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Endocrine > Reproductive Endocrinology > Flashcards

Reproductive Endocrinology Flashcards

1
Q

What hormone is released by the hypothalamus and acts on the pituitary to control the sex hormones?

A

Gonadotrophin Releasing Hormone

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2
Q

What does GnRH do?

A

Responsible for the release of FSH & LH from the anterior pituitary

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3
Q

How is GnRH secreted?

A

In a pulsatile manner - different frequencies in women, constant frequency in men

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4
Q

How does the GnRH frequency change over time in women?

A

High frequency - stimulates LH

Low frequency - stimulates FSH

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5
Q

What controls the change in GnRH frequency in a menstrual cycle?

A

Oestrogen released by the follicle acts on kisspeptin neutrons to increase frequency driving LH

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6
Q

What is the effect of progesterone on GnRH frequency?

A

Reduces frequency

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7
Q

Name the two phases of the menstrual cycle

A
  1. follicular phase (variable length)

2. luteal phase (constant 14 days )

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8
Q

What does release of FSH cause?

A

Stimulation in growth of ovarian follicles which in turn release oestrogen

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9
Q

Describe the effect on the axis when oestrogen is increased

A

Exerts negative feedback to temporarily lower FSH levels

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10
Q

At a certain (set) level of oestrogen what happens to the feedback loop?

A

It exerts positive feedback to increase FSH and cause an LH surge

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11
Q

What is the effect of an LH surge?

A

Leads to ovulation (34-36 hours after) which turns the follicle to the corpus luteum `

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12
Q

What colour is the corpus luteum and why?

A

Yellow due to the abundance of cholesterol the intermediate for progesterone

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13
Q

Name the hormone produced by the corpus luteum what does it do?

A

Progesterone - exerts negative feedback & decreases LH secretion

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14
Q

What is required for the developing embryo to survive in the absence of LH?

A

It needs replaced with HCG - produced by the developing embryo itself

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15
Q

Describe the histology of a follicle

A

Oocyte surrounded by follicular cells - granulosa & theca cells with areas of fluid know as the antrum. Oocyte is surrounded by the zona pellucida (protein layer that prevents polyspermic fertilisation)

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16
Q

What is the effect of progesterone on oocyte release?

A

The increase after LH surge stimulates expression of enzymes that help breakdown the follicular wall leading to release of the oocyte

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17
Q

What happens to granulosa & theca cells under the influence of LH?

A

They transform into luteal cells

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18
Q

State four functions of oestrogen

A
  • increase thickness of vaginal wall
  • regulate LH surge
  • reduce vaginal pH (increase lactic acid)
  • decrease viscosity of cervical mucus to help sperm penetrate
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19
Q

State four functions of progesterone

A
  • maintains thickness of endometrium
  • relaxes myometrium (removal of progesterone = contractions)
  • responsible for infertile thick mucus
  • increases basal body temperature
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20
Q

How can regular menstrual cycles be assessed?

A

midluteal serum progesterone >30nmol/l

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21
Q

What is needed to assess ovulation in irregular menstrual cycles?

A

Further hormone evaluation

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22
Q

What are the three groups of ovulation disorders?

A
  1. Hypothalamic pituitary failure
  2. Hypothalamic pituitary dysfunction
  3. Ovarian Failure
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23
Q

Describe hypothalamic pituitary failure

A

Hypogonadotrophic hypogonadism - low levels of FSH and LH result in an oestrogen deficiency

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24
Q

How can oestrogen deficiency be tested?

A

Negative progesterone challenge test

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25
Q

In group 1 what is the usual presenting complaint

A

amenorrhoea

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26
Q

State the causes of hypothalamic pituitary failure

A
  • stress, anorexia, excessive exercise, tumours, trauma, drugs, kallman’s
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27
Q

What is Kallman’s Disease?

A

Delayed/absent puberty

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28
Q

How are all ovulation disorders initially managed?

A

stabilise weight, modify lifestyle, folic acid, rubella immunity, chalmydia test

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29
Q

How are group 1 ovulation disorders managed?

A

Pulsatile GnRH through a pump
Gonadotrophin daily injections
Both monitored using ultrasound to show response

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30
Q

Describe hypothalamic pituitary dysfunction

A

Normal gonadotrophin & oestrogen levels but other hormone levels abnormal

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31
Q

Name two disorders in group 2 ovulation disorders ``

A
  • Polycystic Ovarian Syndrome

- Hyperprolactinaemia

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32
Q

How is PCOS diagnosed?

A

2/3 of ;
oligo/amenorrhoea
US appearance (lots of underdeveloped follicles)
Clinical/biochemical signs of hyperandrogenism

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33
Q

What are the clinical signs of PCOS?

A

Acne, hirtirsm, olio/amenorrhoea …

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34
Q

Why is insulin resistance more common in women with PCOS?

