Chemical examination of urine

Albuminuria

Protein in the urine is determined using the coagulation reaction. First, a qualitative test for the protein, and then determined the amount. To determine the presence of protein is needed to explore clear urine, therefore when turbidity should be filtered through a filter paper. If turbidity disappears, illuminate urine by adding magnesium sulfate (about 10 d of 100 ml of urine). After shaking the urine filtered again. Besides, Urine should be acidic, however alkaline urine is acidified with two or three drops of acetic acid 5-10%. Turbidity urine is detected in transmitted light on a dark background.

Qualitative tests for protein in the urine is always carried out in two tubes: control and experimental.

To carry out tests with sulfosalicylic acid is used it 15-20 % solution.

Sample Gellera (Ring) carried out with concentrated or 50 % nitric acid, but it is more advisable to use reagent Larionova.

The presence of protein in urine can be detected also by means of the sample indicator paper "AlbuFan", determination is performed according to the instructions.

For the quantitative determination of protein in urine are two methods:

• Brandberg-Roberts-STOLNIK;
• FROM 3 % sulfosalicylic acid.

The basis of the method Brandberg-Roberts-STOLNIK laid's ring experiment with breeding.

To determine the daily proteinuria was collected urine for a day, define therein a protein (biuret test) and the resulting amount of it (g / l) umnozhayut diuresis (liters).

Proteinuria is observed in many diseases. There are true, or renal, and extrarenal proteinuria.

Pochechnaya proteinuria It occurs more frequently and may be organic and functional. The cause of proteinuria is an organic structure of renal parenchymal damage.

Organic renal proteinuria characteristic of acute and chronic glomerulonephritis, nephrosis, stagnation in the kidneys, infectious and renal toxicity, as well as their anomalies, such as polycystic kidney. The highest amount of protein in the urine is observed in NS (60-80 g / l).

Functional renal proteinuria It occurs due to increased permeability of the renal filter or slow blood flow in the renal glomeruli in response to strong external stimuli. Newborn proteinuria observed relatively frequently and is caused by the presence of not yet formed functional renal filter, and, perhaps, birth trauma, or loss of fluid in the first days after birth.

Alimentarnaya proteinuria occurs by ingestion, rich in protein.

Ortostaticheskaya proteinuria diagnosed in children of preschool and school age only in a standing position, and disappear when lying down.

Zastoynaya proteinuria observed in cardiac decompensation activities, and ascites tumors in the peritoneal cavity. Prolonged stagnation of blood can cause damage to the kidneys organic, and in such cases there is an organic renal proteinuria.

Vnepochechnaya proteinuria due to the admixture of urine protein, released during inflammation in the urinary tract and genitals - cystitis, Piel, urethra, prostatitis, vulvovaginal and other diseases. Microscopic when extrarenal proteinuria revealed a large number of white blood cells and bacteria. For every 100*10³ leukocytes in 1 l urine is determined 1 g / L protein. After centrifugation or filtration in the absence of kidney disease protein is not detected in the urine.

Depending on the length renal proteinuria is divided into transient and long-term.

Transient proteinuria is observed in functional and renal toxicity. When nephritis, nephrosis and other organic lesions of the kidney there is a long proteinuria.

The qualitative composition of protein in the urine investigated by the same methods, that serum (fractionation, salting neutral salts, using electrophoresis and ultracentrifugation). The study of protein fractions of urine has diagnostic value in paraproteinemia, including multiple myeloma, and to determine the severity of kidney damage.

Protein body Ben Jones represent mikromolekulyarnye paraproteins molecular weight 45*10³, so that they can easily penetrate the intact kidney filter. The most reliable method of detection of proteins Bence-Jones multiple myeloma, Waldenstrom's disease and the other is the method of electrophoresis.

The urine can detect glucose, laktozu, fructose and other sugars.

Glucose in the urine

Glucose is stored in the urine of a healthy person in a very small quantity (0,17-0.28 Mmol / l) and is not determined by accepted clinical laboratory methods of investigation. To identify the need to examine the glucose urine svezhevypuschennoy, which can be stored in a refrigerator or, or adding a preservative (chloroform, Toluene - 0,1 100-200 ml per ml of urine, timol - 1 kristallik).

