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Human Development > Fertility > Flashcards

Fertility Flashcards

1
Q

Where does the pituitary sit

A

Pituitary fossa in the sella turica

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2
Q

What is the pituitary gland derived from

A

Outward pouching of oral ectderm

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3
Q

What is the anterior pituitary derived from

A

Roof of mouth

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4
Q

What is posterior pituitary derived from

A

Notochord

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5
Q

What nerves passes through the Cavernous sinus

A

III, IV, VI, V1, V2

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6
Q

What is beneath the pitutiary fossa

A

Sphenoid air sinus

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7
Q

What is a microadenoma pituitary tumour

A

Less than 10mm

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8
Q

What a is macroadenoma pituitary tumour

A

Over 10mm, more likely to cause compression

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9
Q

What are macroadenomas caused by

A

NFPA, acromegaly (GH), Cushing’s (overproduction of ACTH), prolactinoma (prolactin producing tumours), TSHoma (thyrotoxicosis)

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10
Q

What does a lesion at the optic chiasm cause

A

Bitemporal hemanopia

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11
Q

How is pituitary hypofunction tested

A

PRL - lactation
TSH - T4, T3
LH - testosterone/estradiol
FSH - spermatogenesis/folliculogenesis
GH - IGF1-1 through insulin tolerance test (causes hypoglycaemia, which body should automatically correct by producing GH, cortisol, adrenaline and glucagon)
ACTH - cortisol through synacthen (synthetic ACTH) or ITT

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12
Q

What if too much ACTH is suspected

A

give dexamethasone as test to see if pituitary gland reacts

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13
Q

What is the treatment for pituitary tumours

A

Conservative, surgery, medical (dopamine agonist therapy in prolactin producing tumours or acromegaly with somatostatin analogues), radiotherapy

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14
Q

When does cortisol peak

A

7am, falls throughout the day. Cortisol to be given in 3 courses in a day.

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15
Q

What is the antrafollicle

A

First follicles seen on US. One antrafollicle is selected to progress to Graafian follicle

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16
Q

What are the 3 stages of the Ovarian cycle

A

Follicular
Ovulatory
Luteal

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17
Q

What is the follicular phase

A
  1. At the start of the cycle levels of FSH rise causing stimulation of a few ovarian follicles.
  2. As follicles mature they compete with each other for dominance.
  3. The 1st follicle to become fully mature will produce large amounts of oestrogen.
  4. This inhibits the growth of the other competing follicles.
  5. The 1 follicle reaching full maturity is called the Graafian follicle (oocyte develops within this).
  6. The Graafian follicle continues to secrete increasing amounts of oestrogen.

.

  1. Oestrogen causes:

Endometrial thickening
Thinning of cervical mucous to allow easier passage of sperm
.

  1. Oestrogen also initially inhibits LH production from the pituitary gland.
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18
Q

What is the ovulatory phase

A

When the ovum is mature, oestrogen reaches a threshold level which conversely causes a sudden spike in LH around day 12.

The high amounts of LH cause the membrane of the Graafian follicle to become thinner.

Within 24-48 hours of the LH surge, the follicle ruptures releasing a secondary oocyte.

The secondary oocyte quickly matures into an ootid and then into a mature ovum.

The ovum is then released into the peritoneal space and is taken into the fallopian tube via fimbriae

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19
Q

What is the luteal phase

A
  1. Once ovulation has occurred the hormones LH and FSH cause the remaining graafian follicle to develop into the corpus luteum.
  2. The corpus luteum then begins to produce the hormone progesterone.
  3. Increased levels of progesterone result in:

Endometrium becoming receptive to implantation of the blastocyst
Increased production of oestrogen by the adrenal glands
Negative feedback causing decreased LH and FSH (both needed to maintain the corpus luteum)
Increase in the woman’s basal body temperature
.
17. As the levels of FSH and LH fall, the corpus luteum degenerates.

  1. This results in progesterone no longer being produced.
  2. The falling level of progesterone triggers menstruation and the entire cycle starts again.
  3. However if an ovum is fertilised it produces hCG which is similar in function to LH.
  4. This prevents degeneration of the corpus luteum (continued production of progesterone).
  5. Continued production of progesterone prevents menstruation.
  6. The placenta eventually takes over the role of the corpus luteum (from 8 weeks).
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20
Q

When does implantation occur

A

begins by day 6-7 after ovulation (day 21 of menstrual cycle) - occurs in the uterus

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21
Q

What happens when oocyte is in fallopian tube

A

It’s propelled by cilia and fallopian tube contractions

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22
Q

What are the 3 stages of the uterine cycle

A 
Menstrual phase (days 1-5)
Proliferative phase (D6-14)
Secretory phase (D15-22):
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23
Q

What happens in the menstrual phase

A

At the end of the luteal phase, the corpus luteum degenerates (if no implantation occurs).

