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Endo > Endocrinology of Infertility > Flashcards

Endocrinology of Infertility Flashcards

1
Q

Which cells within the testes does LH stimulate and what does it make these cells produce?

A

Leydig Cells –> they are stimulated to produce testosterone

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2
Q

Which cells within the testes does FSH stimulate and what does it makes these cells produce?

A

Sertoli cells (in the seminiferous tubules) –> they are stimulated to produce sperm and inhibin A and B

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3
Q

What does inhibin inhibit?

A

Pituitary FSH secretion

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4
Q

What are the three phases of the menstrual cycle?

A

Follicular Phase
Ovulation
Luteal Phase

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5
Q

What does LH stimulate in the ovaries?

A

Oestradiol and progesterone production

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6
Q

What does FSH stimulate in the ovaries?

A

Follicular development and inhibin production

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7
Q

What effect does oestrogen have on the HPG axis in the follicular phase of the menstrual cycle?

A

It has a negative feedback effect – inhibits FSH and LH

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8
Q

What does the leading follicle develop into by around day 10?

A

Graffian Follicle

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9
Q

Once oestrogen reaches a certain level it switches to positive feedback. How does it do this?

A

It increases the GnRH secretion It increases LH sensitivity to GnRH

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10
Q

Define infertility.

A

Inability to conceive after 1 year of regular unprotected sex

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11
Q

What is primary gonadal failure and what effects does it have on the HPG axis?

A

It is a problem with the gonads The testes/ovaries don’t produce enough testosterone/oestrogen so there is no negative feedback on the HPG axis meaning that you get high GnRH, high LH and high FSH.

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12
Q

Describe the levels of the different hormones in the HPG axis in the case of hypothalamic/pituitary disease causing infertility.

A

Low GnRH
Low FSH
Low LH

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13
Q

State some of the clinical features of male hypogonadism.

A 
Loss of libido 
Impotence 
Small testes 
Decreased muscle bulk 
Osteoporosis (testosterone has anabolic action in the bone)
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14
Q

State 5 causes of male hypogonadism.

A 
Hypopituitarism 
Kallmann’s Syndrome (anosmia + low GnRH) 
Illness/underweight
Hyperprolactinaemia 
Androgen receptor deficiency (RARE)
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15
Q

State some congenital and acquired causes of primary gonadal disease.

A

Congenital: Klinefelter’s Syndrome (XXY)
Acquired: Testicular torsion, chemotherapy

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16
Q

What are the main investigations for male hypogonadism?

A

LH, FSH and testosterone (if all are low –> MRI to check pituitary problem) Prolactin Sperm count (azoospermia – absence of sperm in ejaculate; oligospermia – reduced number of sperm in ejaculate) Chromosomal analysis (check for Klinefelter’s)

17
Q

What is given to all patients with hypogonadism?

A

Testosterone to increase muscle bulk and protect against osteoporosis

18
Q

How do you restore fertility in someone with hypothalamic/pituitary disease?

A

Subcutaneous gonadotrophin injections – stimulates testosterone release

19
Q

What is the treatment for hyperprolactinaemia?

A 
Dopamine agonists – bromocriptine and cabergoline 
Pituitary surgery (though this is rarely used because medicine normally works well)
20
Q

State some endogenous sites of production of androgens.

A 
Interstitial leydig cells in the testes 
Adrenal cortex 
Ovaries 
Placenta 
Tumours
21
Q

What are the main actions of testosterone?

A 
Development of the male genital tract 
Maintains fertility in adulthood 
Control of secondary sexual characteristics 
Anabolic effects (muscle, bone)
22
Q

Testosterone is heavily plasma protein bound and it can be converted to other hormones in various tissues. State two products that testosterone can be converted to and the enzymes responsible for these conversions.

A

Converted by 5-alpha-reductase to dihydrotestosterone (DHT), which acts on androgen receptors Converted by aromatase to 17-beta-oestradiol, which acts on oestrogen receptors

23
Q

What type of receptors does DHT and E2 act on?

A

Nuclear receptors

24
Q

What are the clinical uses of testosterone?

A 
Lean body mass 
Muscle size and strength 
Bone formation and bone mass 
Libido and potency
NOTE: it does NOT restore fertility
25
Q

What is the difference between primary and secondary amenorrhoea?

A

Primary Amenorrhoea = failure to develop spontaneous menstruation by the age of 16 years
Secondary Amenorrhoea = absence of menstruation for 3 months in a woman who has previously had cycles

26
Q

What is oligomenorrhoea?

A

Irregularly long, infrequent cycles

27
Q

List some causes of amenorrhoea.

A

Physiological: Pregnancy, Lactation

Ovarian failure: Premature ovarian insufficiency, Oophorectomy, Chemotherapy, Ovarian dysgenesis (Turner’s Syndrome (45 X))

Hypothalamic/pituitary disease : Kallmann’s syndrome

Low BMI

Post-pill amenorrhoea (if you use the pill for a long time and then go off it, it could take a while for the periods to return)

Hyperprolactinaemia

Androgen excess (gonadal tumour)

28
Q

State some investigations for amenorrhoea.

A

Pregnancy test

LH, FSH and Oestradio

Day 21 Progesterone (this should be high (showing that you’re ovulating) because progesterone rises in the second half of the menstrual cycle)
Prolactin

Thyroid function test (both hyper- and hypothyroidism can cause problems with the menstrual cycle)

Androgens (testosterone, androstenedione, DHEAS)

Chromosomal analysis

29
Q

What are the implications on health of polycystic ovarian syndrome (PCOS)?

A

Increased cardiovascular risk Insulin resistance (diabetes)

30
Q

What are the criteria for diagnosing PCOS?

A

They must have at least 2 of the following:
Polycystic ovaries on ultrasound scan
Clinical/biochemical signs of androgen excess
Oligoovulation/anovulation

31
Q

What are the clinical features of PCOS?

A

Hirsuitism
Menstrual irregularities
Increased BMI

32
Q

Describe the treatment for PCOS.

A

METFORMIN – insulin sensitiser
CLOMIFENE – anti-oestrogenic effects in the hypothalamo-pituitary axis – binds to oestrogen receptors in the hypothalamus thereby blocking the negative feedback –> increased GnRH and gonadotrophin secretion
GONADOTROPHIN THERAPY as part of IVF treatment

33
Q

What hypothalamic hormone has a stimulatory effect on prolactin release?

A

Thyrotrophin releasing hormone (TRH)

34
Q

What effect does hyperprolactinaemia have on the HPG axis?

A

It reduces GnRH pulsatility so that it is released basally all the time rather than in regular pulses It will switch off gonadal function via LH actions on the ovaries and testes

35
Q

State some causes of hyperprolactinaemia.

A 
Dopamine antagonists (anti-emetics and anti-psychotics) 
Prolactinoma 
Stalk compression due to pituitary adenoma (so dopamine can’t get to adenohypophysis)
PCOS 
Hypothyroidism 
Oestrogens (OCP)
Pregnancy 
Lactation 
Idiopathic
36
Q

What are the clinical features of hyperprolactinaemia?

A

Galactorrhoea Reduced GnRH and gonadotrophin secretion –> HYPOGONADISM
Prolactinoma: Visual field defect & Headache

Endo (17 decks)

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