Pathophysiology of Digestive System PDF

# PATHOPHYSIOLOGY OF DIGESTIVE SYSTEM ## Chapter 21. PATHOPHYSIOLOGY OF DIGESTIVE SYSTEM The main function of the gastrointestinal system is to break down nutrients into small particles and absorb them into the body. This function is carried out through mechanical processes (grinding and transport...

# PATHOPHYSIOLOGY OF DIGESTIVE SYSTEM ## Chapter 21. PATHOPHYSIOLOGY OF DIGESTIVE SYSTEM The main function of the gastrointestinal system is to break down nutrients into small particles and absorb them into the body. This function is carried out through mechanical processes (grinding and transporting of the food lump in the digestive system) and the action of digestive juices. The digestive system has hormone-producing glands and nerve plexuses (Auerbach and Meissner). In general, the digestive system functions under the control of the autonomic nervous system. Normally, activation of the sympathetic nervous system reduces the motor and secretory functions of the gastrointestinal system, and activation of the parasympathetic nervous system increases them. Insufficiency of digestion is understood as a violation of digestion and absorption of nutrients entering the body. Insufficiency of digestion is divided into two parts: general (total) and selective (partial). With a general deficiency, the digestion of all nutrients is disturbed, and with selective deficiency, the digestion of individual nutrients is disturbed. The classification of the digestive system is based on various principles. According to the anatomical principle, there are digestive disorders in the oral cavity, stomach and intestines; according to the clinical course - acute and chronic; according to the etiology - congenital and acquired; according to the pathophysiological principle, disorders of the motor, secretory, absorption, and other functions of the digestive system are distinguished. Disorders of the activity of one of the divisions of the digestive system affects the activity of other divisions. ### 21.1. General etiology of diseases of the digestive system Various etiological factors are involved in the occurrence of diseases of the digestive system: - alimentary factors (intake of dry and rough, hot and cold, poor quality food, etc.); - physical factors (ionizing radiation, etc.); - chemical factors (salts of heavy metals, poisons, etc.); - biological factors (causative agents of typhoid fever, dysentery, helminth infestations, Helicobacter pylori, etc.); - mental factors (negative emotion, stress, etc.); - social factors (bad habits, etc.); - congenital anomalies of the digestive tract; - tumors, endocrinopathies, postoperative conditions, etc. In addition, the pathology of various systems and organs (blood circulation, liver, kidneys, endocrine glands, etc.); changes in the content of substances (hormones, prostaglandins, peptides, biogenic amines, etc.) that take part in the regulation of the digestive organs; neurogenic influence (sympathetic and parasympathetic nervous system) and other factors can lead to pathology of the digestive system. Conditions that contribute to the effect of etiological factors leading to the onset of pathology of the digestive system include reactivity, gender, age, hereditary predisposition, etc. ### 21.2. Disorders of taste sensitivity and appetite Disturbances in taste sensitivity are manifested in the form of ageusia, hypogeusia, hypergeusia, parageusia, dysgeusia /6/. Decreased taste sensitivity is called hypogeusia, and complete disappearance is called ageusia. With ageusia and hypogeusia, functional and structural disorders of taste analysators occur. Damage to the taste analyzer receptors in chemical burns and glossitis, inflammation of the afferent nerves (lingual or lingo- pharyngeal nerves), damage to the taste center (in encephalitis, cerebral hemorrhage, neuropsychiatric disorders), etc., can serve as an example of this. Hypergeusia is a pathological increase in taste sensitivity, which is observed with an increase in the sensitivity of taste receptors and damage to the taste center (mental disorders, etc.). With parageusia, the sense of taste changes qualitatively. For example, sour foods are perceived as bitter, while sweet foods are perceived as salty. With dysgeusia, the sense of taste is perverted. Dysgeusia may be accompanied by a perversion of appetite. In this case, the patients eat inedible substances (chalk, paper, sand, etc.). #### Appetite disorders. Various substances play a role in the occurrence of the feeling of satiety and hunger. Ghrelin, gastrin, oxytocin, acetylcholine, etc., causing hunger, increase appetite, and leptin, glucose, glucagon, somatostatin, serotonin, adrenaline, etc., causing a feeling of satiety, reduce appetite. For example, depression accompanied by a decrease in serotonin levels leads to the hyperphagia. Appetite disorders include (gr. "orexis" appetite) hyporexia (decreased appetite), anorexia (lack of appetite), hyperorexia (increased appetite) and pararexia (perverted appetite). In an experiment, the animals with damaged ventrolateral nuclei of the hypothalamus (center of hunger) feel no hunger, they refuse to eat, have anorexia. A number of acute diseases (gingivitis, pneumonia, enterocolitis, myocardial infarction, etc.) and chronic intoxication (renal and liver failure, poisoning with mercury and nicotine drugs, alcoholism, etc.), neurogenic and psychogenic pathologies (neuroses, schizophrenia, etc.) are accompanied by decreased appetite. The basis of the pathogenesis of anorexia is a decrease in the excitability of the appetite center. Anorexia leads to weight loss (sometimes up to cachexia), dystrophy, and in severe cases to the immune deficiency. An abnormal increase in appetite is called hyperorexia (bulimia). With bulimia (gr. "bus" - bull, "linos" hunger), food intake increases inadequately, which is called polyphagia. At the same time, the feeling of satiety decreases or does not happen at all (acoria). In an experiment, hyperorexia can be obtained by damaging the ventromedial nuclei of the hypothalamus (center of satiety). Organic and functional changes in the central nervous system (cerebral edema, some types of neurosis, etc.), diseases of the endocrine system (thyrotoxicosis, diabetes mellitus, pancreatic tumors) and other pathologies can cause polyphagia. Perverted appetite is called parorexia. Parorexia means the intake of inedible substances (chalk, coal, etc.). Brain trauma, tumors and cerebral hemorrhages, some mental illnesses are accompanied by parorexia. ### 21.3. Digestional disorders in the oral cavity #### Chewing disorders. In the oral cavity, the food mass is crushed by the teeth and moistened with saliva. Violations of grinding, chewing and moistening the food bolus with saliva leads to impaired digestion in the oral cavity. Violation of the chewing apparatus leads to insufficient grinding of food. The chewing apparatus includes teeth, chewing and lingual muscles, bones to which these muscles are attached. Absence of teeth or their damage (caries, periodontitis, periodontal disease, etc.), violation of the neuromuscular apparatus of the lower jaw (myositis, bulbar paralysis, neuritis, etc.), damage to the jaw joints and bones, inflammation of the mucous membrane of the oral cavity and palate (stomatitis, gingivitis, etc.), damage to the lingual muscle leads to impaired grinding of food. Diseased teeth, being a focus of infection, can lead to sensitization of the body, allergic damage. Damage to the teeth or their absence reduces the pressure on the food during chewing. If the swallowed food is not sufficiently crushed, the mucous membrane of the oral cavity, esophagus, stomach is damaged, the reflex phase of the secretion of digestive juices is disturbed and the rate of digestion decreases. #### Dysfunction of the salivary glands. The salivary glands perform secretory and endocrine functions. As a result of the secretory activity of these glands, saliva is produced. Parotin, neuroleukin, urogastron and other substances, which are formed as a result of the endocrine function of the salivary glands, pass into the blood. Under the action of parotin, calcium is transferred from the blood to the bone tissue and also ensures the growth of teeth. Violation of the formation and secretion of saliva complicates the normal course of digestion in the oral cavity. Saliva protects the oral mucosa from the harmful effects of microorganisms. The saliva contains mucin, ptyalin, lysozyme, kallikrein, nucleases, phosphatases, carbonic anhydrase, sodium, potassium, chlorine, bicarbonate ions, etc. Mucin is a saliva glycoprotein that plays a role in wetting, softening and formation of the food bolus, participates in the digestion of carbohydrates. Lysozyme, which is a proteolytic enzyme, has a bactericidal effect and serves to cleanse the oral cavity and prevent the accumulation of bacteria in the oral cavity. Kallikrein regulates blood circulation in the salivary glands and oral mucosa. Nucleases destroy viruses in the mouth. Under normal conditions, up to 1-2 liters of saliva are secreted per day. An increase in salivary secretion is called hypersalivation (hypersialia), and a decrease is called hyposalivation (hyposialia). The reasons for hypersalivation include: - excitement of the center of salivation in the medulla oblongata (with bulbar paralysis); - irritation of the receptors of the oral mucosa, esophagus and stomach (for example, due to exposure to food); - inflammatory processes in the oral cavity (gingivitis, stomatitis, pulpitis, etc.); - irritation of the parasympathetic nerves that innervate the salivary glands (the action of various drugs, toxins, some vegetative poisons pilocarpine, physostigmine, etc., with various types of encephalitis, neuroses, etc.); - exogenous (mercury, nicotine, etc.) and endogenous (uremia, pregnancy toxicosis, etc.) intoxication, helminthic invasions, etc. With hypersalivation, up to 5-14 liters