The loss of the corpus luteum results in decreased progesterone production.

The decreasing levels of progesterone cause the spiral arteries in the functional endometrium to contract.

The loss of blood supply causes the functional endometrium to become ischaemic and necrotic.

As a result, the functional endometrium is shed and exits out through the vagina.

This is seen as the 3-5 day period of menstruation a woman experiences each month.

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24
Q

What happens in the proliferative phase

A

During the proliferative phase, the endometrium is exposed to an increase in oestrogen levels caused by FSH and LH stimulating the ovaries. This oestrogen causes repair and growth of the functional endometrial layer allowing recovery from the recent menstruation and further proliferation of the endometrium.

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25
Q

What happens in the secretory phase

A

The secretory phase begins once ovulation has occurred.

This phase is driven by progesterone produced by the corpus luteum.

It results in the endometrial glands beginning to secrete various substances.

These secretions make the uterus a more welcoming environment for an embryo to implant.

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26
Q

What happens when GnRH analogues are given in a pulsatile manner

A

Increase production of FSH and LH (and vice versa for continuous)

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27
Q

What does clomid do

A

oestrogen receptive blockers. Disruption of negative feedback of GnRH

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28
Q

What does combined oral contraceptive pill do

A

negative feedback to ant pituitary and GnRH

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29
Q

What causes insensitivity of follicles

A

PCOS

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30
Q

What are the causes of anovulation

A 
Hypothalamic dysfunction (10%) - GnRH production is low or not in pulsatile manner. 
Pituitary dysfunction (10% with hyperprolactinemia) 
Thyroid dysfunction
PCOS - 70% 
Ovarian failure
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31
Q

What effect does obesity have on fertility

A

less fertile, have higher rates of miscarriage, require higher doses of ovulation-inducing agents. Causes insulin resistance, hyperinsulinaemia and hyperandrogenaemia
Weight loss restores ovulation, achieves spontaneous pregnancy

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32
Q

What is clomiphene citrate

A

stimulate endogenous FSH production. Frist line of treatment for those with absent or irregular ovulation but who have normal basal endogenous estradiol

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33
Q

How is PCOS diagnosed

A

12 or more peripheral follicles or increase ovarian volume (greater than 10cm^3)
Oligo-ovulation or anovulation
Clinical and or biochemical signs of hyperandrogenism. Testosterone normal or slightly raised. LH:FSH ratio increased with FSH normal. Free androgen index is usually normal or elevated.

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34
Q

What happens in premature ovarian insufficiency

A

depleted eggs and increased FSH levels below age of 40.
Inhibin B production by small follicles decreases with age, the inhibin suppression of FSH secretion decreases and pituitary glands secretion of FSH increases
An elevated day-3 FHS level in women with menses is highly sensitive and specific for identifying women with a depleted ovarian pool

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35
Q

How is ovarian reserve measured

A

Antral follicle count, measuring AMH

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36
Q

What are the main causes of hyperprolactinemia

A

prolactin secreting pituitary gland tumour and use of psychiatric mediations. Test for hypothyroidism and pregnancy

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37
Q

How is hyperprolactinemia treated

A

Bromocriptine and cabergoline are also used to treat hyperprolactinemia with no known cause

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38
Q

What are the causes of hypogonadotropic hypogonadism

A

low BMI under 20, high intensity exercise, certain dietary patterns including high-fibre, low fat, excessive stress.

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39
Q

What is hypogondotropic hypogonadism

A

Hypogonadism due to impaired secretion of gonadotropin secretion

40
Q

What is the treatment for hypogonadotropic hypogonadism and what are the complications of this

A

Months treatment with hMG (FSH and LH)

Ovarian hyper stimulation syndrome and multiple pregnancies

41
Q

What temperature is best for testes

A

35

42
Q

Describe the anatomy of a testicle

A

Each testicle is divided by fibrous tissue into 200 lobules. Each lobule will contain 4 or 5 seminiferous tubules, containing germinal epithelium producing sperm. Between seminiferous tubules, there are Leydig cells.

