Reproductive System Week 7 Flashcards

1
Q

What is coitus?

A

The act of sexual intercourse that results in the deposition of sperms inside the vagina at the level of the cervix

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2
Q

What happens to the sperm after ejaculation at the cervix?

A

A proportion of sperm enters the uterus and reaches the uterine tubes where they may encounter an ovum released from the ovary

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3
Q

What is conception?

A

Fertilisation of the ovum by a sperm and the subsequent establishment of pregnancy

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4
Q

What are the stages of sexual excitement?

A

Excitement phase, plateau phase, orgasmic phase and resolution phase

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5
Q

What happens during sexual excitement (broadly)?

A

Genital and systemic changes in both sexes

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6
Q

Describe the male sexual response

A

Excitement phase -

  • sensory and psychological stimulation–> limbic system
  • activation of sacral parasympathetic neurones
  • inhibition of thoracolumbar sympathetic neurones
  • ACh -> M3 receptors on endothelial cells –> more intracellular Calcium –> activation of eNOS –> NO production (vasodilator)
  • Arteriolar vasodilation in corpus cavernosa
  • increased penile blood flow
  • penile filling (latency)
  • penile tumescence (erection - reversible) -
  • testes begin to elevate and engorge
  • scrotal skin thickens and tenses

Plateau phase
Activation of sacrospinous reflex
Contraction of bulbospongiosus ischiocavernosus (compresses crus penis and
impedes venous return) → venous engorgement
Rise in intracavernosus pressure → decreased arterial inflow Stimulation of secretionfrom accessory glands:
Cowper’s and Littre’s glands
• Lubricate distal urethra
• Neutralise acidic urine in urethra
• 5% of ejaculate
Corona may become further engorged
Testes become completely engorged and elevated
Loss of erection unlikely

Orgasm:
Emission:
Simulation of thoracolumbar sympathetic reflex
Contraction of smooth muscle in ductus deferens, ampulla, seminal
vesicle and prostate
Internal and external urethral sphincters contract - prevents retrograde ejaculation
Semen is pooled in urethral bulb
Contractions of ampulla of vas deferens
Ejaculation:
Spinal reflex (with cortical control)
Sympathetic Nervous System (L1, L2)
Contraction of glands and ducts (smooth muscle)
Internal urethral sphincter contracts
Filling of the internal urethra stimulates pudendal nerve
–>contractions of the genital organs, the ischiocavernosus and bulbocavernosus muscles –>expulsion of semen
External urethral sphincter relaxes
Contractions of penile urethra
Contraction of anal sphincter

Resolution:
Activation of thoracolumbar sympathetic pathway
Contraction of arteriolar smooth muscle in corpora cavernosa Increased venous return
Detumescence and flaccidity - erection loss
Refractory period
Testes descend and return to unstimulated size
Scrotum thins and resumes wrinkled appearance

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7
Q

Describe the female sexual response

A

Excitement:
Same neuronal responses as male - parasympathetic from sacral plexus
Vaginal lubrication begins (due to vasocongestion)
Inner 2/3 of vagina lengthen and expand
Clitoris engorges with blood
Uterus elevates
Increase in muscle tone, heart rate, and BP
Breast size increases
Nipple becomes erect
Veins become more distinct

Plateau:
Further increase in muscle tone, heart rate and BP
Labia minora deepen in color
Clitoris withdraws under its hood
Bartholin’s gland secretion lubricates vestibule for entry of penis
Orgasmic platform forms in lower 1/3 of vagina - rhythmic contractions
Inner 2/3 of vagina fully extended
Breast same as orgasm phase

Orgasm:
Orgasmic platform (outer 1/3 of vagina) contracts rhythmically 3-15
times
Uterus contracts starting at fundus and moving down, anal sphincter contracts
Clitoris remains retracted under hood
No refractory period - multiple orgasms possible
Greater size increase of breast
Areola increases in size and causes nipple to seem less erect
Sex flush may appear on breasts and upper abdomen

Resolution:
Clitoris descends and engorgement subsides
Labia return to unaroused size and color
Uterus descends to unaroused position
Vagina shortens and narrows back to unaroused state
Breast - areola detumescence nipple appears more erect - disappearance of sex flush, return to unaroused size of breast

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8
Q

What is the G spot?

