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  • Pathophysiology of Mild-Preeclampsia

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    Lohrhen Lheighh Cahreeniyow
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    Mild preeclampsia is caused by an unknown etiologic agent that leads to vasospasm and reduced perfusion, primarily affecting the renal glomeruli and causing proteinuria. This triggers the renin-angiotensin system leading to vasoconstriction, hypertension, fluid retention and edema through aldosterone production and sodium reabsorption. Predisposing factors include advanced age, race, multiple gestation and grand multiparity while precipitating factors can be lifestyle, hydramnios and secondary illnesses.

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    Mild preeclampsia is caused by an unknown etiologic agent that leads to vasospasm and reduced perfusion, primarily affecting the renal glomeruli and causing proteinuria. This triggers the renin-angiotensin system leading to vasoconstriction, hypertension, fluid retention and edema through aldosterone production and sodium reabsorption. Predisposing factors include advanced age, race, multiple gestation and grand multiparity while precipitating factors can be lifestyle, hydramnios and secondary illnesses.

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    26 views1 page

    Pathophysiology of Mild-Preeclampsia

    Uploaded by

    Lohrhen Lheighh Cahreeniyow
    Mild preeclampsia is caused by an unknown etiologic agent that leads to vasospasm and reduced perfusion, primarily affecting the renal glomeruli and causing proteinuria. This triggers the renin-angiotensin system leading to vasoconstriction, hypertension, fluid retention and edema through aldosterone production and sodium reabsorption. Predisposing factors include advanced age, race, multiple gestation and grand multiparity while precipitating factors can be lifestyle, hydramnios and secondary illnesses.

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    PATHOPHYSIOLOGY OF MILD- PREECLAMPSIA

    ` PREDISPOSING FACTORS Age Race Multiple gestation Grand multiparity PRECIPITATING FACTORS Lifestyle Hydramnios Secondary illnesses

    ETIOLOGIC AGENT (unknown)

    VASOSPASM

    REDUCED PERFUSION

    RENAL GLOMERULI AFFECTED PROTEINURIA

    RELEASE OF RENIN

    ANGIOTENSIN I CONVERSION TO ANGIOTENSIN II ALDOSTERONE PRODUCTION SODIUM REABSORPTION

    VASOCONSTRICTION

    RELEASE OFADRENAL HORMONES HYPERTENSION

    FLUID RETENTION

    EDEMA

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