To determine glucose in urine apply qualitative and quantitative tests, most of which are based on the ability of the reducing aldehyde groups of glucose in alkaline medium to recover heavy metals. Reducing properties and others have sugar. Glucose oxidase samples, based on the oxidation of glucose glucose oxidase, are specific and sensitive.

Qualitative reactions determination of glucose in the urine sample are Gaynesa, the test paper "Glyukotest" and express- method using a preset reagents.

Quantitative determination of glucose in the urine can also be produced by several methods.

Polarimetric method for the determination of glucose It based on the ability of glucose to rotate the plane of polarized beam right. In the rotation angle determine the amount of glucose in the urine.

Determining the amount of glucose in the urine color reaction with ortotoluidinom It held as, as the determination of glucose in blood.

Colorimetric method Altgauzena. The principle of the method is, when heated urine, containing glucose with an alkali, there is a color reaction.

There is a modified method of using a medical Altgauzena colorimeter. The most specific method for determining the glucose oxidase is glucose.

Glikozuriâ It may be physiological and pathological. Physiological (alimentarnaâ) glycosuria observed when administered with food -large amounts of carbohydrates. In these cases, the level of glucose in the blood above 9,99 mmol / l, t. it is. exceeds the renal threshold of glucose reabsorption. Pathological renal glycosuria can be and extrarenal.

Renal glycosuria due to the violation of glucose reabsorption in the tubules of nephrons, wherein the blood glucose level normal or slightly reduced. It is observed in chronic nephritis, glycogenosis, acute renal failure, phloridzin poisoning and renal failure as an inherent filter.

Pathological extrarenal glycosuria often due to metabolic disorders and occurs in diabetes, less in the pathology of the pituitary gland (akromegalii, gigantizme, Cushing's syndrome), thyrotoxicosis, pigment cirrhosis, overdose of cortisone, pheochromocytoma, clear cell renal, injury of the central nervous system. In diabetes should be to determine the amount of glucose in the daily amount of urine, It is especially important for prescribing diet and treatment of these patients.

Other urine sugar rare. Galactosuria laktozuriya and found most often in children after ingestion of large amounts of these sugars from food.

Lactose urine

Lactose rotate polarized light to the right and causes the same reduction reaction, that glucose. To diagnose laktozurii can use the following methods.

Fenilozazonovaya sample It based on the, that when heated with phenylhydrazine mono- disaccharides and forms crystals - fenilozazony, shape and properties that can determine the type of sugar. The sample allows differentiation of glucose, lactose and other sugars. Fenilglyukozazony are needles, arranged as brooms and dissolved by heating. Fenillaktozazony forms crystals in the form of hedgehogs and melted by heating.

For the qualitative determination of lactose and maltose recommended sample Velyka.

In determining the angle of rotation of lactose polarimeter beam multiplied by 0,947 and its amount is obtained as a percentage.

Galactose in urine

Galactose is involved in the metabolism of carbohydrates alone after its phosphorylation in liver. In diseases of the liver galactose body is not absorbed and excreted by the kidneys.

The sample with a load of galactose It is used to study the functional state of the liver. Galactosuria can be observed in addition to liver disease in hyperthyroidism, digestive disorders galactosemia and in early childhood or congenital deficiency of galactose metabolism (sample Tollensa).

Fructose in urine

Fructose is also determined in urine polarimetric method (rotate polarized light to the left).

The obtained result is multiplied in a polarimeter for 0,54. If the fructose is present in the urine simultaneously with glucose, the rotation of the polarized beam to the left can not be found.

Fructose in urine is observed in patients with diabetes mellitus (together with glucose), metabolic disorders, ketogeksokinazy congenital deficiency and deficiency fruktozofosfataldolazy.

Ketone (acetone) body

These include acetone, acetoacetic and β-hydroxybutyric acid. Ketone bodies appear in the urine for metabolic disorders. Normally, carbohydrates, fats and proteins are broken down through the intermediate stage to atsetilkoenzima A, that is metabolized to CO₂ and H₂O. For combustion requires the presence of oxaloacetate, formed by the breakdown of carbohydrates. With a lack of carbohydrates atsetilkoenzima quantitative relationship between A and oxaloacetate broken. There is a lack of oxaloacetate. Accumulation atsetilkoenzima A and condensation of its molecules leads eventually to the formation of ketone bodies. With the prevalence of dietary fat and protein ketogenic acetyl coenzyme A accumulates to a greater extent by the relative lack of oxaloacetate and ketone bodies are formed. Carbohydrates and proteins have some influence antiketogeynym.

