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Endocrine & Diabetes > Endocrinology of Female Reproduction > Flashcards

Endocrinology of Female Reproduction Flashcards

1
Q

What is reproduction?

A

-Genetic material is passed on between generations
-New individuals of a species can be produced
=a result of mixing genes from two individuals

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2
Q

Why is infertility becoming more common?

A

-Sexually transmitted infections (chlamydia, gonorrhoea= tubular damage to fallopian tubes so eggs cannot be transported)
-Obesity (overweight/ underweight= hormones off-balanced)
-Tobacco (decreased blood flow in penis)
-Increase in age at childbearing
=Infertility now affects 1 in 7 couples (inability to conceive after 1 year of unprotected sex)
=Sub fertility= inability to conceive after 6 months of unprotected sex

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3
Q

Describe male fertility

A
  • Constant fertility from puberty
  • 300 million per day from puberty
  • Gradual decline with age
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4
Q

Describe female fertility

A
  • Cyclical fertility, 3-5 days a month from puberty
  • 7 million follicles in utero declines to 0 at menopause
  • 400 follicles are ovulated
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5
Q

How is the ovarian reserve formed?

A
  1. Primordial germ cells (precursor to eggs) colonise the gonad
  2. Numbers expand by mitosis (to 7 million)
  3. Germ cells enter, and then arrest, in meiosis (form oogonial cysts, interconnected by cytoplasmic bridges)
  4. Primordial follicles form (granulosa cells wrap oocytes, arrested in diplotene of meiotic prophase 1, only returns at ovulation)
    =relies on connections between chromosomes not decaying over time
  5. Folliculogenesis
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6
Q

What is a follicle and how does it progress?

A
  • Reproductive unit of ovary
  • Egg/ oocyte surrounded by granulosa cells
    1. Primordial= flattened/ squamous single layer granulosa
    2. Primary= squamous to cuboidal, layers, glycoprotein layer zona pellucida (secreted by oocyte)
    3. Secondary= increased no. granulosa cells, theca layer (stroma cells differentiated)
    4. Early-antral follicle= theca differentiated into theca interna (glands, blood vessels) and theca externa (fibrous protective capsule), fluid filled gaps (antral/ follicular, secreted by granulosa cells)
    5. Graafian= all fluid gaps coalesced into follicular antrum, pushes oocyte out into one layer granulosa cell (corona radiata)
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7
Q

Describe the hypothalamic/ pituitary/ gonadal axis

A

-Gonadotrophin-releasing hormone from hypothalamus
-FSH, LH released from anterior pituitary (gonadotrophs)
-Stimulates granulosa cell proliferation and follicle ovulation in the ovaries
=Oestrogens
=Progesterone
=Inhibin
-Negative feedback loop

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8
Q

How are neurosecretory neurones different?

A
  • Synthesise hormones and stores in vesicles
  • Released at terminal when there is an impulse
  • Posterior pituitary (ADH, oxytocin)
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9
Q

What is oxytocin?

A

-Oxytocin has major effects on smooth muscle contraction
=milk ejection
=contraction of uterus during childbirth (myometrium)
-Secretion is stimulated in response to stimulation of nipples or uterine distension.
-Oxytocin is used to induce labour

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10
Q

Describe gonadotropin-releasing hormone

A

-Synthesised by hypothalamic neurons (small), terminate onto portal system
-Pulsatile release
=prevents receptor desensitisation & downregulation
-Responds to ovarian hormonal feedback (oestrogen and progesterone)

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11
Q

What is Kisspeptin?

A

-Small neuropeptide hormones
=feedback onto GnRH neurone themselves, regulate secretion
=Can receive signals from gonads and integrate signals from all over the body (cortisol from adrenal gland, leptin from body fat, environmental cues= shift workers and air hostesses suffer from infertility)

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12
Q

How do these hormones travel through the blood?

A

-Water soluble= travel in blood freely
=Target site= diffusion through binding to receptor, cascade through cAMP
=GnRH, FSH, LH

-Lipid soluble
=Travel bound to transport protein
=Freely diffuse into cell passing through cell membrane into nucleus, transcription factor
=Oestrogen and progesterone

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13
Q

What causes follicle activation?

A

-Gonadotropin regulated growth phase (important at pre-antral follicle and above)
=FSH- antral granulosa cell differentiation, proliferation and function (make oestrogen)
=LH- theca cell androgen production, ovulation (antral expansion as well)
*Gradual decline of primordial follicles not affected by endocrine system

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14
Q

What is Anti-Mullerian hormone?

