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Endocrine physiology > Reproductive tutorial > Flashcards

Reproductive tutorial Flashcards

1
Q

what are the 2 types of endocrine cells in the ovarian follicles and what is their function?

A
  1. thecal cells - they produce androgens in response to LH
  2. granulosa cells - produce estradiol in response to FSH
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2
Q

what are the 2 endocrine cells of the corpus luteum?

A
  1. thecal lutein cells - produce androstenedione
  2. granulosa lutein cells - produce estradiol and progesterone
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3
Q

what enzyme do the granulosa cells express?

A

they have high levels of the enzyme aromatase which converts androgens to estrogens

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4
Q

what enzyme that is present in granulosa cells is not present in thecal cells?

A

aromatase (ie the thecal cells canot convert androgens to estrogens)

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5
Q

what do high LH levels induce in the granulosa cells?

A
  • high LH levels induce receptor upregulation and therefore increase LH responsivness in granulosa cells
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6
Q

What role does the 3beta-HSD-II enzyme have in the liuteal phase of the menstrual cycle?

A

this enzyme leads to an increased progesterone production

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7
Q

Describe the HPO axis in the early follicular phase

A
  • hypothalamus secretes GnRH, which stimulates the release of FSH and LH from anterior pituitary
  • LH acts on the theca cells to produce andrgens and FSH acts on the granulosa cells to produce estradiol
  • the feedback inhibition of LH by estrogen is very weak, thus LH secretion remains constant or slowly increases during the follicular phase
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8
Q

Describe the HPO axis in late follicular phase/ ovualtion of ovarian cycle

A
  • as progesterone is absent in this phase, the high levels of estrogen stimulate pituitary LH (but not FSH) - via positive feedback regulation - leading to the LH surge before ovulation
  • estrogen also acts at the level of the hypothalamus to stimulate GnRH secretion - which accelerates pituitary LH secretion and gives a slight rise in FSH
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9
Q

Describe the HPO axis in the **luteal phase **of the ovarian cycle

A
  • only when both estrogen and progesterone levels are high, is feedback inhibition of LH effective
  • therefore LH levels are low in luteal phase
  • the corpus luteum is dependent on LH for its survival, the falling LH leads to the diminishing of the corpus luteum - unless fertilisation and implantation occur
  • therefore overall there is low estrogen, low LH, lower FSH and high progesterone
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10
Q

what are the 2 main types of endocrine cells in the testis & what is their function?

A
  • sertoli cells- produce AMH, estrogen and inhibin in response to FSH
  • leydig cells - produce testosterone in respone to LH
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11
Q

describe the** HPT axis in men**

A
  • GnRH from the hypothalamus stimulates the secretion of FSH and LH from the pituitary gland
  • FSH acts on the sertoli cells which produce inhibin etc
    * inhibin has a negative feedback effect on the FSH secretion
  • LH acts on the leydig cells which produce tesosterone
  • the testosterone has a negative feedback effect on LH secretion
  • testosterone acts on male reproductive tract and other tissues eg muscle, bone etc
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12
Q

what is primary hypogonadism?

A
  • impaired gonadotrophin responsiveness eg due to FSH and LH receptor mutations
  • defective androgen synthesis eg 5a reductase, 3 beta - hydroxysteroid dehydrogenase etc
  • reduced testosterone and increased GnRH
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13
Q

what type of disorder is 5a reductase defiency?

A
  • autosomal recessive disorder
  • affects only males as DHT has no function in females
  • NOTE 5a reductase converts testosterone into dihydrotestosterone
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14
Q

what are the charactertistics of 5a reductase deficiency?

A
  • male gonads - high freq of crytorchidism - no fall of testes
  • micropenis
  • ambigious or female genitalia eg macroclitoris (hypertrophy of clitoris)
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15
Q

what is secondary hypogonadism?

A
  • GnRH insufficiency
  • may be due to hypopituitarisum - tumours, surgical trauma , andropause etc
  • may be due to hyperprolactinemia
  • may be due to congenital adrenal hyperplasa
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16
Q

what happens to testosterone and gonadotrophin levels in secondary hypogonadism?

A
  • reduction in testosterone
  • reduction in gonadotrophin levels
17
Q

what is Kallman’s syndrome?

A
  • inherited GnRH deficiency
  • mutations in the Kal 1 gene
18
Q

what do mutations of the KAL 1 gene cause?

A
  • they interfere with** migration of GnRH secreting neurons to hypothalamus during development **
  • the mutation can lead to inactivation of these genes and lead to a** greatly reduced population of GnRH secreting neurons**
  • also interfere with migration of olfactory neurons to the olfactory bulb
19
Q

what are the main characteristics of kallman’s syndrome?

