Lecture 16- The placenta Flashcards
1
Q
when does placenta development start
A
Begins to develop in the second week of development
2
Q
Week 2- the week of 2s
A
- 2 distinct cellular layers emerge from
- Outer cell mass
- Inner cell mass
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
4
Q
A
5
Q
- Outer cell mass
A
- foetal membranes–> placenta eventually
- made before inner cell mass
- Syncytiotrophoblast
- Cytotrophoblast
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.
7
Q
inner cell mass become the
A
bilaminar disc
- epiblast
- hypoblast
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*
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
10
Q
A
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
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)
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
14
Q
What does implantation achieve?
A
Establishes the basic unit of exchange
Anchors the placenta
Establishes maternal blood flow within the placenta
15
Q
- Primary villi:
A
early finger-like projections of trophoblast (Syncytiotrophoblast )
16
Q
- Secondary villi:
A
invasion of mesenchyme into core
17
Q
- Tertiary villi:
A
invasion of mesenchyme core by fetal vessels
18
Q
A
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
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
21
Q
Implantation defects
A
- Implantation in the wrong place
- Ectopic pregnancy
- Placenta praevia
- Incomplete invasion
- Placental insufficiency
- Pre-eclampsia
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
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
what controls invasion in implantation
* The decidual reaction provides the balancing forces for the invasive force of the trophoblast
26
the decidual reaction in ectopic pregnancy
no decidua (not endometrium)
- no control
- could burrow through the peritoneal space and cause massive haemorrhage
27
* If the decidual reaction is sub-optimal
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
gross morphology of the fetal aspect of the placenta
29
gross morphology of the maternal aspect of the placenta
* Transport surface
* Cobblestone appearance
30
what are the cobblestoen appearances made of on the maternal aspect of the placenta
Cotyledons--\> functional units containing chorionic villi (thin membrane allowing exchange)
31
structure of chronionic villus
cross section would show
- outer layer of syncytiotrphoblast
- inner layer oc cytotorphoblast
- enothelium of fetal capillaires
32
when is the villus barrier thickest
first trimester
thinnes during third trimester
33
thinning of the palcental barrier during pregnancy
Accounts for the increase in oxygen and nutrients needs of foetus overtime
34
**Umbilical cord vessel and fetal circulation**
*
* Two umbilical arteries
* Deoxygenated blood from fetus to placenta
* One umbilical vein
* Oxygenated blood from placenta to fetus
35
endocrine function of the placenta
* **Protein**
* HCG- human chorionic gonadotrophin
* **Steroid**
* Progesterone
* oestrogen
* when the placenta takes over from the corpus luteum
36
**function of Human chorionic gonadotrophin (hCG)**
* 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
why if HCG pregnancy specific
* Produced by Syncytiotrophoblast therefore is pregnancy specific (pregnancy test marker)
* excreted in maternal urine
38
possible diagnosis when HCG
* Trophoblast diseases cancers derived from the trophoblast up regulation of hCG marker for cancer
* Molar pregnancy (hydatidiform mole)
* choriocarcinoma
39
**Placental steroid hormones**
* Progesterone and oestrogen
* Responsible for maintaining pregnant state
* Placental production taken over from the corpus luteum at the 11th week
40
**Placental hormones influence maternal metabolism : Progesterone**
increased appetite
41
**Placental hormones influence maternal metabolism** : HCG
* increases glucose availability to fetus
42
**Transport function of the placenta**
* **Simple diffusion**
* **Facilitated diffusion**
* **Gas exchange**
* **Active transport**
* **Transfer of passive immunity**
43
* **Simple diffusion**
* * Molecules moving down conc gradient
* Water
* Electrolytes
* Urea and uric acid
* Gases
44
* **Facilitated diffusion**
Applies to glucose transport
45
* **Gas exchange**
* 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
* **Active transport**
* Transporters expressed in Syncytiotrophoblast
* Amino acids
* Iron
* Vitamins
47
* **Transfer of passive immunity**
* 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
summary of blood flow and nutrient transport between the fetus and mother
umbilical arteries- low oxygen
umbilical veins- high oxygen
49
* The placenta is not a true barrier
* 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
**Harmful substances and the placenta**
* **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
## Footnote
**Teratogenesis**
timing is key
52
* Pre-embryonic
* lethal effects
53
Embryonic
* ++ sensitive
* Narrow window for some systems
54
Fetal
* +/- sensisitve
* After embryonic period, risk of structural defects very low except CNS
55
transplacental infections
brucella species
listeria monocytogenes
mycobacterium tuberculosis
leishmania spp
parvovirus
rubella
varicella
cytomegalovirus
malaria (paslmodium falciparum)
