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Semester 4 > repro 2 > Flashcards

repro 2 Flashcards

1
Q

what does the SRY gene code for

A

TF of itself (reinforce) + cascade of TF –> differentiation of male Development

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2
Q

what kind of tissue is genital ridges derived from

A

somatic mesenchymal tissue

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3
Q

what causes mesonephric cells—>vascular tissue/leydig cells/basement membrane in boys

A

the influence of pre-sertoli cells (which themselves express SRY)

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4
Q

what do mullerian/ wolffian ducts differentiate into

A

wolffian duct differentiate to VD + seminal vesicles

Mullerian–> uterine tubes/uterus/upper 1/3rd vagina

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5
Q

what forms the seminiferous tubules/rete testis

A

mesonephric cells

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6
Q

external differentiation of genitalia

A

testosterone
-genital tubercle grows to phallus(glans penis)

  • urethral fold folds to form hollow cylinder - shaft of penis
  • scrotal/genital swellings fuse to become scrotum

absence of testosterone

  • urethral fold folds to become labia minora
  • genital swellings become labia major
  • genital tubercle becomes clitorious
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7
Q

sex reversal

intersex

A

SR = phenotype does not match genotype

Intersex = have components of both tracts/ ambiguous genitalia

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8
Q

5a deficiency inheritance pattern

A

autosomal recessive - higher risk with inter-related marriages

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9
Q

congenital adrenal hyperplasia

A

21-hydroxylase deficiency–> can’t make cortisol/aldosteorne so high production of testosterone

(no cortisol = positive feedback to try make cortisol (high uptake of cholesterol in adrenal) but leads to excess testosterone production )

leading to females–> male like female genitalia & both mullerian and wolffian ducts are present

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10
Q

number of carbons in progesterone, testosterone and oestrogen

A

Progesterone = 21

testosterone = 19
via aromatase
oestrogen = 18

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11
Q

time scale for:

  • wolffian duct development
  • mullerian development
  • regression
A

wolffian develop 4 weeks
mullerian @ 6 weeks

regression

  • mullerian in males - 8 weeks due to AMH
  • wolffian in females - 10 weeks due to lack of testosterone
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12
Q

how is GnRH secreted from hypothalamus

A

travels from neurones via hypophysial portal vessel into anterior pituitary

as a 56 aa with GAP

cleaved by endonuclease at site P to get rid of GAP

to 10aa

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13
Q

why can’t GnRH be given continuously

A

decouples the gpcr with secondary messenger systems

leading to cessation of LH/FSH release from pituitary

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14
Q

gonadotrophins (LH/FSH) are glycoproteins - what subunit limits their concentration

A

beta

alpha is released in excess

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15
Q

precocious puberty girls/boys at what age

A

<8 yrs in girls

<9 yrs in boys

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16
Q

what is adrenarche

A

adrenal maturation (zona reticularis)

Z.R only develops in adrenarche (not apparent in neonates)

high androgen production DHEA/S ONLY–> transported to tissues to produce testosterone/ DHT

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17
Q

type of PSU

A

vellus

  • terminal (beard/facial) only sebaceous glands
  • apocrine (pubic/axillary) apocrine glands too

sebaceous
-scretes sebum via glands under the influence of androgens

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18
Q

how does the GnRH/gonadotrophin pulsatile release change from child–> adult

A

child = nocturnal release

adult = day release too (consistent pulsitile release)

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19
Q

McCune Albright Syndrome

A

example of Peripheral precocious puberty

mutation of Gs–>
activation of adenyl cyclase–> overproduction of sex steroids

present with cafe au lait skin and fibrous dysplasia

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20
Q

puberty delay for girls/boys (age)

A

girls - no secondary characteristics >13yrs / no menarche >18yrs

boys - >14yrs

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21
Q

hypogonadotrophin hypogonadism

hypergondotrophin hypogonadism

leads to DELAYED puberty

A

hypo hypo = Kalmann
-low gonadotrophin from pituitary

hyper hypo = kinefelter 47XXY / turner’s 45XO

  • testes failing to respond to gonadotrophins
  • high LH/FSH due to -ve feedback of low sex steroids
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22
Q

wakening of HPG axis causes increase of LH/FSH

what are their initial actions

A

LH - increase androgen synthesis in both

boys
-LH –> leydig–> testosterone
-FSH–> Sertoli cells –> AMH (in development)
but in puberty it increases growth of testis

girls
-FSH –> folliculogenesis

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23
Q

adrenopause

andropause

A

when DHEA/DHEAS decline after 20-25yrs

decreasing testosterone

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24
Q

what is the name of the sweat gland not associated with hair follicles

(apocrine/sebaceous glands are associated with hair in PSU)

