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RED > L05 - Endocrine Disorders Affecting Reproduction > Flashcards

L05 - 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
  • Continuous GnRH release decreases release of FSH and LH
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2
Q

What is the most common cause of secondary amenorrhoea?

A

Pregnancy

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3
Q

List 3 symptoms of oestrogen deficiency.

A

1 - Hot flushes

2 - Poor libido

3 - Dyspareunia

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4
Q

What factors should be considered 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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5
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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6
Q

List 2 ovarian causes of amenorrhoea.

A

1 - Turner’s syndrome

2 - Premature ovarian failure

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7
Q

List 2 miscellaneous causes of amenorrhoea.

A

1 - PCOS

2 - Thyrotoxicosis

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8
Q

When does leptin secretion increase and why?

A
  • Following weight gain

- Because there is more adipose tissue secreting it

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9
Q

Which cells secrete prolactin and how is its release controlled?

A
  • Lactotrophs
  • It is negatively regulated by tonic release of dopamine
  • TSH also stimulates prolactin release
  • Prolactin inhibits FSH and LH
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10
Q

Why is hyperprolactinaemia difficult to 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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11
Q

What are the symptoms of hyperprolactinaemia in premenopausal women?

A

1 - Oligo/amenorrhoea

2 - Vaginal dryness

3 - Flushes

4 - Sweats

5 - Galactorrhoea

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12
Q

What are the causes of hyperprolactinaemia?

A

1 - Prolactinomas

2 - Compression of the infundibulum and loss of dopamine

3 - Dopamine antagonists

4 - Secondary hypothyroidism

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13
Q

What is premature ovarian insufficiency?

A
  • Elevated LH and FSH (menopause) <45 years of age
  • Oestrogen deficiency
  • Amenorrhoea
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14
Q

What are the causes of premature ovarian insufficiency?

A
  • Congenital causes e.g. Turner’s syndrome (45 XO)
  • Autoimmune diseases e.g. thyroid disorders, Addison’s disease, and diabetes
  • Iatrogenic causes e.g. chemo/radiotherapy, surgery
  • Mutations in the FSH receptor, galactosemia, or Fragile X
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15
Q

How might autoimmune diseases cause premature ovarian insufficiency?

A
  • Likely due to inflammatory infiltration of follicles & production of anti-ovarian antibodies, apoptosis & atrophy
  • Sharing auto antigens between the ovary & adrenals may explain the link between POI & Addison’s
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16
Q

How is premature ovarian insufficiency managed?

A
  • Diagnosed based on serial FSH & oestrogen (E2) levels, karyotyping & FMR1 premutation analysis, screening for autoimmune diseases, DEXA scan (for osteopaenia)
  • Treated with oestrogen replacement (+ progesterone if the patient still has a uterus due to the risk of endometrial hyperplasia with oestrogen alone)
17
Q

What are the signs and symptoms of polycystic ovary syndrome?

A
  • Oligoamenorrhoea
  • Hirsutism
  • Obesity
  • Anovulatory infertility
  • Polycystic ovaries (on ultrasound)
  • Acanthosis nigricans
  • Androgenic alopecia
  • Hyperandrogenism (↑ testosterone, androstenedione (DHEA), & ↑ LH/FSH ratio)
  • Won’t be oestrogen deficient (can be shown by withdrawing progesterone which will lead to menstrual bleeding)
18
Q

How is PCOS diagnosed?

A

2 of the following 3 criteria:

  • Oligo/amenorrhoea
  • Clinical or biochemical signs of hyperandrogenaemia
  • Polycystic ovaries
19
Q

What risks can PCOS cause for pregnancy?

A
  • PCOS presents difficulties in getting pregnant - oligo/amenorrhoea and infertility
  • Large increase in the risk of gestational diabetes and pregnancy related hypertension
  • IVF can be offered, but there is an increased risk of ovarian hyperstimulation syndrome & subsequently fertilisation of more than one egg
20
Q

How can the clinical features of PCOS be treated?

