It is accompanied by a violation of the motor function of the bile. Gallbladder dyskinesia: symptoms and treatment. Causes and risk factors

Inna Lavrenko

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Allows this organ to expel bile produced by the liver into the digestive system when food enters it. Bile is responsible for the breakdown of hard-to-digest fats and contributes to the normal digestive process. That is why good contractility of this important organ of the digestive system is the main indicator of its normal functioning.

Alas, gastroenterologists often encounter such pathologies as impaired motility of this organ and bile ducts, in which the contractile function of the gallbladder deviates from the norm.

This ailment is called dyskinesia, which is a very common disease of this organ. According to medical statistics, women suffer from gallbladder dyskinesia ten times more often than men.

The gallbladder forms the so-called biliary system with the liver. It is located directly below it and is a small oval saccular cavity (reservoir) with a volume of up to 70 cubic centimeters. The length of this organ in adults can reach up to 14 centimeters.

The main functions of the gallbladder:

• accumulation of bile produced by the liver around the clock;
• bringing it to the required consistency;
• delivery of this hepatic secretion to the duodenum when food enters the gastrointestinal tract.

Bile is a biological fluid that participates in the breakdown of heavy animal fats and the release of essential nutrients from the foods entering the body.

The liver is responsible for the production of this fluid, from where it then enters the gallbladder through the common bile duct. There it accumulates, acquires the necessary consistency and, if necessary, is thrown into the digestive tract. This release occurs shortly after food enters the gastrointestinal tract.

Dyskinesia of the gallbladder is a disease (usually of a non-infectious nature), in which there is a violation of the motor (in another way - evacuation) function of this internal organ. This interferes with the normal filling of the bladder with bile, and also disrupts its contractile function.

Women are much more likely to fall ill with this disease, and this is due to the specificity of their hormonal levels and the general structure of the female body. Gallbladder dyskinesia often develops during pregnancy.

If we talk about the share of dyskinesia in the total number of diseases of the biliary system, then it is about 12 percent. This pathology is a functional disorder, and does not cause morphological changes in this internal organ.

Such violations of the gallbladder motility are primary and secondary.

In addition, experts distinguish the following types of this pathology:

• hypotonic;
• hypertensive;
• hypokinetic;
• hyperkinetic dyskinesia.

Hypotension is a decrease in the level of contractility of the gallbladder. For this type of this pathology, difficult bile excretion and difficulties with the accumulation of bile are characteristic.

In contrast, hypertension is characterized by a sharp increase in muscle tone. Such an increase in contractility also disrupts normal bile secretion, since the resulting spasms of the muscles of the walls of this organ lead to chaotic work of the sphincters.

The reasons for the appearance of such pathologies

There are many reasons that cause this functional disruption of the normal functioning of the gallbladder. Dyskinesia in the primary form, as a rule, arises as a result of congenital features of the development of this internal organ. The secondary form of this pathology is mainly provoked by various kinds of concomitant diseases.

The main factors provoking primary gallbladder dyskinesia:

The process of bile secretion is monitored by the nervous and endocrine systems of the human body. The increased activity of the vagus nerve leads to increased contractility of the gallbladder. This pathology occurs due to a failure in the autonomic nervous system. Also, such dyskinesia can be provoked by disturbances in the production of hormones such as gastrin, secretin, cholecystokinin, and so on.

Hypotonic dyskinesia, in which contractility, on the contrary, decreases, as a rule, occurs as a result of the effect of neuropeptides on this internal organ.

Both hypotension and hypertension of the gallbladder can be provoked by improper and inappropriate nutrition. If food intake does not occur regularly, at different times, if a person practices dry food and snacks on the go, as well as in the case of constant consumption of fatty, fried, spicy or simply low-quality foods, this is a sure way to relieve such gallbladder motility disorders. Such violations can also provoke various diets for weight loss and fasting, in which there are long breaks between meals.

Dyskinesias can also develop as a result of a constant stressful state, as a consequence of various kinds of allergic diseases (for example, asthma) and as a consequence of a sedentary sedentary lifestyle. People with asthenic physique are more susceptible to this pathology.

In children, as a rule, dyskinesia is either a consequence of congenital weakening of the muscular system (primary form), or this ailment occurs against the background of concomitant diseases (secondary form). In both children and adult patients, impaired gallbladder motility can be triggered by pancreatitis, gallstone disease, dysentery, salmonellosis, peptic ulcer, gastritis, enterocolitis and various atrophies of the mucous membrane of the digestive system.

The main risk factors for this disease in female patients are various pathological changes in the pelvic organs (for example, salpingitis or adnexitis).

Hypomotor dyskinesia

The clinical picture of this disease of the gallbladder depends on the type of pathology manifested.

Violation of the motility of this internal organ of the hypomotor type is accompanied by the appearance of the following symptoms:

• constant dull pain in the right hypochondrium;
• flatulence;
• constant belching;
• bad breath after belching;
• a feeling of bitterness in the mouth;
• nausea;
• periodic vomiting;
• bloating;
• deterioration in appetite;
• stool disorders (alternating constipation and diarrhea);
• lower heart rate (bradycardia);
• lowering blood pressure;
• an increase in body weight (typical for a chronic form);
• increased sweating;
• hypersalivation.

The majority of patients with dyskinesia of this type complain of constant dull pain syndrome. Pains of varying intensity are present almost constantly, their character can be dull, squeezing or pressing, the intensity of pain increases during movement and decreases at rest. All this is associated with an increase in the value of pressure in the abdominal cavity and a violation of the normal bile outflow. As a rule, such pains do not have a clear localization and are classified as “spilled”. Basically, food intake does not affect the intensity or appearance of pain in these cases.

For dyskinesia, a very characteristic symptom is belching with air, which is provoked by a disturbed function of the nervous system, forcing more swallowing movements.

With the hypokinetic course of this pathology, patients often experience nausea caused by irritation of the receptors of the digestive organs and excitation of the nerve center responsible for vomiting. As a rule, the patient begins to vomit after eating too fatty foods, as well as after overeating or in cases of too rapid absorption of food.

Another characteristic symptom of a deterioration in the muscle tone of the gallbladder is a feeling of bitterness in the mouth (especially in the morning and immediately after a meal). The reason for this is the ingress of bile into the stomach, which is then thrown into the esophagus (which never happens during normal operation of the gallbladder).

Since hypokinetic dyskinesia of the gallbladder provokes the development of fermentation and decay processes in the digestive system, caused by a deficiency of bile that breaks down food, this course of the disease is often accompanied by bloating.

Enzymes such as bile acids are responsible for a good appetite in the human body. In the event of a violation of the process of bile outflow, a deficiency of these substances occurs, and the appetite deteriorates sharply.

Constipation and diarrhea with hypokinetic dyskinesia are rare. Their manifestation is caused by decreased intestinal motility, as well as disturbances in the normal course of the digestive process associated with the normal processing of fats, proteins and carbohydrates.

With stagnation of bile in the gallbladder, the so-called cholestatic syndrome occurs. It is characterized by:

• itching of the skin;
• change in their color (yellowness);
• yellowing of the eye sclera;
• darkening of urine;
• lighter (yellow-green) color of feces.

Symptoms

Hypermotor (or hyperkinetic) dyskinesia of the gallbladder has some characteristic features.

This form of the disease is characterized by the following clinical picture:

1. the occurrence of an intense pain syndrome similar to hepatic colic;
2. significant deterioration in the patient's general well-being;
3. weight loss;
4. decreased appetite;
5. loose stools;
6. nausea;
7. vomit;
8. cardiopalmus;
9. yellowing of the skin;
10. high blood pressure;
11. general weakness;
12. constant malaise;
13. the appearance of plaque on the tongue.

The most common and unpleasant symptom of hypertensive dyskinesia of this internal organ is pain syndrome, which is characterized by the following symptoms:

• duration - up to 30 minutes;
• sharp character;
• occurs in the form of seizures;
• localized in the right hypochondrium;
• provoked by physical stress or stress;
• given to the right hand and right shoulder blade.

The patient quickly loses his appetite, begins to eat poorly, which causes a sharp decrease in body weight. In addition, inadequate breakdown of food nutrients caused by bile deficiency also contributes to weight loss. The subcutaneous fat layer in such patients becomes thinner.

Also, with this type of dyskinesia, the work of the autonomic nervous system is disrupted, which is manifested by mood swings, irritability and sleep disorders.

The appearance on the tongue of a yellowish or greenish plaque can occur with both forms of dyskinesia. In some cases, patients complained of changes in taste sensitivity. In addition, stagnant processes in the gallbladder negatively affect the patient's sexual function, and in women with this pathology, in some cases, the menstrual cycle was disrupted.

Diagnosis of this pathology

Despite the rather typical clinical picture, external symptoms alone are not enough for an accurate diagnosis of gallbladder dyskinesia.

To determine the reasons that provoked the violation of the motility of this organ, laboratory and instrumental studies of the gallbladder itself, its ducts and other organs of the digestive system are prescribed.

Such examinations include:

1. ultrasound examination of the gallbladder, as well as the pancreas and liver;
2. general blood analysis;
3. a blood test for biochemistry;
4. Analysis of urine;
5. coprogram (analysis of feces);
6. laboratory examination of feces for the presence of helminth eggs in it;
7. cholangiography;
8. cholecystography;
9. bile examination (microscopic);
10. duodenal intubation, after which the analysis of gastric juice is performed.

Laboratory studies when making a diagnosis of gallbladder dyskinesia make it possible to identify the following negative changes:

• increased erythrocyte sedimentation rate (ESR);
• an increase in the level of leukocytes;
• an increase in the level of bilirubin;
• increased content of cholesterol, C-reactive protein and bile acids;
• an increase in the level of amylase (typical for cases of the presence of concomitant inflammation of the pancreas).

Also, to make this diagnosis, liver function tests are required.

Also, to clarify this diagnosis, instrumental diagnostic techniques such as cholangiography and cholecystography are used.

Retrograde cholangiopancreatography is also mandatory. To exclude stenosis of the sphincter of Oddi, a manometry procedure is performed.

In order to exclude possible pathologies of the duodenum and stomach, a special examination is carried out, called fibroesophagogastroduodenoscopy.

The method of treating this disease

As a rule, the treatment of this pathology is carried out by conservative methods - with the help of medicines. The choice of drug is based on the type of organ motility disorder. With hypotension of the gallbladder, the following are used:

• drugs that normalize the level of contractility (prokinetics) (for example, Cerucal or Domperidone);
• to improve bile outflow, drugs are used, which are called choleretics (Cholenzym or Allochol);
• to increase the tone of this organ while reducing the tone of the bile ducts, cholekinetic drugs are used.

In addition, to normalize the functioning of the autonomic nervous system, the doctor may prescribe sorbitol, magnesium sulfate, or Eleutherococcus extract. With the hyperkinetic course of this pathology, as a rule, cholekinetics and antispasmodics are used.

