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endo - yr2 > endo of preg > Flashcards

endo of preg Flashcards

1
Q

describe the male reproductive tract *

A

in seminiferous tubules have sertoli

leidig cells between the seminiferous tubules

leidig cells produce testosterone

sertoli cells make oestrogen

spermatozoo go into the middle of the seminiferous tubule and mature under signals from LH and FS

tubular fluid is reabsorbed so concentrated in rete testes and epididymis - induced by oestrogen

nutrients eg fructose secreted into epididymal fluid - needed for long journey and maturation - stimulated by androgens

glycoprotein coat secreted into epididymal fluid - protect sperm from hostile environment - stimulated by androgens

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2
Q

how far to teh spermatozoa travel *

A

100000x their length

from the testes to the fallopian tube

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3
Q

what is in semen *

A

spermatozoa 15-120million

seminal fluid 2-5ml

leucocytes

potentially viruses eg hep b/ hiv

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4
Q

what is the consequence of aromatase deficiency *

A

cannot cobvert testosterone to oestrogen

= igh test = hirsuitism and acne

= low oestrogen = osteoporosis, tall (need oestrogen to fuse epiphyesial plates)

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5
Q

what is important with regards to sperm *

A

percentage of motile sperm in count

number (>15million)

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6
Q

what proportion of sperm are involved in fertilisation *

A

1/100 spermatozoa in ejaculate enter the cervix

1/10 000 cervix to ovum

overall 1/1million reach ovum

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7
Q

where is the seminal fluid produced *

A

small contribution from testes and epididymis, including inositol & glycerylphosphorylcholine

mainly from accessory sex glands - seminal vesicles (including fructose and fibrinogen), prostate (citric acid, Ca2+ chelator, acid phosphatase, fibrinogenase)

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8
Q

why do spermatozoons need activating *

A

when taken from the seminiferous tubule - quiescent and incable of fertilisation

when taken from vas deferens - capable of whiplash movement and some fertilisation - however this is not full activation

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9
Q

what is capacitation *

A

activation of the sperm

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10
Q

where does capacitation occur and why *

A

in the fallopian tube

oestrogen and Ca dependant

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11
Q

what are the 3 things that occur ion capacitation *

A

loss of glycoprotein coat

change in surface membrane characteristics

develop whiplash movement of tail

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12
Q

what is teh acrosome *

A

organelle in sperm

contain enzymes for break down of outer layer of the ovum

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13
Q

describe the acrosome reaction *

A

sperm binds to ZP3 (sperm receptor)

Ca2+ enter the sperm - stimulated by progesterone which is high in the luteal phase as made by corpus luteum

release of hyaluronidase and proteolytic enzymes from acrosome

spermatazoon penetrates zona pellucida (glycoprotein layer of ovum)

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14
Q

descrieb polar bodies *

A

in egg chromosomes divide evenly to make haploid ovum

all cromosome goes into 1 cell

leave polar body - no cytoplasm - so it gets apoptosed

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15
Q

summarise the maturation of the sperm *

A

spermatazoa released into white area?

travel in the semen

1/1 million reach the ovum

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16
Q

where does fertilisation occur *

A

fallopian tube

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17
Q

describe fertilisation *

A

it triggers cortical reaction - cortical granules in ovum release molecules which degrade the zona pellucida eg ZP2 and 3 - this prevents further binding of the sperm as there are no receptors

cell becomes dipoid - as soon as dipoid - zygote starts to divide to form 2 cell conceptus

18
Q

describe the development of the conceptus *

A

conceptus divides as it moves down the fallopian tube

at day 4 - becomes morela

at day 5 - becomes blastocyst with inner cell mass - enters the uterus

19
Q

describe the cycle of follicles in the ovary *

A

primary follicle -> oocyte -> secondary follicle -> ovum -> egg erupts out of the ovary -> follicle degenerates into corpus luteum -> eventually becomes corpus albicans which doesn’t make progesterone

in pregnancy - hCG maintains corpus luteum

hCG is made from the placenta and acts on the LH receptor (LH low in preg because of -ve ffedback from high oestrogen)

20
Q

describe implantation *

A

attacment phase - outer trophoblast cells contact uterine surface epithelium

then: decidualisation pase - progesterone causes change in underlying uterine stromal tissue (need progesterone dominance in the prescence of oestrogen)

