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Karteikarten von Hannah Tribe, aktualisiert more than 1 year ago
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| Frage | Antworten |
| What is the trophoblast? | Cells of the blastocyst that invade the endometrium and myometrium. They are precursors to the placental cells which secrete beta-hCG |
| What is the chorion? | The part becoming the placenta |
| What needs to happen to the morula? | Needs to hatch out of the size-limiting membrane it is surrounded by |
| Towards the end of the luteal phase there is an inflammatory response in the uterus, why is this helpful for pregnancy? | The inflammatory response means there is infiltration of white cells, which allow the appropriate inflammatory response to implantation |
| What is the name of the endometrium during pregnancy? | Decidual endometrium |
| What happens to the trophoblast? | It differentiates and invades the decidua and myometrium. Vasculature develops within the trophoblast and the maternal uterus-placental circulation develops |
| When is the window of implantation and what can happen if the embryo misses it? | Day5-6, will implant ectopically or not at all if missed. |
| What does the trophoblast produce and what does it do? | Produces beta-hCG, which maintains the corpus luteum by acting on LH receptors to stimulate them to produce progesterone. |
| Why is the secretion of beta-hCG so important, especially in the first 6 weeks? | Placental steroidogenesis cannot take place until weeks 7-8 so beta hCG maintains progesterone levels until then. |
| How do pregnancy tests work? | Contain an antibody for beta hCG, so that if a trophoblast has implanted and is producing beta hCG, it will be excreted in the urine and will bind to the antibody on the pregnancy test, showing as a line. |
| Why might measuring serum levels of beta hCG be useful? | Can monitor early complications such as ectopic pregnancy or miscarriage |
| What is the normal pattern of beta hCG levels in the blood? | Between weeks 4-8 levels roughly double every 48 hours. |
| If levels rise slower than expected, what might this show? | Ectopic pregnancy |
| If levels descend, what does this mean? | The pregnancy is failing |
| What are the general functions of the placenta? (4) | 1. Steroidogenesis 2. Provision of important substances from the mother 3. Removal of fetal waste products 4. Barrier between mother and fetus from infection and some drugs |
| Which steroids are made by the placenta? | Oestrogens, progesterone and cortisol |
| What other hormones are made by the placenta? | Human placental lactogen (HPL) and prolactin |
| What is the function of placental progesterone? (4) | 1. Decidualisation of the endometrium 2. Relaxation of the uterus smooth muscle (prevents contraction which can cause miscarriage) 3. Mineralocorticoid effects to cause net fluid gain 4. Breast development (due to large numbers of progesterone receptors on breast tissue) |
| What are the 3 oestrogens and what is the difference between them? | E1 = oestrone (has 1 hydroxyl group) E2 = oestradiol (has 2 hydroxyl groups) E3 = oestrol (has 3 hydroxyl groups) |
| Can the placenta make oestrogens on its own? | No, it relies on androgens from the fetus and maternal adrenal glands. |
| What are the effects of placental oestrogens? (5) | 1. Hypertrophy of the uterus (lots of oestrogen receptors in the uterus, which stimulate growth) 2. Causes metabolic changes such as alteration of glucocorticoid pathway and insulin resistance (oestrogen antagonises insulin so body produces more = hyperinsulinaemia) 3. Cardiovascular changes such as increased fluid volume 4. Breast development 5. Increase in the production of clotting factors in the liver (brings higher risk of DVT) |
| Which of the oestrogens is only made during pregnancy? | Oestrol |
| Why might steroids be given to the mother during premature labour? | So they will cross the placenta and encourage development of the pulmonary surfactant in the fetus. |
| What are the functions of placental cortisol? (3) | 1. Metabolic changes such as insulin resistance 2. Causes maturity of the fetal lungs 3. Mineralocorticoid action |
| What is the theory of the function of placental CRH? | May be involved in initiation of labour |
| What is the function of HPL? | It is similar to GH so causes insulin resistance and hypertension but the role in pregnancy is unclear, may be involved in lactation. |
| What is the function of placental prolactin and how does it differ from pituitary prolactin? | Placental prolactin is not inhibited by dopamine, and levels increase during pregnancy for cause breast development ready for lactation. |
