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Endocrine > Reproduction > Flashcards

Reproduction Flashcards

1
Q

When does oogenesis begin and begin again after suspension?

A

Begins in utero, begins again at puberty

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2
Q

When does oogenesis complete?

A

Fertilisation

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3
Q

When does oogenesis cease?

A

Menopause

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4
Q

What is the primordial germ cell?

A

Earliest recognisable germ cell

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5
Q

When do the primordial germ cells migrate to the genital ridge by?

A

Week 6 of embryo development

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6
Q

What are oogonia?

A

Small diploid cells which on maturation form primordial follicles

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7
Q

What does the presence of two polar bodies signify?

A

Sperm entry and completion of 2nd meiotic division

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8
Q

What are the two phases of the ovarian cycle?

A

Follicular phase and luteal phase

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9
Q

What happens in the follicular phase?

A

Maturation of egg, ready for ovulation at midcycle- ovulation signals end of follicular phase

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10
Q

What happens in luteal phase?

A

Development of corpus luteum. Induces preparation of reproductive tract for pregnancy

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11
Q

What is the primary follicle?

A

A structure made up of the primary oocyte surrounded by a single layer of granulosa cells

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12
Q

How many ovum is a primary follicle capable of producing?

A

1

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13
Q

How does the secondary follicle occur?

A

Oocyte grows and follicle expands and becomes differentiated under hormonal influence. After puberty about 400 will be ovulated, rest undergo atresia. Follicular phase ends with ovulation

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14
Q

What happens to follicular cells left behind after ovulation?

A

They undergo luteinisation- transformation into the corpus luteum

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15
Q

What does the corpus luteum secrete?

A

Progesterone

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16
Q

If no fertilisation occurs, how long will the corpus luteum survive?

A

No longer than 14 days after ovulation

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17
Q

What signals the start of a new follicular phase?

A

Degeneration of corpus luteum

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18
Q

What happens to the corpus luteum if fertilisation occurs?

A

It persists and produces increasing quantities of progesterone and oestrogen until after pregnancy

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19
Q

What is secreted from the hypothalamus that acts on the anterior pituitary?

A

GnRH

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20
Q

What does the anterior pituitary secrete with regards to ovarian action?

A

FSH and LH

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21
Q

What does FSH to do the ovary?

A

Stimulates follicular development, along with LH stimulates secretion of oestradiol and ovulation

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22
Q

What does LH do to the ovary?

A

Stimulates follicle maturation, ovulation and development of corpus luteum

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23
Q

What hormonal secretions happen in the follicular phase?

A

Hypothalamus secretes GnRH, in response Ant Pituitary secretes FSH and some LH. Rescues about 15 follicules- their granulosa and theca cells develop

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24
Q

What do the theca cells of the ‘rescued’ follicles do?

A

Produce androgen which is converted by the granulosa to oestradiol

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25
Q

What does oestradiol do to the uterus?

A

Thickens endometrium/thins cervical mucus

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26
Q

What does oestrogen do to FSH?

A

Suppresses its production by ant. pituitary (dominant follicle selection)

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27
Q

What does granulosa in the dominant follicle express?

A

LH receptor

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28
Q

What does high levels of oestrogen mid cycle cause?

A

Hypothalamus to release GnRH, causes FSH/LH surge from AP

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29
Q

What happens to the corpus luteum at 12 days if there is no hCG production from an embryo?

A

Corpus luteum degenerates forming the corpus albicans, leading to progesterone and oestrogen levels falling

30
Q

What does the developing embryo produce which maintains the corpus luteum?

A

hCG-Human Chorionic Gonadotrophin

31
Q

What does the placenta take over at around 6 weeks?

A

Progesterone production from corpus luteum, it therefore degenerates forming the corpus albicans

32
Q

Where does glandular oestrogen synthesis occur?

A

In the granulosa and theca cells of the ovaries, aswell as the CL

33
Q

What is the pathway of pregnenolone to oestradiol?

A

Pregnenolone diffuses out of granulosa to adjacent theca cells. These cells express 17,20-lyase and 3B-HSD, which mediate pregnenolone to androstenedione conversion via DHEA. Most androstenedione returns to granulosa and is converted to oestrone by aromatase, then is converted to oestradiol by 17B-HSD

34
Q

What is the expression of aromatase and 17B-HSD controlled by?

A

FSH stimulation

35
Q

What does aromatase do outwith gonadal sites?

A

Facilitates peripheral aromatisation of androgens to estrone

36
Q

What is progesterone synthesised by?

A

From pregnenolone by the action of 3B-HSD in the corpus luteum, by the placenta during pregnancy and by the adrenals, as a step in androgen and mineralocorticoid synthesis

37
Q

What is oligomenorrhea?

A

Reduction in frequency of periods to less than 9/year

38
Q

What is primary amenorrhea?

A

Failure of menarche by the age of 16 years

39
Q

What is secondary amenorrhea?

A

Cessation of periods for >6 months in an individual who has previously menstruated

40
Q

What are the causes of primary amenorrhea?

A

Congenital problems (Turner’s, Kallman’s)

41
Q

What are the causes of secondary amenorrhea?

A

Ovarian: PCOS, POF. Uterine: uterine adehsions. Hypothalamic dysfunction: wt loss, over exercise, stress, infiltrative. Pituitary: high PRL, hypopituitarism

42
Q

What should be asked about in the history of secondary amenorrhea?

A

Oestrogen deficiency symptoms: flushing, libido, dyspareunia. Hypothalamic: exercise, wt loss, stress. Features of PCOS/androgen excess: hirsutism/acne. Anosmia: Kallmans. Hypopituitarism/pituitary tumour symptoms: galactorrhea. Drugs associated with hyperprolactinaemia

43
Q

What should be looked for in an examination of a patient with 2’ amenorrhea?

