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Endocrinology > 9. Endocrine Infertility > Flashcards

9. Endocrine Infertility Flashcards

1
Q

Outline the male hypothalamo-pituitary-gonadal axis

A
  • GnRH pulses from hypothalamus
  • Stimulation of LH + FSH release from pituitary
  • LH stimulates leydig cells to produce testosterone
  • FSH stimulates sertoli cells in seminiferous tubules to produce sperm and inhibin A + B
  • Inhibin has negative feedback on pituitary FSH secretion
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2
Q

What are the phases of the menstrual cycle?

A
  • Follicular phase
  • Ovulation
  • Luteal phase
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3
Q

Describe the follicular phase

A
  • GnRH pulses stimulate LH + FSH
  • LH stimulates production of oestradiol and progesterone in the ovaries
  • FSH stimulates follicular development and inhibin
  • Around day 10, leading follicle => Graffian Follicle
  • Oestrogen initially has negative feedback on LH + FSH secretion
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4
Q

Describe ovulation and the luteal phase

A
  • Once oestrogen reaches a certain level, it switches from negative to positive feedback
  • Increases GnRH release and LH sensitivity to GnRH
  • Mid-cycle LH surge
  • Triggers ovulation from the leading follicle
  • Progestrone rises
  • If no implantation - endometrium is shed
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5
Q

Define infertility, and the proportion of couples it can affect

A
  • Inability to conceive after 1 year of regular unprotected sex
  • 1/6 couples can be affected
  • Abnormalities - 30% males, 45% females, 25% unknown
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6
Q

What does primary gonadal failure lead to?

A
  • Testes/ovaries not producing testosterone/oestrogen
  • No negative feedback on HPG axis
  • High GnRH and high LH + FSH
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7
Q

What is hypothalamic/pituitary disease?

A
  • Secondary gonadal failure/hypopituitarism
  • Inability of pituitary to produce FSH + LH - low levels
  • Therefore, low oestradiol/testosterone
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8
Q

What are 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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9
Q

What are the causes of hypothalamic-pituitary disease?

A
  • Hypopituitarism - secondary gonadal failure
  • Kallmann Syndrome - anosmia and low GnRH, due to failure of GnRH and olfactory neurones to migrate from back of brain in development
  • Illness/underweight - low levels of leptin
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10
Q

Give congenital and acquired causes of primary gonadal disease

A
  • Congenital: Klinefelters Syndrome (XXY)

* Acquired: Testicular torsion, chemotherapy

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11
Q

What effect can hyperprolactinaemia have on the gonads?

A

Inhibit gonadal function

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12
Q

How else can low testosterone levels/insensitivity be referred to and why?

A
  • Hypoandrogenism
  • Testosterone = androgen
  • Androgen receptor deficiency is a rare congenital cause of hypogonadism
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13
Q

How do you investigate male hypogonadism?

A
  • LH, FSH and testosterone - if low, MRI of pituitary
  • Prolactin
  • Sperm count: azoospermia = absence, oligospermia = reduced numbers
  • Chromosomal analysis
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14
Q

What is an ICSI?

A
  • Intracytoplasmic sperm injections

* Combats infertility in someone with oligospermia

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15
Q

How can male hypogonadism be treated?

A
  • All patients: replacement testosterone for all patients
  • Hypothalamic/pituitary disease: subcutaneous gonadotrophin injections, inducing spermatogenesis for fertility
  • Hyperprolactinaemia: dopamine agonist, (main influence) negative effect on prolactin release
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16
Q

What are the endogenous sites of androgen production?

A
  • Adrenal cortex
  • Interstitial Leydig cells
  • Ovaries
  • Placenta
  • Tumours
17
Q

What are the main actions of testosterone?

A
  • Development of male genital tract
  • Maintains fertility in adulthood
  • Control of secondary sexual characteristics
  • Anabolic effects
18
Q

How much of testosterone is protein bound

A

98%

19
Q

How is testosterone altered to act on androgen receptors?