43
Q

What is a seminiferous tuble

A

Lined by spermatogonial stem cells (starts production at puberty

44
Q

What is in between spermatogonial stem cells

A

Sertoli cells: provide support, nutrition, protection( Forms a barrier from immune system due to the production of new antigens)

45
Q

How is sperm produced from spermatogonial stem cells

A

two types, dark and pale: undergo mitosis and then meiosis due to haploid nature of sperm. Meiosis I is primary spermatocyte and meiosis II is secondary spermatocyte í spermatid (early and late) í mature sperm (when it reaches the luminal end, it passes into the fluid produced by the Sertoli cells, propelling sperm outside

46
Q

What is spermiogenesis

A

elongation of spermatid into mature sperm, creating a sac full of proteolytic enzymes that can penetrate the egg (acrosome) and a tail piece. Cytoplasm not needed except for mitochondria.

47
Q

How many sperm are produced each day

A

120 million - whole cycle takes 72 days

48
Q

What do sertoli cells do

A

Provide structural support. Create 2 compartments. Provide nutrients for mature sperm. Eliminate degenerate germ cells. Secretes Inhibin, ABP (enhances the function of testosterone), AMH and growth factors

49
Q

What do Leydig cell do

A

surrounds seminiferous tubules. Secrete androgens (C19), mainly testosterone. Mainly molecule is cholesterol. 95% produced in the testicles, 5% in adrenal gland.

50
Q

What are the effects of tesosterone

A

Anabolic male hormone (increase bone and muscle mass)
Primary and secondary sexual characters
Libido and sexual behaviour
Stimulates Sertoli cells and spermatogenesis

51
Q

What produces GnRH

A

Paraventricular and perioptic nuclei in the hypothalamus

52
Q

What does GnRH do

A

reach the pituitary gland to produce FSH and LH

53
Q

What does FSH do in the testes

A

FSH stimulate spermatogonial stem cells by stimulating Sertoli cells to produce ABP, which binds to testosterone to stimulate spermatogenesis, with feedback provided by inhibin produced by Sertoli

54
Q

What does LH do in the testes

A

produce testosterone, which provides feedback to the pituitary.

55
Q

Where does fertilisation take place

A

Ampullary portion of the tube

56
Q

What is sperm capacitation

A

Switching on of sperm - hyperactive
Takes about 4 hours after ejaculation
Cholesterol loss and calcium and bicarbonate influx from vaginal secretions, increasing ATP production.

57
Q

What is the acrosome reaction

A

Triggered by contact with oocyte. Interaction with ZP3 protein on oocyte membrane. Leads to exposure of hyaluronidase and acrosin enzymes. Facilitates oocyte penetration.

58
Q

What occurs in oocyte activation

A

Release of cortical granules - block polyspermic penetration. Resumption of meiosis. Formation of the male and female pronuclei (fertilisation)

59
Q

What happens with too much testosterone

A

suppression of LH and FSH. Spermatogenesis is interrupted.

60
Q

What occurs in Kallman’s syndrome

A

affects development of nuclei of hypothalamus producing GnRH. Less stimulation of the pituitary. Hypogonadotropic hypogonadism

61
Q

What occurs in androgen insensitivity syndrome

A

end organ receptor deficiency - end up with female external features. Testicles remain intraabdominal.

62
Q

What does vasectomy stop spermatogenesis

A

Block vas on both sides so sperm cannot leave testicles. Pressure inside testicles goes up, which creates cracks in the BTB. Immune system produces anti-sperm antibodies. High pressure can lead to seminiferous tubule atrophy.

63
Q

What stage are oocytes arrest at birth

A

P1 of meiosis, Majority of primordial follicles will undergo atresia from birth to menopause

64
Q

What stage do secondary oocytes arrest at

A

metaphase II of Meiosis II

65
Q

When is meiosis II complete

A

Meiosis II only completes when the egg is fertilised at which point the second polar body is extruded to prevent triploidy

66
Q

What do theca cells do

A

LH and produce androgens. Androgens go across to granulosa cells, and are turned to oestrogens under the influence of FSH.

