Digestive System – main symptoms, diarrhea, vomiting, Pathophysiology

In Pathophysiology of The Digestive System, The causes of disorders of the gastrointestinal tract are quite diverse, they are combined into several groups.

  1. Eating disorders, i.e. malnutrition, overeating, or changes in food quality (imbalance in proteins, carbohydrates, or fats).
  2. Violations associated with the pathogenic effects of microbial flora or helminths.
  3. Alcohol and nicotine abuse.
  4. Radiation damage and damage by toxic substances.
  5. Psycho-emotional trauma and stress.
  6. Occupational hazards.
  7. Endocrine disorders, including age-related ones.


MAIN SYMPTOMS OF DIGESTIVE TRACT PATHOLOGY (Pathophysiology of The Digestive System)

  1. Bloating can be acute and chronic, mechanical or biochemical in origin. In young children, the cause is more often an excess of air in the stomach. The most typical mechanical causes are the accumulation of fluid in the abdominal cavity (ascites), diseases accompanied by severe pain and secondary paralytic ileus (peritonitis, renal colic, etc.). At the same time, most of the biochemical causes of bloating are mediated by the influence of acidosis and electrolyte imbalance in the intestine (adrenal insufficiency, cystic fibrosis, galactosemia, etc.).
  2. Abdominal pain is mainly of three types: visceral, peritoneal and radiating. In general, the organs of the abdominal cavity are poorly innervated by the fibers of pain sensitivity, therefore, visceral pain is usually not very specific in nature, poorly localized. The sensation of pain emanating from the internal organs arises due to stretching of the organ bed, and quite fast.

Peritoneal pain is often the result of an inflammatory process, for example, with appendicitis, etc.

Irradiating pain appears as a result of nerve irritation

endings in one of the many branches of the nerve trunk and is felt in one of several areas of distribution of other branches (for example, in liver diseases, pain can “give” to the region of the kidneys, stomach, which made it possible to consider these pain sensations an integral part of viscero-visceral reflexes). The causes of abdominal pain are divided into three large groups.

  1. Gastrointestinal (acute abdomen, inflammatory diseases of the abdominal organs).
  2. Infectious (pneumonia and pleural effusion, parasites, urinary tract infection).
  3. Metabolic (acidosis of any etiology, diabetes, hypoglycemia, hyperlipidemia, intoxication – lead, irritating poisons).

The molecular mechanism of abdominal pain in acidosis is unknown, but ischemia is thought to cause an increase in the concentration of tissue metabolites around nerve endings and thus induce pain.

Diarrhea – In Pathophysiology of The Digestive System, Every year, a huge number of people in the world have diarrhea, in the overwhelming majority of cases of secondary or infectious origin. The intestine is primarily an absorbing and transporting organ that ensures the transfer of substances from the environment to the body. Accordingly, most types of diarrhea are based on one of the following four mechanisms:

  1. osmotic, i.e. due to the presence in the intestinal lumen of an unusual amount of poorly absorbed, osmotically active substances (for example, with deficiency of disaccharidases);
  2. violation of the processes of active transport (absorption) – chloride diarrhea, impaired absorption of glucose and galactose;
  3. secretory, i.e. increased intestinal secretion (infectious enteritis, accumulation of secretory substances – bile salts of fatty acids);
  4. violation of intestinal motility (hypocalcemia, hypothyroidism, adrenal insufficiency, cholinergic drugs).

In Pathophysiology of The Digestive System, Malabsorption in the intestine is manifested primarily by impaired absorption of fats, accompanied by steatorrhea. Since lipids provide about 50% of calorie requirements, this disorder can have serious consequences for growth and general well-being. Penetrating with the help of bile acids into the cells of the intestinal mucosa, fatty acids bind with glycerol, forming esterified fatty acids. They are surrounded by a thin layer of proteins, forming a transport form –

In Pathophysiology of The Digestive System, chylomicrons. Absorption of lipids and fat-soluble vitamins

new depends on the following factors.

  1. Emulsification of lipids, determined by the presence of bile salts.
  2. Digestion of triglycerides catalyzed by pancreatic lipase.
  3. The suction surface of the intestinal mucosa, which is necessary for the formation of chylomicrons.

