Interpretation of clinical stool examination. Stool examination
Blood in stool detected by methods based on the pseudoperoxidase action of hemoglobin. Hemoglobin takes hydrogen from some organic compounds (benzidine, amidopyrine, guaiac gum, orthotoluidine, etc.) and transfers it to hydrogen peroxide, thereby forming coloring compounds.
Benzidine test (Gregersen). To prepare Gregersen's reagent, take basic benzidine on the tip of a knife and dissolve it in 5 ml of a 50% acetic acid solution, add an equal amount of a 3% hydrogen peroxide solution or a 10-fold diluted solution of concentrated hydrogen peroxide (perhydrol).
Undiluted feces are applied in a thick layer to a glass slide, placed in a Petri dish lying on a white background, a few drops of Gregersen's reagent are added and mixed thoroughly. If the reaction is positive, after 1-2 minutes the smear turns green or blue-green. Staining that occurs at a later date is not taken into account.
Instead of hydrogen peroxide, you can use barium peroxide: 0.25 g of basic benzidine and 0.1 g of barium peroxide are dissolved in 5 ml of a 50% acetic acid solution. The reagent is prepared immediately before use. With this technique, the sample is more sensitive.
Test with guaiac resin (Weber van Leen). Compared to the benzidine test, this test is much less sensitive - it detects the presence of less than 5% blood in the stool. Minor bleeding cannot be diagnosed using this test. The test with amidopyrine is more sensitive compared to guaiac.
Express method. The reagents used are orthotolidine (1 part by weight), barium peroxide (1 part by weight), tartaric acid (1 part by weight), calcium carbonate (20 parts by weight). The mixture of reagents is thoroughly ground in a mortar, after which it is tableted or consumed in powder form.
To conduct the study, approximately 0.3 g of powder (at the tip of a knife) is placed on white filter paper and moistened with 2-3 drops of feces diluted with water. In the presence of blood, the powder turns blue after 2 minutes, and a bright blue halo appears around it.
Sample sensitivity: 3-5 red blood cells per field of view (4000-4500 red blood cells per 1 ml).
When detecting hidden blood in stool, it is necessary that the glassware and reagents be chemically clean. For three days before the study, the patient is prescribed a diet that excludes meat, fish, eggs, tomatoes, foods containing chlorophyll, etc. Taking medications containing iron, copper and other heavy metals is prohibited.
Stercobilin. Part of the urobilinogen produced in the intestines is excreted in the feces and is called stercobilinogen. Under the influence of light and atmospheric oxygen, stercobilinogen spontaneously turns into stercobilin. Stercobilin is a stool pigment that gives it a certain color. In the absence of stercobilin in feces, it becomes discolored (clay color).
Reactions to stercobilin are carried out when uncolored stool appears in the patient.
Reaction with mercuric chloride (Schmidt). Sublimate (7 g) is dissolved in 100 ml of distilled water while heating. After cooling, the solution is passed through a paper filter. A small amount of feces is ground in a mortar with 3-4 ml of reagent to the consistency of a liquid slurry, poured into a Petri dish and left for 18-20 hours. In the presence of stercobilin, the feces acquire a pink color, the intensity of the color depends on the pigment content. If there is unchanged bilirubin in the stool, its color may be green due to the formation of biliverdin.
To detect stercobilin, you can also use reaction with zinc acetate. Quantitative determination of stercobilin is carried out using a spectroscope.
The normal content of stercobilin in the daily amount of feces is 2-6 g/l (200-600 mg%).
Determination of stercobilin in the daily amount of feces is important for differentiating parenchymal, mechanical and hemolytic jaundice. With parenchymal jaundice, the content of stercobilin in the feces is reduced, with hemolytic jaundice it is increased, with mechanical jaundice, stercobilin may be completely absent.
The feces are ground with water in a ratio of 1:20 and Fouche's reagent is added dropwise (but not more than the volume of diluted feces). When bilirubin is present, a green or blue color appears.
The reaction with mercuric chloride also reveals the content of bilirubin in feces, but it is less sensitive.
Normally, bilirubin entering the colon with bile is completely reduced to stercobilinogen and stercobilin under the influence of bacterial flora. Therefore, when standing in the air, the feces darken. Unchanged bilirubin appears in the feces with increased peristalsis and, consequently, accelerated evacuation of chyme from the intestines, due to which it does not have time to fully recover. Bilirubin is also found in stool after ingestion of antibiotics and sulfa drugs that suppress the activity of intestinal flora. In infants, unchanged bilirubin is a normal part of stool.
Protein and mucin in feces is determined using Triboulet-Vishnyakov tests. The method is based on the clarification of the liquid as a result of the adsorption of stool particles by coagulated protein or mucin. The reagents used are a saturated solution of mercury dichloride or a 20% solution of trichloroacetic acid, a 20% solution of acetic acid and distilled water.
A lump of feces (1.5 g) is ground in a mortar with a small amount of distilled water, after which water is added to a volume of 50 ml (3% emulsion). If the stool is thin or watery, dilute it in half. The diluted feces are poured approximately equally into three test tubes (15 or 7.5 ml each). To the first of them add 2 ml of a saturated solution of mercury dichloride or 2 ml of a 20% solution of trichloroacetic acid; in the second - 2 ml of 20% acetic acid solution; in the third, control, - 2 ml of distilled water. The tubes are shaken and left at room temperature for 18-24 hours, and then the results are taken into account. With complete clearing of the liquid above the sediment, the reaction is considered strongly positive (+++), with significant clearing - positive (++), with slight clearing - weakly positive (+), with turbidity the same as the control tube - negative (-).
Clearing in the first tube indicates the presence of serum protein, in the second - the presence of mucus (mucin).
Normally, food nucleoproteins are not excreted in feces. If accelerated evacuation of intestinal contents is excluded, protein bodies found in feces are most likely of tissue origin. They indicate the presence of inflammatory and ulcerative processes associated with the destruction of cells of the intestinal wall and exudation of tissue fluid. In diseases of the intestines, this reaction is given particular importance, and a positive reaction is more valuable diagnostically. A negative reaction can also be observed in the presence of an inflammatory process, if stool remains in the colon for a long time, which promotes bacterial breakdown of protein.
Clinical stool analysis (coprogram)- this is one of the important research methods used to diagnose diseases or changes in the digestive organs and reflect the results of treatment of these diseases. During a general clinical examination of stool, its physical and chemical properties are determined, and a microscopic examination is also performed. The analysis includes macroscopic, microscopic and simple chemical studies. Microbiological examination of stool is carried out if an infectious intestinal disease is suspected.
Feces are the contents of the large intestine that are released during bowel movements. In a healthy person, feces contain 75-80% water and 20-25% solid residue. The dense part consists of 1/3 of the remains of ingested food, 1/3 of the remains of the gastrointestinal tract, 1/3 of microbes, about 30% of which are dead.
In most cases, stool analysis is carried out without special preparation of the patient, however, it is recommended 2-3 days before the test to avoid taking medications that change the nature of stool and cause functional disorders of the gastrointestinal tract (iron, bismuth, laxatives).
A decrease in the amount of feces is observed with constipation.
An increase in the amount of feces occurs when:
- gallbladder diseases;
- inflammatory diseases of the small intestine (insufficient digestion, fermentative and putrefactive dyspepsia);
- colitis;
- insufficient pancreatic function (PG).
Shape and consistency feces depend mainly on the water content. Feces normally have a cylindrical shape and a uniform, dense consistency. With constant constipation, due to excessive absorption of water, the feces become very dense and may look like small balls (“sheep feces”). With increased peristalsis (due to insufficient absorption of water) or with abundant secretion of inflammatory exudate and mucus by the intestinal wall, stool becomes unformed, mushy or liquid. Liquid stool contains 90-92% water and occurs when:
- insufficient digestion in the small intestine (accelerated evacuation, putrefactive dyspepsia);
- with nonspecific ulcerative colitis.
Sometimes unformed feces have a pronounced mare-like consistency due to the presence of a large amount of fat in it with impaired pancreatic secretion and changes in bile secretion. Pasty feces also appear in colitis with diarrhea due to increased intestinal motility. Foamy stool occurs in patients with fermentative dyspepsia.
Color The stool of a healthy person has different shades of brown, depending on the presence of stercobilin in the stool. In addition, the color of stool can be influenced by the nature of the food, the intake of medications, and the presence of pathological impurities. With a predominantly dairy diet, the stool is light brown, sometimes yellow; with a meat diet, it is dark brown; with a plant diet, it can be greenish, reddish, or dark. Medicinal substances can also change the color of stool.
The color of stool also changes with diseases of the digestive system (table). With significant bleeding in the upper gastrointestinal tract, the color of the stool is black, tarry (melena), with bleeding from the lower sections, ulcerative colitis - red. When the flow of bile into the intestines stops, the feces become discolored, becoming grayish-white, clayey (“acholic feces”). Stool with pancreatic insufficiency is light yellow in color. Yellow color - with insufficient digestion in the small intestine and fermentative dyspepsia. Light brown - with accelerated evacuation from the large intestine. Dark brown color of feces - with insufficient digestion in the stomach, putrefactive dyspepsia, ulcerative colitis, constipation, increased secretory function of the intestines. In cases of fatty stool, its color is often gray. With typhoid fever, stool takes on the characteristic appearance of “pea soup”; with cholera, it takes on the characteristic appearance of “rice water.”
Change in color of excrement depending on different conditions
| Color | When observed |
| Dark brown | Normal feces on a mixed diet |
| Black-brown | Meat diet |
| Light brown | Plant based diet |
| Brown-red | Unaltered blood |
| Black | Changed blood (bleeding from the upper gastrointestinal tract), when taking bismuth |
| Greenish black | When taking iron supplements |
| Green | With the content of bilirubin and biliverdin under conditions of enhanced peristalsis, with a purely vegetable diet |
| Greenish yellow | During carbohydrate fermentation |
| Golden yellow | With the content of unchanged bilirubin (in infants) |
| Orange-light yellow | Dairy diet |
| White or grayish white | When the flow of bile into the intestines stops |
Smell Stool is normally unpleasant, but not harsh. It depends on the presence of a number of aromatic substances - indole, skatole, phenol, etc., formed as a result of the bacterial breakdown of food residues, mainly protein. With a predominance of meat products in food, the smell of feces intensifies; with a plant and dairy diet, it becomes weaker. With constipation, stool is almost odorless; with diarrhea, the smell is more pungent. Feces have a particularly pungent putrid odor when there is insufficient digestion in the stomach, putrefactive dyspepsia, colitis with constipation, and intestinal movement disorders. A foul odor occurs when the secretion of the pancreas is impaired, there is no flow of bile into the intestines, or its increased secretory function. With fermentative dyspepsia, stool acquires a sour odor. Weak odor - with insufficient digestion, constipation, accelerated evacuation from the small intestine.
Undigested leftovers Normally, food is not macroscopically detected in feces. Food entering the body is almost completely digested by gastrointestinal enzymes, its remains are present in the feces in the form of an undifferentiated fine-grained mass. Severe insufficiency of gastric and pancreatic digestion is accompanied by the release of lumps of undigested food. The presence of undigested meat residues in the stool is called creatorrhoea. A significant amount of fat in the stool is called steatorrhea. In this case, the surface of the stool has a slightly matte sheen and an ointment-like consistency.
Impurities of non-food origin. Mucus is normally contained in small quantities. Mucus, found in the form of strands, flakes, dense formations (often together with blood), indicates inflammation of the intestinal mucosa, appears with ulcerative colitis, fermentative and putrefactive dyspepsia, increased secretory function of the large intestine.
