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ROSA Garcia Application exercise: Case Study

ROSA Garcia Application exercise: Case Study


Complete the case study titled “ROSA Garcia” your response should be thorough, and. Lose to one typed page for three critical thinking questions to receive credit. Include references in APA format.
FYI: please see email and uploaded for case study and questions.

Pre-eclampsia Pathophysiology The normal physiological adaptations to pregnancy are altered in the woman who develops pre-eclampsia. Pre-eclampsia is a multisystem, vasopressive disease process that targets the cardiovascular, hematological, hepatic, renal, and central nervous systems. Pre-eclampsia is associated with a clinical spectrum of events that range from mild to severe with a potential endpoint of eclampsia. Patients do not suddenly “catch” severe pre-eclampsia or develop eclampsia but rather progress in a predictable course through the clinical spectrum. In most cases, the progression is relatively slow, and the disorder may remain mild. In other situations, the disease can progress more rapidly and change from a mild to a severe form in a matter of days or weeks. In the most serious cases, the progression can be rapid: Mild disease at the time of diagnosis evolves to pre-eclampsia with severe features or eclampsia over hours or days (Lavallee, 2015). Hence, the nurse must alert the patient to signs and symptoms that signal a worsening condition and continuously assess the patient for any change. Although the pathophysiology is poorly understood, it is clear that the blueprint for its development is laid down early in pregnancy. Pre-eclampsia is a disease of the placenta because it has been documented in pregnancies that involve trophoblastic tissue but no fetus (i.e., a molar pregnancy). In a normal pregnancy, the endovascular trophoblast cells of the placenta transform uterine spiral arteries to accommodate an increased blood flow. In the presence of pre-eclampsia, the arterial transformation is incomplete. Women with preeclampsia have a distinctive lesion in the placenta termed acute atherosis (fat accumulation in the placental arteries). Their placentas also exhibit a greater degree of infarction (necrosis related to decreased blood supply) than is found in placentas of normotensive women. These pathological changes can lead to decreased placental perfusion and placental hypoxia (Lavallee, 2015; Cunningham et al, 2018). Vasospasm and endothelial cell damage are the major underlying pathophysiological events in pre-eclampsia. Vasospasm may be associated with an elevation in arterial blood pressure and resistance to blood flow. It is unclear whether vasospasm produces damage to the vessels or if damage to the vessels produces vasospasm. Regardless, the restriction of blood flow is associated with endothelial cell damage, and this tissue insult prompts the systemic utilization of platelets and fibrinogen. The widespread vascular changes alter blood flow and result in hypoxic damage to vulnerable organs. Over time, the alterations produce widespread maternal vasospasm that results in decreased perfusion to virtually all organs, including the placenta. Associated physiological events include decreased plasma volume, activation of the coagulation cascade, and alterations in the glomerular endothelium. The increased platelet activation and markers of endothelial activation can predate clinically evident pre-eclampsia by weeks or even months and can lead to HELLP syndrome (Lavallee, 2015; Cunningham et al, 2018) (Fig. 6-8).
• Assessment Tools
SPASMS: A Memory Enhancer When Caring for a Pre-eclampsia Patient S Significant blood pressure changes may occur without warning. P Proteinuria is a serious sign of renal involvement. A Arterioles are affected by vasospasms that result in endothelial damage and leakage of intravascular fluid into the interstitial spaces. Edema results. S Significant laboratory changes (most notably, liver function tests [LFTs] and the platelet count) signal worsening of the disease. M Multiple organ systems can be involved: cardiovascular, hematological, hepatic, renal, and central nervous system. S Symptoms appear after 20 weeks of gestation.
Risk Factors In the United States, the incidence of pre-eclampsia is rising, most likely caused by an increased prevalence of predisposing disorders such as obesity, diabetes, and chronic hypertension. Risk factors associated with pre-eclampsia are presented in Box 6-7.
Classification of Pre-eclampsia and Maternal and Fetal Morbidity and Mortality A number of maternal and fetal complications are likely to develop as the condition worsens. Signs of severe disease include any of the following: ■ Systolic BP greater than or equal to 160 mm Hg or diastolic BP greater than or equal to 110 mm Hg on two occasions at least 4 hours apart while the patient is on bedrest ■ Thrombocytopenia (platelets less than 100 x 109/L) ■ Impaired liver function, as indicated by abnormally elevated blood concentrations of liver enzymes (to twice normal concentration) and/or severe, persistent right upper quadrant (RUQ) or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses
Risk Factors for Pre-eclampsia
• Primigravida (6-8 times greater risk) • Age extremes (less than 19 years and greater than 40 years) • Prpopetatinnal diallptpc

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