Pre Eclampsia Research Paper

During pregnancy, the level of blood-clotting proteins increases, while anti-clotting protein levels decrease. Another possible contributory factor is the enlarged uterus, which puts the lower body veins under additional pressure to return the blood to the heart.

Acute pathological changes, such as organ hemorrhage and necrosis, to women with preeclampsia will revert to normal soon after delivery, which suggests that unique features of pregnancy lead to the change. Previous research supports that preeclampsia is the consequence of reduced placental perfusion, which is suspected to be caused by abnormalities in implantation and vascular remodeling. As a result, there is reduced blood flow to organs other than the placenta, thus causing hemorrhage and necrosis to multiple organ systems including liver, kidney, brain and intervillous space

Insulin is the only hormone in the body that lowers blood glucose levels, as it targets cells and provides for glucose storage as glycogen (Mattson Porth, 2002). Insulin prevents fat and glycogen breakdown and inhibits glycogenesis and increases portent synthesis (Mattson Porth, 2002). The placenta secretes hormones and adipokines, these include tumor necrosis factor (TNF)-α, human placental lactogen, and human placental growth hormone (Alfadhli, 2015). Furthermore, increased oestrogen, progesterone and cortisol during pregnancy add to the disruption of the balance of glucose and insulin levels within the body (Alfadhli, 2015). The body tries to compensate for the insulin resistance by increasing the amount of insulin that is secreted, however women with gestational diabetes can not secrete enough insulin to keep up with the metabolic stress of the insulin resistance causing hyperglycaemia in the bloodstream (Alfadhli, 2015).

We also discussed her 2 other risk factors for preeclampsia including twins and this being her 1st pregnancy. She does have some proteinuria in her urine clearly by the p/c ratio in her urine yesterday. Her BP today is normal and was able to settle back down to normal Perhaps her mild BP in triage was related to her concern at the time for something being wrong with the pregnancy. I would suggest that you follow her BP’s quite closely and certainly if she were to develop HTN or preeclampsia I would consider induction at that time; otherwise, I would try to get as close to 37 weeks as

Sibai, B. (2003). Diagnosis and Management of Gestational Hypertension and Preeclampsia. Obstetrics & Gynecology, 102(1), 181-192.

As the molecular basis of Uterine fibroids are poorly understood, there are several pathogenic factors such as genetic, microRNA, steroids, growth factors, cytokines, chemokines and ECM components that contribute to the development and growth of the disease.

She carried out a risk assessment to identify prelabour risk factors of PPH described by Cathy et al. (2013), such as previous retained placenta, previous caesarean section, placenta praevia, accrete or percreta, antepartum haemorrhage, pre-eclampsia, BMI over 35, increased maternal age, uterine abnormalities, maternal haemoglobin below 9g/dL, grand multiparity. Laura’s risk assessment did not highlight any prelabour risk factor, therefore she was not considered to be a high risk of

Preeclampsia is defined by hypertension and proteinuria during pregnancy. It tends to occur after 20 weeks in gestation.

Preeclampsia is a common hypertensive disorder that occurs only during pregnancy in some individuals. Diagnosis of preeclampsia is made with a new onset of high blood pressure with numbers greater than 140/90 and protein in her urine. Currently the cause of preeclampsia remains unknown. However, preeclampsia is also associated with a decrease in placental perfusion which could restrict uterine growth, decrease fetal movement and cause hypoxia and fetal distress (London, Wieland Ladewig, Davidson, Ball, McGillis Bindler, & Cowen). . Around twelve to twenty-five percent of growth-restricted fetuses and small for gestational age infants along with fifteen to twenty percent of preterm births are correlated with preeclampsia the complications

Preeclampsia is the new onset of hypertension and either proteinuria or end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman. Although most women develop signs of the preeclampsia in late pregnancy with gradual worsening until delivery, a few studies have reported delayed or new-onset postpartum preeclampsia in patients with no antecedent diagnosis of hypertensive disease in the current pregnancy (). Postpartum preeclampsia is defined as the presence of hypertension and proteinuria, occurring up to 4-6 weeks after delivery (yancey, filetti). While the pathophysiology of preeclampsia involves abnormal placental vasculature and altered maternal systemic endothelial function (gilbert, beckmann), postpartum preeclampsia

In contrast to normal pregnancy, there are indications of increased inflammatory responses and also of an immune deviation toward Th1 in the established preeclamptic pregnancy (183). Accompanied by a shift in the direction of Th1-type immunity as identified by the increased IL-2/IL-4 ratio and IFN- γ /IL-4 ratio , there is too increased circulating levels of the pro-inflammatory cytokines IL-6 and TNF-α, also the chemokines IL-8 , interferon-inducible protein-10 (IP-10) and monocyte chemoattractant protein 1 (MCP-1), as well as the adhesion molecules intercellular adhesion molecule 1(ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), in preeclampsia as compared

Laboratory tests were ordered to allow for an appropriate diagnosis. A chemistry panel test and a complete blood count (CBC) with platelets were ordered. A 24-hour urinary protein test was also ordered. Chemistry panels are groups of tests performed on a blood sample that can be used to determine a person’s general health status. For the chemistry panel, a comprehensive metabolic panel (CMP) was done. The 24-hour urinary protein test was ordered in order to obtain a measurement of the protein released in urine over a 24-hour period. The urine tests did not reveal a significant amount of protein in the urine, but the CMP showed the likelihood of hypertension. After further review, M.W. was diagnosed with mild gestational hypertension, a form of pregnancy-induced hypertension (PIH).

The link between SP-A and SP-D and the initiation of an unplanned pre-term labour is supported by observations made by Bernal and Phizackerley. It has been shown that amniotic fluid surfactant is an important intrauterine source of arachidonic acid, and increases the rate of prostaglandin synthesis in the foetal membrane. Foetal surfactant has also been associated with amnion cells contributing archidonate for

PD-ECGF, VEGF) and negative (e.g thrombospondin-1, platelet factor-4) regulatory molecules (Wei, Kuo, Chen, Chou, Lai, Lee & Hsieh, 2003).

Women with APLS are at significant risk for thromboembolism during pregnancy. They may be placed on anticoagulant therapy to prevent thrombus formation.1,20