First of all, they look at the color of the skin and mucous membranes - with anemia, they are usually pale, but in the presence of increased hemolysis, an icteric color appears. In this case, it is necessary to check all signs of hemolysis - the level of indirect bilirubin, the possibility of an increase in the number of reticulocytes, icterus (yellowness) of the sclera.
With iron deficiency anemia, signs of sideropenia develop - dry skin, brittleness, loss of shine of the nails, transverse striation, split ends often appear. (i.e. brittle and easily falling out).
With iron deficiency, tachycardia is noted associated with tissue hypoxia due to a lack of hemoglobin, and, consequently, a decrease in oxygen flow to the tissues.
When examining the surface of the skin, one should pay attention to the possible presence of bruises or pinpoint petechiae. You should always check for increased tissue bleeding. To do this, resort to the pinch symptom. However, this method is very subjective, so it is recommended to check the Rumpel-Leede symptom. To do this, the patient's blood pressure is measured, the systolic and diastolic pressure data are summed up, and the resulting indicator is divided in half, on this figure the inflated cuff on the arm is held for 5 minutes.
If, after that, petechiae remain at the site of the cuff, this indicates an increased fragility of the capillaries. Otherwise, the symptom is negative.
Palpation, percussion and auscultation
It is imperative to palpate all lymph nodes and evaluate them. This will make it possible to suspect a particular diagnosis (even if they increase). In a healthy person, lymph nodes are not palpable or appear in the form of peas, they are not very dense and painless - this is a trace of the transferred inflammatory process in the nearest area (regional lymph nodes). Dense as well as painful lymph nodes indicate an ongoing inflammatory process. Lymph nodes adhered to the skin most often indicate a postponed tuberculous process. In diseases of the blood, the lymph nodes have an average density, they are often quite large (the size of a drain), palpable in the form of a conglomerate of nodes. Usually enlarged lymph nodes have different localization.
The liver is not an organ of hematopoiesis, but with leukemia, its size increases sharply, so it is necessary to carefully determine its size.
The spleen is normally not palpable, it is located on the left and percussion is determined between the ribs IX-XI along the midaxillary line.
The width of the spleen is 4-8 cm. In various pathological conditions, it increases in size, sometimes reaching enormous size and descending into the small pelvis. In this case, a notch is determined along its front edge.
With an increase in the spleen, its size, sensitivity and consistency (dense, bumpy, etc.) are noted. It is also recommended to conduct auscultation, since the appearance of peritoneal friction noise indicates periprocesses (perisplenitis), which is observed in heart attacks, inflammatory diseases, etc. Currently, to clarify the size of the spleen, a study is carried out on an ultrasound machine.
The possibilities of bone marrow research in objective research are very limited. Soreness of bones (especially flat) is noted, especially on palpation and chipping.
Laboratory methods for blood tests
Methods of laboratory research are of paramount importance in the diagnosis of hematological diseases. It should be recalled that in a healthy adult, hematopoiesis is concentrated in the bones, there is about 1.5 kg of active red bone marrow. There is also a yellow (inactive) bone marrow, which becomes capable of hematopoiesis only in pathological conditions - bleeding, leukemia, etc.
Currently, the unitary theory of hematopoiesis has been adopted, according to which blood cells are formed from a single parental cell. It is called the stem. The number of such cells is very limited, they are designed to maintain the genetic continuity of the pool of hematopoietic cells. It is a self-replicating population of cells. They perform the so-called n-divisions, the first of which (up-division) leads to the reproduction of similar cells, the second leads to the formation of one of the same cells, capable only of proliferation, and the other, capable of differentiation. Already from this cell, more mature cells begin to form, capable of transforming into cells of peripheral blood. The exact identification of these cells has not been carried out. It was found that they resemble lymphoid cells.
The possibility of differentiation of hematopoietic cells appeared after the works of Ehrlich and Romanovsky with the use of various paints. Of the bone marrow cells that we can differentiate, it is necessary to indicate the hemocytoblast. Further, segmented forms of granulocytes, etc. In this case, granulocytes differ both in size and shape of the nucleus, and in the composition of intracellular granules - neutrophils, basophils and eosinophils. Mature cells differ in function.
Neutrophils are characterized by mobility and the ability to phagocytosis, basophils are heparinocytes; the number of eosinophils increases with allergies.
Removing cells from the bone marrow is an enzymatic process.
Erythroid cells - erythroblasts, pronormoblasts, basophilic normoblasts, polychromatophilic normoblasts, oxyphilic normoblasts, reticulocytes and mature erythrocytes. A jump over the stage of oxyphilic normoblasts is often noted. There are three ways of maturation of erythroid cells: polychromatophilic - oxyphilic - reticulocyte - erythrocyte; polychromatophilic - reticulocyte - erythrocyte; polychromatophilic - oxyphilic - erythrocyte. The most common type of maturation is the second.
Lymphocytes are produced in the bone marrow and spleen. The bone marrow is examined by puncture of the sternum, the method was developed in Leningrad by MI Arinkin in 1928. At the same time, the handle of the sternum is punctured under local anesthesia and a little bone marrow is aspirated. In the prepared smears, the number of shaped elements is counted and their composition is determined. The ratio of erythroid elements to the rest is 1: 3 (4).
Trepanobiopsy is used in difficult cases for histological examination of points. Puncture of the lymph nodes, liver and spleen is performed when they are enlarged. Usually, they try to identify pathological forms.
Peripheral blood composition. Erythrocytes - 4-5 million, Hb - 80-100 units, reticulocytes - 0.5-1%; the diameter of erythrocytes is 7.5 microns. Less than 6.5 microns - microcytes, more than 8 microns - macrocytes. The appearance of a large number of cells of different diameters is called anisocytosis. The appearance of erythrocytes of various abnormal forms - poikilocytosis. Erythrocytes can change not only in diameter, but also in thickness and volume - microspherocytes, ovalocytes. In various pathological conditions of hemoglobin (hemoglobinopathies), erythrocytes can take on even more bizarre forms - in the form of a crescent, a target, etc.
Leukocytes (from 4-5 thousand to 8-9 x 109 / ml). With a decrease in the number of leukocytes, they talk about leukopenia, with an increase - about leukocytosis. Leukopenia combined with neutropenia is called agranulocytosis.
In the presence of symptoms of increased bleeding, it is necessary to investigate the symptom of a tourniquet or pinch, Rumpel-Leede's symptom. The appearance of a petechial rash indicates a lesion of the vascular factor. Several tests can be used to judge the very process of blood clotting. The simplest is bleeding, determining the time of blood coagulation, for which blood is taken from a vein or finger and the time of clot formation is determined. The retraction of the clot is also determined. Counting the number of platelets (normally 200-300 thousand) is carried out in cases of increased bleeding.
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Basic laboratory tests for liver disease
Performed:
Iliyasova G.
Introduction
Laboratory studies of urine, feces, ascitic fluid and blood are essential in liver diseases.
Analysis of urine
The color of urine with jaundice with the release of bile pigments by the kidneys becomes deep yellow, and with a high content of bile pigments, urine looks like dark beer.
Bile pigments. As a constant sign, bilirubinuria is observed with obstructive jaundice. In parenchymal jaundice, bilirubin does not always appear in the urine; in hemolytic jaundice, it is absent in the urine. Apparently, this, in addition to quantitative relationships, is also explained by the fact that the bilirubin contained in the blood in hemolytic jaundice is of a slightly different structure than in mechanical jaundice.
Bile acids appear in the urine mainly with obstructive jaundice, when it is difficult to excrete them from the biliary tract into the intestines. In parenchymal jaundice, bile acids in the urine can also occasionally occur. With hemolytic jaundice, they do not exist in the urine. The determination of bile acids is not of great importance.
Urobilin. An increase in the content of urobilin in the urine (urobilinuria) indicates the inability of the liver to process all urobilin entering it from the intestine into bilirubin, either due to its increased intake (with increased hemolysis), or - most often - with damage to the function of the liver cells. Therefore, if we exclude cases with increased hemolysis (hemolytic jaundice, pernicious anemia), urobilinuria can serve as one of the most characteristic signs of damage to the hepatic parenchyma. It occurs in many liver diseases - hepatitis, cirrhosis, congestive liver, in acute infections (due to liver damage), etc. Since urobilin is formed from bilirubin in the intestine, the presence of obstructive jaundice with a complete cessation of the outflow of bile into the duodenum prevents urobilinuria even with liver dysfunction.
Amino acids, especially leucine and tyrosine, appear in urine with severe damage to the hepatic parenchyma with impaired formation of urea from protein breakdown products. It is possible that the breakdown of proteins of the liver itself plays a role here. Therefore, leucine and tyrosine are observed in the urine in severe hepatitis and especially in the so-called acute yellow atrophy of the liver.
The amount of ammonia in urine can increase for the same reason - due to a decrease in the formation of urea in severe diffuse liver damage. But it gives little data for judging the function of the liver, since ammonia is formed in the kidneys, its amount in the urine also increases when the alkaline-acid balance changes towards acidosis.
Acetone can appear in urine with severe liver damage, but acetonuria has no diagnostic value in liver disease.