A

Grafenberg spot (Ernest Grafenberg, a
gynaecologist who first publicised G spot in
1950s)
Area of erotic sensitivity located along the
anterior wall of the vagina.
Some women are able to experience orgasm and possibly ejaculation from G spot stimulation.
– G spot tissue is similar to male prostate;
therefore, fluid may be similar to prostatic
component of semen.
Supported by research that showed
presence of enzyme in female ejaculate
characteristic of prostate secretions
Orgasm from G spot stimulation is same as
orgasm from clitoral stimulation, though intensity
may vary depending on the method of
stimulation.

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9
Q

What happens to the female sexual response with age?

A

Some women report reduced desire
Reduced vasocongestion response, causing reduced
vaginal lubrication
Vaginal and urethral tissue lose elasticity
Length and width of vagina decrease; reduced expansile
ability of inner vagina during arousal
Number of orgasmic contractions is often reduced
More rapid resolution

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10
Q

What is a normal amount to be having sex?

A

Normal varies from person to person
10-20% of married couples report engaging in sexual activity a couple of times per year
30% report engaging in sexual activity 2-3 times per week

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11
Q

What is the most common type of sexual dysfunction?

A

Desire - increasing incidence

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12
Q

Name some sexual dysfunctions to do with desire

A

Hypoactivity
Aversion - revulsion or fear of one or more aspects of sex - often a result of assault or abuse
Hyperactive
Nymphomaniac
Kluver Bucci syndrome - bilateral medial temporal lobe lesions from cerebral metastases or head injury etc. –> hyperphagia, hypersexuality, hyperorality, visual agnosia and docility

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13
Q

Describe sexual dysfunctions involving arousal

A

Female - persistent, recurrent inability to attain or maintain lubrication-swelling response - -> lack of lubrication (especially in menopause)
Male - impotence - psychological (descending inhibition of spinal reflexes), tears in fibrous tissue of corpora cavernosa, vascular (atherosclerosis, diabetes), drugs (alcohol, antihypertensives - B blockers and diuretics)

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14
Q

Describe the mechanism of action of viagra

A

Inhibits cGMP breakdown in corpus cavernosum
Increases NO stimulated vasodilation
Increases penile blood flow –> erection

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15
Q

What is an alternative treatment to viagra?

A

Penile implant - reservoir of fluid - pump up by squeezing bulb in scrotum

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16
Q

Describe the properties of normal semen

A
2-4ml
20-200x10^6 sperm per ml
Total sperm per ejaculate >40 X10^6
>60% sperm swimming forward vigorously
<30% abnormal morphology
Liquefaction within 1 hour
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17
Q

When is semen described as abnormal?

A

< 20x10^6 sperm per ml (oligozoospermia)

Or doesnt meet the other criteria for ‘normal’

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18
Q

What are some sperm morphological defects?

A
Giant
Micro sperm
Double head
Double body
Long head
Rough head
Abnormal middle piece
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19
Q

Describe the glandular components of semen

A

Bulbourethral glands - 5% volume

  • alkaline fluid
  • mucous lubricants the tip of the penis and urethral lining

Seminal vesicles - 60% of volume

  • alkaline fluid - neutralises the acid in male urethra and female reproductive tract
  • fructose (ATP production), prostaglandins (increase sperm motility, increase female genital smooth muscle contractions), clotting factors (semenogelin)

Prostate- 25% volume

  • milky, slightly acidic fluid
  • proteolytic enzymes (PSA, pepsinogen - breakdown clotting factors from seminal vesicles, reliquify semen in 10-20 mins)
  • citric acid (ATP production), acid phosphatase
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20
Q

When is the female reproductive tract a hospitable environment for fertilisation and implantation?

A

Days 14-28 - uterine secretory phase - oestrogen and progesterone

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21
Q

How does the female reproductive tract aid in getting the semen to the site of fertilisation?

