The digestive system performs the function of processing food, separating proteins, carbohydrates, minerals and other essential substances, and also ensures their absorption into the bloodstream. Consider the most common diseases of the digestive system.
The digestive organs include:
- esophagus;
- liver;
- gallbladder;
- stomach;
- pancreas;
- intestines.
Interruptions in the normal functioning of these organs can cause serious consequences for the life and activity of a person. The performance of the gastrointestinal tract is closely related to the environment and most diseases are largely dependent on the effects of external factors (viruses, bacteria, etc.).
Remember! To avoid diseases of the gastrointestinal tract, you should not abuse food and drinks. Changes in the digestive process also cause emotional stress.
Abdominal pain can occur in any part of the digestive tract, from the mouth to the intestines. Sometimes pain indicates a minor problem, such as eating too much. In other cases, it can be a signal that a serious illness has begun that requires treatment.
It is difficult or painful digestion. May occur against a background of physical or emotional overload. It can be caused by gastritis, an ulcer, or inflammation of the gallbladder.
The main symptoms of dyspepsia: a feeling of heaviness in the stomach, gas, constipation, diarrhea, nausea. These uncomfortable manifestations can be accompanied by headaches or dizziness. Treatment is prescribed depending on the specific cause of the disease and includes taking medications, introducing a special diet.
Heartburn
Heartburn occurs due to insufficient closure of the sphincter. In this case, gastric acid can be thrown into the esophagus and cause irritation.
There are a number of factors that contribute to heartburn. This is overweight, in which there is squeezing of the abdomen, fatty or spicy foods, alcoholic beverages, caffeine, mint, chocolate, nicotine, citrus juices and tomatoes. The habit of lying down after eating also contributes to the occurrence of heartburn.
Acute abdominal pain is a symptom of various disorders of its functions. Often they arise from infections, obstruction, eating foods that irritate the walls of the digestive tract.
The problem of colic in infants is not well understood, although it is believed that they are caused by increased gas production due to digestive disorders. Renal colic occurs when stones pass from the ureter to the bladder. Colic symptoms are sometimes confused with appendicitis and peritonitis.
From a medical point of view, it is believed that with constipation, the bowel movement occurs less than 3 times a week. Constipation is not a disease, but a symptom of a disease. It can appear when:
- insufficient fluid intake;
- improper diet;
- lack of regularity of the bowel movement;
- in old age;
- lack of physical activity;
- pregnancy.
Constipation can also cause various diseases such as cancer, hormonal disorders, heart disease or kidney failure. In addition, constipation can occur after taking certain medications.
Note! By itself, it is not dangerous, but if this continues for a long time, it can lead to hemorrhoids or anal fissures.
Diarrhea
Diarrhea is a violation of the rhythm of the intestine, accompanying loose stools. The process is the cause of infections, viral or bacterial. May occur when taking toxic substances that irritate the intestines or during emotional stress.
Hernia
A hernia is a prolapse of an organ or part of it through the wall of the cavity. The classification depends on their structure or location.
- An inguinal hernia is a prolapse of part of the intestine through the abdominal wall into the groin area.
- A diaphragmatic hernia, or hernia of the esophagus, is an opening in the diaphragm through which the intestines can enter the chest cavity.
- Umbilical hernia - the penetration of the intestine through the abdominal wall under the skin of the navel.
Hernias usually occur due to excessive stress on weakened walls. An inguinal hernia can occur, for example, when coughing or having a bowel movement. It causes mild pain. Intra-abdominal hernias are very painful. Some hernias can be repaired with light pressure on the prolapsed part of the intestine. It is advisable to provide such assistance to the elderly. Surgery is recommended for young patients.
You should know! If the hernia is pinched, an emergency surgery is necessary, as this can lead to gangrene in a few hours. The operation is performed with the aim of strengthening the cavity of the walls by suturing.
Gastritis is an acute or chronic inflammation of the stomach lining.
- Acute gastritis causes erosion of the surface cells of the mucous membrane, nodules, and sometimes bleeding of the stomach walls.
- Chronic gastritis occurs with the gradual transformation of the mucous membrane into fibrous tissue. The disease is accompanied by a decrease in the rate of gastric emptying and weight loss.
The most common causes of gastritis are smoking, drinking alcohol, stimulating drinks (tea, coffee), excessive secretion of hydrochloric acid into the gastric juice, and various infections, including syphilis, tuberculosis, and some fungal infections.
Recently, scientists have found that the bacteria Helicobacter pylori are present in the mucous membrane of the stomach and duodenum in 80% of patients with gastritis and peptic ulcer disease (stomach and duodenal ulcer). This discovery was revolutionary in the treatment of such diseases, to the point that the use of antibiotics became one of the main directions.
Remember! Psychological stress is of great importance in the occurrence of gastritis.
A spastic process in which episodes of constipation and diarrhea alternate, accompanied by severe abdominal pain and other symptoms of unknown causes, is called irritable bowel syndrome. In some cases, this is due to a malfunction of the smooth muscles of the colon. Up to 30% of patients who seek advice on gastroenterology suffer from this ailment.
Often, the manifestations of diarrhea are associated with stressful situations. In some cases, such a disease can begin after an infectious disease. Proper nutrition is also important. Some patients feel better after adding fiber to their diet. Others argue that the reduction in the diet of carbohydrates and white bread brings relief.
Enteritis
Inflammatory bowel disease - enteritis. May manifest as abdominal pain, tingling, fever, loss of appetite, nausea, diarrhea. Chronic enteritis can be caused by serious medical conditions that require surgery.
Acute enteritis is less severe, but in old people and children it can cause dehydration and even threaten their lives. Enteritis can be caused by chemical irritants, allergies, or emotional stress. But the most common cause is infection (viral or bacterial).
Appendicitis is an acute inflammation of the appendix of the intestine. Which is a tube 1-2 cm in diameter and 5 to 15 cm in length. It is usually located in the lower right square of the abdomen. Its removal does not cause a change in the pathological nature. The most common cause of appendicitis is infection. Without treatment, the wall of the appendix is destroyed and the contents of the intestine are poured into the abdominal cavity, causing peritonitis.
Appendicitis is more common in young adults. But it can appear at any age. Its typical symptoms are abdominal pain (especially in the lower right side), fever, nausea, vomiting, constipation, or diarrhea.
Know! Treatment for appendicitis is to remove it.
Ulcers
Ulcers can occur in the stomach or in the small intestine (duodenum). In addition to pain, ulcers can lead to complications such as bleeding due to erosion of blood vessels. Thinning of the walls of the stomach or intestines or inflammation in the ulcer area causes peritonitis and obstruction of the gastrointestinal tract.
The immediate cause of peptic ulcer disease is the destruction of the mucous membrane of the stomach or intestines under the influence of hydrochloric acid, which is present in the digestive juice of the stomach.
Interesting! It is believed that Helicobacter pylori plays an important role in the development of gastric or duodenal ulcers. Also, a connection was established for its appearance due to an excess amount of hydrochloric acid, genetic predisposition, smoking abuse, psychological stress.
Depending on the cause of the ulcer, appropriate treatment is applied. These can be drugs that block the production of hydrochloric acid. Antibiotics act on the bacteria Helicobacter pylori. Alcohol and caffeine should be avoided during treatment. Although diet is not overriding. In severe cases, surgery is necessary.
Pancreatitis
This inflammation of the pancreas occurs when enzymes are not removed from it, but are activated directly in this gland. The inflammation can be sudden (acute) or progressive (chronic).
- Acute pancreatitis usually involves only "attack", after which the pancreas returns to its normal state.
- In severe form, acute pancreatitis can endanger the patient's life.
