embryo implantment and foetal development Flashcards

(62 cards)

1
Q

how does the hypothalamus stimulate ovaries to release oestrogen/progesterone

A

hypothalamus releases GnRH
- hits receptors in anterior pituitary gland

APG releases LH/FSH
- stimulating ovaries to release oestrogen and progesterone

(positive feedback)

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2
Q

explain the negative feedback in the ovaries

A

with increased progesterone release from ovaries, it will inhibit APG from releasing LH/FSH (thus stop ovaries from releasing oestrogen/progesterone)

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3
Q

only follicle with most receptors chosen to fertilise

A
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4
Q

summarise the ovarian cycle, what hormones are released at what stage, what happens as a result, what gets inhibited or what gorws

A
  1. follicular phase/pre-ovulation
    - day 1-14
    - GnRH–>LH/FSH
    - FSH stimulates ovary folicles to grow
    - follicles release oesgtrogen as they grow
    - initially, increase oestrogen inhibits FSH (negative feedback)
    - but eventually HIGH level oestrogen simulates release of LH (positive feedback)
  2. ovulation
    - day 12-14
    - LH surge = dominant follicle to rupture releasing oocyte/ovum
    - oocyte travel down Fallopian tube
    (burst of follicle = decrease in oestrogen but the ovum itself will secrete oestrogen)
  3. luteal phase
    - day 15-28
    - ruptured follicle forms corpus luteum, this secretes progesterone (thickening the endometrial lining) - and oestrogen
    - progesterone and oestrogen exhibits negative feedback, inhibiting GnRH, FSH and LH
    - if no fertilisation, corpus leuteum degenerates areoung day 24 (decreasing progesterone and oestergen levels), removing the negative feedback thus cycle starts again
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5
Q

why is there need for progesterone to thicken the endometrial lining

A

to prep for implantation of fertilised egg

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6
Q

summarise 3 phases of endometrial cycle and what hormonal release causes what

A
  1. proliferative phase
    - ovarian follicles growing releasing oestrogen
    - growth of endometrium and myometrium. secretion of mucus alongside vagina and uterus
    - day 6-14
  2. secretory phase
    - progesterone softens connective tissue in prep for implantation and promotes secretion of nutrients (endometrium becomes even thicken and more vascularised)
    -oestrogen for growth of endometrium
  3. menstrual phase (if no fertilisation)
    - day 1-5
    - corpus luteum degenerates
    - progesterone/oestrogen support lost
    - uterine prostaglandins –> vasoconstriction –> tissue death
    - blood and endometrial debris lost thru vagina
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7
Q

whats the role of FSH and LH

A

FSH= recruits follicle

LH= causes ovulation

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8
Q

why is it important for the release of progesterone and oestrogen from the corpus collosum (ruptured follicle)

A

to inhibit APG from releasing FSH/LH so another follicle doesnt get recruited

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9
Q

note: fertilisation occurs in Fallopian tube. the corpus luteum is simply a structure in the ovary that forms after ovulation

A
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10
Q

explain how fertilisation causes a missed period and or morning sickness

A
  • blastocysts (early stage of embryo) releases hCG (Human chorionic gonadotropin)
  • hCG is a relaxant + relaxes gut muscles causing morning sickness

-hCG also supports the corpus luteum (which releases progesterone)

  • progesterone (also a relaxant) which maintains the womb (prevents degeneration of lining so missed period occurs)
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11
Q

explain how sperm gets into the egg and fertilises

A
  • sperm penetrates corona radiata
  • binds to ZP3 receptors
  • this triggers release of enzyme from acrosome (in head of sperm) that digests zone pellucid
  • sperm head has DNA, penetrating ovum triggering cortical reaction
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12
Q

what is corona radiata

A

outer layer of follicular (granulosa) cells that form around a developing oocyte in the ovary and remain with it upon ovulation

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13
Q

know: healthy egg membrane prevents additional sperm fertilising egg

  • certain receptors on cell membrane allows ONLY 1 sperm to enter
A
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14
Q

how long after triggering embryonic develpment does the fusion of nuclei from egg and sperm happen

A

1hr

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15
Q

how long can sperm last in females repro tract

A

5 days (but only viable for 48hrs)

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16
Q

after 4 days of fertilisation, the blastocysts develops what feature for better implantation on membrane

A

sticky

  • implantations better on side of uterus not bottom otherwise causing pain and bleeding
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17
Q

explain process of implantation/embedding of embryo into endometrium

A
  • sticky blastocysts sticks to endometrium
  • membrane of trophoblast cells disintegrate
  • endometrium makes prostaglandins increase vascularity locally, increasing nutrients in that specific area
  • embryo gets embedded into endometrium (it divides INTO membrane
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18
Q

what are trophoblasts

A

surface layer of cells of clastocytes

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19
Q

endometrium makes prostaglandins increase vascularity locally, increasing nutrients in that specific area, what do you call this modified endometrium

A

decidua

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20
Q

how long after implantation does the placenta fully develop, what does this mean

A

5 weeks

  • here embryonic heart starts pumping blood into placental villi (heart beating)
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21
Q

what is the placenta responsible for

A

delivering oxygen, nutrients and removal of waste, c02 from foetus

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22
Q

fetal part of placenta secretes hCG and progesterone

  • placenta is endocrine organ producing many hormones
A
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23
Q

the placenta is high permeable to alcohol (and drugs, disease e.g hiv), and can result to foetal alcohol syndrome

A
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24
Q

what is molar / hydatidiform mole pregnancy

A

when the fertilisation of the egg by the sperm goes wrong. This leads to the growth of abnormal cells or clusters of water filled sacs inside the womb.