Young children are especially sensitive in this regard: their total pool of microvilli of the jejunum is less than that of adults. For the normal absorption of fat, the action of pancreatic lipase and cholesterol esterase is of great importance. The causes of intestinal fat absorption disorders can be divided into three groups:

  1. Associated with the pathology of the pancreas: cystic fibrosis, Schwachman’s syndrome, lipase deficiency.
  2. Associated with pathology of the liver and bile ducts: cirrhosis, atresia or obstruction of the bile duct, impaired synthesis of bile acids.
  3. Associated with bowel pathology: blind loop syndrome, chronic infection, parasites, radiation damage, celiac disease, etc.

Vomiting is a complex reflex act of erupting the contents of the stomach (and intestines) out through the mouth. Vomiting is usually preceded by nausea, hypersalivation, tachypnea, and tachycardia.

The vomiting center is located in the medulla oblongata, near the sensory nucleus of the vagus nerve. From a biochemical point of view, the metabolic consequences of vomiting are much more important than the act of vomiting as such, diagnostically relatively insignificant. The consequences of vomiting include dehydration, alkalosis, hyponatremia. The reasons for vomiting are as follows:

  1. Disorders of amino acid metabolism (phenylketonuria, tyrosinemia).
  2. Organic acidemia (lactic acidosis, methylmalonic aciduria).
  3. Violations in the urea cycle (hyperornithinemia, arginine-succinic aciduria, etc.).
  4. Others: galactosemia, adrenogenital syndrome, metabolic acidosis, uremia, cystic fibrosis, porphyria, renal tubular acidosis.

One of the most common disorders of appetite is considered to be its absence – anorexia . More often we are talking about the so-called “anorexia nervosa”, which occurs mainly in girls of puberty and young women (very rarely in boys). This is a serious condition that, if not interrupted, can lead to death. Usually, anorexia nervosa is accompanied by a drop in body weight, amenorrhea, constipation, a decrease in body temperature, and low blood pressure.

Anorexia as such is caused by excess protein and imbalanced mixtures of amino acids. Its mechanism is not exactly known, but its implementation does not depend on the hypothalamus. Anorexia often occurs with liver diseases, for example, hepatitis (but the mechanism of this phenomenon is also not clear), vitamin deficiencies, dehydration, infectious diseases.

Increased appetite (hyperphagia, bulimia) is a kind of painful condition that accompanies diabetes mellitus, some metabolic diseases.

Hyperphagia can be induced in animals by systematic injections of insulin or glucocorticoids. It should be noted that increased appetite without adequate feedback guarantees obesity with all its negative consequences.

Hypersalivation – In Pathophysiology of The Digestive System, increased salivation in case of inflammation of the oral mucosa, pulpitis, periodontitis, during dental procedures, in diseases of the digestive system, pregnancy, the use of parasympathomimetics. The total molar concentration of saliva increases (Gendengain’s law). With hypersalivation, neutralization of gastric juice is likely and, accordingly, indigestion in the stomach. In addition, the loss of a large amount of saliva is fraught with severe disorders of the water-salt balance.

Hyposalivation – In Pathophysiology of The Digestive System, a decrease in salivary secretion during infectious and febrile processes, with dehydration, with the action of atropine-like substances, as well as with inflammation in the salivary glands (sialoadenitis, mumps, submaxillitis). Known severe systemic damage to the salivary and lacrimal glands (Sjogren’s syndrome), characterized by dryness of the mucous membranes of the mouth, eyes and upper respiratory tract. Hyposalivation is sometimes observed with cystic fibrosis and calculous sialoadenitis, inflammation of the ducts (sialodochitis). At the same time, the act of chewing and swallowing becomes more difficult, the development of infectious inflammatory diseases of the oral cavity is initiated.