of saliva are produced per day. Saliva has a slightly alkaline pH. Excessive amounts of saliva dilute gastric juice and neutralize it. The bacteriostatic, bactericidal and peptic activity of the diluted and neutralized gastric juice is reduced. Hypersalivation accelerates the evacuation of gastric contents into the duodenum. With prolonged exposure to saliva on the skin in the lip area, it is damaged (maceration) /2/. The loss of a large amount of saliva during hypersalivation leads to dehydration of the body (hyperosmolar hypohydration, since saliva is hypotonic relative to the blood). Hypersalivation is also protective for the body. Various toxic metabolic products are excreted in the saliva. The causes of hyposalivation include /1/: - damage to the salivary glands (inflammation, surgery, radiation sickness, radiation therapy, etc.); - blockage of the lumen of the salivary gland ducts with a stone or compression of these ducts from the outside by a tumor, edematous fluid, scar tissue; - violation of neurohumoral regulation of saliva secretion (damage to the cerebral cortex, hypothalamus, nerve bundles innervating the salivary glands; the action of some vegetative poisons atropine, scopalamin, etc.; hyperthyroidism, diabetes mellitus, etc.); - prolonged hypohydration (intense sweating, diarrhea, etc.). With hyposalivation, the food lump is not completely moistened with saliva, chewing and the act of swallowing are difficult. A poorly moistened food bolus causes damage to the oral mucosa. Hyposalivation leads to drying out of the oral mucosa xerostomia. Hyposalivation and xerostomia are the main symptoms of Sjogren's syndrome, which is a systemic autoimmune disease, characterized by a decrease in the secretion of the digestive glands /7/. At the same time, dryness also occurs in the synovial membranes (pleura, pericardium). Reduced salivation forms a plaque on the surface of the tongue and gums, consisting of destroyed epithelial cells. This creates favorable conditions for the reproduction of microorganisms in the oral cavity and the development of inflammatory processes here (stomatitis, gingivitis, glossitis, dental caries, etc.). A decrease in the content of lysozyme and other substances with a bactericidal effect in saliva leads to the development of inflammatory processes in the mucous membrane of the oral cavity. #### Violation of the act of swallowing. Difficulty swallowing is called dysphagia (gr. "dys" - violation, "phagein" - eat), and complete disappearance - aphagia. The act of swallowing is a complex physiological process consisting of voluntary and involuntary phases. The reasons for the violation of swallowing include: - pathologies accompanied by a feeling of pain in the oral cavity (inflammation of the oral mucosa, fractures of the jaw, etc.); - damage to the nerves involved in the act of swallowing and the swallowing center (with cerebral hemorrhage, etc.); - pathologies of the mandibular joint and masticatory muscles (arthrosis, arthritis, hyper- and hypotonia of the masticatory muscles, paresis, paralysis, etc.); - violations of the afferent and efferent innervation of the masticatory muscles (inflammation and damage to the trigeminal, vagus, hypoglossal, lingopharyngeal nerves); - pathological processes of the esophagus and pharynx (scar, tumor tissue, diverticulum, etc.); - mental disorders (hysteria, etc.). In case of violation of the act of swallowing, the passage of the food bolus from the esophagus to the stomach becomes difficult. Sometimes, as a result of a violation of the act of swallowing, saliva and food masses entering the respiratory tract, lead to aspiration and related pathologies (aspiration pneumonia, bronchospasm, bronchitis, pulmonary abscess, etc.), and in severe cases - to asphyxia. #### Pathology of the esophagus. An increase in the motor function (peristalsis) of the esophagus is called hyperkinesis, a decrease is called hypokinesis or atony. These disorders are mainly associated with changes in the upper and lower esophageal sphincters. The reasons for impaired motor function include: - violation of the nervous regulation of the motor function of the esophagus. Irritation of the vagus nerve increases the peristalsis of the esophagus, and irritation of the sympathetic nervous system decreases; - violation of humoral regulation of esophageal peristalsis (for example, decreased synthesis of VIP- vasoactive intestinal polypeptide, NO, etc.); - sclerotic damage to the esophagus or its spasm (chemical and thermal burns, dermatomyositis, systemic scleroderma, neurological conditions, etc.). Impaired motor function of the esophagus can be observed with achalasia, gastroesophageal reflux, diffuse esophageal spasm, hiatal hernia and scleroderma. Achalasia is characterized by difficulty in relaxation the lower esophageal sphincter (as a result of its hypertonicity and spasm). This is due to damage to the intramural nerve plexus (plexus myentericus) of the distal esophagus. Due to the violation