Antispasmodics relieve pain. The most famous drugs in this group are No-shpa, Duspatalin, Odeston, Papaverin and Drotaverin. In especially severe cases, it is possible to prescribe anesthetic narcotic drugs.

For the treatment of patients with such a pathology, physiotherapy methods are often used.

The increased tone of the gallbladder helps to normalize electrophoresis with drugs such as Platyphyllin and Papaverine. If the tone is lowered, then electrophoresis with Pilocarpine is used.

For any pathology of the biliary system, patients must follow a diet called "Treatment table No. 5".

The duration of the course of drug therapy for dyskinesia of this organ is several weeks and, as a rule, does without surgery.

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Ilchenko A.A.

GBUZ Central Research Institute of Gastroenterology DZ Moscow

Based on the analysis of the literature and our own experience, the role of the contractile function of the gallbladder (SFGB) in the digestion process is shown. The change in SFGP in various diseases and the reasons for its violation are shown.

Key words: gallbladder, contractile function of the gallbladder, cholecystokinin, gallbladder disease

Introduction

Among the various functions of the gallbladder, the central place is occupied by the contractile function, which, together with the sphincter apparatus of the biliary system, ensures the timely and adequate supply of concentrated bile into the intestine. In the regulation of the motor activity of the biliary tract, the parasympathetic and sympathetic parts of the autonomic nervous system, as well as the endocrine system, which provide synchronized the sequence of contraction and relaxation of the gallbladder and the sphincter apparatus of the biliary tract.

The experiment has shown that moderate irritation of the vagus nerve causes coordinated activity of the gallbladder and sphincters, and strong irritation causes spastic contraction with delayed evacuation of bile. Irritation of the sympathetic nerve helps to relax the gallbladder.

Currently, the leading role in the regulation of the functions of the biliary system, including the motor-evacuation system, belongs to gastrointestinal hormones (cholecystokinin-pancreosimin, gastrin, secretin, motilin, glucagon, etc.).

Under normal physiological conditions, the gallbladder contracts repeatedly throughout the day. In the interdigestive period, the gallbladder deposits hepatic bile, and during food intake, depending on the degree of neurohormonal stimulation, it releases the required amount of bile into the duct system.

Normal contractile function of the gallbladder

It is provided by the fibromuscular sheath, which is represented by smooth muscle bundles mixed with collagen and elastic fibers (Fig. 1). Smooth muscle cells of the bottom and body of the bladder are located in two thin layers at an angle to each other, and in the neck area circularly, therefore, when the bladder contracts, simultaneously with the evacuation of bile, its mixing occurs. 50% of the area occupied by smooth muscle fibers is represented by loose connective tissue. Such a structure is functionally justified, since when the bladder is filled with bile, the connective tissue layers with a large number of elastic fibers are stretched, which protects the muscle fibers and mucous membrane from overstretching and damage (Fig. 2), since when the bladder is filled with bile, the bladder stretches in all planes. At the same time, its volume increases almost 2 times, and the planar dimensions (length and, especially, width) increase by 30-40%.

Rice. 1. The structure of the wall of the human gallbladder.

1- mucous membrane; 2 - fibromuscular membrane; 3 - subserous membrane. Hematoxylin-eosin. Uv. x200.

Rice. 2. Changes in the wall of the gallbladder during computer simulation of stretching during filling with bile. Explanations in the text.

Facilitate the evacuation of bile from the bladder and glands located in its cervical region, which secrete mucins (Fig. 3). Mucins are intended to facilitate the flow of bile in the narrowed space of the neck and cystic duct, as they are easily washed off the surface of the mucous membrane of the neck and, depending on the direction of the flow of bile, enter the lumen of the bladder or the cystic duct. The volume of mucin secretion does not exceed 20 ml per day. With their excessive secretion, for example, with cervical cholecystitis, mucous plugs can form in this place, making it difficult to empty the bladder. In addition, mucins, in combination with an altered chemical composition of bile, can be the nucleus (matrix) of the formation of gallstones.

Rice. 3. Alveolar-tubular glands under the mucous membrane of the cervical region of the gallbladder. Hematoxylin-eosin. Uv. x 200

Full evacuation of bile from the gallbladder is ensured by the synchronous operation of the sphincter apparatus of the biliary tract, mainly the sphincter of Oddi. A feature of the smooth muscles of the sphincter of Oddi is that its myocytes, in comparison with the muscle cells of the gallbladder, contain more g-actin than a-actin. Moreover, the actin of the muscles of the sphincter of Oddi is more similar to the actin of the longitudinal muscular layer of the intestine than, for example, to the actin of the muscles of the lower esophageal sphincter. This fact is of great physiological importance, since the synchronous motility of the sphincter of Oddi and the duodenum provide adequate bile outflow and create the most optimal conditions for digestion.

Regulation of contractions of the gallbladder is carried out by the nervous and hormonal systems. Despite the contradictory information concerning the interaction of the secretion of cholecystokinin and the autonomic nervous system, data were obtained that the nature of the motor-evacuation function of the gallbladder is also determined by the sensitivity of the neuromuscular apparatus of the biliary tract to an increase in the concentration of cholecystokinin under the influence of various choleretic stimuli, and not only by the level of the basal and stimulated secretion of cholecystokinin. The sensitivity of smooth muscles to cholecystokinin in patients with biliary dyskinesias can be influenced by the functional state of the autonomic nervous system, as well as the inflammatory process in the wall of the gallbladder. The ability to influence the mechanisms that change the sensitivity of the gallbladder to an increase in the concentration of cholecystokinin will improve the therapy of motor dysfunctions of the biliary tract and the gallbladder, in particular.

Cholecystokinin (CCK) is the main hormonal stimulus that regulates postprandial contraction of the gallbladder. CCK is produced mainly by I-cells of the small intestine. It has now been established that CCK has a broader biological effect, because occurs in other organs, including the nervous system. "Intestinal" CCK was isolated and isolated by Mutt and Jorpes in 1968. In the gastrointestinal tract, CCK regulates motility, the secretion of pancreatic enzymes, the acid-forming function of the stomach and its emptying, and through the hormones of eating behavior affects the processes of obesity. In the nervous system CCK is involved in angiogenesis, saturation processes, nociception (nociceptors - pain receptors), affects memory and learning processes. In addition, CCK interacts with other neurotransmitters in some areas of the central nervous system. Recent studies have identified a whole family of CCK. The contractile function of the gallbladder (SFZhP) is associated with CCK-8. CCK carries out biological effects through receptor-mediated mechanisms. There are two subtypes of CCK receptors that differ in the structure of protein G - CCK-1 and CCK-2. In the literature, the CCK-1 receptor is also referred to as CCA. The main interaction of CCK is carried out through the receptor subtype A, located on the smooth muscle cell of the gallbladder, the sensitivity of which to CCK is 1000 times greater than to gastrin and does not depend on the age, sex and weight of a person. In the regulation of the motor function of the gallbladder, intestines, exocrine function of the pancreas, as well as in the development of pathological refluxes in GERD, CCK antagonists play, the pharmacological and therapeutic potentials of which have been intensively studied recently. The possibility of selective blockade of CCK antagonists can significantly improve FPG.

Despite the fact that the study of SFWP has a huge history, until now there is no consensus about the norm and methods of its determination.

For a long time, oral cholecystography was considered the classical method for determining FPZhP. A decrease in the size of the gallbladder on the cholecystogram by 1/3 after taking two chicken egg yolks was considered normal. The method had a number of disadvantages - X-ray irradiation, the need to use iodine-containing drugs on the eve of the study, which often had a laxative effect, which was the reason for insufficient contrasting of the gallbladder. In addition, in patients with a "disconnected" gallbladder, it was not contrasted. Insufficient visualization of the bladder with oral cholecystography was also noted in concomitant liver diseases.

Currently, two methods are mainly used to study SFZhP for scientific and practical purposes - dynamic cholescintigraphy and dynamic ultrasonography.

These methods make it possible to give a reliable assessment of FVF and show that normally, after each meal, the gallbladder is rapidly emptied and then refilled with bile.

Transabdominal ultrasonography (TUS) is the main method for assessing FPVP. Modern ultrasound devices equipped with computer programs make it possible to obtain objective criteria characterizing the motor-evacuation function of the biliary tract.

To assess the state of the motor function of the gallbladder, the following indicators are taken into account:

Lean (initial) gallbladder volume (Vн, ml);

The latent period is the time from the moment of taking the choleretic breakfast to the beginning of the contraction of the gallbladder (min);

The presence and severity of the phase of the primary reaction (PR) to the choleretic breakfast (an increase in the volume of the gallbladder due to additional intake of bile (PR, in% in relation to the initial volume of the gallbladder);

The duration of the period of emptying the gallbladder until the minimum volume is reached (DO, min);

The minimum volume of the gallbladder during the period of its emptying (Vm, ml);

Emptying fraction (ejection fraction) - the difference between the initial and minimum volume of the gallbladder (FD, ml);

The coefficient of emptying the gallbladder (KO,%):

KO = (Vn - Vm) / Vn100%;

Volumetric rate of emptying of the gallbladder (CO, ml / min):

CO = (Vn - Vm) / DO;

Relative rate of emptying of the gallbladder (CO,% / min):

CO = KO / DO.

For the clinic, according to TUS data, the most important indicators that allow judging the effectiveness of emptying the gallbladder are the following: emptying fraction, volumetric and relative emptying rate, emptying coefficient. The difficulty in determining the norm is explained by the great variability of both the size of the gallbladder and the degree of its contraction.

According to numerous literary sources, according to ultrasound data, it is customary to consider SFZhP normal if the volume of the bladder decreases by 1 / 3-1 / 2 from the initial one by 30-40 minutes, and the emptying rate is 30-70%. Based on our own experience, we recommend that the volume of the bladder be considered normal if the volume of the bladder by 30-40 minutes has decreased by 1/2 of the initial value, and the rate of emptying is in the range of 50-75%. Thus, if the OR is less than 50%, the TFVP should be considered reduced, and if the CO is more than 75%, it should be considered increased. Based on these indicators, corrective therapy should be prescribed.

Dynamic cholescintigraphy is used to assess the state of SFZhP. However, its accuracy is lower in comparison with ultrasound. In this regard, interesting research conducted by J. Donald et al. 2009 The volunteers underwent simultaneous cholescintigraphy and TUS. The data were analyzed every 5 minutes for 1 hour, and the FVP was assessed by the cholecystokinin test. KO with ultrasound was 66.3% ± 20%, scintigraphy - 49% ± 29%. At the same time, the scintillation of indicators in scintigraphy was wider than in sonography, which required the continuation of the study for another 30 min. In addition, in 5% of the participants, it was not possible to assess the FVF due to the lack of visualization of the bladder after the introduction of the RFP. The authors also showed that TUS is less labor-intensive and less expensive than scintigraphy. Therefore, when evaluating FVD performed using TUS or scintigraphy, it is necessary to keep in mind the results of this comparative study.

