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Semester 4 > repro 2 > Flashcards

repro 2 Flashcards

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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
when is the HPG axis first ever activated (in development)
at 16th gestational week --> 1/2years of age before ceasing again reactivated during gonadarche ~10/11yrs
26
difference between primary and secondary oocyte
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
27
primordial follicle
foetus w/ primary oocyte: granulosa cells surrounding oocyte secrete an acellular layer BASAL LAMINA (protective) like this follicle until--> puberty (folliculogenesis)
28
folliculogenesis (growth of follicles - the primordial ones---> ovulation)
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
29
does taking OCPill preserve your eggs
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
30
when did the Graafian follicle start growing
3 months/3cycles prior to its ovulation month
31
2-cell-2-gonadotrophin theory
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)
32
regular cycle
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
33
when does 1st day of menstrual cycle start
1st day of bleeding for that month
34
what hormone dominates follicular and luteal phase of menstrual cycle
follicular = oestrogen (switching on/off between LH/FSH) luteal = progesterone from corpus luteum (low LH/FSH)
35
what happens at the end of a menstrual cycle
Menstruation / if pregnant the corpus letuem is maintained by hCG (from synctiotrophoblast) and it produces oestrogen + progesterone (initially)
36
when does the endometrium induce progesterone receptors
>4mm after proliferation under oestrogen control
37
endocervical / ectocervical (cervix) cell
endo = columnar mucous cells ecto = non-keratinised stratified squamous cell (like vagina)
38
which layer do uterine fibroids form of uterus
myometrium (therefore also dependent on oestrogen--> grow)
39
where does the oestrogen that increases proliferation of endometrium in follicular phase come from
dominant follicle
40
how long does the egg remain in the uterine tubes for
about 5 days
41
spermatogenesis (division)
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
secretions into seminal fluid
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
ejactulatory duct spermatic cord
ejaculatory duct(2cm) is where the vas deferens combines with the seminal vesicle outflow into the ureter spermatic cord = deep inguinal - testis
44
normal volume of testes
15-25ml
45
where in the testes are sperm most concentrated + where is sperm stored
rete testis stored in epididymis
46
why has the immune system of the body never seen own sperm
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
what are present in between seminiferous tubules
Leydig cells vessels (blood and lymphatics) Interstitual fluid
48
spermiogenesis
spermatids (after meiosis) ---> lose cytoplasm/grow flagella/elongate ---> spermatozoa
49
sperm terminology
spermatogonia(mitosis = diploid) spermatocyte (primary and secondary) after meiosis I spermatid at end of meiosis II primary = diploid secondary = haploid spermatozoa (after spermiogenesis)
50
anabolic steroids consequences
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
somatic control of ejaculation
expulsion of glandular secretions and evacuation of urethra | symp = movement of sperm up spermatic cord--> urethra
52
why is seminal fluid alkaline
to protect sperm from acidic vagina
53
axenome structure
9 fibres with 2 in the middle
54
what medication should you not take in combination with COCP
anti-epileptics = affects metabolism of oestrogen/progesterone broadspectrum antibiotics = may kill microbiome of gut--> affects re-absorption of oestrogen
55
what contraceptives for women who breastfeed
progesterone only methods | no oestrogen - which inhibits lactation
56
diaphragm caps / suction caps
diaphragm around vagina suction around cervix 6 hours before and 6 hours after
57
what hormones are in COCPs
ethinyloestradiol progestogen = compound that acts like progesterone but isn't progesterone
58
IUCDs
``` copper -acts as spermacide -mechanical barrier -sets up inflammatory reaction and PG secretion =hostile environment ```
59
emergency contraception
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
acrosome reaction
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
the 2 x increase in Ca2+ (capicitation / syngamy)
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
``` what do you see on day 0 day 3/4 day 5 day 7 ```
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
testosterone receptor
nuclear receptor = TF | DHT binds more strongly with Testosterone receptor
64
5a-reductase 2 types
type I = scalp/skin | type II = genital skin/prostate
65
5a-reductase inhibitors(-asteride) to who?
balding/prostate cancer
66
danazol cyproterone acetate anti- androgen = flutamide
danazol = androgen derivative that doesn't get converted into oestrogen CA = inhibits peripheral androgen receptors
67
| Unwanted Effects of Testosterone
- hypertension/oedema (sodium,calcium, water retaining actions) - cholestatic jaundice/hepatotoxicity - gynacomastia - testicular atrophy/reduced spermatogenesis - virulisation - balding/acne
68
Cryptorchidism
undescended testes
69
pregnant women water gain
- 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
human placental lactogen
insulin resistance to decrease glucose utilisation --> foetus gets glucose causes high glucose blood levels in 2nd trimester
71
CVS of pregnant women
``` high HR low BP (oestrogen--> NO--> vasodilation) ```
72
decidual cells + what hormone causes decidualisation of the endometrium
cover surface of uterus if pregnant these get filled with glycogen and lipids will become part of MATERNAL placenta progesterone
73
yolk sac and amnion fluid
amnion fluid - will surround foetus yolk sac will cover circulation for the first few days
74
at what week does the placenta take over the corpus luteum
week 7
75
Reduced peripheral resistance and increased flow to what structures (5)
``` skin uterus kidney placenta muscle ```
76
urinary system of pregnant women
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
what suppresses FSH and therefore decreases rate of follicular loss by recruitment
AMH - granulosa cells (after puberty) Inhibin B (follicular phase) / A (luteal phase) - granulosa cells
78
why do you start menopause with short cycles and then later delayed ovulation/absent
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
what is responsible for - hot flushes - breast tenderness - Heavier periods
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
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?
progesterone AMH urinary incontinence
81
how to treat for hot flushes
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
consequences of hyperglycaemia
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
when is it considered miscarriage
<24 weeks
84
what is injected in third stage of labour
syntometrine = artificial oxytocin(short uterine contraction) + ergometrine(sustained contraction) this stage shouldn't be more than 15mins
85
when is oxytocin stimulated
cervix dilation / suckling
86
To reduce or prevent post-partum bleeding
prostaglandins, oxytocin/ergot (Syntometrine) that gets the vessels ligatured.
87
to prevent a premature birth
``` 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)

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