The processing of food in the oral cavity ends with the act of swallowing, ensuring that food enters the stomach. Its violation (dysphagia) is sometimes associated with a disorder of the functions of the trigeminal, hypoglossal, vagus, glossopharyngeal and other nerves, dysfunction of the swallowing muscles, congenital and acquired defects of the hard and soft palate and tonsils. The act of swallowing is impaired in rabies, tetanus and hysteria (spastic muscle paralysis). The final act of swallowing is the movement of food masses along the esophagus under the influence of its peristalsis. This process can be disrupted with spasm or paralysis of the muscular membrane of the esophagus, or with its narrowing (burn, diverticulum, etc.).

In Pathophysiology of The Digestive System, The main functions of the stomach:

  1. reservoir;
  2. secretory;
  3. motor;
  4. suction;
  5. excretory.

In Pathophysiology of The Digestive System, Currently, there are three interrelated phases of gastric secretion: neurogenic (vagal), gastric (gastric) and intestinal, regulated by stimulation of receptors and hormones of the small intestine.

Low acidity of gastric juice is a common condition (in acute and chronic gastritis, stomach tumors, dehydration), but it is difficult to make an accurate diagnosis. When the glands of the stomach lose their ability to secrete HCl and enzymes, they speak of achilia (found in atrophic gastritis, stomach cancer, B 12 anemia ). With a decrease in the bactericidal action of HCl, the development of fermentation and decay processes is possible.

The vagus nerve, gastrin, cholecystokinin, pituitary and adrenal hormones, insulin, and thyroid hormones are capable of stimulating the production of gastric juice (including HCl).

If normally about 2 liters of gastric juice is produced per day, then with hypersecretion it is 0.5-1.5 times more, which is accompanied by hyperchlorhydria (increased HCl). Hypersecretion occurs in gastric ulcer and duodenal ulcer, pylorospasm and pyloric stenosis, alcohol abuse, hot food, and therapy with certain medications.

Strengthening of peristalsis (hyperkinesis) is associated with an increase in the tone of the vagus nerve, ingestion of rough food, alcohol, histamine, choline-like substances and stress. Disorders of humoral regulation play an important role. Normal peristalsis is maintained by motilin produced by enterophinic cells of the small intestine. Its production increases when the pH of the contents of the duodenum rises and is inhibited when it decreases. Hyperkinesis is observed with gastritis and ulcers, with renal or hepatic colic. In this case, the acidity of gastric juice may increase, which, entering the duodenum, causes a prolonged closure of the pylorus and a slowdown in the evacuation of stomach contents (enterogastric reflux).

Decreased peristalsis (hypokinesis) is most often found in gastritis, gastroptosis, weight loss and asthenia, increased fat content in food, unpleasant taste sensations, fear. Gastroinhibiting and vasoactive intestinal peptides inhibit the motor activity of the stomach, secretin – products of the small intestine. Hypokinesis is often accompanied by reflux of gastric contents into the esophagus, heartburn. A severe disorder leading to a violation of the evacuation of food from the stomach is pylorospasm (with peptic ulcer, gastritis, pyloroduodenitis, stomach polyps). It is accompanied by a complex increase in peristalsis and hypertrophy of the muscular membrane of the stomach. Hypertrophic stenosis of the pylorus sometimes joins pylorospasm (especially in children at an early age).

In the intestine, distant (cavity) and membrane (parietal) digestion is carried out.



Congenital Intestinal Hydrolase Deficiency (Pathophysiology of The Digestive System)

1st group: mainly associated with lactase deficiency. Since the disaccharide lactose is found only as a component of milk, this type of disorder is more often observed in infants. Undigested lactose is not available to the body, remains in the intestines and is used by bacteria, supporting the development of pathogenic intestinal flora. Hence, flatulence, diarrhea and vomiting, followed by isotonic dehydration and alkalosis. The disease is facilitated by the loss of amino acids in the urine, which entails a violation of protein metabolism and hypotrophy. The only way out of this situation is to transfer the child to artificial feeding.

Lactose intolerance also occurs in adults. They have so-

after the intake of milk, gastrointestinal disorders develop. Lactose deficiency in such people is formed during ontogenesis, i.e. not immediately after birth. Defects in lactose genes are widespread among the Eastern peoples, in the Central

Noah Asia, among northern peoples, American blacks and Indians.