- The chronic form gradually damages the pancreas and its functions, which leads to organ fibrosis.
Alcoholism or high consumption of fatty foods can be the cause of pancreatitis. The main symptom is pain in the upper abdomen, spreading to the back and lower back, nausea, vomiting, a feeling of pain even with a light touch to the abdomen. Often, such an attack ends in 2-3 days, but in 20% the disease evolves, causing hypotension, respiratory and renal failure. In this case, part of the pancreas dies off.
Chronic pancreatitis is characterized by recurrent recurrent abdominal pain. Diabetes mellitus can provoke the disease. In 80% of cases, it is caused by gallstones. Also affect the occurrence of this disease:
- renal failure;
- hypercalcemia;
- the presence of a tumor;
- abdominal trauma;
- cystic fibrosis;
- bites of a wasp, bee, scorpion, etc.;
- some medications;
- infections.
Treatment for pancreatitis depends on the severity. In 90% of patients with acute pancreatitis, the disease goes away without complications. In other cases, the disease is delayed, becoming chronic. If the condition does not improve within the first hours or days, then, as a rule, the patient is transferred to intensive care.
Cholecystitis
Cholecystitis is called the inflammatory process of the walls of the gallbladder. In this case, micro- and macroscopic changes occur, which develop from simple inflammation to the phase of suppuration.
Symptoms can be varied (abdominal pain, nausea, fever, chills, yellowing of the skin, etc.). Attacks usually last for two or three days, but if not treated, they will continue. The onset of cholecystitis can be sudden or gradual.
There are several reasons that can cause or worsen cholecystitis. This is the presence of stones in the gallbladder, infections in the bile duct, tumors in the liver or pancreas, decreased blood circulation in the gallbladder.
Diverticulitis
A group of disorders of the functions of the colon, in which there is inflammation of the small pockets of the mucous membrane (the inner lining of the intestine). These sacs are called diverticula. When the diverticula are free of complications, asymptomatic diverticulosis is called. But if this causes spasms in the intestines and other symptoms, this disease is called diverticulitis.
Diverticulitis occurs when bowel movements are blocked and the colon becomes inflamed. Diverticulitis symptoms: soreness and fever. In severe cases, there are abscesses, intestinal obstruction.
Sometimes the walls of the large intestine grow together with the small intestine or vagina. This is due to the formed fistulas. In severe cases, the contents of the intestine enter the abdominal cavity, which causes peritonitis.
Chronic liver disease that leads to irreversible destruction of liver cells. Cirrhosis is the final stage of many diseases that affect the liver. Its main consequences are liver failure and increased blood pressure in the vein that carries blood from the stomach and gastrointestinal tract to the liver.
Note! Alcohol and hepatitis B are believed to be the main causes of liver cirrhosis. In countries with low alcohol consumption (for example, Islamic countries), the prevalence of cirrhosis is much lower.
The digestive tract is a vital system in the body. Diseases of this system are usually the result of external factors such as diet and infection. From this we can conclude that in most cases this is the result of one's own inattention and disregard for a healthy diet and hygiene rules.
Many do not pay attention to the symptoms of diseases of the digestive system that have appeared. This leads to the fact that at first they simply bring inconvenience, but over time they turn into serious diseases that are very difficult to cure.
Treatment of gastritis and stomach ulcers is carried out in a complex with the use of medications, diet and traditional medicine. These diseases are the most common types of inflammatory conditions of the mucous membrane ...
Gastritis is an inflammatory disease of the gastric mucosa, in which it is severely irritated, erosions occur, which can eventually lead to an ulcer. There are several different types ...
Gastritis is a fairly common disease in modern times. Now an active and impetuous lifestyle prevails, which does not always allow one to eat rationally and regularly. As a result ...
Gastritis, an inflammatory disease of the gastric mucosa, is an extremely common pathology today that can cause many unpleasant symptoms and lead to other disorders ...
FACTORS DAMAGING THE DIGESTIVE ORGANS
Physical nature:
Coarse, poorly chewed, or unchewed food;
Foreign bodies - buttons, coins, pieces of metal, etc .;
Excessively cold or hot food; -ionizing radiation.
Chemical nature:
Alcohol; -products of tobacco combustion that enter the gastrointestinal tract with saliva;
Medicines such as aspirin, antibiotics. cytostatics;
Toxic substances that penetrate the digestive organs with food - salts of heavy metals, fungal toxins, etc.
Biological nature:
Microorganisms and their toxins; -helminths;
Excess or deficiency of vitamins, such as vitamin C, group B, PP.
Causes of diseases of the digestive system
Each disease of the digestive system has its own specific causes, but among them one can distinguish those that are characteristic of most diseases of the digestive system. All these reasons can be divided into external and internal.
The main ones are, of course, external reasons. These include, first of all, food, liquids, drugs: Unbalanced diet (lack or excess of proteins, fats, carbohydrates) irregular nutrition (every day at different times), frequent eating of “aggressive” components (spicy, salty , hot, etc.), the quality of the products themselves (various additives such as preservatives) - all these are the main causes of diseases of the stomach and intestines and are often the only cause of digestive disorders such as constipation, diarrhea, increased gas production and other digestive disorders. diseases of the digestive system can cause alcohol and its substitutes, carbonated and other drinks containing preservatives and dyes.
And, of course, medicines. Also, external causes of diseases of the digestive system include microorganisms (viruses, bacteria and protozoa that cause specific and non-specific diseases), worms (flukes, tapeworms, roundworms), coming mainly with food or water. Smoking, an independent cause of stomach diseases and intestines are infrequent, but together with insufficient oral hygiene, it causes diseases of the oral cavity (gingivitis, stomatitis, periodontal disease, lip cancer). More external causes of diseases of the stomach and intestines include frequent stress, negative emotions, worries for any reason.
For internal reasons diseases of the digestive system include genetic - this is a predisposition (that is, the presence of a disease of the digestive system in previous generations), disorders of intrauterine development (mutations in the genetic apparatus), autoimmune (when the body, for one reason or another, begins to attack its organs).
Types of digestive disorders:
Violation of the receptor apparatus:
Hypergeusia (Taste disorder, manifested by increased gustatory sensations);
Hypogeusia (decreased gustatory sensitivity).
ageusia (inability to distinguish the taste of substances, due to diseases of the mucous membrane of the tongue and palate).
parageusia (Perversion of gustatory sensitivity, the appearance of gustatory sensations in the absence of an appropriate stimulus. It is observed with damage to the central part of the gustatory analyzer in the cerebral cortex (opercular region and hippocampus) or the pathways of gustatory sensitivity).
dysgeusia (a disorder of taste, characterized by the loss or perversion of the perception of certain gustatory stimuli).
Disorders of the formation and secretion of saliva: hyposalivation (decreased salivary secretion) and hypersalivation (increased salivary secretion)
Pathology of the esophagus: heartburn (a burning sensation, mainly in the lower esophagus, caused by the throwing of acidic gastric contents into the esophagus), belching (the release of gases formed in the stomach through the mouth, sometimes accompanied by the ingestion of particles of stomach contents into the mouth), regurgitation (ejection of food from the esophagus and stomach).
Stomach pathology: Secretory dysfunctions, Motor dysfunctions (see question 52)
Bowel pathology : disorders of the digestive function, absorption function, motor function and barrier-protective.
53. pathology of protein metabolism. Metabolic disorders underlie all functional and organic damage to organs and tissues leading to the onset of the disease. At the same time, metabolic pathology can aggravate the course of the underlying disease, acting as a complicating factor. reasons general violations of protein metabolism is a quantitative or qualitative protein deficiency of primary (exogenous) origin. It may be due to:
1. violation of the breakdown and absorption of proteins in the gastrointestinal tract;
2. slowing down the flow of amino acids into organs and tissues;
3. violation of protein biosynthesis;
4. violation of the interstitial exchange of amino acids;
5. a change in the rate of protein breakdown;
6. pathology of the formation of end products of protein metabolism.