A

-Made by granulosa cells
-Absent in primordial follicles but present at later stages
-Inhibitory effect on follicle development (negative feedback on primordial follicles to keep resources for themselves)
-Unaffected by gonadotropins/steroid hormones
=reliable reflection of growing follicles/ how many left

*In males, stops female duct formation in male reproductive tract

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15
Q

Why is only one follicle selected?

A

-LH receptor
=Oestrogen and FSH induce expression of LH receptor on theca cell
=Most number of LH receptor and in prime position to receive LH hormone= dominant ovulated follicle

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16
Q

What is the relationship between oestrogen and FSH?

A

-As oestrogen is produced by follicles, has negative feedback effect on FSH production in pituitary
-At a certain threshold, effect reverses so positive effect on FSH secretion from pituitary
-Stimulates LH release from pituitary
=Both stimulate LH receptors on theca cells

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17
Q

Describe follicular rupture

A

-Wears away at surface of ovary
-Proteases digest areas
-Releases follicular fluid, egg and cumulus complex
=swept into ovary duct and down into the uterus

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18
Q

Describe the Corpus luteum

A

-Ruptured follicle develops into corpus luteum
=granulosa and theca cells
-Lutein cells – mitochondria, smooth ER, Golgi, lipid droplets, and pigment lutein (yellow colour)
-Luteinisation = progesterone secretion

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19
Q

What happens to the corpus luteum if there is no pregnancy?

A

-Corpus luteum undergoes luteolysis/ regresses due to lack of hCG (become corpus albicans= scar tissue)
=FSH rises
=progesterone and oestrogen drop
=Endometrium shed

20
Q

Describe how hormonal contraception works

A

-Suppresses ovulation via negative feedback of progesterone
=secondary effects on female genital tract (on endometrium)
-Combined pill – oestrogen provides additional feedback & promotes progesterone receptor expression
-During ‘off period’ own HPG axis is awakened

21
Q

How is breast development linked to the placenta?

A
  • Once placenta is birthed, steroidal block on breast development removed
  • Prolactin acts on breast tissue for milk production, blocked by the hormones made by placenta
22
Q

Describe the anatomy of the breast

A

-15 to 20 ducts in adult breast tissue
=Alveola make breast milk
=Sacs surrounded by myoepithelial cells (contractile, contract in response to oxytocin)
-Number of alveola increase in puberty in response to oestrogen

23
Q

How is breast milk made?

A

-Need suckling!
=nerve impulses sent to the brain to maintain prolactin levels
=depends on strength and how long a baby suckles for
-Prolactin release from anterior pituitary, maintained for a few weeks but needs suckling to be maintained
-Alveoli swell and secrete milk

24
Q

How is milk released?

A

-Need suckling!
=nerve impulses sent to the brain
-Boosts oxytocin synthesis & secretion from posterior pituitary
-Myoepithelial cell contraction around alveoli = milk expulsion
-Milk ejection reflex can be conditioned

25
Q

Why is fertility reduced during lactation?

A
  • Lactation can continue for months
  • Menstruation & ovulation re-established by 3-6 months
  • ~50% of unprotected nursing mothers fall pregnant during 9 months of lactation
  • Negative feedback of prolactin on FSH/LH
26
Q

Differentials of high LH

A
  • Premature Ovarian Failure
  • Polycystic Ovarian Syndrome
  • Ashermans syndrome
  • Functional Gonadotroph Tumour
27
Q

Describe Premature Ovarian Failure/Insufficiency

A

-High LH, high FSH, low E2
-Premature menopause or hypergonadotropic hypogonadism
=flushes, difficulty concentrating, vaginal dryness, night sweats
=Cause are genetic (Turners), Familial, Iatrogenic, autoimmune, infection
-USS small ovaries, no follicles

28
Q

Describe PCOS

A

-High LH, normal FSH, normal E2, High testosterone, low SHBG
=weight problems, hirsutism, skin problems, family history, FH diabetes, oligomenorrhoea
-USS polycystic

29
Q

Describe Ashermans syndrome

A

-Normal ovulation but no menstruation due to lack of endometrium
=High LH and high E2
=damage can occur after termination of pregnancy or D and C for miscarriage so scarring/ uterine surgery
=cyclical changes and discomfort
-Trans-vaginal USS ovulation= dominant follicle but thin abnormal endometrium

30
Q

Describe functional gonadotroph tumour

A

-Very rare
=progressive headache, visual field defect
-LH/FSH not subject to feedback will have large numbers of large follicles (USS multiple large follicular cysts on each ovary)

31
Q

What are the differentials for high testosterone?

