Placental Function Flashcards

1
Q

Where does the placenta come from?

A

• Begins to develop in the second week of development
• Early development there is focus on ensuring development of the “fetal membranes”
– i.e. the sacs supporting the embryo/fetus
– and the placenta
• There cannot be a healthy pregnancy without a healthy placenta - starts from process of implantation - weds to be just right

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2
Q

Decsribe the beginning of implantation

A

Blastocyst hatches from within zona pelluicda. Outer cell mass contact with endometrium. Syncitioprophoblast contact endometrium surface epithelium. Entire conceptus buried in endometrium by week 2 . Gives acces to glands and blood vessels

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3
Q

What happens by the end of week 2

A
• the conceptus has implanted 
• the embryo and its  two cavities
– amniotic cavity &
– yolk sac will be
• suspended
– connecting stalk within a 
• supporting sac
– chorionic cavity
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4
Q

Wat is the fate o the embryonic sacs

A

• The yolk sac disappears • The amniotic sac enlarges
• The chorionic sac is occupied by the expanding amniotic sac
Amniotic sac warapped around embryo . Grows with embryo. The amniotic sac grows to fill space in chorionic sac. Given amniochorion membrane (this ruptured in labor)

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5
Q

What does implantation achieve

A

• establishes the basic unit of exchange - the chorionic villus - folds of chorionic membrane to give big SA for transport
– primary villi: early finger-like projections of trophoblast
– secondary villi: invasion of mesenchyme into core
– tertiary villi: invasion of mesenchyme core by fetal vessels
• anchor the placenta
• establish maternal blood flow within the placenta

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6
Q

Decsribe implantation continued

A

• implantation is interstitial
– the uterine epithelium is breached and the conceptus implants within the stroma
• the placental membrane becomes progressively thinner as the needs of the fetus increase
• in the human one layer of trophoblast ultimately separates maternal blood
from fetal capillary wall - minimise barrier to 2 cellular layers - optimum exchange
– But the two circulations never mix (foetus is genetically distinct from mother)

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7
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
Cytotrophobast are a stem cell layer for sycitiotrophoblast 0 they will merge to keep expanding the syncitiotopphoblast.  Then get mesenchymal in the core of villi - mesoderm derivatives - fetal capillaries begin to develop in the centre of chorionic villi.
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8
Q

What are plantation defects

A
• I Implantation in the wrong place
– Ectopic pregnancy
– Placenta praevia 
• II Incomplete invasion
– placental insufficiency
– pre-eclampsia
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9
Q

What is an ectopic pregnancy and placenta prevail

A

 implantation at site other than uterine body (most commonly Fallopian tube) - barrier to zygote
 can be peritoneal or ovarian
 can very quickly become life- threatening emergency

 implantation in the lower uterine segment
 can cause haemorrhage in pregnancy
 can require C-section delivery

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10
Q

How is invasio controlled

A

• Transformation of the endometrium over the course of implantation in the presence of a conceptus
– Becomes the decidua
Interaction between trophoblast and decidua
• The decidual reaction provides the balancing force for the invasive force of
the trophoblast - balance between invasion and managing invasive force. Checks invasion is sufficiently deep to maintain pregancy, but also makes sure it doesnt go too far
– ectopic pregnancy = no decidua therefore no control
• If the decidual reaction is sub-optimal
– Can lead to a range of adverse pregnancy outcomes

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11
Q

What are examples of how invasion goes wrong

A

See slide 0 Shallow invasio - over zealous decidual reaction - preeclampsia -
When trophoblast invades too far, into myometrium - placenta accretion

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12
Q

Describe the gross morphology of a placenta

A

See slide

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13
Q

Describe the structural changes of the chorionic villus between. The second and thirst trimester

A

Fist trimester - thicker barrier - more layers to cross - lots of cytorophoblast ready to grow s in TIII - placenta stil growing.
By third trimester - need barrier optimised and thinner - get rid of complete cytoprophoblast layer - dotted around to repair hold. Only a few. Eliminates one cellular layer. Then capillaries pushed out to edge of villi, 2 cellular layers up against each other. Minimise barrier for transport a

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14
Q

Decsribe how maternal blood contacts the chorionic villus

A

Thick main stem villi - branch out. At the tip of the villus trees there are anchoring. Villi - open ended tip - spill cytotrophoblast cells out of tips to create big wide trophoblast cell around placental membrane around amniochorion - enclose conceptus within decidua.. endometrial veins and arteries eel endometrium. These vessels are transformed into high flow low resistance circulation - hey spill maternal blood into blood lake” in cotyledon.