A

Body habitus: Turners. Visual fields/anosmia. Breast development. Hirsutism/acne/androgen excess

44
Q

How should amenorrhea be investigated?

A

LH/FSH/Oestradiol. TFT, PRL. Additional: ovarian US +-endometrial thickness. Testosterone if hirsutism. PFTs +MRI pituitary. Karyotype

45
Q

How is female hypogonadism identified?

A

Low levels of oestrogen

46
Q

What is seen in primary hypogonadism?

A

Problem with ovaries. High LH/FSH-hypergonadotrophic hypogonadism. e.g. POF

47
Q

What is seen in secondary hypogonadism?

A

Problem with hypothalamus/pituitary. Low LH/FSH: hypogonadotrophic hypogonadism. e.g. high PRL, hypopituitarism

48
Q

How does POF present?

A

Amenorrhea, oestrogen deficiency and elevated gonadotrophins occuring

49
Q

How is POF diagnosed?

A

FSH >30 on 2 separate occasions > 1 month apart

50
Q

What are the causes of POF?

A 
Chromosomal abnormalities (e.g. Turner’s syndrome, Fragile X)
Gene mutations (e.g. FSH receptor/LH receptor)
Autoimmune disease (e.g. association with Addison’s, thyroid, APS1/2)
Iatrogenic (radiotherapy/chemotherapy)
51
Q

What are the causes of 2’ hypogonadism?

A

Hypothalamic problem: Functional hypothalamic disorders, Kallman’s syndrome, Idiopathic hypogonadotrophic hypogonadism (IHH). Pituitary problems. Miscellaneous: Prader-Willi, Haemachromatosis

52
Q

What can cause functional hypothalamic amenorrhea?

A 
Weight change
Stress
Exercise
Anabolic steroids
Systemic illness
Iatrogenic (surgery/radiotherapy)
Recreational drugs
Head Trauma
Infiltrative disorders e.g sarcoidosis
53
Q

How is idiopathic hypogonadotrophic hypogonadism identified?

A

By absent or delayed sexual development associated with inappropriate low levels of gonadotrophin and sex hormone levels in absence of anatomical / functional defects of hypothalamic-pituitary gonadal axis

54
Q

What is Kallman’s syndrome?

A

A genetic disorder characterised by a loss of GnRH secretion and anosmia or hyposmia

55
Q

What are the ovarian causes of amenorrhea?

A

PCOS, ovarian failure, congenital problem with ovarian development

56
Q

What are the causes of hirsutism?

A

PCOS, familial, idiopathic, non-classical congenital adrenal hyperplasia, adrenal or ovarian tumour

57
Q

What is congenital adrenal hyperplasia?

A

CAH is an inherited group of disorders characterised by a deficiency in one of the enzymes necessary for cortisol synthesis-90% dye to 21a-hydroxylase deficiency. Autosomal recessive. Varied clinical presentation

58
Q

What is the genetic abnormality in Turner’s?

A

Females only have 1 x chromosome

59
Q

What are the key clinical features of Turner’s?

A

Short stature, webbed neck, shield chest with wide spaced nipples, cubitus valgus. Failure to progress though puberty

60
Q

What are the CVS complications of Turner’s?

A

Coarctation of aorta, bicuspid aortic valve, hypoplastic left heart

61
Q

What are the GI complications of Turner’s?

A

Bleed (vascular malformation), increased IBD

62
Q

What are some non CVS/GI complications of Turner’s?

A

Lymphoedema, AI hypothyroidism, osteoporosis, scoliosis, otitis media, renal abnormalities

63
Q

How does male 1’ hypogonadism present?

A

Low testosterone with high LH/FSH, Acquired and congenital causes

64
Q

How does male 2’ hypogonadism present?

A

Low testosterone with inappropriate low LH/FSH. Pit/hypothalamic disease

65
Q

What is the karyotype in Klinefelter’s?

A

47 XXY

66
Q

What are the clinical featres of Klinefelter’s?

A 
Reduced testicular volume
Gynaecomastia
Eunuchoidism
(intellectual dysfunction in 40%)
(azoospermia)
67
Q

What are the congenital/idiopathic causes of 2’ hypogonadism?

A

Idiopathic hypogonadotrophic hypogonadism (IHH) including Kallman’s syndrome (i.e. with anosmia)
Congenital adrenal hyperplasia

68
Q

What are the functional causes of 2’ hypogonadism?

A

Exercise, weight change, stress, systemic illness
Infiltrative disorders – sarcoid, haemachromatosis,
Cranial irradiation / trauma
Drugs (e.g. anabolic steroids, opiates)
Hyperprolactinaemia
Hypothalamic or Pituitary tumours / surgery
Prader-Willi syndrome

69
Q

What are the benefits of testosterone replacement?

A

Improved sexual function, bone health, body composition/muscle strength, QOL and cognition, insulin sensitivity and diabetes. Will not aid fertility (may act as contraceptive)

70
Q

What are the causes of gynaecomastia?

A

Physiological
Drugs: Oestrogens, testosterone, spironolactone, digoxin +many more
Hypogonadism
Tumours; Oestrogen/androgen testicular or adrenal origin, hCG secreting (e.g. germinoma)
Endocrine disorders (e.g. thyrotoxicosis, Cushings)
Systemic illness
Hereditary disorders

71
Q

What investigations are carried out in gynaecomastia?

A

Testosterone, LH/FSH. Oestradiol, PRL, AFP, HCG, LFTs, SHBG. Breast imaging, testicular/adrenal imaging

72
Q

What is the treatment of gynaecomastia?

A

Address underlying cause. Reassurance. Surgery, medication (e.g. anti-oestrogens)

Endocrine (14 decks)

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