Blood is also a pathological impurity. Its presence is associated with a violation of the integrity of the gastrointestinal mucosa; it appears in ulcerative colitis, dysentery, hemorrhoids, polyps and rectal fissure. Minor bleeding from the upper gastrointestinal tract is not detected macroscopically.
Pus is found in ulcerative processes mainly in the lower intestines.
Stones of origin can be bile, pancreatic and intestinal (coprolites). Gallstones can be cholesterol, calcareous, bilirubin or mixed. They are discovered after an attack of biliary colic, sometimes after a few days or without previous colic. Pancreatic stones are small in size (about the size of a pea), have an uneven surface and consist mainly of lime carbonate or phosphate. Coprolites are dark brown in color, they are divided into false, formed from feces compacted in the area of the kinks of the large intestine, and true, consisting of an organic core and layered mineral salts (phosphates, poorly soluble drugs, undigested food residues).
The objective of this study is to determine the reaction of feces, “occult blood”, stercobilin, bilirubin, soluble protein, total nitrogen, the amount of fatty products, organic acids, ammonia, enzymes, etc.
Fecal reaction Normal pH is 6.0-8.0. Depends mainly on the vital activity of the intestinal microbial flora: the predominance of fermentation processes shifts the reaction to the acidic side, and the intensification of rotting processes - to the alkaline side. A slightly alkaline stool reaction is determined by insufficient digestion in the small intestine, alkaline - by insufficient digestion in the stomach, impaired gastric secretion, insufficient pancreatic function, colitis with constipation, ulcerative colitis, increased secretory function of the large intestine, constipation. With protein foods, the reaction becomes alkaline due to increased proteolytic putrefactive flora; with carbohydrate foods, the reaction becomes acidic (due to the activation of fermentative - iodophilic flora).
Bile pigments. The study aims to determine the presence (absence) of stercobilin or unchanged bilirubin in the stool. An increase in the amount of stercobilin is observed in hemolytic jaundice, a decrease in the excretion of stercobilin is characteristic of parenchymal jaundice (acute and chronic hepatitis, cirrhosis of the liver), cholangitis. The absence of stercobilin in feces (acholic feces) is characteristic of obstructive jaundice, but transient acholia is observed in severe hepatitis and cirrhosis of the liver.
In the differential diagnosis of jaundice, the determination of fecal stercobilin over time and the ratio of bilirubin reduction products in feces and urine are important. The ratio of daily fecal stercobilin / daily amount of urobilin bodies in urine is normally 10:1 - 20:1, with parenchymal jaundice it decreases to 1:1 due to a decrease in stercobilin excretion and an increase in urobilinuria, and with hemolytic jaundice it sharply increases to 300:1 - 500 :1 due to an increase in stercobilin excretion, outstripping the rate of increase in urobilinuria.
Bilirubin appears with increased peristalsis and accelerated evacuation from the intestines, long-term use of antibiotics and sulfonamides (due to suppression of intestinal microflora).
Soluble protein determined by putrefactive dyspepsia, ulcerative colitis, increased secretory function of the large intestine, bleeding, inflammatory processes.
Blood in stool. Normally, healthy people do not find blood in their stool. Hidden blood is blood that does not change the color of stool and is not detectable macroscopically or microscopically. Determination of blood in stool is important for identifying ulcerations and tumor processes in the gastrointestinal tract, especially if they are accompanied by minor bleeding that does not change the color of stool (so-called hidden bleeding). A positive stool reaction to occult blood can be determined by:
- peptic ulcer of the stomach and duodenum (DPC);
- tumors of the esophagus, stomach, intestines;
- intestinal tuberculosis;
- nonspecific ulcerative colitis;
- helminthic infestation;
- varicose veins of the esophagus with portal hypertension syndrome;
- hemorrhagic diathesis;
- typhoid fever.
Preparing a patient for a benzidine test
For 3 days, the patient is prescribed a diet that excludes meat, liver, blood sausage and all foods containing iron (green plants, apples, bell peppers, spinach, white beans, cucumbers, etc.), i.e. foods that have catalytic properties. Serial testing for occult blood is recommended.
Food grade elements.
Muscle fibers in the feces of a healthy person on a normal diet, they are rare or not detected. The detection of muscle fibers in large quantities indicates insufficient digestion of meat foods, impaired pancreatic secretion, and impaired absorption in the intestines. The presence of muscle fibers in feces is accompanied by a picture of putrefactive dyspepsia.
Connective tissue fibers are not normally detected. They are detected by poor chewing of food, consumption of undercooked meat, as well as gastrogenic dyspepsia and insufficient pancreatic function.
Fat and its breakdown products. Normally, fat supplied with food in moderate amounts is absorbed almost completely (90-95%), so a small amount of soap may be found in feces with an almost complete absence of neutral fat. The detection of a significant amount of neutral fat and its breakdown products indicates a violation of the digestion and absorption of fat. Neutral fat is found in case of insufficient pancreatic function, fatty acids - in the absence of bile supply, insufficient digestion in the small intestine, accelerated evacuation from the small intestine, fermentative dyspepsia, insufficient secretion of the pancreas, accelerated evacuation from the large intestine.
Soap noted in feces in large quantities under the same conditions, but mainly with constipation.
Plant fiber and starch. There are 2 types of fiber: digestible and indigestible. Indigestible fiber is not broken down in the intestines and is excreted in the same amount. It mainly includes supporting fiber (the skin of vegetables, fruits, vessels and plant hairs).
Digestible fiber is the pulpy parenchymal cells of vegetables and fruits and consists of round cells with a thin shell and a cellular structure. Digestible fiber is detected in insufficient gastric digestion, putrefactive dyspepsia, lack of bile intake, insufficient digestion in the small intestine, accelerated evacuation from the large intestine, fermentative dyspepsia, impaired pancreatic secretion, ulcerative colitis.
Starch grains are not normally detected. The presence of starch in feces (amilorrhea) indicates insufficiency of digestion in the stomach and small intestine, fermentative dyspepsia, impaired pancreatic secretion, and accelerated evacuation from the large intestine.
Cellular elements in mucus. Cellular elements (intestinal epithelium, blood cells, macrophages, tumor cells) are found in feces containing mucus. Mucus takes the form of strands of varying sizes, consisting of a grayish structureless substance containing columnar epithelial cells, bacteria, and sometimes blood cells or food debris. Mucus is detected in colitis with constipation, with ulcerations, fermentative and putrefactive dyspepsia, increased secretory function of the large intestine.
The appearance of cylindrical epithelial (intestinal) cells in large groups and layers indicates inflammation of the mucous membrane of the large intestine.
Leukocytes are detected during ulcerative processes in the colon, paraintestinal abscess. White blood cells in the mucus coming from the small intestine have time to break down.
With amoebic dysentery and ulcerative colitis, a large number of eosinophils are found in the stool.
Unchanged red blood cells are found in feces during bleeding from the large intestine (ulcerative processes), dysentery, hemorrhoids, polyps and rectal fissures. If blood is released from higher lying parts of the intestine, then the red blood cells are either completely destroyed or take on the character of shadows.
Macrophages are found in some inflammatory processes, especially in dysentery (bacillary).
Cells of malignant tumors can enter the stool when the tumor is located in the rectum.
Crystal formations found in putrefactive dyspepsia in feces with a sharply alkaline reaction. Calcium oxalate crystals are found in feces when the acidity of gastric juice decreases. Charcot-Leyden crystals are often found in mucus in combination with eosinophils, this indicates allergic inflammation of the intestines, amoebiasis, balantidiasis, and helminthic infestation. Hemosiderin crystals are often detected after intestinal bleeding, with ulcerative colitis.
Bacteria and fungi are found in large quantities in the intestines and perform a number of important functions: vitamin-forming, protective, digestive due to the content of various enzymes. Activation of any one group in the intestine (putrefactive, fermentative or pathogenic) leads to a change in the normal ratio of microflora - dysbiosis. Dysbacteriosis complicates the course of most gastrointestinal diseases (chronic enteritis, chronic colitis, Achilles gastritis, chronic pancreatitis). Drug dysbacteriosis (fungal, staphylococcal, Pseudomonas aeruginosa, Proteus), which develops during treatment with antibacterial drugs, is often severe and, if diagnosed untimely, often leads to sepsis and shock with a fatal outcome. The diagnosis of dysbacteriosis is made on the basis of bacteriological examination of stool.
Microscopically, the intestinal flora is not differentiated even in stained preparations. Bacterioscopically it is possible to differentiate iodophilic flora and tuberculosis bacillus. Iodophilic flora is found in stool preparations with insufficient digestion in the small intestine, accelerated evacuation from the large intestine, fermentative dyspepsia, and impaired pancreatic secretion.
Of the fungal flora, the most important is the detection of Candida type fungi, which appear in the stool and multiply when the normal intestinal microflora is suppressed (for example, with prolonged treatment with antibiotics).
With normal human nutrition, the nature of feces depends on a number of important factors:
- enzymatic breakdown of foods at various stages of digestion;
- absorption of food digestion products in the intestines;
- condition of the colon (its motor function and mucous membrane);
- vital activity of intestinal flora.
Violation of any of these factors leads to a change in digestive function in one or another part of the gastrointestinal tract, which is accompanied by the characteristic properties of feces, called scatological syndromes.
Feces during normal digestion.
The color is brown, the reaction is slightly alkaline or neutral, the consistency is soft, the shape is cylindrical. Microscopically: indigestible plant fiber - a moderate amount, altered muscle fibers - single, soap - a little.
Feces due to insufficiency of gastric digestion.
The color is dark brown, the reaction is alkaline, the consistency is dense or mushy, the feces are formed or unformed depending on the consistency. Microscopically: a lot of indigestible fiber (in layers), starch, unchanged muscle fibers, scraps of connective tissue soap - a moderate amount, iodophilic flora - a little.
Feces with pancreatic insufficiency.
Quantity up to 1 kg, color - grayish-yellow, alkaline reaction, ointment-like consistency. Microscopically: digestible and indigestible fiber - moderate amount, starch, unchanged muscle fibers (creatorrhoea), neutral fat - a lot (stetorrhoea), iodophilic flora - a little.
Feces in the absence of bile flow.
The amount is greater than normal, the color is grayish-white, the reaction is sour, the consistency is solid (greasy). The reaction to stercobilin is negative. Microscopically: digestible fiber and starch - a little, modified muscle fibers - a little, neutral fat - a little, fatty acids - a large amount.
Feces due to insufficient digestion in the small intestine (accelerated evacuation or inflammation).
The color is yellow, the reaction is alkaline, the consistency is liquid or semi-liquid, the reaction to bilirubin is positive. Microscopically: digestible fiber and starch - a lot, modified and unchanged muscle fibers - a moderate amount, neutral fat, fatty acids and soaps - a moderate amount, iodophilic flora - a little.
Feces due to insufficient digestion in the large intestine:
- fermentative dyspepsia. The color is yellow or light brown, the reaction is sharply acidic, the consistency is mushy, foamy, there is a little mucus. Microscopically: digestible fiber and starch - a lot, muscle fibers - a little, soap - a little, iodophilic flora - a lot;
- putrefactive dyspepsia. The color is dark brown, the reaction is alkaline, the consistency is liquid, there is a little mucus. Microscopically: digestible fiber, starch, modified muscle fibers, a little soap.