A

LOOK UP ANSWER

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35
Q

How is PCOS infertility managed?

A

Depends on symptoms/needs of patients

  1. Clomifere citrate tablets
  2. Gonadotrophin therapy
  3. Laparoscopic ovarian diathermy
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36
Q

Describe the mechanism of action of clomifere citrate

A

Anti-oestrogen, stimulates LH & FSH

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37
Q

What drug can be added to clomifere citrate?

A

Metformin

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38
Q

What is the main risk for gonadotrophin therapy?

A

Multiple pregnancy

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39
Q

What is the difference between monozygotic & dizygotic twins?

A

dizygotic - come from two fertilised ova

monozygotic - come from an egg splitting

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40
Q

Describe monochorinic twins

A

Twins that share a placenta - three times increased risk of perinatal mortality

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41
Q

What signs indicate chrionicity?

A

Lambda sign - dichorionic

T sign - monochorionic

42
Q

Describe twin - twin transfusion syndrome

A

Unbalanced vascular communication within placenta bed - one big baby & one small baby. Most successful treatment is intra-uterine surgery

43
Q

What long term consequences are linked to prematurity?

A
  • ADHD
  • Lower IQ
  • Language problems
44
Q

After what length of time on IVF is there a risk of ovarian cancer?

A

12 months

45
Q

How does hyperprolactinaemia often present?

A

amenorrhoea, galactorrhoea, visual field problems

46
Q

What is the treatment for hyperprolactinaemia?

A

Dopamine agonist

47
Q

Describe ovarian failure

A

High gonadotrophin & low oestrogen - menopause

48
Q

What causes ovarian failure?

A
  • genetic (turner’s syndrome, fragile X, XX gonadal agenesis)
  • autoimmune
  • oophorectomy
  • chemotherapy/radiotherapy
  • family history
49
Q

How is ovarian failure managed?

A

Hormone Replacement Therapy (OCP)
Assisted conception
Counselling

50
Q

Where do FSH and LH act on in the male reproductive tract?

A

FSH - Sertoli cells

LH - Leydig cells

51
Q

What do sertoli cells do?

A

Produce androgen binding protein leading to local testosterone production & spermatogenesis
Produce Inhibit which exerts negative feedback on the hypothalamus to decrease GnRH

52
Q

What do leydig cells do?

A

produce testosterone from cholesterol leading to local production, release into the body & spermatogenesis

53
Q

Describe the function of the blood testes barrier

A

Separates the immune cells from stem cells to stop the immune cells attacking the new cells

54
Q

State two functions of testosterone

A
  • maintains the integrity of the blood testes barrier

- releases mature spermatozoa from sertoli cells by influencing peritubular myeloid cells

55
Q

What proteins does testosterone bind to?

A

SHBG & Albumin

56
Q

Define hypogonadism

A

clinical syndrome comprising of signs, symptoms & biochemical evidence of testosterone deficiency

57
Q

What is meant by primary hypogonadism?

A

Testes are primarily affected, decreased testosterone results in a decrease in negative feedback.

58
Q

State the biochemistry of primary hypogonadism

A

Low testosterone, anterior pituitary secretes higher amounts of LH/FSH
‘hypergonadotrophic hypogonadism’

59
Q

What is meant by secondary hypogonadism?

A

hypothalamus/pituitary affected despite testes being capable of normal function

60
Q

State the biochemistry of secondary hypogonadism

A

Low FSH/LH and low testosterone

‘hypogonadotrophic hypogonadism’

61
Q

Name three congenital causes of primary hypogonadism

A
  • klinefelter’s syndrome
  • cryptorchidism (undescended testes)
  • Y-chromosome micro deletions (lack of male characteristics)
62
Q

What causes klinefelter’s syndrome?

A

Nondisjunction - unequal division of chromosomes between cells

63
Q

How is klinefelter’s syndrome diagnosed?

A

Karyotyping

64
Q

Name some clinical features of klinefelter’s syndrome

A

Infertility, small firm testes, cryptorchidism, learning difficulties, ‘female’ like body structure, little chest hair & breast development

65
Q

State some acquired causes of primary hypogonadism

A

trauma, chemotherapy/radiation, varicocele, mumps, infiltrative disease, certain medications

66
Q

Name two congenital causes of secondary hypogonadism

A

Kallmann’s Syndrome

Prader Willi Syndrome

67
Q

Describe Prader Willi Syndrome

A

Excessive appetite, increased consumption, loss of GnRH & lack of sexual development

68
Q

Describe Kallmann’s Syndrome

A

Genetic disorder characterised by GnRH deficiency & hypo/anosmia (reduced/no sense of smell)

69
Q

What are the signs & symptoms of hypogonadism in pre-pubertal onset?

A

Small male sexual organs, decreased body hair, high pitched voice, low libido, gynaecomastia, ‘enuchoidal’ habitus, decreased muscle & bone mass

70
Q

What are the signs & symptoms of hypogonadism in post-pubertal onset?

