REPRODUCTION Flashcards
Late luteal early follicular stage
Menstrual cycle
Low progesterone and high FSH
Mid follicular stage
Menstrual cycle
High Oestrogen = negative feedback
Low FSH
Mid cycle stage
Menstrual cycle
Oestrogen = positive feedback
Increase LH
Mid luteal stage
Menstrual cycle
Increase progesterone = negative feedback
Decrease LH & FSH
Describe the steps for follicle selection/dominant follicle
- high FSH - recruit antral follicles that are at the right stage to continue growth.
- Oestradiol levels increase and FSH levels fall
- Follicle that survives the decline of FSH becomes the dominant follicle
- As FSH fall, LH increases - dominant follicle requires LHR on GCs
Steps of ovulation
Occurs with release of cumulus oocyte complex
- Oocyte with cumulus extruded from ovary
- Follicular fluid pours into Pouch of Douglas
- Egg ‘collected’ by fimbria of fallopian tube
- Egg progresses down tube by peristalsis and action of cilia
Describe the structure of the testes
Basement membrane - primary germ cells or spermatogonia
Walls of tubule made of sertoli cells - tight junctions between = adluminal compartments.
Spaces between tubules are filled with blood and lymphatic vessels, leydig cells and interstitial fluid
Sperm stages during spermatogenesis
Spermatogonia Primary spermatocytes Secondary spermatocytes Spermatids Spermatozoa
Capacitation
Partly achieved by removing the sperm from seminal fluid. Uterine or tubal fluid may contain factors which promote capacitation
Acrosome reaction
Occurs in contact with zona cumulus complex
Acrosomal membrane on the sperm head fuses releasing enzymes that cut through the complex
Acrosin
Bound to the inner acrosomal membrane - digests the zona pellucida so the sperm can enter
What happens in endometrial proliferative phase
Stimulated by oestrogen
Stromal cell division, ciliated surface. Glands expand, increase vascularity
When endometrium >4mm induction of progesterone receptors and small muscular contractions of myometrium
What happens in endometrial secretory phase
2-3 days after ovulation, gradual rise in progesterone causes reduction in cell division.
Oedema, increase vascular permeability, arterioles contract
Myometrial cells enlarge and movement suppressed
What happens in menstruation
Prostaglandin release cause constriction of spiral arteries. Hypoxia lead to necrosis.
Vessels dilate and bleeding ensues.
Proteolytic enzymes from dying tissue.
Changes in cells lining uterine tubes
Epithelial cells - high numbers of oestrogen receptors and undergo differentiation
Cilia beat and secretory cells are active along with muscle layer contractions
After a few days exposure to progesterone the oestrogen receptors are suppressed.
What is the ectocervix covered with
Non-keratinised stratified squamous epithelium - resembling the squamous epithelium lining the vagina
Cervix follicular phase
Oestrogen in follicular phase - change in vascularity of cervix and oedema
Change in mucous
Cervix luteal phase
Progesterone cause reduced secretion and viscous mucus
Glycoproteins form mesh like structure - acts as a barrier
Cardiovascular risks of COCP
HBP
Clotting disorders
Migraines - cannot have COCP due to concerns of stroke
GI risks of COCP
Insulin resistance
Weight gain
Crohns disease
Hepatic risks of COCP
Hormone metabolisms
congenital nonhemolytic jaundice
gall stones
What does IUCD do
Copper IUCD inserted into the uterus.
Destroy spermatoza
Prevent implantation - inflammatory reaction and prostaglandin secretion as well as mechanical effect
Risks of IUCD
Miscarriage if left in situ if pregnant
Ectopic
May be expelled if incorrectly inserted
Uterus may be perforated - need to know orientation of the uterus before insertion
Contraindications of IUCD
Current pelvic inflammatory disease
Suspected or known pregnancy
Unexplained vaginal bleeding
Abnormalities of the uterine cavity
Changes in glucose in 1st trimester
Pancreatic beta cells increase in number - plasma insulin increases, fasting serum glucose decrease
Changes in glucose in 2nd trimester
hPL cause insulin resistance - less glucose in stores = increased availability in serum glucose (more crosses placenta)
Changes in CVS in pregnancy
Increase CO
Increased HR and SV
Changes in vessels in pregnancy
Increased CO and vasodilation by steroids = reduced peripheral resistance
Increased flow to uterus, placenta, muscle, kidney and skin
Stages of implantation
- Apposition
- Attachment
- Invasion
Day 7-8 in implantation time line
Blastocyst attach to the surface of decidua basalis.
