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Y2S2- Genetics, Renal, Endocrine > Repro > Flashcards

Repro Flashcards

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Biology 101 flashcards
1
Q

subfertility and infertility definitions

A

inability to conceive after 6months or 1year of unprotected sex

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2
Q

sperm and egg fertility comparison

A

sperm- constant fertility from puberty, gradual decline with age
egg- cyclical fertility, 7M follicles in utero declines to 0 at menopause

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3
Q

formation of ovarian reserve of follicles

A
  1. primordial germ cells colonise the gonad and numbers expand by meiosis
  2. germ cells enter and then arrest in, meiosis which begins again at ovulation
  3. primordial follicles form
  4. folliculogenesis
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4
Q

stages of follicle development

A
  1. primordial follicle- oocyte with squamous granulosa cells
  2. primary follicle- oocyte with stratified cuboidal granulosa cells
  3. secondary follicle- stroma and theca cells
  4. early antral follicle- theca external and interna with blood vessels
  5. graafian follicle ready to be ovulated
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5
Q

feedback loop of FSH LH

A
  1. hypothalamus secretes GnRH
  2. stimulates anterior pituitary to secrete FSH and LH
  3. oestrogen, progesterones negatively feedback from follicle to inhibit AP and hypothalamus
    inhibins negatively feedback on FSH only
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6
Q

oxytocin effects

A

smooth muscle contraction:
- milk ejection
- contraction of uterus during childbirth: used to induce labour
- during orgasm
Secretion stimulated in response to stimulation of nipples or uterine distension

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7
Q

why does GnRH have a pulsatile release?

A

prevent receptor desensitisation and downregulation

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8
Q

kisspeptin

A

neuropeptide that feeds back on GnRH neurons and regulate secretion

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9
Q

water soluble hormones

A

GnRH, FSH, LH

travel through blood freely and bind to cell surface receptor

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10
Q

lipid soluble hormones

A

oestrogen, progesterone

travel attached to transport protein and freely diffuse into cell

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11
Q

gonadotrophin regulated growth phase

A

from preantral follicle to preovulatory follicle
FSH- astral granulosa cell differentiation, proliferation & function, can make oestrogen
LH- theca cell androgen production, ovulation

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12
Q

AMH

A

anti-mullerian hormone
made by granulosa cells, absent in primordial follicle but present at later stages

has an inhibitory effect on follicle development- neg feedback on small follicles from more developed follicle
unaffected by GnRH/steroid hormones
reliable reflection of growing follicles- decreases over age

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13
Q

which follicles are selected to be ovulated?

A

estrogen and LH induce expression of LH receptor on theca cells
↳ follicle with largest #of LH receptors is ovulated and others die

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14
Q

hormones when follicle begins growth

A

FSH increase, oestrogen increase

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15
Q

When do FSH levels drop during follicle growth?

A

when oestrogen levels are high due to negative feedback causing endometrial thickening

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16
Q

what does the oestrogen peak cause?

A

LH release from the pituitary and suddenly has stimulatory effect on FSH secretion
oestrogen and FSH stimulate LH binding sites on granulosa cells

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17
Q

LH surge on day 14

A

ovulation

oestrogen drops as follicle is gone, corpus luteum produces some

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18
Q

hormones in luteal phase of menstruation

A

drop on FSH/LH as progesterone levels rise completing the endometrium

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19
Q

corpus luteum

A

made fo granulosa and theca cells, lutein cells contain lipid droplets and pigment lutein which give yellow colour, secrete progesterone

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20
Q

hormones when no pregnancy is detected in menstrual cycle

A

CL regresses, FSH rise, progesterone and oestrogen drop as endometrium shed

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21
Q

hCG

A

produced by blastocysts which bind to LH receptors and maintain progesterone if preggo and surpasses maternal immune rejection of placenta

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22
Q

how does hormonal contraception work?

A

suppresses ovulation via negative feedback of progesterone- secondary effects on female genital tract
HPG axis can be awakened in off period

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23
Q

combined pill mechanism

A

oestrogen provides additional feedback and promotes progesterone receptor expression

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24
Q

when can the breast produce milk?

A

once the placenta is delivered

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25
Q

myoepithelial cells in breast

A

contract on signal from oxytocin and expel milk from ducts

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26
Q

milk ejection reflex

A

suckling breast stimualtes prolactin release and oxytocin synthesis and secretion
myoepithelial cell contraction -> milk expulsion

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27
Q

why is fertility reducing during lactation?

