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Endo > 9. Endocrine Infertility > Flashcards

9. Endocrine Infertility Flashcards

1
Q

Describe the hypothalamo-gonadotrophin axis during the follicular and ovulation phase

A

Follicular phase: Same as men - FSH/LH stimulates the ovaries to release oestradiol + progesterone which have NEGATIVE feedback on hypothalamus + pituitary

Ovulation phase: High oestradiol levels has POSITIVE feedback on the hypothalamus, causing a SURGE in LH/FSH

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2
Q

What happens in the luteal phase?

A

If implantation doesn’t occur, endometrium is shed -> menstruation

If implantation occurs -> pregnancy

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3
Q

Definition of infertility?

A

Inability to conceive after 1 year of regular unprotected sex

1:6 couples affected
Male abnormalities (30%)
Female abnormalities (45%)
Unknown abnormalities (25%)
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4
Q

What is primary gonadal failure?

A

Failure of the testes/ovaries -> LOW testosterone/oestradiol
So LESS negative feedback onto hypothalamus ->
HIGH GnRH -> High FSH/LH

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5
Q

What is secondary gonadal failure? (hypothalamus/pituitary disease)

A

Failure of hypothalamus/pituitary to release GnRH

LOW FSH/LH -> Low testosterone/oestradiol

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6
Q

Features of male hypogonadism

A
  • Loss of libido
  • Impotence
  • Small testes
  • Decreased muscle bulk
  • Osteoporosis
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7
Q

Causes of male primary hypogonadism?

A

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

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8
Q

Causes of male secondary hypogonadism?

A

Hypo/pituitary disease:

  • Hypopituitarism
  • Kallman’s syndrome - genetic disorder (anosmia + low GnRH)
  • Illness/underweight
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9
Q

Other causes of male hypogonadism?

A

Hyperprolactinaemia

Congenital Androgen receptor deficiency (rare)

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10
Q

Investigations for male hypogonadism?

A
  1. FSH, LH, testosterone - if ALL LOW -> MRI pituitary
    If FSH/LH are high, problem with gonads
  2. Prolactin levels
  3. Sperm count:
    Azoospermia = absence of sperm in ejaculate
    Oligospermia = reduced sperm
  4. Chromosomal analysis (Klinefelters XXY)
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11
Q

Treatment for male hypogonadism?

A

Testosterone replacement

To reactivate spermatogenesis (fertility) -> sc gonadotrophins (FSH/LH) injection

Hyperprolactinaemia - D2 agonist

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12
Q

Where are the endogenous sites of androgen production?

A
  1. Leydig cells (testes)
  2. Adrenal cortex
  3. Ovaries
  4. Placenta
  5. Tumours
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13
Q

What are the main actions of testosterone?

A
  1. Development of male genital tract
  2. Maintains fertility in adulthood
  3. Control of secondary sexual characteristics
  4. Anabolic effects (muscle, bone)
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14
Q

What is tissue-specific processing of testosterone?

A

In muscle/bone:
Converted by 5a-reductase into DHT (Dihydrotestosterone)
DHT acts via Androgen receptors

In brain/adipose tissue:
Converted by aromatase into 17b-oestradiol (E2)
E2 acts via oestrogen receptors

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15
Q

What are the clinical uses of testosterone?

A

Increases:

  • Lean body mass
  • Muscle strength/size
  • Bone formation/mass
  • Libido/potency

It does NOT restore fertility - that can be achieved by gondaotrophin treatment which will activate spermatogenesis

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16
Q

What are the 3 causes of infertility in females?

A
  1. Amenorrhoea
  2. Polycystic Ovarian Syndrome (PCOS)
  3. Hyperprolactinaemia
17
Q

What are the types of amenorrhoea?

A
  1. Primary amenorrhoea = failure to begin spontaneous menstruation by 16yrs
  2. Secondary amenorrhoea = no menstruation for 3 months in woman who’s previously had normal cycles
  3. Oligomenorrhoea = irregular long cycles
18
Q

Causes of amenorrhoea at the level of gonads?

A 
Pregnancy/lactation
Ovarian failure
- Premature ovarian failure
- Ovariectomy/chemo
- Ovarian dysgenesis (Turner's 45 XO, missing X chromosome)
19
Q

Clinical features of Turners syndrome?

A

Short stature
Gonadal dysgenesis
Wide carrying angle

20
Q

Causes of amenorrhoea at the level of hypo/pituitary?

A

Gonadotrophin failure:

  • Hypo/pit disease
  • Kallmann’s syndrome (XXY)
  • Low BMI
  • Post pill

Hyperprolactinaemia

Gonadal tumour -> androgen excess (RARE)

21
Q

Investigations for amenorrhoea?

A
  1. Pregnancy test
  2. FSH/LH/oestradiol
  3. Day 21 progesterone (should be high if ovulating. If not, that means no LH surge -> no ovulation -> low day 21 progesterone)
  4. Prolactin, thyroid function tests
  5. Androgen levels (testosterone, DHEAS)
  6. Chromosomal analysis (Turners 45 XO)
  7. Ultrasound ovaries/uterus
22
Q

Treatment for amenorrhoea?

A

Treat the cause (e.g. low weight)

Primary ovarian failure - HRT to treat infertility

Hypo/pit disease: HRT if not interested in fertility, for fertility give FSH/LH (part of IVF treatment)

23
Q

Incidence of PCOS?

A

1 in 12 women of reproductive age

24
Q

What is PCOS associated with?

A

Increased risk of CVD and insulin resistance

25
Q

Diagnosis of PCOS?

A
  1. Polycystic ovaries on ultrasound
  2. Oligo-/anovulation
  3. Clinical/biochemical androgen excess
26
Q

Clinical features of PCOS?

A

Hirsutism
Menstrual cycle disturbance
Increased BMI

27
Q

Treatment of PCOS infertility?

A

Metformin (drug for insulin resistance in T2DM)
Clomiphene
Gonadotrophin therapy as part of IVF

28
Q

MOA of clomiphene?

A

Anti-oestrogenic

Binds to oestrogen receptors in hypothalamus
Blocks negative feedback -> INCREASED GnRH release

29
Q

Action of prolactin?

A

Stimulates lactation

In high amounts:
REDUCES GnRH pulsatility
INHIBITS LH action on ovary/testis

30
Q

Causes of hyperprolactinaemia?

A
  1. Dopamine antagonists - Anti-emetics + anti-psychotics
  2. Prolactinoma
  3. Stalk compression due to pituitary adenoma

Minor causes: PCOS, hypothyroidism, pregnancy

31
Q

Clinical features of hyperprolactinaemia?

A
  1. Galactorrhoea
  2. Reduced GnRH secretion/LH action -> HYPOGONADISM
  3. Prolactinoma -> headache, visual field defect
32
Q

Treatment of hyperprolactinaemia?

A
  1. Treat the cause (e.g. stop drugs)
  2. Dopamine agonist (bromocriptine, cabergoline)

For prolactinoma - dopamine agonist therapy very effective - surgery rarely needed

Endo (13 decks)

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