Stool examination
Stool staining. With a decrease in the release of bilirubin into the intestine (due to liver damage or mechanical obstruction to the outflow of bile), the color of the feces turns pale. With the complete cessation of the access of bile into the intestines, the feces are completely discolored and resemble clay in appearance (acholic stool). With an increased release of bile pigments into the intestine (bile pleochromia), the color of the feces darkens.
The complete absence of stercobilin in the stool is determined more precisely by chemical means, since, on the one hand, small amounts of stercobilin may not stain feces, on the other hand, some food products can impart color to feces, despite the absence of stercobilin.
The quantitative determination of stercobilin in feces gives more accurate data on the course of bile metabolism, but has no significant practical value.
The presence of fatty acids and neutral fats on microscopic examination of feces indicates the absence of the effect of bile acids emulsifying fats and is observed simultaneously with discoloration of the stool when bile does not enter the intestine.
analysis laboratory research disease liver
Examination of ascitic fluid
The study of ascitic fluid obtained during a test puncture is important for the differential diagnosis between ascites and exudative peritonitis. The specific gravity is below 1015, the protein content is not more than 3% and the presence of mainly endothelial cells in the sediment indicate the presence of transudate, not exudate.
Blood test
In a more detailed study of the hepatic patient, some methods of blood examination are of certain importance.
The amount of bilirubin in the blood (bilirubinemia)
Bilirubin. Bilirubin is the main bile pigment and is formed when hemoglobin breaks down. In the blood, bilirubin binds to albumin. In hepatocytes, bilirubin is conjugated with glucuronic acid, and in conjugated form it is excreted in the bile. An increase in the amount of bilirubin in the blood (hyperbilirubinemia) develops as a result of increased production of bilirubin, a decrease in the intensity of its capture and / or conjugation in the liver, and a decrease in bile excretion. Violation of the synthesis of bilirubin, its capture by hepatocytes and / or conjugation leads to an increase in the level of its Free (indirect) Fraction in the blood. Inhibition of the excretion of Direct (bound) bilirubin leads to an increase in its level in the blood serum and the appearance of bilirubin in the urine (bilirubinuria is not observed with an isolated increase in the free fraction of bilirubin and, therefore, can be considered as a marker of direct bilirubinemia). Bilirubinuria is an early sign of liver damage and biliary tract, and in acute viral hepatitis (AVH) may occur before the development of Jaundice. This is important for practical drug addiction, since in a number of cases drug addicts are admitted to the clinic for treatment of the underlying disease in the acute phase of viral hepatitis with a latent (subclinical) course. The diagnosis of AVH is complicated by the fact that the disease often proceeds in an anicteric form, and the clinical symptoms of hepatitis (for example, general weakness) can be masked by the general severity of the withdrawal state and the side effects of the drugs used to stop it.
Liver enzymes. For laboratory diagnostics of hepatobiliary diseases, data on the level of the content in the blood of patients of such enzymes as transaminases (aminotransferases), alkaline phosphatase and gamma-glutamyl transpeptidase are important.
Aspartate transaminase (ACT) It is present in many parenchymal organs (liver, myocardium, brain, kidneys, skeletal muscles), therefore, an increase in its serum activity is not a specific enough diagnostic sign. Despite the nonspecificity, a significant increase in the level of ACT in the blood (more than 500 IU / L) indicates the development of acute viral or toxic hepatitis (if the diagnosis of acute myocardial infarction is excluded). The degree of increase in ACT does not correlate with the severity of the pathological process and has no prognostic value. Normalization of serum ACT levels on retest usually indicates recovery and can be considered a criterion for the effectiveness of therapy.
Alanine transaminase (ALT) Contained mainly in hepatocytes, therefore, an increase in its serum content is a more specific sign of hepatobiliary lesion than an increase in ACT. Typically, with liver damage, serum ACT increases less than ALT (ACT / ALT< 1). Исключением является острый алкогольный гепатит, при котором это соотношение меняется (ACT/АЛТ >2). This circumstance is usually explained by the increased need for pyridoxal-5 "-phosphate as an ALT cofactor (for patients with alcoholism, a deficiency of pyridoxal-5" -phosphate is characteristic, limiting the production of ALT). A very characteristic sign of alcoholic liver damage is an ACT / ALT ratio> 3 with a significant increase in serum GGT levels (twice the increase in alkaline phosphatase).
Alkaline phosphatase (ALP). It is more correct to talk about alkaline phosphatases as a group of isoenzymes. They participate in the reactions of hydrolysis of ether bonds of organic phosphates with the formation of an organic radical and inorganic phosphate. ALP enter the blood serum from the liver, bone tissue, intestines and placenta. The serum level of enzymes increases significantly with impaired bile formation and therefore is considered as one of the laboratory markers of cholestasis, and the indicator increases approximately fourfold, regardless of the form of cholestasis (intrahepatic or extrahepatic). To a lesser extent, the content of enzymes in the blood increases with hepatocellular lesions. A significant increase in the level of alkaline phosphatase in the blood is observed in primary biliary cirrhosis, primary sclerosing cholangitis, subhepatic jaundice, drug hepatitis with cholestatic syndrome, cholestatic variant of acute alcoholic hepatitis. An increase in serum alkaline phosphatase activity in liver diseases is explained by an increased synthesis of enzymes in hepatocytes, which depends on the block of intestinal-hepatic circulation of bile acids, and a delay in its entry into bile. An isolated increase in alkaline phosphatase is observed in hepatocellular carcinoma (HCC), metastatic liver cancer, amyloidosis, sarcoidosis, Hodgkin's lymphoma. It is believed that an isolated increase in alkaline phosphatase, especially in old age, without other laboratory or clinical symptoms, is not an alarming sign and does not represent an indication for a more in-depth examination. Typically, this laboratory phenomenon is due to an increase in the bone fraction of the enzyme.
Gamma Glutamyl Transpeptidase (GGT). An increase in the serum GGT level is observed in various diseases of the liver and biliary tract, as well as in obstruction of the common bile duct. It is believed that the predominant increase (in comparison with transaminases) of this enzyme in hepatitis indicates the toxic nature of the disease. The increase in GGT in drug addicts is a highly sensitive, but as a result of this nonspecific marker of any toxic (including drug) effects on hepatocytes. An increase in GGT in the blood of patients with alcoholism and drug addiction (in comparison with previous indicators) in the absence of drug therapy may be an indirect sign of the resumption of alcohol intake, non-alcoholic psychoactive substances, or unauthorized use of psychotropic drugs in the post-withdrawal period and in remission of the disease.
Blood proteins. An important laboratory indicator of liver damage is the content of plasma albumin. In narcological practice, a decrease in the level of albumin is often revealed, which develops as a result of inhibition of the synthetic function of the liver in hepatocellular lesions, as well as alimentary disorders characteristic of patients with alcoholism.
Prothrombin index (PTI). It reflects the prothrombin activity of the blood and is determined by the formula: where A is the prothrombin time of the blood of a healthy person, B is the prothrombin time of the blood under study. Prothrombin time is the time of clot formation in plasma with an excess of thromboplastin and optimal calcium content. The prothrombin time reflects the activity of the factors of the prothrombin complex synthesized in the liver.
Immunological studies. For laboratory diagnostics in hepatology, the study of markers of viral hepatitis (including immunoglobulins) is important.
Immunoglobulins. Immunoglobulins are serum proteins (predominantly γ-globulins) and are divided into 5 classes: IgA, IgM, IgG, IgD and IgE. Individual classes of immunoglobulins have different origins and biological significance, and their ratio changes in different diseases. With liver damage, there is usually an increase in the level of all classes of immunoglobulins with some differences that are of differential diagnostic value. Thus, primary biliary cirrhosis is characterized by a predominant increase in IgM with a moderate increase in fractions of other classes. An increase in IgA is a relatively specific marker of alcoholic liver damage. On the contrary, a decrease in IgA is characteristic of long-term drug-induced liver damage of the cholestatic type. In chronic active hepatitis (CAH), as a rule, there is an increase in IgG and, to a lesser extent, IgM.
Markers of viral hepatitis. The following markers of viral hepatitis are distinguished: antigens (which are structural and non-structural proteins of viral particles), nucleic acids and antibodies produced when antigens enter the blood of patients.
Enzyme-linked immunosorbent assay (ELISA). The method is based on the determination of the antigen-antibody complex by introducing an enzymatic label into one of the reagents and is important for the diagnosis of viral hepatitis.
Radioimmunoassay (RIA) It is also based on the determination of the antigen-antibody complex, but at the same time, not an enzymatic, but a radioactive label is combined with the reaction component. The method has high sensitivity and is also used in the diagnosis of viral hepatitis.
Polymerase chain reaction (PCR). A method for the diagnosis of viral hepatitis, based on the detection of nucleic acids (RNA and DNA) of hepatitis viruses. The method is based on a process identical to the natural replication of the virus nucleic acid. During PCR, denaturation of the desired nucleic acid, its reverse transcription (RNA -> DNA or the opposite reaction) and amplification (from the English Amplification - increase, amplification) or chain synthesis, which practically corresponds to the natural replication of viruses, occurs sequentially. PCR is distinguished by high sensitivity and specificity in the detection of viral components and allows one to judge the presence of an active viral infection (in contrast to serological methods, which only make it possible to ascertain a past or current infection).