A

Normal skeletal proportions but decreased sexual characteristics (libido, pubic hair, testicular volume, gynaecomastia, bone/muscle mass)

71
Q

How is hypogonadism diagnosed?

A

AM testosterone

LH/FSH Measurements

72
Q

How is testosterone calculated?

A

By measuring total testosterone & SHBG to work out free testosterone

73
Q

What are the three methods of testosterone replacement therapy?

A
  • Gel
  • Long-acting injection
  • Short-acting injection
74
Q

Describe the testosterone gel

A

Applied daily, mimics circadian rhythm but can cause skin irritation & risk of inter-personal contact

75
Q

Describe the long acting testosterone injection

A

‘nebido’
Given c. every 10 weeks, difficult to withdraw side effects if they are experienced, coughing post injection may occur but it maintains steady testosterone levels

76
Q

Describe the short acting testosterone injection

A

‘sustanon’
Variable testosterone levels, coughing may occur post injection but can be self administered, easier to withdraw if side effects experienced

77
Q

What are the contraindications for testosterone replacement therapy?

A

Hormone responsive cancer
Possibility of prostate cancer
Haematocrit >50%
Severe sleep apnoea/heart failure

78
Q

What three things should be monitored throughout testosterone replacement treatment?

A
  • testosterone concentration
  • PSA & DRE (cancer markers)
  • Haematocrit
79
Q

Why is the incidence of infertility increasing?

A

Older women, chlamydia, obesity, awareness of treatment, change in attitude

80
Q

Define infertility

A

Failure to achieve a clinical pregnancy after 12 months or more of regular unprotected intercourse in a couple who have never had a child

81
Q

What is the difference between primary and secondary infertility?

A

Primary - couple never conceived

Secondary - couple have conceived but pregnancy was unsuccessful

82
Q

Name some factors that affect fertility

A
  • age
  • previous pregnancies
  • less than 3 years trying
  • intercourse around ovulation
  • BMI
  • alcohol/smoking
  • recreational drugs
83
Q

Describe the implications of a hydrosalpinx

A

Damage causes accumulation of fluid which inhibits the cilia & leads to complete obstruction/ectopic pregnancy

84
Q

What are the features of a hydrosalpinx?

A

Abdominal pain, discharge, excitation, dysmenorrhoea

85
Q

What test could be done in a male who is suspected to be infertile?

A

Semen analysis, hormone biochemistry, chromosome analysis, biopsy/Ultrasound

86
Q

What tests are done on women at the infertility clinic?

A
  • swab for chlamydia
  • cervical smear
  • blood test for rubella immunity
  • midluteal progesterone
  • tubal patency test
87
Q

What are the two types of tubal patency tests?

A
  • hysterosalpingiogram

- laparoscopy

88
Q

Describe a hysterosalpingiogram

A

Visualisation of the tube by radiography & dye used if no known risk factors or laparoscopy contraindicated

89
Q

When is laparoscopy used?

A

Possible tubal/pelvic disease, known pathology/suggestive history or abnormal HSG

90
Q

What other tests can be used to investigate infertility in women?

A

Hysteroscopy
Pelvic Ultrasound
Endocrine profile
Chromosome Analysis

91
Q

What is the very first aspect of infertility management?

A

Lifestyle Advice

92
Q

What lifestyle advice is given to infertile couples?

A
  • Lose weight
  • Stop smoking, drugs & methadone
  • Drink alcohol & caffeine in moderation
  • Folic acid 400 micrograms/day
  • Vitamin D 10 micrograms/day
  • Need tested for chlamydia & rubella immunity
93
Q

What are the two different aims of reproductive surgery?

A
  • Treat infertility

- Enhance IVF treatment

94
Q

What can be done surgically to treat infertility?

A
  • correction of adhesions
  • removal of chocolate cysts in ovary
  • unblock tube
  • treat grade 1 & 2 endometriosis
95
Q

How is proximal tubal obstruction treated?

A

Selective salpingography & catheterisation/cannulation to improve chances of pregnancy

96
Q

What is removal of tissue (fibroids & polyps) called?

A

Measure

97
Q

How is a uterine septum treated?

A

Resection

98
Q

What are the four types of fibroid?

A
  • pendunculated
  • submucous
  • subserous
  • intramural
99
Q

Do all fibroids need removed?

A

No - it is very patient dependent. Submucosal fibroids should be treated as they are impacting uterine cavity.

100
Q

What are the seven steps of IVF?

A
  1. Ovarian stimulation
  2. Monitoring
  3. Ovulation induction
  4. Oocyte retrieval (in theatre)
  5. Preparation of sperm
  6. IVF - to produce blastocyst
  7. Embryo transfer & luteal support

Endocrine (17 decks)

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