A
  • PCOS
  • CAH (congenital adrenal hyperplasia)
  • Androgen secreting tumour (ovary or adrenal sites)
  • Exogenous testosterone/ steroids
32
Q

Describe CAH

A

-Relative block to enzyme that makes cortisol (21-hydroxylase)
=precursors for cortisol build up and are converted into potent androgens
=ACTH high so hyperplasia of adrenal gland
-Incomplete block is late onset, complete is neonate in crisis
=sudden and severe onset
=can be virilised (breasts atrophy, voice deepen, hair loss and clitoromegaly), late menarche, oligomenorrhoea
=image with MRI, CT or USS/ 17-a-OH progesterone (mainly adrenal origin)/ Synacthen test

33
Q

How do we investigate doping?

A

-Low LH due to negative feedback
=In doping look for pattern of other androgens and metabolites and they will be different from PCOS where there is a spectrum with several forms of androgen elevated

34
Q

What are the differentials of low oestradiol?

A
  • Hypogonadotropic hypogonadism
  • Hyperprolactinaemia
  • Premature Ovarian Failure
  • Exogenous hormones
35
Q

Describe hypogonadotropic hypogonadism

A

-Low LH, low FSH, low E2, normal PRL
=often symptom free (childlike in hormonal status)
=low body fat in anorexia and over exercise, acute stress and chronic stress (severe illness)
=bone scan and hormones

36
Q

Describe hyperprolactinaemia

A

-Low LH, low FSH, Low E2, high prolactin
=galactorrhoea
=bitemporal hemianopia, tunnel vision= microadenoma (MRI)
=drug treatment (antipsychotics and antiemetics are dopamine antagonists)
=hypothyroidism (thyroid function test)

37
Q

Describe exogenous hormones

A

=contraceptive depo provera causes prolonged amenorrhoea with low E2

38
Q

Risk of POF

A

-Osteoporosis

=Acceleration of heart disease to male levels

39
Q

Management of POF

A

-Oestrogen replacement
=combined pill
=donor egg (and primed with oestradiol followed by progesterone)

40
Q

Management of Ashermans syndrome

A
  • Main treatment for pregnancy
  • Hysteroscopy and curettage to break down adhesions and copper coil to hold sides of uterus apart for endometrium to regrow and work normally (remove after 4 months)
41
Q

Risk of PCOS

A

-Hormone imbalance exaggerated by weight and insulin resistance
-Associated with metabolic imbalance such that there are higher concentrations of insulin
=more likely to be T2DM
-Thick endometrium
(unopposed E2)= heavy bleed and risk of hyperplasia

42
Q

Management of PCOS

A

-Weight loss
-Lowering insulin with metabolic approach (metformin)
-Hormonal treatment
=contraceptive pill
=raise FSH for pregnancy (injections/ clomifene, tamoxifen oestrogen antagonists)- only for 5 days at start

43
Q

Management of CAH

A

-Suppress ACTH by low dose glucocorticoids (dexamethasone)

=Replace glucocorticoids and reduce drive to androgens

44
Q

Management of hypogonadotropic hypogonadism

A

-Lifestyle modification
-Oestrogen replacement (COCP, sequential HRT)
=headache, nausea, tender breasts so counselling
-Pulsatile GnRH/ LH and FSH injections for pregnancy

45
Q

Management of hyperprolactinaemia

A 
-Dopamine agonist
=shrink microadenoma
=bromocriptine (daily)
=cabergoline (weekly)
-Surgery if pressing on optic chiasma
46
Q

Examples of anti-oestrogen drugs

A
  • Ovulation induction = clomifene blocks oestrogen receptors at anterior pituitary
  • Treat oestrogen sensitive breast cancer = Tamoxifen
  • Letrozole can be used for either as aromatase inhibitor
47
Q

What are the C numbers for hormones?

A

-Oestrogens C18
-Androgens C19
-Progesterone C21
-Corticosteroids C21
=glucocorticoids (cortisol, prednisolone, dexamethasone)
=mineralocorticoids (aldosterone, fludrocortisone)

Endocrine & Diabetes (45 decks)

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