of peristalsis, the transition of the swallowed food bolus into the stomach is difficult. The retention of food in the esophagus for a long time leads to the multiplication of bacteria here, the dilation of the lumen of the esophagus above the level of the lower esophageal sphincter, ulceration of its mucous membrane, the occurrence of retrosternal pain, weight loss, the return of food to the oral cavity (regurgitation), and in severe cases - to the development aspiration pneumonia and esophageal perforation (fig. 21.1) /8/. Diffuse esophageal spasm develops as a result of the absence of the inhibitory effect on the activity of the smooth muscles of the esophagus. It leads to the uncoordinated contractions of the esophagus. Repeated intense contractions of the smooth muscles of the esophagus are observed, and restrosternal pain and dysphagia develop. Retrosternal pain resembles angina pain and disappears after taking nitrates. Scleroderma is a systemic disease from the group of collagenoses. In this disease, the smooth muscle layer of the esophagus wall and its lower sphincter is replaced by collagenous fibrous tissue. As a result, the peristalsis of the esophagus is disturbed and the tonicity of its lower sphincter decreases (hypotonia). With this pathology, dysphagia and gastroesophageal reflux occur (fig. 21.2) /8/. Gastroesophageal reflux is the return of gastric contents to the esophagus. Decreased pressure in the lower esophageal sphincter leads to the development of gastroesophageal reflux. The decrease in pressure here is associated with primary defects of the sphincter musculature and a violation of the nervous regulation of sphincter function. A weakening of the evacuation function of the stomach, an increase in gastric acidity and other causes also play a role in the development of gastroesophageal reflux (fig. 21.3) /8/. One of the main symptoms of gastroesophageal reflux is the appearance of retrosternal burning sensation, that is, heartburn (pyrosis). Due to frequent reflux, inflammation and ulceration of the mucous membrane of the distal esophagus may occur. Inflammation of the mucous membrane of the low part of the esophagus is called reflux esophagitis. Occasionally, metaplasia of the esophageal mucosa occurs - the replacement of squamous epithelial cells with columnar epithelial cells. It is called Barrett esophagus (fig. 21.4.). This process can be complicated by adenocarcinoma. Impaired esophageal motility causes food stagnation, partial dilation and thinning of the esophageal wall (diverticulum). Food masses lingering in the diverticulum rot. Thinning of the diverticulum wall can lead to subsequent perforation. During various pathologies of the esophagus, accompanied by an increase of the intrabdominal and intragastric pressure, a hiatal hernia occurs. Heavy physical work, and congenital or acquired defects of connective tissue and diaphragm also play a role in the formation of a hiatal hernia. ### 21.4. Gastric disorders Digestive disorders in the stomach are associated with changes in its secretory, motility (motor), reservoir, absorption, excretory, barrier and protective functions. Impairment of the secretory function of the stomach is manifested by changes in the quantity and quality of gastric juice. Increased secretion of gastric juice is called hypersecretion, decreased secretion hyposecretion; increased total acidity of gastric juice is called hyperaciditis, decreased - hypoaciditis; an increase in the amount of free hydrochloric acid is called hyperchlorhydria, and a decrease in it is called hypochlorhydria. Glands located in the gastric mucosa secrete hydrochloric acid, pepsinogen, gastromucoprotein (internal factor of Castle), mucus and gastrin. The secretion of hydrochloric acid in the stomach is regulated by endocrine and nerve mechanisms. Histamine synthesized in enterochromaffin-like cells of the stomach increases the secretion of hydrochloric acid. Gastrin, acetylcholine, etc. stimulate the release of histamine. Gastrin improves blood circulation in the stomach, increases the secretion of pepsinogen, the contraction of muscular layer of the stomach. Irritation of the vagus nerve, foods rich in protein and calcium, alcohol, etc. increase secretion of gastrin. Hydrochloric acid, somatostatin, secretin, glucagon, vasoactive intestinal peptide (VIP), prostaglandin E, gastric-inhibitory peptide (GIP) also known as glucose-dependent insulinotropic peptide, etc. reduce secretion of gastrin (fig. 21.5). Gastrin-releasing peptide (GRP, bombesin), ghrelin and other substances are also secreted in the stomach. The GRP stimulates the secretion of gastrin, pepsinogen and HCl. The effect of ghrelin is associated with leptin released from adipose tissue. The appetite increases with an increase in ghrelin, decreases with decreasing. Causes of hypersecretion include: - hereditary excess number of secretory cells in the stomach; - hypertrophy or hyperplasia of enterochromaffin-like cells (hypertrophic