A

Site of fertilisation - ampulla
Site of deposition - cervix
Oxytocin stimulates uterine contractions

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22
Q

Describe how the cervical mucous changes over the uterine cycle

A

Days 7-14 - oestrogen only - abundant, clear non-viscous cervical mucous
Days 14-28 - oestrogen and progesterone - thick, sticky mucous plug - prevents infection from reaching uterus

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23
Q

Describe the nuclear maturation of the oocyte

A

Oocyte undergoes meiosis I
Nuclear membrane of oocyte disappears
First polar body separates and enters the perivitelline space
Second meiotic division takes place - stops in metaphase II

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24
Q

Describe the cytoplasmic maturation of the oocyte

A

Mitochondria dispersed throughout the cytoplasm
Endoplasmic reticulum - accumulates in oocyte cortex, protein and lipid synthesis creates cortical granules
The granules are initially dispersed throughout the cytoplasm but become cortical as the oocyte matures
Lipid droplets provide energy for meiosis, maturation, fertilisation and early embryo development
Cytoskeleton microfilaments migrate towards oocyte cortex

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25
Q

How many sperm are required to get pregnant?

A

Average 200-300 million per ejaculate
300 reach fertilisation site
299+ sacrificed to disperse the zona pellucida
1 sperm required for fertilisation

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26
Q

How long do sperm survive in the female genital tract?

A

Up to 5 days

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27
Q

How long do oocytes survive?

A

6-24 hours before phagocytosis

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28
Q

When is the fertile period?

A

Sperm deposition can be up to 3 days prior to ovulation or on the day of ovulation
The oocyte takes 3-4 days to travel from the ovary to the body of the uterus (cilia and Fallopian tube peristalsis)
Fertilisation is in the Fallopian tube

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29
Q

How long does it take the oocyte to travel to the uterus?

A

The oocyte takes 3-4 days to travel from the ovary to the body of the uterus (cilia and Fallopian tube peristalsis)

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30
Q

Describe how sperm further mature in the female genital tract before fertilisation can occur

A

Sperm undergo further maturation for 6-8 hours after deposition in the female genital tract (capacitation)
Sperm cell membrane changes in the female genital tract environment to allow fusion with the oocyte cell surface - removal of protein coat and acrosomal enzymes are exposed which can digest through the zona pellucida
Tail movement changes from beat to whip-like action (3mm/hour)
Sperm need to penetrate corona radiata (follicular cells)
And zona pellucida (glycoprotein membrane) of the ovum

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31
Q

Describe how the acrosome reaction begins and what it involves

A

When sperm contacts the corona radiata has an intact acrosome
Pushes through the corona radiata using the force produced by the tail
Proteins on sperm head bind to ZP3 proteins of zona pellucida
Triggers acrosome reaction:
Key signalling mechanism nvolves intracellular calcium
Acrosomal enzymes digest path through ZP
One sperm penetrates –> fusion of plasma membranes of oocyte and sperm
Sperm moves into cytoplasm –> zygote
Cortical reaction prevents polyspermy

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32
Q

Describe the plasma membrane of the oocyte

A

Can be divided into two major regions:

  • the part that directly overlies the metaphase chromosomes is smooth and devoid of microvilli
  • the rest is rich in micro villas protrusions - where sperm bind and fuse
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33
Q

Describe the fast block and slow block to polyspermy

A

Fast block:
Electrical change in oocyte membrane
Na channels open (resting potential is -75mV, fertilisation potential is +20mV)
Wave of depolarisation starts at point of entry of sperm and propagates across the cytoplasm

Slow block:
Calcium released from endoplasmic reticulum induces local exocytosis of cortical granules
Granules release enzymes to stimulate adjacent cortical granules to undergo exocytosis
Wave of exocytosis occurs around oocyte in 3 dimensions from original point of entry of sperm

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34
Q

What is syngamy?

A

The union of male and female pronuclei to form a diploid zygote nucleus (46 chromosomes)
Oocyte completes meiosis II, expels second polar body, and the male and female pronuclei migrate towards each other to fuse

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35
Q

What is polyploidy and how can it occur?