A

negative feedback fo prolactin on FSH/LH

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28
Q

difference between early and premature menopause

A

early- <45

premature- <40 (premature ovarian insufficiency)

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29
Q

causes of premature menopause

A
  • idiopathic
  • autoimmune- Addisons, thyroid
  • surgery/ chemo/ radiotherapy
  • chromosomal/infecitons/ metabolic
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30
Q

management of early menopause

A

treat with oestrogen replacement

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31
Q

Biochemical profile of post-menopausal women

A

low estradiol
high FSH (main marker)
high LH

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32
Q

predictors of menopause

A

FSH – day 3 raised level
•AMH – anti-Mullerian hormone: declines with age and useful marker of ovarian reserve
•Inhibin B - declines with age and protein hormone marker of ovarian reserve
•Ovarian antral follicle count by ultrasound

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33
Q

vasomotor symptoms of lack of oestrogen

A

Hot flushes and night sweats • Palpitations, faintness

• Severe sleep deprivation

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34
Q

Urogenital ageing

A

Vaginal dryness and dyspareunia

• Bladder neck symptoms: urgency, urge incontinence, nocturia, recurrent urinary infections

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35
Q

HRT hormones that can be given

A

• Estrogen- improve symptoms but don’t restore fertility
• Progestogen - for endometrial protection
• Testosterone
oral, skin (transdermal) patches and gels, subdermal
implant, intra-uterine progestogen
Prescribed for menopausal symptom

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36
Q

benefits of HRT

A

improve QOL, protection against osteoporosis (provided HRT is taken long enough) and bowel cancer

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37
Q

risks of HRT

A

• Small extra risk of breast cancer with prolonged duration of use
• Increased risk of venous thromboembolism: x2 fold increase
• Small excess risk of stroke
(last 2 for tablets not transdermal patches)

38
Q

erectile dysfunction marker of cardiovascular disease

A

especially predictive of CV in men younger than 60 and in those with diabetes

39
Q

Testicular dysgenesis syndrome

A

condition characterised by:
- cryptorchism, hypospadias
- testis GC cancer, low sperm count, low-norm testosterone levels
(penis may be reduced in size)

40
Q

what can cause cryptoorchism and hypospadias?

A

deficiencies in fetal androgens

41
Q

what is cryptorchidism

A

A congenital undescended testis is one that has failed to reach the bottom of the scrotum by 3 months of age- dependant on there being enough androgens

42
Q

Reasons for correction of cryptorchidism

A

Reduce risk of infertility
Allows the testes to be examined for testicular cancer
Avoid testicular torsion
Cosmetic appearance

43
Q

cryptorchidism link to cancer

A

Males with undescended testis are 40 times as likely to develop testicular cancer (seminoma) as males without undescended testis
After the age of 2 years in untreated individuals the Sertoli cells will degrade

44
Q

assisted reproduction effectiveness with age

A

increasingly ineffective with age

45
Q

why do Sertoli cells have an impact on sperm count?

A

each Sertoli cell can only support a fixed number of germ cells during their 10 week development into sperm, mainly determined during fetal/early postnatal life

46
Q

AGD

A

anogenital distance, between anal opening and base of penis/vaginal opening
determined by fetal androgen exposure

47
Q

male AGD is

A

twice that of female

48
Q

masculinisation programming window

A

male- female difference in AGD was induced by androgen exposure specifically in the MPW, TDS orginate in 1st trimester MPW (8-12w)

49
Q

factors via mother in TDS

A

smoking, medications, lifestyle, diet

50
Q

hypospadias is characterised by:

A

Hypospadias is characterised by

  • a ventral urethral meatus
  • a hooded prepuce
  • chordee (ventral curvature of the penis) in more severe forms
  • the urethral meatus may open more proximally in the more severe variants. However, 75% of the openings are distally located.
51
Q

Turner’s syndrome (45 XO)

A

Women with Turner’s syndrome run out of eggs as a neonate and therefore have streak ovaries in adult life.
cannot produce ovarian oestrogen in response to the increasing LH and FSH during puberty- puberty induced at appropriate time

52
Q

hypogonadotropic hypogonadal anovulation

A

LH and FSH are low because there is not enough GnRH being secreted from the hypothalamus- low test and oestrogen
notably hypothalamic amenorrhoea- excessive exercise, anorexia

53
Q

hyperprolactinemia

A

Prolactin inbibits gonadotrophin secretin locally. This results in low LH, low FSH and low oestradiol
symptoms: galactorrhea

54
Q

visual defect caused by pituitary tumour

A

bitemporal hemianopia

55
Q

oligomenorrhoea

A

fewer than six to eight periods per year

56
Q

hypergonadotropic hypoestrogenic anovulation

A

hypogonadism due to an impaired response of the gonads to the GnRH, FSH and LH, and in turn a lack of sex steroid hormone production

57
Q

normogonadotropic normoestrogenic anovulation

A

PCOS- high LH and androgens with normal/low FSH and estradiol
hyperinsulinaemia also seen

58
Q

PCOS symptoms

A

hisuitism, acne, oily skin, menstrual disturbances: oligomenorrhea and amenorrhoea, obesity, acanthosis nigricans (due to insulin resistance)

59
Q

PCOS physiology

A

normal FSH and oestrogen stimulates growth of follicles but high androgens pause growth and inability to ovulate
high LH stimulates androgen production- ovary has many arrested follicles looking polycystic
overlap with metabolic syndrome

60
Q

treatment of PCOS

A

COCP- suppresses hormones
weight control
additional testosterone blocking drugs- cyproterone acetate

61
Q

diagnosis of PCOS

A

transvaginal USS

62
Q

finding on examination of premature menopause

A

atrophic vaginitis

63
Q

Which hormone is required to maintain progesterone production during the menstrual cycle?

