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Year 2 - endocrinology > Endocrine infertility > Flashcards

Endocrine infertility Flashcards

1
Q

What is the axis in males?

A

GnRH -> LH/FSH -> testosterone (feedback)

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2
Q

What is the phases of the menstrual cycle?

A

Follicular phase, Ovulation, Luteal phase

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3
Q

What happens in the follicular phase?

A
  • Positive feedback from the hypothalamus to stimulate hormone release
  • Followed by negative feedback onto both the pituitary and hypothalamus
  • As the follicle grows you get positive feedback (as oestradiol levels rise, it induces positive feedback at the hypothalamus)
  • There is an increase in GnRH, and a big LH surge (ovulation)
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4
Q

What happens if implantation doesn’t occur?

A

endometrium is shed (menstruation) – energy consuming

otherwise the endometrium keeps growing (cancer disposition)

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5
Q

What is infertility?

A

Infertility: inability to conceive after 1 year of regular unprotected sex

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6
Q

How many people are affected by infertility and who are the abnormalities in which % of the time?

A

1:6 couples

Caused by abnormalities in males (30%) or females (45%), or unknown (25%)

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7
Q

How can you tell whether there is primary or secondary gonadal failure?

A

blood profile

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8
Q

What is primary gonadal failure and what will the hormone levels be?

A

Ovaries and testes not working

  • If testes aren’t working, there is low testosterone as less negative feedback -> increased LH/FSH
  • If the ovaries aren’t working, there is low oestradiol -> increased LH/FSH
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9
Q

What is secondary gonadal failure?

A

Hypothalamus or pituitary gland not working

  • If the problem is with the hypothalamus/pituitary -> LH and FSH are going to be low
  • Testosterone and oestradiol will still be low (in conjunction with low LH/FSH)
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10
Q

What are the clinical features of male hypogonadism?

A
  • Loss of libido
  • Impotence
  • Small testes
  • Decrease muscle bulk
  • Osteoporosis
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11
Q

What are the causes of male hypogonadism?

A
  1. Hypothalamic-pituitary disease
    - Hypopituitarism
    - Kallman’s syndrome (anosmia & low GnRH)
    - Illness/underweight (sufficient nutrition required for reproduction)
  2. Primary gonadal disease (problems at the gonads themselves)
    - Congenital: Klinefelter’s syndrome (XXY) – extra X chromosome -> hypogonadal
    - Acquired: Testicular torsion (-> necrosis), Chemotherapy
  3. Hyperprolactinaemia
  4. Androgen receptor deficiency
    Rare – born without the androgen receptor
    (Testosterone binds via androgen receptors to carry out its actions)
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12
Q

What is Kallman’s syndrome?

Features?

A
  • GnRH neurones don’t migrate and develop properly -> no GnRH released (so pituitary stimulation)
  • Also have anosmia (lack of smell) – GnRH neurones and olfactory neurones migrate together in embryogenesis from the base of the brain upwards
  • Pre-pubertal phenotype
  • Testes originally undescended
  • Stature low-normal
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13
Q

How can male hypogonadism be investigated?

A
  • Check the LH, FSH and testosterone: If they are all low, it suggests secondary failure -> MRI pituitary
  • Check prolactin (high prolactin switches of the gonadal axis)
  • Check sperm count, appearance of sperm, and their motility
  • Chromosomal analysis (Klinefelter’s XXY)
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14
Q

What is azoospermia and oligospermia?

A

Azoospermia = absence of sperm in ejaculate (producing zero sperm)

Oligospermia = reduced numbers of sperm in ejaculate

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15
Q

How is male hypogonadism treated?

A
  • Replacement testosterone for all patients (tablets, injections) – this will not make you fertile. This will increase their muscle bulk and protect against osteoporosis
  • For fertility: if hypothalamic/pituitary disease, you need gonadotrophins to stimulate testosterone release. You need to give subcutaneous gonadotrophin injections to induce spermatogenesis (stimulates the testes)
  • Hyperprolactinaemia -> dopamine agonist. Dopamine is the main hypothalamic influence over prolactin release. It has a negative effect on prolactin release
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16
Q

What are the endogenous sites of androgen production?

A
  • Interstitial Leydig cells of the testes
  • Adrenal cortex (males and females)
  • Ovaries
  • Placenta
  • Tumours
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17
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)
18
Q

How does testosterone circulate in the body?

A

Most (98%) of the testosterone in our system is bound to binding proteins.

19
Q

How is testosterone converted?

A

There are two enzymes involved in conversion of testosterone. 5α-reductase converts testosterone into the active form (DHT). DHT binds to androgen receptors.

Aromatase is found in the brain and adipose tissue. It converts testosterone to 17b-Oestradiol (E2) which acts via the oestrogen receptors

20
Q

Why may obese males be infertile?

A

Due to over-conversion of testosterone to oestradiol

21
Q

How do DHT and E2 act?

A

Via nuclear receptors – much slower action than G proteins

22
Q

What are the clinical uses of testosterone in adulthood?

A
  • Lean body mass (due to anabolic activity)
  • Muscle size and strength
  • Bone formation and bone mass (in young men)
  • Libido and potency
23
Q

Why does testosterone not restore fertility?

A

Treatment with gonadotrophins to restore normal spermatogenesis

24
Q

What are some disorders in females?

A
  1. Amenorrhoea
  2. Polycystic Ovarian Syndrome (PCOS)
  3. Hyperprolactinaemia
25
Q

What is amenorrhoea?

A

ABSENCE OF PERIOD

26
Q

What is primary, secondary amenorrhoea and oligomenorrhoea?

