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Reproductive system > Lecture 16- The placenta > Flashcards

Lecture 16- The placenta Flashcards

1
Q

when does placenta development start

A

Begins to develop in the second week of development

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2
Q

Week 2- the week of 2s

A
  • 2 distinct cellular layers emerge from
    • Outer cell mass
    • Inner cell mass
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3
Q

Syncytiotrophoblast

A
  • epithelial covering of the highly vascular embryonic placental villi, which invades the wall of the uterus to establish nutrient circulation between the embryo and the mother.
  • makes human chorionic gonadotropin
  • maintains corpus luteum
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4
Q
A
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5
Q
  • Outer cell mass
A
  • foetal membranes–> placenta eventually
  • made before inner cell mass
    • Syncytiotrophoblast
    • Cytotrophoblast
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6
Q

cytotrophoblast

A

is the inner layer of the trophoblast. It is interior to the syncytiotrophoblast and external to the wall of the blastocyst in a developing embryo.

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7
Q

inner cell mass become the

A

bilaminar disc

  • epiblast
  • hypoblast
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8
Q

epiblast

A
  • amniotic cavity forms above this
  • becomes the trilaminar disc

* primitive node facilitates migration and invagination of epiblast cells under the epiblast layer*

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9
Q

hypoblast

A

Yolk sac forms beneath here

Replacement of hypoblast and creation of 2 new layers forming the trilaminar disc

  • Ectoderm
  • Mesoderm
  • Endoderm
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10
Q
A
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11
Q
  • Implantation
A
  • Starts day 6
  • There has to be movement/interface between the blastocyst (early embryo) and the maternal endometrium
  • Syncytiotrophoblast move into endometrial layer
  • By day 9 Syncytiotrophoblast has embedded embryo fully into the endometrial wall
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12
Q

By the end of the 2nd week

A
  • Conceptus implanted
  • Has 2 cavities
    • Amniotic cavity and yolk sac
  • Will be
    • Suspended (via the connecting stalk)

within the supporting sac (chorionic cavity)

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13
Q

Fate of the embryonic spaces

A
  • Yolk sac disappears
  • Amniotic sac enlarges
    • Will break during labour- waters breaking
  • Chorionic sac is occupied by the expanding amniotic sac
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14
Q

What does implantation achieve?

A

Establishes the basic unit of exchange

Anchors the placenta

Establishes maternal blood flow within the placenta

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15
Q
  • Primary villi:
A

early finger-like projections of trophoblast (Syncytiotrophoblast )

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16
Q
  • Secondary villi:
A

invasion of mesenchyme into core

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17
Q
  • Tertiary villi:
A

invasion of mesenchyme core by fetal vessels

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18
Q
A
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19
Q
  • Placental membrane becomes ………….. as the needs of fetus increases (think alveolar membrane)
A
  • Placental membrane becomes thinner
  • Optimal movement of nutrients in and waste out
  • In the human one layer of trophoblast ultimately separates maternal blood from fetal capillary wall
    • But the two circulations never mix
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20
Q

What is a chorionic villus

A
  • The placenta is a specialisation of the chorionic membrane
    • Chorion frondosum
  • Finger-like projections
    • Trophoblast
    • Inner connective tissue core- fetal vessels
    • Very good for exchange
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21
Q

Implantation defects

A
  1. Implantation in the wrong place
    • Ectopic pregnancy
    • Placenta praevia
  2. Incomplete invasion
    • Placental insufficiency
    • Pre-eclampsia
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22
Q

ectopic pregnancy

A
  • implantation at site other than uterine body (most commonly the fallopian tube)
  • can be peritoneal or ovarian
  • can very quickly become life-threatening emergency
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23
Q

placenta praevia

A
  • implantation in the lower uterine segment
  • can cause haemorrhage in pregnancy
  • can require C-section delivery
24
Q

what does the endometrium become in the presence of the cocneptus

A

the decidua (controls invasion during implantatation)

25
Q

what controls invasion in implantation

A
  • The decidual reaction provides the balancing forces for the invasive force of the trophoblast
26
Q

the decidual reaction in ectopic pregnancy

A

no decidua (not endometrium)

  • no control
  • could burrow through the peritoneal space and cause massive haemorrhage
27
Q
  • If the decidual reaction is sub-optimal
A

Can lead to a range of adverse pregnancy outcomes

  • pre-eclampsia= invasion too shallow
  • premature decidual sensecence - rpeterm birth/fetal death
  • deferred implantation- placental insufficiency
28
Q

gross morphology of the fetal aspect of the placenta

A
29
Q

gross morphology of the maternal aspect of the placenta

A
  • Transport surface
  • Cobblestone appearance
30
Q

what are the cobblestoen appearances made of on the maternal aspect of the placenta