A
  • hypogonadotrophic hypogonadism - low GnRH and testosterone etc
  • infertility
  • absent / partial puvertal maturation
  • 50% of cases have anosmia or hyposmia - reduced sense of smell NB distinguishing feature
20
Q

what is hyperprolactinemia?

A
  • very high levels of prolactin in the blood - can affect males and females
21
Q

what are the main causes of hyperprolactinemia?

A
  • 40% of cases due to a benign pituitary adenoma that is secreting prolactin
  • other pituitary tumours that lower dopamine levels (and therefore increase prolactin levels) can also cause hyperprolactinemia
22
Q

What effect does hyperprolactinemia have on gonadal function?

A
  • it supresses LH and FSH secretion by suppressing GnRH secretion
23
Q

what are the symptoms associated with hyperprolactinemia in males vsfemales

A
  • in males, there is infertility and loss of labido
  • in females there is galactorrhea and amernorrhea
24
Q

what type of disorder is androgen insensitivity syndrome?

A
  • x linked recessive disorder
  • mutation in the androgen receptor gene - therefore inactivating it
25
Q

what are the 3 types if androgen insensitivity syndrome?

A

complete - female genitalia, development of breasts, testes have not descended
partial - ambigious genitalia
mild - male genitalia, delayed puberty, sub/infertile

26
Q

what are the characteristics of androgen insensitivity syndrome?

A
  • failure of male genital development and impaired secondary sexual develoment
  • wolffian structures may be absent, underdeveloped or normal
  • female internal reproductive glands never present
  • male gonads / testes have a high freq of cryptorchidism
27
Q

how can secondary hypercortisolism (cushings) cause problems reproductivly?

A
  • secondary hypercortisolism due to pituitary or extrapituitary excess of ACTH
  • ACTH stimulates cortisol and DHEA production
  • therefore there is increased negative feedback from androgens to hypothalamus and therefore less FSH and LH being secreted
  • can cause amenorrhea in females and sub/infertility in males
28
Q

what is congenital hyperplasia?

A
  • a disorder of sexual development due to excess adrenal androgen secretion
29
Q

what symptoms can congenital adrenal hyperplasia cause in males?

A
  • accelerated puberty in men
  • high incidence of infertility
30
Q

what symptoms can congenital adrenal hyperplasia cause in women?

A
  • ambigious genitalia
  • excessive facial nhair
  • menstrual irregulatory
  • anoovulation- ie no ovulation
31
Q

Describe sheehan’s syndrome

A
  • due to a lot of blood loss during childbirth - which causes infarction and necrosis of pituitary gland - which can cause hypopituitarism and hypothyroidism, hypocortisolism and hypogonadotrophism
  • may present immediately or may be assymptomatic for years
32
Q

how is sheehans syndrome treated?

A
  • they are given hormone replacement therapy - T4 , cortisone, gonadotrophins (if normal ovarian cycling is desired)
33
Q

what is PCOS?

A
  • most common form of chronic anoovulation in women of reproductive age
34
Q

what are the clinical features of PCOS?

A
  • hyperandrogenism - high levels of androgens
  • amenorrhea / anovulation
  • hirsutism - facial hair
  • insulin resistance / hyperinsulinemia NB - type II diabetes
  • obesity
35
Q

A 25 year old woman, who was referred to the OBGYN department by her GP after complaining about not having a period for the last 6 months. she is also seeing a dermatologist for the treatment of acne and she has had 2 treatments of hair removal on her face. There is a family history of type II diabetes and obesity. Her blood shows normal FSH, high LH, high insulin, hyperglycemia, high testosterone levels , normal DHEA levels… what is the most probable diagnosis?

A
  • PCOS
  • high levels of androgens - normal FSH and high LH - points strongly to PCOS
  • amenorrhea - hyperandrogenism
  • high levels of glucose and insulin in the blood suggests insulin resistance - key for PCOS
  • patients age also key
  • family history of diabetes and obesity
36
Q

do the laboratory findings for this womens blood allow us to exclude other syndromes of hyperandrogenism?

remember - high testosterone, low FSH, high LH, normal DHEA etc

A
  • yes to some degree
  • the key observation here is that normal DHEA is seen - therefore you can exclude congenital adrenal hyperplasia
  • can also exclude 5a reductase defiency - only affects males
  • can exclude androgen insensitivity - as she had normal ovarian cycles prior to this

Endocrine physiology (19 decks)

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