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15
Q

Describe the fetal circulation vessels

A

• Two umbilical arteries
– Deoxygenated blood from fetus to placenta
• One umbilical vein
– Oxygenated blood from placenta to fetus
High pO2 in maternal blood lake, low in fetal circulation.

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16
Q

What are hormones reduced by the placenta

A

Steroid hormones - produced by placentas - takes over from corpus luteum:

  • progesterone
  • oestrogen

Protein hormones:
human chorionic gonadotrophin (hCG) human chorionic somatomammotrophin human chorionic thyrotrophin
human chorionic corticotrophin

17
Q

What is the role of hcg in pregnancy

A

Maintains corpus luteum until placenta can take over
• produced during the first 2 months of pregnancy
• supports the secretory function of corpus luteum
• produced by syncytiotrophoblast therefore is pregnancy specific
• excreted in maternal urine therefore used as the basis for pregnancy testing
• trophoblast disease
– molar pregnancy (hydatidiform mole)
– choriocarcinoma

18
Q

What is the role of steroid hormones

A
  • progesterone and oestrogen
  • responsible for maintaining the pregnant state - suppression of hpo axis - development of Mary glans - preparing for both of baby
  • placental production takes over from corpus luteum by the 11th week
19
Q

How do placental hormones influence maternal metabolism

A

• Progesterone
– increased appetite - fat stores to help lactation
• hCS / hPL
– increases glucose availability to fetus - mothers tissue sbecome insulin resistance - glucose crosses placenta very quickly and easily

20
Q

What are the transport function of the placenta

A

• Simple diffusion
– molecules moving down a concentration gradient
• water • electrolytes • urea & uric acid • gases
• Facilitated diffusion
– applies to glucose transport

21
Q

Decsribe gas exchange in the placenta

A

• simple diffusion
• flow-limited, not diffusion-limited - need to make sure flow is optimised
• fetal O2 stores, are small therefore maintenance of adequate flow essential
• NB!!
– adequate uteroplacental circulation

22
Q

Decsribe active transport in the placenta

A

• specific “transporters” expressed by the syncytiotrophoblast
– amino acids
– iron
– vitamins

23
Q

Decsribe the transfer of passive immunity

A

• fetal (and newborn) immune system is immature
• receptor-mediated process, maturing as pregnancy progresses
• immunoglobulin class-specific
• IgG only
• IgG concentrations in fetal plasma exceed those in maternal circulation
Oly receptors for IgG
Foetus “borrows” antibodies from mother. As pregnancy proceeds, much more immunoglobulins cross placenta

24
Q

Describe the basis of the pathophysiology of placental transport

A

• the placenta is not a true “barrier”
• teratogens can access the fetus via the placenta - Teratogens = agents athat can interfere with normal physiological processes
• unintentional outcomes from physiological process
– Haemolytic disease of the newborn secondary to Rhesus incompatibility of
mother and fetus
Transfer of antibodies - anti thesis antibodies ban go across placenta and trigger destruction of RBCs in the baby

25
Q

What are harmful substances to the placenta

A

• thalidomide
– Limb defects - stops limb buds from growing to whole length
• Alcohol
– FAS and ARND
— alcohol can go straight through placenta
• therapeutic drugs
– Anti-epileptic drugs
– Warfarin
– ACE inhibitors
• drugs of abuse eg opioids, cocaine, etc, transported across placenta a
– Dependency in the fetus and newborn
• maternal smoking - not necessarily teratogen, but can have negative effect on placenta

26
Q

Scribe teh timing of teratogenesis

A
• Timing is key 
• Pre-embryonic
– lethal effects 
• Embryonic (weeks 3-8)
– ++ sensitive
– narrow windows for some systems 
• Fetal
– +/- sensitive 
- less bc structures just growing and maturing lower risk of structural defects 
• After embryonic period, risk of structural defects very low 
– Except CNS
27
Q

Describe infectio in pregnancy

A

See slide