Disorders of protein breakdown and absorption. In the digestive tract, proteins are broken down under the influence of proteolytic enzymes. At the same time, on the one hand, protein substances and other nitrogenous compounds lose their specific features.
The main causes insufficient breakdown of proteins - a quantitative decrease in the secretion of hydrochloric acid and enzymes, a decrease in the activity of proteolytic enzymes (pepsin, trypsin, chymotrypsin) and the associated insufficient formation of amino acids, a decrease in the time of their exposure (acceleration of peristalsis).
In addition to general manifestations of amino acid metabolism disorders, there may be specific disorders associated with the absence of a specific amino acid. So, a lack of lysine (especially in a developing organism) retards growth and general development, lowers the content of hemoglobin and erythrocytes in the blood. With a lack of tryptophan in the body, hypochromic anemia occurs. Arginine deficiency leads to impaired spermatogenesis, and histidine - to the development of eczema, growth retardation, inhibition of hemoglobin synthesis.
In addition, insufficient digestion of protein in the upper parts of the gastrointestinal tract is accompanied by an increase in the transfer of products of its incomplete breakdown into the large intestine and an increase in the process of bacterial breakdown of amino acids. This leads to an increase in the formation of poisonous aromatic compounds (indole, skatole, phenol, cresol) and the development of general intoxication of the body with these decay products.
Slowing down the flow of amino acids into organs and tissues... Since a number of amino acids are the starting material for the formation of biogenic amines, their retention in the blood creates conditions for the accumulation of the corresponding proteinogenic amines in tissues and blood and the manifestation of their pathogenic effect on various organs and systems. The increased content of tyrosine in the blood promotes the accumulation of tyramine, which is involved in the pathogenesis of malignant hypertension. A prolonged increase in the amount of histidine leads to an increase in the concentration of histamine, which contributes to impaired blood circulation and capillary permeability. In addition, an increase in the content of amino acids in the blood is manifested by an increase in their excretion in the urine and the formation of a special form of metabolic disorders - aminoaciduria. Aminoaciduria can be general, associated with an increase in the concentration of several amino acids in the blood, or selective - with an increase in the content of any one amino acid in the blood.
Violation of protein synthesis... The synthesis of protein structures in the body is the central link in protein metabolism. Even small violations of the specificity of protein biosynthesis can lead to profound pathological changes in the body.
The absence of at least one (out of 20) essential amino acids in cells stops protein synthesis in general.
Violation of the rate of synthesis protein may be due to a disorder in the function of the corresponding genetic structures on which this synthesis takes place (DNA transcription, translation).
Damage to the genetic apparatus can be both hereditary and acquired, arising under the influence of various mutagenic factors (ionizing radiation, ultraviolet rays, etc.). Some antibiotics can cause protein synthesis impairment. So, "errors" in reading the genetic code can occur under the influence of streptomycin, neomycin and a number of other antibiotics. Tetracyclines inhibit the addition of new amino acids to the growing polypeptide chain. Mitomycin inhibits protein synthesis due to the alkylation of DNA (the formation of strong covalent bonds between its chains), preventing the splitting of DNA strands.
Qualitative and quantitative disorders of protein biosynthesis are distinguished. The importance of qualitative changes in protein biosynthesis in the pathogenesis of various diseases can be judged by the example of some types of anemias with the appearance of pathological hemoglobins. Replacement of only one amino acid residue (glutamine) in the hemoglobin molecule with valine leads to a serious disease - sickle cell anemia.
Of particular interest are quantitative changes in the biosynthesis of proteins of organs and blood, leading to a shift in the ratios of individual fractions of proteins in the blood serum - dysproteinemia. There are two forms of dysproteinemia: hyperproteinemia (an increase in the content of all or certain types of proteins) and hypoproteinemia (a decrease in the content of all or individual proteins). Thus, a number of liver diseases (cirrhosis, hepatitis), kidneys (nephritis, nephrosis) are accompanied by a pronounced decrease in the albumin content. A number of infectious diseases accompanied by extensive inflammatory processes lead to an increase in the content of gamma globulins. The development of dysproteinemia is accompanied, as a rule, by serious shifts in the homeostasis of the body (violation of oncotic pressure, water exchange). A significant decrease in the synthesis of proteins, especially albumin and gamma globulins, leads to a sharp decrease in the body's resistance to infection, a decrease in immunological resistance. The importance of hypoproteinemia in the form of hypoalbuminemia is also determined by the fact that albumin forms more or less strong complexes with various substances, ensuring their transport between various organs and transfer through cell membranes with the participation of specific receptors. It is known that salts of iron and copper (extremely toxic to the body) at pH of blood serum are difficult to dissolve and their transport is possible only in the form of complexes with specific serum proteins (transferrin and ceruloplasmin), which prevents intoxication with these salts. About half of the calcium is retained in the blood in the form associated with serum albumin. In this case, a certain dynamic balance is established in the blood between the bound form of calcium and its ionized compounds. In all diseases accompanied by a decrease in the content of albumin (kidney disease), the ability to regulate the concentration of ionized calcium in the blood is also weakened. In addition, albumins are carriers of certain components of carbohydrate metabolism (glucoproteins) and the main carriers of free (non-esterified) fatty acids and a number of hormones.
With liver and kidney damage, a number of acute and chronic inflammatory processes (rheumatism, infectious myocardium, pneumonia), the body begins to synthesize special proteins with altered properties or unusual norm. A classic example of diseases caused by the presence of abnormal proteins are those associated with the presence of abnormal hemoglobin (hemoglobinosis). Blood clotting disorders occur when pathological fibrinogens appear. Unusual blood proteins include cryoglobulins, which can precipitate at temperatures below 37 ° C, leading to blood clots. Their appearance is accompanied by nephrosis, cirrhosis of the liver and other diseases.
Pathology of interstitial protein metabolism (violation amino acid metabolism).
The central place in the interstitial exchange of proteins is occupied by the transamination reaction, as the main source of the formation of new amino acids. Violation of transamination can occur as a result of a deficiency in the body of vitamin B -6. This is due to the fact that the phosphorylated form of vitamin B-6 - phosphopyrodoxal is an active group of transaminases - specific transamination enzymes between amino and keto acids. Pregnancy, long-term intake of sulfonamides inhibit the synthesis of vitamin B6 and can serve as the basis for a violation of amino acid metabolism. Finally, the reason for the decrease in transamination activity can be the inhibition of the activity of transaminases due to a violation of the synthesis of these enzymes (during protein starvation), or a violation of the regulation of their activity by a number of hormones.
The processes of transamination of amino acids are closely related to the processes of oxidative deamination, during which the enzymatic elimination of ammonia from amino acids is carried out. Deamination determines both the formation of end products of protein metabolism and the entry of amino acids into energy metabolism. Weakening of deamination can occur due to a violation of oxidative processes in tissues (hypoxia, hypovitaminosis C, PP, B2). However, the most dramatic violation of deamination occurs with a decrease in the activity of amine oxidases, either due to a weakening of their synthesis (diffuse liver damage, protein deficiency), or as a result of a relative lack of their activity (an increase in the content of free amino acids in the blood). The consequence of a violation of the oxidative deamination of amino acids will be a weakening of urea formation, an increase in the concentration of amino acids and an increase in their excretion in the urine - aminoaciduria.