To assess the motor function of the gallbladder, various cholecystokinetic tests (choleretic breakfasts) are performed. As a choleretic breakfast, 20.0 g of sorbitol with 100 ml of water or intravenous administration of cholecystokinin at a dose of 20 mg / kg of body weight are used. Studies show that the cholecystokinetic effect after the use of sorbitol or cholecystokinin does not differ statistically significantly.

In practice, a sandwich with bread and 10 g of butter or 200 ml of 10% cream, two egg yolks, or 50 ml of vegetable oil are also used to assess the FVF. It should be noted that in different patients the response to the same choleretic breakfast can differ significantly, and the emptying time lasts from 60-80 to 150-225 minutes with multiple repeated phases of contractile activity of the smooth muscles of the gallbladder. Therefore, when comparing SFZhP, for the assessment of which various stimuli were used, this factor should also be taken into account, especially in studies conducted for scientific purposes. For this, a prerequisite in the research protocol is an indication of the choleretic breakfast used.

In practice, sorbitol is often used as a chocecystokinetic test, with a voiding period of 15 to 55 minutes, and our experience has shown that 10% cream can be successfully used to solve both scientific and practical problems in which an assessment of FPG is necessary (200 ml). The use of standardized cholecystokinetic tests in population studies is especially important.

The contractile function of the gallbladder in pathology

The contractile function of the gallbladder is impaired in both functional and organic pathology of the biliary tract, as well as diseases of other digestive organs and systems.

Biliary dysfunction and, hypokinesia, in particular, can be of a primary or secondary nature.

The reasons for the primary dysfunction of the gallbladder of the hypokinetic type are: a decrease in the sensitivity of the smooth muscles of the gallbladder to neurohumoral stimulation, an increase in resistance from the cystic duct as a result of impaired patency or motor discoordination between the gallbladder and the Lutkens sphincter, anatomical features of the structure of the gallbladder outlet and neck of the gallbladder. enlarged Hartman's pocket, elongated and convoluted neck of the gallbladder, pronounced Heister's spiral flap), impeding bile outflow from it, congenital abnormalities of smooth muscle cells of the gallbladder, irregular nutrition and a sedentary lifestyle.

The causes of secondary dysfunction of the gallbladder in a hypokinetic type are: inflammatory diseases of the gallbladder (acute and chronic cholecystitis), cholecystosis (cholecystosteatosis, steatocholecystitis, lymphoplasmacytic cholecystitis, xanthogranulomatous cholecystitis, neurofibromatosis, gallbladder disease and other liver diseases) hepatitis, cirrhosis of the liver), stomach and duodenum (chronic gastritis with reduced secretory function, chronic duodenitis, peptic ulcer localized in the duodenum), pancreas (chronic pancreatitis with endocrine dysfunction), diseases accompanied by impaired cholesterol cholesterol metabolism ( cholesterosis of the gallbladder), bowel disease (celiac disease, Crohn's disease), surgical interventions (vagotomy, resection of the stomach and duodenum, extensive resection of the small intestine), long-term adherence to a strict diet, irregular food intake with intervals, endocrine diseases (hypothyroidism, diabetes mellitus), high levels of estrogen in the blood (pregnancy, taking contraceptives, the second phase of the menstrual cycle), long-term therapy with myotropic antispasmodics and somatostatin, systemic diseases (systemic lupus erythematosus, scleroderma) and other causes.

These reasons explain the widespread occurrence of gallbladder hypokinesia and justify the need for its correction. The criterion for the appointment of conservative therapy is a decrease in the rate of emptying of the gallbladder below 50%.

Functional disorders of the biliary tract occur after emotional stress, overwork and other reasons. The influence of psychogenic factors on the function of the biliary tract is realized through the interaction of cortical and subcortical formations with the nerve centers of the medulla oblongata, hypothalamus, complex nervous and local hormonal relationships between the central nervous system and the digestive system.

The classification of functional disorders of the gallbladder, based on X-ray examination and proposed by L.D. Lindenbraten in 1980, retains its significance at the present time. According to this classification, it distinguishes the hyperkinetic and hypokinetic form of gallbladder dyskinesia. The previously described methods with sequential stimulation with cholecystokinin, xylitol, or a balanced food load are used to diagnose SFGP in functional diseases of the biliary tract. Evaluation of SFZhP cannot be carried out in isolation from the study of the state of the tone of the sphincter of Oddi. It should be remembered that hypokinesia of the gallbladder in some cases can be secondary in nature and is due to hypertonicity of the sphincter of Oddi. In these cases, it is necessary to have information about its functional state. Dysfunction of the sphincter of Oddi can be determined using radioisotope studies, staged chromatic duodenal intubation, or direct manometry. The relief of dysfunction of the sphincter of Oddis with the help of selective antispasmodics in these cases leads to the restoration of a reduced SFP.

Organic pathology of the gallbladder in the overwhelming majority of cases is accompanied by a decrease in FPG. Consider the state of SFZhP in the most common biliary pathology.

In acute and chronic cholecystitis, there is a thickening of the gallbladder wall, which is clearly detected by ultrasound. Despite the fact that the CCK level does not decrease, the muscular membrane involved in the inflammatory process does not provide adequate evacuation of bile from the bladder. There is a direct correlation between the abatement of the inflammatory process in the wall of the gallbladder and the restoration of its contractile function. However, the long-term inflammatory process is accompanied by the secretion of inflammatory mediators, primarily pro-inflammatory cytokines, which negatively affect the contraction of myocytes.

In gallstone disease (GSD), the state of the contractile function of the gallbladder has been studied in sufficient detail, since decreased FPVP is one of the factors contributing to the formation of gallstones. As a rule, patients with cholesterol gallstones have an increased volume of the bladder on an empty stomach, a low rate of emptying after a food load. Moreover, these indicators do not depend on whether the patient has small or large stones or only lithogenic bile.

It should be noted that, despite the presence of stones in the gallbladder and impaired motor function, inflammation in the wall of the gallbladder in gallstones, even at stage II of the disease (according to the classification of gallstones developed by the Central Research Institute of Geology, is usually absent or weakly expressed and therefore cannot be considered the main cause decrease in contractile function. Research carried out in the clinic showed that hypokinesia of the gallbladder develops already at the initial stage of the formation of cholesterol gallstones, although it is not accompanied by an increase in the volume of the gallbladder on an empty stomach.

It was found that the degree of decrease in the emptying of the gallbladder is in direct proportion to the concentration of cholesterol in the bile of the gallbladder. Moreover, this dependence persists in healthy individuals, in the absence of gall stones. These results of the study suggest that excess cholesterol molecules in bile act on the gallbladder wall as a myotoxic agent.

In vitro studies comparing the contractile function of the gallbladder in patients with cholesterol gallstones and control have revealed abnormalities in the binding of agonists, for example, cholecystokinin to the CCK-1 receptors of the plasma membrane, a decrease in the contraction of isolated smooth muscle cells or isolated smooth muscle bands of the gallbladder.

As you know, CCK modulates the contractions of the gallbladder, the sphincter of Oddi. This effect is realized through the activation of smooth muscles as a result of interaction with CCK-1 receptors (CCK-1Rs). In an experiment on mice lacking CCK-1Rs (line 129 / SvEv), which for 12 weeks were fed a standard or lithogenic diet (containing 1% cholesterol, 0.5% bile acids and 15% milk fat), it was found that regardless of the diet received in animals lacking CCK-1Rs, there was a greater volume of the gallbladder, predisposing to bile stasis, as well as a significant slowdown in the transit of small intestinal contents, which led to increased absorption of cholesterol and increased secretion of cholesterol into bile. Increased cholesterol levels in bile, together with gallbladder hypokinesia, promoted nucleation, growth, and agglomeration of cholesterol monohydrate crystals, which in turn led to more frequent detection of cholesterol gallstones in mice lacking CCK-1Rs. ... This gave reason to believe that the receptor-mediated mechanism is leading in reducing the contractile function of the gallbladder. Indeed, subsequent studies did not reveal any disturbances in the intracellular mechanisms of contraction of the smooth muscles of the human gallbladder in the presence of cholesterol gallstones.

Violation of SFGP, caused by excess cholesterol in bile and its effect on smooth muscle cell membranes, is detected at an early stage of gallstone formation.In this regard, it becomes clear why emptying of the gallbladder is reduced generically to the formation of gallstones when bile is only oversaturated with cholesterol.

These studies provided a strong basis for confirming the hypothesis that an increase in the concentration of cholesterol in bile and its increased absorption from the gallbladder cavity lead to smooth muscle dysfunction. In addition, it was found that the absorption of cholesterol by the wall of the gallbladder is accompanied by an increase in the stiffness of the sarcolem membrane of the myocyte. Therefore, when CCK binds to a receptor on a smooth muscle cell, its G-proteins are not activated and the contractility of the gallbladder decreases.

At the early stage of gallstone formation, the violation of the contractility of the gallbladder is still reversible. However, if, against this background, an acute or exacerbation of chronic inflammation in the wall of the gallbladder joins, it is not necessary to count on the restoration of SFZhP.

In contrast to the above, there is an opinion that hypokinesia of the gallbladder may precede cholecystolithiasis. The congestion caused by hypofunction of the gallbladder provides the necessary time for the nucleation of crystals and the growth of gallstones in the mucin gel. In addition, a viscous mucin gel that forms in the gallbladder cavity can contribute to the development of hypokinesia, because. with difficulty pushed through the cystic duct. In the presence of mucin and biliary sludge containing calcium, pigments and glycoproteins, conditions are quickly created for the nucleation of cholesterol or precipitation of calcium bilirubinate.

This opinion is supported by the high incidence of cholelithiasis in patients receiving complete parenteral nutrition and emphasizes the importance of hypokinesia and stagnation of bile in the gallbladder for the formation of gallstones. So, for example, in Crohn's disease, the frequency of detection of gall stones reaches 27%, and in patients on complete parenteral nutrition - 49%. This is due to the fact that during parenteral nutrition, the gallbladder is not emptied, since the food irritant for the release of CCK is excluded. Stagnation of bile contributes to the formation of biliary sludge, and subsequently, stones in the gallbladder. On the contrary, daily intravenous administration of CCK can completely prevent impairment of gallbladder motility and eliminate the inevitable risk of biliary sludge and gallstone formation. In addition, delayed emptying and increased gallbladder volume, which occur, for example, during pregnancy or with oral contraception, also predispose to gallstones.

However, it should be noted that a decrease in FPVP even with multiple gallstones is not always a mandatory attribute. We observed patients with multiple calculi in the gallbladder, in whom SFGP did not suffer (Fig. 4).

