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4 RED > 5 Endocrine Disorders Affecting Reproduction > Flashcards

5 Endocrine Disorders Affecting Reproduction Flashcards

1
Q

How are Androgens converted to oestrogen in females?

A

by aromatids in the granulosa cells

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2
Q

What causes pulsatile secretion of LH?

A

pulsatile secretion of GnRH

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3
Q

What happens if you give a female constant continuous GnRH?

When might you do this?

A

completely downregulates LH and FSH

controlling cycles in IVF

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4
Q

What are the 3 main things that can go wrong in the hypothalamo-pituitary-gonadal axis in the female?

A

central pathology (lack of LH/FSH secretion, other disease)

Gonadal damage (failure of germ cell production, lack off sex steroid production)

polycuystic ovary syndrome

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5
Q

What is Oligomenorrhoea?

A

irregular cycle < 9 period/year or 42-day cycles

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6
Q

What is primary amenorrhoea?

A

failure of menarche after age 16

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7
Q

What is secondary amenorrhoea?

A

absent periods for 6 months after menarche

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8
Q

What are the 5 key types of presentations we look for with endocrine disorders affecting reproduction in females?

A 
menstrual issues
oestrogen deficiency
hirsutism (also acne, androgenic alopecia)
Weight gain/loss
Galactorrhoea
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9
Q

What are the key causes of amenorrhoea?

A

RULE OUT PREGNANCY
central:
-hypothalamic (anorexia, exercise, stress)
-pituitary (hyperprolactinaemia, pituitary adenoma)
-hypogonadotropic hypogonadism

ovarian causes:

  • Turner’s syndrome
  • premature ovarian failure
  • polycystic ovary syndrome
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10
Q

What is prolactin synthesised by?

How is this controlled?

A

lactotrophs (AP)

+ TRH
- Dopamine

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11
Q

What happens to lactation when dopamine production is stopped?

A

it increases!

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12
Q

What is the effect of prolactin on LH and FSH?

A

inhibitory

therefore testosterone and oestrogen inhibited too

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13
Q

When do prolactin levels peak?

A

in sleep

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14
Q

What are the clinical features of physiological hyperprolactinaemia in pre-menopausal women?

A

hypogonadism (oligo/amenorrhoea, estrogen deficiency symptoms)
Galactorrhoea

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15
Q

Why might post-menopausal women and men have physiologcial hyperprolactinaemia?

A

hyogonadism

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16
Q

What might cause pathological hyperprolactinaemia?

A

pituitary tumours
loss of inhibitory effect
Drugs (DA antagonists)
hypothyroidism

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17
Q

How might loss of inhibitory effect cause pathological hyperprolicatinaemia?

A

pituitary stalk compression / disconnection

stop getting dopamine inhibition

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18
Q

Which drugs might act as DA antagonists?

A

Phenothiazines
metoclopramide
TCAs
verapamil

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19
Q

What are the 3 key features of Premature Ovarian insufficiency?

A

Amenorrhoea
Oestrogen deficiency
Elevated LH, FSH

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20
Q

What are the 4 key causes of Premature Ovarian insufficiency?

A

Congenital (Turner’s syndrome)
Autoimmune (Addison’s, DM)
Iatrogenic (chemo/rediotherapy, surgery)
genetic (FSHR mutations, FMR1 gene premutation)

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21
Q

What proporiton of premature ovarian insufficiency cases are autoimmune?

A

2-10%

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22
Q

What is the mechanism of autoimmune POI?

A

inflammatory infiltration of follicles and production of anti-ovarian Ab
apoptosis and atrophy

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23
Q

What might explain the link between Addison’s and POI?

A

sharing of auto-antigens between ovary and adrenals

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24
Q

How might mutations in the FMR1 gene cause POI?

A

increases risk of developing FXPOI

an X-linked dominant pattern

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25
Q

How is POI managed?

A

screening for AI diseases
DEXA scan
Manage with oestrogen

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26
Q

How is PCOS diagnosed?

A

Rotterdam diagnostic criteria - 2 of the following…
oligo/amenorrhoea
any sign of hyperandrogenaemia
polycystic ovaries

27
Q

What are the key clinical features of PCOS?