A

eccrine

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25
Q

when is the HPG axis first ever activated (in development)

A

at 16th gestational week –> 1/2years of age

before ceasing again

reactivated during gonadarche ~10/11yrs

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26
Q

difference between primary and secondary oocyte

A

primary - arrested in meiosis I anaphase (during development)

therefore in primary = 46 chromosomes

secondary - after meiosis I completes in LH surge when 1st polar body gets extruded

secondary = 23 chromosomes

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27
Q

primordial follicle

A

foetus w/ primary oocyte:

granulosa cells surrounding oocyte secrete an acellular layer BASAL LAMINA (protective)

like this follicle until–> puberty (folliculogenesis)

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28
Q

folliculogenesis (growth of follicles - the primordial ones—> ovulation)

A

pre-antral phase (gonadotrophin independent)

  • growing of the follicle
  • ZP from granulosa (sign of growth) around oocyte
  • 2nd outer layer of basal lamina differentiate into theca cells

antral phase - gonadotrophin dependent (FSH)

  • as it grows the gaps between granulosa cells increase and fluid enters = antrum
  • antrum surrounds the oocyte+zp+cumulous cells
  • surrounding antrum = theca/basal lamina/granulosa cells

= cumulous oocyte complex

follicle recruitment

  • right size can respond to FSH–> recruited = antral follicles
  • then only 1 is selected to ovulated = Graafian follicle
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29
Q

does taking OCPill preserve your eggs

A

no

OCP does suppress FSH

however pre-antral phase is independent to FSH - so follicles will still grow but will not survive/progress as they will require FSH –> die

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30
Q

when did the Graafian follicle start growing

A

3 months/3cycles prior to its ovulation month

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31
Q

2-cell-2-gonadotrophin theory

A

the dominant follicle (Graafian)

  • highly vascularised theca cells—> LH
  • causes androgen synthesis
  • release to–> granulosa cells + body
  • production of oestrogen
  • oestrogen causes HPG feedback/drives granulosa cell multiplication( dominant follicle growth)
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32
Q

regular cycle

A

within 4days difference in duration month to month eg. 28 and 32 days

ask for 1st day of bleeding of previous month and then this month

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33
Q

when does 1st day of menstrual cycle start

A

1st day of bleeding for that month

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34
Q

what hormone dominates follicular and luteal phase of menstrual cycle

A

follicular = oestrogen
(switching on/off between LH/FSH)

luteal = progesterone from corpus luteum
(low LH/FSH)

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35
Q

what happens at the end of a menstrual cycle

A

Menstruation / if pregnant the corpus letuem is maintained by hCG (from synctiotrophoblast) and it produces oestrogen + progesterone (initially)

36
Q

when does the endometrium induce progesterone receptors

A

> 4mm after proliferation under oestrogen control

37
Q

endocervical / ectocervical (cervix) cell

A

endo = columnar mucous cells

ecto = non-keratinised stratified squamous cell (like vagina)

38
Q

which layer do uterine fibroids form of uterus

A

myometrium (therefore also dependent on oestrogen–> grow)

39
Q

where does the oestrogen that increases proliferation of endometrium in follicular phase come from

A

dominant follicle

40
Q

how long does the egg remain in the uterine tubes for

A

about 5 days

41
Q

spermatogenesis (division)

A

PGCs
A- proliferation by mitosis (diploid) -> spermatocytes (primary)

  1. B/Ap - meiosis: primary spermatoctyes(diploid) —> 2ndary spermatocytes(Haploid)—->spermatids(haploid)
  2. spermiogenesis = spermatids–>spermatazoa
42
Q

secretions into seminal fluid

A
  1. bulbs-urethral (Cower’s) to clear/lubricate/neutralise acid because fluid is alkaline(high in salt)
  2. seminal vesicle (50-70%)- fructose
  3. prostate(milky) - proteolytic enzymes + high zinc (anti-bacterial)
43
Q

ejactulatory duct

spermatic cord

A

ejaculatory duct(2cm) is where the vas deferens combines with the seminal vesicle outflow into the ureter

spermatic cord = deep inguinal - testis

44
Q

normal volume of testes

A

15-25ml

45
Q

where in the testes are sperm most concentrated

+ where is sperm stored

A

rete testis

stored in epididymis

46
Q

why has the immune system of the body never seen own sperm

A

Sertoli cells separate the inside of the tubule to the interstitial space.

