UNIT 7 REVISION DOCUMENT Flashcards
implantation process
1) Apposition – unstable adherence of blastocyst to uterine lining
2) Attachment – endometrial epithelial cells and trophoblast cells connect via integrins, causing a strong adhesion
3) Trophoblast differentiation – differentiates into cytotrophoblast and syncytiotrophoblast, this invades the wall of the uterus
4) Invasion
5) Maternal recognition
how is the placenta devleoped
- Blastocyst implants on the endometrium
- Syncytiotrophoblast grows into the endometrium
- Froms finger like projections called the chorionic villi, containing fetal blood vessels
- Chorion fundosum: is the chorionic villi nearest the connecting stalk of the developing embryo, most vascular, contain mesoderm, these proliferate and become the placenta, connecting stalk becomes the umbilical cord
- Umbilical cord: contains 2 arteries and 1 vein, arteries carry blood frombaby to the placenta and is deoxygenated
hormones secreted by the anterior pituitary
FSH
LH
ACTH
TSH
Prolactin
Ignore
GH
what forms blood testes barrier
tight junctions between sertoli cells
oogenesis
- Oogonia
- Mitotic division starts before 12 weeks
- Producing primary oocytes which begin meiosis
- Meiotic arrest – metaphase 1 until puberty
- Primary oocytes go through remainder of meiosis I to make secondary and polar body
- Secondary oocytes go through meiosis 2 producing 1 ovum and 1 polar body (Large ovum as it takes everything needed for production of foetus mitochondria)
- Group of oogonia in ovaries
- Some die and become theca cells and granulosa cells
- Granulosa cells form follicle around ovum
- Theca cells inside the follicle and provide nutrition to maturing ovum
- Once ovum is mature follicle opens and ovulation happens
- Follicle the degrades forming corpus luteum
- Corpus luteum responsible for making progesterone and inhibiting GnRH and therefore LH and FSH
- Eventually degrades
spermatogenesis
- Occurs in the seminiferous tubules in testes
- Spermatogonia are the initial pool of the diploid cells
Type A – replenish pool of spermatogonia
Type B – form mature sperm - Type B spermatagonia repliocate by mitosis to form identical diploid cells linked by cytoplasm bridges these are primary spermatocytes
- Primary spermatocytes undergo meiosis
- Meiosis I produces secondary spermatocytes
- Meiosis II produces spermatids
- Bridges break and spermatids released into lumen of seminiferous tubule – spermiation
- Spermatids undergo spermeogenesis
- Cells travel to rete testis – concentrates the sperm (removes excess water)
- Move to epididymis where they are stored and have final maturation
follicularp hase
follicular phase= start to day 14
- When follicles reach the secondary follicle stage, they develop receptors for FSH. To develop after the secondary follicle stage, they require stimulation from FSH
- As the follicles grow, the granulosa cells secrete increasing amount of oestrogen which has a negative feedback on the pituitary gland, decreasing LH and FSH. Increasing oestrogen also makes the cervical mucus more permeable, allowing sperm to penetrate the cervix around the time of ovulation
- One follicle develops further than the others, becoming the dominant follicle
- LH spikes just before ovulation, causing the dominant follicle to release an ovum from the ovary
- Ovulation happens 14 days before the end of the cycle
luteal phase
- Luteal phase= 14 to 28
- Follicle which release the ovum then collapses and becomes the corpus luteum
- The corpus luteum secretes high levels of progesterone to maintain the endometrial lining and thicken the cervical mucus
- Corpus luteum also secretes a small amount of oestrogen
- At fertilisation, the syncytiotrophoblast of the embryo secrete HCG which maintains the corpus luteum
- If no fertilisation, the corpus luteum degenerates causing a fall in oestrogen and progesterone
- This causes the endometrium to break down and menstruation occurs
- The stromal cells of endometrium release prostaglandins which encourage the breakdown of the endometrium
- Menstruation starts on day 1 of the menstrual cycle
- Negative feedback from oestrogen and progesterone on the hypothalamus and pituitary gland ceases, allowing LH and FSH levels to rise so the cycle restarts
first sign of puberty in females
breast development
first sign of puberty in males
testicular development
male puberty
female puberty
hypothalamic pituitary testicular axis
LH to Leydig cells to testosterone release
FSH to Sertoli cells to spermatogenesis
Testosterone has negative feedback effect on hypothalamus and anterior pituitary gland
hypothalamic pituitary ovarian axis
LH to theca cells to androgen release
Androgens diffuse from theca cells to granulosa cells
FSH to granulosa cells to convert androgen to oestrogen
sperm transport
S – Seminiferous tubules
R – Rete testis
E – Efferent ducts
E – Epididymis
V – Vas deferens
E – Ejaculatory duct
N – Nothing
U – Urethra
P- Penile Urethra
placental physiology
Storage
Endocrine
Respiration
Protection
Excretion
Nutrition
Transport
stages of labour
- spontaneous onset, gestation 37 weeks plus, vertex presentation & completed within ~ 18 hours with no complications.