Rice. 4. TUS. Cholecystolithiasis (multiple stones in the gallbladder with an acoustic shadow). Study of the contractile function of the gallbladder after a standard choleretic breakfast (cream 10% - 200ml):

a - before stimulation;

b - after 40 min KO 57%;

c - after 1 hour KO 60%

Conclusion: Normal FPVP

With cholesterosis of the gallbladder (CGD), as well as with gallstone disease, there is an oversaturation of bile with cholesterol. This makes it possible to explain not only the deposition of cholesterol in the wall of the gallbladder, but also the frequent combination of CGD with cholecystolithiasis. A decrease in FPG is a factor contributing to the progression of gallbladder cholesterosis and the formation of gallstones. According to Yu.N. Orlova, with CGD, 40.2% of patients have a decrease in FPG that does not depend on its form. The ejection fraction of the gallbladder was significantly lower in CGD combined with biliary sludge and cholecystolithiasis. Against the background of urso therapy, there is an increase in the ejection fraction of the gallbladder in 95.2% of patients in the absence of cholecystolithiasis (on average by 21.2%) and in 83.3% in combination with cholecystolithiasis (on average by 12.9%).

SFZhP in non-alcoholic fatty gallbladder disease. Obesity, which has taken on the nature of an epidemic, has provided a steady upward trend in the number of patients with cholesterol gallstones. However, in recent years, information has appeared that cholecystectomy has increasingly begun to be performed for chronic cholecystitis, in the absence of stones in the gallbladder, and the frequency of such operations has more than doubled in recent years. According to J. Majeski, the number of patients operated on for chronic acalculous cholecystitis increased to 20-25%. No convincing explanation has been found for this phenomenon. Due to the fact that the disease is more common among women, partly the reason was attributed to the influence of estrogen and progesterone, which reduce SFGP. The study of the problem of obesity and, in particular, non-alcoholic fatty gallbladder disease (NAFGD), has made it possible to answer many questions. The term NAFLG was coined on the basis of studies showing that, like non-alcoholic fatty liver disease, NAFLG has similar stages: gallbladder steatosis, steatocholecystitis, and gallbladder cancer.

The first experimental studies on leptin-deficient and leptin-resistant obese mice showed that they have an increased volume of the gallbladder, which does not respond to the administration of neurostimulants, cholecystokinetic agents. Subsequent studies found that in mice with congenital obesity and in mice that were fed a diet high in fat, the amount of lipids in the gallbladder wall increased. The study of SFGP of the bladder revealed a relationship: it was lowest in mice with a high lipid content in its wall. The results of experimental studies on animals made it possible to draw a fundamental conclusion: leptin-deficient obesity and / or a diet high in fat cause non-alcoholic fatty gallbladder disease. which is manifested by a decrease in TFVP.

As mentioned above, an increase in cholesterol in cell membranes and an increase in the ratio of cholesterol / phospholipids in them, affect smooth muscle cells, changing the fluidity of the membranes. Back in 1996, P. Yu et al. reported that animals fed a cholesterol diet increased cholesterol in the gallbladder wall and decreased phospholipids, which was accompanied by an increase in the cholesterol / phospholipid ratio.

More recently, Q. Chen et al. showed that smooth muscle cells of human gallbladders with cholesterol stones have an increased cholesterol content and an increased cholesterol / phospholipid ratio compared to the gallbladders of patients with pigment stones. They also demonstrated a decrease in membrane fluidity in cholesterol cholecystolithiasis and a decrease in gallbladder muscle cell contraction with an increase in the cholesterol / phospholipid ratio.

Thus, it can be concluded that the deposition of lipids in the wall of the gallbladder is accompanied by a decrease in its contractile function and, in some patients, may be the cause of cholecystectomy.

SFZhP with adenomyomatosis. Most of the pathological processes in the wall of the gallbladder are accompanied by a decrease in SFGP. The exception is adenomyomatosis (AMM) - an acquired, hyperplastic lesion of the gallbladder, characterized by excessive proliferation of the superficial epithelium with invagination into the hyperplastic muscular membrane and the formation of internal false diverticula - Rokitansky-Ashoff sinuses. AMM belongs to the group of hyperplastic cholecystosis - diseases, the development of which is based on degenerative and proliferative changes in the wall of the gallbladder of a non-inflammatory nature. AMM of the gallbladder is commonly referred to as a rare disease. However, the frequency of AMM according to our data (11000 ultrasound and 2300 cholecystectomies) is 16% and 33%, respectively.

It is important to note that an increase in FPGP in AMM is one of the characteristic ultrasound criteria that justify the diagnosis. The reason for the increase in SFGP in adenomyomatosis is explained by hypertrophy of the muscular membrane. It should be noted that CO of more than 75% is observed only with a diffuse form of AMM and a macroscopically visible thickening of the gallbladder wall. Focal and segmental forms of AMM do not have a significant effect on SFZhP. The initial manifestations of AMM, which are found only on histological examination, also do not affect the state of the SFGP. SFGP does not decrease even when AMM is combined with cholecystolithiasis. In these cases, SFGP in the formation of gallstones is likely to play a secondary role.

Only in some cases with AMM it is possible to reveal a decrease in FPVP. This may be due to the presence of an extensive adenoma localized in the bottom, a cancerous or sclerotic process in the wall of the gallbladder. SFZhP also decreases in the diffuse form of AMM with a predominant lesion in the cervical region. In these cases, contraction of the gallbladder in the cervical region can also make it difficult to empty. The combination of AMM with other types of hyperplastic cholecystosis (lymphoplasmacytic and xanthogranulomatous cholecystitis, gallbladder steatosis and steatocholecystitis, etc.) also has a negative effect on SFGP.

Conclusion

SFZhP, providing an adequate outflow of concentrated bile, promotes complete digestion in the small intestine. The choice of the method for determining the FPI and the correct interpretation of the results obtained make it possible to substantiate the need for corrective therapy. Knowledge of the causes of FVD disorders enables the doctor to choose the most optimal treatment option and monitor its effectiveness.

Literature

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2. Schjoldager BT. Role of CCK in gallbladder function. Ann N Y Acad Sci. 1994 Mar 23; 713: 207-18.

3. Herranz R. Cholecystokinin antagonists: Pharmacological and therapeutic potential. Med Res Rev. 2003 Sep; 23 (5): 559-605.

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5. Barr RG, Kido T, Grajo JR. Comparison of sonography and scintigraphy in the evaluation of gallbladder functional studies with cholecystokinin. J UltrasoundMed. 2009 Sep; 28 (9): 1143-7.

6. Ilchenko A.A., Maksimov V.A., Chernyshev A.L. and other Staged chromatic duodenal sounding. Guidelines. - Moscow. - 2004 .-- 26 p.

7. Ilchenko A.A. Diseases of the gallbladder and biliary tract. A guide for doctors. - 2nd ed., Rev. and add. - M .: LLC "Publishing House" Medical Information Agency ", 2011. - 880 p.

8. Ilchenko A.A. 10 years of classification of gallstone disease (TsNIIG): the main results of scientific and practical application. - Experimental and clinical gastroenterology. - 2012. - No. 4. - p. 3-10.

9. Wang DQ, Schmitz F, Kopin AS, Carey MC. Targeted disruption of the murine cholecystokin-1 receptor promotes intestinal cholesterol absorption and susceptibility to cholesterol cholelithiasis. J Clin Invest. 2004 Aug; 114 (4): 521-8.

10. Ivanchenkova R.A., Izmailova T.F., Metelskaya V.A. and other Cholesterosis of the gallbladder. Clinic, diagnostics, treatment. Wedge. Honey. - 1997. - No. 5: 46-51.

11. Orlova Yu.N. Cholesterosis of the gallbladder. Clinical and sonographic examination. Abstract of the thesis. ... Candidate of Medical Sciences. - M .: 2003 .-- 30 p.

12. Joahanning JM, Gruenberg JC. The changing face of cholecystectomy. Am Surg 1998; 64: 643-647.

13. Patel NA, Lamb JJ, Hogle NJ, Fowler DL. Therapeutic efficacy of laparoscopic cholecystectomy in the treatment of biliary dyskinesia. Am J Surg 2004; 187: 209-212.

14. Majeski J. Gallbladder ejection fraction: an accurate evaluation of symptomatic acalculous gallbladder disease. Int Surg 2003; 88: 95-99.

15. Yu P, Chen Q, Biancani P, Behar J. Membrane cholesterol alters gallbladder muscle contractility in prairie dogs. Am J Physiol 1996; 271: G56-G61.

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17. Ilchenko A.A., Orlova Yu.N., Bystrovskaya E.V. and other Adenomyomatosis of the gallbladder. Analysis of 215 operational cases. Experiment and wedge gastroenterol. - 2013. - No. 4. - Accepted for publication.

The contractile function of the gallbladder

Under normal physiological conditions, the gallbladder contracts repeatedly throughout the day. Between meals, the gallbladder deposits hepatic bile (the average volume is approximately 25-30 ml in healthy individuals), and during meals it secretes different amounts of bile, depending on the degree of neurohormonal stimulation.

Dynamic cholescintigraphy and ultrasonography make it possible to give a reliable assessment of the contractile function of the gallbladder and show that after each meal, the gallbladder is quickly emptied and then refilled with bile. On the contrary, in patients with cholesterol gallstones, an increased volume of the gallbladder on an empty stomach and a low rate of emptying after a food load are often noted. Moreover, these indicators do not depend on whether patients have small or large stones, or only lithogenic bile.

It should be noted that, despite the presence of stones in the gallbladder, it is a violation of motor function, inflammation in the wall of the gallbladder is either absent or moderate and therefore cannot be considered the main reason for a decrease in contractile function. Studies carried out in the clinic have shown that hypokinesia of the gallbladder develops already at the stage of formation of cholesterol gallstones, although it is not yet accompanied by an increase in the volume of the gallbladder on an empty stomach. The reduced contractile function of the gallbladder persists after successful extracorporeal shock wave lithotripsy, as well as in some patients after oral litholytic therapy with bile acids.

It was found that the degree of decrease in the emptying of the gallbladder is in direct proportion to the concentration of cholesterol in the bile of the gallbladder. Moreover, this dependence persists in healthy individuals in the absence of gall stones. These results of the study suggest that excess cholesterol molecules in bile act on the gallbladder wall as a myotoxic agent.

In vitro studies comparing the contractile function of the gallbladder in patients with cholesterol gallstones and in control subjects revealed abnormalities in the binding of agonists, for example, cholecystokinin (CCK) to CCK-1 receptors of the plasma membrane, a decrease in the contraction of isolated smooth muscle cells or isolated smooth muscle bands of the bile bubble.