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 previously had cycles

Oligomenorrhoea = irregular long cycles

27
Q

What are the causes of amenorrhoea?

A

Pregnancy – commonest cause of amenorrhoea

Lactation – higher prolactin stops menstruation

Ovarian Failure:
Premature ovarian failure,
ovariectomy, chemotherapy, ovarian dysgenesis (Turner’s Syndrome – 45 X)

Gonadotrophin Failure:
Hypothalamic/pituitary disease, Kallmann’s syndrome, low BMI (leptin deficiency), post-pill amenorrhoea (downregulates the hypothalamus and pituitary)

Hyperprolactinaemia

Androgen excess: gonadal tumour – easy to diagnose because testosterone will be in excess

28
Q

What is the relationship between the pill and amenorrhoea?

A

Use of pill for a long time -> periods wont come back for 12 months after cessation

This is why it is advised that you stop using the pill every 4 years

29
Q

What are the symptoms Turner’s syndrome?

A
  • Short stature
  • Cubitus Valgus (forearm angled away from body to a greater degree when fully extended)
  • Gonadal dysgenesis (defective development)

1:5000 live female births – relatively common

30
Q

How is amenorrhoea investigated?

A
  • Pregnancy Test
  • LH, FSH and Oestradiol blood measurements (hypothalamic/pituitary disease)
  • Day 21 Progesterone
    There should be a rise in progesterone around this time to show that they are ovulating
    Someone with a low day 21 progesterone, they have not ovulated in that cycle
  • Prolactin measurement
  • Thyroid function test (hyper- and hypothyroidism can cause problems with periods)
  • Androgens (testosterone, androstenedione, DHEAS) – can be high in PCOS
  • Chromosomal Analysis (Turner’s)
  • Ultrasound Scan Ovaries/Uterus
31
Q

What is the treatment for amenorrhoea?

A
  • Treat the cause (e.g. low weight)
  • rimary Ovarian Failure – HRT, infertile
  • Hypothalamic/pituitary disease: HRT for oestrogen replacement (won’t make women fertile), for fertility: gonadotrophins (LH and FSH) – part of IVF treatment
32
Q

How common is PCOS and what is it associated with (risk)?

A

Very common: 1 in 12 women of reproductive age

Associated with:

  • Increased cardiovascular risk
  • Insulin resistance (diabetes)
33
Q

How is PCOS diagnosed?

A

You need two of the following:

  • Polycystic ovaries on the ultrasound scan
  • Oligoovulation or anovulation – irregular ovulation (difficult to diagnose)
  • Clinical/biochemical androgen excess: E.g. increased growth of hair in a male pattern
34
Q

What are the clinical features of PCOS?

A
  • Hirsutism – excess hair growth in a male pattern
  • Menstrual cycle disturbance
  • Increased BMI
35
Q

What is the treatment for PCOS and how do they work?

A

Metformin
Insulin sensitiser used in type II diabetes – improves insulin sensitivity. This is meant to prevent the onset of diabetes in PCOS

Clomiphene – a fertility drug
Anti-oestrogenic effect in the hypothalamo-pituitary axis. Binds to oestrogen receptors in the hypothalamus thereby blocking the negative feedback. This results in an increase in GnRH and gonadotrophin secretion. This is used in short periods to kick-start the HPG axis – 5 day course with clomiphene

  • If this all fails then gonadotrophin therapy as part of IVF treatment
36
Q

What problem do people with PCOS have and how can this be dealt with (follicles)?
What is a risk of this?

A

People with PCOS have lots of follicles but they can’t get them out normally
If these drugs don’t work, you can super-stimulate follicles with IVF
Over-stimulation can run life-threatening complications: ovarian hyper-stimulation syndrome

37
Q

What is prolactin? Which sex experiences higher levels?

A
  • Prolactin is normally involved in breast-milk production
  • High prolactin happens more commonly in women than men
  • Men have normal limits throughout life
38
Q

How is prolactin secretion normally controlled and how is this different to what happens during pregnancy and breast feeding?

A
  • Prolactin secretion has a predominantly negative control
  • Dopamine negatively controls prolactin because it inhibits secretion from the pituitary gland
  • Dopamine release is reduced in pregnancy.
  • TRH has a weak stimulatory effect on prolactin secretion but the predominant regulator is dopamine
  • Excess prolactin switches off GnRH pulsatility and stops LH acting on the ovaries and testes to prevent another pregnancy
39
Q

What are the causes of hyperprolactinaemia?

A
  • Dopamine antagonist drugs (commonest cause)
    Anti-emetics (metoclopramide) – anti-sickness tablets
    Anti-psychotics (phenothiazines)
  • Prolactinoma (another common cause - pituitary tumour producing prolactin)
  • Stalk compression due to pituitary adenoma
    A tumour mass blocks the secretion of the dopamine coming from the hypothalamus, therefore prolactin secretion is not inhibited
  • PCOS (may give a mild hyperprolactinaemia)
  • Hypothyroidism
    (primary hypothyroidism gives a high TRH -> stimulates prolactin)
  • Oestrogens (OCP), pregnancy, lactation
  • Idiopathic
40
Q

What are the clinical features of hyperprolactinaemia?

A
  • Galactorrhoea – breast milk expression
  • Reduced GnRH secretion / LH action -> hypogonadism
  • Prolactinoma (headaches and visual field defect)
41
Q

What is the treatment for hyperprolactinaemia?

A
  1. Treat the cause – stop drugs
  2. Dopamine agonist
    - Bromocriptine
    - Cabergoline

Pituitary surgery is rarely needed.

Year 2 - endocrinology (18 decks)

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