Pregnancy induced Hypertension- Pathogenesis and pathological changes

Pathogenesis & pathological changes seen in pregnancy induced hypertension.

1. Pathogenesis & Pathological changes Ameer Salman

2. pathogenesis of pre-eclampsia/ eclampsia Changes that occur during pregnancy contribute to the development of preeclampsia: Vasospasm Absence of remodelling of spiral arteries Increased production of anti-angiogenic factors Retention of sodium

3. Vasospasm resistance to blood flow development of arterial hypertension also exerts damaging effects on vessels

4. Absence of remodelling of spiral arteries In preeclampsia, cytotrophoblast cells infiltrate the decidual portion of the spiral arteries, but fail to penetrate the myometrial segment spiral arteries fail to develop into large, tortuous vascular channels- resulting in placental hypoperfusion (hypoperfused, ischemic placenta releases several factors into maternal bloodstream causing maternall endothelial dysfunction

5. Absence of remodelling of spiral arteries

6. Increased production of anti-angiogenic factors A number of pro-angiogenic factors are elaborated by placenta, like: VEGF- Vascular endothelial growth factor P1GF- Placental growth factor sEng- Soluble endoglins Balance among the above factors play a vital role for normal placental development. Increased production antiangiogenic factors- disturbs the balance-systemic endothelial dysfunction.

7. Retention of sodium In normal pregnancy, there is marked increase in- plasma volume, GFR & renal blood flow. Whereas in preeclampsia, it is characterised by- Reduced plasma volume Reduced GFR Reduced renal blood flow Hence, there is sodium retention and shift of sodium into the arterial walls- increased sensitivity to press or agents in preeclampsia.

8. Pathological changes

9. Impact of preeclampsia/eclampsia can be seen in most of the vital structures, such as: Liver Kidneys Placenta Brain

10. Liver Smooth surface with mottled appearance- numerous scattered areas of subcapsular hemorrhage. Microscopically, Fibrin thrombi in the portal capillaries (periphery of the lobules) Surrounding peripheral thrombi- areas of haemorrhage and necrosis (periportal hemorrhagic necrosis)

11. Kidneys In PID, there is an association with renal lesion. Enlarged glomeruli invading into the neck of the tubules (Renal biopsy & electron microscopy) Microscopically, Endothelial cells are swollen, possibly blocking the lumen of the capillaries. Cytoplasm shows vacuolation, droplet formation & deposition. These causes glomerular endotheliosis

12. 👎🏼 GFR Proteinuria 👎🏼 Renal blood flow Renal tubular necrosis is common in women with eclampsia. Tubular necrosis can lead to Acute renal failure.

13. Placenta Vasospasm--->decreased uteroplacental blood flow--> Anoxia--->liberation of thromboplastic substances---> intravascular coagulation

14. Brain Gross haemorrhages due to ruptured arteries caused by severe hypertension can be seen. Other findings that can be found include: Cerebral edema Hyperaemia Focal anemia Thrombosis

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