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Pregnancy

From Mediwikis

Events Leading up to Pregnancy

Oogenesis

This is the process of creating female gametes. Oogonia transform into millions of primary oocytes before birth which die over time and are never replaced. Every month a primary oocyte reaches maturity. This is the enlarged primary oocyte. Over the course of Meiosis it divides twice (meiosis) into a total of four cells. The daughter cells either become the next stage in development for the oocyte or become polar bodies which are discarded. Oestrogen dominance establishes which cell is chose to be the egg and which cells are polar bodies i.e. the cells which produce the most oestrogen survive. The first division results in either a secondary oocyte or the first polar body. Both undergo division again however the first polar body only produces second polar bodies while the secondary oocyte produces a second polar body and the mature ovum. In summary the stages of development for an egg go: Oogonia (pre natal) to primary oocytes to enlarged primary oocyte to secondary oocyte to ovum.

Ovulation

Primary follicle if primary due to oestrogen dominance. Follicle left behind mid cycle as egg released into Fallopian tube (ovulation). Once ovulation occurs the follicle transforms into the corpus luteum which excretes hormones and eventually becomes the corpus albicans once is has secreted its contents.

Uterine cycle

This starts with the follicular phase. This is before ovulation occurs. The lining is very thin during the early stage the menstrual stage. As it builds at around day five you start the proliferation phase. This increase in uterus wall lining is stimulated by oestrogen produced by the more mature follicle. After ovulation you have the secretory phase which starts at day 15. This is when when the endometrium is thick and has increased vascularisation and increased glands and secretion. Once Corpus Luteum dies there's no more oestrogen and progesterone so lining enters menstrual phase and falls apart.

Hormones

Gonadotropin releasing hormone: Released by hypothalamus, effects pituitary glands to release gonadotropin hormones such as FSH and LH. Oestrogen: Released by multiple locations in the ovary, stimulates growth of myometrium, develops duct system in the breasts. It also causes relaxation of pelvic ligaments and increases LDL uptake to augment progesterone synthesis. It and progesterone stop production of gonadotropins. There is an exception to this, as oestrogen builds during the follicular phase of the menstrual cycle it eventually reaches critical concentration. At this point LH and FSH concentrations surge as oestrogen stimulates their release. Progesterone: Released by yellow body, maintains uterine lining, inhibits uterine contractions, causes alveolar pouching, modulates levels of hCG and hCS and is a substrate for synthesis of cortisol and aldosterone. It also causes respiratory stimulation which is important to keep the heightened levels of oxygen in the blood required to adequately perfuse the fetus. Human chorionic somatomammotropin. Secreted by syncytiotrophiblast. High levels in maternal blood but low in fetal. Similar action to growth hormone. Essentially it's job is to ensure the fetus has adequate nutrition. It does this by increasing lipolysis and decreasing levels of maternal insulin. This increases maternal blood sugar levels so the fetus can be better supplied with glucose. This can also result in diabetes though. Follicle stimulating hormone: Released by the pituitary gland this stimulates the formation of a follicle. Luteunising hormone: Relesed by pituitary gland this stimulates the conversion of the follicle to the yellow body/ Human chorionic gonadotropin: Secreted by the syncytiotrophoblast this promotes the maintenance of the yellow body and allows it to secrete progesterone in the first trimester before hormone control is taken over by the placenta.

Spermatogenesis

Testosterone can cross blood-testis barrier freely and is a major testicular androgen, stimulating sperm production. One primary spermatocyte forms 4 sperm cells. These undergo mitotic and then meiotic then cytospecialisation to form sperm.

Fertilisation

Ovulation occurs somewhere mid cycle. Sperm can persist in the female tract for up to 48 hours. Sperm parts: head, mid-piece, tail-piece. Acrosomal vesicle at the top just round the nucleus. Mitochondria in a spiral. Flagellum. Pheromones like allurin attract sperm towards egg. After a while capacitance occurs, whip like movement of flagellum.

Capacitation

Membrane of sperm binds (acrosomal vesicle) to zona pellucida and acrosomal reaction takes place. Sperm penetrates through ZP to fuse with plasma membrane of ovum. ZP hardens after it to prevent polyspermy. Once sperm is inside egg enzymes are activated to start formation of blastocyst.