Biochemical syndromes. To diagnose liver damage, it is important to ascertain the so-called biochemical (laboratory) syndromes:
cytolytic
cholestatic
hepatocellular failure.
Cytolytic syndrome. Indicates a violation of the integrity of the cell membranes of hepatocytes and the entry of membrane fragments, cell organelles and cytosol components into the extracellular matrix and blood of patients. Cytolytic syndrome is manifested by hyperbilirubinemia and increased serum activity of ACT and ALT in the serum and reflects the massive necrosis of hepatocytes. Cytolytic syndrome is observed in acute hepatitis (including viral, alcoholic and medicinal), with exacerbation of chronic hepatitis and decompensation of liver cirrhosis.
Cholestatic syndrome As a laboratory phenomenon, it corresponds to the clinical syndrome of cholestasis. Cholestatic syndrome is manifested by hyperbilirubinemia (not always), an increase in the serum activity of alkaline phosphatase and GGT, an increase in blood cholesterol levels with the disappearance of urobilin in the urine. In a narcological clinic, cholestatic biochemical syndrome is detected in alcoholic liver damage, acute and chronic viral hepatitis, as well as drug and toxic liver damage. The severity of the syndrome determines the severity and duration of the course of intra - and extrahepatic cholestasis.
Hepatocellular failure syndrome Represents a set of laboratory parameters reflecting a violation of the synthetic, metabolic and antitoxic functions of hepatocytes.
The syndrome is manifested by hypoproteinemia (primarily hypoalbuminemia), a deficiency of prothrombin and coagulation factors II, V and VII with a decrease in PTI, a decrease in the clearance of drugs and their metabolites, as well as products of biogenic reactions (ammonia, phenols, amino acids) with an increase in their content in blood.
The amount of cholesterol in the blood does not have a particular diagnostic value, it is usually slightly increased in obstructive jaundice and cholelithiasis.
Determination of the resistance of erythrocytes is of known importance in the diagnosis of liver diseases, since it is normal or increased in obstructive jaundice and decreased in hemolytic jaundice.
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Laboratory research methods
Sputum examination. Sputum is a pathological discharge of the respiratory organs, which is thrown out when coughing. The phlegm may contain mucus, serous fluid, blood cells and respiratory tract cells, protozoa, rarely helminths and their eggs. Sputum examination helps to establish the nature of the pathological process in the respiratory organs, and in some cases to determine its etiology.
The sputum for research should be taken in the morning, fresh, if possible before meals and after rinsing the mouth. Only for the detection of mycobacterium tuberculosis, sputum can be collected within 1-2 days (if the patient excretes little of it). In stale sputum, saprophytic microflora multiplies, shaped elements are destroyed. To collect sputum, special jars (spittoons) with screw caps and measuring divisions are used.
The study of sputum begins with its examination, first in a transparent jar, and then in a Petri dish, which is placed alternately on a black and white background. The following signs are noted. The nature, color and consistency of sputum. Mucous sputum is usually colorless, viscous, found in acute bronchitis. Serous sputum is also colorless, liquid, foamy, observed with pulmonary edema. Mucopurulent sputum, yellow or greenish, viscous, occurs in chronic bronchitis, tuberculosis, etc. Pure purulent sputum is homogeneous, semi-liquid, greenish-yellow, characteristic of a lung abscess when it breaks out. Bloody sputum can be either purely bloody with pulmonary bleeding (tuberculosis, cancer, bronchiectasis), and mixed, for example, mucopurulent blood streaked (with bronchiectasis), serous-bloody foamy (with pulmonary edema), muco-bloody (with lung infarction or congestion
in the system of the pulmonary circulation), purulent-bloody, semi-liquid, brownish-gray (with gangrene and lung abscess). If blood from the respiratory tract is not released immediately, but remains in them for a long time, its hemoglobin turns into hemosiderin and gives the sputum a rusty color (typical for croupous pneumonia).
When standing, sputum may exfoliate. Chronic suppurative processes are characterized by three-layer sputum: the upper layer is mucopurulent, the middle is serous, and the lower is purulent. Sometimes purulent sputum is divided into two layers - serous and purulent.
Smell. More often absent. The foul smell of freshly secreted sputum depends on the putrefactive decay of tissue (gangrene, disintegrating cancer) or on the decomposition of sputum proteins when it is retained in the cavities (abscess, bronchiectasis). Individual elements visible to the naked eye. In sputum can be found
Kurshman's spirals in the form of small dense twisted whitish filaments; fibrin clots - whitish and reddish tree-branched elastic formations found in fibrinous bronchitis, rarely in pneumonia; "Lentils" - small greenish-yellow dense lumps, consisting of calcified elastic fibers, crystals of cholesterol and soaps, and containing mycobacterium tuberculosis; Dietrich's plugs, similar to "lentils" in appearance and composition, but not containing tuberculous mycobacteria and emitting a fetid odor when crushed (found in gangrene, chronic abscess, putrid bronchitis); grain from-
messages found during the disintegration of old tuberculous foci; druses of actinomycetes in the form of small yellowish grains resembling semolina; necrotic pieces of lung tissue and tumors; leftover food.
Reaction of the environment. In sputum, the reaction of the medium is usually alkaline; it becomes sour with the decomposition of sputum and from the admixture of gastric juice, which helps to differentiate hemoptysis from bloody vomiting.
Microscopic examination of sputum. It is produced in both native and colored preparations. For the former, purulent, bloody, crumbly lumps, crimped white threads are taken from the material poured into the Petri dish and transferred to a glass slide in such an amount that a thin translucent preparation is formed when covered with a cover glass.
It is viewed first at low magnification for the initial orientation and search for the Kurshman spirals, and then at high magnification to differentiate the shaped elements. Kurshman's spirals are cords of mucus, consisting of a central dense axial thread and a spiral-like mantle enveloping it, in which leukocytes (often eosinophilic) and Charcot-Leiden crystals are interspersed (Fig. 27). Kurshman's spirals appear in
sputum with bronchial spasm, most often with bronchial asthma, less often with pneumonia, lung cancer. With a large increase in the native preparation, you can find leukocytes, a small amount of which is present in any sputum, and a large number in inflammatory and especially suppurative processes; eosinophils (Fig. 28) can be distinguished in the native preparation by the uniform large shiny granularity, but it is easier to recognize them when stained. Erythrocytes appear when the lung tissue is destroyed, pneumonia, stagnation in the pulmonary circulation, pulmonary infarction, etc.
Squamous epithelium enters the sputum mainly from the oral cavity and has no diagnostic value. Cylindrical ciliated epithelium is present in a small amount in any sputum, in a large amount - in case of respiratory tract lesions (bronchitis, bronchial asthma). Alveolar macrophages are large cells (2-3 times more leukocytes) of reticulohistiocytic origin. Their cytoplasm contains abundant inclusions. They may be
colorless (myelin grains), black from coal particles (dust cells) (Fig. 29) or yellow-brown from hemosiderin (heart disease cells, siderophages). Alveolar macrophages are found in small numbers in any sputum, their content increases in inflammatory diseases. Cells of heart defects (Fig. 30) are found when erythrocytes enter the alveolar cavity (with stagnation in the pulmonary circulation, especially with mitral stenosis, pulmonary infarction, as well as with croupous pneumonia and hemosiderosis). For more reliable
Their definitions put the so-called reaction to Prussian blue: a little sputum is placed on a glass slide, 1-2 drops of a 5% solution of yellow blood salt are poured, after 2-3 minutes - the same amount of 2% hydrochloric acid solution, mixed and covered with a cover glass. After a few minutes, the hemosiderin grains turn out to be blue.
Malignant tumor cells often end up in sputum, especially if the tumor grows endobronchially or disintegrates. In the native preparation, these cells are distinguished by their atypism: they are mostly large, have an ugly shape, a large nucleus, and sometimes several nuclei. In chronic inflammatory processes in the bronchi, the epithelium lining them, metaplastic, acquires atypical features and may resemble tumor cells. Therefore, it is possible to define cells as tumor cells only if complexes of atypical and, moreover, polymorphic cells are found, especially if they are located on a fibrous base or together with elastic fibers.
