Morphology of the Fallopian Tube in Pregnancy
When pregnancy develops outside the uterine cavity—specifically in the fallopian tube—specific histological changes occur. Chorionic villi deeply penetrate the tubal wall, reaching the thickness of its muscular layer. Extravillous trophoblast cells and fibrinoid deposits are found within these tissues. Unlike the endometrium, the decidual reaction in the mucosa of the fallopian tubes is weakly expressed and insignificant.
Gestosis: Epidemiology and Risk Factors
Gestosis (previously referred to as late pregnancy toxemia) is a frequent pregnancy-specific pathology. Global clinical practice still lacks a unified terminology for this condition. The disease is classified according to its severity, with eclampsia representing its most severe form.
Superimposed gestosis is also distinguished—a pathology developing in pregnant women with pre-existing somatic disorders. The average incidence of gestosis ranges between 10% and 15%, although some studies report figures up to 30%.
Major risk factors for gestosis include:
- Overweight and obesity
- Renal disease
- Arterial hypertension and related comorbidities
- Unfavorable socioeconomic conditions
- Maternal age: risk increases in pregnant individuals under 17 and over 30 years old.
Pathogenesis: Gestational Transformation of Spiral Arteries
The exact etiology of gestosis remains incompletely understood, but it is well established that the condition is driven by the presence of placental tissue; delivery of the placenta leads to the resolution of the disease. Impaired trophoblast invasion is considered the cornerstone of pathogenesis.
Physiological Norm In a normal pregnancy, extraplacental trophoblast deeply invades the endometrium and myometrium. Gestational transformation of the spiral arteries occurs: their muscular and elastic tunics are destroyed and replaced by a wide layer of fibrinoid. Invasive extravillous trophoblast cells accumulate around the artery within the decidual tissue. As a result, vessel diameter increases 10- to 15-fold. The loss of the muscular layer renders these arteries unresponsive to circulating maternal vasoconstrictors, ensuring a stable and adequate blood supply to the placenta.
Pathology in Gestosis In gestosis, trophoblast invasion into the endometrium and myometrium is disrupted. Gestational transformation of the spiral arteries fails to occur. Histologically, the vascular lumen remains narrow, and the vessel wall layers (muscular and elastic) are preserved—devoid of fibrinoid necrosis and trophoblast invasion. Against the background of these changes, atherosis may develop—a specific vascular pathology characterized by excessive fibrinoid accumulation and the presence of numerous lipid-laden foamy macrophages.
Humoral Alterations and Systemic Vascular Spasm
The absence of gestational transformation and the narrow lumen of the spiral arteries trigger a biological compensatory reaction. The body attempts to raise blood pressure and enhance blood flow to the placenta to prevent fetal hypoxia.
Vascular inadequacy induces placental ischemia, triggering an acute imbalance of vasoactive substances in the pregnant individual:
- Increased secretion of vasoconstrictive factors: Thromboxane A2, prostaglandin F, angiotensin, and endothelin are actively released into the bloodstream.
- Decreased production of vasodilatory agents: Levels of prostacyclin (prostaglandin I2), prostaglandin E, and nitric oxide drop.
The consequence of this humoral shift is generalized vascular spasm, which serves as the core driver of the clinical presentation of gestosis.