Implantation

Histiotrophic nutrition is the nutrition from the fluid in the uterus while haemotrophic nutrition is from the mothers blood. There is more on this exact process in the placenta article however the uterus lining gets increased vasculatisation, increased permeability and oedema.

Pregnancy

Oestrogen, progesterone and relaxin maintains lining of uterus and widens pelvis. Corpus luteum maintains the lining of the uterus and survives due to production of human chorionic gonadotropin (hCG) produced and secreted by syncytiotrophiblast. It's in the blood at day 6 and in urine at day 14. It is luteinising and luteotrophic. After a while the placenta takes over hormone control so hCG falls.

Physical signs are amenorrhea (lack of cycle), nausea during huge peak of hCG, increased sensitivity of breasts and increased frequency of mictuition (urine). Other changes are increase in bulk of uterus due to hypertrphy of myometrial cells and from 12 week onwards this can be felt. Cervix becomes softer and uterine ligaments stretch and thicken. Blood flow through ovarian arteries increase. Occasionally you get odema, this is normal but can be pathological is IVC rises by five litres. There is a rise in cardiac output. Body fat increase for energy stores for the 3rd trimester where they are used.

You can get gestational diabetes due to pregnancy.The mother gets high resistance to insulin so impaired glucose tolerance this is designed to divert glucose to fetus by keeping the blood glucose concentration in the maternal blood high meaning it will diffuse into the fetal blood at the placenta. If you get diabetes it will increase size of the baby. Cortisol and hCS are insulin antagonisers as well. Low lipid metabolism so again lipid concentration gradient in favour of fetus.

Physiological changes

Increase in cardiac output proportional to the amount of babies. Accelerates up until 20 weeks then maintain. Blood plasma volume increases by 50% so you get physiological anaemia and the platelets decrease as they are diluted. RBC and platelet count stay constant. Women often on iron and folate for these reasons. Folate also decreases chance of NTD.

The blood is also made hypercoagulable to combat blood loss in pregnancy. Increase by 50% in ventilation. Arterial O2 increases and CO2 decreases and there is low HCO3. So pH of blood rises slightly. Blood pressure decreases during the end of the first trimester and then rises towards delivery. Placenta increases insulin resistance. HBG means glucose in urine. Risk of gestational diabetes.

Increase in plasma flow through kidneys and fall in the kidney failure markers. Means threshold to say someone had kidney problems is lower for pregnancy. Kidneys are leaky. Water and sodium are retained while glucose and protein are leaked. Liver function increased.


Labour

Stage one is increase in uterine contraction. Stage two is total cervix dilation Stage three is delivery of placenta.

Cervical composition changes, oestrogen, relaxin and prostoglandins along with collagenase are produced to break down collagen and cause inflammatory response to soften uterus and cervix. Different oxygen haemoglobin dissociation curves helps oxygen exchange as fetal haemoglobin has a much higher tolerance to hypoxia and much higher affintiy. Bohr effect as well as CO2 travels in mothers blood.

The change to independent life is quite considerable. Lung development is very important. You have to change from dependent to independent life. Change from maternal circulation to infant circulation causes babies to be blue when they are first born. Persistent fetal circulation could damage baby but babies have fetal haemoglobin which has a higher affinity for oxygen which protects the baby from ischaemic damage.

Lactation

Mammogenesis is creation of mammary glands Lactogenesis is lactation function, initiated near parturition Galactopoeisis is maintenance and enhancement of established lactation.

The first milk produced, colostrum, has a higher protein, minerals, fat solvable vitamins and antibodies than mature milk.

In early pregnancy there aren't many alveoli (lactiverous ducts) they enlarge and acquire lumen. Once you give birth they enlarge again. After your stop feeding they undergo involution. Milk fat secreted via exocytosis.

Prolactin maintains lactation, prolactin produced by baby suckling. Oxytocin is released on suckling which causes myoepithelial cells to contract and release milk, also causes lower dopamine and so higher prolactin. Also the receptors in the nipple trigger the hypothalamus to increase secretion of prolactin releasing hormone to cause the anterior pituitary gland to secrete more. Once lactation ceases the mammary gland undergoes involution and the cycle can start again with a new pregnancy. This is because prolactin inhibits GnRH and therefore the action of gonadotrphins on the ovaries.