- Latent phase of labour: presence of uterine contractions, cervical dilatation, effacement up to 4cm
- Active phase of labour: regular contractions and progressive dilatation beyond 4cm
different foetal positoins in utero
cervical ripening
- Occurs in response to oestrogen, relaxin and prostaglandins breaking down cervical connective tissue
- Relative decrease in progesterone in relation to oestrogen increases the excitability of the uterine musculature as well as mechanical stretching of the uterus as the fetus grows. This increases contractility
ferguson reflex
after 36 weeks there is an increase in oxytocin receptors so the uterus respond to the release of oxytocin form the posterior pituitary, contractions cause positive feedback releasing more oxytocin and stronger contractions
uterine layers
- Perimetrium – outermost serous layer (visceral peritoneum)
- Myometrium – middle layer, interlacing layers of smooth muscle
- Endometrium – mucosal lining of uterine cavity, changes thickness during menstrual cycle
corticotropin releasing hormone
- in response to stress hypothalamus releases CRH
- travels to the anterior pituitary
- stimulates release of adrenocorticotropic hormone
- ACTH travels to adrenal cortex
- stimulate release of cortisol and other steroids that liberate energy stores to cope with the stress
- CRH increases but binding porting decreases
- CRH stimulates PG released and potentially action of oxytocin in stimulating myometrium contractions
delivery stages
- Descent
- Engagement
- Neck flexion
- Internal rotation
- Crowning
- Extension of the presenting part
- Restitution
- External rotation
- Lateral flexion
two main hormones involved in breast feeding
prolactin and oxytocin
prolactin function
- Stimulus: baby’s sucking action
- Stretch receptors in breast send impulses to the hypothalamus
- Inhibits prolactin-inhibiting hormone (PIH)
- Stimulates prolactin-releasing hormone (PRH)
- Increased PRH causes release of prolactin from anterior pituitary
- Prolactin circulates to the alveoli of the mammary gland to stimulate lactation
oxytocin function
- Once the milk is formed , oxytocin causes the ejection
- Stimulus: baby’s sucking action
- Stretch receptors in breast send impulses to the hypothalamus
- Stimulates the production of oxytocin
- Oxytocin circulates to the myoepithelial cells surrounding the mammary glands
- Allows contraction of the myoepithelial cells to force milk out of the ducts where it can be suckled by the baby
prolactin receptor theory
prolactin in the blood rises, more circulating prolactin= greater activation of prolactin receptors= greater number of primed receptor sites= greater number of functional lactocytes = max triggering of mothering response
feedback inhibtor of lactation
supply and demand establishment, breats become full due to ineffective milk removal, FIL slows synthesis by signalling to cells to stop production
hormones that change in pregnancy
oestrogen
progesterone
hCG
prolactin
relaxin
oxytocin
prostaglandins
oestrogen
produced throughout pregnancy, regulates levels of progesterone, prepares the uterus for baby (stimulates growth of uterine mass), prepares the breasts for lactation, induces synthesis of receptors for oxytocin, first 2 months = supplied by corpus luteum, then by placenta.
