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RED > Endocrine Disorders Affecting Reproduction > Flashcards

Endocrine Disorders Affecting Reproduction Flashcards

1
Q

Describe the pattern of GnRH release.

What is the consequence of this?

A
  • GnRH is released in a pulsatile manner throughout the day.

- This results in pulsatile FSH and LH release.

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2
Q

What is the consequence of continuous GnRH release?

A

Continuous GnRH release decreases release of FSH and LH.

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3
Q

List the 3 categories of causes of HPG axis dysfunction.

A

1 - Central pathology.

2 - Gonadal damage.

3 - PCOS.

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4
Q

What is the most common cause of secondary amenorrhoea?

A

Pregnancy.

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5
Q

List 3 symptoms of oestrogen deficiency.

A

1 - Hot flushes.

2 - Poor libido.

3 - Dyspareunia.

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6
Q

List 7 factors to consider when assessing the function of the HPG axis in females.

A

1 - Menstrual history (oligomenorrhoea / amenorrhoea).

2 - Oestrogen deficiency.

3 - Hirsutism.

4 - Acne.

5 - Androgenic alopecia.

6 - Weight changes.

7 - Galactorrhoea.

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7
Q

List 3 central causes of amenorrhoea.

A

1 - Hypothalamic responses due to anorexia excessive exercise and stress.

2 - Pituitary tumours.

3 - Hypogonadotropic hypogonadism (failure of FSH / LH secretion).

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8
Q

List 2 ovarian causes of amenorrhoea.

A

1 - Turner’s syndrome.

2 - Premature ovarian failure.

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9
Q

List 2 miscellaneous causes of amenorrhoea.

A

1 - PCOS.

2 - Thyrotoxicosis.

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10
Q

When does leptin secretion increase?

Why?

A
  • Following weight gain.

- Because there is more adipose tissue secreting it.

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11
Q

List the anterior pituitary hormones.

A

1 - ACTH.

2 - TSH.

3 - GH.

4 - LH.

5 - FSH.

6 - Prolactin.

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12
Q

Which cells release prolactin?

A

Lactotrophs.

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13
Q

How is prolactin release controlled?

A

It is constantly negatively regulated by dopamine.

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14
Q

What effect does prolactin have on other anterior pituitary hormones?

A

Prolactin negatively regulates FSH and LH.

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15
Q

What is the effect of thyrotropin-releasing hormone on prolactin?

A

Thyrotropin-releasing hormone stimulates the release if prolactin from the anterior pituitary (as well as thyroid-stimulating hormone).

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16
Q

What is the average upper limit of prolactin concentration?

A

500mu/L.

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17
Q

Why is hyperprolactinaemia difficult is diagnose in postmenopausal women?

A
  • Because prolactin inhibits FSH and LH, therefore oestrogen production.
  • The effects of a lack of oestrogen are normally the indicators of hyperprolactinaemia.
  • In postmenopausal women, oestrogen isn’t being released anyway.
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18
Q

List the symptoms of hyperprolactinaemia in premenopausal women.

A

1 - Oligo/amenorrhoea.

2 - Vaginal dryness.

3 - Flushes.

4 - Sweats.

5 - Galactorrhoea.

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19
Q

List 4 causes of hyperprolactinaemia.

A

1 - Prolactinomas.

2 - Space-occupying lesions.

3 - Dopamine antagonists.

4 - Secondary hypothyroidism.

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20
Q

Why might a space-occupying lesion cause hyperprolactinaemia?

A

Because the pituitary stalk might become compressed / disconnected, causing loss of inhibitory signalling by the hypothalamus.

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21
Q

Define premature ovarian insufficiency.

A

Elevated LH and FSH (menopause) <45 years of age.

22
Q

List 4 causes of premature ovarian insufficiency.

A

1 - Turner’s syndrome.

2 - Fragile X syndrome.

3 - Autoimmune disease against the ovaries.

4 - Iatrogenic (chemotherapy, radiotherapy, surgery etc.).

5 - Mutations in the FSHR.

23
Q

Summarise the pathophysiology of Addison’s disease, Hashimoto’s disease, Cushing’s disease and Grave’s disease.

A
  • Addison’s disease is hypoadrenalism due to an autoimmune response to the adrenal cortex.
  • Hashimoto’s disease is hypothyroidism due to an autoimmune response to the thyroid gland.
  • Cushing’s disease is hyperadrenalism due to an adrenal tumour or a pituitary tumour.
  • Grave’s disease is hyperthyroidism due to autoantibodies that stimulate the TSH receptor.
24
Q

Describe the mechanism of autoimmune premature ovarian insufficiency.

A

Antiovarian antibodies cause inflammatory infiltration of the ovaries, leading to apoptosis and atrophy.

25
Q

Why is there a link between autoimmune premature ovarian insufficiency and Addison’s?

A

Because the autoantibodies might target the same autoantigens in the adrenal gland as in the ovaries.

26
Q

What is the treatment of premature ovarian insufficiency?

A

Oestrogen replacement.

27
Q

List 5 signs and symptoms of polycystic ovary syndrome.

A

1 - Oligo/ amenorrhoea.

2 - Hirsutism.

3 - Obesity.

4 - Infertility (due to anovulation).