gastritis); - increased gastrin secretion; - increased tonicity of the vagus nerve (constitutional vagotonia, some forms of neurosis, etc); - effects of various drugs (ascorbic acid, glucocorticoids, etc.). It is known that the acidic contents of the stomach pass into the duodenum in portions, causing a reflex spasm of the sphincter of the pyloric part of the stomach. After neutralizing of the portion of food bolus that passed into the duodenum, the sphincter opens again, and the next portion of the gastric contents passes into the duodenum, and the process is repeated. Hypersecretion, on the other hand, takes more time to neutralize the portion that passes into the duodenum due to the excessive acidity of the stomach contents. Therefore, the duration of digestion of food in the stomach increases, belching, heartburn and sometimes vomiting and pain occur. The amount of content passing into the intestine is reduced. Intestinal peristalsis weakens and constipation occurs. One of the pathologies associated with hypersecretion of gastric juice is Zollinger-Ellison syndrome (gastrinoma). Zollinger-Ellison syndrome is characterized by the development of a gastrin-producing tumor in the pancreas (65-75%) and other organs (stomach, liver, spleen, lymph nodes, etc.). Gastrin secretion by tumor cells causes persistent hypersecretion in the stomach. In turn, it leads to the development of peptic ulcer, diarrhea, maldigestion and malabsorption. Such peptic ulcers are refractory to therapy and are prone to complications (perforation, penetration and bleeding). The acid content in the intestine damages its mucous membrane, resulting in the development of malabsorption syndrome. Causes of hyposecretion include: - hereditary lack of gastric secretory cells; - hypoplasia of enterochromaffin-like cells (hypo- and atrophic chronic gastritis, etc.); - decrease in gastric secretion; - decreased tonicity of the vagus nerve (constitutional sympathotonia, some forms of neurosis); - protein, vitamin starvation, as well as the effects of various drugs. Due to the low content of hydrochloric acid in the gastric juice, less time is spent on neutralizing the food bolus entering the duodenum. As a result, the evacuation of unchanged food lump into the duodenum is accelerated, it does not mix completely with the intestinal and pancreatic juices. Transport of undigested food to the lower parts of the intestine is accelerated. It irritates the receptors of the intestinal wall, increases peristalsis and causes diarrhea. Lack of hydrochloric acid and pepsin in gastric juice is called achilia. Achilia can be of functional (stress, avitaminosis) and organic (atrophic gastritis) origin. #### Disorders of gastric motility include disturbances in gastric muscle tonicity, peristalsis, and evacuation of gastric contents. An increase in stomach muscle tonicity is called hypertension, a decrease is called hypotension, and a loss is called atony. When the tonicity of the stomach muscles changes, the digestion of food in the stomach and its transfer to the duodenum is impaired. Accelerated gastric peristalsis is called hyperkinesis, and weakening is called hypokinesis. Separately or combined pathology of gastric muscle tonicity and peristalsis either reduces or increases the evacuation of food lump. Activation of the vagus nerve increases the motor function of the stomach, and the activation of the sympathetic nervous system reduces it. Cholecystokinin, a GIP, reduces the motility of the stomach, and motilin, gastrin, increases it. Many pathological processes in the stomach (erosion, ulcers, scars, tumors, etc.) can also change the motility of the stomach.. Impaired gastric motility and secretory function lead to many pathological syndromes. These include early satiety syndrome, heartburn, belching, hiccups, nausea, vomiting and dumping syndrome /1/. Early satiety syndrome is caused by a decrease in the tonicity and motor function of the antrum of the stomach. In this case, eating a small amount of food leads to a feeling of heaviness and fullness in the stomach. Heartburn (pyrosis) is characterized by a burning sensation in the epigastrium, along the esophagus (mainly in the lower part of the esophagus), behind the sternum. Pyrosis is caused by the return of acidic gastric mass to the esophagus (reflux) when the tonicity of the cardial sphincter of the stomach and esophageal sphincter is weakened. Belching (eructatio) is when gases (air, small amounts of food) from the stomach enters the esophagus and from there into the mouth. Thus, when food remains in the stomach for a long time, fermentation and putrefaction processes take place. Carbon dioxide, methane, hydrogen sulfide, ammonia, and other gases are formed in the stomach. Excessive accumulation of gases in the stomach increases the intragastric pressure. The muscles of the stomach, anterior abdominal wall and diaphragm contract reflexively, and gases enter the oral cavity. Spasm of the pyloric part of the stomach