Placenta

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  • Created by: Becca
  • Created on: 29-12-13 17:47
What are the functions of the placenta?
Movement of essential nutrients/O2->baby/CO2->mum, barrier between mum & embryo (protection from infection, phagocytosis of unwanted material), functions as endocrine organ, helps produce amniotic fluid to cushion baby & maternal recognition of baby
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What are the two types of materno-foetal transport?
Diffusion: blood gases/Na/H2O/electrolytes/urea/fatty acids/bilirubin/steroids. Active transport: hexose sugars/amino acids/water soluble vitamins/nucleotides/cholesterol/Ca/glucose (foetus has little capacity for gluconeogenesis)
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What does receptor transport involve? Give examples
Mediated endocytosis & transcytosis e.g. maternal IgG using Fc receptor or iron using transferrin receptor
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What is the umbilical blood supply? How can this cause obstetric problems?
2 arteries: take de-oxygenated blood from foetus to placenta. 1 vein: takes oxygenated blood back to foetus. Problems: coiling around foetus, true knots (stop foetal circulation), cardiovascular malformations (only 1 artery forms)
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What happens during 1st trimester of placental development?
Implantation: syncytium forms, cytotrophoblast invasion, cytotrophoblast shell, achoring villi. Established materno-foetal circulation: lacuna formation, spiral artery remodelling. Development of chorionic villi & establishment of foetal circulation
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What happens during 2nd & 3rd trimester of placental development?
2nd: arborization (tree-like branching) of chorionic villi, maturity of capillary plexus, vascular pruning, blood flow regulation (no NS/lymphatics). 3rd: formation of terminal villous capillaries (maximum transport) & terminal villi (max exchange)
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What happens during vascular pruning & vessel identity?
Under influence of vascular endothelial growth factor (VEGF), angiopoietin-1, fetal blood flow & high maternal oxygen levels: artery-vein specification, smooth muscle & pericyte wrapping of endothelium, maturation of junctions (between endothelium)
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How do terminal villous capillaries & terminal villi develop?
Looped angiogenesis: in response to fetal growth, existing blood vessels elongate in restricted space leading them to coil & bulge out of villous tissue. These bulges with surrounding trophoblast are terminal villi (maximum materno-foetal exchange)
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How are terminal villous capillaries optimised for nutrient exchange?
Proximity to maternal blood, dilated lumen & abutting of syncytium with endothelium (exchange plate)
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How does the materno-foetal barrier form?
Possession of syncytial layer, continuous endothelium with restrictive intercellular tight & adherens junctions (size/charge selective, nutrients go through endothelial cells), presence of macrophages in stroma
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How does the materno-foetal barrier help transport?
Increases surface area of exchange: extensive branching of chorionic villi/vascular network, development of highly coiled terminal villous capillaries, formation of microvilli on syncytiotrophoblast, increased surface area for receptors/transporters
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How is the diffusion distance in terminal villi reduced?
Fetal capillaries dilated & close to syncytiotrophoblast (ST, elongates & thins). Close apposition of fetal endothelium to ST & reduction in stromal tissue between. Dispersal of intermediate layer of cytotrophoblasts so cant hinder diffusion pathway
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What is the mechanism behind extrusion of excess accumulated nuclei in ST to maternal circulation?
A form of nuclear apoptosis, results in aggregation & pinching off nuclei with syncytial knots into maternal circulation. Syncytial debris is phagocytosed by maternal immune cells
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What are some complications of pregnancy?
Pre-eclampsia, type 1/2 diabetes, gestational diabetes, addictions, infections (rubella, HIV etc) & maternal nutrition changes
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What does incomplete invasion lead to? What are the different types?
Miscarriages! Pre-eclampsia: shallow invasion, reduced invasion of spiral arteries, reduced maternal blood flow. Pre-eclampsia with intra-uterina growth restrictions: increase fetal vascular resistance, reduce villous branching/microvilli, small baby
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What does diabetes mellitus in pregnancy cause?
Increased placental angiogenesis & villous growth, basement membrane thickening, leaky blood vessels, maternal hyperglycaemia, fetal hyperglycemia/hyperinsulemia, fetal programming
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What are the terms for insufficient & excessive amniotic fluid?
Oligohydramnios: insufficient amniotic fluid (renal agenesis - fetal kidney is principal source of amniotic fluid). Polyhydramnios: excessive fluid (no swallowing, oesophageal atresia)
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Other cards in this set

Card 2

Front

What are the two types of materno-foetal transport?

Back

Diffusion: blood gases/Na/H2O/electrolytes/urea/fatty acids/bilirubin/steroids. Active transport: hexose sugars/amino acids/water soluble vitamins/nucleotides/cholesterol/Ca/glucose (foetus has little capacity for gluconeogenesis)

Card 3

Front

What does receptor transport involve? Give examples

Back

Preview of the front of card 3

Card 4

Front

What is the umbilical blood supply? How can this cause obstetric problems?

Back

Preview of the front of card 4

Card 5

Front

What happens during 1st trimester of placental development?

Back

Preview of the front of card 5
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