67
Q

How is menopause defined

A

Defined as LMP over 45. Retrospective after one year of amenorrhoea (or based on symptoms for women without a uterus). No laboratory tests over 45.
FSH high >30 due to lack of oestrogen and inhibin from granulosa cells
Oestradiol low <203
Aged 54, over 80% thought to be postmenopausal

68
Q

What is perimenopause

A

period around the last menstrual period. Vasomotor symptoms plus irregular bleeding

69
Q

What happens with limited pool of oocytes

A

Reduction in oestrogen, FSH increases (lack of inhibitory feedback from oestrogen on hypothalamus)
Leads to -> anovulatory cycles, menstrual irregularities, menorrhagia, physical changes, psychological changes

70
Q

What are the symptoms of hypo-oestrogenism

A

hot flush/night sweat, headaches, palpitations, leg cramps, uro-genital symptoms, reduced libido, mood change
Can be measured with Greene climacteric scale

71
Q

How does menopause cause osteoporosis

A

Oestrogens are crucial for the maintenance of bone mass in both males and females, acting to suppress bone resorption by osteoclasts and to promote bone formation by osteoblasts. DEXA state for osteopenia and osteoporosis

72
Q

What are the CV effects of menopause

A

Coronary artery disease, stroke, venous thromboembolism, pulmonary embolism

73
Q

What are the HRT options

A

oral, transdermal, implant or local. Implants can cause tachyphylaxis

74
Q

What does oestrogen do in HRT

A

reverse symptoms and effects of low oestrogen (if given alone, can cause endometrial hyperplasia, with risk of developing into carcinoma). Contraindicated for px with history of DVT or breast cancer.

75
Q

What does progesterone do in HRT

A

necessary to protect the endometrium if uterus present, not required in women without a uterus (anti-proliferative hormone)

76
Q

What does testosterone do in HRT

A

increases overall energy and sexual desire

77
Q

What are non-hormonal options for menopause

A

lifestyle, Replens, alpha 2 agonists (clonidine for bad vasomotor symptoms), SSRIs, Gabapentin (joint ache and muscle aches)

78
Q

What are the causes of idiopathic POI

A

cytogenetics (50% due to Turner’s), FMR1 premutation screening (trinucleotide repeat CGG in FMR1, X-linked dominant inheritance. Full mutation leads to fragile X metnal retardation), anti-adrenal (need to look for Addison’s - adrenal glands do not produce enough steroid hormones) and anti-thyroid antibodies

79
Q

What percentage of couples achieve conception within 12 months of trying

A

84 (49% of remaining will achieve conception within 24 months.
14% of remaining will achieve conception within 36 months)

80
Q

What is the definition of infertility

A

A woman of reproductive age who has not conceived after 1 year of unprotected sexual intercourse

81
Q

What causes subfertility

A

Male factor, anovulation, tubal factor, subtle factors not detectable on routine (25%)

For secondary infertility, tubal factor is biggest cause (40%)

82
Q

What is ideal semen volume

A

Volume >1.5ml
Density >15*10^6
Motility >40% progressively motile
Morphology >4% normal

83
Q

How is pelvic anatomy and Fallopian tube patency assessed

A

Laparoscopy and dye: gold standard in tubal patency evaluation
HSG - X-Ray with injection of contrast
Hycosy - US

84
Q

What is ovarian reserve

A

measures to assess ovarian reserve used to predict the likelihood of a successful response to ovarian stimulation with assisted reproduction treatment, although seem to have poor correlation with pregnancy outcomes

85
Q

How many eggs at birth

A

2 million

86
Q

How many eggs before birth

A

7 million

87
Q

How many eggs at first period

A

0.4 million

88
Q

How many eggs at menopause

A

Less than 1000

89
Q

What is Group I anovulation

A

hypothalamic pituitary failure (hypothalamic amenorrhoea or hypogonadotropic hypogonadism)

90
Q

What is Group II anovulation

A

hypothalamic-pituitary-ovarian dysfunction (PCOS)

91
Q

What is Group III anovulation

A

ovarian failure

92
Q

What is obstructive azoospermia

A

normal sized testes and FSH level. Post infection, post vasectomy, congenital absence of vas deferens

93
Q

What is non-obstructive azoospermia

A

small testes, raised FSH. Testicular failure

94
Q

What does ICSI do

A

Sperm retrival
Local anaesthetic, outpx procedure, samples may be stored for future cycles
Percutaneous epididymal sperm aspiration
Testicular sperm extraction

95
Q

What are causes of tubal damage

A

Infection (PID, STI), surgery, ectopic prengnacy, endometriosis

96
Q

Why and how is AMH measured

A

Blood test - produced by granulosa cells. Can be measured anytime in the cycle, also accurate in women receiving hormonal contraception.

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