Intermediate exchange of a number of amino acids occurs not only in the form of transamination and oxidative deamination, but also by decarboxylation (loss of CO2 from the carboxyl group) with the formation of the corresponding amines, called "biogenic amines". So, during the decarboxylation of histidine, histamine is formed, tyrosine - tyramine, 5-hydroxytryptophan - serotin, etc. All these amines are biologically active and have a pronounced pharmacological effect on blood vessels.
Change in the rate of protein breakdown. A significant increase in the rate of breakdown of tissue and blood proteins is observed with an increase in body temperature, extensive inflammatory processes, severe trauma, hypoxia, malignant tumors, etc., which is associated either with the action of bacterial toxins (in case of infection), or with a significant increase in the activity of proteolytic blood enzymes (with hypoxia), or the toxic effect of tissue decay products (with injuries). In most cases, the acceleration of protein breakdown is accompanied by the development of a negative nitrogen balance in the body due to the predominance of protein breakdown processes over their biosynthesis.
Pathology of the final stage of protein metabolism. The main end products of protein metabolism are ammonia and urea. The pathology of the final stage of protein metabolism can be manifested by a violation of the formation of final products, or a violation of their excretion.
The main mechanism for the binding of ammonia is the formation of urea in the citrulline-arginineornithine cycle. Disorders of urea formation can occur as a result of a decrease in the activity of the enzyme systems involved in this process (hepatitis, liver cirrhosis), general protein deficiency. When urea formation is impaired, ammonia accumulates in the blood and tissues and the concentration of free amino acids increases, which is accompanied by the development of hyperazotemia. In severe forms of hepatitis and cirrhosis of the liver, when its urea-forming function is sharply impaired, pronounced ammonia intoxication develops (dysfunction of the central nervous system).
In other organs and tissues (muscles, nervous tissue), ammonia binds in the amidation reaction with the addition of free dicarboxylic amino acids to the carboxyl group. The main substrate is glutamic acid.
Another end product of protein metabolism, formed during the oxidation of creatine (nitrogenous substance of muscles) is creatinine. During fasting, vitamin E deficiency, febrile infectious diseases, thyrotoxicosis and a number of other diseases, creatinuria indicates a violation of creatine metabolism.
In case of impaired renal excretory function (nephritis), urea and other nitrogenous products are retained in the blood. Residual nitrogen increases - hyperazotemia develops. The extreme degree of impaired excretion of nitrogenous metabolites is uremia.
With simultaneous damage to the liver and kidneys, a violation of the formation and excretion of the end products of protein metabolism occurs.
In pediatric practice, hereditary aminoacidopathies are of particular importance, the list of which today includes about 60 different nosological forms. By the type of inheritance, almost all of them are autosomal recessive. The pathogenesis is due to the lack of one or another enzyme that catabolizes and anabolizes amino acids. A common biochemical sign of aminoacidopathies is tissue acidosis and aminoaciduria. The most common hereditary metabolic defects are four enzymopathies, which are associated with each other by a common pathway of amino acid metabolism: phenylketonuria, tyrosinemia, albinism, and alcaptonuria.
54. pathology of carbohydrate metabolism make up the obligatory and most of human food (about 500 g / day). Carbohydrates are the most easily mobilized and utilized material. They are deposited as glycogen, fat. During carbohydrate metabolism, NADPH H2 is formed. Carbohydrates play a special role in the energy of the central nervous system, since glucose is the only source of energy for the brain.
Disorder of carbohydrate metabolism may be due to impaired digestion and absorption in the digestive tract. Exogenous carbohydrates enter the body in the form of poly-, di- and monosaccharides. Their splitting mainly occurs in the duodenum and small intestine, the juices of which contain active amylolytic enzymes (amylase, maltase, sucrase, lactase, invertase, etc.). Carbohydrates are broken down into monosaccharides and absorbed. If the production of amylolytic enzymes is insufficient, then di - and polysaccharides supplied with food are not broken down to monosaccharides and are not absorbed. Absorption of glucose suffers when its phosphorylation in the intestinal wall is disturbed. This disorder is based on the deficiency of the enzyme hexokinase, which develops in severe inflammatory processes in the intestine, in case of poisoning with monoiodoacetate, phloridzin. Non-phosphorylated glucose does not pass through the intestinal wall and is not absorbed. Carbohydrate starvation may develop.
Violation of the synthesis and breakdown of glycogen... A pathological increase in the breakdown of glycogen occurs with strong excitation of the central nervous system, with an increase in the activity of hormones that stimulate glycogenolysis (STH, adrenaline, glucagon, thyroxine). An increase in the breakdown of glycogen with a simultaneous increase in muscle glucose uptake occurs with severe muscle stress. The synthesis of glycogen can change towards a decrease or pathological increase.
Decreased glycogen synthesis occurs with severe damage to liver cells (hepatitis, liver poisoning), when their glycogen-forming function is impaired. The synthesis of glycogen decreases during hypoxia, since under conditions of hypoxia, the formation of ATP, which is necessary for the synthesis of glycogen, decreases.
Hyperglycemia- an increase in blood sugar levels above normal. It can develop under physiological conditions; in this case, it has an adaptive value, since it ensures the delivery of energetic material to the tissues. Depending on the etiological factor, the following types of hyperglycemia are distinguished.
Alimentary hyperglycemia that develops after taking a large amount of easily digestible carbohydrates (sugar, sweets, flour products, etc.).
Neurogenic (emotional) hyperglycemia - with emotional arousal, stress, pain, ether anesthesia.
Hormonal hyperglycemia accompany dysfunctions of the endocrine glands, whose hormones are involved in the regulation of carbohydrate metabolism.
Hyperglycemia with insulin hormone deficiency is the most pronounced and persistent. It can be pancreatic (absolute) and extrapancreatic (relative).
Pancreatic insulin deficiency develops when the insular apparatus of the pancreas is destroyed or damaged. A common cause is local hypoxia of the islets of Langerhans in atherosclerosis, vasospasm. In this case, the formation of disulfide bonds in insulin is disrupted and insulin loses its activity - it does not have a hypoglycemic effect.
The destruction of the pancreas by tumors, damage to it by an infectious process (tuberculosis, syphilis) can lead to insulin deficiency. Insulin production can be disrupted in pancreatitis - acute inflammatory and degenerative processes in the pancreas.
The insular apparatus is overstrained and can be depleted with excessive and frequent consumption of easily digestible carbohydrates (sugar, candy), with overeating, which leads to alimentary hyperglycemia.
A number of drugs (thiazide groups, corticosteroids, etc.) can cause impaired glucose tolerance, and in persons predisposed to diabetes, they can be a trigger factor in the development of this disease.
Extrapancreatic insulin deficiency... It can be caused by an excessive connection of insulin with transporting proteins in the blood. Protein-bound insulin is active only on adipose tissue. It provides the transition of glucose to fat, inhibits lipolysis. In this case, the so-called obese diabetes develops.
With diabetes mellitus, all types of metabolism are disrupted.
Disorders of carbohydrate metabolism determine the characteristic symptom of diabetes - persistent severe hyperglycemia. It is determined by the following features of carbohydrate metabolism in diabetes mellitus: a decrease in the passage of glucose through cell membranes and its assimilation by tissues; slowing down the synthesis of glycogen and accelerating its breakdown; increased gluconeogenesis - the formation of glucose from lactate, pyruvate, amino acids and other products of non-carbohydrate metabolism; inhibition of the transition of glucose to fat.