5 - Polycystic ovaries on ultrasound.

28
Q

What proportion of premenopausal women have PCOS?

A

10%.

29
Q

List 3 hormonal changes in women with PCOS.

A

1 - Increased testosterone.

2 - Increased androstenedione.

3 - Increased LH.

  • Not oestrogen deficient.
30
Q

Why is LH increased in PCOS?

What is the effect of LH hypersecretion?

A
  • It is increased as a result of increased frequency of hypothalamic gonadotropin-releasing hormone pulses.
  • Increased LH leads to an increase in androgen production by the theca cells within the ovary.
31
Q

What is the cycle of clinical features causing PCOS?

How is this used to treat PCOS?

A

Each of these factors upregulate each other:

1 - Anovulation.

2 - Insulin resistance.

3 - Androgen excess.

4 - Obesity.

  • Treatment involved breaking this cycle, usually by losing weight.
32
Q

List 2 risks of PCOS regarding pregnancy.

A

1 - The risk of gestational diabetes is ten times increased in pregnant women with PCOS.

2 - The risk of pregnancy-related hypertension is equally high in women with PCOS.

3 - There is an increased risk of ovarian hyperstimulation syndrome, and subsequently fertilisation of more than one egg.

33
Q

Describe the mechanism of action of Dianette as an oral contraceptive.

A
  • It contains ethinyl oestradiol, a synthetic oestrogen.

- It also contains cyproterone acetate, an anti-androgen that acts on the endometrium like progesterone.

34
Q

Describe the mechanism of action of Yasmin as an oral contraceptive.

A
  • It contains ethinyl oestradiol, a synthetic oestrogen.

- It also contains drospirenone, a synthetic progesterone.

35
Q

What is androgen insensitivity syndrome?

A

A spectrum of disorders due to mutations in the androgen receptor, where patients are genetically male but have female characteristics. This can include:

1 - Complete androgen insensitivity syndrome.

2 - Incomplete androgen sensitivity syndrome.

3 - Reifensteins syndrome.

36
Q

List 5 symptoms of complete androgen insensitivity syndrome.

A

1 - Female external genitalia.

2 - Short vagina.

3 - No uterus.

4 - Absent prostate.

5 - Gynaecomastia.

37
Q

Why might androgen insensitivity syndrome present as an inguinal hernia?

A

Because undescended testes cause inguinal bulging.

38
Q

Why do patients with androgen insensitivity syndrome have high LH?

A

Because there is no negative feedback mechanism as LH cannot stimulate androgen production at the ovaries.

39
Q

Why do patients with androgen insensitivity syndrome have high oestrogen?

A

1 - Due to LH-driven gonad secretion.

2 - Due to aromatisation of testosterone, which is also high in androgen insensitivity syndrome.

40
Q

What is 5-alpha-reductase deficiency?

A

A condition in which genetic females are unable to convert testosterone to dihydrotestosterone, resulting in slightly masculine characteristics.

41
Q

Is testosterone decrease with age pathological or physiological?

A

Physiological - decrease is normal.

42
Q

List 6 causes of male primary hypogonadism (hypergonadotropic hypogonadism where the problem is in the testes).

A

1 - Trauma.

2 - Cancer treatment.

3 - Undescended testes.

4 - Infections.

5 - Chromosomal abnormalities such as Klinefelter’s syndrome.

6 - Systemic diseases such as liver cirrhosis.

43
Q

List 6 causes of male secondary hypogonadism (hypogonadotropic hypogonadism where the problem is in the brain).

A

1 - Pituitary tumours.

2 - Hyperprolactinaemia.

3 - Hypothalamic disorders such as craniopharyngioma pituitary tumour and Kallmann syndrome.

4 - Systemic diseases such as liver cirrhosis.

5 - Obesity.

6 - Androgen abuse.

44
Q

List 8 symptoms of hypogonadism in males.

A

1 - Delayed puberty.

2 - Reduced libido.

3 - Gynaecomastia.

4 - Loss of body hair.

5 - Decreased muscle mass.

6 - Female fat distribution.

7 - Osteoporosis.

8 - Infertility.

45
Q

If FSH and LH are high, is this indicative of primary or secondary hypogonadism?

Why?

A
  • Primary hypogonadism.
  • Because the brain is able to release signals to the testes, but a signal is not being relayed back to the brain, so the problem is with the testes.
46
Q

What is the karyotype of Klinefelter’s syndrome?

A

47 XXY.

47
Q

List 6 symptoms of Klinefelter’s syndrome.

A

1 - Small testes.

2 - Azoospermia.

3 - Gynaecomastia.

4 - Reduced sexual hair.

5 - Osteoporosis.

6 - Tall stature.

48
Q

Give an example of a genetic cause of primary male hypogonadism other than Klinefelter’s syndrome.

A

Myotonic dystrophy.

49
Q

What is the treatment for hypergonadotropic hypogonadism?

A

Testosterone replacement.

50
Q

Why does androgen abuse cause hypogonadism?

A

Because the exogenous testosterone blocks FSH and LH production.

51
Q

List 5 symptoms of androgen abuse.

A

1 - Psychological changes.

2 - Prostate cancer.

3 - Atrophy of the testes.

4 - Azoospermia.

5 - Polycythaemia.

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