Feces during the inflammatory process in the large intestine:
- colitis with constipation - the color is dark brown, the reaction is alkaline, the consistency is solid in the form of “sheep feces”. Microscopically: mucus - a moderate amount, altered muscle fibers, soap - a little;
- colitis with diarrhea (see “digestive insufficiency in the large intestine”);
- dysentery, ulcerative colitis and other lesions of the large intestine. Feces contain an admixture of blood, mucus, and pus. Microscopically: in the mucus there are leukocytes, erythrocytes, and cylindrical epithelium in varying quantities.
Detection of intestinal protozoa |
Normally, protozoa are not found in the stool of a healthy person. In the human body, protozoa are found in the form of a vegetative form - active, mobile, vital, easily susceptible to the influence of the external environment (for example, cooling) and therefore quickly dying after being excreted from the intestine, and in the form of cysts resistant to external influences. In formalized feces, protozoa are mainly found in encysted form. Encystment is the characteristic ability of protozoa to become rounded and covered with a dense shell, turning into a cyst. The cyst is much more resistant to adverse environmental conditions than the vegetative form. Under favorable conditions, the protozoa emerge from the cyst and begin to reproduce.
Most intestinal protozoa are non-pathogenic, but some can cause disease (amoebiasis, giardiasis, etc.).
To identify protozoa, freshly excreted feces are examined (no later than 15-20 minutes after defecation), since vegetative forms quickly die in the external environment. Cysts in feces last longer, so they can be detected 3-6 hours after defecation.
Research for helminthiasis.
Normally, worm eggs are not found in a healthy person.
- cestodes - unarmed and armed tapeworm, wide tapeworm, small tapeworm;
- trematodes - liver fluke, cat fluke, schistosomes;
- nematodes - roundworms, whipworm, tominx, necator, hookworm.
Geohelminths develop without changing hosts. Their eggs or larvae mature to the invasive stage (capable of causing infection) in the external environment, mainly in the soil. Geohelminths include roundworms, whipworms, and hookworms. Eggs or larvae of geohelminths that mature in the external environment enter the body of the final host through the mouth, some actively penetrate the skin.
Biohelminths develop with a change of hosts: along with the definitive host, they have an intermediate host, in whose body the larval form develops, and some of them also have an additional host to complete the development of the larvae. The larvae enter the body of the definitive host in different ways, but most often this occurs through consumption of cattle meat (intermediate host), as well as through an accidentally infected intermediate host (rat tapeworm).
The effect of helminths on the human body is varied. Helminths sensitize the host's body and cause allergic reactions, having a toxic effect on the liver, central nervous system and other organs; mechanically damage tissues and blood vessels. They can cause toxic and toxic-allergic effects (roundworms, trichinella), and have a mechanical effect, injuring the intestinal wall. Some helminths (hookworms) can cause bleeding and lead to anemia, and also facilitate the penetration of pathogenic microorganisms from the intestines into the blood. Roundworms can close the lumen of the intestine and excretory ducts of the liver and pancreas. Also, all helminths use nutrients from the host’s intestines, which leads to metabolic disorders and vitamin deficiency (for example, with infestation by the broad tapeworm).
The diagnosis of helminthiasis is made on the basis of positive laboratory tests of feces, scrapings from the perianal folds, as well as urine, sputum, duodenal contents, muscle tissue - for Trichinella larvae, blood - for microfilariae, skin sections - to identify cysticerci. In some cases, ophthalmoscopy is used for diagnosis.
FECAL EXAMINATION
Feces are the final product formed as a result of complex biochemical processes and absorption of the final products of digestion in the intestine. Stool analysis is an important diagnostic area that allows making a diagnosis, monitoring the development of the disease and treatment, and initially identifying pathological processes. Examination of the intestinal region is necessary when examining patients suffering from diseases of the digestive system; it allows one to judge some pathological processes in the digestive organs and, to a certain extent, makes it possible to assess the state of enzymatic function.
RULES FOR COLLECTION OF MATERIAL
Preliminary preparation of the subject for a general stool analysis (macroscopic, chemical and microscopic examination) consists of eating food with a dosed content of proteins, fats and carbohydrates for 3-4 days (3-4 bowel movements). The Schmidt diet and the Pevzner diet meet these requirements.
Schmidt's diet is gentle, includes 1-1.5 liters of milk, 2-3 soft-boiled eggs, 125 g of lightly fried minced meat, 200-250 g of mashed potatoes, mucous broth (40 g of oatmeal), 100 g of white bread or crackers, 50 g of butter, total calorie content 2250 kcal. After its consumption, during normal digestion, food residues are not found in the feces.
The Pevzner diet is based on the principle of maximum nutritional load for a healthy person. It is a common diet for healthy people, which is convenient in outpatient settings. It consists of 400 g of white and black bread, 250 g of fried meat, 100 g of butter, 40 g of sugar, buckwheat and rice porridge, fried potatoes, salad, sauerkraut, dried fruit compote and fresh apples. Calorie content reaches 3250 kcal. After its administration in healthy people, microscopic examination reveals only a few altered muscle fibers in rare fields of vision. This diet allows you to identify even a small degree of disruption of the digestive and evacuation capacity of the gastrointestinal system.
When preparing a patient for a study for hidden bleeding, fish, meat, all types of green vegetables, tomatoes, eggs, and medications containing iron (that is, catalysts that cause a false-positive reaction to blood) are excluded from the diet.
Feces are collected after spontaneous bowel movements in a specially designed container. You cannot send material for research after an enema, taking medications that affect peristalsis (beladona, pilocarpine, etc.), after taking castor or vaseline oil, after administering suppositories, or drugs that affect the color of stool (iron, bismuth, barium sulfate). The stool should not contain urine. Delivered to the clinical diagnostic laboratory immediately or no later than 10-12 hours after defecation, subject to storage in the refrigerator.
In the laboratory, feces are subjected to chemical analysis, macroscopic and microscopic examination.
CHEMICAL ANALYSIS OF FOCUS USING DIAGNOSTIC TEST STRIPS OF THE COMPANY "BIOSENSOR AN"
A chemical study of feces consists of determining the pH, identifying a hidden inflammatory process (mucus, inflammatory exudate), detecting hidden bleeding, diagnosing obstruction of the biliary system, and testing for dysbacteriosis. To carry out these studies, it is possible to use reagent test strips that allow you to determine the pH of feces, the presence of protein, blood, stercobilin, bilirubin, and leukocytes.
To carry out chemical analysis using reagent strips and microscopic examination of feces, it is necessary to prepare a fecal emulsion.
PREPARATION OF FECAL EMULSION
Place a small amount of feces (the size of a hazelnut) in a centrifuge tube and, gradually adding distilled water, rub with a glass rod until the consistency of “thick syrup” (dilution 1:6 - 1:10).
For chemical analysis of feces, it is advisable to use reagent strips: Uripolian - to determine pH and protein; Urigem - for determining red blood cells and hemoglobin; Uripolian-2 - for the detection of bilirubin and urobilinogen. For chemical analysis of stool, you can use multifunctional Uripolian-7 strips (blood, ketones, bilirubin, urobilinogen, glucose, protein, pH). However, a test for ketones is not used when conducting a chemical examination of feces.
RULES FOR WORKING WITH REAGENT TEST STRIPS
1. Carefully place fecal emulsion
2. Using a glass rod, apply the emulsion to the corner of the reagent field. Do not cover the entire reagent sensory field with fecal emulsion;
3. Immediately start the stopwatch;
4. Observe a change or appearance of color in the reagent sensory field near the fecal emulsion;
5. After the time specified in the instructions for this test, compare the color of the reagent touch zone with the value on the package label.
pH
Clinical aspects
Normally, in practically healthy people on a mixed diet, the stool reaction is neutral or slightly alkaline (pH 6.8-7.6) and is due to the vital activity of the normal bacterial flora of the colon.
An acidic reaction (pH 5.5-6.7) is observed when the absorption of fatty acids in the small intestine is impaired.
Sharp - acidic (pH less than 5.5) occurs with fermentative dyspepsia, in which carbon dioxide and organic acids are formed as a result of activation of fermentative flora (normal and pathological).
An alkaline reaction (pH 8.0-8.5) is observed during the rotting of food proteins (not digested in the stomach and small intestine) and inflammatory exudate as a result of activation of putrefactive flora and the formation of ammonia and other alkaline components in the large intestine.
Strongly alkaline (pH more than 8.5) - for putrefactive dyspepsia (colitis).
Principle of the method
The reagent sensory zone, impregnated with the indicator bromothymol blue, changes color depending on the concentration of hydrogen ions in feces in the pH range from 5 to 9.
Sensitivity
When compared with the color of the indicator scale on the container, the pH value of the sample can be determined with an accuracy of 0.5 pH units.
Test score
The color of the reactive zone of the strip changes depending on the pH of the fecal emulsion being tested. The color of the reactive zone is compared with a color scale immediately after applying the sample to the strip. The color of individual scale squares corresponds to pH values 5-6-7-8-9. If the color of the reactive zone falls between two colored squares, then the results can be normalized to whole values or to intermediate values with a range of 0.5 units.
5,0 6 ,0 6,5 7 ,0 7,5 8 ,0 9.0 pH units
PROTEIN
Clinical aspects
There is no protein in the stool of a healthy person. A positive reaction to protein indicates the presence of inflammatory exudate, mucus, undigested food protein, and bleeding.
Protein in stool is detected when:
Stomach damage (gastritis, ulcer, cancer);
Damage to the duodenum (duodenitis, cancer of the papilla of Vater, ulcer);
Damage to the small intestine (enteritis, celiac disease);
Damage to the colon (fermentative colitis, putrefactive, ulcerative, polyposis, cancer, dysbacteriosis, increased secretory function of the colon);
Damage to the rectum (hemorrhoids, fissure, cancer, proctitis).
Test principle
The test is based on the principle of "protein error indicator". The reactive sensory zone contains an acid buffer and a special indicator (bromophenol blue), which in the presence of proteins changes color from yellow through green to blue.
Sensitivity and spec digitality
The test is highly sensitive to the protein and reacts to its presence in stool at concentrations as low as 0.10-0.15 mg/ml of fecal emulsion.
If the stool reaction is alkaline or sharply alkaline (pH 8.0-10.0), in order to avoid a false-positive reaction, it is necessary to acidify the stool emulsion with a few drops of 30% CH3COOH to pH 7.0-7.5.
Test score
A change in the color of the reagent sensory field occurs immediately after application of the test material and is compared with the color of the colored areas on the container after 60 seconds.
Reagent field coloring:
light green – the reaction to protein is weakly positive;
green – positive;
dark green or green-blue – sharply positive.
0,00,1 0,3 1,0 3,0 ≥ 10,0 g/l
0.0 10 30 100 300 ≥ 1000 mg/dL
BLOOD
Clinical aspects
A positive reaction to blood (hemoglobin) indicates bleeding from any part of the digestive tract (gums, varicose veins of the esophagus and rectum, affected by an inflammatory process or malignant neoplasm of the gastric and intestinal mucosa). Blood in the stool appears with hemorrhagic diathesis, ulcers, polyposis, hemorrhoids. Using diagnostic strips, the so-called “occult blood” is detected, which is not detected during macroscopic examination.
Test principle
The reagent zone is impregnated with cumyl hydroperoxide, citric acid buffer and reagents that enhance the color reaction. Cumyl hydroperoxide provides a positive reaction with hemoglobin and myoglobin. The test is based on the pseudoperoxidase effect of hemoglobin, which catalyzes the oxidation of the chromogen by stabilized organic hydroperoxide.
Sensitivity and Specificity
The test is specific and gives a positive result in the presence of hemoglobin and myoglobin, has a very high sensitivity to hemoglobin. The reaction is positive in the presence of 4000-5000 red blood cells in 1 ml of fecal emulsion. The reaction can be positive in the presence of bacterial and fungal peroxidases.