| What is the general trend in hormones during pregnancy? | Levels increase in the blood. |
| Why else might levels of free drugs/hormones in the circulation rise? | Levels of binding proteins such as albumin fall, so more hormones travel un-bound. |
| What maternal substances are transferred to the fetus across the placenta? (7) | 1. Oxygen 2. Carbohydrates 3. Fats 4. Amino Acids 5. Vitamins 6. Minerals 7. IgG antibodies |
| What waste substances are removed from the fetus through the placenta? (4) | 1. CO2 2. Urea 3. Ammonia 4. Minerals |
| What features of the placenta make it so good at its function? (3) | 1. Large blood supply with low pressure allows increased diffusion 2. Large surface area in contact with the maternal blood 3. Highly efficient transfer system |
| What is the name of the functional unit of the placenta? | Cotyledon |
| What are the functions of the amniotic cavity? (3) | 1. Homeostasis of temperature, fluid and ions 2. Vital for development of certain fetal structures (e.g. lungs) 3. Protective barrier |
| What are some disorders of the placenta? (5) | 1. Miscarriage 2. Pre-eclampsia 3. Hydatidiform mole 4. Placental insufficiency 5. Transfer of drugs or toxins |
| What is a hydatidiform mole? | An abnormal conception resulting from a sperm fertilising an empty ovum and implanting. It can be detected on ultrasound and needs to be removed. |
| What are some disorders of the amnion? (3) | 1. Polyhydramnios (excessive amniotic fluid) 2. Oligohydramnios (too little amniotic fluid) 3. Premature rupture of membranes |
| What are the effects of placental steroids on the mother? (6) | 1. increases the RAAS to increase fluid volume 2. Causes slightly faster, deeper breathing in the respiratory centre 3. Smooth muscle of the GI tract relaxes (increases constipation) 4. Net effect of vasodilation so BP usually goes down during pregnancy 5. Increases uterine contractions (counteracted by progesterone) 6. Inhibition of prolactin action |
| When do these effects stop? | As soon as the placenta is delivered |
| What is the normal total gain in weight of the mother during pregnancy? | 12.5-13kg |
| What is the average increase in cardiac output during pregnancy? | 40-50% |
| By how much does the basal metabolic rate increase during pregnancy? | In mid-gestation by 350 kcal/day, then 250 kcal/day by late gestation |
| What happens in the first trimester in regards to glucose? (3) | 1. Increased number of beta cells in the pancreas 2. Increase in levels of plasma insulin 3. Decrease in fasting serum glucose (because it is laid down as stores [glycogen] and used by muscle) |
| What happens in the second trimester with regards to glucose? (2) | 1. HPL causes insulin resistance (so less glucose gets laid down in stores) 2. There is an increased in serum glucose which can cause diabetes |
| Where does the water gain come from? | 1. Increased plasma volume 2. Fetus 3. Placenta 4. Amniotic fluid 5. Oedema (due to capillary leakage, e.g. in ankles. In lungs is dangerous) 6. Uterine muscle 7. Mammary gland |
| What causes the increased plasma volume? (3) | 1. Increased RAAS due to oestrogens and progesterone, so sodium and water is retained 2. Decreased thirst threshold 3. Decreased plasma oncotic pressure due to lower albumin levels, so favours movement of fluid into the interstitial space |
| What causes pregnant women to breathe more deeply? | 1. The respiratory centre becomes more sensitive to CO2 2. Ribcage is displaced upwards and flares outwards |
| What does this mean for PO2 and PCO2? | PO2 increases, and PCO2 decreases so mothers normally have a slight respiratory alkalosis |
| What effect does this have on the fetus? | The difference between maternal oxygen and CO2 facilitates efficient gas transfer across the placenta. |
| Why can pregnant women appear anaemic on blood tests? | Because there is a haemodilution - increased blood volume and so dilution of Hb so concentration decreases. |
| What is the effect of the alteration in clotting factors? | The blood is hypercoagulable, so ESR increases , there is increased fibrinogen for when the placenta separates, but this puts the mum at increased risk of thrombosis. |
| What are the properties of fetal blood? | It has increased fetal Hb and the dissociation curve shifts to the left, to encourage maternal Hb to give up its oxygen. |
| What effect does smoking have on fetal blood? | Smoking increases the levels of carboxy-Hb which reduces the shift to the left in the fetal dissociation curve, so fetus experiences hypoxia |
