the zona and impairs the ability of sperm to bind to it.
  • The third event involves resumption of the second meiotic division of the egg. The second polar body is formed and extruded from the egg, thereby assuring that the female pronucleus is haploid. Again, the diploid zygote is protected.
21
Q

How are both capacitation and the acrosomal reaction induced?

A

Both capacitation and the acrosomal reaction are induced by an **influx of calcium and rise in cAMP in the spermatozoa. **

22
Q

How long do Spermatozoa and Oocytes survive for in the tract? What is the fertile period? Describe transport of oocyte to the site of fertilisation

A

Survival of fertile gametes in tract

[*] Spermatozoa 48-72 hours (up to 3/4 days)

[*] Oocytes (6-24 hours max)

[*] Fertie period: serum deposition up to 3 days prior to ovulation or day of ovulation

[*] Oocyte transport: beating cilia, peristalsis of Fallopian tube

By the time of ovulation, the ovum (primary oocyte) in the ovulatory follicle has completed its first meiotic division to form a secondary oocyte (containing haploid number of chromosomes and the bulk of the cytoplasm of the primary oocyte).

[*] The remaining haploid chromosomes are contained in a structure called the first polar body.

The secondary oocyte, surrounded by follicular cells (cumulus) embedded in a gelatinous matrix, is released from an ovulatory follicle and picked up by the fimbria of the uterine tube and guided into its lumen by the ciliary movements of the lining cells towards the ampulla, the site of fertilisation, where the oocyte and the sperms come together.

23
Q

What happens after fertilisation?

A
  • During fertilisation, only one sperm penetrates the cytoplasm of the ovum. The nucleus of the sperm (which makes up the bulk of the sperm head) fuses with the nucleus of the ovum. The product of this fusion is called the zygote.
  • The entry of the sperm into the ovum sets off a series of events in the ovum that prevent other sperms from entering the ovum and ensuring that the zygote contains diploid chromosomes for the normal development to proceed.
  • Within a few hours, the zygote begins to divide by a series of metabolic changes and rapid mitotic cell divisions known as cleavage, to form a ball of cells called the morula and then a hollow structure, the blastocyst. It takes approximately 3 days (awaiting rise in progesterone for smooth muscle relaxation) to reach blastocyst stage. During this transformation process it is gradually transported along the uterine tube towards the uterus.

[*] Cleavage results in increased number of cells 16-32 without growth (does not increase in size – still needs to get through the Fallopian tubes)

[*] Totipotency

[*] Monozygotic/identical twins are when one zygote splits into two.

  • The blastocyst comprises of the earliest rudiments of both the embryo itself (called the inner cell mass) and the placenta (the trophoblast cells).

[*] Loss of totipotency

[*] Fluid-filled cavity

24
Q

Describe the process of implantation

A

By the time the blastocyst enters the uterine cavity (4-5 days after fertilisation), the endometrium is ready to receive it for pregnancy to be established. After up to 3 days in the uterine cavity (nourished by intrauterine fluid), the blastocyst attaches itself to the uterine endometrium. This process is called implantation and involves an interaction between the sticky trophoblast cells and the lining epithelium of the uterus (hCG). The posterior 2/3rds of the wall is the most common site.

[*] Further embedding of the blastocyst into the endometrium is dependent upon the invasive property of the trophoblast, which by now has an outer syncytium called the syncytiotrophoblast differentiated from the underlying cellular cytotrophoblast.

[*] Implantation commences 6 days after ovulation and by the 10th day after fertilisation, the blastocyst is fully embedded within the endometrium.

[*] Zygote => Blastocyst: Days 14 to 21 of uterine cycle

[*] Progesterone priming of endometrium has occurred – so uterus is ready for conceptus

[*] If the conceptus is to survive more than 14 days after ovulation, the ovarian corpus luteum must contain to secrete progesterone. Human chorionic gonadotrophin (hCG) produced by the developing trophoblast and secreted into the maternal bloodstream acts like luteinizing hormone, supporting the corpus luteum by inhibiting luteal regression.

The cellular interactions of the blastocyst and the endometrium and the establishment of the relationship between the embryonic and maternal tissues lead to the establishment of the early placenta.

25
Q

Describe ectopic pregnancy

A

[*] Failure of transport of egg

[*] Embeds into uterine tube, ovary or abdomen

[*] Embryo dies (~6-8 weeks – due to insufficient blood supply)

[*] Severe risk of maternal haemorrhage e.g. uterine arteries may be involved.

26
Q

What is meant by Contraception, Infertility and what are the classifications of contraceptives?