2nd group: sucrose intolerance associated with a deficiency of the enzyme – sucrase. Pathogenesis is determined by the powerful development of intestinal flora and enteritis. Clinically manifests itself when the baby switches to mixed feeding and milk sugar (lactose) is replaced by sucrose. The result is chronic diarrhea, malnutrition, in severe cases, death.

3rd group: maltose intolerance. The condition is determined by maltase deficiency, the clinical manifestations are similar to those of the 1st and 2nd groups. Elimination of the corresponding disaccharide from food is recommended. The appearance of disaccharides in fecal masses is of diagnostic value.

Generalized malabsorption disorders are as follows:

  1. Associated with villous atrophy – (i.e., reduced suction surface area). The condition is induced by hypersensitivity to gluten (gluten enteropathy), with tropical sprue, idiopathic steatorrhea.
  2. Associated with surgical resection of a large part of the small intestine.
  3. Associated with extensive infiltration and inflammation of the intestinal mucosa (usually against the background of altered microflora).
  4. After gastrectomy.
  5. In carcinoid syndrome, which is associated with the formation of an excess of serotonin by tumors containing argentophilic cells, usually arising in the small intestine, as well as their metastases, usually localized in the liver. Lack of absorption is apparently due to stimulation of peristalsis by serotonin and rapid passage of food.
  6. Associated with diseases of the pancreas. Malabsorption is due to insufficient digestion and affects mainly high molecular weight compounds.

In Pathophysiology of The Digestive System, The motor function of the intestine in pathology is usually either enhanced or weakened. Strengthening occurs with inflammation (enteritis, colitis) under the influence of mechanical or chemical stimuli of poorly digested food, under the influence of bacterial toxins, with a disorder of nervous and humoral regulation. Increasing the tone of the vagus nerve stimulates motor skills, as well as serotonin, gastrin, motilin. Vasoactive intestinal peptide inhibits it. The clinical expression of these effects is diarrhea, which in some cases plays a protective role. However, prolonged and profuse diarrhea sometimes ends in exsicosis and even collapse.

The weakening of peristalsis occurs with a small amount of food with insufficient fiber content, with increased digestion of it in the upper gastrointestinal tract, with reduced excitability of the vagus nerve center. Constipation forms. Stagnation of fecal masses, fermentation, decay, flatulence – this is a set of disorders that accompany the weakening of intestinal motility.

Under certain conditions (colitis, enteritis, intestinal obstruction), the barrier function of the intestine decreases and its condition

but-pathogenic flora has a toxic effect due to the activation of decarboxylation of amino acids. Toxic amines are formed – cadaverine, tyramine, indole, skatole, which are usually not

a lot, but with pathology due to fermentation and fermentation, their level increases sharply. In such cases, they talk about intestinal autointoxication. The death of the microflora itself (for example, with prolonged antibiotic therapy) leads to the development of dysbiosis – severe dyspeptic disorders; their therapy in some cases is very difficult.



GASTRIC and duodenal ulcer (Pathophysiology of The Digestive System)

In Pathophysiology of The Digestive System, In the etiology of peptic ulcer disease, extreme or extreme effects on the body are important – severe mental stress, overexertion (confirmed by statistics from the Second World War). A certain role is played by local adverse effects on the stomach and inaccuracies in nutrition (irregular food intake, excessively hot food, alcohol, nicotine, spicy food), hereditary predisposition, the predominance of parasympathetic tone, hypokinesia.

The pathogenesis of the disease is complex and is still largely unclear. There is an interpretation of an ulcer as a psychosomatic disease –

cortico-visceral theory of Bykov-Kurtsin. According to her, the triggering factor of pathology is a disorder of higher nervous activity under the influence of unfavorable extero- and interoceptive signals. The relationship between the cerebral cortex and the subcortical centers for the regulation of autonomic functions is disrupted. The secretion of HCl increases, microcirculation in the wall of the stomach and duodenum is disturbed, dystrophic processes develop. Under the influence of stress hormones (primarily glucocorticoids), the adhesiveness of mucosal cells is disrupted,

digestion of the mucous membrane by pepsin begins. Ulcerogenic effect

the effect of glucocorticoids is realized through an inhibitory effect on the synthesis of prostaglandins, which in turn inhibit the secretion of HCl in the stomach.