| What is the effect of pregnancy on the mother's heart? (4) | 1. it is pushed to the side 2. A high-volume flow murmur can be heard 3. Increased HR and SV 4. Reduced difference between the arterial and venous oxygen level |
| What effect does pregnancy have on the mother's blood vessels? (3) | 1. Reduced TPR causes net decrease in BP despite rise in CO 2. There is increased blood flow to the uterus/placenta, muscles, kidneys and skin 3. Neoangiogenesis in the skin to assist with heat loss (spider naevi) |
| What effect does pregnancy have on the GI tract? (3) | 1. Increased appetite and thirst 2. Reduced motility of the GIT, leading to constipation 3. Relaxation of the lower oesophageal sphincter, leading to reflux (as well as due to large uterus pushing up) |
| Why is folic acid supplementation advised before conception and during the first trimester? | Folic acid is needed for DNA replication, growth and blood cells, and there is lots of mitosis occurring in the beginning of pregnancy, so levels need to be high. Deficiency can result in neural tube defects such as spina bifida. |
| What changes occur in the urinary system during pregnancy? (2) | 1. The urinary tract dilates and relaxes, allowing stasis of urine and therefore higher chance of persistent UTIs 2. Increased blood flow to the kidney causes increased GFR and increased clearance of creatinine, urea and uric acid. |
| What would be the most likely problem if a pregnant woman's creatinine or urea levels were high? | They have renal impairment |
| What happens to a pregnant woman's micturition habits at the different stages of pregnancy? | In the early stages, the uterus is enlarging but still in the pelvis so is compressing the bladder = increased frequency. In the mid-stages, the uterus expands above the pelvic brim so micturition returns to normal. In late stages, the fetal head descends into the pelvis again and compresses the bladder = increased frequency |
| What happens to the lower uterine segment (isthmus of uterus) by the late stages of pregnancy? | 1. Becomes thinner 2. Becomes more fibrous 3. Becomes less muscular |
| What happens to the cervix during pregnancy? (3) | 1. Becomes more vascularised 2. From 8 weeks, is softer and turns bluer 3. Glands proliferate so mucosal layer is much thicker and mucus production is increased |
| What causes the cervix to become soft? | Prostaglandins breakdown collagen and cause water to be drawn in. |
| What changes occur on delivery? (4) | 1. Rapid decrease in steroids 2. Reversal of endocrine changes 3. Loss of oedema of uterine muscle but size reverts more slowly 4. Removal of steroids allows action of prolactin on the breast. |
| What are some common minor symptoms of pregnancy? (11) | 1. Tiredness 2. Nausea/vomiting 3. Constipation 4. Heartburn 5. Breast tenderness 6. Frequency of urination 7. Backache 8. Piles 9. Headache 10. Heat intolerance 11. Being emotional |
| What are some complications which can occur in the first trimester? (3) | 1. Miscarriage (possibly in up to 40% of pregnancy) 2. Ectopic pregnancy (0.5-2%) 3. Hyperemesis gravidarum (2-5%) |
| What can be some complications to the mother in the second and third trimesters?(5) | 1. UTI 2. Anaemia 3. Pre-eclampsia 4. Gestational Diabetes 5. Antepartum Haemorrhage |
| What are some common complications to the fetus in the second and third trimesters? (3) | 1. Premature labour 2. Intrauterine Growth Restriction (IUGR) 3. Macrosomia |
| Why are UTI's a common problem during pregnancy and why can they be a problem? | Pregnant women have relative urinary stasis (due to increased relaxation of the bladder smooth muscle due to effect of progesterone, plus the increased fluid load), and immunosuppression (to prevent immune attack on the fetus) cause increased incidence of UTIs. They can be associated with obstetric problems such as pre-term delivery. |
| Why is the physiological Hb range in pregnancy lower than that in non-pregnant women? | The increase in plasma volume is larger than the increase in red cell volume, so there is a dilution of the Hb, making it appear as a lower concentration. |
| How is anaemia in pregnancy managed? | Hb levels checked at booking, 28 and 36 weeks. Cause of anaemia must be investigated and treated (e.g. give iron tablets if iron deficient, or folate/B12 supplements). Give blood transfusion if Hb <7 or if anaemia is symptomatic. |
| What is the definition of gestational diabetes? | Diabetes mellitis diagnosed or recognised for the first time at more than 20 weeks gestation. |