(trophoblast tissue overgrows and shows as cysts)

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25
how long does it take the placenta to take over from the corpus luteum
10-12 weeks
26
what 4 things are secreted by placenta
oestrogen progesterone hCG Human placental lactogen
27
function of human placental lactose from placental
responsible for movement of glucose into embryo for growth
28
how long is average full term for growth of baby
37/38 weeks
29
3 most common congenital anomalies are: heart, neurotube defects down syndrom
30
what is a teratogen
agent or factor causing malformation of embryo
31
give some examples of a teratogen
thalidomide (causes loss of limbs) (from drugs treating skin cancer) infections (rubella, heart defect causing) alcohol drugs
32
what genetic factor affect kids
maternal age chromosomal abnormalities mutant genes
33
Down syndrome risk increases with maternal age
34
what is gastroschisis/exompholos (type of defect visible at birth)
abdominal wall doesnt close (intestines spill out)
35
what is achondroplasia
dominant inherited abnormality to convert cartilage to bone
36
what is the most critical period of development
week 3-8 (during embryo development) - very susceptible to pathogens etc - major congenital anomalies
37
define the terms ectoderm, mesoderm, endoderm (3 germ layers)
ectoderm = structure maintain contact with outside e.g nose, eyes,CNS mesoderm = peritoneal, pleural, etc endoderm = GI tract, respiratory tract, epithelial lining etc
38
neural tube defects sensitive across what period of development
3-16 weeks
39
what is neurulation
formations of neural tube - starts thickening at neural plat at cranial end of embryo
40
ectoderm folds and joins to form neural tube, what sends signals to control this
notochord - an embryonic midline structure common to all members of the phylum Chordata, providing both mechanical and signaling cues to the developing embryo
41
what 3 things may cause neural tube defects
- anti epileptic meds - maternal diabetes - hyperthermia e.g sauna
42
what medication/supplement is take to prevent neural defect
folic acid
43
what is spina bifida and its different variations
neural tube fails to close at its length - spin bifida aperta (spinal cord and nerves open to outside) - spina bifida occulta (covered with skin - spina bifida cystica / meningocele/ mylomeninocele (covered with just surrounding membrane)
44
spina bifida occulta, meningocele, myelomeningocele are the same issue increasing in severity, describe the difference
occulta = no closing of neural tube but no sac/bulge meningocele = no closing of neural tube and bulging myelomeningocele = no closing of neural tube and bulging with spinal cord and nerves in the bluge
45
what is Arnold chiari malformation
lower part of brain pushes down into spinal canal (cerebellum and brain stem pushing into foramen magnum)
46
what is hydrocephalus
accumulation fo cerebrospinal fluid in brain
47
how do you detect and diagnose nerutal tube defects - how long does it take fo ultrasound to pick it up on screen
antenatal screening - positive if elevated alpha fetoprotein levels - 12 - 20 weeks
48
what signals for segregation of brain into fore, mid,hind brain and facial development
homeobox genes / hox gene
49
what are the names for the fore, mid, hind Brian in development
fore = prosencephalon mid = mesencephalon hind = rhombencephalon
50
whats anencephaly
no closure of neural tube at top end 100% fatality
51
failure of fusion b/w maxillary prominence and inter maxillary segments during the 7th week results in what disorder
cleft lip
52
what week does the intermaxillary process form the philtrum of the upper lip
14th
53
whats frontonasal dysplasia
is a congenital malformation of the midface.
54
why are there minor anomalies occurring during metal development week 9-36?
hox gene mainly only in action during embryo development which controls many things such as facial development and Brian development/segmentation
55
what day of development does heart begin beating and blood flow
day 22-24 heart beating blood flow starts week 4
56
whats the issue with heart defects such as septal defect
mixed oxygenated and deoxygenated blood
57
what is persistent trunks arteriosus and hypopplastic left heart
- PTA congenital defect where pulmonary trunk and aorta fails to divide properly - Hypoplastic left heart syndrome is a rare congenital heart defect in which the left side of the heart is severely underdeveloped and incapable of supporting the systemic circulation
58
failure of what process during development causes syndactyly (webbed tigers)
apoptosis (programmed cell death)
59
what cells form skeletal and muscular parts of the limbs
lateral plate cells = skeletal formation myotome = muscular components
60
formation of limb buds = proliferation of somatic lateral plate mesoderm and myotome cells (stops muscle and skeletal formation)
61
formation of limbs buds secrete FGF 7/10, this stimulates what
Apical ectodermal ridge (AER) - determines pattern of limb - formation of early skeleton - muscles tendons vasculature
62
what are the following limb develpment anomalies: meromelia Amelia polydactyly triphalageal dysplasias
mero = reduction of limb Amelia = missing limb poly = extra digits tri = 3 phalangeal bones (not 2) (so as long as normal finger) dysplasia = fusion of limb/disproportional growth