The significance of hyperglycemia in the pathogenesis of diabetes mellitus is twofold. It plays a certain adaptive role, since it inhibits the breakdown of glycogen and partly increases its synthesis. Glucose penetrates into tissues more easily, and they do not experience a sharp lack of carbohydrates. Hyperglycemia also has a negative meaning. With it, the flow of glucose into the cells of insulin-independent tissues (lens, liver cells, beta cells of the islets of Langerhans, nervous tissue, erythrocytes, the aortic wall) sharply increases. Excess glucose is not phosphorylated, but is converted to sorbitol and fructose. These are osmotically active substances that disrupt the metabolism in these tissues and cause their damage. With hyperglycemia, the concentration of gluco- and mucoproteins increases, which easily fall out in the connective tissue, contributing to the formation of hyaline.
With hyperglycemia exceeding 8 mol / l, glucose begins to pass into the final urine - glucosuria develops. This is a manifestation of the decompensation of carbohydrate metabolism.
In diabetes mellitus, the processes of phosphorylation and dephosphorylation of glucose in the tubules cannot cope with the excess of glucose in the primary urine. In addition, in diabetes, the activity of hexokinase is reduced, so the renal threshold for glucose is lower than normal. Glucosuria develops. In severe forms of diabetes mellitus, the sugar content in urine can reach 8-10%. The osmotic pressure of the urine rises, and therefore a lot of water passes into the final urine. During the day, 5-10 liters or more of urine (polyuria) with a high relative density due to sugar is released. As a result of polyuria, dehydration of the body develops, and as a result, increased thirst (polydipsia).
At a very high blood sugar level (30-50 mol / l and above), the osmotic pressure of the blood rises sharply. The result is dehydration of the body. Hyperosmolar coma may develop. The condition of the patients with her is extremely difficult. Consciousness is absent. Signs of tissue dehydration are sharply expressed (eyeballs soft on palpation). With very high hyperglycemia, the level of ketone bodies is close to normal. As a result of dehydration, kidney damage occurs, their function is impaired up to the development of renal failure.
55. Pathological changes in fat metabolism can occur at its various stages: in violation of the processes of digestion and absorption of fats; in violation of the transport of fat and its transfer to tissues; in violation of fat oxidation in tissues; in violation of intermediate fat metabolism; in violation of the metabolism of fat in adipose tissue (excessive or insufficient formation and deposition).
Disruption of the process of digestion and absorption of fats is observed:
1.with a lack of pancreatic lipase,
2. with a deficiency of bile acids (inflammation of the gallbladder, blockage of the bile duct, liver disease). Fat emulsification, pancreatic lipase activation and the formation of the outer shell of mixed micelles, in which the higher fatty acids and monoglycerides are transferred from the site of fat hydrolysis to the absorbing surface of the intestinal epithelium, are disrupted;
3.with increased peristalsis of the small intestine and lesions of the epithelium of the small intestines by infectious and toxic agents
4. with an excess of calcium and magnesium ions in food, when water-insoluble salts of bile acids are formed - soaps;
5. with avitaminosis A and B, lack of choline, as well as in violation of the phosphorylation process (fat absorption is inhibited).
As a result of impaired fat absorption, steatorrhea develops (feces contain a lot of higher fatty acids and unsplit fat). Calcium is lost along with fat.
Fatty infiltration and fatty degeneration.
If the fat entering the cells is not broken down, oxidized, or removed from it, this indicates fatty infiltration. If it is combined with a violation of the protoplasmic structure and its protein component, then they speak of fatty degeneration. The common cause of fatty infiltration and fatty degeneration is considered to be the suppression of the activity of oxidative and hydrolytic enzymes of fat metabolism (in case of poisoning with arsenic, chloroform, in vitamin deficiencies, etc.).
Fatty infiltration develops when:
1) alimentary and transport hyperlipemia;
2) violation of the formation of phospholipids;
3) excess cholesterol.
Violation of intermediate fat metabolism leads to ketosis, which manifests itself in an increase in the level of ketone bodies in the blood (ketonemia) and their excretion in an increased amount in the urine (ketonuria).
Causes of ketosis:
1) deficiency of carbohydrates in the body;
2) stress, in which, due to the activation of the sympathetic system, the body's carbohydrate reserves are depleted;
3) when the liver is damaged by toxicoinfectious factors, its ability to synthesize and store glycogen is impaired, there is an increase in the intake of NEFA into the liver and the development of ketosis;
4) deficiency of vitamin E, which slows down the oxidation of higher fatty acids;
5) suppression of the oxidation of ketone bodies in the Krebs cycle;
6) violation of the resynthesis of ketone bodies into higher fatty acids with a lack of hydrogen sources.
A pronounced ketosis leads to intoxication of the body (central nervous system), the electrolyte balance is disturbed due to the loss of sodium in the urine (sodium forms salts with acetoacetic and β-hydroxybutyric acids), acidosis develops; a decrease in blood sodium levels can cause secondary aldosteronism. All this characterizes the diabetic coma.
Violation of fat metabolism in adipose tissue. Obesity - it is the tendency of the body to excessive weight gain under the influence of certain conditions. In this case, the body weight increases due to the abnormal accumulation of fat in the depot.
There are three types of obesity by etiology.: alimentary, hormonal, cerebral. The role of heredity in the pathogenesis of obesity is essential. Obesity develops as a result of the following three main pathogenetic factors:
1) increased food intake (carbohydrates, fats) with inappropriate energy expenditure of fat;
2) insufficient use (mobilization) of the fat depot as an energy source;
3) excessive formation of fat from carbohydrates.
Obesity consequences:
1) impaired glucose tolerance,
2) hyperlipemia due to TG and cholesterol, more often pre-β-lipoproteinemia,
3) hyperinsulinemia,
4) an increase in the excretion of glucocorticoids in the urine, in contrast to patients with Cushing's syndrome, the ratio of excretion of glucocorticoids and creatinine remains normal in obese,
5) after exercise, during sleep, after the introduction of arginine, there are less fluctuations in the concentration of STH in the plasma,
6) decreased insulin sensitivity of enlarged adipocytes and muscles,
7) an increase in the content of NEFA in the blood - an increased consumption of them by the muscles,
8) hypertrophied lipocytes react more strongly to norepinephrine and other lipolytic substances.
Patients with obesity often develop cardiovascular diseases, hypertension, cholelithiasis (bile in obesity turns out to be lithogenic, i.e. it contains few detergents that dissolve cholesterol esters). Obese people do not tolerate anesthesia and surgery well. Thromboembolism often occurs as a postoperative complication. One of the most serious complications of obesity is diabetes mellitus. With obesity, the likelihood of cirrhosis of the liver is increased, women who are obese are more likely to develop endometrial cancer, because their adipose tissue is more likely to metabolize androstenedione to estrone. With obesity, shortness of breath is observed, because massive subcutaneous fat deposits restrict the movement of the chest, the accumulation of fat in the abdominal cavity prevents the diaphragm from dropping. The need for oxygen is increased, but gas exchange is difficult, the relative pulmonary insufficiency increases, and frequent shallow breathing develops.
Overfeeding a baby during the first year of life contributes to the development of hyperplastic (multicellular) obesity (an abnormal increase in the number of fat cells). This obesity has a poor prognosis for weight loss. It is constantly combined with hypertrophy and is observed in high obesity. Obesity that develops in older childhood is hypertrophic (an increase in the volume of fat cells). It is usually the result of overeating.
With normal (according to energy expenditure) functions of the food center, the cause of obesity may be insufficient use of fat from fat depots as an energy source. This can occur with a decrease in the tone of the sympathetic and an increase in the tone of the parasympathetic nervous system, with an inhibitory effect of the cerebral cortex on the centers of the sympathetic part of the diencephalic region. In the nerve branches of adipose tissue, the phenomena of interstitial neuritis are found.