Test score
It is necessary to pay special attention to the speed at which the color appears. A positive, rapid green or dark green color that appears in the first seconds indicates the presence of red blood cells or hemoglobin. The appearance of a positive color after 30 seconds or more is observed in the presence of a large number of muscle fibers (undigested protein food), which is usually confirmed by microscopic examination of stool. The combination of a positive protein reaction with a rapid positive blood reaction (hemoglobin) confirms the presence of damage to the gastrointestinal mucosa.
UROBILINOGEN (STERCOBILINOGEN)
Clinical aspects
Stercobilinogen and urobilinogen are the end products of hemoglobin catabolism in the intestine. It is very difficult to distinguish analytically between urobilinogen and stercobilinogen, so the term “urobilinogen” combines both of these substances. Urobilinogen is absorbed in significant quantities in the small intestine. Stercobilinogen is formed from bilirubin in the colon as a result of the activity of normal bacterial flora (Figure No. 5). The feces of a healthy person contain stercobilinogen and stercobilin; 40 - 280 mg of them are excreted in feces per day. Stercobilinogen is colorless. Stercobilin colors feces brown.
Stercobilin and stercobilinogen are absent in feces due to obstruction of the biliary tract. The feces become colorless.
The content of stercobilin in feces decreases with parenchymal hepatitis and cholangitis; during the period of intrahepatic stagnation, feces are also colorless. In acute pancreatitis, stercobilinogen is released in the stool (light gray stool).
The content of stercobilin in feces increases in hemolytic anemia.
Test principle
Determination of the level of stercobilinogen is based on the principle of the Ehrlich reaction of azo coupling of a stabilized diazonium salt with stercobilinogen in an acidic environment. The colorless reaction zone becomes pink or red in the presence of stercobilinogen.
Sensitivity and Specificity
The test is specific for urobilinogen and stercobilinogen. A positive reaction is observed at a stercobilinogen concentration of 3-4 μg/ml of fecal emulsion.
The reagent sensory zone in the presence of a large amount of bilirubin becomes yellow no earlier than 60 seconds later and then turns green. This has virtually no effect on the determination of stercobilinogen content, since a pink color in the presence of stercobilinogen appears in the first 60 seconds.
Test score
In the presence of stercobilinogen, a positive pink or crimson color appears immediately or within the first 60 seconds. The absence of color indicates obstruction of the biliary system, pink or pale pink color indicates incomplete obstruction, bright pink or crimson color indicates normal.
negative positive
3.5 17.5 35.0 70.0 140.0≥ 210.0 µmol/l
BILIRUBIN
Clinical aspects
Normally, bilirubin is found in the meconium and feces of a breastfed baby until about 3 months of age. By this time, normal bacterial flora appears in the gastrointestinal tract, which partially reduces bilirubin to stercobilinogen. By 7-8 months of life, bilirubin is completely oxidized by intestinal flora to stercobilinogen-stercobilin. In a healthy child 9 months and older, only stercobilinogen-stercobilin is present in the feces.
The detection of bilirubin in the stool indicates a pathology: rapid evacuation of food through the intestines, severe dysbiosis (lack of normal bacterial flora in the colon, suppression of intestinal microflora with long-term use of antibiotics and sulfa drugs).
The combination of stercobilin with bilirubin indicates the appearance of pathological flora in the colon and its displacement of normal flora (latent, sluggish dysbiosis) or the rapid evacuation of chyme through the intestines.
Test principle
The method is based on the azo coupling reaction in an acidic environment. The reactive zone contains p-nitrophenyldiazonium-p-toluenesulfonate, sodium bicarbonate and sulfosalicylic acid. Upon contact with bilirubin, a purple-red color appears after 30 seconds, the intensity of which depends on the amount of bilirubin detected.
Specificity and sensitivity
The test is specific for conjugated bilirubin. The coloring of the reactive sensory zone appears already at a bilirubin concentration of 2.5 - 3.0 μg/ml of fecal emulsion.
Ascorbic acid in very high concentrations (approximately 500 mg/l) causes a faint pink color, which can be taken as a positive test. In the presence of stercobilinogen in very high concentrations (over 60 μg/ml), the color of the bilirubin-responsive reactive zone takes on a pale orange hue. In this case, it is recommended to read the test 90-120 seconds after wetting the reactive zone, when the purple-red color characteristic of bilirubin appears.
Test score
In the presence of bilirubin, the reagent sensory zone or within 30-60 seconds turns lilac, lilac-pink or purple-red depending on the amount of conjugated bilirubin. The result is assessed accordingly as weakly positive, positive or strongly positive.
negative positive
0,0 9 ,0 17 ,0 ≥ 50.0 µmol/l
neg + ++ +++
MACROSCOPIC EXAMINATION OF FECAL
Quantity
A healthy person excretes 100-200 g of feces in 24 hours. The predominance of protein foods in the diet is accompanied by a decrease, while vegetable foods are accompanied by an increase in the amount of feces.
Less than normal - for constipation
More than normal - if there is a violation of the flow of bile, insufficient digestion in the small intestine (fermentative and putrefactive dyspepsia, inflammatory processes), with colitis with diarrhea, colitis with ulcerations, accelerated evacuation from the small and large intestines.
Up to 1 kg or more - with pancreatic insufficiency.
Consistency
The consistency of stool depends on the content of water, mucus and fat. The normal water content is 80-85% and depends on the time the stool remains in the distal colon, where it is absorbed. With constipation, the water content decreases to 70-75%, with diarrhea it increases to 90-95%. Hypersecretion of mucus in the colon and inflammatory exudate give the stool a liquid consistency. In the presence of large amounts of unchanged or broken down fat, the stool becomes ointment-like or doughy.
Dense, shaped - in addition to the norm, it occurs with insufficiency of gastric digestion.
Ointment-like - characteristic of impaired pancreatic secretion and lack of bile flow.
Liquid - with insufficient digestion in the small intestine (enteritis, accelerated evacuation) and large intestine (colitis with ulceration, putrefactive colitis or increased secretory function).
Pasty - with fermentative dyspepsia, colitis with diarrhea and accelerated evacuation from the colon, chronic enteritis.
Foamy - with fermentative colitis.
Sheep - for colitis with constipation.
Ribbon-shaped, pencil-shaped - with sphincter spasm, hemorrhoids, tumors of the sigmoid or rectum.
The color of normal stool is brown, due to the presence of stercobilin. With dairy foods, the color of stool is less intense, yellow; with meat foods, it is dark brown. The color of stool is affected by pigments from plant foods and medications. The color of feces changes due to pathological processes in the gastrointestinal system.
Black or tarry - with gastrointestinal bleeding.
Dark brown - with insufficiency of gastric digestion, putrefactive dyspepsia, colitis with constipation, colitis with ulceration, increased secretory function of the colon, constipation.
Light brown - with accelerated evacuation from the colon.
Reddish - with colitis with ulcerations.
Yellow - with insufficient digestion in the small intestine and fermentative dyspepsia, movement disorders.
Gray, light yellow - with pancreatic insufficiency. White - with intrahepatal stagnation or complete obstruction of the common bile duct.
Smell
The odor of feces is normally due to the presence of protein breakdown products (indole, skatole, phenol, ortho- and para-cresols). With an abundance of proteins in food, the smell intensifies; with constipation, it almost completely disappears, since some of the aromatic substances are absorbed.
Putrefactive - with insufficiency of gastric digestion, putrefactive dyspepsia, ulcerative colitis due to the formation of hydrogen sulfide and methyl mercaptans.
Fetid (smell of rancid oil) - due to impaired pancreatic secretion, lack of bile flow (bacterial decomposition of fat and fatty acids).
Weak - with insufficient digestion in the large intestine, constipation, accelerated evacuation through the intestines.
Sour - for fermentative dyspepsia due to volatile organic acids (butyric, acetic, valeric).
Butyric acid - in case of malabsorption in the small intestine and accelerated evacuation.
Leftover undigested food
Undigested protein, vegetable and fatty foods are revealed in the fecal emulsion in a Petri dish against a dark and light background. The pulpy part of plant food is visible in the form of transparent, colorless, mucus-like round lumps, sometimes painted in one color or another. The detection of digested fiber indicates rapid evacuation of food or the absence of hydrochloric acid in the gastric juice. Undigested fiber has no diagnostic value. Undigested meat is presented in the form of whitish shreds of fibrous structure (muscle fibers, ligaments, cartilage, fascia, blood vessels).
MICROSCOPIC EXAMINATION OF FECAL
PREPARATION OF PREPARATIONS FOR MICROSCOPY
1. Drug
A drop of fecal emulsion is applied to a glass slide and covered with a coverslip. In this preparation, during microscopic examination, against the background of fecal detritus, the remains of undigested protein food are differentiated - connective tissue (Fig. No. 14), muscle fibers with and without striations (Fig. No. 15), remains of undigested carbohydrate food (digested fiber), remains of undigested and split fat - drops, needles, lumps (Fig. No. 16). In the same preparation, mucus and the leukocytes, red blood cells, columnar epithelium, helminth eggs, protozoan cysts and vegetative individuals contained in it are examined.
2. Drug
A drop of fecal emulsion and the same drop of Lugol's solution (1 g of iodine, 2 g of potassium iodide and 50 ml of water) are applied to a glass slide, mixed and covered with a coverslip. This drug is intended to detect undigested (black, dark blue) or partially digested (blue or cyan - amylodextrin; pink, reddish or violet erythrodextrin) extracellular or intracellular starch and iodophilic flora, which is stained black and brown with iodine (Fig. 17) .
3. Drug
A drop of fecal emulsion and a drop of 20-30% acetic acid are applied to a glass slide, mixed, and covered with a coverslip. The drug is intended for the diagnosis of needles and lumps of fatty acid salts (soaps). If in the native preparation the needles and lumps do not turn into drops (fatty acids) when heated, then preparation III is brought to a boil over the flame of an alcohol lamp and microscopically examined under high magnification. The formation of droplets after boiling indicates the presence of fatty acid salts (soaps) in the feces.
4. Drug
Apply a drop of fecal emulsion and a drop of 0.5% aqueous solution of methylene blue to a glass slide, mix and cover with a coverslip. This preparation is intended to differentiate neutral fat droplets from fatty acid droplets. Drops of fatty acids are stained with methylene blue in an intense blue color, while drops of neutral fat remain colorless (Fig. No. 18).
5. Drug
Prepare in the presence of mucus, mucous-bloody, purulent masses, or tissue shreds. Selected tissue scraps and mucus are washed in saline, applied to a glass slide and covered with a coverslip. This drug is intended for the detection of leukocytes (neutrophils, eosinophils), erythrocytes, columnar epithelium, elements of malignant neoplasms, protozoa, etc.
|
Rice. No. 14. Native preparation of fecal emulsion: connective tissue remains of blood vessels, ligaments, fascia, cartilage, eaten meat 400x magnification. |
|
Rice. No. 15. Native preparation: Muscle fibers covered with connective tissue - sarcolemma (with striations) and without striations. 400x magnification. |
|
Rice. No. 16. Native preparation: split fat, represented by lumps and needles (salts of fatty acids and fatty acids). 400x magnification. |
|
Rice. 17. Preparation: with Lugol’s raster: starch undigested into doamylodextrin (blue) and split into erythrodextrin (pink), located inside the cells of digestible fiber. Normal iodophilic flora (clostridia) and pathological rods and cocci, stained black with Lugol's solution. 400x magnification. |
|
Rice. 18. Native preparation: drops of neutral fat and fatty acids). Preparation with methylene blue: drops of non-neutral fat are colorless, drops of fatty acids are colored blue. 400x magnification. |
SCATROLOGICAL SYNDROMES (MICROSCOPIC STUDY)
Normal stool
Against the background of a large amount of detritus, there are single muscle fibers devoid of striations (sarcolemmas) and a meager amount of fatty acid salts (soaps) in rare fields of vision.