A

Embryo contains three or more pronuclei

Entry of more than one sperm or failure of extrusion of second polar body

36
Q

Describe cleavage

A

A series of rapid mitotic divisions and metabolic changes for upcoming cell division and embryogenesis
Increasing number of cells (16-32 blastomeres) of decreasing size - no increase in size of fertilised ovum
Totipotency - each cell has the capacity to become anything (can become an entire individual)

37
Q

What’s the difference between monozygotic and dizygotic twins?

A

Monozygotic - during cleavage the totipotent cells become divided into 2 separate independent cell masses (25-35% of twins follow separation after first cleavage)
Dizygotic - 2 eggs ovulate, 2 eggs fertilised

38
Q

Why is cleavage important?

A

Generation of a large number of cells that can undergo differentiation and gastrulation to form organs
Increase in the nuclear/cytoplasmic ratio - one nucleus couldn’t transcribe sufficient mRNA to support the entire zygote, No G1 (duplication of organelles and cytosol) or G2 (protein synthesis) stages in cleavage, cleavage is asynchronous (not all blastomeres divide at the same time)

39
Q

Describe compaction

A

8 cell stage

Blastomeres undergo polarisation and form tight junctions to create inner embryo environment

40
Q

What is a morula?

A

16 blastomere stage
3-4 days following fertilisation
Embryo passes into uterus

41
Q

What is ectopic pregnancy and what are the clinical consequences?

A

Failure of morula to enter the uterus
Implantation in Fallopian tube, ovary or peritoneal cavity
Risk of maternal haemorrhage
Embryo is non-viable

42
Q

Describe the blastocyst stage

A

5 days after fertilisation
Fluid-filled cavity develops in morula (blastocoele) –> blastocyst
Loss of totipotency
Inner cell mass (embryoblast) –> embryo
Outer cell mass (trophoblast) –> contributes to formation of placenta and produces hCG

43
Q

Describe the hatching process

A

Local digestion of zona pellucida by enzyme produced in trophoblast cells
Opposite the inner cell mass (minimises risk of damage to embryo)
After hatching, blastocyst begins process of implantation

44
Q

Describe implantation

A

Zygote to blastocyst - days 14-21 of uterine cycle
Progesterone priming of endometrium
Conceptus nourished in intrauterine fluid - 2-3days ‘floating’ in uterus
Trophoblast overlying inner cell mass is sticky - adheres to endometrium
Implantation commences 6 days after ovulation

45
Q

What proportion of couples who have unprotected sex could be expected to conceive within a year?

A

75%

46
Q

In Western Europe populations, what proportion of primary infertility is due to problems with the male partner?

A

30%

47
Q

List the possible points in the female reproductive system where problems may lead to
infertility. Write beside each the approximate proportions of women in which each type of problem is identified as the cause

A

Failure to ovulate - 28%
Fallopian tube problems - 22%
Uterine problems - 11%
Cervical problems - 3%

48
Q

What are the likeliest causes of erectile dysfunction in young men?

A

Psychological
Endocrine (e.g., diabetes)
Neurological
Alcohol

49
Q

Which hormone provides evidence that ovulation has occurred, when and from where should you measure it?

A
Progesterone 
Day 21 (at peak of progesterone curve) in blood
50
Q

Why is it useful to keep a daily record of body temperature on rising in the morning?
Why does the temperature have to be taken at the same time each day?

A

Progesterone elevates basal temperature

Circadian rhythm of body temperature will confuse results if not same time of day

51
Q

What are the clinical signs of hyperprolactinaemia, what are the consequences of this condition for fertility and how can it be treated?

A

Production of small quantities of milk
Infertility
Bromocryptine - dopamine agonist (prolactin inhibitory hormone)

52
Q

How, in principle, might you test whether uterine tubes are patent?

A

Passage of radio-opaque dye from uterine cavity, hysterosalpingography

53
Q

What particular feature in a patient’s history might lead you to suspect that the uterine
tubes could be blocked?

A

Previous pelvic infection

54
Q

What properties of cervical mucus facilitate sperm survival and transport?

A

Alkalinity, lowered viscosity

55
Q

How might you establish whether cervical sperm transport is disturbed?