A
  • 5 α-reductase converts it into dihydrotestosterone (DHT)

* Goes into nucleus - nuclear receptors

20
Q

How is testosterone altered to act on oestrogen receptors?

A
  • Aromatase converts it into 17β-oestradiol (E2)

* Goes into nucleus - nuclear receptors

21
Q

What are the clinical uses of testosterone?

A 
• Lean body mass
• Muscle size and strength
• Bone formation and bone mass
• Libido and potency
(• will not restore fertility)
22
Q

What is primary amenorrhoea?

A

Failure to develop spontaneous menstruation by age 16

23
Q

What is secondary amenorrhoea?

A
  • Absence of menstruation for 3 months in a woman who has previously had cycles
  • Probably not congenital
24
Q

What is oligomenorrhoea?

A

Irregular long cycles

25
Q

What are the causes of amenorrhoea?

A 
• Pregnancy
• Lactation
• Ovarian failure
- premature ovarian insufficiency
- oophorectomy/ovariectomy
- chemotherapy
- ovarian dysgenesis - Turner's syndrome
• Gonadotrophin failure (can also be caused by the pill)
26
Q

What are some of the features of Turner’s syndrome?

A
  • Short stature
  • Cubitus Valgus (angled forearm)
  • Gonadal dysgenesis
27
Q

How can amenorrhoea be investigated?

A
  • Pregnancy test
  • LH, FSH and oestradiol
  • Day 21 progesterone - rises in second half of menstrual cycle
  • Prolactin
  • Thyroid function test - hyper/hypothyroidism can cause problems
  • Androgens
  • Chromosomal analysis
  • Ultrasound
28
Q

How can amenorrhoea be treated?

A 
• Treat the cause
• Primary ovarian failure - hormone replacement therapy (HRT)
• Hypothalamic/pituitary disease
- HRT for oestrogen replacements
- Gonadotrophins for fertility
29
Q

Who gets polycystic ovarian syndrome (PCOS) and what is it associated with?

A
  • 1/12 women of reproductive age

* Associated with increased cardiovascular risk and insulin resistance (diabetes)

30
Q

What are the criteria to diagnose PCOS?

A

• 2 of the following:

  • polycystic ovaries on ultrasound
  • oligoovulation/anovulation
  • androgen excess
31
Q

What are the clinical features of PCOS?

A
  • Hirsuitism
  • Menstrual cycle disturbance
  • Increased BMI
32
Q

How is PCOS treated (fertility)?

A

• Metformin - insulin sensitiser
• Clomiphene
- anti-oestrogenic effect in hypothalamo-pituitary axis
- Binds to oestrogen receptors in hypothalamus, blocking negative feedback
- Increase in GnRH and gonadotrophin secretion
• Gonadotrophin therapy

33
Q

What happens if prolactin secretion is dysregulated?

A
  • Gonadal function switched off via LH actions on the ovaries and testes
  • Reduced GnRH pulsatility - released all the time rather than in pulses
34
Q

What are the causes of hyperprolactinaemia?

A
  • Dopamine antagonists: anti-emetics and anti-psychotics (more likely as it’s used long term)
  • Prolactinoma
  • Stalk compression due to adenoma - dopamine can’t get through
  • PCOS
  • Hypothydroidism
  • Oestrogens (pill), pregnancy, lactation
  • Idiopathic
35
Q

What are the clinical features of hyperprolactinaemia?

A
  • Galactorrhoea
  • Hypogonadism - due to reduced GnRH secretion/LH action
  • Prolactinoma - headache, visual field defect
36
Q

How can hyperprolactinaemia be treated?

A
  • Treat the cause e.g. stop taking drugs causing the problem if possible, surgery
  • Dopamine agonists - bromocriptine, cabergoline (also decreases tumour if prolactinoma)

Endocrinology (17 decks)

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