**3. Pathogenesis and risk factors**

The pathogenesis of hemorrhoids is still largely unknown. Hemorrhoids occur based on the theory of varicose veins, as in the case of leg varicose veins, but in the case of hemorrhoids, they occur in the anus. This theory has been abandoned because various studies have shown that varicose veins and hemorrhoids are different entities. There was no increase in the incidence of hemorrhoids in patients with portal hypertension. The theories of vascular hyperplasia and hypertrophy of the anal sphincter are not supported by the evidence. Today, the theory of the sliding of the anal cushions is widely accepted [2, 4]**.**

As it has been stated in the physiology of the anus and rectum, the anal cushion plays a role in protecting the anal canal during defecation. After the stool comes out, the anus cushions will return to their place due to the work of the Treitz muscles.

#### *Prolapsing Hemorrhoids DOI: http://dx.doi.org/10.5772/intechopen.104554*

In constipation, there will be difficulty in defecating. The patient will push a lot so that the anal cushions are often forced to shift distally. Over time, it will be followed by damage to the supporting tissue, so that the anal cushions cannot return to their own position. Prolapsing anal cushions will be followed by venous dilatation, vascular thrombosis, degeneration of fibroelastic tissue, and damage to the Treitz muscles. Inflammatory reactions are also seen in the vascular wall and the surrounding supporting tissues**,** ulceration, ischemia, and thrombosis [4].

Several enzymes play a role in the degradation of the supporting tissues of the anal pads. Matrix metalloproteinase (MMP), a zinc-dependent proteinase, is the most potent enzyme and is capable of degrading elastin, fibronectin, and collagen. MMP-9 is overexpressed in hemorrhoids and degrades elastin fibers. Activation of MMP-2 and MMP-9 by thrombin, plasmin or other proteinases results in damage to the capillary bed and stimulates the vascular proliferative activity of TGF (transforming growth factor). This also explains the thinning of the tunica media in the sphincter-like structures that control blood flow from the arteries to the venous plexus. Hemorrhoids have an overexpressed endoglin attachment site with TGF. Microvascular density also increases, influenced by Vascular Endothelial Growth Factors (VEGF), which increases, especially when there is thrombosis [4].

Morphological and hemodynamic studies showed that in hemorrhoids there was an increase in the diameter of the branches of the superior rectal artery, the amount of blood flowing and its flow rate increased significantly. There is a correlation between the diameter of the arterial branches and the degree of hemorrhoids [6]. Physiological changes in the anal canal in hemorrhoids have also been reported. Anal canal pressure at rest in patients with prolapsed and unprolapsed hemorrhoids was higher than in normal people, without internal anal sphincter hypertrophy. This pressure will decrease after hemorrhoidectomy is performed, so it can be said that this increase in pressure is due to the effect of hemorrhoids, not the cause [7]**.**

Constipation is widely believed to be a risk factor for the occurrence of hemorrhoids, through the sliding mechanism of the anal cushion, as previously stated, but diarrhea has also been reported to increase the risk of hemorrhoids**,** through an unclear mechanism. Pregnancy is also a predisposing factor for hemorrhoids due to increased intra-abdominal pressure causing congestion of the anal cushion, and the patient can recover after delivery. Many other risk factors have been reported for the occurrence of hemorrhoids, such as a low-fiber diet, spicy foods, and drinking alcohol [2, 4, 7].
