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高血压英文ppt精品课件hypertensive disorders in pregnancy (2)

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高血压英文ppt精品课件hypertensive disorders in pregnancy (2)

Hypertensive Disorders in Pregnancy, ,Scope,Terminology and classification Risk factors Etiology Pathophysiology Prediction and prevention Management,Incidence,3.7 % of pregnancies 16% of pregnancy-related deaths Eclampsia 1 in 2000 deliveries,Classification by the working group of the NHBPEP (2000),1. Gestational hypertension 2. Preeclampsia 3. Eclampsia 4. Preeclampsia superimposed on chronic hypertension (superimposed preeclampsia) 5. Chronic hypertension,Gestational hypertension,BP >= 140/90 mmHg for first time during pregnancy No proteinuria BP returns to normal < 12 wk postpartum Final diagnosis made only postpartum May have other S&S of preeclampsia , eg. epigastric discomfort or thrombocytopenia,Preeclampsia,Minimum criteria BP >= 140/90 mmHg after 20 wk gestation Proteinuria >= 300 mg/24hr or >=1+ dipstickMild preeclampsia Severe preeclampsia,Severe preeclampsia,BP >= 160/110 mmHg Proteinuria 5 g/24hr or >= 2+ dipstick (persistent) Cr > 1.2 mg/dl Platelets < 100,000 /mm3 Microangiopathic hemolysis Elevated ALT or AST Persistent headache , visual disturbance , epigastric pain,Eclampsia,Seizures that cannot be attributed to other causes in a woman with preeclampsia Seizures are generalized May appear before , during or after labor 10% develop after 48 hr postpartum,Superimposed preeclampsia,New onset proteinuria >= 300mg/24 hr in hypertensive women but no proteinuria before 20 wk A sudden increase in proteinuria or BP or platelet count < 100,000 in women with hypertension and proteinuria before 20 wk,Chronic hypertension,BP >= 140/90 mmHg before pregnancy or diagnosed before 20 wk , not attributable to GTD or Hypertension first diagnosed after 20 wk and persistent after 12 wk postpartum,Diagnosis,Gestational HT,Also called transient HT Final Dx : after delivery , by exclusion BP : resting BP , Korotkoff phase V is used to defined diastolic pressure GHT may later develop preeclampsia 10% of eclamptic seizures develop before overt proteinuria is identified BP rise , increase both mother and fetus risks,Preeclampsia,Described as “pregnancy-specific syndrome of reduced organ perfusion secondary to vasospasm and endothelial activation” Proteinuria & glomerular pathology develop late in the course , pathophysiologic process begin as early as implantation,Preeclampsia,Diastolic hypertension >= 95 , increase fetal death rate 3 fold Worsening proteinuria resulted in increasing preterm delivery Epigastric pain from hepatocellular necrosis , ischemia and edema that stretches Glisson capsule Thrombocytopenia from platelet activation & aggregation , microangiopathic hemolysis induced by severe vasospasm,Preeclampsia,Hemoglobinemia , Hburia , Hyperbilirubinemia : indicative of severe disease Cardiac dysfunction , pulm edema , obvious IUGR : indicative of severe disease Severity of preeclampsia assess by freq & intensity of abnormalities,Superimposed preeclampsia,1. Hypertension (>=140/90) is documented antecedent to pregnancy 2. Hypertension is detected before 20 wk , unless there is GTD 3. Hypertension persists long after delivery Additional previous Hx or family Hx of HT End organ damage : LVH , retinal change Risk abruption , IUGR , preterm & death,Underlying causes of CHT,Essential familial hypertension Obesity Arterial abnormalities Endocrine disorders Glomerulonephritis Renoprival hypertension Connective tissue disease PCKD ARF,Risk factors for preeclampsia,Nulliparous Advanced maternal age Race and ethnicity (genetic predisposition & envoronmental factor) Multifetal gestation Obesity BMI > 35 kg/m2,Etiology,Theory account for the observation : hypertensive disorder more likely to develop in : 1. exposed to chorionic villi for first time 2. exposed superabundance of chorionic villi (Twin ,mole) 3. Preexisting vascular disease 4. Genetic predisposition,Etiology,1. Abnormal trophoblastic invasion of uterine vessels 2. Immunological intolerance between maternal and fetoplacental tissues 3. Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy 4. Dietary deficiencies 5. Genetic influences,Abnormal trophoblastic invasion,Normal implantation , uterine spiral arteries undergo extensive remodeling as they are invaded by endovascular trophoblasts Incomplete invasion (decidual vessels , not myometrial vessels) : preeclampsia,Abnormal trophoblastic invasion,Atherosis : pathology,Endothelial damage Insudation of plasma constituents into vessel walls Proliferation of myointimal cells Medial necrosis Lipid accumulation in myointimal cells & macrophages Aneurysmal dilatation Obstruction of spiral arteriole,Placental growth factors : implications for abnormal placentation,Placental growth factors : regulate vascular endothelial cell and trophoblast function Highly expressed in trophoblasts during normal pregnancy Significantly decreased in preeclampsia Asso with placental bed hypoxia & ischemia (Abnormal placentation)J Soc Gyn Investig 2003 : 10 : 178-88,

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