and the openness of the esophagus-gastric sphincter contribute to the process of belching. Hiccups (singultus) is a reflex act accompanied by a spasm of the diaphragm, a convulsive contraction of the stomach and a sudden strong inspiration, which occurs simultaneously with narrowing of the laryngeal cleft. Hiccups occur with direct irritation of the mediastinum, pleura, diaphragm and diaphragmatic nerve in diseases of the peritoneum. Nausea is an unpleasant subjective feeling and is often accompanied by vomiting. Nausea occurs due to the excitation of the vomiting center. In most cases, nausea is accompanied by general weakness, sweating, increased salivation, coldness of the extremities, blanching of the skin, decreased blood pressure, etc. These changes are associated with dysfunction of the autonomic nervous system. Vomiting is an involuntary reflex act. During vomiting, the contents of the stomach (sometimes the intestines) are expelled from the oral cavity. Vomiting begins with deep inspiration, the soft palate is raised, the epiglottis is lowered, and the nasopharyngeal junction is closed. The stomach and its pyloric part are contracted, the esophagus is shortened and dilated, and the sphincter between the esophagus and the stomach is fully opened. Strong contraction of the abdominal muscles and diaphragm increases the intraabdominal and intragastric pressure. The contents of the stomach are expelled into the oral cavity with the opposite peristalsis, and from there outwards. Narrowing of the larynx and closing of the nasopharyngeal junction prevents passage of vomit mass into the respiratory tract and nasal cavity. Passage of vomit mass into the respiratory tract may cause aspiration pneumonia. According to its origin, vomiting can be central, peripheral and gastric. Diseases of the central nervous system (meningitis, encephalitis, brain tumors, increased intracranial pressure, etc.), the exposure to nicotine, poisons, toxins, drugs, toxic metabolic products (uremia, ketoacidosis), unpleasant odors, pregnancy toxicosis, etc. irritate the vomiting center (at the bottom of the IV ventricle in the medulla oblongata) and it leads to vomiting (vomiting of central origin). Vomiting is observed during the transmission of impulses from reflexogenic zones (for example, diseases of the larynx, ileocecal part of the intestine, peritoneal cavity, gallbladder, liver, kidney, diseases of the vestibular system, coronary pathologies, etc.) to the vomiting center by peripheral nerves and it leads to vomiting (vomiting of peripheral origin). Irritation of gastric receptors with poor quality food, alcohol, toxic substances, diseases of the gastrointestinal tract etc. cause vomiting of gastric origin. In some cases, vomiting caused by poor quality or indigestible food, toxic substances has protective character, because it cleans the gastrointestinal tract from these substances. Prolonged, frequent vomiting leads to the loosing of Na+, K+, H+ ions, gastric juice, etc. from the body, causes dehydration, hypovolemia, acid-base imbalance (metabolic alkalosis occur). Dumping syndrome is a reflex process that occurs in patients after gastric resection as a result of rapid filling of the small intestine. Food bolus from the resected stomach is rapidly evacuated to the small intestine, intestinal motility increases reflexively, and diarrhea is observed. Fluid loss results in hypovolemia and blood pressure drops. Dumping syndrome can cause redness of the face, weakness, increased sweating, tachycardia, abdominal pain, headache, dizziness, tremors, hypotension, and sometimes unconscoesness, collapse. After a meal, blood sugar increases the secretion of insulin. The hyperglycemia is soon replaced by hypoglycemia. Dumping syndrome is characterized by impaired digestion of fats, absorption of fat-soluble vitamins (vitamins A, D, E, K), iron, lack of endogenous factor of Castle secreted from the stomach, etc. These processes create conditions for the development of various diseases. #### Impaired absorption function of the stomach. Normally, water, alcohol and electrolytes are absorbed from the stomach. Absorption of proteins and toxic substances from the stomach during the destruction of the stomach wall, its inflammation, atony and violation of the barrier function of the stomach, leads to the development of immunopathological processes in the body (allergic reactions, etc.). When the reservoir function of the stomach is impaired, peristalsis and subsequent evacuation of gastric contents weaken, the stomach cavity expands and the wall becomes thinner. Due to the processes of putrefaction and fermentation of the food lump, which remains in the stomach for a long time, the amount of gas formed increases. It causes belching, heartburn, and other symptoms. #### Impaired excretory function of the stomach. The excretory function of the stomach serves to cleanse the body of toxic substances. Normally, some end products of metabolism (creatinine, urea, uric