Elastic fibers (Fig. 31) appear in sputum during the breakdown of lung tissue: tuberculosis, cancer, abscess. Elastic fibers have the form of thin double-circuit filaments of the same thickness throughout, dichotomously branching. They are often found in ring-shaped bundles that retain their alveolar location. Since these fibers are not found in every drop of sputum, to facilitate the search, they resort to their concentration. For this purpose, an equal or double amount of 10% caustic alkali solution is added to several milliliters of sputum and heated until the mucus dissolves. In this case, all the formed elements of sputum dissolve, except for elastic fibers. After cooling, the liquid is ntrifuged, adding 3-5 drops of a 1% alcohol solution of eosin to it, the precipitate is microscoped. Elastic fibers retain the character described above and stand out well with a bright red color. Actinomycetes are searched for by choosing small dense yellowish grains from sputum - druses. In a druse, crushed under a cover glass in a drop of glycerin or alkali, under a microscope, the central part, consisting of a mycelium plexus, and the surrounding zone of radiant flask-shaped formations are visible. When the crushed drusen is stained according to Gram, the mycelium becomes purple, and the cones become pink. Of the other fungi found in sputum, the most important is Candida albicans, which affects the lungs with prolonged antibiotic treatment and in very weak people. In the native preparation, budding yeast-like cells and branched mycelium are found, on which spores are arranged in whorls. From crystals in sputum, Charcot-Leiden crystals are found: colorless octahedra of various sizes, resembling a compass needle in shape. They consist of a protein released during the breakdown of eosinophils, therefore they are found in sputum containing many eosinophils, and more of them in stale sputum. After pulmonary bleeding, if blood is not immediately released with sputum, hematoidin crystals can be found - rhombic or needle-like formations of a yellow-brown color.
Microscopy of stained preparations. Produced to study the microbial flora of sputum and some of its cells. Of these, the most important is the determination of the cells of malignant tumors. For this purpose, a smear from a suspicious material found in a native preparation, made with care so as not to crush cells, is fixed in methanol or Nikiforov's mixture and stained according to Romanovsky-Giemsa (or other differential stain). Opulent cells are characterized by polymorphism in size and shape, the presence of individual very large cells, large, often hyperchromic and along with them hypochromic nuclei, sometimes multiple, irregular in shape with large nucleoli; homogeneous, sometimes vacuolated cytoplasm in some of the cells is sharply basophilic; figures of mitosis are not uncommon. The most convincing are the complexes of polymorphic cells of this nature. To recognize eosinophilic leukocytes, a smear stained according to Romanovsky-Giemsa or sequentially with 1% eosin solution (2-3 min) and 0.2% methylene blue solution (V2-1 min) is suitable. Single eosinophils can be found in any sputum: in large numbers (up to 50-90% of all leukocytes), they are found in bronchial asthma, eosinophilic infiltrates, helminthic invasions of the lungs, etc.
Bacterioscopic examination... For this test, smears are prepared by rubbing a lump of phlegm between two glass slides. The dried smear is fixed by slowly passing it 3 times through the flame of a gas burner, and stained: for the search for mycobacterium tuberculosis according to Ziehl-Nielsen, in other cases - according to Gram. Stain according to Ziehl-Nielsen. A piece of filter paper, equal in area, is applied to a fixed smear, Tsil's carbolic fuchsin is poured onto it and heated over a low flame until vapors appear. Then the paper is removed, the preparation is washed with water and dipped for discoloration in a 3% solution of hydrochloric acid in 9 ° alcohol (or in a 5-10% sulfuric acid solution), washed well again with water, painted over for 1 / 2-1 min 0.5 % methylene blue solution and washed with water. Acid-resistant bacteria firmly retain the adopted color: they do not discolor and remain red against the blue background of the other elements of sputum, discolored in acid and acquiring an additional color.
In cases where during bacterioscopy due to the small number of mycobacteria of tuberculosis (Fig. 32) it is not possible to detect them, they resort to a number of additional studies. So, in luminescence microscopy, a smear made in the usual way and fixed is stained with a luminescent dye (rhodamine, acridine orange), and then with another dye (acid fuchsin, methylene blue), which quenches the background luminescence. In the ultraviolet light of a fluorescent microscope, mycobacteria glow so brightly that they can be seen using a dry lens (40x), covering a much larger field of view than an immersion one. Methods
accumulations allow concentrating mycobacterium tuberculosis. The most widely used method is flotation, in which sputum homogenized with alkali is shaken with toluene, xylene or gasoline, the smallest drops of which, floating up, capture mycobacteria. The settled creamy hydrocarbon layer is sucked off with a pipette and applied drop by drop onto the heated glass at the same place. After drying, the preparation is fixed and stained according to Ziehl-Nielsen. Another method of accumulation is electrophoresis: when a direct current passes through the liquefied sputum, mycobacteria of tuberculosis rush to the cathode, from the surface of which smears are made and stained according to Ziehl-Nielsen. Oaska by Gram. A strip of filter paper is placed on a smear fixed on a fire, on which pouring
Gentian violet carbolic solution. After 1-2 minutes, the paper is discarded, a smear is poured for 2 minutes
Lugol's solution, then it is poured off and the preparation is immersed in 96 ° alcohol for 7 g-1 min (until the dye ceases to leave), washed with water and painted over for 1 min with a solution of carbolic fuchsin diluted 10 times.
In a Gram-stained preparation, a number of microorganisms can be differentiated: gram-positive capsular pneumococcus, streptococcus and staphylococcus, gram-negative Klebsiella (capsular diplobacillus Friedlander), small Pfeiffer's bacillus, etc. (Fig. 33). All these mi-
small amounts of microorganisms are present in the respiratory tract of healthy people and only under unfavorable conditions for the body can they become pathogenic and cause pneumonia, lung abscess, bronchitis, etc. In these cases, they are found in sputum in large quantities.
Bacteriological examination(sowing sputum on nutrient media). Used when bacterioscopic examination does not detect the suspected pathogen. Bacteriological research allows you to identify the type of microbes, determine their virulence and drug resistance, which is necessary for the correct selection of medications. Finally, in some cases, when it is not possible to detect the pathogen by simpler methods, the sputum obtained from the patient is infected with experimental animals.
Pleural fluid examination... In the pleural cavity of a healthy person, there is a small amount of fluid similar in composition to lymph, which facilitates the sliding of the pleural sheets during breathing. The volume of pleural fluid can increase (effusion) both in violation of blood and lymph circulation in the lungs - non-inflammatory effusion, or transudate, and in inflammatory changes in the pleura - exudate. Exudate can be clinically caused by a primary infection of the pleura or be concomitant with some common infections and with a number of diseases of the lungs and mediastinum (rheumatism, heart attack, lung cancer and tuberculosis, lymphogranulomatosis, etc.). The study of pleural fluid is carried out for the following purposes: 1)
determining its nature (transudate, exudate, pus, blood, chyle fluid); 2) studying the cellular composition of the fluid, giving information about the nature of the pathological process, and sometimes (when finding tumor cells) - about the diagnosis; 3) detection in case of infectious nature of the lesion of the pathogen and determination of its sensitivity to antibiotics. Analysis
pleural fluid consists of macroscopic, physicochemical, microscopic and, in some cases, microbiological and biological studies.
Macroscopic examination. The appearance of the pleural fluid depends mainly on its cellular and partly on the chemical composition. There are effusions serous, serous-fibrinous, fibrinous, serous-purulent, purulent, putrid, hemorrhagic, chyle and chyle-like.
Transudate and serous exudate are transparent or slightly opalescent. Clouding of exudate is caused by an abundance of leukocytes (serous-purulent and purulent exudate), erythrocytes (hemorrhagic exudate), fat droplets (chyle exudate), cellular detritus (chyle-like exudate). The character of the cells is recognized by microscopy. The chylous nature of the exudate is determined by the test with ether - when it is added, the turbidity disappears. Such an effusion is
caught by lymph congestion or destruction of the thoracic lymphatic duct by a tumor or injury. The exudate takes a chyle-like appearance during fatty degeneration of cells contained in abundant quantities. In both cases, the fat is stained with Sudan III. The color of the transudate is pale yellow, serous exudate - from pale to golden yellow, with jaundice - to deep yellow. Purulent exudate is grayish-whitish, greenish-yellow, with an admixture of blood - with a red tint or, more often, brownish-gray; putrid exudate has the same color. Hemorrhagic effusion, depending on the amount of blood and the duration of its presence in the pleura, can have different shades: from pink to dark red and brown. With hemolysis, the effusion becomes lacquered. Chylous exudate is like diluted milk.
The consistency of the transudate and exudate is usually liquid in most cases. Purulent exudate is thick, creamy, sometimes with difficulty passes through the puncture needle. Pus from the old encapsulated empyema can be puree, crumbly, with flakes of fibrin.
The smell (unpleasant, fetid) is possessed only by the putrid exudate observed with gangrene of the lung. This smell is due to the breakdown of protein produced by enzymes of the anaerobic flora.
General blood analysis
Hemoglobin (Hb) is a blood pigment and the main respiratory protein in the blood that transports oxygen to organs and tissues.
Hemoglobin is normal:
For men - 130–160 g / l;
In women, it is 120–140 g / l.
A decrease in the concentration of Hb in the blood indicates anemia of one degree or another (a drop in its concentration to 40 g / l requires urgent measures, and the minimum content of Hb, at which a person's life continues, is 10 g / l).
Erythrocytes are normal:
For men: from 4.5 · 1012 to 5.3 · 1012 / l (or 4.5–5.3 T / l);
In women: from 3.8 · 1012 to 5.1 · 1012 / l (or 3.8-5.1 t / l).
A decrease in the number of erythrocytes below 3.5 G / l characterizes the development of anemia syndrome. The presence of aniso- and poikilocytosis indicates destructive disorders in erythrocytes. In healthy people, erythrocyte diameters range from 5 to 9 microns, with an average of 7.2 microns. The erythrocytometric curve (Price-Jones curve) is a graph of the distribution of erythrocytes along their diameter, where the abscissa represents the erythrocyte diameters (μm), and the ordinate represents the percentage of erythrocytes of the corresponding size.
