Gastric ulcers for alcohol abuse
Introduction
One of the most important functions that are carried out within our body is the assimilation of food to convert them into energy necessary for the development of daily activities and vital functions. The system responsible for fulfilling this function is the digestive that consists of organs such as the oral cavity, esophagus, thin intestine and large intestine. The organ responsible for unfolding food for absorption is stomach through the production of gastric juices composed of enzymes such as pepsin. Under normal conditions, the stomach coating protects the stomach from any damage caused by acidity produced by gastric juices. However, there are conditions that can alter the balance existing in this organ. Within these we can mention excessive alcohol consumption, which generates irritation and inflammation in the stomach lining because the corresponding mechanisms cannot be adapted to excess acidity. If this dysfunctionality is maintained, the appearance of lesions in the mucosa to which ulcers is probably.
The peptic ulcer is a condition of the gastrointestinal mucosa that spreads through mucosae muscularis and is maintained due to gastric juice activity. We find two types: the gastric ulcer (which develops in the stomach) and the duodenal ulcer (which is presented in the duodenum). This research will focus solely on knowing how gastric ulcers occur based on alcohol excess consumption, as well as finding out what structures are particularly damaged and how the tissue alteration occurs at the stomach level.
Objectives
General objective
Determine how excessive alcohol consumption causes ulcers in the stomach.
Specific objectives
- Know the topographic and descriptive anatomy of the stomach.
- Know the location of the lesion in the digestive tract.
- Histologically identify the condition of the gastric mucosa.
- Explain the physiology of the ulcer.
- Investigate how alcohol components alter the function of the gastric mucosa.
Gastric ulcer caused by alcohol consumption
Stomach generalities: affected organ
The stomach is a dilated segment of the digestive tract in the form of a muscular bag located in the curve between the esophagus and the duodenum occupying the upper left of the abdomen under the diaphragm. It measures 25 cm long, 10 to 12 cm wide and 8 to 9 cm in anteroposterior direction (Rouviere, 2005).
Presents the form of a capital J. The curved party out is called the major curvature and is directed down and to the left. The part of the stomach curved inwards, in the opposite part of the stomach, is directed up and right and is called minor curvature (Rouviere, 2005).
In the stomach we can identify two faces: one previous and one posterior, separated from each other by the edges or curvatures of the stomach. The stomach communicates superiorly with the esophagus by means.
The stomach has a driving function that is performed by the attachment of the anterior and posterior faces of the mucosa, forming the gastric channel followed by the liquids that arrive through the cardias. In addition, functionally constitutes the reservoir where the crushing of the food initiated in the oral cavity ends where its digestion begins. This process is carried out thanks to the secretion of the gastric glands. The Piloric portion consists of mucous and endocrine glands that secrete gastrine. This hormone makes the gastric secretion of the descending part of the stomach and enzymes necessary for digestion (Rouviere, 2005).
Stomach biochemistry
The normal volume of stomach fluid is 20 to 100 ml and its pH is very acidic taking values of 1.5 to 3.5 (Medlineplus, 2018). With food intake, parietal cells secrete hydrochloric acid in 160 mmol/l concentrations, equivalent to a pH of 0.8 Although in a state of rest this value can vary between 1–3 in adults and about 4 in babies. The proportion of acid secretion varies widely according to each person and depends on several factors such as age and sex (Barraguirre, 2018).
The acidity of the stomach is controlled by several hormones, among which acetylcholine, histamine, secretin, prostaglandin E2 and the aforementioned gastrin stand out. The normal values of the latter are usually less than 100 pg/ml. However, by increasing its normal levels, it can cause an increase in acid secretion and lead to ulcers formation (Medline Plus, 2018). Something similar happens with histamine because its repeated action on stomach H2 receptors also increases gastric secretion leading to the formation of stomach ulcers (structural biochemistry and applied to medicine, 2013).
Histologically the stomach is formed by four layers:
First, the mucosa presents simple epithelium of high cylindrical cells that form very compact folds. In these folds some cavities are distinguished in which the gastric glands flow. The coating epithelium is formed by mucus secretory cells that lubricate the surface of the mucosa and protect it from possible injuries (Animal Histology Atlas, 2019).