Since the processes of fat mobilization from the depot are under the control of hormonal and humoral factors, the violation of the production of these factors leads to a restriction of the use of fat. This is observed with an insufficiency of the thyroid gland and pituitary gland.
Increased secretion of glucocorticoids causes hyperglycemia by enhancing gluconeogenesis. An increase in the concentration of glucose in the blood decreases the release of fat from the depot and increases the absorption of NEFA and HM by the adipose tissue.
The main action of insulin:
● on carbohydrate metabolism - activates glycogen synthetase (promotes glycogen synthesis), activates hexokinase, inhibits gluconeogenesis, promotes glucose transport across the cell membrane;
● on fat metabolism - inhibits lipolysis in fat depots, activates the transition of carbohydrates to fat, inhibits the formation of ketone bodies, stimulates the breakdown of ketone bodies in the liver;
● on protein metabolism - enhances the transport of amino acids into the cell, provides energy for protein synthesis, inhibits the oxidation of amino acids, inhibits protein breakdown;
● on water-salt metabolism - enhances the absorption of potassium by the liver and muscles, ensures the reabsorption of sodium in the kidney tubules, promotes water retention in the body.
Obesity ( lat. adipositas - literally: "obesity" and lat. obesitas - literally: fullness, obesity, fattening) - fat deposition, an increase in body weight due to adipose tissue. Adipose tissue can be deposited both in places of physiological deposits, and in the area of the mammary glands, thighs, and abdomen.
Obesity divided into degrees(by the amount of adipose tissue) and on types(depending on the reasons that led to its development). Obesity leads to an increased risk of diabetes mellitus, hypertension and other diseases associated with being overweight. The causes of excess weight also affect the spread of adipose tissue, the characteristics of the adipose tissue (softness, firmness, percentage of fluid content), as well as the presence or absence of skin changes (stretching, enlarged pores, so-called "cellulite").
Obesity can develop as a result of:
Imbalance between food intake and energy expended, that is, increased food intake and reduced energy expenditure;
Obesity of non-endocrine pathology appears due to disturbances in the systems of the pancreas, liver, small and large intestines;
Genetic disorders.
Obesity contributing factors
Sedentary lifestyle
Genetic factors, in particular:
Increased activity of lipogenesis enzymes
Decreased activity of lipolysis enzymes
Increased intake of easily digestible carbohydrates:
drinking sweet drinks
a diet rich in sugars
Certain diseases, in particular endocrine diseases (hypogonadism, hypothyroidism, insulinoma)
Eating disorders (for example, binge eating disorder), in the Russian literature called eating disorders, a psychological disorder leading to an eating disorder
Tendency to stress
Lack of sleep
Psychotropic drugs
In the process of evolution, the human body has adapted to accumulate a supply of nutrients in conditions of abundance of food in order to spend this supply in conditions of a forced absence or restriction of food - a kind of evolutionary advantage that made it possible to survive. In ancient times, completeness was considered a sign of well-being, wealth, fertility and health.
There are differences in the distribution of excess body fat and in the presence or absence of symptoms of damage to the nervous or endocrine system.
Most common alimentary obesity , usually in individuals with a hereditary predisposition to obesity. It develops when the caloric content of food exceeds the energy consumption of the body, and is usually noted in several members of the same family. This type of obesity often affects middle-aged and elderly women who lead a sedentary lifestyle. When collecting an anamnesis with a detailed clarification of the daily diet, it is usually established that patients are systematically overeating. Alimentary obesity is characterized by a gradual increase in body weight. Subcutaneous adipose tissue is evenly distributed, sometimes to a greater extent accumulates in the abdomen and thighs. There are no signs of damage to the endocrine glands.
Hypothalamic obesity observed in diseases of the central nervous system with damage to the hypothalamus (with tumors, in the outcome of injuries, infections). This type of obesity is characterized by the rapid development of obesity. Fat deposition is noted mainly on the abdomen (in the form of an apron), buttocks, and thighs. Often there are trophic changes in the skin: dryness, white or pink streaks of stretching (striae). Clinical symptoms (for example, headache, sleep disorders) and neurological examination of the patient are usually able to establish the pathology of the brain. As a manifestation of hypothalamic disorders, along with obesity, various signs of autonomic dysfunction are observed - an increase in blood pressure, sweating disorders, etc.
Endocrine obesity develops in patients with certain endocrine diseases (for example, hypothyroidism, Itsenko-Cushing's disease), the symptoms of which prevail in the clinical picture. On examination, along with obesity, which is usually characterized by uneven deposition of fat on the body, other signs of hormonal disorders (for example, masculinization or feminization, gynecomastia, hirsutism) are detected, striae are found on the skin.
A kind of obesity is the so-called painful lipomatosis (Derkum's disease), which is characterized by the presence of fatty nodes, painful on palpation.
Prevention of obesity consists in the elimination of physical inactivity and a balanced diet. In children, it is necessary to adhere to the rules of feeding and regular monitoring of the physical development of the child by systematic measurement of height and body weight (especially with a constitutional predisposition to obesity). Early detection and treatment of diseases associated with hypothalamic and endocrine obesity is important.
Diseases of the digestive tract are distinguished by the variety of their clinical and morphological signs. They include independent primary diseases, which are studied by a science called gastroenterology, as well as others, secondary, which are a manifestation of a number of diseases of an infectious and non-infectious nature, acquired or hereditary origin. These diseases can be based on various general pathological processes, such as alteration, inflammation, hyper- and dysplastic processes, autoimmune disorders and, finally, tumors.
INFLAMMATORY DISEASES OF THE STOMACH
Inflammatory processes in the stomach, indicated gastritis(from the Greek. gaster- stomach), as well as in other organs, can be adrift acute and chronic. The pathogenesis of chronic gastritis is complex. Until recently, it was believed that in one of the forms of chronic gastritis - type A, autoimmune reactions are observed, and in the second form (non-immune type B gastritis), inflammation occurs as a result of prolonged exposure to various nonspecific irritants, such as exogenous (for example, hot drinks or acute spices), or endogenous (for example, bile reflux). It has now been proven that type B chronic gastritis is a response to bacterial infection. Gastritis, which develops as a result of bile reflux, is excluded from this group.
ACUTE GASTRITIS
Acute gastritis most often develops after exposure to various factors:
1. chemical substances(alcohol, poor quality food);
2. some medicinal substances(non-steroidal anti-inflammatory substances containing aspirin).
3. eating spicy, cold or hot food.
4. Helicobacter pylori.
5. other infections(salmonella, staphylococcus, etc.).
6. toxic products of endogenous origin(with uremia).
By the area of the lesion, they are distinguished:
ü acute diffuse gastritis;
ü acute focal gastritis (fundal, antral, pyloroantral and pyloroduodenal).
Depending on the severity of the lesion, changes in the mucosa range from vasodilation and edema lamina propria before erosion and hemorrhage. Erosion is a section of the mucous membrane with partial violation of the epithelium, while in the ulcer there is a violation of the muscle layer of the mucous membrane. Erosions in acute gastritis are usually multiple, so bleeding from them can be very dangerous. However, it usually heals quickly (within 24-48 hours) by regeneration. With frequent relapses of acute gastritis, chronic gastritis can develop.
CHRONIC GASTRITIS
Currently, the following forms of chronic gastritis are distinguished:
q autoimmune chronic gastritis;
q Helicobacter-associated chronic gastritis;
q chemical reflux gastritis;
q other forms of gastritis.
