7. Conception and Contraception Flashcards

1
Q

What is the normal volume of ejaculate?

A

2-4ml.

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2
Q

What are the main constituents of semen?

A

Testes: sperm, >40 x 10^6 per ejaculate.
Seminal vesicles = 60% of volume: alkaline fluid, fructose, prostaglandins, clotting factors (fibrinogen).
Prostate gland = 25% of volume: milky + acidic fluid, proteolytic enzymes, citric acid, phophotase.
Bulbourethral glands/Cowper’s glands = small volume: alkaline fluid, mucous.

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3
Q

Describe the physiological process involved in emission.

A

Emission = movement of ejaculate into the prostatic urethra before ejaculation. This is from peristalsis of the vas deferens and secretions from the seminal vesicles.

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4
Q

What are the stimulants in erection of the penis?

A

Psychogenic, tactile (sensory afferents of penis and perineum).

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5
Q

What are the efferents involved in erection of the penis?

A

Soamtic and autonomic effects - pelvic nerve (PNS), and pudendal nerve (somatic).

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6
Q

Outline the haemodynamic changes in erection.

A

Inhibition of sympathetic arterial vasoconstrictor nerves, activation of parasympathetic nervous system via pelvic nerve, activation of non-adrenergic + non-cholinergic nerves to arteries releasing NO, NO diffuses into and causes relaxation of vascular muscle.

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7
Q

How does activation of parasympathetic nervous system via pelvic nerve contribute to erection?

A

Release of ACh -> M3 receptors.
Rise in [Ca2+] -> activation of NO.
NOS -> formation of NO.

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8
Q

How does NO cause relaxation of vascular smooth muscle once it’s diffused in?

A

NO -> cGMP -> Ca2+ taken up into stores so lower [Ca2+] meaning less actin-myosin cross-bridges formed.

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9
Q

How do the corpa cavernosa change in erection?

A

Central arteries straighten and enlarge lumen so more blood can flow into and dilate the cavernous spaces.

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10
Q

How does the corpus spongiosum change in erection?

A

Dilates a bit, not too much otherwise the urethra would be closed off.

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11
Q

How do the bulbospongiosus and ischiocavernosus muscles contribute to erections?

A

Compress veins egressing from corpora cavernosa, impeding return of venous blood. Helps engorge the corpa cavernosa to become engorged with blood -> turgid.

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12
Q

What are the causes of erectile dysfunction?

A

Physchological - descending inhibition of spinal reflexes, tears in fibrous tissue of corpa cavernosa, vascular (arterial and venous, most common), factors blocking NO (alcohol, anti-hypertensives, diabetes).

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13
Q

What can be used to treat erectile dysfunction and how does it work?

A

Viagra - inhibits breakdown of cGMP, maintain erection.

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14
Q

What are the physiological changes in the female that facilitate coitus?

A

Vaginal lubrication, swelling and engorgement of the external genitalia, internal enlargement of the vagina, cervical mucus.

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15
Q

How does cervical mucus change under the influence of oestrogen compared to progesterone and oestrogen?

A

Oestrogen - abundant, clear, non-viscous mucous.

Progesterone + oestrogen - thick, sticky mucous plug.

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16
Q

What is the mechanism of ejaculation?

A

Spinal reflex. Sympathetic nervous system control (L1, L2). Contraction of glands and ducts by smooth muscle, bladder internal sphincter contracts to prevent entry of semen into bladder, rhythmic striatal muscle contractions (of pelvic floor, ischiocavernosus, bulbospongiosus, hip and anal muscles).

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17
Q

How does sperm travel through the cervix and uterus?

A

Most sperm are lost in the vagina. Those that enter uterus travel 15-20cm to reach uterine tube, which takes a few hours. The sperm themselves have propulsive capacity so move by this and currents in fluid from ciliated cells in the uterine tract.

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18
Q

How does sperm change after ejaculation?

A

Semen coagulates after ejaculation then re-liquifies after 10-20 minutes.

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19
Q

What are capacitation and acrosomal reactions of sperm induce dby?

A

Influx of calcium and rise in cAMP in spermatozoa.

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20
Q

What is the process of capacitation?

A

Maturation of sperm in the female reproductive tract (6-8 hours): sperm cell membrane changes to allow fusion with oocyte cell surface (removal of glycoprotein coat), tail movement changes from beating to whip-like action, sperm become responsive to signals from the oocyte.

21
Q

What is the acrosomal reaction?

A

Capacitated sperm come into contact with oocyte zona pellucida, membranes fuse then acrosome swells and liberates its contents by exocytosis, proteolytic enzymes and further binding facilitae pentration of zona pellucida by sperm.

