Pregnancy induced Hypertension- Pathogenesis and pathological changes

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PATHOGENESI S & PATHOLOGICA L CHANGES Ameer Salman

Transcript of Pregnancy induced Hypertension- Pathogenesis and pathological changes

PATHOGENESIS &

PATHOLOGICAL CHANGES

Ameer

Salman

PATHOGENESIS OF PRE-ECLAMPSIA/

ECLAMPSIAChanges 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

VASOSPASM

➤ resistance to blood flow

➤development of arterial

hypertension

➤also exerts damaging

effects on vessels

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

Absence of remodelling of spiral arteries

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.

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.

PATHOLOGICAL

CHANGES

Impact of preeclampsia/eclampsia can be seen in most of

the vital structures, such as:

➤ Liver

➤ Kidneys

➤ Placenta

➤ Brain

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)

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

👎🏼

GFR

Proteinuri

a

👎🏼 Renal blood

flow

• Renal tubular necrosis is common in women with

eclampsia.

• Tubular necrosis can lead to Acute renal failure.

PLACENTA

• Vasospasm--->decreased uteroplacental blood flow-->

Anoxia--->liberation of thromboplastic substances--->

intravascular coagulation

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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