A

anovulation
insulin resistance
obesity
androgen XS

28
Q

How is Hisutism classified?

A

Ferriman Gallwey Score

29
Q

How is obesity / oligo/amenorrhoea in PCOS treated?

A

metformin

lifestyle modifications

30
Q

How is anovulatory infertility in PCOS treated?

A

metformin

31
Q

How is hirsutism in PCOS treated?

A

Yasmin
Vaniqua cream
cosmetic removal
sprinolactone

32
Q

What are the types of 21-hydroxylase deficiency?

A

classic (simple vrilising / salt wasting)

non-classical (cryptic)

33
Q

When might classic 21-hydroxylase deficiency present?

A

neonateal / infancy

34
Q

When might nonclassical 21-hydroxylase deficiency present?

A

childhood / adult

35
Q

What are the features of complete androgen insensitivity?

A 
female external genitalia
short, blind - ending vagina
no uterus / testes
absent prostate
gynaecomastia
36
Q

What happens to LH, Testosterone, and E2 lvels in adrogen insensitivity syndrome?

A

elevated

37
Q

What is the karyotype of people with complete androgen insensitivity?

A

46XY but ‘female’

38
Q

How might people with 5alpha-reductase deficiency present?

A

females but 46XY
abdominal testes
primary amenorrhoea
virilisation at puberty

39
Q

What is the effect of 5alpha-reductase deficiency?

A

unable to convert T to DHT (more andorgenic form)

40
Q

Which cells in the male produce testosterone?

A

Leydig cells

41
Q

Which cells does FSH act on in males?

A

Sertoli cells

42
Q

What might an increased FSH level cause in males?

A

inhibition of apoptosis of spermatogonia

43
Q

How do testosterone levels change with age?

A

fall

44
Q

How might hypogonadism present in males?

A 
delayed puberty
gynaecomastia
 - body hair/muscle mass
osteoporosis
infertility
45
Q

What are the key groups of causes of primary male hypogonadism?

A 
trauma
chemo/radiotherapy
undescended testes
infection/inflammation/infiltration
chromosomal anomalies
systemic diseases
46
Q

What is another name for undescended testes?

A

cryptorchidism

47
Q

Name a chromosomal anomaly causing primary hypogonadism in males

A

Klinefelter syndrome

48
Q

Name 4 systemic diseases causing primary hypogonadism in males

A

liver cirrhosis
renal failure
thyroid dysfunction
myotonic dystrophy

49
Q

Name 6 key causes of secondary male hypogonadism

A 
pituitary tumours
hyperprolactinaemia
hypothalamic disorders
systemic disease
obesity
androgen us/abuse
50
Q

Name 3 hypothalamic disorders causing secondary male hypogonadism

A

Craniopharyngioma
Kallman’s syndrome
GnRH therapy

51
Q

How would you investigate male hypogonadism?

A

clinical examination
LH, FSH, testosterone
further investigations (liver function, prolactin…)

52
Q

What might indicate primary male hypogonadism?

A

High LH and FSH

53
Q

What might indicate secondary male hypogonadism?

A

Low LH and FSH

54
Q

What is the karyotype of Klinefelter’s syndrome?

A

47 XXY

55
Q

What type of cancer are those with Klinefelter syndrome at higher risk of?

A

breast cancer (by 20%)

56
Q

What are the features of myotonic dystrophy?

A 
AD
myotonia
mental retardation
fontral bladness
cataracts
primary gonadal failure
57
Q

What might Kallman’s syndrome otherwise be called?

A

Idiopathic Hypogonadaotropic Hypogonadism

58
Q

What is the basis of Kallman’s syndrome?

A

failure of migration of GnRH neurones

59
Q

What is the genetic cause of Kallman’s syndrome?

A

X-linked AR/AD

mutations in Kal-1, FGF-Receptor 1

60
Q

Name a testosterone replacement tablet

A

testosterone undecanoate

61
Q

Name a transdermal testosterone patch

A

Testogel

62
Q

What might an increased FSH suggest about male infertility?

A

germ cell failure

63
Q

What might a normal FSH and testis size suggest about male infertility?

A

obstructive uropathy

64
Q

What might a low FSH and LH suggest about male infertility?

A

endocrine causes (pituitary / hypothalamic disease)

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