As you know, CCK modulates the contractions of the gallbladder, the sphincter of Oddi. This effect is realized through the activation of smooth muscles as a result of interaction with CCK-1 receptors (CCK-1Rs). In an experiment on mice lacking CCK-1Rs (line 129 / SvEv). which within 12 weeks. fed a standard or lithogenic diet (containing 1% cholesterol, 0.5% bile acids and 15% milk fat), it was found that, regardless of the diet received, animals lacking CCK-1Rs had a larger gallbladder volume, predisposing to bile stasis , as well as a significant slowdown in the transit of small intestinal contents, which led to increased absorption of cholesterol and increased secretion of cholesterol into bile. Increased cholesterol levels in bile, together with gallbladder hypokinesia, promoted nucleation, growth, and agglomeration of cholesterol monohydrate crystals, which in turn led to more frequent presence of cholesterol gallstones in mice lacking CCK-1Rs. This gave reason to believe that the receptor-mediated mechanism is leading in a decrease in the contractile function of the gallbladder. Indeed, subsequent studies did not reveal any disturbances in the intracellular mechanisms of contraction of the smooth muscles of the human gallbladder in the presence of cholesterol gallstones.

Violation of the contractile function of the gallbladder, due to the excessive content of cholesterol in bile and its effect on the membranes of smooth muscle cells, is noted already at an early stage of the formation of gallstones. In this regard, it becomes clear why the emptying of the gallbladder is reduced even before the formation of gallstones, when bile is only oversaturated with cholesterol.

These studies provided a strong basis for confirming the hypothesis that an increase in the concentration of cholesterol and bile and an increased absorption from the gallbladder cavity leads to smooth muscle dysfunction. In addition, it was found that the absorption of cholesterol by the wall of the gallbladder is accompanied by an increase in the rigidity of the sarcolemmic membrane of the myocyte. Therefore, when CCK binds to a receptor on a smooth muscle cell, G-proteins are not activated and the contractility of the gallbladder decreases.

At the early stage of gallstone formation, the violation of the contractility of the gallbladder is still reversible. However, if against this background an acute inflammation or exacerbation of a chronic inflammation in the wall of the gallbladder joins, it is not necessary to count on the restoration of its contractile function.

In contrast to the above, it is believed that hypokinesia of the gallbladder may precede cholecystolithiasis. The congestion caused by hypofunction of the gallbladder provides the necessary time for the nucleation of crystals and the growth of gallstones in the mucin gel. It is also a viscous mucin gel that forms in the gallbladder cavity. may contribute to hypokinesia, as it is difficult to push through the cystic duct. In the presence of mucin and biliary sludge containing calcium, pigments and glycoproteins, conditions are quickly created for the nucleation of cholesterol or precipitation of calcium bilirubinate.

This opinion is supported by the high incidence of cholelithiasis in patients receiving total parenteral nutrition, and emphasizes the importance of hypokinesia and stagnation of bile in the gallbladder for the formation of gallstones. So, for example, in Crohn's disease, the frequency of gallstones reaches 27%, and in patients on complete parenteral nutrition - 49%. This is due to the fact that during parenteral nutrition, the gallbladder is not emptied, since the food irritant for the release of CCK is excluded. Stagnation of bile contributes to the formation of biliary sludge, and subsequently, stones in the gallbladder. In contrast, daily intravenous administration of CCK can completely prevent impairment of gallbladder motility and eliminate the inevitable risk of biliary sludge and gallstones formation. In addition, it is known that delayed emptying and increased gallbladder volume, which occur during pregnancy and with oral contraception, also predispose to the formation of gallstones.

Concentration function of the gallbladder

In contrast to the contractile function, the concentration function of the gallbladder in its pathology suffers in the last turn. Due to the absorption of water by the mucous membrane of the gallbladder, the concentration of the main components of bile increases significantly compared to. hepatic bile. However, the ratios of the various components in the gallbladder are not equivalent to the hepatic portion.

According to numerous studies, the bile of the gallbladder of animals or patients with cholesterol gallstones contains higher concentrations of proteins in comparison with the bile of patients without stones or with pigment stones.

Analysis of the composition of hepatic and gallbladder bile obtained from patients with cholesterol gallstones during cholecystectomy showed that only mucin, total protein, IgG and aminopeptidase N content in the bile of the gallbladder increases, causing a pronounced pronucleating effect. At the same time, the concentration of haptoglobin, α1-acid glycoprotein, IgM and IgA was decreased in most patients. This suggested that such changes in concentration indicators cannot be explained only by water absorption, but are due to absorption by the gallbladder epithelium.

Thus, the preserved concentration function of the gallbladder contributes to an increase in the level of proteins that cause a pronuclear effect, and therefore is an additional factor that increases the risk of gallstones formation.

As a result of water absorption, the concentration of lipids in the gallbladder also increases. Normally, the mucous membrane of the gallbladder carries out differential absorption of cholesterol, phospholipids and bile acids, as a result of which the saturation of bile with cholesterol decreases. In this case, cholesterol molecules from oversaturated bile are absorbed continuously by the mucous membrane of the gallbladder with cholesterol gallstones. In the presence of cholesterol gallstones, the gallbladder epithelium loses its ability to selectively absorb cholesterol and bile phospholipids, which can contribute to the formation of gallstones, maintaining bile oversaturation. The process is aggravated by the associated hypokinesia of the gallbladder.

The outcome of cholesterol absorbed by the gallbladder is similar to that found in the development of an atherosclerotic plaque. Unesterified cholesterol molecules are quickly dispersed in muscle fibers, since the gallbladder does not have a pronounced muscle layer under the mucous membrane. Due to the fact that the gallbladder does not synthesize lipoproteins for the transport of cholesterol to the plasma, "excess" unesterified cholesterol molecules can be removed from the mucous and muscular membranes of the gallbladder only by esterification and their subsequent storage or by reverse diffusion into bile. It should be noted that in the presence of lithogenic bile, the reverse diffusion of cholesterol molecules is blocked, since the bile of the gallbladder is continuously saturated despite daily fluctuations.

In addition, “extra” cholesterol molecules absorbed from lithogenic bile can cause proliferative and inflammatory changes in the gallbladder mucosa. In experiments on dogs fed with food containing 1–2% cholesterol, infiltration of the mucous membrane with polymorphonuclear leukocytes occurred within 2 weeks. Acute and chronic inflammatory changes are accompanied by impaired blood flow in the mucous membrane. It remains unclear which factor in lithogenic bile is the trigger that triggers these inflammatory reactions. However, all these changes are noted before microscopic stones are found.

As noted above, the absorption of cholesterol by the mucous membrane of the gallbladder is accompanied by hypokinesia. In vitro studies show that gallbladder muscle dysfunction is associated with a 2-fold increase in the sarcolemma in comparison with the norm in the ratio of cholesterol and phospholipids in patients with cholelithiasis and animals receiving a lithogenic diet. This ratio can be restored to normal if isolated muscle cells are cultured with cholesterol-free liposomes.

These data help to understand the development of gallbladder hypokinesia in the presence of lithogenic bile. Since non-esterified cholesterol molecules are inserted into the membrane of muscle cells, their increased content in comparison with phospholipid molecules leads to an increase in muscle fiber rigidity and a decrease in the response of the muscle cell to CCK.

Intestinal factors and nucleation

Numerous epidemiological and clinical studies convincingly demonstrate that the incidence of cholesterol gallstones in North America and European countries, whose populations consume food with high cholesterol content, is significantly higher than in developing countries. Previously, cholesterol gallstones were relatively rare in Japan. However, over the past 50 years, food preferences have changed, residents have become more committed to European cuisine, which has led to an increase in cholesterol cholelithiasis. A similar trend is observed in China in connection with the Europeanization of the traditional Chinese diet, i.e. with excessive consumption of food high in cholesterol.

However, studies regarding the effect of poverty cholesterol on bile lipid levels have yielded conflicting results. It has been established that an increased content of cholesterol in food does not always cause oversaturation of bile with cholesterol. Experimental studies have shown that high absorption of cholesterol in the intestine positively correlates with the frequency of the formation of cholesterol gallstones. C57L / S mice (susceptible to the lithogenic diet) have significantly higher intestinal cholesterol uptake and more cholesterol gallstones than AKR mice (resistant to lithogenic diet). This is due to the different metabolism of chylomicron remnants in C57L / S and AKR mice. Cholesterol molecules, absorbed in the small intestine, are the main source for hypersecretion into bile in mice sensitive to a lithogenic diet.

Thus, the high content of cholesterol in the diet and its high absorption in the intestine are two independent factors that increase the risk of the formation of cholesterol gallstones.

In addition, slowing bowel motility may play a role in the formation of gallstones. It has been established that a delay or slowdown in the transit of intestinal contents is accompanied by an increased absorption of cholesterol and the intestines, its increased secretion into bile and an increase in the prevalence of gallstones.

As you know, bile acids secreted into the duodenum are reabsorbed in the ileum due to active transport and returned to the liver. A significant slowdown in intestinal transit increases the level of secondary bile acids, which can increase the lithogenic properties of bile. The relationship between decreased intestinal motility, increased levels of deoxycholates in bile and lithogenicity of bile has been noted in studies both in mice and in humans. So. Clinical studies have shown that in patients with acromegaly treated with octreotide (a known risk factor for cholesterol gallstone disease), due to a decrease in the transit of intestinal contents, the level of deoxycholates in the bile increases and cholesterol precipitation in the gallbladder is noted. An increase in deoxycholates in bile is associated with an increased amount of gram-positive anaerobic bacteria in the colon with 7α-dehydroxylase activity. The concentration of deoxycholates and cholesterol in bile decreases after antibiotic therapy, which decreases the activity of fecal 7α-dehydroxylase.

These studies have suggested that chronic intestinal infection is a potential factor in the pathogenesis of cholesterol gallstones. As noted above, recent studies in mice have shown that the enterohepatic species, but not Helicobacter pylon, are responsible for the nucleation of cholesterol from oversaturated bile. These Helicobacter species have been identified in the bile and gallbladder tissue of Chilean patients with chronic cholecystitis. However, further research is needed to resolve the question of whether there is a pathogenetic relationship between chronic enteritis and the formation of cholesterol gallstones.

In addition, it was found that in patients with Crohn's disease, as well as in individuals. who have undergone bowel resection or complete colectomy, there is an oversaturation of bile with cholesterol, and they have a tendency to precipitate cholesterol crystals and an increased risk of the formation of bile stones. This is due to the fact. that part of the bile acids is turned off from the EHC, and therefore their secretion into bile decreases, as a result of which the solubilization of cholesterol decreases.

Attaching great importance to intestinal factors in cholesterol cholelithiasis, some authors propose to attribute gallstone disease to the group of intestinal diseases.