Anisochromia - a change in the color of red blood cells - depends on the hemoglobin content in them. Polychromasia - the simultaneous perception of acidic and basic colors by erythrocytes - indicates enhanced blood regeneration. A certain diagnostic value has a change in the properties of erythrocytes to resist various destructive influences - osmotic, thermal, mechanical.
Reticulocytes are young forms of erythrocytes that retain granularity (remnants of the basophilic substance of the cytoplasm). In healthy people, it is normal - 0.5-1% of reticulocytes.
The color index (CP) depends on the volume of erythrocytes and the degree of their saturation with hemoglobin. Normal - 0.8-1.1. The color indicator is important for judging normo-, hypo- or hyperchromia of erythrocytes.
Leukocytes - from 4.5 · 109 to 8.1 · 109 / L (or 4.5–8.1 G / L). A decrease in the number of leukocytes below 4.0 G / L characterizes the development of leukopenia syndrome, and an increase above 9.0 G / L characterizes the syndrome of leukocytosis (Table 1.3).
The erythrocyte sedimentation rate (ESR) is not a specific indicator for any disease, since it depends on the qualitative and quantitative changes in blood plasma proteins, the amount of bile acids and pigments in the blood, the state of acid-base balance, blood viscosity and the number of red blood cells.
Normal ESR (micro-method modified by T.P. Panchenkov):
For men: 2-10 mm / h;
For women: 2-15 mm / h.
An increase in ESR is detected in various inflammatory processes, intoxications, acute and chronic infections, with myocardial infarction, tumors, after blood loss and surgical interventions. A particularly pronounced increase in ESR is observed in hemoblastosis (myeloma, Waldenstrom's disease, etc.), malignant neoplasms, chronic active hepatitis, liver cirrhosis, tuberculosis, amyloidosis, collagenoses.
A decrease in ESR is observed with erythremia and symptomatic erythrocytosis, viral hepatitis, obstructive jaundice, hyperproteinemia, intake of salicylates, calcium chloride.
Platelets are platelets that provide primary hemostasis, as well as activating plasma coagulation factors, which have antiheparin and antifibrinolytic activity.
Platelets are normal: 200 · 109-400 · 109 / l (200-400) · 109 / l
Anemia, or anemia, is a group of diseases characterized by a decrease in the content of Hb or Hb and the number of erythrocytes per unit of blood volume (Table 1.4). Leukemias (leukemias) - tumor systemic blood diseases occurring with damage to the bone marrow (Table 1.5).
Pigment Metabolism Study Evaluation
Bilirubin is a pigment formed during the oxidative breakdown of hemoglobin and other chromoproteins in the RES. Before entering the liver, bilirubin formed after the breakdown of heme is combined with a protein, therefore it gives an indirect reaction with a diazo-reactive (it needs to be preheated) - hence the name - indirect:
Unconjugated - unbound bilirubin. In the liver, bilirubin binds to glucuronic acid, and since this bond is fragile, the reaction with the diazo reactive is direct (direct - bound - conjugated bilirubin).
The normal content of total bilirubin in serum is from 5.13 to 20.5 μmol / l, of which 75-80% is accounted for by indirect (unconjugated) bilirubin. Jaundice is visualized when the bilirubin level is above 34.2 μmol / L.
Increase in the level of bilirubin in the blood:
Damage to the liver parenchyma (infections, toxins, alcohol, medicines);
Increased hemolysis of erythrocytes;
Violation of the outflow of bile from the biliary tract into the intestines;
Loss of an enzyme link providing biosynthesis of bilirubin glucuronide.
Table 1.3
Norms of absolute and relative (percentage) content of certain types of leukocytes (table unchanged)
Table 1.4
Peripheral blood picture for anemia (table unchanged)
Table 1.5
Peripheral blood picture in leukemia
|
Disease: |
Indicators: |
|
undifferentiated |
The number of leukocytes varies widely - from leukopenia to leukocytosis, always blastemia (the appearance of blast cells in the peripheral blood or the content of blasts more than 5% in the bone marrow). Characterized by leukemic failure (the absence of intermediate maturing forms in the leukocyte formula. Normochromic or hyperchromic anemia, erythrocytes (1.0-1.5) · 1012 / l; macroanisocytosis of erythrocytes; Нb reduced to 20-60 g / l. Thrombocytopenia (up to critical level). |
|
Chronic lymphocytic leukemia |
A pronounced leukocytosis with an absolute predominance of lymphocytes (80–95%) is possible, mostly small and medium, but there may be prolymphocytes and lymphoblasts. Shadows of Botkin-Gumprecht (incompetent lymphocytes crushed during the preparation of a blood smear). Anemia is characteristic of an exacerbation of the disease |
|
Chronic myeloid leukemia |
The number of leukocytes can range from aleukemic and subleukemic parameters to the sharpest hyperleukocytosis. In the leukocyte formula, a shift of granulopoiesis to metamyelocytes, myelocytes, promyelocytes and myeloblasts. There are all transitional forms of the granular row (there is no leukemic gap). A combined increase in eosinophils and basophils (eosinophilic-basophilic association) is one of the diagnostic signs of the initial stage of leukemia. Platelet count initially rises, but then decreases |
|
Polycythemia true (erythremia, Vakez disease) |
Pancytosis is an increase in red blood counts in combination with neutrophilic leukocytosis and thrombocytosis. Increase in hemoglobin content - from 180 to 260 g / l |
The study of bilirubin fractions is important for the differential diagnosis of parenchymal, obstructive and hemolytic jaundice. In hepatic jaundice (hepatitis, cirrhosis), two fractions of bilirubin are detected in the blood, usually with a sharp predominance of direct. Significant indirect hyperbilirubinemia in parenchymal jaundice (over 34.2 μmol / l) indicates severe liver damage with impaired glucuronization processes and is a poor prognostic sign. In obstructive jaundice, hyperbilirubinemia is mainly due to the direct fraction, however, in severe forms of congestive jaundice, the content of indirect bilirubin also increases.
With hemolytic jaundice - a sharp increase in indirect bilirubin due to its increased formation during hemolysis.
Blood proteins
The normal content of total blood protein is 60–80 g / l.
Hypoproteinemia (a decrease in the total amount of protein) occurs due to:
Insufficient protein intake (starvation);
Increased protein loss (with kidney disease, blood loss, neoplasms);
Protein synthesis disorders (liver disease).
Hyperproteinemia (increased total protein) occurs due to:
Dehydration (trauma, burns, cholera);
Paraproteinemia (multiple myeloma, Waldenstram's disease).
Proteins are divided into fractions by electrophoresis:
Albumin (normal 50–70%) - hypoalbuminemia and hyperalbuminemia due to the same reasons as hypo- and hyperproteinemia.
Globulins (normally 11–21%) are proteins of the acute phase, reflecting the intensity of inflammatory processes.
The main proteins of the acute phase are C-reactive protein, 1-glycoprotein, ceruloplasmin, haptoglobin.
Globulinemia is observed in chronic inflammatory diseases, tumors and their metastasis, trauma, heart attacks, rheumatism.
Globulins (normally 8–18%) increase in hyperlipoproteinemia (atherosclerosis, diabetes mellitus, hypothyroidism, nephrotic syndrome);
Globulins (normally 15-25%) increase due to the production of antibodies after an infectious disease, as well as in conditions leading to the depletion of the immune system: allergies, chronic inflammatory diseases, tumors and their metastasis, long-term therapy with steroid hormones, AIDS.
C-reactive protein (CRP) is an acute phase protein that is a product of tissue breakdown in various inflammatory and necrotic processes. In healthy people, the reaction to CRP is negative. The reaction is positive for rheumatism, septic endocarditis, myocardial infarction, diffuse connective tissue diseases, systemic vasculitis, tuberculosis, cancer, peritonitis, multiple myeloma.
Rheumatoid factor (RF) is an antibody that can belong to the IgM or IgG class (as an exception, to the IgA class). The reaction is positive in rheumatism, infectious nonspecific polyarthritis, rheumatoid arthritis, systemic lupus erythematosus, periarteritis nodosa, liver cirrhosis, subacute infective endocarditis.
Fibrinogen (Plasma Factor 1) - is synthesized in the liver. Normal plasma concentration (by the method of R.A. Rutberg) is 5.9–11.7 μmol / l.
Decreased fibrinogen - liver failure, increased fibrin formation when fibrinolytic substances enter the bloodstream (amniotic fluid embolism, snake bite), with cachexia, B12- (folic) deficiency anemia, erythremia, severe toxicosis, shock. An increase in fibrinogen is observed in myocardial infarction, acute infections, diffuse connective tissue diseases, burns, and multiple myeloma.
Residual nitrogen
These are nitrogen compounds that remain in the blood after protein precipitation.
Normal values: 14.3-28.6 mmol / L. Increase in residual nitrogen content:
Retention (in case of impaired renal function in chronic glomerulonephritis, pyelonephritis, urolithiasis (Urolithiasis), benign prostatic hyperplasia);
Production (associated with increased formation of nitrogenous toxins during fever and the decay of tumors).