Insufficiency of gastric digestion
Ahilia (achlorhydria) - a large number of muscle fibers covered with sarcolemma (with striations) and located predominantly in layers (creatorrhea), connective tissue, layers of digested fiber and calcium oxalate crystals.
Hyperchlorhydria - a large number of sarcolemma-covered, scattered muscle fibers (creatorrhea) and connective tissue.
Rapid evacuation of food from the stomach - scattered muscle fibers with and without striations.
Pancreatic insufficiency.
A large amount of neutral fat (steatorrhoea), digested (without striations) muscle fibers (creatorrhoea).
Impaired bile secretion (acholia).
With the rapid evacuation of chyme through the intestines, a large amount of fatty acids is revealed (steatorrhea).
For constipation, steatorrhea is represented by soaps (fatty acids react with ions K, Ca, Mg, Na, P inorg., forming salts of fatty acids - soaps). Steatorrhea with acholia is explained by the lack of bile acids that promote the absorption of fatty acids.
Malabsorption in the small intestine.
Malabsorption in the small intestine of any etiology is characterized by steatorrhea, expressed to a greater or lesser extent, and represented by fatty acids during diarrhea or salts of fatty acids during normal evacuation of chyme through the intestines or constipation.
Digestive insufficiency in the large intestine.
Fermentative dysbiosis (overdose of carbohydrates) - a large amount of digested fiber. In a preparation with Lugol's solution, starch located intra- and extracellularly and normal iodophilic flora (clostridium) are revealed. The transition of fermentative dysbiosis to dysbacteriosis (colitis) is characterized by the appearance of mucus with leukocytes and cylindrical epithelium, while the mucus is usually mixed with fecal detritus and the appearance of pathological iodophilic flora (small cocci, small and large rod flora).
Putrefactive dyspepsia (colitis) - triplet phosphate crystals indicate a shift in pH to the alkaline side and an increased process of putrefaction in the colon.
Ulcerative colitis.
In freshly isolated mucopurulent-bloody masses against the background of neutrophils, erythrocytes and cylindrical epithelium, one can detect vegetative forms of pathogenic protozoa (Ent. histolytica, Bal. coli), sometimes eosinophils and Charcot-Leyden crystals (allergic nonspecific colitis or allergic reaction to protozoa).
Delayed evacuation of the colon (constipation, spastic colitis).
Constipation and spastic colitis are characterized by microscopy by a large amount of detritus and undigested fiber. The detection of mucus containing dystrophically altered cellular elements (leukocytes and columnar epithelium) indicates the presence of an inflammatory process.
FEATURES OF DIGESTION AND COPROGRAM OF INFANTS IN NORMAL AND IN PATHOLOGY
The fetal digestive tract begins to function at 16-20 weeks of intrauterine development. During this period, the swallowing reflex is well expressed, the salivary glands produce amylase, and the stomach produces pepsinogen. The developing fetus swallows amniotic fluid, which is similar in chemical composition to interstitial fluid (tissue and spinal fluid), containing protein and glucose.
The pH of a newborn's stomach is 6.0, decreases to 1.0 - 2.0 in the first 6-12 hours of life, by the end of the first week it rises to 4.0, then gradually decreases to 3.0. Pepsin does not play a significant role in protein digestion in the newborn. Enzymatic processing of breast milk protein occurs in the duodenum and small intestine.
The intestines of an infant are 8 times the length of his body. As a result of the sequential connection of pancreatic enzymes (trypsin, chemotrypsin) and proteolytic enzymes of the small intestine, almost complete utilization of milk protein occurs. A breastfed baby absorbs up to 98% of amino acids.
Lipolysis during breastfeeding in the first week of life occurs in the stomach cavity due to lipase in mother's milk. The maximum effect of milk lipase is achieved at pH 6.0 - 7.0. Further lipolysis occurs in the duodenum under the action of pancreatic lipase. Already in the first weeks and months of a child’s life, 90-95% of the broken down fat is absorbed in the small intestine.
The hydrolysis of carbohydrates in the oral cavity and stomach of a newborn is insignificant and is mainly concentrated in the small intestine, where lactose, sucrose and maltose are broken down on the surface of the microvilli of the brush border of enterocytes.
Original feces (meconium)
The discharge of meconium occurs 8-10 hours after birth and continues for 2-3 days in the amount of 70-100 g. The consistency of meconium is sticky, viscous, thick, dark green in color, no odor; pH 5.0-6.0;
the reaction to bilirubin is positive.
The first portion of meconium acts as a plug; it consists of mucus, against which one can see layers of keratinized squamous epithelium, single cells of the cylindrical epithelium of the rectum, drops of neutral fat, representing the original lubricant, cholesterol and bilirubin crystals.
Bacterial flora appears in the feces of a newborn only during subsequent bowel movements.
Meconium is recommended to be examined in maternity hospitals to diagnose the intestinal form of cystic fibrosis in newborns. To do this, you can use the ALBU-FAN diagnostic strip. The diagnosis is based on the increased amount of albumin in cystic fibrosis. The colorless reagent field takes on a green or dark green color 1 minute after lowering into meconium. The diagnostic value is low, false-positive results are about 90%, confirmation of the diagnosis requires microscopic analysis of stool in infants.
Feces of a healthy baby while breastfeeding
The amount of feces in the first month of life is 15 g, and then gradually increases to 40-50 g for 1-3 bowel movements per day. This is a homogeneous, unformed mass, semi-viscous or semi-liquid, golden-yellow, yellow or yellow-green in color with a slightly sour odor, pH 4.8-5.8
The acidic environment of feces is explained by the vital activity of abundant saccharolytic flora, pronounced enzymatic processes and a high lactose content.
The reaction to bilirubin remains positive until 5 months of age, then, in parallel with bilirubin, stercobilin begins to be detected as a result of the restorative effect of the normal bacterial flora of the colon. By 6-8 months of age, only stercobilin is detected in the feces.
Microscopic examination of feces against the background of detritus reveals single drops of neutral fat and a meager amount of fatty acid salts. Mucus is present in small quantities in the feces of an infant, mixed with it and contains no more than 8-10 leukocytes in the field of view.
Feces of a healthy baby with artificial feeding
The amount of feces is 30-40 g per day. The color is light or pale yellow, when standing in air it becomes gray or colorless, but can take on brown or yellowish-brown shades depending on the nature of the food, pH 6.8-7.5 (neutral or slightly alkaline reaction). The smell is unpleasant, slightly putrid due to the rotting of cow's milk casein.
Microscopic examination reveals a slightly increased amount of fatty acid salts. In a meager amount of mucus mixed with feces, single leukocytes are found.
Acute enteritis in an infant is accompanied by a shift in pH to the alkaline or sharply alkaline side and a positive reaction to the blood. The feces become liquid or semi-liquid with a lot of mucus. Lumps of mucus in liquid feces indicate the occurrence of follicular enteritis. Microscopic examination reveals fatty acids and mucus strands containing leukocytes.
The appearance of drops of neutral fat indicates insufficient supply of lipase due to swelling of the duodenal mucosa.
If the symptoms of acute enteritis are eliminated, the nature of the infant's stool has returned to normal, but microscopic examination reveals a large amount of fatty acid salts (soaps) - this indicates a continuing violation of intestinal absorption (chronic enteritis). At the same time, ions of potassium, calcium, phosphorus, sodium, etc. are removed from the body, which can quickly lead to rickets.
Intestinal malabsorption caused by congenital failure of enterocytes and enzymatic deficiency
Celiac enteropathy (celiac disease or celiac disease). Develops with congenital deficiency of 1-glutamyl peptidase and is characterized by impaired breakdown of gluten. During the breakdown of gluten, glutamine is formed, which causes an allergic reaction and inhibits the regeneration of the epithelium of the small intestine.
Celiac disease manifests itself in children from the moment they are fed mealy substances containing gluten (wheat and rye flour, rice, oats).
Liquid feces of a steatorrheic nature are excreted up to 5-10 times a day in the color of “mastic” with a disgusting musty odor. The stool reaction is slightly acidic or neutral (pH 6.5 - 7.0).
Bilirubin and stercobilin are determined according to the age of the child. On microscopic examination, fatty acids (steatorrhoea) indicate malabsorption in the small intestine.
Disucrose deficiency syndrome (carbohydrate intolerance)
The syndrome is caused by the absence of lactose and, less commonly, sucrase in the small intestine of the newborn. Lactose deficiency (breast milk lactose intolerance) is determined in the first days of a newborn’s life. An infant produces watery or liquid stool 8-10 times a day, yellow in color with a sour odor. Stool pH is 5.0-6.0, the reaction to bilirubin is positive.
Microscopic examination shows fatty acids (steatorrhoea). Unabsorbed lactose enters the colon, undergoes fermentation by saccharolytic flora, resulting in the formation of a huge amount of lactic acid, which irritates the mucous membrane of the colon and increases its permeability, as a result of which lactose is partially absorbed with water and is found in the urine.
A-beta lipoproteinemia (acanthocytosis)
Hereditary inability to synthesize beta-lipoproteins is detected in early childhood. In the peripheral blood of patients, acanthocytes and the absence of beta lipoproteins are detected. The feces are liquid, light yellow and golden yellow in color with an acidic reaction (pH 5.0-6.0) and the presence of bilirubin. A coating of fat is clearly visible on the surface of liquid feces. Microscopic examination shows fatty acids (steatorrhoea).
Cystic fibrosis or cystic fibrosis (intestinal form)
A hereditary disease characterized by disruption of the secretory function of the pancreas, glands of the stomach and intestines. Infants suffer from polyfecal: frequent, copious, mushy stools with a strong fetid odor, gray, shiny, greasy, the reaction is neutral or slightly acidic (pH 6.5-7.0). Grease stains form on diapers and are difficult to wash off. In older children (6-7 months), there may be a tendency to constipation - the feces are dense, shaped, sometimes “sheep-like”, but always pale in color, greasy, with a fetid odor. Fat is sometimes released in drops at the end of a bowel movement. Possible intestinal obstruction.
Microscopic examination reveals drops of neutral fat (steatorrhea), which confirms cystic degeneration of the pancreas (lack of lipase) in 80-88% of cases of the disease. Cystic degeneration of the digestive glands of the stomach and small intestine manifests itself during the transition from breastfeeding to mixed feeding and is confirmed by microscopic examination by a large number of undigested muscle fibers, connective tissue, digested fiber, starch and drops of neutral fat. This indicates a violation of hydrolysis, proteolysis and lipolysis.
Exudative enteropathy.
The disease is characterized by loss of plasma proteins by the gastrointestinal tract and is accompanied by impaired intestinal absorption.
State budgetary educational institution
higher professional education
"Omsk State Medical Academy"
Ministry of Health of the Russian Federation
Department of Propaedeutics of Internal Diseases
Laboratory and instrumental methods for diagnosing diseases of the gastrointestinal tract
S.S. Bunova, L.B. Rybkina, E.V. Usacheva
Study guide for students
UDC 616.34-07(075.8)
BBK 54.13-4ya73
This textbook presents laboratory and instrumental methods for diagnosing diseases of the gastrointestinal tract and outlines their diagnostic capabilities. The material is presented in a simple accessible form. The textbook contains 39 pictures, 3 tables, which will facilitate the assimilation of the material when working independently. The proposed textbook complements the textbook on propaedeutics of internal diseases. The presented test tasks are intended to consolidate the assimilation of the presented material.