Thus, significant advances have been made in the study of the formation of gallstones. However, evaluating the results of experimental and clinical studies, it should be noted that the mechanisms of cholesterol nucleation at the molecular level are still not fully understood, since the study of nucleation processes is limited by the list of available laboratory methods. In this regard, it can be assumed that new informative technologies will give a more accurate answer to many questions of biliary lithogenesis.

Dyskinesia of the gallbladder is considered a fairly common pathology, which is characterized by a violation of the functioning of this organ, which causes an insufficient outflow of bile into the duodenum. The disease can be both primary and secondary, which is why the reasons for its formation will differ. Often they are congenital anomalies or other ailments of the digestive system.

The clinical picture will also depend on the type of disease. Such a disorder has nonspecific symptoms, for example, pain in the area under the right ribs, bouts of nausea and vomiting, and an unpleasant taste in the mouth.

A wide range of instrumental diagnostic procedures will help to make the correct diagnosis and determine the type of ailment. However, laboratory tests may be required, and the information obtained by the gastroenterologist during the examination is also taken into account.

Ways to treat dyskinesia are always limited to conservative treatments such as medication, diet therapy, and folk remedies.

Etiology

Depending on the factors that led to dyskinesia of the gallbladder and biliary tract, the disease is divided into primary and secondary.

The most common sources of development of the first type of ailment are:

• doubling or narrowing of this organ or cystic ducts;
• the formation of scars and constrictions;
• improper motor activity of smooth muscle cells;
• dysfunction of the ANS, which can develop due to acute or chronic;
• increase or decrease in the production of cholecystokinin;
• congenital failure of the muscles of the gallbladder and bile ducts;
• poor diet, in particular overeating, irregular meals, or excessive addiction to fatty foods. It is for this reason that sparing nutrition for dyskinesia is not the last place in the treatment;
• the presence in a person of any stage or, conversely, a lack of body weight;
• sedentary lifestyle.

Secondary DVP develops against the background of diseases already occurring in the human body, which makes it difficult to establish the correct diagnosis, since the symptoms of the main ailment prevail over the signs of malfunctioning of the gallbladder.

In addition, gastroenterologists have put forward a theory that the development of such a disease can be affected by the improper functioning of liver cells, which is why they initially produce bile with a changed composition.

In a child, this disease can be caused by:

• perinatal CNS lesions, such as trauma during childbirth;
• or ;
• or ;
• psychoemotional disorders and gastrointestinal diseases.

Classification

For the time and reasons for development, gallbladder dyskinesia is divided into:

• primary- this type is associated either with congenital anomalies or with disorders that affect only the functioning of this organ, and not its structural integrity. In such cases, no violations will be observed during instrumental examinations;
• secondary- is formed during life and is associated with the course of other acquired serious diseases.

There is also a division of pathology regarding the features of motor activity, i.e., muscle contraction of the affected organ:

• hypertensive gallbladder dyskinesia- at the same time, the contractile activity of the biliary system is increased. Most often found in children and young people;
• hypomotor dyskinesia of the gallbladder- has the opposite picture and is characterized by a decreased activity of the biliary system. Most often diagnosed in women over forty years old;
• mixed.

Symptoms

The clinical signs of the disease will differ depending on the form in which dyskinesia of the gallbladder and bile ducts proceeds. However, there is a group of symptoms that can be attributed to both increased and decreased activity of the biliary system.

Hypotonic dyskinesia has the following symptoms:

• pain under the right ribs - the pain is constant, dull and aching. May intensify during meals or immediately after eating;
• belching, which in some cases is accompanied by an unpleasant odor - often occurs after meals, less often - between meals;
• attacks of nausea, ending with vomiting - in some cases, bile impurities are present in the vomit. It is very often the result of overeating or eating a lot of fatty foods;
• a feeling of bitterness in the mouth is the most characteristic symptom of an ailment. Appears mainly in the morning, after a meal or excessive physical activity;
• an increase in the size of the abdomen, which is often complemented by pain;
• decreased appetite or complete aversion to food - occurs against the background of the fact that a large number of symptoms appear during or after the absorption of food;
• violation of the act of defecation - constipation occurs more often than diarrhea and occurs after a short period of time after a meal;
• weight gain - in cases of hypokinetic dyskinesia, obesity is not only a cause, but also a symptom;
• a decrease in blood pressure indicators, which occurs against the background of a decrease in heart rate;
• increased production of saliva and sweat;
• pathological redness of the skin of the face.

The hyperkinetic type of dyskinesia is represented by the following symptoms:

• pain syndrome - pain is sharp, intense and colicky, localized in the area of ​​the right hypochondrium. The duration of the attack is often half an hour and can be repeated several times throughout the day;
• irradiation of pain to the right side of the back, scapula or upper limb. Less commonly, pain is observed, expressed with angina pectoris or with scoliosis;
• a constant feeling of heaviness under the right ribs;
• a complete lack of appetite, against the background of which there is a decrease in body weight;
• nausea and vomiting that accompany an attack of intestinal colic;
• disorder of the act of defecation - in contrast to hypotonic dyskinesia of the gallbladder, diarrhea predominates in the hypertensive form;
• rapid heartbeat;
• increased sweating;
• headache;
• irritability and sleep disturbance;
• an increase in blood tone;
• aching pains in the heart;
• rapid fatigability.

Signs that are observed regardless of the type of course of the disease:

• Acquisition of a yellowish tint by the skin, mucous membranes of the mouth and sclera;
• overlapping of the tongue with a bloom of white and yellow;
• discoloration of feces;
• darkening of urine;
• an increase in the size of the liver;
• severe itching of the skin;
• decreased sexual activity;
• violation of the menstrual cycle in women.

Dyskinesia of the gallbladder in a child proceeds in the same way as in adults, but it is worth noting that in this age category, the hypotonic form is quite rare.

Diagnostics

The gastroenterologist knows what dyskinesia is, how to diagnose it and prescribe treatment. All diagnostic measures are aimed at differentiating the hypermotor type of the disease from the hypomotor form.

The first stage of establishing the correct diagnosis includes manipulations performed directly by the clinician, including:

• the study of the life history and medical history of not only the patient, but also his close relatives - because the likelihood of a genetic predisposition is not excluded;
• a thorough examination aimed at palpating the anterior wall of the peritoneum in the area under the right ribs, assessing the condition of the skin and measuring blood pressure;
• conducting a detailed survey of the patient - to draw up a complete symptomatic picture, since each type has characteristic signs.

Laboratory diagnostic measures are limited to:

Instrumental diagnostics is based on the implementation of such procedures:

• Ultrasound and MRI of the affected organ are the most informative diagnostic methods;
• cholecystography;
• dynamic scintigraphy;
• sphincter of Oddi manometry;
• FEGDS;
• duodenal intubation;
• RCPG;
• CT scan of the bile ducts.

Treatment

Despite the variety of symptoms, the treatment of gallbladder dyskinesia will be carried out using conservative methods.

The basis of therapy is a diet for gallbladder dyskinesia, based on the following rules:

• frequent and fractional food intake;
• complete rejection of spicy and fatty foods, smoked meats and preservatives;
• reducing the daily volume of salt consumption to 3 grams;
• cooking food only by cooking and stewing, baking and steaming;
• intake of a large amount of mineral water without gas.

The rest of the nutritional advice is provided by the attending physician according to dietary table number five.

Drug treatment is carried out by taking the following drugs:

• choleretics;
• cholespasmolytics;
• enzyme substances;
• neurotropic medications, which are prescribed by a psychotherapist, in particular, "Novo-Passit".

Dyskinesia of the gallbladder and biliary tract is successfully eliminated with the help of physiotherapy procedures, including:

• diadynamic therapy;
• electrophoresis;
• acupuncture;
• hirudotherapy.

Conservative treatment in children and adults also includes:

• duodenal intubation;
• closed tubazh;
• acupressure;
• the use of traditional medicine, but only after consulting with the attending physician, since the use of medicinal herbs is necessary depending on the variant of the course of the disease. With hypotonic dyskinesia, oregano, immortelle and corn silk are useful, and with hypertensive dyskinesia - mint, licorice and chamomile;
• spa therapy.

Surgical intervention is inappropriate to use for gallbladder dyskinesia.

Possible complications

Ignoring the symptoms or self-treatment with folk remedies can lead to the development of a large number of consequences. These include:

• and cholecystitis;
• gastritis and gallstone disease;
• duodenitis;
• a strong decrease in body weight up to exhaustion.

Prevention and prognosis

To reduce the likelihood of such an ailment, you must adhere to such simple rules.

Dyskinesia of the gallbladder and biliary tract is a disease in which there is a violation of the motility (movement) and tone of the gallbladder, as well as its ducts.

Some statistics

Among all diseases of the gallbladder and bile ducts, dyskinesia is 12, 5%.

Women suffer from this ailment about 10 times more often than men. That is due to the peculiarities of the hormonal and metabolic processes of the female body (for example, changes during pregnancy, taking oral contraceptives). Young women with asthenic constitution are especially susceptible to ailment.

Among children, adolescents are most often affected.

In 2/3 of all cases, it is a secondary disease that develops against the background of lesions of the gastrointestinal tract (colitis, peptic ulcer of the duodenum and / or stomach, pancreatitis, gastritis).

The most common (about 60-70% of all cases) is the hypotonic form. In modern medicine, the disease was first described by surgeons in 1903-1909, who operated on a patient with severe pain in the right hypochondrium. However, having opened the abdominal cavity, they did not find any stones or inflammation in the gallbladder. After that, the disease began to be carefully studied by therapists.

However, even in ancient times it was noticed that there is a connection between negative emotions of a person and a disease of the gallbladder, as well as its ducts. Therefore, such people were called "bile".

In addition, everyone knows about four types of temperament, which are described in medical treatises by ancient doctors.

For example, anger and irritability indicate an excess of energy at the point of the gallbladder - a hypertensive variant of dyskinesia (choleric type of temperament). That is, the wall of the gallbladder is tense and is strongly contracted.

Whereas bitterness, lethargy and a tendency to depression indicate a lack of energy at the point of the gallbladder - a hypotonic variant of dyskinesia (melancholic type of temperament). That is, the wall of the gallbladder is sluggish and does not contract well.

Anatomy and physiology of the gallbladder

Gall bladder- a hollow organ. It is usually located on the right upper abdomen at about the midpoint of the lower hypochondrium (below the last rib).

The length of the gallbladder ranges from 5 to 14 cm, and the width - from 3 to 5 cm. Its capacity on an empty stomach is from 30 to 80 ml. However, with stagnation of bile, its volume increases.

Normally, the gallbladder has an elongated pear-shaped shape (with wide and narrow ends). However, sometimes its shape is rather bizarre: spindle-shaped, elongated, doubled, with an inflection or internal bridges, and so on.

The gallbladder has three parts - the bottom, the body, and the neck (narrow part). The cystic duct departs from the neck, which is further connected to the hepatic duct, forming a common bile duct. In turn, the common bile duct opens into the duodenum cavity (12 PC) in the Vater's nipple, which is surrounded by the sphincter (muscle ring) of Oddi.