Reduced residual nitrogen content:
With severe liver failure or liver necrosis.
Blood urea - 50% residual nitrogen; formed in the liver from ammonia and carbon dioxide.
Normal values:
Children under 14 years old - 1.8–6.4 mmol / l;
Adults under 60 years old - 3.5–8.3 mmol / l;
Adults over 60 years old - 2.9-7.5 mmol / l.
An increase in urea is the main sign of kidney failure, but it happens with increased protein breakdown and fluid loss.
Decrease in urea - with liver diseases due to impaired synthesis of urea, with drug poisoning, low-protein diet. Blood creatinine - 7.5% of residual nitrogen; synthesized in the liver, kidneys, pancreas and transported to muscle tissue. Normal serum creatinine values are 50–115 µmol / L, but significant age-related variations should be kept in mind.
The concentration of creatinine in the blood is a fairly constant value, therefore, endogenous creatinine clearance is used to assess glomerular filtration. An increase in creatinine content occurs when:
Acute and chronic renal failure;
Urolithiasis.
Uric acid is the end product of the breakdown of purine bases.
Normal values:
In men - 214–458 μmol / l;
In women - 149–404 µmol / L.
Hyperuricemia (increased uric acid content) occurs when:
Gout;
Leukemia, B 12 deficiency anemias;
Polycythemia;
Acute infections;
Liver disease;
Severe form of diabetes mellitus;
Psoriasis, eczema;
Kidney disease;
Long-term therapy with non-steroidal and steroidal anti-inflammatory drugs.
Blood glucose is the main indicator of carbohydrate metabolism.
Normal fasting glucose values:
Plasma - 3.3 - 5.5 mmol / l;
Capillary whole blood - 3.88–5.55 mmol / l.
Hypoglycemia (a decrease in glucose below 3.3 mmol / l in adults) occurs when:
Prolonged fasting;
Malabsorption, liver failure;
Violation of the secretion of counterinsular hormones (hypopituitarism, chronic insufficiency of the adrenal cortex);
Hypothyroidism;
Stroke;
Overdose of insulin and oral diabetic drugs;
Violation of the diet in patients with diabetes mellitus;
Insulinoma.
Hyperglycemia (an increase in glucose above 6 mmol / l in adults) occurs when:
Physiological conditions (alimentary, emotional);
Diabetes mellitus (subject to an empty stomach content of 7 mmol / l or more and daily fluctuations after a meal up to 11 mmol / l); if diabetes mellitus is suspected and in risk groups, a glucose tolerance oral test is performed;
Hyperthyroidism;
Adrenocorticism;
Hypopituitarism.
State budgetary educational institution
higher professional education
"Omsk State Medical Academy"
Ministry of Health of the Russian Federation
Department of Propedeutics 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 54.13-4y73
This tutorial presents laboratory and instrumental methods for diagnosing diseases of the gastrointestinal tract, outlines their diagnostic capabilities. The material is presented in a simple accessible form. The manual contains 39 figures, 3 tables, which will facilitate the assimilation of the material during independent work. The proposed study guide supplements the textbook on internal medicine propaedeutics. The presented test tasks are aimed at consolidating 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 Business.
Foreword
List of abbreviations
Chapter 2. Data of instrumental research methods in diseases of the gastrointestinal tract
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 (radiography) of the esophagus and stomach
2.2. Computed tomography and multispiral computed tomography of the abdominal organs
2.3. Plain X-ray of the abdominal organs and examination of the passage of barium through the intestine
2.4. Irrigoscopy
3. Ultrasonic research methods
3.1. Ultrasound of the stomach
3.2. Intestinal ultrasound (endorectal ultrasonography)
4. Methods of functional diagnostics
4.2. Study of gastric secretion - aspiration-titration method (fractional study of gastric secretion using a thin probe)
Self-study tests
Bibliography
Foreword
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 pathology of the digestive system 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 extremely important in the diagnosis of gastrointestinal diseases. path, as they often proceed 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 course of the disease, monitoring the effectiveness of treatment and prognosis.
This tutorial 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 the traditional, firmly established research, new modern methods of 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, study of blood serum using the GastroPanel, method diagnostics of stomach cancer using a serum tumor marker, modern methods for diagnosing Helicobacter pylori infection, capsule endoscopy, computed tomography and multispiral 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-linked immunosorbent assay, which have taken a firm place on the diagnostic platform and allow screening, monitoring of certain pathologies and solving complex clinical problems.
Scatological research has not yet lost its significance in assessing the digestive capacity of the organs of the digestive system, for the selection of adequate enzyme replacement therapy. This method is easy to perform, does not require large material costs and special laboratory equipment, and is available in every medical institution. In addition, this manual details the main scatological syndromes.
For a better understanding of the diagnostic capabilities of laboratory and instrumental research methods and the interpretation of the results obtained, 39 figures and 3 tables are presented in the textbook. In the final part of the manual, test tasks for self-preparation are given.
List of abbreviations
| TANK | - blood chemistry |
| BDS | - large duodenal papilla |
| KDP | - duodenum |
| ZhVP | - biliary tract |
| ZhKB | - cholelithiasis |
| Gastrointestinal tract | - gastrointestinal tract |
| ELISA | - linked immunosorbent assay |
| CT scan | - CT scan |
| MSCT | - multispiral computed tomography |
| OAK | - general blood analysis |
| OAM | - general urine analysis |
| OBP | - abdominal organs |
| n / a | - line of sight |
| PCR | - polymerase chain reaction |
| burn | - gastric mucosa |
| soe | - erythrocyte sedimentation rate |
| Tf | - transferrin in feces |
| Ultrasound | - ultrasound procedure |
| FEGDS | - fibroesophagogastroduodenoscopy |
| HP | - Helicobacter pylori |
| Hb | - hemoglobin in feces |
| HC1 | - hydrochloric acid |
Chapter 1. Data of 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. The study of feces for eggs of worms and cysts of protozoa:
2. Special research methods
2.1. Stool research methods
2.1.1. Coprological examination (coprogram)
| Coprogram indicators | Coprogram indicators are normal | Changes in coprogram indicators in gastrointestinal diseases |
| Macroscopic examination | ||
| Feces | 100-200 g per day. With the predominance of protein food in the diet, the amount of feces decreases, plant food - increases. 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 - polyfeces) is typical for diarrhea. - A small amount of stool (less than 100 g per day) is characteristic of constipation. |
| Stool consistency | Moderately dense (rather dense) | - Dense consistency - with persistent constipation due to excessive absorption of water - Liquid or mushy consistency of feces - with increased peristalsis (due to insufficient absorption of water) or with abundant release of inflammatory exudate and mucus by the intestinal wall - Oily consistency - in the presence of a large amount of neutral fat (for example, in chronic pancreatitis with exocrine insufficiency) - Foamy consistency - with increased fermentation processes in the colon and the formation of a large amount of carbon dioxide |
| The shape of the feces | Cylindrical | - The form of feces in the form of "large lumps" - with prolonged stay of feces in the colon (hypomotor dysfunction of the colon in people with a sedentary lifestyle or do not use rough food, as well as in colon cancer, diverticular disease) - The shape in the form of small lumps - "sheep feces" indicates a spastic state of the intestine, during fasting, gastric ulcer and duodenal ulcer, reflex nature after appendectomy, with hemorrhoids, anal fissure - Ribbon-like or "pencil" shape - for diseases accompanied by stenosis or severe and prolonged spasm of the rectum, for tumors of the rectum - Unformed feces - maldigestion and malabsorption syndrome The Bristol Stool Scale (Fig. 1) is a medical classification of human stool forms developed by Meyers Hayton at the University of Bristol, published in 1997. Type 1 and 2 characterize constipation Types 3 and 4 - Normal Stools Type 5, 6 and 7 - diarrhea |
| Smell | Fecal (normal) | - Prolonged 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, valerian) - Increased decay processes (putrefactive dyspepsia, disintegration of intestinal tumors) cause a fetid odor as a result of the formation of hydrogen sulfide and methyl mercaptan |
| Colour | Brown (when eating dairy food - a yellowish brown color, meat - dark brown). Taking plant foods and some medications can change the color of feces (beets - reddish; blueberries, black currants, blackberries, coffee, cocoa - dark brown; bismuth, iron stains feces 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 bilirubin secretion, the flow of bile into the intestine stops or decreases, which leads to discoloration of feces, it becomes grayish-white, clayey (acholic feces) - With 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 colon and rectum (tumor, ulcers, hemorrhoids), depending on the degree of bleeding, the feces have a more or less pronounced red color - In cholera, intestinal discharge is a gray inflammatory exudate with flakes of fibrin 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 of deep pink or red color |
| Slime | Absent (or scarce) | - When the distal colon (especially the rectum) is affected, mucus is in the form of lumps, strands, ribbons or vitreous mass - With enteritis, mucus is soft, viscous, mixing with feces, gives it a jelly-like appearance - The mucus that covers the formed feces from the outside in the form of thin lumps, occurs with constipation and with inflammation of the large intestine |