21
Q

what do the 2 different parts of the blastocyst become *

A

inner cells mass = embryo

trophoblast cells - placenta

22
Q

what factors are important for attachment (part of implantation) *

A

leukaemia inhibitory factor (LIF) - from the endometrial sectretory glands and possible blastocyst - stimulates adhesion of blastocyst to endometrial cells

interleukin 11 - from endometrial cells - released into te uterine fluid

many others eg HB-EGF

23
Q

what is important in decidualisation *

A

interleukin 11

histamine

prostaglandins TGFbeta (promote angiogenesis)

24
Q

what occurs in decidualisation (part of implantation)

A

glandular epithelial secretion

glycogen accumulation in stromal cell cytoplasm (below epi)

growth of capillaries

increased vascular permeability - oedema

25
Q

describe the hormone changes and their effects in pregnancy *

A

hCG - first thing to increase - maintain corpus luteum, acts on LH receptor = increase in progesterone and oestrogen

then placenta take over oestrogen and progesterone production so hCG falls because dont need corpus luteum to be stimulated

human placental lactogen increases (produced by placenta) - causes change in metabolism - makes mothers insulin resistant = increase glucose - promote nutrients to foetus

26
Q

describe hormones in ivf

A

FSH given to increase the number of follicles

hCG given to trigger ovulation

27
Q

describe progesterone and oestrogen production during pregnancy *

A

for first 40 days - they’re made uin the corpus luteum stimulated by hCG (which is produced by the tropoblasts) - act on lh receptors - negative feedback mean inibit lH and FSH production - oestrogen and prog essential for developing fdetoplacental unit

from day 40 - placenta produces oestrogen and progesterone

sex steroids are mede from cholesterol precurser -> through androgen to oestrogen

foetal and maternal DHEAS

28
Q

what hormones increase in pregnancy and why *

A

ACTH

adrenal steroids - becasue of ACTH increase

prolactin

igf 1 - stimulated by placental gh variant

iodothyronines - cg stimulate thyroid becasue they sare an a subunit with TSH

pth related peptides made by breast tissue = ca increase - mobilise from bone tissue to make sure there is enoug for the foetus

29
Q

effect of prolactin increase in preg in clinical asssessments 8

A

mean cant use prolactin to assess size of prolactinoma - normally size is related to level of prolactin

in preg - lactotroph ypertrophy

so have to assess visual fields instead

30
Q

what hormones decrease in pregnancy *

A

gonadotrophins - negative feedback from oestrogenb

pituitary gh

tsh - hcg does job of tsh

31
Q

summarise the endocrine control of parturition *

A

oestrogen and oxytocin stimulate the oxytocin recepetor on myometrium and endometrial cells

progesterone inhibits it

oxytocin causes uterine contraction, cervical dilation and milk ejection

32
Q

why do you get galactorrhoea from prolactinoma *

A

too muc milk produced - leaks out with minimal stimulation

33
Q

describe the endocrine control of lactation *

A

suckling stim - activate neuronal pathways - stimulate teh hypothalamus

= stim of pit

= adenohypophesis - produce prolactin (milk production), neurohypophysis produce oxytocin (milk ejection)

increased prolactin switch off reproductive axis by binding to kisspeptin neurons in the hypothalamus = reeduction in kisspeptic stimulating gnRH neurons

34
Q

how does oestrogen inhibit the reproductive axis *

A

act on ERa receptor on kisspeptin neurons

35
Q

effects of high prolactin 8

A

amenorrhoea

low libido and testosterone

becauyse reproductive axis switched off

36
Q

why is reproductive axis switched off in anorexia

A

less leptin bind to kisspeptin neurons - switch of axis

37
Q

wy do marathon runners have low testosterone *

A

becasue of nipple stim = high prolactin = switch of reproductive axis

38
Q

does decidualisation provide nutrients for implanting blastocyst *

A

yes

39
Q

what is the main oestrogen produced by the feto-placental unit *

A

oestriol

40
Q

summarise partuition *

A

The foetal hypothalamus releases CRH, which causes ACTH release from the foetal adenohypophysis and cortisol release from the foetal adrenals

This leads to steroid precursor production, and the placenta converts these to oestrogen, with progesterone as a by-product.

Oestrogen activates phospholipase A2 in the uterus, which converts arachidonic acid into PGF

PGF2A causes the release of calcium ions (Ca2+) from microsomes in the uterus

Oxytocin binding to the oxytocin receptor causes the formation of Ca2+-calmodulin, which forms Ca2+-calmodulin-myosin kinase

The formation of actin-myosin causes contraction of the uterus

endo - yr2 (24 decks)

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