The structure of the gallbladder wall

• The mucous membrane is composed of epithelial and various glandular cells that produce mucus. It forms multiple folds that form the Lutkens-Martynov sphincter at the neck of the gallbladder, which prevents the release of bile before certain stages of digestion.


• The muscular layer, which is mainly composed of smooth muscle fibers located circularly (circular)


• The connective tissue sheath covers the outside of the gallbladder. It contains blood vessels.

Gallbladder Tasks

• Accumulation, concentration and storage of bile produced in the liver


• Excretion of bile into the lumen of the duodenum as needed

Bile is produced by liver cells continuously (from 0.6 to 1.5 liters per day). Then it enters the intrahepatic ducts, and from them into the gallbladder. In the gallbladder, bile is concentrated due to the absorption of excess water, sodium and chlorine from the cells of the epithelium of the mucous membrane.

The mechanism of excretion of bile from the gallbladder

The most important neurohumoral factors regulating this complex process are:

• The autonomic nervous system (sympathetic and parasympathetic divisions), which regulates the work of almost all internal organs

  Normally, when the vagus nerve (vagus) is activated, which provides the sensory and motor innervation of most internal organs, the gallbladder contracts, and the sphincter of Oddi relaxes. In case of violation of the coordination in the work of the sympathetic and parasympathetic divisions of the autonomic nervous system, this mechanism is disturbed.

• Intestinal hormones (motilin, cholecystokinin-pancreosimin, gastrin, secretin, glucagon), which are produced in the gastrointestinal tract during meals

  When exposed to cholecystokinin in normal doses, the gallbladder contracts, and the sphincter of Oddi relaxes (in large doses, gallbladder motility is inhibited). Gastrin, secretin, glucagon have the same effect as cholecystokinin, but less pronounced.

• Neuropeptides (neurotensin, vasointestinal polypeptide and others) are a type of protein molecule that has the properties of hormones

  They interfere with the contraction of the gallbladder.

  As a result of the close interaction of these factors during a meal, the muscle layer of the gallbladder contracts 1-2 times, increasing the pressure in it to 200-300 mm of water column. Therefore, the sphincter of Lutkens-Martynov relaxes, and bile enters the cystic duct. Further, bile enters the common bile duct, and then through the sphincter of Oddi - to 12 PCs. When diseases occur, this mechanism is disrupted.

The main functions of bile in digestion

• Creates the necessary conditions in 12 PCs for the loss of pepsin (the main enzyme of gastric juice) of its properties
• Participates in the breakdown of fats, promoting their absorption, as well as the assimilation of fat-soluble vitamins (A, E, D)
• Improves the motor function (motility) of the small intestine and increases appetite
• Stimulates the secretion of mucus and the production of intestinal hormones: motilin, cholecystokinin-pancreosemin and others
• Activates enzymes necessary for the digestion of proteins (trypsin and lipase - enzymes of pancreatic juice)
• Promotes the multiplication of epithelial cells of the intestinal mucosa
• Possesses antibacterial properties, which weaken with stagnation of bile

Causes of gallbladder dyskinesia

Distinguish between primary and secondary dyskinesia of the gallbladder and biliary tract (BDT), depending on the causes that led to the disease.

Also, a theory is currently being considered about a disruption in the work of liver cells, so they initially produce bile, the composition of which has already been changed.

Primary dyskinesia of the gallbladder and biliary tract

At the onset of the disease, there are only functional disorders that are not detected by research methods (ultrasound, X-ray). However, as the disease progresses, structural changes develop in the gallbladder and its ducts.

Most Common Causes of Primary VDD

Secondary dyskinesia of the gallbladder and biliary tract

It occurs against the background of already developed diseases or conditions. The changes are clearly visible with the applied research methods.

The most common causes of secondary DVP

Symptoms of gallbladder dyskinesia

Depends on the type of violation of the motor activity of the gallbladder and its ducts.

Types of JVP

• Hypotonic (hypomotor) dyskinesia develops with insufficient contractility of the gallbladder and its ducts. It occurs in patients with a predominance of the tone of the sympathetic nervous system (normally dominates during the day), which lowers the tone and motor activity of the gastrointestinal tract, as well as the gallbladder and its ducts. Most often people over 40 suffer from this form of the disease.
• Hypertensive (hypermotor) dyskinesia develops with increased contractility of the gallbladder and biliary tract. It occurs in people with a predominance of the parasympathetic nervous system (normally dominates at night), which enhances the motor function and tone of the gastrointestinal tract, as well as the gallbladder and its ducts. Most often, adolescents and young people suffer from this form of the disease.
• Hypotonic-hyperkinetic dyskinesia is a mixed variant of the course of the disease. The patient has symptoms of both hypotonic and hypertensive forms of dyskinesia in varying degrees of severity.

Signs of gallbladder dyskinesia

Symptom	Manifestations	Development mechanism
Hypotonic dyskinesia
Pain	Constant, prolonged, dull, bursting, aching. It is located in the right hypochondrium, but does not have a clear localization. As a rule, it gets worse during a meal or immediately after it.	The bottom of the gallbladder is stretched, which is caused by stagnation of bile due to insufficient production of cholecystokinin in the gastrointestinal tract.
Belching - involuntary release of gas from the stomach into the oral cavity with a characteristic sound, and sometimes a smell	It usually occurs after meals, but sometimes between meals.	The regulation of the gallbladder by the nervous system is impaired, so the patient makes more swallowing movements, swallowing air while eating. As a result, the pressure in the stomach rises. Therefore, the muscular wall of the stomach contracts, and the tone of the exit sphincter decreases - and air is expelled.
Nausea and / or vomiting (sometimes with an admixture of bile, if there is a reflux of bile from 12 PCs into the stomach)	More often occurs after eating and nutritional errors: eating fatty foods, fast food, overeating and others	Due to impaired motility, nerve receptors in the gastrointestinal tract are irritated, which send an impulse to the vomiting center (located in the brain). From it, impulses are sent back to the digestive tract and diaphragm, leading to a contraction of their muscles and the occurrence of reverse movements. Also, with bacterial and viral infections, helminthiases, the vomiting center is irritated by their waste products (toxins).
Bitterness in the mouth (most common in hypotonic dyskinesia)	Mostly in the morning, after eating or exercising.	Motility is impaired, and the sphincters of the gastrointestinal tract relax. As a result, antiperistaltic movements appear (food moves in the opposite direction). Therefore, bile from 12 PC enters the stomach, then into the esophagus, and then into the oral cavity.
Bloating (flatulence)	There is a feeling of fullness of the abdomen at the height of digestion, which is often accompanied by pain. After discharge of gases, the pain subsides.	Digestion is impaired due to insufficient bile. As a result, the processes of decay and fermentation in the lumen of the small intestine are intensified. Therefore, gases are emitted in large quantities.
Decreased appetite		Bile stagnates due to the poor contractility of the gallbladder. Therefore, it is not enough allocated in the lumen of 12 PCs.
Diarrhea (rare)	Typically occurs shortly after a meal.	With insufficient bile, digestion is disturbed: proteins, fats and carbohydrates are poorly broken down. As a result, the cells of the mucous membrane of the small intestine are irritated, which increase the excretion of water, sodium and chlorine. At the same time, their absorption is reduced. Therefore, the volume of the food bolus increases, and its movement through the intestines is accelerated.
Constipation (occurs frequently)	Stool is absent for more than 48 hours or there is a systematic inadequate bowel movement.	It occurs due to a slowdown in the movement of the food lump through the intestines due to spasm or relaxation of the tone of the intestinal wall. Therefore, the re-absorption of water is increased. In this case, the feces decrease in volume, and their density increases. In addition, there is a lack of bile acids (contained in bile), which normally have a stimulating effect on the intestinal muscles.
Obesity	Develops with a long course of the disease or is the cause of its occurrence	Due to insufficient bile, the process of digestion and the breakdown of fats is disrupted. Therefore, the production of insulin by the pancreas increases. As a result, the synthesis of fats and their accumulation in the fat cells of the subcutaneous fat, as well as on the internal organs, increase.
	Decrease in heart rate, lowering blood pressure, facial flushing, sweating, increased salivation.	The mechanism of development is complex and not fully understood. However, it is believed that there is a low resistance of the heart and blood vessels to stress. Therefore, during it, less oxygen is supplied to the brain, organs and tissues. As a result, the balance between the sympathetic and parasympathetic nervous systems is disturbed, and the internal organs receive the wrong commands to work.
Hypertensive dyskinesia
Pain	The pain is intense, colicky, arising acutely in the right hypochondrium after stress or emotional stress (most often), errors in nutrition, physical exertion. The pain lasts from 20 to 30 minutes, repeats several times during the day. Often she gives the right side to the back, shoulder blade or arm. However, sometimes the pain radiates to the left (to the region of the heart), simulating an attack of angina pectoris. In the period between attacks, as a rule, a feeling of heaviness in the right hypochondrium remains.	The pain is associated with a sharp contraction of the gallbladder with an increased tone of the sphincters of Oddi and Lutkens-Martynov, so bile does not leave.
Decreased appetite	Bile is a stimulant of appetite, intestinal motility and the production of intestinal hormones.	The gallbladder is in a spasmodic state and contracts unnecessarily. However, at the same time, the sphincters, which are responsible for the timely flow of bile into 12 PCs, do not work or relax between meals. Therefore, bile in insufficient or large quantities enters 12 PCs.
Decrease in body weight (develops often)	The subcutaneous fat layer becomes thinner, muscle mass decreases.	Due to the secretion of bile between meals, foods are poorly broken down. Therefore, proteins, carbohydrates, fats, vitamins and minerals are not absorbed in sufficient quantities. In addition, due to decreased appetite, patients do not eat enough.
Nausea and vomiting	Often they accompany the attack of biliary colic itself, and outside the attack they are usually absent.	Receptors of the gastrointestinal tract are irritated due to impaired motility, therefore nerve impulses are sent from them to the vomiting center (located in the brain). Back from it, impulses are sent to the receptors of the gastrointestinal tract and diaphragm, the intercostal muscles, so they contract, spewing out the gastric contents.
Diarrhea (common)	As a rule, it occurs shortly after a meal or during an attack.	Bile enters the lumen of the small intestine in large quantities between meals (asynchronously). As a result, bile acids in bile inhibit absorption, and also increase the secretion of water and salts (sodium, chlorine), causing an increase in the volume of feces and accelerating their movement through the intestines.
Symptoms of a disorder in the functioning of the autonomic nervous system (the center is in the brain)	During an attack, sweating, heart palpitations, general weakness, headache appear, and blood pressure rises. Outside the attack, irritability, fatigue, sleep disturbances, increased blood pressure, aching pain in the heart, palpitations and other symptoms are noted.	The development mechanisms have not been fully established. It is assumed that the disease is based on the lability of the nervous system due to the weakness of the heart and blood vessels, which at the time of stress poorly supply organs, tissues and the brain with blood. Therefore, the autonomic nervous system gives the wrong commands to the vessels, gastrointestinal tract, internal organs, as well as the gallbladder and its ducts.
Signs that can develop with both forms of DVP with the same manifestations
Yellowness of the skin and visible mucous membranes (rarely develops)	It appears with a pronounced violation of the outflow of bile (stone, narrowing of the common bile duct). In this case, the feces are colorless, and the urine is colored dark.	With stagnation of bile, bilirubin (a pigment contained in bile) is absorbed into the bloodstream and spreads throughout the body, settling in the skin and mucous membranes, giving them an icteric hue. Since bile does not enter the digestive tract, the feces become colorless.
Plaque on the tongue (can develop with other diseases: colitis, gastritis and others)	It can be white or with a yellowish tinge with reverse bile flow (most often occurs with hypotonic dyskinesia). If the plaque is pronounced, then the patients may experience a feeling of discomfort on the tongue and dullness of taste.	It appears as a result of a violation of the processes of keratinization (transformation of mucosal cells into scales) and desquamation of the epithelium from the surface of the tongue. It occurs due to a violation of the transfer of nutrients to the tongue.

