**7. Physiopathology of preeclampsia**

Preeclampsia is a syndrome that compromises all maternal organs and systems. The etiology of hypertensive disorders in pregnancy remains to be identified since searching for their origin has led to an infinite number of hypotheses that encompass practically all maternal and fetal organs.

Its physiopathology has not been totally elucidated, and it is no different in the *adolescent* patient than in the rest of the affected population.

Several factors have been implicated in its physiopathology such as oxidative stress, the inflammatory response, abnormal circulatory adaptation, metabolic abnormalities, and even abnormalities in placental development, releasing circulating factors that interfere with vascular endothelial growth factor (VEGF) and placental growth factor (PGF).

Aside from the physiopathogenic factors to be discussed ahead, many factors predisposing to preeclampsia have been reported, such as extreme ages (very young or older), nulliparity, obesity, smoking, a history of preeclampsia in a previous pregnancy, etc. Other less studied factors include some infections, asthma, and the time period between pregnancies [20].

#### **7.1 Systemic endothelial dysfunction**

Endothelial abnormality leads to dysfunction in the control of muscle tone in blood vessels which, in turn, may cause hypertension, edema due to increased permeability, and also proteinuria.

Likewise, the abnormal expression of procoagulant factors by the endothelium favors the development of coagulopathy. All of these abnormalities injure target organs such as the kidney, the liver, the central nervous system, and the placenta. Women with previous vascular disease are at greater risk of developing preeclampsia, quite possibly a result of preestablished vascular injury.

**131**

following:

*Adolescence and Preeclampsia*

*DOI: http://dx.doi.org/10.5772/intechopen.86147*

*7.1.1 First phase: abnormal placentation and placental ischemia*

is not considered complete until weeks 18–20 of gestation.

marker of pseudovasculogenesis, decreased alarmingly.

*7.1.2 Second phase: systemic endothelial dysfunction*

glomerular endotheliosis.

onset of preeclampsia symptoms.

develops in its presence and symptoms rapidly remit after delivery.

The placenta plays a pivotal role in the development of preeclampsia since it only

During the development of normal placentation, the cytotrophoblast invades the spiral arteries which leads to their remodeling; they will have low resistance and high elasticity or capacitance. This cytotrophoblastic vascular invasion not only affects the most superficial layers but reaches the muscle tunica. Trophoblast penetration has also been reported as incomplete and is not invasive in patients with preeclampsia; after complete remodeling of the spiral arteries, placental perfusion decreases. Although remodeling of the spiral arteries begins in the first trimester, it

Recently, great importance has been attributed to angiogenesis because of molecules such as VEGF, angiopectin, and other proteins in the ephrin family. The invasive trophoblast expresses VEGF, P1GF, VEGF, and their respective receptors. Likewise, in in vitro studies in which these signals were blocked, integrin alpha-1, a

As previously mentioned, systemic endothelial dysfunction in these patients may explain all or almost all of the clinical signs, such as hypertension, proteinuria, or abnormalities in target organs such as the liver, the central nervous system, or the kidneys. Among the various findings upholding this theory, we can mention the

• The plasma elevation in some biomarkers, such as fibronectin, factor VIII, and thrombomodulin, reflects endothelial cell injury in patients with preeclampsia.

• Vasodilation mediated by flow has also been reported in the vessels of women

• Decreased production of vasodilators such as prostacyclins or an increase in

• In these patients, renal biopsies show diffuse glomerular injury caused by

• Likewise, the serum of women with preeclampsia has been shown to activate the endothelium in in vitro studies using endothelial cells from the umbilical veins.

An important factor for future consideration is that the increased concentrations of sFlt-1 generally precede, by 5 weeks, the development of clinical manifestations and appear to be most elevated in the initial phase of severe preeclampsia. However, neither PlGF nor VEGF, measured during gestation, appears to decrease prior to the

Most recently, decreases in urinary PIGF have been described before the development of preeclampsia. Some authors have speculated that sFlt-1 plays a beneficial role in fetal circulation and that preeclampsia is a reflection of a maladaptive effect of its release into the maternal circulation. Thus, in the setting of some spiral arterioles with increased resistance, vasoconstriction of the nonplacental maternal circulation would theoretically increase the cardiac output percentage reaching the

with preeclampsia, suggesting altered endothelial function.

the production of angiotensin II also suggests endothelial injury.

*Prediction of Maternal and Fetal Syndrome of Preeclampsia*

and that cannot be explained by another underlying cause.

**6.6 Chronic hypertension and pregnancy-induced hypertension**

sia; values return to baseline after the tenth day postpartum.

It is defined as the presence of seizures or coma in a patient with preeclampsia,

BP > 140/90 mm Hg before pregnancy or the same obtained values on two separate occasions prior to week 20 of gestation or persistent hypertension after the

It is defined as an increase in SAP greater than 30 mm Hg or an increase greater than 15 mm Hg in DAP, on two separate occasions, prior to week 20 of gestation,

This is hypertension developing in the postpartum without previous preeclamp-

Preeclampsia is a syndrome that compromises all maternal organs and systems. The etiology of hypertensive disorders in pregnancy remains to be identified since searching for their origin has led to an infinite number of hypotheses that

Its physiopathology has not been totally elucidated, and it is no different in the

Several factors have been implicated in its physiopathology such as oxidative stress, the inflammatory response, abnormal circulatory adaptation, metabolic abnormalities, and even abnormalities in placental development, releasing circulating factors that interfere with vascular endothelial growth factor (VEGF) and

Aside from the physiopathogenic factors to be discussed ahead, many factors predisposing to preeclampsia have been reported, such as extreme ages (very young or older), nulliparity, obesity, smoking, a history of preeclampsia in a previous pregnancy, etc. Other less studied factors include some infections, asthma, and the

Endothelial abnormality leads to dysfunction in the control of muscle tone in blood vessels which, in turn, may cause hypertension, edema due to increased

Likewise, the abnormal expression of procoagulant factors by the endothelium favors the development of coagulopathy. All of these abnormalities injure target organs such as the kidney, the liver, the central nervous system, and the placenta. Women with previous vascular disease are at greater risk of developing preeclamp-

**6.4 Eclampsia**

**6.5 Chronic hypertension**

sixth week postpartum.

initial proteinuria, and generalized edema.

**6.7 Transient or late arterial hypertension**

**7. Physiopathology of preeclampsia**

placental growth factor (PGF).

time period between pregnancies [20].

**7.1 Systemic endothelial dysfunction**

permeability, and also proteinuria.

encompass practically all maternal and fetal organs.

*adolescent* patient than in the rest of the affected population.

sia, quite possibly a result of preestablished vascular injury.

**130**