This manual is intended for students studying in the following specialties: 060101 – General Medicine, 060103 – Pediatrics, 060105 – Medical and preventive medicine.
Preface
List of abbreviations
Chapter 2. Data from instrumental research methods for gastrointestinal diseases
1. Endoscopic research methods
1.1. Fibroesophagogastroduodenoscopy
1.2. Sigmoidoscopy
1.3. Colonoscopy
1.4. Enteroscopy
1.5. Capsule endoscopy
1.6. Chromoscopy (chromoendoscopy)
1.7. Diagnostic laparoscopy
2. X-ray research methods
2.1. Fluoroscopy (x-ray) of the esophagus and stomach
2.2. Computed tomography and multislice computed tomography of the abdominal organs
2.3. Survey radiography of the abdominal organs and study of the passage of barium through the intestines
2.4. Irrigoscopy
3. Ultrasound research methods
3.1. Ultrasound of the stomach
3.2. Ultrasound of the intestines (endorectal ultrasonography)
4. Functional diagnostic methods
4.2. Study of gastric secretion - aspiration-titration method (fractional study of gastric secretion using a thin probe)
Test tasks for self-study
Bibliography
Preface
Diseases of the gastrointestinal tract occupy one of the first places in the structure of morbidity, especially among young people of working age; the number of patients with pathologies of the digestive organs continues to increase. This is due to many factors: the prevalence of Helicobacter pylori infection in Russia, smoking, alcohol consumption, stress factors, the use of non-steroidal anti-inflammatory drugs, antibacterial and hormonal drugs, cytostatics, etc. Laboratory and instrumental research methods are an extremely important point in the diagnosis of gastrointestinal diseases tract, since they often occur latently, without obvious clinical signs. In addition, laboratory and instrumental methods for diseases of the esophagus, stomach and intestines are the main methods for monitoring the dynamics of the disease, monitoring the effectiveness of treatment and prognosis.
This textbook presents the diagnostic capabilities of laboratory and instrumental methods for diagnosing diseases of the esophagus, stomach and intestines, including general clinical and special laboratory research methods, endoscopic, radiological, ultrasound methods and methods of functional diagnostics.
Along with traditional studies that have become firmly established in practice, new modern methods for diagnosing diseases of the gastrointestinal tract were considered: quantitative determination of transferrin and hemoglobin in feces, determination of a marker of inflammation of the intestinal mucosa - fecal calprotectin, blood serum testing using the "GastroPanel", method diagnosing stomach cancer using a tumor marker in blood serum, modern methods for diagnosing Helicobacter pylori infection, capsule endoscopy, computed tomography and multislice computed tomography of the abdominal organs, ultrasound examination of the stomach and intestines (endorectal ultrasonography) and many others.
Currently, the potential of laboratory services has significantly increased as a result of the introduction of new laboratory technologies: polymerase chain reaction, immunochemical and enzyme immunoassays, which have taken a strong place on the diagnostic platform and allow screening, monitoring of certain pathologies and solving complex clinical problems.
Coprological research has not yet lost its importance in assessing the digestive capacity of the digestive system organs, for the selection of adequate enzyme replacement therapy. This method is easy to perform, does not require large material costs or special laboratory equipment, and is available in every medical institution. In addition, this manual describes in detail the main scatological syndromes.
For a better understanding of the diagnostic capabilities of laboratory and instrumental research methods and interpretation of the results obtained, the textbook presents 39 figures and 3 tables. The final part of the manual contains test tasks for self-preparation.
List of abbreviations
| TANK | - blood chemistry |
| BDS | – major duodenal papilla |
| DPK | - duodenum |
| ZhVP | – bile ducts |
| ZhKB | - cholelithiasis |
| Gastrointestinal tract | – gastrointestinal tract |
| ELISA | - linked immunosorbent assay |
| CT | - CT scan |
| MSCT | – multislice computed tomography |
| OAK | - general blood analysis |
| OAM | - general urine analysis |
| OBP | – abdominal organs |
| p/z | - line of sight |
| PCR | – polymerase chain reaction |
| sozh | – gastric mucosa |
| soe | - erythrocyte sedimentation rate |
| Tf | – transferrin in feces |
| Ultrasound | - ultrasonography |
| FEGDS | - fibroesophagogastroduodenoscopy |
| HP | – Helicobacter pylori |
| Hb | – hemoglobin in stool |
| NS1 | – hydrochloric acid |
Chapter 1. Data from laboratory research methods for diseases
1. Screening research methods
1.1. General blood analysis
1.2. General urine analysis
1.3. Blood chemistry
1.4. Examination of stool for worm eggs and protozoan cysts:
2. Special research methods
2.1. Stool research methods
2.1.1. Coprological research (coprogram)
| Coprogram indicators | Coprogram indicators are normal | Changes in coprogram indicators in gastrointestinal diseases |
| Macroscopic examination | ||
| Amount of feces | 100-200 g per day. When protein foods predominate in the diet, the amount of feces decreases, while vegetable feces increase. With a vegetarian diet, the amount of feces can reach 400-500 g. | - Excretion of feces in a large volume (more than 300 g per day - polyfecal matter) is characteristic of diarrhea. - A small volume of feces (less than 100 g per day) is characteristic of constipation. |
| Stool consistency | Moderately dense (dense) | - Thick consistency - with constant constipation due to excess water absorption - Liquid or mushy consistency of stool - with increased peristalsis (due to insufficient absorption of water) or with abundant secretion of inflammatory exudate and mucus by the intestinal wall - Ointment-like consistency - in the presence of a large amount of neutral fat (for example, in chronic pancreatitis with exocrine insufficiency) - Foamy consistency - with enhanced fermentation processes in the colon and the formation of large amounts of carbon dioxide |
| Shape of feces | Cylindrical | - The form of stool in the form of “large lumps” - with a long stay of stool in the colon (hypomotor dysfunction of the colon in people with a sedentary lifestyle or who do not eat roughage, as well as in cases of colon cancer, diverticular disease) - Shape in the form of small lumps - “sheep feces” indicates a spastic state of the intestines, during fasting, stomach and duodenal ulcers, a reflex nature after appendectomy, with hemorrhoids, anal fissure - Ribbon or “pencil” shape - for diseases accompanied by stenosis or severe and prolonged spasm of the rectum, for rectal tumors - Unformed feces - maldigestion and malabsorption syndrome. The Bristol Stool Form Scale (Fig. 1) is a medical classification of the forms of human feces, developed by Meyers Hayton at the University of Bristol, published in 1997. Types 1 and 2 characterize constipation Types 3 and 4 - normal stool Type 5, 6 and 7 - diarrhea |
| Smell | Fecal (regular) | - Long-term retention of feces in the colon (constipation) leads to the absorption of aromatic substances and the smell almost completely disappears - During fermentation processes, the smell of feces is sour due to volatile fatty acids (butyric, acetic, valeric) - Intensified putrefaction processes (putrefactive dyspepsia, decay of intestinal tumors) cause the appearance of a fetid odor as a result of the formation of hydrogen sulfide and methyl mercaptan |
| Color | Brown (when eating dairy foods - yellowish-brown, meat - dark brown). Ingestion of plant foods and some medications can change the color of stool (beets - reddish; blueberries, blackcurrants, blackberries, coffee, cocoa - dark brown; bismuth, iron color stool black) | - With obstruction of the biliary tract (stone, tumor, spasm or stenosis of the sphincter of Oddi) or with liver failure (acute hepatitis, cirrhosis of the liver), leading to a violation of the secretion of bilirubin, the flow of bile into the intestine stops or decreases, which leads to discoloration of stool, it becomes grayish-white, clayey (acholic feces) - In case of exocrine pancreatic insufficiency - gray, since stercobilinogen is not oxidized to stercobilin - Bleeding from the stomach, esophagus and small intestine is accompanied by the appearance of black stool - “tarry” (Melena) - When bleeding from the distal parts of the colon and rectum (tumor, ulcers, hemorrhoids), depending on the degree of bleeding, the stool has a more or less pronounced red color - In cholera, intestinal discharge is a gray inflammatory exudate with fibrin flakes and pieces of the colon mucosa (“rice water”) - Dysentery is accompanied by the secretion of mucus, pus and scarlet blood - Intestinal discharge with amoebiasis may have a jelly-like character, deep pink or red. |
| Slime | Absent (or in scant quantity) | - When the distal colon (especially the rectum) is affected, mucus occurs in the form of lumps, strands, ribbons or a glassy mass - With enteritis, the mucus is soft, viscous, mixing with feces, giving it a jelly-like appearance - Mucus covering the outside of formed stool in the form of thin lumps, occurs with constipation and inflammation of the large intestine |
| Blood | Absent | - When bleeding from the distal parts of the colon, the blood is located in the form of streaks, shreds and clots on formed stool - Scarlet blood occurs when bleeding from the lower parts of the sigmoid and rectum (hemorrhoids, fissures, ulcers, tumors) - Changed blood from the upper part of the digestive system (esophagus, stomach, duodenum), mixing with feces, colors it black (“tarry” feces, melena) - Blood in the stool can be detected in infectious diseases (dysentery), ulcerative colitis, Crohn's disease, disintegrating colon tumors in the form of streaks, clots, up to profuse bleeding |
| Pus | Absent | - Pus on the surface of the stool is determined by severe inflammation and ulceration of the colon mucosa (ulcerative colitis, dysentery, disintegration of an intestinal tumor, intestinal tuberculosis), often together with blood and mucus - Large amounts of pus without mucus are observed when opening paraintestinal abscesses |
| Leftover undigested food (lientorrhea) | None | Severe insufficiency of gastric and pancreatic digestion is accompanied by the release of undigested food residues |
Chemical research |
||
| Reaction | Neutral, less often slightly alkaline or slightly acidic | - An acidic reaction (pH 5.0-6.5) is observed when iodophilic flora is activated, producing carbon dioxide and organic acids (fermentative dyspepsia) - Alkaline reaction (pH 8.0-10.0) occurs with increased processes of protein putrefaction in the large intestine, activation of putrefactive flora that produces ammonia (putrefactive dyspepsia) |
| Reaction to blood (Gregersen reaction) | Negative | A positive reaction to blood indicates bleeding in any part of the gastrointestinal tract (bleeding from the gums, rupture of varicose veins of the esophagus, erosive and ulcerative lesions of the gastrointestinal tract, tumors of any part of the gastrointestinal tract in the stage of decay) |
| Reaction to stercobilin | Positive | - The absence or sharp decrease in the amount of stercobilin in the feces (the reaction to stercobilin is negative) indicates obstruction of the common bile duct with a stone, compression by a tumor, stricture, stenosis of the common bile duct or a sharp decrease in liver function (for example, in acute viral hepatitis) - An increase in the amount of stercobilin in feces occurs with massive hemolysis of red blood cells (hemolytic jaundice) or increased bile secretion |
| Reaction to bilirubin | Negative, because the vital activity of the normal bacterial flora of the colon ensures the process of restoration of bilirubin into stercobilinogen, and then into stercobilin | The detection of unchanged bilirubin in the stool of an adult indicates a disruption in the process of bilirubin recovery in the intestine under the influence of microbial flora. Bilirubin can appear during rapid evacuation of food (sharp increase in intestinal motility), severe dysbiosis (syndrome of bacterial overgrowth in the colon) after taking antibacterial drugs |