Diagnostics of the dyskinesia of the gallbladder and biliary tract

The objectives are to determine the type of biliary dyskinesia and to identify concomitant diseases that may support their dysfunction.

Ultrasound examination (ultrasound)

Allows you to determine the shape and presence of congenital malformations of the gallbladder, as well as the degree of its emptying.

Basic X-ray examinations

They are the leading methods in the diagnosis of diseases of the gallbladder and biliary tract.

1. Cholecystography

   Based on the ingestion of preparations containing iodine (Biliselectan, Holevid, Iodobil and others).

   Indications

   • Study of the structure and identification of the presence of stones in the gallbladder
   • Study of the excretory and accumulative (concentration) functions of the gallbladder, as well as its extensibility.
   Flaw

   The inability to determine the state of the biliary tract, since they are not visible on the images.

   Methodology

   The patient on the eve of the study at 19.00 takes two raw eggs. Starting at 21.00, he takes a contrast agent at intervals of 30 minutes with water. The contrast agent is absorbed into the bloodstream in the intestines, and then secreted by the liver cells.

   In the morning on an empty stomach, several survey images of the right side of the abdomen are made. Then the patient is offered a choleretic breakfast (as a rule, this is the yolk of an egg) and a series of images is taken again.

   Interpretation of results

   In hypertensive form, the gallbladder sharply and rapidly contracts from the original volume: by 75% in the first 5-15 minutes, by 90% in the next 1.5-2 hours. Then for a long time it is in this state, not emptying due to the fact that there is a spasm of the sphincter of Oddi.

   With a hypotonic form, the gallbladder is enlarged, and its contraction after a choleretic breakfast is very slow from the initial volume: by 20-30% within 15 minutes and remains so for three to four hours.



2. Infusion cholecystography

   The method is based on the intravenous administration of a contrast agent containing iodine, which accumulates in the gallbladder and its ducts.

   Indications

   Determination of the tone of the sphincter of Oddi.

   Methodology

   A patient in the morning on an empty stomach in the X-ray room on the table is injected intravenously with a Bilignost solution for 15-20 minutes. And at the same time, a solution of morphine is injected to artificially reduce the sphincter of Oddi. After 15-20 minutes, a picture is taken, which shows the gallbladder and its extrahepatic ducts. Normally, the width of the common bile duct is 3-7 mm.

   Interpretation of results

   In case of insufficiency of the sphincter of Oddi, the contrast agent enters 12 PCs at 15-20 minutes after administration with the width of the common bile duct 9 mm or more.



3. Cholangiography

   It is carried out to study the bile ducts after the introduction of a contrast agent into them.

   Indications

   • Suspected severe narrowing of the bile duct
   • Jaundice of the skin and mucous membranes caused by blockage of the bile duct by a stone or compression of it by a tumor
   • Severe and prolonged pain syndrome
   Basic techniques for diagnosing dyskinesia
   
   
   If necessary, during the procedure, small stones are removed from the lumen of the common bile duct, and a tube is installed into it to facilitate the outflow of bile.
4. Duodenal intubation

   Purpose - the study of bile, as well as the function of the gallbladder and its ducts,

   On an empty stomach, a probe is inserted into 12 PCs through the oral cavity and stomach. Then it is laid on the right side and bile is obtained in portions:

   • The first phase ("A" portion) is a mixture of pancreatic juice and 12 PCs. It is collected from the moment the probe is inserted to the introduction of the stimulant (magnesium sulfate solution). Normally, 15-20 ml of a golden-yellow secret is obtained in 10-20 minutes.
   • The second phase is the period of time from the moment the stimulant (choleretic) is introduced until the next portion of bile appears (the phase of the closed sphincter of Oddi). Normally, the duration is from 3 to 6 minutes.
   • The third phase is getting the contents of the cystic duct. Normally, about 3-5 ml of secretion is obtained in 3-5 minutes.
   • The fourth phase (portion "B") - getting the contents of the gallbladder. Bile is thick, dark brown in color. Normally, from 30 to 50 ml of bile is released in 15-25 minutes.
   • The fifth phase (portion "C") is hepatic, during which a light yellow liquid bile is obtained from the intrahepatic bile ducts.
   Interpretation of results

   Treatment of diseases that lead to the development of dyskinesia is carried out:

   • Helminthic invasion (eg, giardiasis or opisthorchiasis)
   • Peptic ulcer (using two or three component schemes)
   • Fighting infection (prescribing antibiotics)
   • Removal of stones from the gallbladder and treatment of other ailments
   Outside the period of exacerbations:
   • Mineral waters are used: in case of hypertonic variant - waters of low mineralization (Slavyanovskaya, Narzan, Essentuki 2 or 4), with hypotonic - waters of high mineralization (Arzani, Essentuki 17).
   
   
   • It is recommended to stay in a sanatorium with a bias for the treatment of diseases of the digestive system.

   Diet for gallbladder dyskinesia

   Compliance with a diet is the basis for success in treating the disease, it is prescribed for a long time (from 3-4 months to a year).

   Target- sparing the liver, biliary tract and gastrointestinal tract, as well as normalizing their function.

   During an exacerbation of the disease with any type of dyskinesia, the following are excluded:

   • Fatty meats (goose, duck) and fish (sardine, sturgeon, halibut)
   • Smoked, fried, fatty, salty, sour and spicy foods
   • Alcohol, rich broths, spices, onions, garlic, radishes, sorrel
   • Confectionery with cream, muffins, chocolate, carbonated drinks, cocoa, black coffee
   • Foods that increase gas formation: peas, beans, rye bread
   • Cream, whole milk
   • Canned foods and marinades
   It is recommended to eat fractionally (5-6 times a day) and in small portions.

   Culinary processing:

   • Products are boiled, baked or steamed: meatballs, steam cutlets, and so on.
   
   
   • In the first days of an exacerbation, it is recommended to eat foods in a liquid, mashed or minced form. As the acute symptoms disappear, this is not required.
   Features of the diet for hypomotor dyskinesia

   Allowed for consumption

   • Yesterday's bread made from rye or wheat flour of the second grade
   • Lactic acid products no more than 6% fat: sour cream, cottage cheese, kefir
   • Low-fat meats (beef) and fish (hake, pollock, pike perch), poultry (chicken)
   • Vegetables in any form
   • No more than one yolk per day
   • Boiled low-fat sausages and sausages
   • Vegetable fats and butter
   • Honey, sugar, caramel, marmalade, candy
   • Fruit and vegetable juices, as well as fruits and berries of non-acidic varieties (apples, apricots and others)
   • Tea, coffee with milk
   • Any cereals and pasta
   • Vegetable broth soups
   Features of the diet for hypermathic dyskinesia

   The same foods are allowed to be consumed as in hypomotor dyskinesia, but the following are excluded:

   • Sausages and sausages (even boiled)
   • Sugar, caramel
   • Pork, veal
   • Egg yolk
   • Fresh berries, vegetables and fruits

   Traditional methods of treating dyskinesia

   A good addition to the main treatment with medicines, especially after reducing the acute symptoms of the disease.
   
   

   Infusions and decoctions	How to cook and take	What effect to expect
   Hypotonic dyskinesia
   A decoction of immortelle flowers	3 tbsp Pour flowers into an enamel bowl, pour a glass of boiling water. Then heat in a water bath for 30 minutes, stirring constantly. Remove from heat, let cool, then drain. Take half a glass 20-30 minutes before meals. The course is 2-3 weeks.	Strengthens the contraction of the gallbladder and improves the flow of bile Normalizes the composition of bile Improves the digestive tract Disinfects locally
   Infusion of corn silk	1 tsp Pour the chopped raw materials with a glass of boiling water and let it brew for 30 minutes. Then strain and take 3 tbsp. l. three times a day half an hour before meals. The course is 2-3 weeks.	Liquefy bile and eliminate its stagnation Lowers blood bilirubin and cholesterol levels
   Oregano herb infusion	Pour in 2 tablespoons. crushed raw materials 200 ml of boiling water. Express after 20-30 minutes. Take the entire infusion throughout the day in three doses 30 minutes before meals. The course is 1 month or more.	Strengthens the motor activity of the intestines and biliary tract Has a local anti-inflammatory and choleretic effect Normalizes the work of the nervous system
   Hypertensive dyskinesia
   Peppermint infusion	2 tsp peppermint and pour 200 ml of boiling water. Let it brew for 30 minutes, then decant. Take 1/3 cup 20 minutes before meals, twice daily. The course is 3-4 weeks.	Reduces pain and nausea Relaxes the muscles of the bile ducts and sphincters, facilitating the outflow of bile Improves Digestion and Appetite Has a local anti-inflammatory effect
   Licorice root decoction	2 tsp Pour 200 ml of boiling water over the crushed raw materials, place in a water bath for 20 minutes. Let it cool, then strain and bring to the original volume with boiled water. Take 1/3 cup 30 minutes before meals three times a day. The course is 2-3 weeks.	Relaxes the smooth muscles of the gallbladder and its ducts
   For both types of dyskinesia
   Decoction or tea from chamomile flowers	1 tsp pour 200 ml of boiling water over dry chamomile flowers. Express after 3-5 minutes. Drink for a long time three times a day, like tea.	Reduces bloating Improves the digestive tract Helps reduce or eliminate belching Normalizes the work of the nervous system, helps fight insomnia Accelerates the healing of wounds on the mucous membranes (ulcers, erosions) Fights locally against pathogenic microbes Increases appetite