Hemorrhoids causes

Hemorrhoids are abnormal varicose dilatations of the venous plexus in the rectal submucous membrane. The disease is frequent between 30 and 60 years and statistics suggest that this disease affects more than 1 million individuals per year.

Anatomically, the hemorrhoidal plexus is formed by the veins of the rectal submucous membrane, organized in the internal and external hemorrhoidal plexus, situated under the pectineal line. The first signs of hemorrhoidal disease usually appear in the superior hemorrhoidal plexus. Lack of the venous valves at this level acts in such a way that standing up and any pressure increase in the portal system reverberates over the internal hemorrhoidal plexus. Once appeared, the internal hemorrhoids determines a chronic dilatation of the veins, accompanied by clinical suffer and turgor of the interior hemorrhoidal plexus, which leads to the appearance of the external hemorrhoids. Dilatation of the external hemorrhoidal veins after constitution of the internal hemorrhoids is actually a hemodynamic decompensation phenomenon.

There are two types of hemorrhoids , with identical appearance, but with different causes of production: the primary or essential hemorrhoids and the secondary hemorrhoids. While the first category appears mainly because of deterioration of the elastic tissue in the walls of the veins of the mucous and submucous of the anal canal leading to high venous pressure at this level, the second category appears in the context of other disease and may sometimes be the first symptom of it.

Both essential and secondary hemorrhoids can also be internal (inside the rectum, not visible on the outside) or external (outside the anus). The external prolapsing position is most commonly known or associated by patients with definition of the hemorrhoids.

Etiology of the essential hemorrhoids

Alteration of the venous wall is the main factor in the pathological process which determines the appearance of the primary or essential hemorrhoids. The pathological modifications in the venous wall determine dilatation of the vascular lumen, which then leads the venous stasis. There are a series of genetic factors that generate or favor this pathological process:

  1. Hereditary factors could have the same role as in the varicose disease. They are responsible for the low quality of the collagen tissue, interfering with the quality of the venous wall, which is weaker in this case and thus not able to maintain the proper pressure in the venous system at this level and leading to dilatation of the lumen. This explains the association between hemorrhoids and other collagen related disease such as varicocele, weakness hernia or scoliosis.
  2. Inflammatory factors: the source of the inflammation is usually represented by inflammation of the rectum, Morgagni crypts or Hermann glands. Secondary to the inflammatory process the elastic tissue in the walls of the veins is progressively altered and replaced with fibrous tissue.
  3. Other etiological factors are represented by: obesity, arterial hypertension, chronic constipation (straining results in prolapsed of this tissue to the outside of the anal canal, creating external hemorrhoids), diarrhea, sitting on a chair for long periods, alimentation rich in alcohol, fat and poor in fiber, spices, sauces, which can determine chronic hepatitis and then lead to hemorrhoids because of the increased pressure in the veins of the lower rectum. Pulmonary disease associated with prolonged cough (such as chronic obstructive bronchial and pulmonary pathology) can also lead to the appearance of the hemorrhoids, determined by the increase in pressure at the level of the rectum veins during the cough.
Etiology of the secondary hemorrhoids

Secondary hemorrhoids are usually the result of another disease, located in the pelvis or in another part of the body, which causes hypertension at the level of the lower rectum. Thus, the causes that generate secondary or symptomatic hemorrhoids must be well known.

Modifications of the venous walls in the hemorrhoidal plexus and the stasis secondary to the pelvic venous hypertension are in a reciprocal pathological interdependence. Pelvic venous hypertension can be determined by appearance at this level of pelvic or genital tumors (uterine fibroma, ovarian tumors, prostate adenoma or tumors) that come in contact with the veins and compress them during their growth. In the malignant rectum tumors, in cardiac insufficiency and in pregnancy secondary hemorrhoids appear as well.

Also, the portal hypertension reverberates early over the avalvular veins of the superior hemorrhoidal plexus. In hepatic cirrhosis (usually associated with alcohol abuse, hepatitis, lack of certain enzymes or right cardiac insufficiency) or pancreatic tumors (demonstrated to be related to smoking) that determine a portal hypertension syndrome, secondary hemorrhoids appear as epiphenomena.