| Blood | Absent | - When bleeding from the distal colon, the blood is located in the form of streaks, clumps and clots on the formed feces - Red blood occurs when bleeding from the lower parts of the sigmoid and rectum (hemorrhoids, fissures, ulcers, tumors) - Altered blood from the upper digestive system (esophagus, stomach, duodenum), mixing with feces, stains it black ("tarry" feces, melena) - Blood in the feces can be found 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 feces is determined with severe inflammation and ulceration of the mucous membrane of the colon (ulcerative colitis, dysentery, disintegration of intestinal tumors, intestinal tuberculosis) often together with blood and mucus - Pus in large quantities without mucus is observed when paraintestinal abscesses are opened |
| Remains of undigested food (lientorea) | Absent | Severe failure 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 with the activation of the iodophilic flora, which forms carbon dioxide and organic acids (fermentative dyspepsia) - An alkaline reaction (pH 8.0-10.0) takes place with enhanced processes of decay of proteins in the colon, activation of the putrefactive flora that forms ammonia (putrefactive dyspepsia) |
| Blood reaction (Gregersen reaction) | Negative | A positive blood reaction 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 decay stage) |
| Stercobilin reaction | Positive | - The absence or a 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, its compression by a tumor, strictures, 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 the feces occurs with massive hemolysis of erythrocytes (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 the recovery of bilirubin into stercobilinogen, and then into stercobilin | The detection of unchanged bilirubin in the feces of an adult indicates a violation of the process of recovery of bilirubin in the intestine under the influence of the microbial flora. Bilirubin can appear with rapid evacuation of food (a 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 detect a latent inflammatory process. Detection of soluble protein in feces indicates inflammation of the intestinal mucosa (ulcerative colitis, Crohn's disease) |
Microscopic examination |
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| Muscle fibers: Striated (unchanged, undigested) | Absent Absent (or single in the field of view) | A large number of altered and unchanged muscle fibers in the feces ( Torheatorrhea) indicates a violation of proteolysis (protein digestion): - in conditions accompanied by achlorhydria (absence of HCl freedoms in gastric juice) and achilia (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 intestine - in case of violation of the exocrine function of the pancreas - with putrid dyspepsia |
| Connective tissue (remnants of undigested vessels, ligaments, fascia, cartilage) | Absent | The presence of connective tissue in the feces indicates a lack of proteolytic enzymes of the stomach and is observed with hypo- and achlorhydria, achilia |
| Fat neutral Fatty acid Fatty acid salts (soaps) | Absent or meager number fatty salts acids | Impaired digestion of fats and the appearance in the feces of large amounts of neutral fat, fatty acids and soaps is called Steatorrhea. - with a decrease in lipase activity (exocrine pancreatic insufficiency, mechanical obstruction to the outflow of pancreatic juice), steatorrhea is represented by neutral fat. - in case of violation of the flow of bile into the duodenum (violation of the process of emulsification of fat in the small intestine) and in violation of absorption of fatty acids in the small intestine, fatty acids or salts of fatty acids (soap) are found in the feces |
| Vegetable fiber (digestible) is found in the pulp of vegetables, fruits, legumes and grains. Indigestible fiber (peel of fruits and vegetables, hairs of plants, epidermis of cereals) has no diagnostic value, since there are no enzymes in the human digestive system that break down it | Single cells in f / s | It is found in large quantities with the rapid evacuation of food from the stomach, achlorhydria, achilia, with the syndrome of bacterial overgrowth in the colon (a pronounced decrease in normal microflora and an increase in pathogenic microflora in the colon) |
| Starch | Absent (or single starch cells) | The presence of a large amount of starch in the feces is called amilorrhea and is observed more often with increased intestinal peristalsis, fermentative dyspepsia, less often - with exocrine insufficiency of pancreatic digestion |
| Iodophilic microflora (clostridia) | Single in rare f / s (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 are regarded as fermentative dysbiosis. |
| Epithelium | Absent or single cells of columnar epithelium in the field of view | A large number of columnar epithelium in feces is observed in acute and chronic colitis of various etiologies |
| Leukocytes | There are no or single neutrophils in the field of view | A large number of leukocytes (usually neutrophils) is observed in acute and chronic enteritis and colitis of various etiologies, ulcerative necrotic lesions of the intestinal mucosa, intestinal tuberculosis, dysentery |
| Erythrocytes | Absent | - the appearance of little changed erythrocytes in the feces indicates the presence of bleeding from the large intestine, mainly from its distal parts (ulceration of the mucous membrane, disintegrating tumor of the rectum and sigmoid colon, cracks in the anus, hemorrhoids) - with bleeding from the proximal colon, erythrocytes are destroyed and not detected by microscopy - a large number of red blood cells in combination with leukocytes and columnar epithelium is characteristic of necrotic ulcerative lesions of the colon mucosa (ulcerative colitis, Crohn's disease with colon lesions), polyposis and malignant neoplasms of the colon |
| Worm eggs | Absent | Eggs of roundworm, broad tapeworm, etc. indicate the corresponding helminthic invasion |
| Pathogenic protozoa | Absent | Cysts of dysentery amoeba, lamblia, etc. indicate the corresponding invasion of protozoa |
| Yeast cells | Absent | Found in feces during treatment with antibiotics and corticosteroids. Identification of the fungus Candida albicans is carried out by sowing 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 food, normally HCl of gastric juice dissolves to form calcium chloride. Crystal detection is a sign of achlorhydria |
| Crystals of triple phosphates (phosphate ammonia-magnesia) | Absent | It is formed in the colon during the breakdown of lecithin, nuclein and other products of protein putrefaction. Crystals of triple phosphates found in feces (pH 8.5-10.0) immediately after defecation indicate increased putrefaction in the colon |
Scatological syndromes
Insufficient chewing syndrome
The syndrome of insufficient chewing reveals the insufficiency of the act of chewing food (detection of food particles in the feces that are visible to the naked eye).
Causes of insufficient chewing syndrome:
- lack of molars
- multiple dental caries with their destruction
Syndrome of insufficiency of digestion in the stomach (gastrogenic scatological syndrome)
Gastrogenic scatological syndrome develops as a result of a violation of the formation of hydrochloric acid and pepsinogen in the coolant.
Causes of gastrogenic scatological syndrome:
- atrophic gastritis
- stomach cancer
- conditions after gastric resection
- erosion in the stomach
- stomach ulcer
- Zollinger-Ellison syndrome
The presence of digestible fiber in the feces is an indicator of a decrease in the amount of free HCl and a violation of gastric digestion. During normal gastric digestion, the digestible fiber is macerated (softened) by the free HCl of the gastric juice and becomes available for the enzymes of the pancreas and intestines and is not found in feces.
Pancreatic digestion insufficiency syndrome (pancreatogenic scatological syndrome)
A true indicator of pancreatic digestion failure is the appearance of neutral fat in the stool (steatorrhea), since lipases do not hydrolyze fats.
There are muscle fibers without striations (creatorrhea), the presence of starch is possible, polyfecalia is characteristic; soft, ointment consistency; unformed feces; color gray; pungent, offensive odor, positive reaction to stercobilin.
Causes of pancreatogenic coprological syndrome:
- chronic pancreatitis with exocrine insufficiency
- pancreas cancer
- conditions after resection of the pancreas
- cystic fibrosis with exocrine pancreatic insufficiency
Syndrome of insufficiency of bile secretion (hypo- or acholia) or hepatogenous scatological syndrome
Hepathogenic scatological syndrome develops due to the absence of bile ( acholia) or its insufficient receipt ( hypocholia) in the KDP. As a result, bile acids, which 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 peristalsis, stimulated by bile and its bactericidal effect, also decreases.
The surface of the feces becomes dull, granular due to the increased content of fat droplets, the consistency is ointment, grayish-white, the reaction to stercobilin is negative.
Microscopic examination: a large amount of fatty acids and their salts (soaps) - products of incomplete breakdown.
Causes of hepatogenic coprological syndrome:
- diseases of the gastrointestinal tract (gallstones, obstruction of the common bile duct with a stone (choledocholithiasis), compression of the common bile duct and OBD by a tumor of the pancreatic head, pronounced strictures, stenosis of the common bile duct)
- liver diseases (acute and chronic hepatitis, liver cirrhosis, liver cancer)
Small intestine digestive disorder (enteral scatological syndrome)
Enteral scatological syndrome develops under the influence of two factors:
- insufficiency of enzymatic activity of the secretion of the small intestine
- decreased absorption of the final products of hydrolysis of nutrients
- insufficiency of chewing syndrome gastric insufficiency
- lack of separation or flow of bile into the duodenum
- helminthic invasions 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, celiac disease
Colon digestive disorder
Causes of the syndrome of digestive disorders in the colon:
- violation of the evacuation function of the colon - constipation, spastic dyskinesia of the colon
- inflammatory bowel disease (ulcerative colitis, Crohn's disease)
- insufficiency of digestion in the colon by the type of 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), there is a decrease in the amount of feces, the consistency is liquid, the feces are unformed, there are pathological impurities: mucus, pus, blood; sharply positive reaction to blood and the Vishnyakov-Triboulet reaction; a large number of columnar epithelium, leukocytes and erythrocytes.