Table 1
Types of chronic gastritis
|
Etiology |
Pathogenetic mechanism |
Histological changes |
Associated clinical changes |
|
Autoimmune |
Antibodies against parietal cells and receptors for external factor Kastl. |
Atrophy of the glands in the body of the stomach. Intestinal metaplasia. |
Pernicious anemia. |
|
Bacterial infection |
Cytotoxins. |
Active chronic inflammation. |
Peptic ulcers. |
|
Chemical damage |
Direct damage. |
Hyperplasia of the pit epithelium. |
Peptic ulcers. |
Other forms of gastritis
The following types of chronic gastritis are distinguished separately:
v lymphocytic;
v eosinophilic;
v granulomatous.
At lymphocytic gastritis the main histological manifestation is the presence of numerous mature lymphocytes in the surface layers of the epithelium. This form is sometimes found in patients with specific erosions along the enlarged folds of the mucous membrane. Etiology and relationship with Helicobacter-associated gastritis has not been identified.
Eosinophilic gastritis characterized by mucosal edema and the presence of numerous eosinophils in the inflammatory infiltrate. It is assumed that eosinophilic gastritis is an allergic response to a food antigen to which the patient is sensitized.
Granulomatous gastritis is a rare form of gastritis in which epithelioid cell granulomas form. These granulomas can be a manifestation of Crohn's disease or sarcoidosis, but in rare cases it is cryptogenic.
STOMACH AND DUAL PURPOSE
Peptic ulceration - This is a violation of the integrity of the epithelial cover and underlying tissues of the digestive tract as a result of damage to them by acid and pepsin. According to the clinical course, ulcers are divided into acute and chronic.
Acute ulcers
Reasons for development:
- Severe acute gastritis.
- Severe stress (extensive trauma, surgery).
- A pronounced increase in acidity.
- Poisoning.
- Sepsis.
- Multiple organ failure.
Morphology. Multiple, often combined with chronic ulcers. The diameter does not exceed 1 cm, but giant ulcers are also found. Macroscopically oval, rounded, the bottom of which is covered with grayish-yellow necrotic masses, when rejected, their defect has a gray-red color with arosed blood vessels. The edges of the ulcer are soft. After the healing of an acute ulcer, a flat, stellate, re-epithelialized scar remains.
Chronic ulcers
Chronic ulcers can be caused by:
- Infection Helicobacter pylori.
- Chemical influences, including steroid drugs and non-steroidal anti-inflammatory drugs.
- Chronic distress syndrome.
Chronic peptic ulcers most often form at the junction of various types of mucous membranes. So, for example, in the stomach, ulcers are observed at the place of transition of the body to the antrum, in the duodenum - in the proximal area on the border with the pylorus, in the esophagus - in the stratified epithelium in front of the esophageal-gastric junction, postoperative ulcers are localized in the stoma (in the anastomosis ). That is, ulcers appear where acid and pepsin come into contact with the unprotected mucous membrane.
Pathogenesis. The main role in the development of ulcers is played not by acidity, but by the ratio of factors of aggression and factors of mucous protection. It is believed that in the genesis of duodenal ulcer, the main role is played by the increase in factors of aggression, and in the development of gastric ulcer in the first place is a decrease in protective factors. With a decrease in the latter, ulcers may develop even with low acidity.
Stomach ulcer. Ulceration occurs as a result of either a violation and destruction of the mucous barrier, or a violation of the integrity of the epithelium. As a result of bile reflux, the mucous barrier is easily destroyed by its components. Acid and bile together destroy the surface epithelium, increasing the permeability and vulnerability of the mucous membrane. This leads to congestion and swelling in lamina propria, which is observed with reflux gastritis.
The epithelial barrier can also be disrupted by the use of NSAIDs. they disrupt the synthesis of prostaglandins, which normally protect the epithelium. Also, infection plays a significant role in the destruction of the epithelium. Helicobacter pylori, in which both cytotoxins and ammonium ions and an inflammatory reaction have a destructive effect.
Duodenal ulcer. Factors that damage the anti-acid defense in the stomach usually do not affect the duodenum: Helicobacter pylori does not populate the duodenal mucosa, the mucosa is resistant to the action of bile and alkaline ions of pancreatic juice, drugs are significantly diluted and absorbed before entering the intestine. but Helicobacter pylori affects ulceration, because infection contributes to gastric hypersecretion, which causes the development of gastric metaplasia in the duodenum, and then colonization of metaplastic epithelium occurs Helicobacter pylori, which leads to the development of chronic inflammation, which also provokes ulceration.
Morphological changes.
Macroscopically chronic ulcers are usually round or oval in shape. Their sizes, as a rule, do not exceed 2 cm in diameter, however, cases have been described when ulcers reached 10 cm in diameter or more. The depth of the ulcer is different, sometimes it reaches the serous membrane. The edges of the ulcer are clear, dense and rise above the normal surface, the pyloric edge of the ulcer is shallow (terraced), and the cardiac edge is subdued.
During an exacerbation microscopically four zones are distinguished at the bottom of the ulcer:
- Exudation
- Fibrinoid necrosis
- Granulation tissue
- Fibrous tissue (fibrinoid changes and significant narrowing of blood vessels as a result of intimal proliferation and sclerosis are often observed in the vessels).
During the period of remission, scar tissue is found at the edges of the ulcer. The mucous membrane is thickened at the edges, hyperplastic.
Complications.
Ulceratively destructive:
- 1. perforation the walls of the stomach or duodenum, while the contents of the digestive tract are poured into the abdominal cavity, which leads to the development of peritonitis.
- penetration - perforation of the ulcer occurs in the closer lying organs, for example, the pancreas or liver.
- bleeding , which can be lethal.
Inflammatory:
- 1. gastritis, perigastritis.
- 2. duodenitis, periduodenitis.
Ulcerative cicatricial:
- 1. stenosis.
- 2. deformations .
Malignancy of stomach ulcers (duodenal ulcers are very rarely malignant).
Combined complications.
APPENDICITIS
Appendicitis - primary inflammation of the appendix of the cecum with a kind of clinical syndrome. Therefore, not every inflammation of the appendix in the clinical and anatomical terms should be considered as appendicitis (for example, when the inflammatory process spreads from nearby organs, with its tuberculous lesion, etc.)
There are two clinical and anatomical forms of appendicitis: acute and chronic.
Acute appendicitis is the most common cause of emergency operations in surgery. It occurs in all age groups, but is most common in adolescents.
The most common causes of acute appendicitis are obstruction of the appendix coprolitis or an enlarged submucosa as a result of lymphoid hyperplasia, as well as with an inflection of the appendix. At the same time, in the distal segment, an increased multiplication of microorganisms occurs, such as Escherichia coli, Streptococcus faecalis and anaerobic bacteria. These bacteria then invade the lining and other lining of the appendix, causing acute inflammation.
Pathological changes. It is customary to distinguish between the following main morphological forms of acute appendicitis:
1) simple;
2) superficial;
3) destructive (which, in turn, is divided into phlegmonous, apostematous, phlegmonous-ulcerative, gangrenous).
All these forms, in essence, are a morphological reflection of the phases of an acute inflammatory process in the appendix, which ultimately ends in necrosis. The duration of this process is 2-4 days.
For acute simple appendicitis characterized by the presence of stasis in the capillaries and venules, edema, hemorrhages, marginal leukocyte standing, leukodiapedesis, most often in the distal appendix. Externally, the appendix appears normal, however, the diagnosis is confirmed by histological examination.
Acute superficial appendicitis characterized by the presence in the distal focus of exudative purulent inflammation in the mucous membrane, designated as primary affect. The changes inherent in simple or superficial appendicitis may be reversible. However, as a rule, they progress, and develops destructive appendicitis.
