Fertilisation, pregnancy and birth Flashcards

1
Q

Features of the oocyte

A
  1. Expanded cumulus cell matrix, to aid passage along fimbria
  2. Zona pellucida, with ZP3 surface receptor for sperm
  3. Stalled in second meitotic division
  4. Able to decondense sperm nucleus
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2
Q

The oviduct features

A
  • High levels of muscular activity
  • Fimbriated and closely opposed ciliated epithelia
  • Secretions produced possibly to provide for pre-implantation embryo
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3
Q

Sexual behaviour in men

A
  1. Arousal: arteriolar vasodilation via parasympathetic NO and cGMP. Veins compress and pressurised blood stiffens penis = erection.
  2. Plateau: distension of penis and teste, mucus bulbourethral gland secretion.
  3. Orgasm: contraction of vas seminal vesicles, prostate and relaxation of urethral sphnicter, under sympathetic control = emission. Then ejaculation as perineal striated muscle and anal sphincter rhythmically contract
  4. Refractory period and resolution to non-aroused state.
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4
Q

Viagra

A

Sildenafil = competitive inhibitor of phosphodiesterase 5 => maintenance of cGMP and specific to penis. Maintained vasodilation and hence erection.

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5
Q

Sperm features

A
  1. Haploid DNA
  2. Flagellating tail, propelling sperm at about 1-3mm/min (female sperm are slightly larger so somewhat slower)
  3. Receptors for ZP and oocyte
  4. Able to fuse and activate as egg (have to be galactosyltransferase modified in the epididymis)
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6
Q

Recognition of egg

A

ZP3 recognised by receptor on sperm head. Binding triggers acrosome reaction. Hydrolases released and contents will break down surrounding ZP. Stimulated by ANP and progesterone from cumulus cells. Sperm penetration.

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7
Q

Cortical reaction

A

PLC zeta (a specific sperm phosphoplipase) is released into the oocyte, acting via IP3 pathway to stimulate Ca2+ oscillations, which then stimulates cortical granule exocytosis. This blocks polyspermy (coagulating the ZP), further meitotic division and pronuclear development.

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8
Q

Proliferative phase

A

During oestrogen release in follicular phase

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9
Q

Secretory phase

A

Due to progesterone release following ovulation.

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10
Q

Blastocyst attachment

A
  • Uterine mucins down-regulated
  • Trophoectoderm attaches via heparan sulphate proteoglycans
  • Trophoectoderm undergoes EMT
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11
Q

Decidualisation

A

-Invasion of blastocyst into uterine wall triggers decidual reaction
- Basal lamina broken down in the endometrial stroma
- Becomes oedematous and highly vascular and glandular
HOXa10 required in stroma for decidualisation.
-? Triggered by progesterone

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12
Q

hCG secretion

A

Preserves progesterone secretion.

  • Initially by the corpus luteum
  • Then by syncytiotrophoblast, still stimulating progesterone production in a positive feedback loop.
  • Particular hCG variations are associated with different conditions. eg. hyperglycosylated hCG-H is potentially a marker in individuals with Down’s Syndrom.e
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13
Q

Pregnancy time frames

A

40 weeks from last menstrual period (normally 38 gestation). Divided into trimesters but really 3 phases:

1st: below 10 days
2nd: 3-8 weeks
3rd: 8 weeks to term

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14
Q

Requirements for successful pregnancy

A
  1. Fetal respiration, nutrition and excretion
  2. Control of placental blood flow
  3. Uterine partial quiescence during development
  4. Prevent maternal rejection of fetus
  5. Control of hormones reaching the fetus
  6. Preparation of uterine and breast for birth and post-birth
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15
Q

Braxton Hick’s contractions

A

False uterine spasms during pregnancy. Asynchronous and occur as cervix softens via collagenolysis.

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16
Q

Phases of fetal nutrition

A
  1. Yolk proteins in oocyte
  2. Secretions of oviduct and uterus prior to implantation
  3. Digestion of specialised endometrium
  4. Products from maternal blood via placenta.
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17
Q

Structure of placenta

A

Analogous to many bunches of grapes dropped into bath of maternal blood = fetal villi structures bathed in maternal blood.
Disc shaped, with cotyledons attached to mother, with very smooth surface.
Disc shaped, although depending on development of cotyledons around spiral arteries.
Normally found on upper posterior aspect of uterine wall.

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18
Q

Developmental of placental villi

A
  1. PRIMARY: cytotophoblast growth attachments into endometrial wall
  2. SECONDARY: out-growth of mesodermal core
    TERTIARY: invasion of fetal blood vessels
    COMPLEX PLACENTAL VILLI: many branches and eventual convoluted knot with terminal dilation where flow is slow.
    Cytotrophoblast and syncytiotrophoblast thin to increase efficiency on transpoirt.
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19
Q

Chorionic somatomammotrophin

A

= placental lactogen. Produced by fetus.

GH and PRL activity. COnverts glucose to FFas and ketones used by placenta and fetus

20
Q

Relaxin

A

Produced by fetus. Relaxes pelvic joint, ligaments and uterus. Role in angiogenesis?

21
Q

Fetal protection from steroids

A

Placental 11beta-OH steroid dehydrogenase protects fromo glucocorticosiuds before term. Otherwise long-term stress response in fetus in adult life.

22
Q

Other maternal hormone changes

A

Increased size of pituitary (pressure on optic chiasm), thyroid and adrenal glands.
INcreased cortisol, T3, T4, calcium homeostasis control. Increased oestrogen and progesterone.

