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| Question | Answer |
| how many weeks is a normal human pregnancy | around 38 weeks |
| how is a human pregnancy split up? | into trimesters made up of 3 months each |
| in which stage of the menstural cycle is the endometrium peaking in nutrient excretion | mid luteal phase (around the phase youd expect implantation in ) |
| what hormones are high in the mid leuteal phase and why | progesterone and oestrogen which is coming from the corpus luteum to promote development of the placenta |
| is there any FSH or LH produced mid luteal phase? explain | no because progesterone suppresses the HPG axis to prevent ovulation again |
| what happens if there is no blastocyst implantation | drop in progesterone allows HPG axis to continue and the endometrium to shed |
| what is a receptive endometruim | one which is producing lots of nutreints for any implanting blastocyst |
| give the layers of the endometrium | basal layer (always present) functional layer (released then builds up again) |
| how long is the window of implantation | 4 days around day 18-24 of the cycle |
| what do the cilia on the epithelium of the endometrium do to aid implantaiotn | help transport the blastocyst to an implantation site from the filopian tube |
| does the endometrium always have cilia | no it undergoes a hugh conformational change to develop them around say 16 |
| where does fertilisation occur | in the filopian tube |
| where do the first divisions happen if fertalisation happens | in the filopean tube as its traveling down to the uterus |
| what is the foetus known as by the time it enters the uterus and why | blastocyst because it has divided enough to gain polarity |
| what needs to happen to the blastoyst before it can implant | it needs to hatch out of the zona |
| what are the apposition, adhesion and invasion stages of implantation | -apposition is blastocyst loosly associating with uterine wall - adhesion is firm attachment - invasion is enzyme driven degradation of the glycogen endometrial stroma |
| what are used for firm adhesion of the blastocyst to the endometruim | intergrins |
| what is decidulisation | the morphological change of the endometrium from fibroblast like cells to polygonal |
| what causes decidualisation | blastocyst attachment causing oedema, changes in extracellular matrix and angiogeniss |
| what inflamatory cells are involved in decidualisation | uterine NK cells |
| what are stored and produced by the endometrium after decidualisation | stored glycogen and lipids secreted prolactin, tissue factor, VEGF etc |
| give the structure oft he placenta | - large chamber at top for maternal blood flow which coats layer of placental cells - chambers of placenta - umbilical veins and arteries at top |
| does the mother and babies blood mix | no nutreints diffuses across instead |
| how is maternal and baby blood situated ? | in close contact just seperated by a few layers of tissue allowing for efficient nutreint transfer |
| how is decidualisation independant of implantatoin | is triggered by rise in progesterone from corpus luteum rather than form the blastocyst itself |
| where does the invading blastocyst develop | enclosed in a layer of uterine tissue |
| what drives cell differntiation in the blastocyst | growth factors and oxygen |
| how does the blasocyst get its nutreints | it eats into uterine tissue |
| what 3 main trophoblasts are produced by the trophectoderm | cytotrophoblasts syncytiotrophoblasts extravillious cytotrophoblasts |
| how does the placenta form a syncitium | by fusing membranes to form a single unit |
| how does the placenta develop immune tolerance | communicates with immune cells to make sure you dont get immune reaction |
| during early development how does nutreients get there? | through diffusion because tehre is no specific blood supply for the embryo |
| is the blastocyst in a low or high O2 environment | low O2 environment which is good because prevents oxidative stresss |
| what is histiotroph | extracelluar matrix which accumulates between the maternal and placenta |
| what do terminal placental vili look like | they are knoted structures with high surface area - contain blood vessel's to allow for efficient exchange |
| how do placental vili become terminally specialised | thin down to improve exchange |
| what actually is the purpose of placental vili | to allow for exchange of the maternal blood with the foetal blood |
| give the pathway of blood form mother ot baby | maternal blood comes through spiral artery and diffuses through to endometrial veins where |