Sertoli cells create an adluminal compartment for developing sperm by forming tight junctions between them

This forms a blood-testis barrier.

this leads to vasectomy = dangerous (if get into blood, the body will make Ab against sperm)

47
Q

what are present in between seminiferous tubules

A

Leydig cells
vessels (blood and lymphatics)
Interstitual fluid

48
Q

spermiogenesis

A

spermatids (after meiosis) —> lose cytoplasm/grow flagella/elongate —> spermatozoa

49
Q

sperm terminology

A

spermatogonia(mitosis = diploid)

spermatocyte (primary and secondary) after meiosis I
spermatid at end of meiosis II
primary = diploid
secondary = haploid

spermatozoa (after spermiogenesis)

50
Q

anabolic steroids consequences

A

reduced LH –> reduced testosterone (but since you are injecting steroid = little effects)

reduced FSH—> testicular atrophy (maintins Sertoli population)

there is some aromatase in men - if VERY high levels of testosterone–> oestrogen–> growth of breast tissue

51
Q

somatic control of ejaculation

A

expulsion of glandular secretions and evacuation of urethra

symp = movement of sperm up spermatic cord–> urethra

52
Q

why is seminal fluid alkaline

A

to protect sperm from acidic vagina

53
Q

axenome structure

A

9 fibres with 2 in the middle

54
Q

what medication should you not take in combination with COCP

A

anti-epileptics = affects metabolism of oestrogen/progesterone

broadspectrum antibiotics = may kill microbiome of gut–> affects re-absorption of oestrogen

55
Q

what contraceptives for women who breastfeed

A

progesterone only methods

no oestrogen - which inhibits lactation

56
Q

diaphragm caps / suction caps

A

diaphragm around vagina

suction around cervix

6 hours before and 6 hours after

57
Q

what hormones are in COCPs

A

ethinyloestradiol

progestogen = compound that acts like progesterone but isn’t progesterone

58
Q

IUCDs

A 
copper
-acts as spermacide
-mechanical barrier
-sets up inflammatory reaction and PG secretion
=hostile environment
59
Q

emergency contraception

A

copper IUCDs - up to 5 days

  • if in 1st part of cycle - prevents fertilisation
  • 2nd part of cycle - prevents implantation

pills - up to 72 hrs-5days

  • levonelle 2 tablets
  • ellaone
  • Schering PC4(old)
60
Q

acrosome reaction

A

burst
release of hyalurondiase
digests cumulus cells/corona radiata
sperm binds to ZP3 on zona pellucida

THEN true acrosome reaction = enzyme acrosin digests zona pellucida for sperm to enter

61
Q

the 2 x increase in Ca2+ (capicitation / syngamy)

A

CatSPER open in high alkaline near egg (voltage gated)
-calcium to beat tail more forcefully

sperm enters and has PLC-zeta –> PIP pathway
-calcium for cortical reaction (prevent polyspermy/complete meiosis II of oocyte)

62
Q 
what do you see on
day 0
day 3/4
day 5
day 7
A

day 0 = fertilisation(ampulla)
2pronucleis with 2 polar bodies outside

day 3/4 = 6-8 cells = morula

day 5 = blastocyst = blastocele+trophoblasts(placenta)

day 7 = implantation

63
Q

testosterone receptor

A

nuclear receptor = TF

DHT binds more strongly with Testosterone receptor

64
Q

5a-reductase 2 types

A

type I = scalp/skin

type II = genital skin/prostate

65
Q

5a-reductase inhibitors(-asteride) to who?