progesterone
prevents miscarriage builds up endometrium for support of placenta, inhibits uterine contractility – so fetus is not expelled prematurely. Increases throughout pregnancy. First 2 months = supplied by the corpus luteum.
hcg
stimulates Oestrogen / progesterone production by ovary, pregnancy test hormone – diminishes once the placenta is mature enough to take over oestrogen / progesterone production.
prolactin
produced by the anterior pituitary gland, increases cells that produce milk, prevent ovulation (unreliably), after birth, oestrogen and progesterone levels decrease, allowing prolactin to stimulate milk production (also controlled by suckling)
relaxin
high in early pregnancy, produced by ovary and placenta, helps limit uterine activity, softens cervix & involved in cervical ripening for delivery.
oxytocin
triggers ‘caring’ reproductive behaviour, responsible for uterine contractions during pregnancy and labour (drug used to induce labour).
prostaglandins
PGF2a = main one (PGE2 10x more powerful). Tissue hormones – role in initiation of labour; synthetic prostaglandins used to induce labour.
what are the domains of maternal adaptation
CVS
resp
GI
skin
biochem
CVS
Increased CO, Decreased systemic BP, Decreased total peripheral resistance, Increased uterine blood flow, Increased blood volume, Increased plasma and blood cell mass, Varicose veins
resp
: Increased alveolar ventilation
gi
Increased acid reflux, Gastroparesis (delayed emptying)
skin changes
Linea nigra, Striae gravidarum, Darkened areola
biochemical
Weight gain – maternal and fetoplacental. Obese women don’t put much weight on as have fat stores, Increased protein and lipid synthesis, Insulin resistance
what are the different follicles made
- Primordial follicle
- Small primary follicle
- Secondary/ preantral follicle
- Antral follicle then ovlulation
- Luteinization
- Corpus leuteum
- Leutolysis/regression of follicle
phases of follicular development
pre antral
antral
pre ovulatory
pre antral
gonadotrophin independent
proliferation in granulosa cells
oocyte increases in size and activity
secretes ZP
cytoplasmic processes between granulosa cells and oocyte
development of theca cell layters and blood supply
antra l
gonadotrophin dpeendent
granulosa cells secrete follicular fluid, coalesce in the antrum to increase the follicular size
synthetic activity in oocyte maintained
morphological changes in the follicle
pre ovulatory phase
lh and progesterone dependent
meitotic maturation and expulsion of the first polar body
withdrawal of cytoplasmic processes
oocyte synthesis of cortical granules
rapid expansion of volume of antral fluid
lh stimulated progesterone secretion by granulosa cells
hormone stimulated protease activity
foeta lcircualtion
blood flows right atrium to right ventricle
but also through the foramen ovale to the LA and LV
ductus arteriosus connects the pulmonary artery to the aorta and therefore bypases the lungs due to increased pressure
allows right to left shunt and by pass the lungs
umbilical vein to the lvier becomes the ductus venosus and joins the IVC
circulation at birth
decreased pulmonary resistance
increased systemic pressure
foramen ovale closes
foetal lungs
full of amniotic fluid
onset of labour increases glucocorticoids, catecholamines and ADH meaning secretion of lung fluid stops
crying clears the fluid
what stimulates production of type 2 pneumocytes
cortisol and TSH
nutritional supply to the foetus in utero
cortisol triggers storage of glycogen in the liver
when maternal glucose supply is good the insulin triggers storage of gluycose not required for growth as fat
nutritional supply at birth
decreased plasma glucos
by releasing glycogen stores but only lasts 12 hours
glucose metabolism begins
increased foetal stress increases catecholamine and glucagon
decreased insulin= mobilisation of glycogen
gluconeogenesis 2 hours after birth
by PEPCK activity, allows lactate recycling and hepatic gluconeogenesis
12 hours ketogenesis occurs