22
Q

What is a secondary oocyte?

A

Haploid number of chromosomes and bulk of cytoplasm from first meiotic division of ovulatory follicle.

23
Q

What is the first polar body?

A

From first meiotic division of ovulatory follicle, remaining haploid number of chromosomes.

24
Q

What happens to the secondary oocyte?

A

Surrounded by follicular celled embedded in a gelatinous matrix, released from ovulatory follicle and picked up by fimbria of uterine tube and guided into lumen by ciliary movements of epithelial cells towards ampulla, site of fertilisation.

25
Q

What is the zygote?

A

The result of fusion of the nuclei from one ovum and one sperm.

26
Q

What is cleavage?

A

Division by a series of mitotic cell divisions within a few hours to form the morula.

27
Q

What is the blastocyst?

A

Hollow structure from further division of the morula.

28
Q

When does implantation happen?

A

After 4-5 days as the blastocyst enters the uterine cavity.

29
Q

What is ectopic pregnancy?

A

Failure of transport of egg, embeds in uterine tube/ovary/abdomen, embryo dies, risk of maternal haemorrhage.

30
Q

What is natural conception?

A

Abstinence of coitus interruptus (but there are sperm in pre-ejaculate).

31
Q

What is a vasectomy?

A

Operative that divides vas deferens bilaterally so sperm are prevented from entering ejaculate so it is free of sperm.

32
Q

What are barrier methods of contraception?

A

Prevent sperm reaching cervix.
Condoms - also provide STI protection.
Diaphragm - lies diagonally across cervix, needs correct fitting, doesn’t completely occlude passage of sperm, holds sperm in acid environment of vagina to reduce survival time.
Cap - fits across cervix.

33
Q

What are the effects of progesterone in relation to conception.

A

Makes thick, hostile cervical mucus plug to prevent sperm from entering uterus, also negatively feedbacks on hypothalamus/pituitary/gonadal axis to decrease frequency of GnRH pulses to inhibit follicular development.

34
Q

What are the effects of oestrogen in relation to conception?

A

Negatively feedbacks of anterior pituitary so loss of positive feedback mid-cycle and no LH surge.

35
Q

What are the types of hormonal contraceptive?

A

Combined OCP (progesterone and oestrogen), progesterone only pill (POP), depot progesterone (3 monthly injections), progesterone implants.

36
Q

What are intrauterine contraceptive devices?

A

Inert copped - interferes with endometrial enzymes and implantation, may affect sperm transport into fallopian tube.
Progesterone impregnated.

37
Q

What are post-coital methods of contraception?

A

Combined oestrogen/progesterone or progesterone only at HIGH dose up to 72 hours post intercourse, disrupts ovulation or blocks implantation, may impair luteal function.

38
Q

What is infertility?

A

Failure to conceive within 1 year.

39
Q

What is primary and secondary infertility?

A

Primary - no previous pregnancy.

Secondary - previous pregnancy, successful or not.

40
Q

What are the causes of male infertility?

A

Abnormal sperm production (testicular disease), obstruction of ducts (infection, vasectomy), hypothalamic/pituitary dysfunction.

41
Q

What are the groups of causes of female infertility?

A

Anovulation, tubal occlusion, polycystic ovarian syndrome.

42
Q

What are the causes of anovulation?

A

Hypothalamic - hyperprolactinaemia, weight loss, exercise, stress.
Pituitary - pituitary tumours, necrosis.
Ovarian - ovarian failure, menopause, radiotherapy, chemotherapy.

43
Q

How can ovulation be induced

A

Anti-oestrogen - reduces negative feedback to hypothalamus/pituitary, increases GnRH and FSH.
Goandotrophins - FSH administration.
GnRH agonists - pulsatile to mimic secretion.

44
Q

What causes tubal occlusion?

A

Sterilisation, PID.

45
Q

How is tubal occlusion diagnosed?

A

Laparoscopy, hysterosalpingogram.

46
Q

How is tubal occlusion treated?

A

Tubal surgery, assisted contraception.

47
Q

What is polycystic ovarian syndrome?

A

Increased androgen secretion, raised LH/FSH ratio, insulin resistance, multiple small ovarian cysts.

48
Q

What questions need to be answered before deciding how infertility is managed?

A

Regular, unprotected intercourse? Ovulating? - regular menstrual cycle? Patent tubes - history of infection/sterilisation, hysterosalpingogram. Adequate sperm count?

49
Q

How is infertility treated?

A

Induce ovulation, overcome tubal occlusion by surgery of IVF, artificial insemination by donor/intra-cytoplasmic sperm infection is inadequate sperm.