In Pathophysiology of The Digestive System, The pathogenetic significance of infectious and allergic processes cannot be denied. It is assumed that the disease begins with the ingestion of Campylobacter pyloridis into the stomach. Further, the bacterium invades the protective layer of mucus and attaches to the apical part of the epithelial cells. The most actively colonized by bacteria is the antrum of the stomach and the duodenal bulb, where there are favorable conditions for them. Due to the adhesion of bacteria on the epithelial cells, a local immune response is formed, i.e. the production of antibodies of different types. Moreover, certain immunoglobulins are highly specific in relation to bacterial antigens and do not give cross-reactions with any representative of the intestinal flora.

In Pathophysiology of The Digestive System, Leukocytes (mainly polymorphonuclear neutrophils) rush into the affected mucosa. Infiltrating it, they cause a characteristic inflammatory reaction, manifested by edema, hyperemia, trophic disturbance, which precedes degenerative changes in the mucous membrane. Erosion forms on the surface, and then an ulcer.

Proof of this point of view on the pathogenesis of peptic ulcer

nor – high efficiency of a number of antibacterial

and acid-lowering drugs.

The background for the previously described pathogenetic reactions are humoral disorders (an increase in the level of histamine, gastrin, insulin).

Protective factors of the gastric mucosa:

  1. Digestive enzymes are isolated inside cells in the form of zymogens (granules) – inactive pepsinogen, trypsinogen, chymotrypsin, etc.
  2. Being in the lumen of the gastrointestinal tract, enzymes hardly penetrate back into the cells of the mucous membrane, since the cell membranes

we have a selective permeability and are covered with a protective layer of mucins (mucus). Probably, with a peptic ulcer,

there is a violation between protective and damaging factors, which leads to a breakdown in the permeability of the protective layer of membranes, activation of proteases directly in the cells of the mucous membrane.

DISORDER OF THE SECRETARY FUNCTION OF THE PANCREAS

In Pathophysiology of The Digestive System, Inflammatory processes in the tissue of the pancreas lead to the development of pancreatitis, acute and chronic. In the etiology of acute pancreatitis, significant importance is attached to alcohol abuse, overeating, excess fatty foods, gallstones and polyps of the pancreatic lumen, mechanical damage, infections and intoxications. As a result, there is an increase in the secretion of pancreatic juice and a violation of its outflow from the pancreas.

The key role in this is played by the activation of phospholipase A2, which causes the destruction of the cell membrane with the release of enzymes from them, which results in autolysis (self-digestion) of the gland tissue, necrosis of its individual areas, the launch of the kinin system, followed by disruption of hemodynamics, respiration, etc. In severe cases, it develops pancreatic shock. Violations of the blood supply to the gland and immunopathological processes play a certain role in the pathogenesis of pancreatitis.

With a decrease in the endocrine function of the pancreas, cystic fibrosis is likely (in patients with impaired metabolism of fat and protein), manifested by chronic steatorrhea and severe hypotrophy, since the absorption of partially digested foods becomes impossible.

A special section of the gastrointestinal tract pathology is made up of diseases of the operated stomach. As a rule, after gastrectomy (partial or total), the malabsorption is negligible. However, the rapid evacuation of the contents from the small residual stomach into the duodenum is fraught with dumping syndrome and hypoglycemia.

With dumping syndrome, soon after a meal, the patient experiences a feeling of discomfort in the abdomen, fainting, and nausea. It is believed that the syndrome is caused by a sudden movement of fluid into the duodenum, which has a high osmotic pressure. Before this excessive load is eliminated by absorption, water flows in accordance with an osmotic gradient from the extracellular fluid into the intestinal lumen. A decrease in plasma volume causes fainting, while an increase in the volume of liquid contents is accompanied by a feeling of discomfort in the abdomen.

Dumping syndrome is accompanied by hypoglycemia if food rich in glucose enters the duodenum faster than usual. In this case, the rate of glucose absorption is very high. A sharp increase in plasma glucose concentration causes the release of insulin, as a result, its content there quickly drops, and symptoms of hypoglycemia often appear, which are typically observed 2 hours after a meal.



 

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