We can distinguish our own histological characteristics in some areas such as cardias that presents a simple prismatic epithelium. In this portion there are mucous cells of gastrin;which is the hormone responsible for the mobility of the stomach and the activation of secretory cells (Animal Histology Atlas, 2019).
Second, the submucosa is formed by lax connective tissue in which plasma lymphocytes and cells, blood and lymphatic vessels are included (Animal Histology Atlas, 2019).
Then, the muscle layer consisting of three layers of smooth muscle comes;an oblique internal, a circular intermediate and a longitudinal external. Which fulfill the function of contracting the stomach to digest food (Atlas of Animal Histology, 2019). And finally a serous layer that is the continuation of the peritoneum of the abdominal and visceral cavity (Animal Histology Atlas, 2019).
Gastric ulcer: generalities
Gastric ulcer also known as peptic ulcer can be defined as an open sore that develops in the internal stomach coating (Mayoclinic, 2018). In our country, from a study conducted with 60 patients it was shown that the cause of peptic ulcer in 43% of them was alcohol consumption. Stomach pain, nausea and vomiting (especially after eating) are presented as associated symptoms of this disease, although in some cases the patient may not present symptoms during a prolonged period of time (Vargas, 2015).
Pathological anatomy
The ulcerative lesion consists of a loss of localized substance of the mucosa and, in a variable degree, of the remaining layers of the gastric wall. The gastric ulcer is usually rounded or oval although it can be linear, and its diameter is generally less than 3cm. It can appear in any portion of the stomach, but in more than half of the cases, it is located along the minor curvature, near the union of the body with the gastric antro (Rozman, 2013).
According to their location, according to Johnson we can classify them in (Ameg, S.F.)
- Grade I: Ulcer located in the minor curvature. It is related to a normal acid expense, constitutes 50 to 60% of gastric ulcers.
- Grade II: Gastric and duodenal location ulcer. It is related to a normal acid expense, it constitutes 20% of gastric ulcers.
- Grade III: Pre -pyloric location ulcer. It is related to a normal acid expense, constitutes 20% of gastric ulcers.
- Grade IV: ulcer in the gastric or high background of the minor curvature. Its frequency is equal to or less than 10%.
- Grade V: secondary ulcer to prolonged use of NSAIDs. It has a high risk of drilling and bleeding, commonly asymptomatic.
Histologically, gastrointestinal mucosa lesions are classified as:
- Erosions: They are superficial and rounded lesions, less than 5mm in diameter, margins little on high, brown or reddened background, and usually multiple. Histologically, the loss of tissue is limited to the mucosa, where neutrophic, neutrophils and red blood cells are observed with a polymorphonuclear infiltrate on the periphery (Rozman, 2013).
- Acute ulcer: they are unique or multiple lesions of similar appearance, but larger than erosions. Histologically, they are deeper and extend at least to the mucosae muscularis. At the bottom of the ulcer, some granulation tissue with low fibroblastic reaction can be observed. Peripheral coating and glandular epithelia show an active aspect because from them regeneration occurs (Rozman, 2013).
- Chronic ulcer: It is characterized by the existence of fibrosis at its base, which will determine the healing of the area. Histologically, it penetrates the mucosa, the submucosa, and usually to a greater or lesser degree in the muscle layer. It presents four very characteristic layers that are outside: a superficial layer of fibrinoleucitarian exudate;a layer of eosinophilic necrotic tissue;Very vascularized granulation tissue with fibroblasts and abundant inflammatory cellsmocyte and polymorphonuclear and, finally, a layer of very variable thick fibrosis (Rozman, 2013).
PHYSIOLOGY OF THE ULCERA
The most admitted concept to explain the physiology of the gastric ulcer is that it is a consequence of an imbalance caused between the aggressive and defensive factors that regulate the function of the gastric mucosa (Vadibia, 2013).
The stomach produces a powerful acid, hydrochloric acid, to unfold food. As protection against this acid, the stomach has a barrier that has the inner part of the stomach. This barrier consists of pre -epithelial, epithelial and sub -epithelial components (Vadibia, 2013).