A

Post coital test – collect cervical mucus soon after copulation

56
Q

How in principle would you set about inducing ovulation in a woman whose cycles are anovulatory? Suggest which types of drugs or hormones might be used and why

A

Use an anti-oestrogen to reduce inhibition of FSH & LH e.g., clomiphene given for a few days prior to expected time of ovulation

57
Q

In polycystic ovarian syndrome (PCOS), exposure of follicles to androgens may lead to
inhibition of FSH, but not LH secretion. From what you know of the control of gonadotrophin secretion, by what mechanism might FSH secretion be inhibited selectively? Why might there be no LH surges in this condition?

A

Follicles may still secrete inhibin which selectively inhibits FSH, thus reducing FSH in respect to LH (hence, ratio changed)
Androgens may suppress LH surges (consider the role of testosterone in the male which inhibits LH release from the pituitary).

58
Q

What features of excess androgens may be present in PCOS?

A

hirsutism (which can be blocked by anti-androgen therapy) oily skin / acne

59
Q

Why is there an increased risk of endometrial malignancy in prolonged and untreated PCOS?

A

Due to sustained oestrogen stimulation of the endometrium

60
Q

What effect does progesterone have on the HPG axis before and after ovulation?

A

Moderate/high dose - enhances the negative feedback of oestrogen before ovulation, reduce LH and FSH secretion
- inhibits the positive feedback of oestrogen at ovulation –> no LH surge –> no ovulation

At lower doses - does not inhibit the LH surge - ovulation still likely - however thickens cervical mucous - harder for sperm to penetrate

61
Q

Describe some natural methods of contraception and their advantages and disadvantages

A

Fertility awareness methods - use of fertility indicators to identify fertile points of menstrual cycle - cervical secretions (large amounts of thin, watery mucous when fertile), basal body temperature (progesterone increases it), length of menstrual cycle:

Lactational amenorrhoea method - breastfeeding delays the return of ovulation following childbirth - only effective for 6 months following birth - suppresses GnRH release (doesnt work if also using bottle)

Advantages - no hormones, no contraindications
Disadvantages - not as effective, unreliable

62
Q

Describe some barrier methods of contraception and their advantages and disadvantages

A

Male/female condoms - physical barrier, prevents entrance of sperm into cervix:
Advantages - Can help prevent against STIs
Disadvantages - male condoms - sensitivity/allergy to latex
Female condoms - not widely available

Female diaphragm/cap - physical barrier, prevents entry of sperm into cervix, also used with spermicide so additional chemical barrier:
Advantages - Can be inserted anytime before intercourse
Disadvantages - Need to use with spermicide (can cause a local reaction)

63
Q

Describe some prevention of ovulation methods of contraception and their advantages and disadvantages

A

Combined oral contraceptive pill - pill containing both oestrogen and progestogen (synthetic progesterone) - taken for either 21 days followed by 7 day break or 21 days followed by 7 days of dummy pill:
principal action - prevents ovulation
secondary actions - reduces endometrial sensitivity to inhibit implantation, thickens cervical mucous to inhibit penetration of sperm
Advantages - can relieve menstrual disorders, reduces risk of ovarian cysts and cancer
Disadvantages - user dependent (same time everyday), side effects (breakthrough bleeding, breast tenderness, mood disturbance), increased risk of venous thromboembolism and myocardial infarction, many contraindications (previous stroke etc.)

Progesterone depot - progestogen - administered via SC or IM injection which is slowly released into circulation - can last between 8-13 weeks
Principal action - prevents ovulation
Secondary actions - reduces endometrial sensitivity to inhibit implantation, thickens cervical mucous to inhibit penetration of sperm
Advantages - convenient (no pill everyday), can also relieve menstrual disorders
Disadvantages - altered and irregular bleeding is common, delayed return of fertility for up to a year after stopping, not quickly reversible, small loss of bone mineral density and possible increase in fracture risk (not for <18s)

Progesterone implant - progestogen containing 4cm rod - inserted subdermally int he upper arm - can last up to 3 years
Principal action - prevents ovulation
Secondary actions - reduces endometrial sensitivity to inhibit implantation, thickens cervical mucous to inhibit penetration of sperm
Advantages - long duration of action, convenient, can also relieve menstrual disorders
Disadvantages - small procedure required to fit and remove the implant, local adverse effects can occur (migration, infection), can cause changes in bleeding pattern

