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Gestational Hypertension - Coggle Diagram
Gestational Hypertension
Pathophysiology
it is thought to be related to a mechanism of reduced placental perfusion inducing systemic vascular endothelial dysfunction.
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The resultant placental hypoxia induces a cascade of inflammatory events, disrupting the balance of angiogenic factors, and inducing platelet aggregation, all of which result in endothelial dysfunction manifested clinically as the preeclampsia syndrome.
Angiogenic imbalances associated with the development of preeclampsia include decreased concentrations of angiogenic factors such as the vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) and increased concentration of their antagonist, the placental soluble fms-like tyrosine kinase 1 (sFlt-1).
impeding the binding of VEGF and PIGF to their receptors is a factor in the reduction of nitric oxide synthesis, a crucial factor in vascular remodeling and vasodilation, which may otherwise be able to ameliorate placental ischemia
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risk factors
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Multiple fetuses (twins, triplets)
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Nursing care
Bedrest, either at home or in the hospital, may be recommended
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Continued laboratory testing of urine and blood (for changes that may signal worsening of gestational hypertension)
Medications, called corticosteroids, that may help to mature the lungs of the fetus (lung immaturity is a major problem of premature babies)