By the end of the first day, leukocyte infiltrate (neutrophils predominate) spreads to the entire thickness of the wall of the appendix (phlegmonous appendicitis). Macroscopically, the inflamed appendix looks edematous and red, its surface is often covered with fibrinous-purulent exudate. Sometimes, against this background, small multiple abscesses are revealed, in which case such appendicitis is designated as apostematous. Acute inflammation of the mucous membrane leads to the formation of ulcers and inflammation of the muscle layer - this is phlegmonous-ulcerative appendicitis... Purulent-destructive changes come to the end with development gangrenous appendicitis... The process in this form is thickened, the wall of its gray-dirty color, structureless with a fetid odor, pus is released from the lumen. Microscopically, there are extensive foci of necrosis with colonies of microbes, hemorrhages, blood clots in the vessels. The mucous membrane is desquamated almost throughout.
Complications.
"Appendicular infiltrate"
peritonitis
distant abscesses (for example, in the rectal-cystic and subphrenic spaces)
thrombophlebitis of the portal vein with the formation of multiple pylephlebitic liver abscesses.
Chronic appendicitis characterized by the presence of sclerotic and atrophic processes, against the background of which signs of inflammatory and destructive changes can be detected. Adhesions appear with the surrounding tissues. With cicatricial obliteration of the proximal section, serous fluid can accumulate in the lumen of the appendix and a cyst forms - dropsy of the appendix. If the contents of the cyst are mucus, this complication is referred to as mucocele. If such a cyst ruptures and the contents enter the abdominal cavity, the implantation of cells on the peritoneum and the development of formations resembling a tumor is possible - pseudomyxoma peritoneum.
NONSPECIFIC ULCERATIVE COLITIS
NUC is a nonspecific inflammatory disease of the colon that usually develops in the rectum and then spreads proximally.
Etiology. It is assumed that there is a clear genetic predisposition to ulcerative colitis; this genetic defect can affect both the immune response and the structure of the intestinal mucosa. So in ulcerative colitis, the genes HLA-DR2 and some cytokines play an important role. There is an increase in the synthesis of IgG 2 compared to IgG 1. An increase in the permeability of the mucous membrane and a change in the composition of mucus glycoproteins are found.
Now there is evidence that NUC develops as a result of autoimmune processes, and mucosal damage occurs through inadequate activation of T cells and mediated damage by cytokines, proteases and oxygen radicals synthesized by macrophages and neutrophils.
In a normal state, the immune system of the mucous membrane is tolerant to external antigens located in the intestinal lumen; this tolerance is maintained by the interaction of the intestinal epithelium and T-suppressors. A change in the state of epithelial cells, leading to an acquired increase in the synthesis of MHC class II molecules (HLA-DR), activates T-helpers, which leads to the development of cascade immune and biochemical reactions under the influence of cytokines. The most likely antigen or triggering factor is the microorganisms that colonize the intestines. The start of this process can be significantly influenced by stress, inflammation of the intestinal mucosa, and smoking.
Regardless of the cause, it has been proven that mucosal damage in NUC occurs as a result of the accumulation of polymorphonuclear leukocytes in the mucosa, which secrete proteases, nitric oxide and free radicals.
Morphology. With NUC, a consistent and continuous type of lesion is observed. Usually, the lesion initially occurs in the rectum, where the maximum severity of changes is observed, and then spreads to the sigmoid and colon (Fig. 1).
Rice. 1. Pathological changes in ulcerative colitis
Ulcers have jagged edges and can coalesce; they spread horizontally to areas that are still intact, forming extensive lesions. Usually, ulcers are superficial, involve the mucous and submucous membranes, however, in severe cases, all layers of the intestine can be damaged, up to perforation. In the intact mucosa, pronounced hyperemia is found, bleeding often occurs from ulcers.
Microscopically infiltration of the mucous membrane by cells of acute and chronic inflammation is determined. Polymorphonuclear leukocytes are found in the interstitium; however, in some crypts they form aggregates (crypt abscesses). Widespread degenerative changes in both surface epithelial cells and crypts develop, and the synthesis of mucins is sharply reduced. In the acute period, complete destruction of the crypts can be observed. Then their regeneration begins, the newly formed crypts are distinguished by significant expansion and often have connections with neighboring crypts. So, with a biopsy of the rectum, atrophy and significant expansion of crypts are found, in which signs of epithelial metaplasia are sometimes found. NUC is a precancerous disease, therefore epithelial dysplasia is found in some areas.
table 2
Complications of ulcerative colitis
|
Complication |
The main symptoms of diseases of the digestive system are abdominal pain, appetite disturbances, unpleasant taste in the mouth, belching, heartburn, nausea, vomiting, upset stools. Pain should be distinguished by its intensity, localization and their relationship with food intake. Low-intensity, but constant pain is more characteristic of chronic gastritis. With a peptic ulcer, the pain is more intense, they are quite clearly associated with the intake of food. Very severe pain occurs with gallstone disease. Appetite disturbance is largely associated with gastric secretion and acidity levels. With increased secretion, appetite can even be increased (gastritis with high acidity, peptic ulcer, which is often accompanied by increased secretion of gastric contents and high acidity). With a decrease in secretion, appetite is reduced (gyno- and anacid, as well as achilic gastritis). There is a perversion of appetite (in particular, with stomach cancer), when the patient does not tolerate (disgust) certain foods. An unpleasant taste in the mouth is noted with lesions of the gastric mucosa, bitterness in the mouth - with diseases of the liver and gallbladder, and a metallic taste with some food poisoning. Belching is a sudden entry of stomach contents into the mouth, accompanied by a characteristic sound - belching. Belching with food eaten 12 hours or more ago is of especially great diagnostic value; this is a sign of a violation of the evacuation function of the stomach. "Empty" belching - belching with air - is observed with a decrease or absence of hydrochloric acid in the gastric contents, and belching with a rotten egg - when Achilles is combined with a violation of the evacuation function of the stomach (the smell of hydrogen sulfide in this case depends on the increased breakdown of proteins in the stomach). Heartburn refers to the sensation of severe burning in the upper part of the epigastric region, under the xiphoid process and behind the sternum (which corresponds to the lower segment of the esophagus). In most cases, heartburn is associated with the throwing of acidic gastric contents from the stomach into the esophagus. Nausea is an unpleasant sensation in the epigastric region. Most often it happens with diseases of the stomach with low acidity. Sometimes nausea precedes vomiting. Vomiting is of great importance for the diagnosis of diseases of the digestive system. Vomiting mixed with food debris eaten the day before may indicate a significant violation of the evacuation activity of the stomach (pyloric stenosis?). Vomiting with an admixture of "coffee grounds" is observed with gastric bleeding, vomiting in the morning mixed with mucus - with Chronic gastritis, with an admixture of bile - with pathology of the biliary tract. For the recognition of diseases of the digestive system, the symptoms detected when feeling the abdomen are of great importance. So, it is important to identify pain points; they are located in the epigastric region with peptic ulcer and gastritis, in the right hypochondrium with diseases of the liver and gallbladder, to the left of the navel with pathological changes in the pancreas, etc. In the diagnosis of diseases of the digestive system, tapping and partly listening are used. So, light beating with the ends of the fingers on the anterior abdominal wall can reveal a "splash noise", which speaks of stagnation of fluid in the stomach, while listening to determine the noise of intestinal peristalsis, etc. The palpation method allows you to identify the symptoms of "acute abdomen". A number of symptoms are established using instrumental, laboratory and other research methods. Thus, X-ray examination reveals one of the characteristic symptoms of peptic ulcer disease - a "niche" symptom, with the help of duodenal intubation - a number of important symptoms of gallbladder diseases, the gastrobiopsy method allows detecting stomach cancer in the early stages of development.