| why are the maternal blood vessles remodelled | to establish as low resistance high flow blood supply to the intervillous space |
| how is the resistance reduced through spiral artery remodelling | - arteries are transformed to gain larger diameters by removing the thick muscle coat - means the arteries no longer respond to vasoactive substances |
| why do cells from trophoblast populations migrate away? | to establish immune tolerance |
| how are the maternal blood vessles remodelled | placenta eats into the spiral artery and aided by NK cells the vessles are remodelled |
| through what process is the smooth muscle of the spiral arteries lost | through apoptosis |
| what makes the remodelled spiral arteries rigid | deposition of extracellualr matrix |
| what are the major functions of the placenta | transport metabolism endocrine immune privilege |
| what happens in the haemotrophic phase around weeks 12-14 | the placenta gains a firm blood supply so no longer relies on diffusion for nutrients |
| what happens to the mother to compensate for increased oxygen and nutrient demand from the foetus | - maternal CO increases - blood volume increases increased vent rate |
| what hormone causes increased blood volume in pregnant women | progesterone |
| here is a piccy which kinda explains the nutrient exchange... idfk really | |
| what % of the oxygen delivered to the placenta is used just to support itself? | 40% |
| do drugs pass across the blood placenta barrier? | yes which is why women shouldnt drink when pregnant |
| what is thicker? the layers between the maternal blood and placental circulation or the alveoli walls in the lungs? | the placental barrier |
| is Hb conc higher in maternal or baby | 40% higher in foetal blood |
| compare the affinity of foetal Hb for O2 to adult Hb for O2 | foetal Hb has higher affinity allowing it to saturate in more hypoxic environments |
| does the O2 saturation curve of the foetus shift to the left or right? | to the left because will have higher satutarion at any given O2 |
| is the Bohr effect stronger or weaker in a foetus? | - stronger so that there is greater uptake of O2 to Hb at lower PO2's - causes higher pH of foetal blood |
| how is glucose taken up by the placenta | through insulin INSENSITIVE hexose transporters (GLUT3 and GLUT1) |
| what is glucose metabolised to in the foetis and why | metabolised to lactate which the foetus can use as a food source |
| how are amino acids transported into the fetus and why | by active transport because the fetal blood has higher conc of amino acids so is going up a conc grad |
| how does the foetus regulate the maternal amino acid metabolism | through progesterone |
| what is the primary placental barrier | the syncytiotrophoblast layer |
| give the structure of the syncytiotrophoblast layer | - highly envaginated giving high SA - lots of GLUT transporters present for glucose transport |
| how are fatty acids transported across the placental barrier | through diffusion as theyre lipid soluble |
| what can poor Exravillus invasion of maternal spiral arteries cause? | - pre-eclampsia - poor implantation (shallow) - poor immune tolerance - no modification of blood vessles - poor vili growth (smaller SA) - no breakdown of spiral arteries |
| what happens if the spiral arteries arent modified properly | - can cause high resistance low flow rate leading to lots of O2 transfer which can cause oxidative stress - the vessles still have vasoregulation causing intermittant pulsatile flow |
| compare normal to pathological placental blood flow | - normally even perfusion and nutrient transfer - pathological shows no remodelling causing high resistance flow with uneven distribution |
| what does IUGR stand for | interuterine growth restriction |
| what do vili look like during IUGR | no branches blind ended bili no terminal buds IDFK |
| compare the angiogenesis of normal vili compared to in IUGR | - normally there is good capillerisation - in IUGR there is reduced angiogenesis within the vili whcih compramises transfer |
| give the effects and symptoms of IUGR | - associated with pregnancy induced hypertension and early PE - oxygen has to transfer through simple diffusion causing foetal hypoxia - reduced fatty acid transfer |
| is glucose transfer affect by IUGR | no not normally |
| what happens to ion transfer during IUGR and whats the effect on pH | reduced ion transport causing acidosis and reduction in important ions |
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