| Vishnyakov-Triboulet reaction (for soluble protein) | Negative | The Vishnyakov-Triboulet reaction is used to identify a hidden inflammatory process. Detection of soluble protein in stool indicates inflammation of the intestinal mucosa (ulcerative colitis, Crohn's disease) |
Microscopic examination |
||
| Muscle fibers: With striations (unchanged, undigested) | None Absent (or only a few in sight) | A large number of changed and unchanged muscle fibers in the feces ( Torheatorrhea) indicates a violation of proteolysis (digestion of proteins): - in conditions accompanied by achlorhydria (lack of free HCl in gastric juice) and achylia (complete absence of secretion of HCl, pepsin and other components of gastric juice): atrophic pangastritis, condition after gastric resection - with accelerated evacuation of food chyme from the intestines - in case of violation of the exocrine function of the pancreas - for putrefactive dyspepsia |
| Connective tissue (remnants of undigested vessels, ligaments, fascia, cartilage) | Absent | The presence of connective tissue in the stool indicates a deficiency of proteolytic enzymes of the stomach and is observed with hypo- and achlorhydria, achylia |
| Fat neutral Fatty acid Salts of fatty acids (soaps) | None or meager quantity fatty salts acids | Impaired digestion of fats and the appearance in the stool of large amounts of neutral fat, fatty acids and soaps is called Steatorrhea. - with a decrease in lipase activity (exocrine pancreatic insufficiency, a mechanical obstruction to the outflow of pancreatic juice), steatorrhea is represented by neutral fat. - if there is a violation of the flow of bile into the duodenum (a violation of the process of emulsification of fat in the small intestine) and if the absorption of fatty acids in the small intestine is impaired, fatty acids or salts of fatty acids (soaps) are found in the feces |
| Plant fiber (digestible) is found in the pulp of vegetables, fruits, legumes and grains. Indigestible fiber (the skin of fruits and vegetables, plant hairs, the epidermis of cereals) has no diagnostic value, since there are no enzymes in the human digestive system that break it down | Single cells in p/z | Occurs in large quantities during rapid evacuation of food from the stomach, achlorhydria, achylia, and with bacterial overgrowth syndrome in the colon (a marked decrease in normal microflora and an increase in pathogenic microflora in the colon) |
| Starch | Absent (or single starch cells) | The presence of large amounts of starch in feces is called amilorrhea and is observed more often with increased intestinal motility, fermentative dyspepsia, less often with exocrine insufficiency of pancreatic digestion |
| Iodophilic microflora (clostridia) | Single in rare p/z (normally iodophilic flora lives in the ileocecal region of the colon) | With a large amount of carbohydrates, clostridia multiply intensively. A large number of clostridia is regarded as fermentative dysbiosis |
| Epithelium | Absent or single cells of columnar epithelium in the p/z | A large amount of columnar epithelium in the feces is observed in acute and chronic colitis of various etiologies |
| Leukocytes | Absent or single neutrophils in the p/z | A large number of leukocytes (usually neutrophils) are observed in acute and chronic enteritis and colitis of various etiologies, ulcerative necrotic lesions of the intestinal mucosa, intestinal tuberculosis, dysentery |
| Red blood cells | None | - the appearance of slightly changed red blood cells in the feces indicates the presence of bleeding from the colon, mainly from its distal parts (ulceration of the mucous membrane, disintegrating tumor of the rectum and sigmoid colon, anal fissures, hemorrhoids) - during bleeding from the proximal colon, red blood cells are destroyed and are not detected by microscopy - a large number of red blood cells in combination with leukocytes and cylindrical epithelium is characteristic of ulcerative necrotic lesions of the colon mucosa (ulcerative colitis, Crohn's disease with damage to the colon), polyposis and malignant neoplasms of the colon |
| Worm eggs | None | Eggs of roundworms, tapeworms, etc. indicate a corresponding helminthic infestation |
| Pathogenic protozoa | None | Cysts of dysenteric amoeba, lamblia, etc. indicate corresponding invasion by protozoa |
| Yeast cells | None | Found in feces during treatment with antibiotics and corticosteroids. Identification of the fungus Candida albicans is carried out by culturing on special media (Sabouraud's medium, Microstix Candida) and indicates a fungal infection of the intestine |
| Calcium oxalate (oxalic lime crystals) | Absent | They enter the gastrointestinal system with plant foods and normally dissolve in the HCl of gastric juice to form calcium chloride. Detection of crystals is a sign of achlorhydria |
| Triple phosphate crystals (ammonium phosphate magnesium) | None | It is formed in the large intestine during the breakdown of lecithin, nuclein and other products of protein decay. Triple phosphate crystals found in feces (pH 8.5-10.0) immediately after defecation indicate increased putrefaction in the colon |
Scatological syndromes
Chewing deficiency syndrome
Mastication deficiency syndrome reveals insufficiency in the act of chewing food (detection of food particles in the stool, visible to the naked eye).
Causes of chewing deficiency syndrome:
- missing molars
- multiple dental caries with their destruction
Digestive insufficiency syndrome in the stomach (gastrogenic scatological syndrome)
Gastrogenic coprological syndrome develops as a result of impaired formation of hydrochloric acid and pepsinogen in the coolant.
Causes of gastrogenic scatological syndrome:
- atrophic gastritis
- stomach cancer
- conditions after gastrectomy
- erosions in the stomach
- stomach ulcer
- Zollinger-Ellison syndrome
The presence of digestible fiber in feces is an indicator of a decrease in the amount of free HCl and impaired gastric digestion. During normal gastric digestion, digestible fiber is macerated (softened) by free HCl of gastric juice and becomes accessible to pancreatic and intestinal enzymes and is not found in feces.
Pancreatic digestive insufficiency syndrome (pancreatogenic scatological syndrome)
A true indicator of pancreatic digestive insufficiency is the appearance of neutral fat in the stool (steatorrhea), since lipases do not hydrolyze fats.
There are muscle fibers without striations (creatorrea), the presence of starch is possible, and polyfecal matter is characteristic; soft, ointment-like consistency; unformed feces; color gray; pungent, fetid odor, the reaction to stercobilin is positive.
Causes of pancreatogenic scatological syndrome:
- chronic pancreatitis with exocrine insufficiency
- pancreas cancer
- conditions after pancreatectomy
- cystic fibrosis with exocrine pancreatic insufficiency
Bile deficiency syndrome (hypo- or acholia) or hepatogenic scatological syndrome
Hepatogenic coprological syndrome develops due to the lack of bile ( acholia) or its insufficient supply ( hypocholia) in the KDP. As a result, bile acids that participate in the emulsification of fats and activate lipase do not enter the intestine, which is accompanied by impaired absorption of fatty acids in the small intestine. At the same time, intestinal motility, stimulated by bile, and its bactericidal effect are also reduced.
The surface of the stool becomes matte, granular due to the increased content of fat droplets, the consistency is ointment-like, grayish-white in color, the reaction to stercobilin is negative.
Microscopic examination reveals a large amount of fatty acids and their salts (soaps) - products of incomplete breakdown.
Causes of hepatogenic scatological syndrome:
- diseases of the gallbladder (gallstones, obstruction of the common bile duct with a stone (choledocholithiasis), compression of the common bile duct and bile duct by a tumor of the head of the pancreas, severe strictures, stenosis of the common bile duct)
- liver diseases (acute and chronic hepatitis, liver cirrhosis, liver cancer)
Syndrome of indigestion in the small intestine (enteral scatological syndrome)
Enteral coprological syndrome develops under the influence of two factors:
- insufficiency of enzymatic activity of small intestinal secretions
- decreased absorption of end products of hydrolysis of nutrients
- mastication insufficiency syndrome gastric digestion insufficiency
- insufficiency of separation or entry of bile into the duodenum
- helminthic infestations of the small intestine and gallbladder
- inflammatory diseases of the small intestine (enteritis of various etiologies), ulcerative lesions of the small intestine
- endocrine diseases that cause increased intestinal motility (thyrotoxicosis)
- diseases of the mesenteric glands (tuberculosis, lymphogranulomatosis, syphilis, lymphosarcoma)
- Crohn's disease affecting the small intestine
- disaccharidase deficiency, gluten enteropathy (celiac disease)
Colon indigestion syndrome
Causes of indigestion syndrome in the colon:
- violation of the evacuation function of the colon - constipation, spastic dyskinesia of the colon
- inflammatory bowel diseases (ulcerative colitis, Crohn's disease)
- insufficiency of digestion in the large intestine, such as fermentative and putrefactive dyspepsia
- massive intestinal damage by helminths, protozoa
A sign of colitis will be the appearance of mucus with leukocytes and columnar epithelium. With inflammation of the distal colon (ulcerative colitis), a decrease in the amount of feces is observed, the consistency is liquid, the feces are unformed, pathological impurities are present: mucus, pus, blood; sharply positive reaction to blood and Vishnyakov-Triboulet reaction; a large number of columnar epithelium, leukocytes and erythrocytes.
Insufficiency of digestion in the large intestine according to the type of fermentative and putrefactive dyspepsia:
- Fermentative dyspepsia(dysbiosis, bacterial overgrowth syndrome in the colon) occurs due to impaired digestion of carbohydrates and is accompanied by an increase in the amount of iodophilic flora. Fermentation processes occur with an acidic pH environment (4.5-6.0). The stool is copious, liquid, foamy with a sour odor. Mucus mixed with feces. In addition, fermentative dyspepsia is characterized by the presence of large amounts of digestible fiber and starch in the feces.
- Putrid dyspepsia more common in people suffering from gastritis with secretory insufficiency (due to the lack of free hydrochloric acid, food is not properly processed in the stomach). The digestion of proteins is disrupted, their decomposition occurs, and the resulting products irritate the intestinal mucosa and increase the secretion of fluid and mucus. Mucus is a good breeding ground for microbial flora. In putrefactive processes, feces have a liquid consistency, dark brown color, an alkaline reaction with a sharp, putrid odor and a large number of muscle fibers under microscopy.
2.1.2. Bacteriological examination of stool
Bacteriological examination of stool- sowing feces on nutrient media for the purpose of qualitative analysis and quantitative determination of normal intestinal microflora, as well as opportunistic and pathogenic forms of microorganisms.Bacteriological culture of stool is used to diagnose intestinal bacterial overgrowth syndrome (intestinal dysbiosis), intestinal infections and monitor the effectiveness of their treatment:
- quantitative assessment of microflora (bifido- and lactic acid bacteria, clostridia, opportunistic and pathogenic microflora, fungi) with determination of sensitivity to antibiotics and phages
- identification of pathogens of intestinal infections (Shigella, Salmonella, Proteus, Pseudomonas, Yersinia enterocolitica, Campylobacter jejuni, E.coli, Candida, rotaviruses, adenoviruses)
2.1.3. Markers of damage to the intestinal mucosa:
A. examination of feces for occult blood (Gregersen reaction)
B. determination of transferrin (Tf) and hemoglobin (Hb) in feces
A. Examination of feces for occult blood (Gregersen reaction):
Hidden blood is blood that does not change the color of stool and is not detectable macroscopically or microscopically. The Gregersen reaction for detecting occult blood is based on the property of blood pigment to accelerate oxidative processes (chemical study).