Trophoblast cells assemble to form SYNCYTIOTROPHOBLAST to facilitate invasion of decidua basalis
Day 9-11 in implantation time line
Syncytiotrophoblast further invades the decidua basalis and by day 11 it is almost buried in the decidua
Day 12 in implantation time line
Decidual reaction occurs - high levels of progesterone result in enlargement and coating of the decidual cells in glycogen and lipid rich fluid.
Fluid is taken up by syncytiotrophoblast and help sustain blastocyst before placenta is formed
Day 14 in implantation time line
Primary villi form all round blastocyst
Lacunae form
Blood vessels merge with the lacunae - maternal arteries and veins grow into decidua basalis
Blood filled lacunae merge into single pool of blood = junctional zone
How are primary villi formed
Cells of syncytiotrophoblast protrude to form tree like structures
How are lacunae formed
Decidual cells between primary villi begin to clear out, leaving behind spaces
What is the junctional zone
Blood filled with lacunae merge into single large pool of blood connected to multiple arteries and veins
Day 17 in implantation/placenta time line
Foetal mesoderm cells start to form blood vessels within the villi – a basic network of arteries, veins, and capillaries. Capillaries connect with blood vessels in the umbilical cord
Villi grow and develop into chorionic frondosum.
At this point, endothelial cell wall and syncytiotrophoblast (villi) lining separate maternal and foetal RBCs
4th and 5th month of placenta timeline
Decidual septa form as they divide placenta into 15-20 regions = COTYLEDONS
Maternal spiral arteries supply blood to each cotyledon, facilitates maternal foetal exchange
Pre-eclampsia
Result in placental insufficiency – inadequate maternal blood flow to the placenta during pregnancy
Causes new onset maternal hypertension and proteinuria
Symptoms range from mild to life threatening
Characterised by the narrowing of maternal spiral arteries supplying blood to the placenta
Risk factors of pre-eclampsia
1st pregnancy
Hypertension, diabetes, obesity
Hypertension - decreased blood flow in kidney and lead to proteinuria
Pre-eclampsia + seizures = eclampsia
Cause of Placenta abruption
Degradation of maternal arteries supplying blood to the placenta. Degenerated vessels rupture causing haemorrhage and separation of the placenta
Complications - maternal of placenta abruption
Hypovolemic shock
Sheehan syndrome
Renal failure
Disseminated intravascular coagulation (from release of thromboplastin)
Complications - foteal of placenta abruption
Intrauterine hypoxia and asphyxia
Premature birth
Placenta previa
Placenta implants in lower uterus, fully or partially covering the internal cervical os
Associated with increased chances of pre-term birth and foetal hypoxia
Risk factors of placenta previa
Previous caesarean delivery Previous uterine/endometrial surgery Uterine fibroids Previous placenta previa Smoking and recreational drug use
Hormonal changes in pregnancy
Low ratio of oestrogen: progesterone to supress maturation of other follicles in the ovary
Placenta synthesised oestrogens from foetal androgens from foetal adrenal cortex
Placenta synthesised progesterone from maternal cholesterol
Spermatogonia
Germ cell on basement membrane, capable of mitotic or meiotic division into spermatocytes or more spermatogonia by mitosis. They are diploid
Primary spermatocytes
Move into adluminal compartment and duplicate their DNA into sister chromatids which exchange genetic material before entering meiosis I. 46XY diploid
Secondary spermatocytes
Have undergone meiosis I to give 23X + 23Y haploid number of chromosomes arranged as sister chromatids
Spermatids
Meiosis II occurs to give 4 haploid spermatids. Round spermatid to elongated spermatid differentiation
Spermatoza
Mature sperm extruded into the lumen
Sexual determination
Genetically controlled process dependent on the switch on the Y chromosome
Chromosomal determination of male or female
Sexual differentiation
Process by which internal and external genitalia develop as male or female
Primordial germ cells become
Sperm or oocytes
Primitive sex cords become
Sertoli cells or granulosa cells