A
  • Contraception: How to process of conception may be modified to prevent it’s occurrence
  • Infertility: Possible abnormalities of the process of conception that may prevent it’s occurrence.
  • Classifications of Contraceptives
  1. Natural
  2. Preventing Sperm from Entering Ejaculate Vasectomy
  3. Barrier methods: prevent sperm from reaching the cervix
  4. Prevention of ovulation
  5. Inhibit Sperm transport along Fallopian tube (Various methods)
  6. Inhibition of sperm passing through cervix
  7. Inhibition of implantation
27
Q

Describe Natural Contraception

A

[*] Abstinence

[*] Coitus interruptus

  • But there may be sperm in pre-ejaculate

[*] Rhythm method

  • Avoid having intercourse during the fertile period
  • Need regular cycle
  • Assume maximum sperm survival of 7 days (average 3-4 days), ovum survival of 1 day. So for a regular 28 day cycle with ovulation on day 14 or 15, the ‘fertile period’ is day 7-16 of cycle.
  • Can use home ovulation kits (look at basal body temperature, cervical mucus changes) to work this out
28
Q

Describe Preventing Sperm from Entering Ejaculate Vasectomy

A

[*] Prevent sperm from entering ejaculate

[*] Divide vas deferens bilaterally

[*] Ensure ejaculate is free of sperm before relying on it for contraception via semen analysis

  • Check a few months later
  • Can be a permanent method of sterilisation
29
Q

Describe Barrier Methods to prevent the sperm from reaching the cervix

A

[*] Condoms

  • Readily available
  • Also protects against STIs
  • Effective if used correctly

[*] Diaphragm

  • Lies diagonally across the cervix
  • Needs correct fitting
  • Does not completely occlude the passage of sperm (if does not fit properly)
  • Holds sperm in the acid environment of vagina and reduces survival time
  • Needs woman to be motivated

[*] Cap – fits across cervix (physical barrier) but not very common

[*] Spermicide: most effective used in conjunction with barrier methods

30
Q

Describe Prevention of Ovulation? What are the types of hormonal contraceptives?

A

[*] Progesterone

  • Thick, ‘hostile’ cervical mucus plug
    • Prevents sperm from entering uterus
    • Main contraceptive action of progesterone
  • Negative feedback to hypothalamus/pituitary
    • Decreases frequency of GnRH pulses
    • Inhibits follicular development

[*] Oestrogen

  • Oestrogen negatively feeds back on anterior pituitary
  • Loss of positive feedback mid-cycle – no LH surge

[*] Types of Hormonal Contraceptive

Combined OCP (progesterone and oestrogen)

  • Negative feedback to hypothalamus/pituitary – inhibits follicular development
  • Oestrogen – loss of positive feedback midcycle, so no LH surge
  • So provides contraception at 2 levels

Progesterone only pill (POP)

  • Low-dose progesterone only
  • May inhibit ovulation

Depot Progesterone

  • 3 monthly infections of progesterone
  • Negative feedback effect to inhibit ovulation

Progesterone implants

  • May inhibit ovulation
  • Implants placed within arm, releasing small amounts of progesterone
31
Q

Describe the various methods in inhibiting transport of sperm along the Fallopian tubes

A

[*] Sterilisation: occlude fallopian tubes

  • Clips
  • Rings
  • Ligation
  • Clips and rings are normally permanent
  • May rarely (1:300-500) recanalise => often resulting in an ectopic pregnancy
32
Q

Describe inhibition of sperm passing through cervix

A

[*] Affect cervical mucus – thick ‘hostile’ mucus, progesterone mediated

  • Combined OCP
  • Depot progesterone
  • Progesterone implant
  • Progesterone only pill

Main mode of action of POP and implant

33
Q

Describe Inhibition of Implantation

A

[*] Hormonal Contraception: affect receptivity of endometrium (preventing endometrium preparation for implantation). Direct effect. Plus absence of corpus luteum prevents preparation of endometrium for implantation.

  • OCP
  • Progesterone implant
  • POP
  • Depot progesterone

[*] Post-Coital Contraception (emergency)

  • Combined oestrogen/progesterone high dose (or progesterone only)
  • Up to 72 hours after intercourse
  • May disrupt ovulation
  • Blocks implantation
  • May also impair luteal function

[*] Intrauterine Contraceptive Device (may also be used as post-coital contraception up to 5 days after ovulation but can be used as a routine method on contraception)

  • The IUD is a small T-shaped device, placed into the uterine cavity and attached to a nylon thread that hangs into the vagina, allowing the user to confirm that it remains in place. The modern IUD provides safe, long-acting, highlgy effective and rapidly reversible contraception with few side effects.
  • The precise contraceptive mechanism of IUD is not known, but is thought to work by preventing fertilization as well as causing the endometrium to be inhospitable for implantation.
  • Can be inert, or copper containing, or progesterone impregnated
  • Copper

Interferes with endometrial enzymes
Interferes with implantation
May also interfere with sperm transport into fallopian tube

Side effects of copper IUD include increased menstrual bleeding, iron-deficiency anaemia and dysmenorrhoea.