acid, etc.) enter the stomach from the gastric mucosa and are neutralized by digestive enzymes and excreted through the gut. In many chronic kidney diseases, renal failure, the amount of urea, creatinine, etc. in the gastric juice increases. It can lead to development of uremic gastritis. The barrier function of the stomach is provided through the secretion of mucus from the mucous membrane, bicarbonates (HCO 3) with a neutralizing effect. The mucus protects mucous membrane of the stomach against the effects of hydrochloric acid, pepsin, and other substances. One of the main features of the barrier function of the stomach is the strong connection between the epithelial cells of the mucous membrane. Disruption of this function can lead to various diseases (ulcers, etc.). ### 21.5. Ulcer disease of the stomach and duodenum Ulcer is a chronic, relapsing disease characterized by damage to the mucous membranes of the stomach and duodenum. Peptic ulcer disease has seasonal character, may worsen in spring and autumn. According to its localization, ulcers can occur in the the junction of the esophagus into the stomach, in the pyloric part and corpus of the stomach, in the duodenum. In modern times, Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID) are the main etiological factors of peptic ulcer disease. Neuropsychiatric factors (stress, shock, burns, operative intervention), alcohol, smoking, gastric secretion tumors, duodeno-gastric or esophageal-gastric reflux, hypersecretion of hydrochloric acid, delayed evacuation of gastric contents, liver cirrhosis, chronic renal failure also plays a role in the development of peptic ulcer disease. The basis of the pathogenesis of ulcers is a violation of the relationship between the defense factors that protect the gastrointestinal mucosa and the aggression factors that damage it (fig. 21.6) /9/. Protective factors include mucus, bicarbonates (excreted from the stomach, duodenum, and pancreas), the ability of mucosal epithelial cells to regenerate, and the blood supply to the gastrointestinal mucosa, prostaglandins E2. Aggressive factors include Helicobacter pylori, increased acidity and proteolytic activity of gastric juice, impaired motility of the stomach and duodenum, etc. Helicobacter pylori is a gram-negative anaerobic microorganism, that cannot survive in acidic conditions. H.pylori secretes a urease to adapt to an acidic environment. Urease breaks down urea in the stomach, forming ammonia and CO2. Ammonia creates an alkalic pH around the bacterium, the mucin is broke down, and the bacterium adheres to the epithelial cells of the antral part of the stomach. Bacteria multiply intensively in the antral part of the stomach. Phospholipase, secreted by bacteria, damages the epithelial cells of the mucous membrane, allowing H.pylori to penetrate deeper. Ammonia reduces the synthesis of somatostatin by reducing the number of D-cells in the antral part of the stomach, and increases gastrin secretion by irritating G-cells. Increased secretion of gastrin leads to hypersecretion of hydrochloric acid. As a result, the damage to the gastric mucosa deepens. Histamine and serotonin, which are released from gastric enterochromaffin-like cells, also play an important role in the pathogenesis of ulcers. Histamine stimulates the secretion of hydrochloric acid through irritation of H2-receptors and increases the permeability of mucous membrane vessels. Microcirculatory disorders damage the mucous membrane and contribute to the development of ulcers. Long-term therapy by the anti-inflammatory steroids reduces the synthesis of prostaglandins, the formation of mucus, the blood supply to the mucous membrane and the ability of epithelial cells to regenerate. The formation of ulcers during stress is associated with activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal system, an increase in the amount of catecholamines and glucocorticoids. Smoking increases the secretion of hydrochloric acid and pepsinogen, slows the evacuation of gastric contents, increases the occurrence of duodeno-gastric and gastroesophageal reflux. The synthesis of prostaglandins and the blood supply to the mucous membrane is reduced. Epigastric pain, dyspeptic disorders (heartburn, nausea, vomiting, etc.), asthenovegetative symptoms (weakness, fatigue, tachycardia, etc.) are observed in peptic ulcer disease. Ulcer disease is may result in granulation (restoration) of the damaged area, scarring, angiogenesis in the scar tissue, etc. Complications of ulcers include bleeding from the ulcer, perforation, penetration (into small omentum, pancreas, and other organs), obstruction (stenosis), malignancy, posthemorrhagic anemia, fistulas (duodenal ulcer most often opens into the bile ducts, and stomach ulcer - into the colon). ### 21.6. Digestion disorders in the bowels The intestines perform secretory, absorption, incretory, excretory and motility functions. Digestive disorders in the intestines are associated with changes in these