A

LH

64
Q

What problem limited the development of IVF as we know it now?

A

premature LH surge

65
Q

_ increase bleeding at menstruation

A

prostaglandins

66
Q

When is the best time in an average 28-day menstrual cycle to do a blood test for ovulation?

A

Day 21- progesterone from CL is measured to confirm ovulation

67
Q

estrogen agonists uses

A
  • HRT: treat post-menopausal atrophic vaginitis, after hysterectomy or induction of puberty
  • COCP
68
Q

Continuous combined HRT

A

estrogen and progestagen are taken continually. It is used two years after the menopause and does not cause vaginal bleeding.

69
Q

sequential HRT

A

estrogen is given followed by two weeks of progestogen. This causes regular periods (after progestogen withdrawal).

  • used for younger women with hypogonadotrophic hypogonadism or in the climacteric.
  • not contraceptive but will have less side effects than the oral contraceptive pill
70
Q

oestrogen side effects

A

nausea, headaches and breast tenderness

71
Q

COCP side effects

A

headaches, nausea, weight gain, reduce libido, prevent lactation, associated with thromboembolism

72
Q

why can’t women with a uterus be given oestrogen alone?

A

cause continued proliferation of the endometrium and this can cause heavy irregular bleeding or pathologies such as endometrial hyperplasia and endometrial cancer

73
Q

oestrogen antagonist

A
  • ovulation induction (clomifene)- Anti-estrogens for ovulation induction in PCOS are only used for 5 days each month at the beginning of the cycle to allow the endometrium and potential for the LH surge to recover.
  • breast cancer (tamoxifen)
74
Q

progesterone agonist

A
  • menstrual induction- PCOS
  • heavy menstrual bleeding- reduce endometrial thickness
  • progesterone replacement in IVF
75
Q

types of progesterone contraception

A
  • progestagen only contraception
  • depo contraception- IM, inhibits gonadotrophins
  • implant contraception
  • intrauterine system- coil causes endometrial atrophy
  • post coital contraception- makes endometrium less receptive
76
Q

progesterone vs oestrogen contraception

A

most of the serious side effect of the combined contraceptive pill are because of the estrogen, progesterone alone is a safer contraceptive and used in higher risk women. However, unlike the combined pill which gives a regular cycle, progesterone only contraception causes irregular bleeding which can be frequent

77
Q

progesterone antagonist

A
  • termination of pregnancy
  • post coital contraception
  • shrink fibroid growth
78
Q

androgen agonist

A

HRT- increase energy & libido

79
Q

androgen antagonist

A

treatment of hirsuitism (cyproterone acetate, finasteride)- need effective contraception also

80
Q

cyproterone acetate

A

androgen antagonist and progesterone agonist

81
Q

which 2 drugs are used for termination of pregnancy?

A

progesterone antagonist (mifepristone) and second stage prostaglandin E (agonist)

82
Q

FSH agonist

A
  • ovulation induction

- superovulation- collect multiple eggs in IVF treatment

83
Q

FSH antagonist

A

gonadotrophin suppression

84
Q

LH agonist

A
  • superovulation

- ovulation

85
Q

LH antagonist

A
  • IVF- prevent a premature LH surge
86
Q

oxytocin antagonist

A

prevention fo preterm labour (atosiban)- stop uterine contractions

87
Q

oxytocin agonist

A
  • augmentation fo labour

- post-partum haemorrhage- solve uterine atony

88
Q

prostaglandin agonist in inducing labour

A

Vaginal prostaglandin E2 gel- cervical ripening and myometrium contractions

89
Q

prostaglandin antagonist

A
  • treatment of heavy menstrual bleeding (mefenamic acid)

- premature labour (indomethacin)- SE: premature closure of the fetal ductus

90
Q 
Which peptide hormones are produced from:
arcuate nucleus 
preoptic nucleus 
supraoptic nucleus 
paraventricular nucleus 
periventricular nucleus
A 
GHRH, dopamine
GnRH
AVP, oxytocin
AVP, oxytocin, CRH, TRH
somatostatin
91
Q

Kallman syndrome

A

50% of hypogonadotropic hypogonadism cases defined by a delay or absence in onset of puberty and an impaired or absent sense of smell
presentation in males is characterised by low gonadotrophins & testosterone and small external genitalia, with small or undescended testis

Y2S2- Genetics, Renal, Endocrine (6 decks)

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