Compared to women using no form of contraception, women with IUDs have a reduced risk of ectopic pregnancy.

34
Q

Compare the effects of different contraceptives

A
35
Q

Differentiate between primary and secondary infertility

A

[*] Infertility is the failure to conceive within 1 year and affects ~15% of couples

  • Almost 90% of couples conceive within first 2 years of trying.

[*] Primary Infertility: no previous pregnancy

[*] Secondary Infertility: previous pregnancy, successful or not

36
Q

Describe male causes of infertility

A

[*] 20 – 25% of cases

[*] Abnormal sperm production e.g. due to Testicular disease

[*] Obstruction of ducts e.g. due to Infection, vasectomy (potentially reversible)

[*] Hypothalamic / Pituitary dysfunction

  • Hypothalamic dysfunction is quite a common cause of azoospermia
  • Pituitary dysfunction can often be treated with external administration of FSH/LH – can then often conceive naturally but takes a long time

[*] Cystic Fibrosis: congenital absence of vas deferens

37
Q

Describe causes of infertility in females

A

[*] 45-60% of cases

[*] Coital problems

[*] Anovulation (15-20%)

  • Occasional anovulatory cycles normal, especially at the extremes of reproductive life.
  • Usually very irregular periods
  • Hypothalmic causes: hyperprolactinaemia, weight loss, exercise, stress
  • Pituitary causes: pituitary tumour, necrosis, Sheehan’s syndrome (hypopituitarism caused by ischaemic necrosis due to blood loss and hypovolemaic shock during and after child birth)
  • Ovarian causes: ovarian failure, menopause, radiotherapy, chemotherapy
  • Differentiate causes by looking at hormone levels
  • Diagnosis of anovulation: serum progesterone level in mid-luteal phase (~day 21 if someone is ovulatory). Serum progesterone normally peaks 7 days before start of menses but if cycles are shorter, 21-7 = measure at 14 days or cycles are longer, add 7 days. If slightly varied, get 2 tests done but no point doing test in irregular delayed periods.
38
Q

Describe ways to induce ovulation

A

Anti-oestrogen:

  • Reduce negative feedback to hypothalamus/pituitary
  • Increase GnRH
  • Increases FSH
  • E.g. Clomiphene citrate is an oestrogen partial agonist/antagonist that acts at the level of the hypothalamus and pituitary gland to block oestrogenic negative feedback. This increases gonadotrophin secretion.
  • Aromatase inhibitors act to reduce circulating oestrogen levels, again blocking negative feedback centrally and promoting gonadotrophin production and release.

Gonadotrophins

  • FSH administration to stimulate ovaries for folliculargenesis. Used in IVF and assisted fertility treatment
  • GnRH agonists
    • Pulsatile to mimic secretion
    • Normally used to induce puberty rather than fertility treatment
39
Q

Describe tubal occlusion causes of infertility

A

[*] Tubal occlusion (15-40%)

  • Causes: sterilisation (potentially reversible), PID, scarring from infection (likely irreversible), endometriosis (e.g. endometrium in the pelvis or ovaries causes lots of scar tissue formation => adhesions, preventing normal function)
  • Diagnosis: laparoscopy and dye insufflation, hysterosalpingogram (HSG test, used with X-ray)
  • Treatment: tubal surgery (reanasotomosis – recanalization is possible), assisted conception (IVF)
40
Q

Describe PCOS

A

~15-20% have PCOS or polycystic ovaries (2 different)

  • Uncertain pathogenesis – originates pituitary or ovarian level?
  • Increased androgen secretion (from theca cells)
  • Raised LH/FSH ratio (due to negative feedback and lack of ovulation)
  • Insulin resistance (generally throughout the body – metabolic syndrome)
  • Multiple small ovarian cysts
  • Anovulation – often amenorrhoea or oligomenorrhoea
  • Features: irregular periods (long delays in between) in history, symptoms of excessive hair growth (male pattern baldness) or hyperandrogenism, ultrasound appearance ‘bead of pearls’ of Graafian follicles (usually more than 12, arranged at the periphery of the ovary). Only 2 out of 3 criteria needed to make diagnosis.
41
Q

How many cases in infertility are due to unknown reasons?

A

Unexplained 20-30% of cases (everything found is normal)

42
Q

Describe the management and treatment for infertility

A

Management of Infertility - investigation

[*] Regular, unprotected intercourse?

[*] Ovulating?

  • Regular menstrual cycle?
  • Day 21 Progesterone?

[*] Patent tubes?

  • History of infection/sterilisation
  • Hysterosalpingogram or by dye insufflation and laparoscopy

[*] Adequate sperm count?

Treatment of Infertility

[*] Induce ovulation

[*] Overcome tubal occlusion by surgery or IVF

If inadequate sperm then

  • Artificial insemination by donor
  • Intra-cytoplasmic sperm injection