Preepithelial elements
It includes a layer of mucus and bicarbonate that acts as a physicochemical barrier against multiple molecules. The entire surface of the gastric mucosa between the glands has a continuous layer of surface mucous cells, responsible for secreting a viscous mucus to cover epithelial cells. The thickness of this layer is almost always greater than 3mm (Díaz-Casasola, 2015). The main components are mucin (glycoproteins), bicarbonate (HCO3−), lipids and water (95%) (Díaz-Casasola, 2015).
The gastric mucus is arranged in two layers:
- The inner layer or visible mucus: forms a gelatinous coating with a high concentration of bicarbonate to maintain a neutral pH (7.0), protecting the mucosa from corrosive acid, delaying the retrograde diffusion of hydrogen ions (H+) and maintaining bicarbonate secreted by the epithelium (Díaz-Casasola, 2015).
- The outer layer or soluble mucus: it is responsible for the constant release of nitric oxide (NO) and the union with harmful agents, mix with food and detach (Díaz-Casasola, 2015).
Epithelial elements
Epithelial cells provide protection through various factors. Among these are ionic conveyors that maintain intracellular pH, mucus, bicarbonate and thermal shock proteins. The latter prevent protein denaturation, protecting factors cells such as temperature increase, cytotoxic agents or oxidative stress. Exhibition of the mucosa to various aggressor agents can cause an imbalance between loss and cell renewal (Díaz-Casasola, 2015).
Subepitelial elements
Subepithelial microvasculature has the most important protective effect of gastric mucosa. It is in charge of maintaining uninterrupted blood flow to epithelial cells, serving as a means of transporting nutrients and waste products, in addition to being a signaglandin producing source of important prostaglandins. These substances are responsible for stimulating protective mechanisms (Díaz-Casasola, 2015).
The constant consumption of alcoholic beverages increases the production of gastric acid causing stomach irritation and inflammation (apocatastasis, 2018).
When this happens, acid can lose weight the inner wall of the digestive system and create an open lesion known as ulcer. Therefore, ulcers appear when hydrochloric acid comes into contact with stomach walls (apocatastasis, 2018).
The epithelial cells of the stomach secrete mucosa in response to the irritation of the epithelial coating and as a result of cholinergic stimulation. The superficial portion of the gastric mucosa exists in the form of a gelatinous layer, waterproofing to acid and pepsin. Other gastric cells secrete bicarbonate, which helps regulate acid near the mucosa, this is the case of type E prostaglandins that have an important role of protection because they not only increase bicarbonate production, but also increase secretionMucosa (Philip or Katz, 2018).
When the acid enters the cell, certain additional mechanisms are launched to reduce the wound. Within epithelial cells, ions are released in the cell basolateral membrane to regulate intracellular pH through excess hydrogen ions elimination. Through the restitution process, healthy cells migrate to the affected site. The blood flow of the membrane removes the acid that spreads through the damaged mucosa and provides bicarbonate to the surface of the epithelial cells (Philip or Katz, 2018).
Although the mucosa has all these protection mechanisms, excessive and frequent alcohol consumption does not allow them to be carried out properly because this drink produces the inhibition of these defense methods. For this reason, there are cases of gastric -type ulcers (Philip or Katz, 2018).
conclusion
In conclusion, excessive alcohol consumption is a factor that can generate the gastric ulcer because due to its high level of acidity it causes alterations in normal stomach functioning. This organ in itself already contains an acidic secretion with the purpose of digestboth the generation of an ulcer. This is because excess alcohol inhibits normal mucosa work and does not allow you to exercise your protection property. It has been found that lesions of this type are located in different areas of the stomach being more repeat offered in the minor curvature, and of course it can be mentioned that from the histological point of view the most affected layer of the stomach is the mucosa.
In other words, under normal conditions, we have seen that there is a balance between acid secretion and gastrointestinal mucosa defense. The damage to the mucosa (which is the gastric ulcer) occurs when the balance between aggressive factors and defense mechanisms alters. In this case, the aggressive factor has been excessive alcohol consumption because this substance not only causes the increase in gastric secretion but also interrupts the mechanism of defense of the mucosa preventing mucus, bicarbonate, cell restitution and finallyEpithelial regeneration.
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