Mesonephric cells become
Leydig cells or theca cells
Gonadal dysgenesis - AIS
Testosterone is made but has no effect
Testis form and make AMH - regression of Mullerian ducts
Complete AIS
Appear female at birth but is XY - undescended testes
Primary amenorrhoea and lack of body hair
5 alpha reductase deficiency
Testosterone made but not DHT
Testes form and make AMH - Wolffian ducts develop
External structures do not develop
AUTOSOMAL RECESSIVE
Turner syndrome
Females missing X chromosome
Uterus and tubes are present but small, other defects in growth and development
Congenital adrenal hyperplasia (CAH)
No SRY, No testes, No AMH
Masculinised external genitalia, but androgen levels not high enough to save Wolffian ducts
Possibility of ‘salt wasting’ due to lack of aldosterone
Pathway block leading to CAH
Failure to synthesise cortisol - (by 21 hydroxylase)
No negative feedback so CRH will stimulate pituitary to release ACTH
Regulation of uterus by neurotransmitter
Sympathetic innervation
Expression of alpha and beta adrenoreceptors
alpha adrenoreceptor agonist = contraction
beta adrenoreceptor = relaxation
Regulation of uterus by sex hormones
Progesterone inhibit contraction
Oestrogen increases contraction
Hormones in a non pregnant uterus
Weak contractions
Strong contractions during menstruation - decrease progesterone, increase prostaglandin
Hormones in pregnant uterus
Weak and uncoordinated contraction - high progesterone
Strong and coordinated contraction at parturition - high oestrogen
Oestrogen/progesterone ratio during parturition
Increases
Oestrogen increases while progesterone decreases gap junction expression in myometrium
Oestrogen/progesterone also found in ICC
Regulation by prostaglandins
Myo- and endo-metrium synthesise PGE2 and PGF2α – promoted by oestrogens
Both prostaglandins induce myometrial contraction
Role in dysmenorrhoea (severe menstrual pain), menorrhagia (severe menstrual blood loss), pain after parturition - NSAIDs are effective – decreased contraction and pain
Act together to:
Coordinate increased frequency/force of contractions
Increase gap junctions
Soften cervix
Prostaglandin analogues
dinoprostone (PGE2)
Carboprost (PGF2α)
Misoprostol (PGE1)
Uses of prostaglandin
Induction of labour - before term
Postpartum bleeding
Softening of cervix
Concerns of prostaglandins
Dinoprostone can cause systemic vasodilation
Potential for CVS collapse
PGs - hypertonus and foetal distress
What is oxytocin
Non-peptide hormone synthesised in hypothalamus and released from posterior pituitary gland
Effective at term
Regulation by oxytocin
Oestrogen released after parturition produce - increase oxytocin release, oxytocin receptors and increase gap junctions.
Oxytocin also synthesises prostaglandins
Pharmacological actions of sythetic versions of oxytocin
Low conc. of oxytocin analogue – increase frequency and force of contractions.
High concentrations cause hypertonus – may cause foetal distress
Synthetic versions of oxytocin
Syntocinon and pitocin
Uses of synthetic versions of oxytocin
Induction of labour at term – does not soften cervix
Treat/prevent post-partum haemorrhage
Syntometrine – oxytocin (rapid)/ergot (prolonged) combination
Action of ergot
Powerful and prolonged uterine contractions - but only when myometrium is relaxed
Mechanism of ergot
Stimulate alpha adrenoreceptors and 5HT receptors
Uses of ergot
Post partum bleeding - not induction
Myometrial relaxants
May be used in premature birth - delay delivery by 48hrs
Beta adrenoreceptor stimulants
Salbutamol
Relax uterine contractions - direct action to myometrium
Used to reduce strength of contraction in premature labour
May occur as a side effect of drugs used in asthma
Ca2+ channel antagonist
Nifedipine
Used in hypertension
Or mg sulfate
Oxytocin receptor antagonists
Retosiban
COX inhibitors
NSAIDs
What to use for induction of labour
Oxytocin
What to use for Induction labour/termination in early term
Prostaglandins
What to use for post partum bleeding
Prostaglandins
Oxytocin
Ergots
What to use to prevent premature birth
Beta 2 adrenoreceptor agonists
Ca2+ channel blockers, Mg sulphate
Oxytocin inhibitors
