妊高症英文课件

病 例 张平，女，36岁，以“停经九个月，胎动五个月 ，双下肢浮肿两周，头晕眼花一小时。”为主诉入 院。早孕反应及胎动如期出现，两周前无明显诱因 双下肢浮肿，休息后无好转。一小时前出现头晕眼 花。既往无高血压，慢性肾炎病史。 查体：T36.7，P78次/分，BP175/110mmHg, 心肺听诊无异常，腹膨隆，足月腹型，LOA，浮肿 +。 实验室检查：血常规示PL258G/L，HGB108g / L，HCT0.45。尿常规示蛋白+。 辅助检查：B超示BPD9.0cm，FL7.2cm，胎盘钙 化级。NST有反应型。 Hypertensive disorder complicating pregnancy 妊娠期高血压疾病 Preeclampsia Preeclampsia is defined as the combination of high blood pressure (hypertension), swelling (edema), and protein in the urine (albuminuria, proteinuria) developing after the 20th week of pregnancy. nMild preeclampsia is characterized by a systolic BP greater than 140 mm Hg or a diastolic BP greater than 90 mm Hg in a pregnant patient with minimal proteinuria(300mg/d )and pathologic edema. nSevere preeclampsia A systolic BP greater than 160 mm Hg or a diastolic BP greater than 110 mm Hg with significant proteinuria (5.0 g/d) and evidence of end-organ damage. Serum creatinine106mol/L, Platelet:100x109/L elevated LDH, ALT or AST Risk factors extremes of maternal age, primigravida, multiple gestations, molar pregnancy, diabetes mellitus (DM), renal disease, connective tissue disease, vascular disease, prior history of preeclampsia or eclampsia, and family history of preeclampsia or eclampsia. nThe fetus is a semi-allograft to the mother. Immune interaction between decidual leukocytes and invading cytotrophoblast cells is essential for normal trophoblast invasion and development. Immune maladaptation may cause shallow invasion of spiral arteries by endovascular cytotrophoblast cells and endothelial cell dysfunction mediated by an increased decidual release of cytokines, proteolytic enzymes, and free radical species. n Genetic gactor nDevelopment of preeclampsia-eclampsia may be based on a single recessive gene or a dominant gene with incomplete penetrance. Penetrance may be dependent on fetal genotype. The possibility of genetic imprinting should be considered in future genetic investigations of preeclampsia. npreeclampsia is a disease of first pregnancies. The protective effect of multiparity, however, is lost with change of partner. Also, exposure to semen provides protection against developing preeclampsia. Analogous to altered paternity, artificial donor insemination and oocyte donation are reported to result in a substantial increase of preeclampsia. Thus, epidemiologic studies strongly suggest that immune maladaptation is involved in the etiology of preeclampsia. nNormal placental development involves progressive loss of the musculoelastic tissue in the spiral arteries that feed the vessels of the intervillous spaces, which results in uterine blood flow increases of nearly 25% during the first trimester. In women destined to develop preeclampsia, this physiologic dilatation of the spiral arteries does not occur because the placental trophoblast cells do not invade the spiral arteries. In severe cases, other pathologic changes also occur. Accumulation of fat-laden macrophages with fibrinoid necrosis (ie, acute atherosis), disruption of the basement membranes, platelet deposition, mural thrombi, and proliferation of intimal and smooth muscle cells all decrease the luminal diameter. nThe narrowed and damaged spiral arteries become thrombosed, resulting in placental infarction and necrosis. Uteroplacental blood flow then is reduced by 50-75%. The anatomical reduction in blood flow may be complicated by vasospasm of the uteroplacental bed. nDecreased placental perfusion is thought to lead to fetoplacental ischemia. The ischemic placenta may produce a circulating agent, which is currently unidentified but causes the widespread dysfunction of the maternal vascular endothelium that leads to the systemic manifestations of preeclampsia Pathophysiologic changes Pathological deterioration of function I a numner of organs and systems has been identified as a consequence of Generalized vasospasm Pathologic changes in main organs nBrain : blindness n cerebral edema n cerebral hemmorage ncardiovascular change n increased cardiac after load n myocardial ischemia,edema n pulmonary edema Pathologic changes in main organs nLiver : periportal hemorrhagic necrosis （门脉周围出血坏死） nkidneys :endothelial edema of glomerulus nplacenta : atherosclerosis low placental perfusion nBlood volume: hemoconcentration nHematological changes n thrombocytopenia nendocrine and metabolic changes diagnosis nHistory hypertension proteinuria nsign edema symptom convulsion , coma blood examination n axillary liver and renal functions examination funduscopy of eyes others Differential diagnosis nEssential hypertension and chronic nephritis nconvulsive disorders nthe screening test : mean arterial blood pressure roll over test blood variation calcium amount in urine Management nGestional hypertension A rest B diet C medication : phnobarbital （苯巴比妥） diazepam（安定） preeclampsia nA. Hospitalization nB. antispasm medication magnesium sulfate（硫酸镁） nB sedative drugs diazepam nC antihypertensive drugs nD expansive volume treatment albumin （白蛋白） plasma （血浆） whole blood（全血） nE D