A positive fecal occult blood reaction can occur when:
- erosive and ulcerative lesions of the gastrointestinal tract
- tumors of the stomach and intestines in the decay stage
- infestations by helminths that injure the intestinal wall
- rupture of varicose veins of the esophagus, cardia of the stomach, rectum (liver cirrhosis)
- blood entering the digestive tract from the mouth and larynx
- impurities in the stool of blood from hemorrhoids and anal fissures
B. Determination of transferrin (Tf) and hemoglobin (Hb) in feces(quantitative method (iFOB)) - identification of lesions of the intestinal mucosa. This test is much more sensitive than the fecal occult blood test. Transferrin persists for a longer time than hemoglobin in feces. An increase in transferrin levels indicates damage to the upper intestine, and hemoglobin indicates damage to the lower intestines. If both indicators are high, then this indicates the extent of the damage: the higher the indicator, the greater the depth or affected area.
These tests are of great importance in the diagnosis of colorectal cancer, as they can detect cancer both in the early stages (I and II) and in later stages (III and IV).
Indications for the determination of transferrin (Tf) and hemoglobin (Hb) in feces:
- bowel cancer and suspicion of it
- screening for colorectal cancer - as a preventive examination for people over 40 years of age (once a year)
- monitoring the condition of the intestine after surgery (especially in the presence of a tumor process)
- intestinal polyps and suspicion of their presence
- chronic colitis, including ulcerative colitis
- Crohn's disease and suspicion of it
- examination of first- and second-degree family members who have been diagnosed with cancer or intestinal polyposis
2.1.4. Determination of a marker of inflammation of the intestinal mucosa - fecal calprotectin
Calprotectin is a calcium-binding protein secreted by neutrophils and monocytes. Calprotectin is a marker of leukocyte activity and inflammation in the intestine.
Indications for the determination of calprotectin in feces:
- detection of acute inflammatory processes in the intestines
- monitoring of inflammation activity during treatment for inflammatory bowel diseases (Crohn's disease, ulcerative colitis)
- differential diagnosis of organic intestinal diseases from functionally caused ones (for example, irritable bowel syndrome)
2.2. Blood serum examination using GastroPanel
"GastroPanel" is a set of specific laboratory tests that can detect the presence of coolant atrophy, assess the risk of developing stomach cancer and peptic ulcers, and determine HP infection. This panel includes:
- gastrin-17 (G-17)
- pepsinogen-I (PGI)
- pepsinogen-II (PGII)
- specific antibodies - immunoglobulins class G (IgG) to Helicobacter pylori
Intragastric pH measurements are presented in Table 2.
Table 2. Intragastric pH-metry indicators
| Gastric body pH | hyperacid state | normoacid state | hypoacid state | anacid state |
| basal period | <1,5 | 1,6-2,0 | 2,1-6,0 | >6,0 |
| after stimulation | <1,2 | 1,2-2,0 |
2,1-3,0 3,1-5,0 (very weak reaction) |
>5,1 |
| pH of the antrum of the stomach | alkalization compensation | decreased alkalizing function | subcompensation for alkalization | decompensation of alkalization |
| basal period | >5,0 | - | 2,0-4,9 | <2,0 |
| after stimulation | >6,0 | 4,0-5,9 | 2,0-3,9 | <2,0 |
4.2. Study of gastric secretion– aspiration-titration method (fractional study of gastric secretion using a thin probe).
The technique includes two stages:
- Study of basal secretion
- Stimulated secretion assay
Study of stimulated secretion: parenteral stimulants of gastric secretion (histamine or pentagastrin - a synthetic analogue of gastrin) are currently used. So, after studying secretion in the basal phase, the patient is injected subcutaneously with histamine (0.01 mg/kg of the patient’s body weight - submaximal stimulation of the parietal cells of the coolant fluid or 0.04 mg/kg of the patient’s body weight - maximum stimulation of the parietal cells of the coolant fluid) or pentagastrin (6 mg /kg of patient's body weight). Gastric juice is then collected every 15 minutes. The resulting 4 servings within an hour constitute the volume of juice in the second phase of secretion - the phase of stimulated secretion.
Physical properties of gastric juice: normal gastric juice is almost colorless and odorless. Its yellowish or greenish color usually indicates an admixture of bile (duodenogastric reflux), and a reddish or brownish color indicates an admixture of blood (bleeding). The appearance of an unpleasant putrefactive odor indicates a significant disruption of gastric evacuation (pyloric stenosis) and the resulting putrefactive breakdown of proteins. Normal gastric juice contains only a small amount of mucus. An increase in mucus impurities indicates inflammation of the coolant, and the appearance of food residues in the resulting portions indicates serious disturbances in gastric evacuation (pyloric stenosis).
Normal gastric secretion indicators are presented in Table 3.
Table 3. Indicators of gastric secretion are normal
| Indicators | Normal values |
| Determination of clock voltage – amount of gastric juice produced by the stomach within an hour |
Basal secretion phase: 50-100 ml per hour - 100-150 ml per hour (submaximal histamine stimulation) - 180-220 ml per hour (maximum histamine stimulation) |
| Determination of flow rate HCl free. – amount of HCl, released into the lumen of the stomach per hour and expressed in milligram equivalents |
Basal secretion phase: 1-4.5 mEq/l/hour Stimulated secretion phase: - 6.5-12 meq/l/hour (submaximal histamine stimulation) - 16-24 meq/l/hour (maximum histamine stimulation) |
| Microscopic examination of gastric juice | Leukocytes (neutrophils) single in the field of view Single cylindrical epithelium in the field of view Slime + |
Interpretation of research results
1. Clock voltage change:
- an increase in the amount of gastric juice indicates hypersecretion (erosive antral gastritis, ulcer of the antrum or duodenum, Zollinger-Ellison syndrome) or a violation of the evacuation of food from the stomach (pyloric stenosis)
- a decrease in the amount of gastric juice indicates hyposecretion (atrophic pangastritis, stomach cancer) or accelerated evacuation of food from the stomach (motor diarrhea)
- normoacid state (normoaciditas)
- hyperacidity (hyperaciditas) - ulcer of the antrum or duodenum, Zollinger-Ellison syndrome
- hypoacid condition (hypoaciditas) - atrophic pangastritis, stomach cancer
- anacid state (anaciditas), or complete absence of free HCl after maximum stimulation with pentagastrin or histamine.
Disadvantages of the aspiration-titration method that limit its use in practice:
- removal of gastric juice disrupts the normal working conditions of the stomach; it is of little physiological value
- Some of the stomach contents are inevitably removed through the pylorus
- secretion and acidity indicators do not correspond to actual ones (as a rule, they are underestimated)
- the secretory function of the stomach increases, since the probe itself is an irritant of the gastric glands
- the aspiration method provokes the occurrence of duodenogastric reflux
- it is impossible to determine night secretion and the circadian rhythm of secretion
- it is impossible to assess acid formation after eating
- varicose veins of the esophagus and stomach
- burns, diverticula, strictures, stenosis of the esophagus
- bleeding from the upper gastrointestinal tract (esophagus, stomach, duodenum)
- aortic aneurysm
- heart defects, cardiac arrhythmias, arterial hypertension, severe forms of coronary insufficiency
Test tasks for self-study
Select one or more correct answers.
1. Special laboratory tests for gastrointestinal diseases
- scatological research
- general blood analysis
- blood serum examination using GastroPanel
- bacteriological examination of stool
- general urine analysis
- neutrophilic leukocytosis
- thrombocytosis
- anemia
- erythrocytosis
- acceleration of ESR
- gastric ulcer complicated by bleeding
- condition after gastric resection
- chronic duodenitis
- cancer of the cecum in the decay stage
- opisthorchiasis
- hypoproteinemia
- hyperproteinemia
- hyperlipidemia
- hypolipidemia
- hypokalemia
- positive reaction to stercobilin
- positive reaction to bilirubin
- positive Vishnyakov-Triboulet reaction (for soluble protein)
- microscopy shows a small amount of neutral fat
- microscopy shows a small amount of digested muscle fibers
- acholic feces
- "tarry" stool
- Gregersen's strongly positive reaction
- anemia
- polyfecal
- muscle fibers
- stool color
- reaction to stercobilin
- stool consistency
- reaction to bilirubin
- reaction to stercobilin
- connective tissue
- shape of stool
- reaction to bilirubin
- Gregersen reaction
- amount of stool
- neutral fat
- vegetable fiber (digestible)
- leukocytes
- red blood cells
- ahilia
- appendectomy
- hyperchlorhydria
- exocrine pancreatic insufficiency
- normal coprogram
- cholidocolithiasis
- stomach tumor
- tumor of the head of the pancreas
- cirrhosis of the liver
- atrophic gastritis
- Gregersen reaction
- transferrin in feces
- reaction to bilirubin
- hemoglobin in stool
- reaction to stercobilin
- morphological study of biopsy samples of the gastric mucosa
- X-ray
- urease breath test with 13C-urea
- rapid urease test
- bacteriological
- fibroesophagogastroduodenoscopy
- irrigoscopy
- colonoscopy
- fluoroscopy of the stomach
- sigmoidoscopy
- irrigoscopy
- sigmoidoscopy
- enteroscopy
- computed tomography of the abdominal organs
- fluoroscopy of the stomach
- short-term
- aspiration
- endoscopic
- X-ray
- daily allowance
- gastrin-17
- hourly voltage
- determination of IgG antibodies to Helicobacter pylori
- flow-hour of free HCl
- pepsinogen-I
19. A large number of changed and unchanged muscle fibers in feces is called___________
20 A large amount of starch in feces is called ____________
Answers to test tasks
| 1. | 1, 3, 4 | 6. | 2, 3, 4 | 11. | 1, 3, 4 | 16. | 1, 3, 5 |
| 2. | 1, 3, 5 | 7. | 2, 4 | 12. | 1, 2, 4 | 17. | 2, 4 |
| 3. | 1, 2, 4 | 8. | 1, 4, 5 | 13. | 1, 3, 4, 5 | 18. | steatorrhea |
| 4. | 1, 4, 5 | 9. | 2, 3, 4, 5 | 14. | 1, 3, 5 | 19. | creatororrhea |
| 5. | 1, 5 | 10. | 4 | 15. | 1, 4, 5 | 20. | amilorrhea |
Bibliography
- Vasilenko V.Kh., Grebenev A.L., Golochevskaya V.S., Pletneva N.G., Sheptulin A.A. Propaedeutics of internal diseases / Ed. A.L. Grebeneva. Textbook. – 5th edition, revised and expanded. - M.: Medicine, 2001 – 592 p.
- Molostova V.V., Denisova I.A., Yurgel V.V. Scatological research in health and pathology: educational and methodological manual / Ed. Z.Sh. Golevtsova. – Omsk: Publishing House Omsk State Medical Academy, 2008. – 56 p.
- Molostova V.V., Golevtsova Z.Sh. Methods for studying the acid-forming function of the stomach: educational manual. Supplemented and revised. – Omsk: Publishing House Om-GMA, 2009. – 37 p.
- Aruin L.I., Kononov A.V., Mozgovoy S.I. International classification of chronic gastritis: what should be accepted and what is in doubt // Pathology Archives. – 2009. – Volume 71 – No. 4 – P. 11–18.
- Roytberg G.E., Strutynsky A.V. Internal illnesses. Laboratory and instrumental diagnostics: textbook. – Moscow: Publishing house MEDpress-inform, 2013. – 816 p.
- Electronic library of Omsk State Medical Academy. Access mode: weblib.omsk-osma.ru/.
- Electronic library system "KnigaFond". Access mode: htwww. knigafund.ru
- Electronic library system of the 1st Moscow State Medical University named after. I.M. Sechenov. Access mode: www. scsml.rssi.ru
- Scientific electronic library (eLibrary). Access mode: http://elibrary.ru
- Journal of Consilium Medicum. Access mode: www. consilium-medicum.com
