Etiology of hypertension in pregnancy:
Potential causes include:
1. Abnormal trophoblastic invasion of uterine vessels.
2. Immunological intolerance between maternal and fetomaternal tissues.
3. Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy.
4. Dietary deficiencies.
5. Genetic influences.
Pathogenesis:
Vasospasm:
Causes resistance and subsequent hypertension.
Diminished blood flow lead to necrosis, hemorrhage and other end organ disturbances.
Endothelial cell activation:
Intact endothelium has anti coagulant properties.
Unknown factors likely from placenta provoke activation and dysfunction of the vascular endothelium.
Damaged endothelium secrete substances that promote coagulation, increase the sensitivity to vasopressors.
Increased pressor resopnses:
More sensitive to angiotensin II.
Decreased ratio of prostacyclin and thromboxaneA2.
Decreased endothelial nitricoxide synthase expression.
Increased endothelin -1, a potent vasoconstictor.
Decreased bioavialability of VEGF.
-Hypertension in pregnancy-classification
-Hypertension in pregnancy-gestational hypertension
-Preeclampsia
-Eclampsia, preeclamsia superimposed on chronic hypertension
-Chronic hypertension
-Hypertension in pregnancy-etiology and pathogenesis
-Pathology
-Mild hypertension in pregnancy-prevention and management
-Severe hypertension in pregnancy-management
-Severe preeclampsia in pregnancy-management
-Complications of hypertension
-Antihypertensive therapy- centrally acting drugs
-Antihypertensive therapy-beta blockers, calcium channel blockers
-Antihypertensive therapy-alpha blockers, vasodilator, diuretics, ACE inhibitors
-Acute severe hypertension - treatment
-Eclampsia - signs and symptoms
-Eclampsia - management
Potential causes include:
1. Abnormal trophoblastic invasion of uterine vessels.
2. Immunological intolerance between maternal and fetomaternal tissues.
3. Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy.
4. Dietary deficiencies.
5. Genetic influences.
Pathogenesis:
Vasospasm:
Causes resistance and subsequent hypertension.
Diminished blood flow lead to necrosis, hemorrhage and other end organ disturbances.
Endothelial cell activation:
Intact endothelium has anti coagulant properties.
Unknown factors likely from placenta provoke activation and dysfunction of the vascular endothelium.
Damaged endothelium secrete substances that promote coagulation, increase the sensitivity to vasopressors.
Increased pressor resopnses:
More sensitive to angiotensin II.
Decreased ratio of prostacyclin and thromboxaneA2.
Decreased endothelial nitricoxide synthase expression.
Increased endothelin -1, a potent vasoconstictor.
Decreased bioavialability of VEGF.
-Hypertension in pregnancy-classification
-Hypertension in pregnancy-gestational hypertension
-Preeclampsia
-Eclampsia, preeclamsia superimposed on chronic hypertension
-Chronic hypertension
-Hypertension in pregnancy-etiology and pathogenesis
-Pathology
-Mild hypertension in pregnancy-prevention and management
-Severe hypertension in pregnancy-management
-Severe preeclampsia in pregnancy-management
-Complications of hypertension
-Antihypertensive therapy- centrally acting drugs
-Antihypertensive therapy-beta blockers, calcium channel blockers
-Antihypertensive therapy-alpha blockers, vasodilator, diuretics, ACE inhibitors
-Acute severe hypertension - treatment
-Eclampsia - signs and symptoms
-Eclampsia - management
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