| What are the 2 main effects of maternal hyperglycaemia during pregnancy? | Maternal hyperglycaemia causes fetal hyperglycaemia as well, which causes: 1. Fetal glycosuria 2. Fetal hyperinsulinaemia (pancreas beta cell hyperplasia) |
| What is the consequence of fetal glycosuria? | Excess water from fetal urine enters the amniotic sac, causing polyhydramnios |
| What are the consequences of fetal hyperinsulinaemia? (4) | 1. Macrosomia 2. Inhibition of pulmonary surfactant 3. Neonatal hypoglycaemia 4. Polycythaemia |
| What are the consequences of polyhydramnios? (3) | 1. Malpresentation of the fetus 2. Cord prolapse 3. Postpartum haemorrhage (due to overstretched uterus causing inefficient contractions) |
| What is the consequence of polycythaemia? | Jaundice, caused by the breakdown of the excessive number of red cells |
| What is the consequence of inhibition of pulmonary surfactant? | fetal respiratory distress syndrome |
| What is the effect of the hyperinsulinaemia and what are its consequences? | High insulin and high glucose cause anabolism which cause macrosomia of the fetus and hyperplacentation. This leads to prolonged labour which increases the risk of shoulder dystocia and the need for operative delivery. Also increases the risk of ante- and post-partum haemorrhage. |
| What are some other effects of GDM on the mother? (5) | 1. Increased infection 2. Hypoglycaemia due to a tighter regime 3. Deterioration in nephropathy (reverses after pregnancy) 4. Doubled risk of progression of retinopathy 5. 50% increased lifetime risk of getting Non-insulin dependent diabetes mellitis |
| What are the other complications on the fetus in GDM? | The placenta becomes damaged by hyperglycaemia which causes less efficient oxygen exchange and therefore fetal hypoxia. It can cause late intra-uterine death or fetal distress. |
| What are some aims of management of GDM? (6) | 1. Counselling 2. Achieve normal glucose levels, with appropriate management of diet and insulin 3. Metformin 4. Ultrasound monitoring to detect congenital abnormalities and assess for correct fetal growth or polyhydramnios 5. Screen for pre-eclampsia 6. Plan the appropriate timing for delivery |
| Which decisions must be made when deciding the timing of delivery? | 1. Compare risks of intra-uterine death vs. risk of respiratory distress 2. Compare risks of macrosomia and consequent shoulder dystocia vs. the risk of C-section |
| What is the definition of pre-eclampsia (PET)? | A significant rise in BP above 140/90 later than 20 weeks gestation on more than one occasion (at least 4 hours apart), with significant proteinuria. May also be signs of end organ damage due to infarction by small thromboses. |
| What is another symptom that can be observed linked with pre-eclampsia but is not a requirement for diagnosis? | Oedema - particularly worrying if facial or sacral |
| What is the difference between pre-eclampsia and pregnancy-induced hypertension? | PIH will not also present with proteinuria. |
| Why is BP normally slightly reduced during pregnancy? | Because despite the increase in CO, there is a larger decrease in TPR to accommodate increased placental flow, so net effect is reduced BP |
| So why does BP rise in pre-eclampsia? | There is a systemic vasospasm causing significantly increased TPR, which causes the rise in BP. (BP= CO x TPR) |
| Why might pre-eclampsia be described as "tight, leaky sticky disease"? | Tight because of the vasoconstriction effect. Leaky because of the increased permeability of the glomerular basement membranes, allowing proteins through the Bowman's capsule (proteinuria), and capillaries, causing odema. Sticky due to activation of the endothelium causing increased risk of thrombosis. |
| What are 3 possible pathophysiologies of pre-eclampsia? | 1. Immunological - abnormal immune reaction to implantation of trophoblast (which forms the placenta) 2. Vasospastic substances or lack of vasodilators, or altered sensitivity to the RAAS 3. Mineral/vitamin deficiencies |
| What are the effects of PET on the fetus? | Reduced fetal perfusion, causing reduced nutrient/waste transfer and reduced fetal renal perfusion. The inefficent transfer causes hypoxia and poor nutrition which can lead to fetal death. The reduced fetal renal perfusion causes decreased production of fetal urine which leads to oligohydramnios. |
| When giving treatment management, what is a sign that they are improving? | Increased urine output |
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