functions. Normally, the digestive process in the intestines consists of the secretion of digestive juices, hydrolysis of nutrients, absorption from the intestines into the blood and lymph. The normal digestive functions in the intestines include the intraluminal digestion and the mucosal absorption (membrane digestion). In the process of intraluminal digestion in the lumen of intestine, large-molecule substances are broken down. Mucosal absorption takes place in the enterocytes of the intestinal tract. Here, the hydrolyzed substances undergo the next absorption process. The intestine plays an important role in the absorption of fats, proteins, carbohydrates, water and electrolytes, and secretes various hormones (secretin, cholecystokinin, gastrointestinal peptide - bombesin, vasoactive intestinal peptide (VIP), enteroglucagon, motilin, peptide Y, etc.). Hydrochloric acid provides the secretion in the duodenum of secretin, as well as fats and aminoacids provide the secretion of cholecystokinin. Secretin, cholecystokinin, affects the pancreas and promotes the secretion of bicarbonates and enzymes, respectively. Impaired biliary excretion and pancreatic secretion also lead to digestive disorders in the duodenum. #### Disturbance of bile excretion. Bile is formed in liver cells and accumulates in the gallbladder. Up to 500 ml of bile is excreted into the duodenum per day. The bile consists of bile acids and bile pigments, cholesterol, alkaline phosphatase, etc. Insufficient excretion of bile into the duodenum is called hypocholia, and complete rupture is called acholia. Obstruction of the common bile duct (ductus choledochus) by stones, worms, its inflammation, dyskinesia of the bile ducts, its constriction by tumor, scar tissue, enlarged lymph nodes, etc., impaired neural and humoral regulation of the gallbladder and disorders of bile formation in the liver reduce bile secretion. Under the influence of secretin, the passage of bile from the liver to the bile ducts increases, and under the influence of cholecystokinin and vagus nerve accelerates the contraction of gallbladder, the relaxation of the Oddi's sphincter, and the excretion of pancreatic enzymes. If the formation or excretion of bile is impaired, it is difficult to emulsify and absorb fats. Impaired digestion and absorption of fats leads to steatorrhea. Steatorrhea (gr. stear, atos - fat; rhoe - flow) is the excess output of undigested fats in the feces /1/. When the bile is not enough, it becomes difficult to absorb fatty acids, cholesterol, fat-soluble vitamins and the activity of proteolytic and amylolytic enzymes decreases. As a result, the digestion of proteins and carbohydrates is disturbed, there is a deficiency of fat-soluble vitamins; the intensification of putrefaction and fermentation processes in the intestines creates favorable conditions for the growth of bacteria, flatulence and constipation. #### Disorders of the secretory activity of the pancreas. Exocrine function of the pancreas plays an important role in the digestive process. Pancreatic juice contains enzymes involved in the digestion of carbohydrates, fats, proteins, and bicarbonates that neutralize food bolus that passes from the stomach to the duodenum. Normally, trypsin, chymotrypsin are involved in the breakdown of proteins, pancreatic amylase - carbohydrates, lipase - lipids, cholesterolesterase - cholesterol esters, phospholipase - phospholipids. The reasons for the decrease in the secretion of the pancreas are: - resection of the pancreas, its necrosis, sclerosis, etc; - obstruction of the pancreas duct by stones, its compression by tumors, scar tissue and dyskinesia; - disorders of the nervous and humoral regulation of the gland, etc. During the reduction of pancreatic secretion, digestion of fats, proteins, carbohydrates is disturbed, steatorrhea and creatorrhea (finding muscle fibers in the stool) are observed. Alcohol, hyperlipidemia, hereditary predisposition, trauma, ischemia, obstruction of the pancreatic duct, reflux of bile into the pancreas duct, infectious factors, various drugs, etc. factors play a key role in the development of inflammatory diseases of the pancreas. Normally, the pancreatic and common bile ducts open into the duodenum through the hepatic-pancreatic ampulla (Vater's ampulla). The pressure in the pancreatic duct is two times greater than the pressure in the common bile duct. Therefore, neither bile nor intestinal contents can pass into the pancreatic duct. In some pathologies (bowel obstruction with ileus, loss of tonicity of the Oddi's sphincter, etc.) bile or duodenal contents may enter the pancreatic duct (reflux). In this case, enzymes are activated inside the pancreas. Activation in one area of the gland quickly spreads to the entire gland. Trypsinogen is activated and converted to trypsin. Trypsin and other proteases penetrate in to the blood and caused inflammation of the interstitial tissue of the pancreas by activating the proteolytic systems of blood