A
  • Obesity, oligo/amenorrhoea treated with metformin & lifestyle changes
  • Hirsutism = male hormone-dependent hair growth, treated with Yasmin, Vaniqua cream, cosmetic removal, spironolactone
  • Anovulatory infertility treated with metformin or metformin combined with clomiphene (selective oestrogen receptor modulator) or letrozole (aromatase inhibitor)
  • Anti-androgenic oral contraceptives e.g. Dianette or Yasmin
21
Q

What is androgen insensitivity syndrome?

A
  • A spectrum of disorders due to a mutation in the androgen receptor which can lead to anything between a poorly virilised infertile man to men with complete testicular feminisation (46XY “females”)
22
Q

What are the signs and symptoms of complete androgen insensitivity syndrome and how might patients present?

A
  • Female external genitalia
  • Short blind-ending vagina
  • No uterus
  • Abdominal/ inguinal testes
  • Absent prostate
  • Absent pubic and axillary hair
  • Gynaecomastia

Patients would usually present with symptoms of an inguinal hernia (testes), and/or primary amenorrhoea

23
Q

What hormone levels would a patient with androgen insensitivity syndrome have?

A
  • Elevated levels of LH, testosterone & oestrogen

- Due to testosterone aromatisation & LH-driven gonad secretion

24
Q

What is 5-alpha-reductase deficiency?

A
  • A lack of 5α-reductase results in an inability to convert testosterone to DHT, meaning that there is a lack of virilisation of the external genitalia
  • This causes a female external appearance with a normal male karyotype (46XY)
  • At puberty, patients will present with primary amenorrhoea and virilisation
25
Q

How do testosterone levels vary with age?

A

Testosterone decreases with age

26
Q

What are the causes of male primary hypogonadism?

A

1 - Trauma - surgery & torsion

2 - Chemo & radiotherapy

3 - Cryptorchidism

4 - Infections, inflammation & infiltration - orchitis (mumps), iron, varicocele

5 - Chromosomal abnormalities - Klinefelter’s syndrome

6 - Systemic diseases - liver cirrhosis, renal failure, thyroid dysfunction, myotonic dystrophy

27
Q

What are the causes of male secondary hypogonadism?

A

1 - Pituitary tumours

2 - Hyperprolactinaemia

3 - Hypothalamic disorder - craniopharyngioma, Kallman’s syndrome, GnRH therapy

4 - Systemic diseases

5 - Obesity

6 - Androgen use & abuse

28
Q

What are the symptoms of hypogonadism in males?

A

1 - Delayed puberty

2 - Loss of libido (not erectile dysfunction as this is not related to testosterone)

3 - Gynaecomastia

4 - Loss of body hair and reduced shaving frequency

5 - Decreased muscle mass and female fat distribution

6 - Osteoporosis

7 - Infertility ± reduced testicular volume

29
Q

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

Why?

A
  • Primary hypogonadism (hypergonadotropic hypogonadism where the problem is in the testes)
  • There is no negative feedback
30
Q

What is the karyotype of Klinefelter’s syndrome and what are the symptoms?

A

47XXY

  • Firm, pea-sized testes
  • Feminisation - azoospermia, gynaecomastia, reduced secondary sex characteristics
  • Osteoporosis, tall stature, reduced IQ
  • Increased risk breast cancer
31
Q

What is Kallmann syndrome?

A

Idiopathic hypogonadotropic hypogonadism due to the failure of GnRH neurones to migrate in foetal development

32
Q

What is the treatment for endocrine causes of male infertility?

A

Testosterone replacement

33
Q

Why does androgen abuse cause hypogonadism?

A

Androgen abuse causes hypogonadism due to a negative feedback suppression of natural androgen production

34
Q

What are the symptoms of androgen abuse?

A
  • Psychological changes
  • Prostate cancer
  • Atrophy of testes
  • Azoospermia
  • Polycythaemia

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