Lack of digestion in the large intestine by the type of fermentative and putrefactive dyspepsia:
- Fermentative dyspepsia(dysbiosis, syndrome of bacterial overgrowth in the colon) occurs due to impaired digestion of carbohydrates and is accompanied by an increase in the amount of iodophilic flora. Fermentation processes proceed with an acidic pH of the medium (4.5-6.0). Stools copious, thin, frothy with a sour odor. The mucus is mixed with the 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 persons 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 impaired, their decomposition occurs, the resulting products irritate the intestinal mucosa, increase the release of fluid and mucus. Mucus is a good breeding ground for microbial flora. With putrefactive processes, feces of a liquid consistency, dark brown, alkaline reaction with a sharp, putrid odor and a large number of muscle fibers under microscopy.
2.1.2. Bacteriological examination of feces
Bacteriological examination of feces- 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 feces culture is used to diagnose the syndrome of bacterial overgrowth in the intestine (intestinal dysbiosis), intestinal infections and monitor the effectiveness of their treatment:
- quantitative assessment of microflora (bifidobacteria 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. study of feces for occult blood (Gregersen reaction)
B. determination of transferrin (Tf) and hemoglobin (Hb) in feces
A. Study of feces for occult blood (Gregersen reaction):
Latent blood is called blood that does not change the color of feces and is not determined macro- and microscopically. The Gregersen reaction for detecting occult blood is based on the property of blood pigment to accelerate oxidative processes (chemical research).
A positive fecal occult blood reaction can be noted when:
- erosive and ulcerative lesions of the gastrointestinal tract
- tumors of the stomach, intestines in the decay stage
- invasion by helminths that injure the intestinal wall
- rupture of varicose veins of the esophagus, cardiac part of the stomach, rectum (cirrhosis of the liver)
- ingestion of blood from the oral cavity and larynx into the digestive tract
- impurities to feces of blood from hemorrhoids and cracks in the anus
B. Determination of transferrin (Tf) and hemoglobin (Hb) in feces(quantitative method (iFOB)) - detection of lesions of the intestinal mucosa. This test is far superior in sensitivity to the fecal occult blood test. Transferrin persists for a longer time than hemoglobin in feces. An increase in transferrin content indicates damage to the upper intestine, and hemoglobin - to the lower intestine. If both indicators are high, then this indicates the extent of the lesion: the higher the indicator, the greater the depth, or the 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 at 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 of persons over 40 years old (once a year)
- monitoring the state 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 family members of the first and second degree of relationship, 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 that is 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:
- identification of acute inflammatory processes in the intestine
- monitoring the activity of inflammation during treatment for inflammatory bowel diseases (Crohn's disease, ulcerative colitis)
- differential diagnosis of organic bowel diseases from functionally determined ones (for example, irritable bowel syndrome)
2.2. Study of blood serum using the "GastroPanel"
"GastroPanel" is a set of certain laboratory tests that can detect the presence of coolant atrophy, assess the risk of developing stomach cancer and peptic ulcer disease, and determine HP infection. This panel includes:
- gastrin-17 (G-17)
- pepsinogen-I (PGI)
- pepsinogen-II (PGII)
- specific antibodies - class G immunoglobulins (IgG) to Helicobacter pylori
Indicators of intragastric pH-metry are presented in table 2.
Table 2. Indicators of intragastric pH-metry
| body pH of the stomach | hyperacid state | normoacid condition | hypoacid condition | anacid condition |
| 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 |
| antrum pH | alkalinization compensation | decreased alkalizing function | alkalinization subcompensation | alkalinization decompensation |
| 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 Study
Investigation of stimulated secretion: parenteral stimulants of gastric secretion (histamine or pentagastrin - a synthetic analogue of gastrin) are currently used. So, after the study of 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 coolant parietal cells or 0.04 mg / kg of the patient's body weight - the maximum stimulation of the coolant parietal cells) or pentagastrin (6 mg / kg of patient's body weight). Gastric juice is then collected every 15 minutes. Received 4 portions within an hour make up the volume of juice in the second phase of secretion - the phase of stimulated secretion.
Physical properties of gastric juice: Normal gastric juice is practically colorless and odorless. Its yellowish or greenish color usually indicates an admixture of bile (duodenogastric reflux), and reddish or brownish - about an admixture of blood (bleeding). The appearance of an unpleasant putrefactive odor indicates a significant violation of evacuation from the stomach (pyloric stenosis) and the resulting putrefactive decay of proteins. Normal gastric juice contains only a small amount of mucus. An increase in mucus impurity indicates inflammation of the coolant, and the appearance of food residues in the received portions also indicates serious violations of gastric evacuation (pyloric stenosis).
Normal gastric secretion indices are presented in Table 3.
Table 3. Indicators of gastric secretion in norm
| Indicators | Normal values |
| Determination of clock voltage - the amount of gastric juice, produced by the stomach for an hour |
Basal secretion phase: 50-100 ml per hour - 100-150 ml per hour (submaximal stimulation with histamine) - 180-220 ml per hour (maximum stimulation with histamine) |
| Determination of the debit-hour of HCl freedoms. - the 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 stimulation with histamine) - 16-24 meq / l / hour (maximum stimulation with histamine) |
| 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. Changing the clock voltage:
- an increase in the amount of gastric juice indicates hypersecretion (erosive antral gastritis, ulcer of the antrum of the stomach or duodenum, Zollinger-Ellison syndrome) or a violation of the evacuation of food from the stomach (pylorus 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)
- normoacidny state (normoaciditas)
- hyperacid state (hyperaciditas) - an ulcer of the antrum of the stomach or duodenum, Zollinger-Ellison syndrome
- hypoacid state (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, which limit its application in practice:
- removal of gastric juice disrupts the normal working conditions of the stomach, it is of little physiological
- some of the stomach contents are inevitably removed through the pylorus
- secretion and acidity indicators do not correspond to the actual ones (as a rule, they are underestimated)
- the secretory function of the stomach increases, since the probe itself is an irritant to the glands of the stomach
- the aspiration method provokes the occurrence of duodenogastric reflux
- it is impossible to determine the night secretion and the circadian rhythm of secretion
- it is impossible to assess acid production after a meal
- varicose veins of the esophagus and stomach
- burns, diverticula, strictures, esophageal stenosis
- bleeding from the upper gastrointestinal tract (esophagus, stomach, duodenum)
- aortic aneurysm
- heart defects, heart rhythm disturbances, arterial hypertension, severe forms of coronary insufficiency
Self-study tests
Choose one or more correct answers.
1. Special laboratory tests for gastrointestinal diseases
- scatological examination
- general blood analysis
- study of blood serum using the "GastroPanel"
- bacteriological examination of feces
- 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 for bilirubin
- positive Vishnyakov-Triboulet reaction (for soluble protein)
- small amount of neutral fat on microscopy
- microscopic examination of a small amount of digested muscle fibers
- acholic feces
- "Tarry" feces
- overwhelmingly positive Gregersen reaction
- anemia
- polyfecal
- muscle fibers
- feces color
- reaction to stercobilin
- stool consistency
- reaction to bilirubin
- reaction to stercobilin
- connective tissue
- feces shape
- reaction to bilirubin
- Gregersen reaction
- the amount of feces
- neutral fat
- vegetable fiber (digestible)
- leukocytes
- erythrocytes
- achilia
- appendectomy
- hyperchlorhydria
- exocrine pancreatic insufficiency
- normal coprogram
- cholidocholithiasis
- stomach swelling
- pancreatic head tumor
- cirrhosis of the liver
- atrophic gastritis
- Gregersen reaction
- transferrin in feces
- reaction to bilirubin
- hemoglobin in feces
- reaction to stercobilin
- morphological examination of biopsies of the gastric mucosa
- radiological
- 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
- radiological
- daily
- gastrin-17
- clock voltage
- determination of IgG antibodies to Helicobacter pylori
- debit-hour free HCl
- pepsinogen-I
19. A large number of altered and unchanged muscle fibers in the 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. | creatorrhea |
| 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. Propedeutics of Internal Diseases / Ed. A.L. Grebenev. Textbook. - 5th edition, revised and enlarged. - M .: Medicine, 2001 - 592 p.
- Molostova V.V., Denisova I.A., Yurgel V.V. Scatological research in norm and pathology: teaching aid / Ed. Z.Sh. Golevtsova. - Omsk: Publishing house of OmGMA, 2008 .-- 56 p.
- Molostova V.V., Golevtsova Z.Sh. Methods for studying the acid-forming function of the stomach: teaching aid. 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 taken and what is in doubt // Archives of pathology. - 2009. - Volume 71 - №4 - P. 11-18.
- Roitberg G.E., Strutynsky A.V. Internal illnesses. Laboratory and instrumental diagnostics: textbook. - Moscow: Publishing house MEDpress-inform, 2013 .-- 816 p.
- Electronic library of OmGMA. 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 M.V. I.M.Sechenov. Access mode: www. scsml.rssi.ru
- Scientific electronic library (eLibrary). Access mode: http: // elibrary.ru
- Consilium Medicum Magazine. Access mode: www. consilium-medicum.com
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