64
Q

Describe inhibition of sperm transport methods of contraception

A

Progesterone only pill - pill containing progestogen only at a low dose, taken everyday
Principal action - thickens cervical mucous, making it impenetrable to sperm
Ovulation usually not prevented
Advantages - can be used where the COCP is contraindicated
Disadvantages - menstrual problems are common, must be taken at the same time everyday (error for forgotten pills is only 3 hours late)

65
Q

Describe inhibition of implantation methods of contraception

A

Intrauterine system - small plastic device containing slow release progestogen - placed in uterus - can last between 3-5 years
Principal action - reduces endometrial proliferation and prevents implantation
Secondary actions - thickens cervical mucous
Ovulation usually not prevented
Advantages - convenient, long duration of action, can also relieve menstrual disorders
Disadvantages - Insertion may be unpleasant, IUS displacement/expulsion may occur, menstrual irregularity common in the first 6 months, risk of uterine perforation is ~2/1000 insertions

Intrauterine device - small device made of plastic with added copper that is placed in the uterus - lasts between 5-10 years
Principal action - copper is toxic to sperm and ovum - prevents fertilisation
Secondary actions - copper causes endometrial inflammatory reaction - prevents implantation, reduces penetration of sperm due to effect of copper on cervical mucous
Advantages - convenient, long duration of action, can also be used as emergency contraception (up to 5 days after unprotected intercourse)
Disadvantages - insertion may be unpleasant, IUD displacement/expulsion may occur, periods may be heavier, longer or more painful, risk of uterine perforation is ~2/1000 insertions

66
Q

Describe sterilisation methods of contraception

A

Male - vasectomy - vas deferens interrupted to prevent sperm from entering ejaculate - performed under LA - confirm success by post-operative semen analysis approx 12-16 weeks following surgery

Female - tubal ligation/clipping - Fallopian tubes cut or blocked to stop the ovum from travelling from ovary to uterus - done under LA or GA

Advantages - permanent, no hormonal side effects
Disadvantages - male failure rate 1/2000, female failure rate 2-5/1000, should not be chosen if any doubt about having children in the future - not widely reversible

67
Q

What is infertility?

A

Failure of conception in a couple having regular, unprotected coitus for one year

68
Q

What is primary infertility?

A

No previous pregnancy

69
Q

What is secondary infertility?

A

Previous pregnancy, successful or not

70
Q

How many people have trouble conceiving in the UK?

A

1/7 couples - 3.5 million people in the UK

71
Q

What history would you take from a female with fertility issues?

A
Age
Duration of infertility
Menstrual cycle - length and predictability of cycle, age of menarche
Tubal or pelvic surgery
PID
Menorrhagia
Pelvic pain
Sexual history - any infections
72
Q

What history would you take from a male with fertility issues?

A

General health
Alcohol/smoking
Previous surgery/injury to the testes
Drug history
Sexual history and previous infections (STIs)
Sexual dysfunction (erectile dysfunction etc.)

73
Q

What would you include in your examination of a patient with fertility issues?

A

BMI
Signs of secondary sexual characteristics
Galatorrhoea (spontaneous flow of milk from breast unassociated with child birth)- hyperprolactinaemia
Pelvic examination - feel for structural abnormalities

Do not usually perform male examination in absence of relevant history - potentially look at testicular size and check for descent

74
Q

What are the statistics relating to the aetiology of infertility?

A
Male factors - 30%
Ovulation disorders - 25%
Tubal damage - 20%
Uterine or peritoneal disease - <10%
Other factors including unexplained infertility - 25%
75
Q

What are the most common male factors involved in infertility?

A

Idiopathic oligospermia (most common)
Varicocoele - bag of worms - increased temperature causes damage to sperm
Abnormal sperm production- e.g. testicular disease
Hypothalamic/ pituitary dysfunction - high levels of prolactin inhibit production of GnRH
Ductal obstruction (post-infective epididymitis, post-vasectomy)
Failure to deliver sperm to the vagina (hypospadias, impotence)

76
Q

How can ovulatory disorders be classified?