A

balding/prostate cancer

66
Q

danazol

cyproterone acetate

anti- androgen = flutamide

A

danazol = androgen derivative that doesn’t get converted into oestrogen

CA = inhibits peripheral androgen receptors

67
Q

Unwanted Effects of Testosterone

A
  • hypertension/oedema (sodium,calcium, water retaining actions)
  • cholestatic jaundice/hepatotoxicity
  • gynacomastia
  • testicular atrophy/reduced spermatogenesis
  • virulisation
  • balding/acne
68
Q

Cryptorchidism

A

undescended testes

69
Q

pregnant women water gain

A
  • E2/Prog = water retaining mineralocorticoid actions
  • RAAS placental renin + E2 up regulates Angiotensinogen synthesis in liver (without vasoconstriction due to AngII resistant to AT2 receptor by VEGF/progesterone)
  • connective tissue/ligaments take on more water
  • resetting osmostat (drinking more)
70
Q

human placental lactogen

A

insulin resistance to decrease glucose utilisation –> foetus gets glucose

causes high glucose blood levels in 2nd trimester

71
Q

CVS of pregnant women

A 
high HR
low BP (oestrogen--> NO--> vasodilation)
72
Q

decidual cells

+ what hormone causes decidualisation of the endometrium

A

cover surface of uterus
if pregnant these get filled with glycogen and lipids

will become part of MATERNAL placenta

progesterone

73
Q

yolk sac and amnion fluid

A

amnion fluid - will surround foetus

yolk sac will cover circulation for the first few days

74
Q

at what week does the placenta take over the corpus luteum

A

week 7

75
Q

Reduced peripheral resistance and increased flow to what structures (5)

A 
skin
uterus
kidney
placenta 
muscle
76
Q

urinary system of pregnant women

A

relaxin from placenta/CL–> formation of endothelin which mediates dilation of renal arteries by nitric oxide synthesis

baby pushing on bladder

increased risk of UTI

progesterone + VEGF–> increased resistance of AngII–> less vasoconstriction and more vasodilation–> higher GFR

77
Q

what suppresses FSH and therefore decreases rate of follicular loss by recruitment

A

AMH - granulosa cells (after puberty)

Inhibin B (follicular phase) / A (luteal phase) - granulosa cells

78
Q

why do you start menopause with short cycles and then later delayed ovulation/absent

A

short cycles
-less Inhibin B so less suppression of FSH so in follicular phase you get high FSH–> high oestrogen–>LH surge at earlier stages
(reduced follicular phase)

delayed ovulation

  • despite having high FSH
  • FSH receptors loss sensitivity = faulty granulosa cells
  • oestrogen levels don’t rise high enough to induce LH surge
79
Q

what is responsible for

  • hot flushes
  • breast tenderness
  • Heavier periods
A

hot flushes: steep decline in oestrogen - disturbs serotonin levels- resetting of the thermoregulatory nucleus (in the brain stem) and this leads to excess heat loss.

breast tenderness: due to the transient increases in oestrogen

heavier periods: longer oestrogen stimulation(because faulty granulosa receptors–> no dominant follicle recruited) of the endometrium causing it to proliferate + no progesterone from CL because no dominant follicle recruited

80
Q

Which hormone is no longer produced after the menopause?

Which hormone decreases first during a woman’s reproductive life?

Which symptom is not associated with the menopause?

A

progesterone

AMH

urinary incontinence

81
Q

how to treat for hot flushes

A

HRT with oestrogen

but if patient has a risk of stroke/thrombosis we avoid giving steroids and we give SSRI (antidepressant) eg. sertraline

Tibolone =synthetic oestrogen + progesterone (no need to give progesterone with it)

82
Q

consequences of hyperglycaemia

A

polycythaemia (high RBC due to poor functioning placenta)—-> juandice as later there is too much so RBCs broken down

resp distress as hyperglycaemia inhibits surfactant production

neonatal hypoglycaemia

glycosuria–> polyhydramnios –> uncomfortable for mother

baby = macrosomia
(start producing insulin–> increased storage of sugars in fat stores)

83
Q

when is it considered miscarriage

A

<24 weeks

84
Q

what is injected in third stage of labour

A

syntometrine = artificial oxytocin(short uterine contraction) + ergometrine(sustained contraction)

this stage shouldn’t be more than 15mins

85
Q

when is oxytocin stimulated

A

cervix dilation / suckling

86
Q

To reduce or prevent post-partum bleeding

A

prostaglandins, oxytocin/ergot (Syntometrine) that gets the vessels ligatured.

87
Q

to prevent a premature birth

A 
b2-adrenoceptor agonist eg. salbutamol
Ca2+ blockers
Mg sulfate 
oxytocin inhibitors 
oxytocin receptor antagonist eg. retosiban

COX inhibitors NSAIDs (but can get into foetal circulation)

Semester 4 (10 decks)

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