23
Q

Oestrogen in pregnancy

A
  • Growth of uterus
  • Breast development
  • Connective tissue made more pliable
  • Water retention
  • Sodium retention
  • Vasodilation
24
Q

Progesterone in pregnancy

A

-Formation of breast alveoli
-Quiescence of smooth muscle activity generally = nausea, constipation, reduced bladder and ureter tone.
-Reduced diastolic BP
Heart burn due to relaxation of cardiac sphincter
Altered taste and appetite.

25
Q

Increasing placental efficiency (as fetal growth outstrips)

A
  • Branching of villi and brush border on syncytiotrophoblast to increase SA
  • Decreasing villous diameter from 150um in early pregnancy to 40um in later
    Thinning of placental barrier to only 1-2um in late pregnancy.
26
Q

Massive obstetric haemorrhage

A

Largest direct cause of maternal death. 2003-2009, 661,000 women died from haemorrhage worldwide.

27
Q

Fetal growth restriction

A

Individual growth potential failed to be achieved.
-possivle intrauterine fetal death
- cerebral palsy
preterm delivery
poor neurodevelopment
Neurological and cardiovascular sequelae in adulthood

28
Q

Pre-eclampsia

A

Multisystem disorder, caused by placental dysfunction, and possible autoimmune reaction - restricts fetal growth, and hypertension, renal issues, oedema, heptaic problems and seizures in mother.

29
Q

Excessive implantation

A

May be in uterus, or spread throughout body (choriocarcinoma caused by hydatiform mole).
- Deep invasion = placenta percreta, or increta. Increasing due to high caesarians and invasion into scar tissue.

30
Q

Hormones decreasing contractility

A

Progesterone and relaxin

31
Q

Hormones increasing contractility

A

Oestrogens, prostaglandins, oxytocin

32
Q

Requirements for parturition (birth)

A

Fetus should be appropriately mature, and have functioning lungs, gut and liver.
Uterus must change from relaxed state to forceful expulsive contractions
Cervix must change allowing fetal passage.

33
Q

Uterus relaxation -> contraction

A

Dependent on the balance between oestrogens and progesterone.
Considerable protein remodelling, particularly in increasing intracellular Ca2+ and gap junctions so contraction can occur in synchrony (muscle more like cardiac than smooth).
Uterine smooth muscle cells must have appropriate receptors on which contractile ignals (prostaglandins E and F and oxytocin) can act.

34
Q

Discovery of parturition signals.

A

Experiments in sheep, as first noted that sheep eating toxic weed caysed non delivery of fetus, and atrophy of adrenal glands. Sheep have linear progression as fetal hypothalamus produces CRH, then fetal cortisol, stimulating a rise in placental oestrogen, so a fall in progesterone and increase in prostaglandins. Sheep fetus determines time of birth rather than the mother. More complicated in humans as hCG is involved and there are multiple feedback signal.

35
Q

Positive feedback loop for parturition in humans

A

Fetal hypothalamus and placenta synthesise CRH.
Stimulates fetal ACTH production.
ACTH acts at fetal adrenal glands leading to producition of cortisol and DHEA.
Cortisol matures fetal lungs and livers, and increases placental CRH.
DHEA converted to oesrtogens in placenta, stimulates oxytocin receptor upregulation, formation of gap junctions and synthesis of prostaglandins.

36
Q

Pro-labour signals

A

Switch from anti-inflammatory to pro-inflammatory cytokines.
Increased oestrogen
Inflammation due to increased prostaglandins
Mechanical irritation of the cervix.

37
Q

Stages of labour

A

0 uterine tranquility and refraction
1 uterine awakening, initiation of parturition to complete cervical dilation.
2 active labour, from complete cervical dilation to delivery of newborn
3 delivery of fetys to placental expulsion and final contraction

38
Q

The Ferguson reflex

A

Once cervix is stretched, very hard to halt loop due to positive feedback loop unless the placenta is removed.
Stretch of cervix -> oxytocin secretion -. uterine contraction -> movement of fetus further into cervix.

39
Q

Development of breast ducts and alveoli

A

Duct and alveoli growth driven by oestradiol, GH and progesterone.
From mid-pregnancy, alveoli grow and form lumen.
Oestrogen and progesterone suppress milk formation an promote growth.

40
Q

Hormones in breast lactation system

A

Oestrogen: stimulated milk duct system to grow and differentiation. High levels inhibit lactation.
Progesterone: influences growth size in alveoli, also inhibitoroy to milk production
Prolactin: contributes to increased growth and differentiation of ductal structures
Human placental lactogen: important in breast, nipple and areola growth.

41
Q

Colustrum

A

the initial secretion after childbirth = thin, yellow milk-like fluid which is rich in protein and carbohydrate, but low in electrolytes and fat (as neonatal gut cannot handle) rich in IgM and IgA.

42
Q

Components and production of milk

A

Lactalbumin, casein synthesised in RER. Lactose and salts also secreted into vesicles.
Amino acids, glucose/galactorse + water and ions.
Fat droplets form in SER, then IgA and IgM secreted in via transcytosis.

43
Q

Milk ejection reflex

A
  1. SUckling stimulus from nipple conveyed by afferent nerves to oxytocin and dopamine neurons in the hypothalamus
  2. Oxytocin release from the posterior pituitary causes myoepithelial cells to eject milk
  3. Dopamine reduction increases prolactin secretion, so milk production increases
44
Q

Oxytocin as a pheromone

A

Promotes bonding between mother and child

45
Q

Lactational amenhorraea

A

Prolactin secretion inhibits GnRH from the hypothalamus and so LH and FSH from posterior pituitary. Hence ovulation suppressed.

46
Q

Galactorrhea

A

Production of milk unrelated to child birth. Potentially due to lactotroph tumours, or antipsychotics (eg haloperidol) which suppress dopamine release.