endocrinology Flashcards

1
Q

3 connective tissues around testes

A

tunica vasculosa => has BVs

tunica albuginea => forms septa to separate lobules

tunica vaginalis => covers testes + epidydimis

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2
Q

seminal fluid composition

A

fructose
citric acid nutrient
bicarbonate (neutralise vaginal acidity)
fibrinogen (thickener)
fibrinolytic enzymes

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3
Q

testes lobules

A

each lobule = 1-4 coiled seminiferous tubules which have closed loops (meiosis of sperm)

drain into the rete testis → epidydimis for storage → vas deferens

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4
Q

seminiferous tubule structure

A

surrounded by tunica propria (BM)

cells become more differentiated closer to lumen

spermatogonia (round nuclei) => primary spermatocytes => secondary => sprematids

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5
Q

primary vs secondary spermocytes

A

primary:
larger nuclei - round + filled with dense chromosomes
in extended prophase of first mitotic division

secondary:
rarely seen
almost immediately undergo second meiotic division to become spermatids

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6
Q

sertoli cells

A

in sn-tubules - just above spermatogonia

large, pale, irregular nuclei w/prominent nucleolous

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7
Q

functions of sertoli cells

A

support development of sperm
assist sperm movement to centre
transfer nutrients from capillaries to sperm
phagocytosis of damaged sperm
hormone synthesis (AMH, ABP, inhibinB, acitivin)

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8
Q

leydig cells

A

between seminiferous tubules

pale cytoplasm

hormone synthesis: cholesterol used to make testosterone/androsterone/dihydroepiandrosterone when stimulate by LH

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9
Q

oocyte development through life

A

2nd trimenster: oogonia → primary oocytes → enter the 1st meiotic division (prophase)
granulosa cells surround oocyte to form primordial follicles

menarche: some primordial follicles recommence growth partly dependent on FSH → secondary oocytes released

secondary oocyte + sperm → calcium influx → stimulates 2nd meiotic division → ova (ovum) – the functional gamete

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10
Q

follicle layers (in->out)

A

ovum
follicular fluid
granulosa cells
theca cells

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11
Q

theca cell function

A

support folliculogenesis
hormone synthesis (LH stimulates androgen synthesis)

final cell type to die in atresia

if ovulate: hormone-dependent differentiation into luteinized thecal cells of corpus luteum

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12
Q

granulosa cells

A

hormone synthesis

turn into granulosa lutein cells that produce relacin + progesterone after ovulation

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13
Q

Hyperprolactinaemia

A

prolactin binds prolactin receptors on kisspeptin neurones

inhibits kisspeptin release

decreases all downstream hormones as master regulator (kisspeptin) is switched off

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14
Q

side effects of hyperprolactinaemia

A

Oligomenorrhoea (in females - infrequent periods)
low libido
infertility
osteoporosis (loss of bone mineral density)

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15
Q

semen formation + voyage

A

in efferent ducts of testes:
tubular fluid reabsorbed
increased conc of semen
induced by oestrogen

epidydimis:
nutrients + glycoproteins secreted into epidydimal fluid
induced by androgens

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16
Q

how is oestrogen formed in males

A

testosterone => oestrogen by aromatase

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17
Q

Aromatase deficiency

A

raises testosterone levels

lack of oestrogen

reduced bone mineral density + osteoporosis, taller (oestrogen needed for closure of growth plates in long bones)

18
Q

Capacitation

A

process by which sperm achieve fertilising capability
only occurs in the female reproductive tract

loss of GP coat => new surface characteristics => whiplash movements develop

19
Q

why capacitation only in female tract

A

ionic & proteolytic environment
Oestrogen and Ca2+ dependent

20
Q

Acrosome

A

sperm organelle containing enzymes and can bind to the Zona Pellucida

21
Q

acrosome reaction

A

sperm => ZP3 on ovum

Ca2+ influx into the sperm stimulated by progesterone

release of hyaluronidase (breaks down polysaccharides) & proteolytic enzymes from the acrosome

spermatozoon penetrates the Zona Pellucida

22
Q

what happens in fertilisation

A

cortical reaction triggered => ZP degradation by molecules from cortical granule

stops other sperm binding

diploid zygote forms
apoptosis + expulsion of second polar body

23
Q

Polar body

A

small haploid cell as oocyte cytoplasm does not divide evenly - undergoes apoptosis

24
Q

attachment phase of implantation

A

outer trophoblast cells contact uterine surface epithelium => involves Leukaemia inhibitory factor, Interleukin-11

25
Q

decidualisation phase of implantation

A

endometrial changes due to progesterone
glandular epithelial secretion
glycoprotein accumulation in stromal cell cytoplasm
capillary growth
increased vascular permeability

26
Q

Gonadarche

A

activation of gonads by HPG axis

27
Q

Thelarche

A

breast development

28
Q

menarche

A

development of menstrual cycles

29
Q

spermarche

A

Spermatogenesis

30
Q

Adrenarche

A

adrenal androgen production (starts ~2yrs before gonadarche)

31
Q

Pubarche

A

pubic hair

32
Q

Mini puberty (what is it, what happens in it, lack)

A

activation of the HPG axis during late pregnancy/early neonatal life

GnRH → testicle descent, penile length, Sertoli cell maturation and behaviour

lack = Cryptorchidism (failure of testicles to descend), responding to treatments, gender preferences

33
Q

Amenorrhoea

A

Absence of Periods

primary = not started after 16 years

secondary = start but then stop for at least 3-6 months e.g. pregnancy/PCOS

34
Q

Hypogonadism

A

decreased function of the gonads

decreased oestrogen in a woman/testosterone in a man

primary = issue with gonads, secondary = - decreased function of hypothalamus or pituitary gland

35
Q

what is menopause

A

Primary hypogonadism

reduced function of ovaries → reduced -ve feedback on hypothalamus and pituitary gland → high LH/FSH → decreased oestogen

36
Q

Early Menopause

A

Premature Ovarian Insufficiency (POI)
same symptoms as menopause

due to: utoimmunity, genetics (Fragile X Syndrome/Turner’s Syndrome (one X chromosome)), previous cancer therapy

37
Q

Menopause Hormone Therapy (MHT)

A

oestrogen replacement: oestrogen stimulates endometrium to proliferate

add progesterone: (if endometrium is intact) to prevent risk of Endometrial Hyperplasia/Cancer

38
Q

Andropause

A

Testosterone levels decrease slightly with age

39
Q

Free hormone hypothesis for andropause

A

majority of testosterone in blood strongly bound to SHBG (sex hormone binding globulin) - transports testosterone in blood
binds so strongly that its inactive + unavailable

albumin also binds large proportion => bioavailable

free testosterone = very small proportion - unbound + shows effect

40
Q

testosterone in prostate/scalp

A

5-alpha-reductase converts testosterone to di-hydro-testosterone (DHT)

binds androgen receptor strongly

prostate cancer: 5-alpha-reductase inhibitors would prevent increase in DHT → prevents growth of cancer

41
Q

testosterone in fat tissue

A

aromatase converts androgens into oestrogen (testosterone → oestradiol, or androstenedione → oestrone)

Breast cancer: aromatase inhibitor ensures they don’t convert their testosterone into oestrogens → prevents growth of cancer