A

Cotyledons–> functional units containing chorionic villi (thin membrane allowing exchange)

31
Q

structure of chronionic villus

A

cross section would show

  • outer layer of syncytiotrphoblast
  • inner layer oc cytotorphoblast
  • enothelium of fetal capillaires
32
Q

when is the villus barrier thickest

A

first trimester

thinnes during third trimester

33
Q

thinning of the palcental barrier during pregnancy

A

Accounts for the increase in oxygen and nutrients needs of foetus overtime

34
Q

Umbilical cord vessel and fetal circulation

*

A
  • Two umbilical arteries
    • Deoxygenated blood from fetus to placenta
  • One umbilical vein
    • Oxygenated blood from placenta to fetus
35
Q

endocrine function of the placenta

A
  • Protein
    • HCG- human chorionic gonadotrophin
  • Steroid
    • Progesterone
    • oestrogen
      • when the placenta takes over from the corpus luteum
36
Q

function of Human chorionic gonadotrophin (hCG)

A
  • Produced during the first 2 months of pregnancy
  • Supports the secretory function of the corpus luteum (oestrogen and progesterone- which will then be produced by the placenta)
37
Q

why if HCG pregnancy specific

A
  • Produced by Syncytiotrophoblast therefore is pregnancy specific (pregnancy test marker)
  • excreted in maternal urine
38
Q

possible diagnosis when HCG

A
  • Trophoblast diseases cancers derived from the trophoblast  up regulation of hCG marker for cancer
    • Molar pregnancy (hydatidiform mole)
    • choriocarcinoma
39
Q

Placental steroid hormones

A
  • Progesterone and oestrogen
  • Responsible for maintaining pregnant state
  • Placental production taken over from the corpus luteum at the 11th week
40
Q

Placental hormones influence maternal metabolism : Progesterone

A

increased appetite

41
Q

Placental hormones influence maternal metabolism : HCG

A
  • increases glucose availability to fetus
42
Q

Transport function of the placenta

A
  • Simple diffusion
  • Facilitated diffusion
  • Gas exchange
  • Active transport
  • Transfer of passive immunity
43
Q
  • Simple diffusion
A
    • Molecules moving down conc gradient
      * Water
      * Electrolytes
      * Urea and uric acid
      * Gases
44
Q
  • Facilitated diffusion
A

Applies to glucose transport

45
Q
  • Gas exchange
A
  • Simple diffusion
  • Flow-limited (need good blood supply), not diffusion limited
  • Fetal O2 stores are very small therefore maintenance of adequate flow is essential (contractions can limit fetal placental flow)
46
Q
  • Active transport
A
  • Transporters expressed in Syncytiotrophoblast
    • Amino acids
    • Iron
    • Vitamins
47
Q
  • Transfer of passive immunity
A
  • Fetal immune system is immature
  • Receptor-mediated process, maturing as pregnancy progresses
  • Immunoglobulin class-specific
  • IgG only
    • IgG conc in fetal plasma exceeds those in maternal circulation
48
Q

summary of blood flow and nutrient transport between the fetus and mother

A

umbilical arteries- low oxygen

umbilical veins- high oxygen

49
Q
  • The placenta is not a true barrier
A
  • Teratogens can access the fetus via the placenta
  • Unintentional outcomes from physiological process
    • Haemolytic disease of the new-born secondary to rhesus incompatibility of mother and the fetus
50
Q

Harmful substances and the placenta

A
  • Thalidomide
    • Limb defects
  • Alcohol (small molecule can diffuse across placenta)
    • Foetal alcohol syndrome (FAS)
    • Alcohol related neurological delay(ARND)
  • Therapeutic drugs
    • Anti-epileptic drugs
    • Warfarin
    • ACE inhibitors
  • Drugs of abuse
    • Dependency in the fetus and new-born
  • Maternal smoking
    • Intrauterine growth deficiency
51
Q

Teratogenesis

A

timing is key

52
Q
  • Pre-embryonic
A
  • lethal effects
53
Q

Embryonic

A
  • ++ sensitive
  • Narrow window for some systems
54
Q

Fetal

A
  • +/- sensisitve
  • After embryonic period, risk of structural defects very low except CNS
55
Q

transplacental infections

A

brucella species

listeria monocytogenes

mycobacterium tuberculosis

leishmania spp

parvovirus

rubella

varicella

cytomegalovirus

malaria (paslmodium falciparum)

Reproductive system (28 decks)

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