A

Group 1 - hypothalamic-pituitary failure - hypogonadotrophic hypogonadism - not enough GnRH or acquired (weight loss, anorexia), hyperprolactinaemia
Group 2 - hypothalamic-pituitary-ovarian dysfunction - eugonadotrophic - polycystic ovarian syndrome, congenital adrenal hyperplasia - anovulation
Group 3 - ovarian failure - hypergonadotrophic hypogonadism - early menopause, turner syndrome, cancer/chemo/radiotherapy, surgery

77
Q

Describe polycystic ovary syndrome

A

Syndrome consisting of polycystic ovaries and systemic features resulting from elevated androgens
Unknown pathophysiology but appears to have a genetic component
- increased androgen secretion
- raised LH/FSH ratio - follicles secrete inhibin
- insulin resistance
- multiple small ovarian cysts - lots of follicles arrested at early antral stage
- anovulation - amenorrhoea or oligomenorrhoea

Clinical features:
- hirsuitism 
- acne
- obesity
- male-pattern baldness
- oligomenorrhoea
- psychological history - mood swings, depression and anxiety 
Rotterdam diagnostic criteria:
2/3 of the following:
12 or more follicles on ultrasound
Oligoovulation or anovulation
Clinical and/or biochemical signs of hyperandrogenism
Exclusion of other causes of androgen excess
78
Q

What are the common causes of tubal damage?

A
Past pelvic infection e.g. Chlamydia
Previous pregnancies e.g. Ectopic
Pelvic surgery
Endometriosis
Mullerian developmental anomaly
79
Q

What are the causes of uterine or peritoneal disease?

A

Endometriosis
Ashermans syndrome - adhesions or fibrosis of endometrium
Uterine fibroids - myometrium benign tumour
Cervical stenosis - trauma, genetic, STIs, cervical cancer
Cervical hostility - due to infection or female sperm antibodies - acidic cervix

80
Q

Describe endometriosis

A
Presence of endometrial tissue in sites other than the uterine cavity - most commonly in the pelvic cavity 
10-15% of women
Clinical features:
- dysmenorrhea
-dyspaureunia - painful sex
- chronic pelvic pain
- infertility

Laparoscopy
Management - contraceptive pill if dont want pregnancy, NSAIDs, IVF if want to conceive

81
Q

What are some other factors involved in infertility?

A

Unexplained infertility
Poorly controlled diabetes - common in Leicestershire and in polycystic ovary syndrome
Coital problems
Multifactorial - 5-10% of cases

82
Q

Who should be referred for further investigations regarding infertility?

A

A woman of reproductive age who hasnt conceived after 1 year of unprotected vaginal sexual intercourse - in the absence of any known cause of infertility
A woman of reproductive age who is using artificial insemination to conceive with either a partner or donor sperm - who has not conceived after 6 cycles of treatment - in the absence of any known cause of infertility

Early referral for :
Women >36 years
Known clinical cause of infertility or a history of predisposing factors for infertility

83
Q

What investigations are used for females with fertility issues?

A
Follicular phase LH, FSH (day 2)
Luteal phase progesterone (day 21) if ovulating regularly
Prolactin, androgens, TFTs
Cervical smear
Pelvic USS
Test of tubal patency
84
Q

What investigations are used for males with fertility issues?

A

Sperm analysis - motility, morphology, count
Antisperm antibodies - if testicular blood barrier is dysfunctional e.g. Due to trauma
FSH/LH/testosterone
USS
Karyotype
Cystic fibrosis - congenital absence of ductus deferens
Testicular biopsy

85
Q

What are the figures for normal semen?

A
Volume >2ml
PH 7.2-7.8
Sperm count >20 million per ml
Motility >50%
Morphology >50%
86
Q

Describe the management of fertility issues

A

Depends on the cause

Induction of ovulation:
Clomifene citrate - reduces negative feedback of oestrogen on hypothalamus
Gonadotropins
GnRH agonists
Weight loss/gain
Dopamine agonists
Ovum donation

Tubal occlusion:
Tubal surgery (re-anastomosis)
Assisted conception

Male factors:
Artificial insemination by donor 
Intracytoplasmic sperm injection
GnRH agonist
Dopamine agonist