The urine ketone bodies appear in ketonemia. To detect them using sample Lange, LEGAL, Lestrade. The basis of these samples is their property in an alkaline medium to give a color reaction with sodium nitroprusside (formation of complex compounds reddish brown).

The urine of a healthy person contains a minimal amount of ketone bodies, are not detected by the above methods. Ketone bodies appear in severe diabetes, and fasting, fever, glycoprivous (ketogenic) diet, postoperatively, as well as glycogen storage disease, hyperinsulinism, Renal glycosuria (loss of carbohydrates), akromegalii, Cushing's disease. Ketonuria central origin is in the subarachnoid hemorrhage, traumatic brain injuries, strong excitation or stimulation of the central nervous system (ketonemicheskaya vomiting in children) , when the RVOT and pride.

Bilirubin in the urine

Bilirubin in the human body is formed by the breakdown of hemoglobin, erythrocytes in the system of mononuclear phagocytes. Due to this catabolic fractions 80-85 provides education % total bilirubin in body. The destruction of old erythrocytes hemoglobin is the main, but not the only source of bilirubin. Bilirubin can be synthesized from hemoglobin in the formation of erythrocytes in the bone marrow, the formation of excess heme towards globin, decay of young red blood cells to the degeneration of the blood, direct synthesis of bile pigments or precursors of protoporphyrin. Resulting from these sources is called bilirubin early, or hematopoietic, Faction. It is about 11% total bilirubin. This process of bilirubin increases sharply in a significantly altered erythropoiesis. So, congenital porphyria, Pernicious, sickle cell, hemorrhagic anemia, thalassemia value of early fractions reaches 40 80%.

Bilirubin may also be formed from sources negemoglobinovyh: myoglobin, catalase, peroxidase, cytochrome C in their decay, this fraction does not exceed 5 % total bilirubin.

Thus, Bilirubin is the main source of hemoglobin. Conversion of the latter to bile pigments occurs as follows. Initially, the gem of hemoglobin is oxidized to iron-complex pigment - verdogematin, wherein between I and II pyrrole rings oxidized methine group, wherein there is a rupture of the porphyrin ring to form verdohemoglobin - Green pigment. Later verdohemoglobin enzymatically cleaved into biliverdin, globin and iron. Iron is deposited in the liver in the form of hemosiderin, globin used by the body for the purposes of Plastic. Biliverdin restored in bilirubin - orange pigment, insoluble, having cytotoxic properties, especially towards the nervous tissue.

Because the cells of the mononuclear phagocyte bilirubin from the bloodstream to the liver. Transport of bilirubin, formed on the periphery, carried out in conjunction with albumin. Albumin binding capacity is quite substantial: 1 mol albumin binds 2 please bilirubin. Therefore, even if pronounced jaundice bilirubin albumin complete saturation occurs. Allowed, that only newborn and premature infants in connection with shortages of albumin binding capacity may be exhausted.

The binding and transport the bilirubin to limit the possibility of tissue penetration. The specific function of the liver is the absorption or capture of bilirubin from the blood and its further excretion through the intestine. Inside the liver cells bilirubin falls, previously freed from ties with protein. In Ca2 hepatocytes with participation of gljukuroniltransferazy enzyme occurs conjugation of bilirubin, t. it is. his connection with one or two molecules of glucuronic acid, resulting in bilirubingljukuronidy-bilirubinmonogljukuronid (BMG) and bilirubindigljukuronid (BDG). Bilirubingljukuronidy -associated, fraction of conjugated bilirubin, soluble in water. The transformation of free bilirubin in bilirubingljukuronidy is a sine qua non for their subsequent excretion in bile capillaries. Free bilirubin directly into the bile does not fall. In human bile svejesobranna detected only conjugates bilirubin. With full block mechanism of conjugation bile contains almost no bilirubin and therefore has a pale yellow colour.

Basic conjugate is BDG. Its content in bile of healthy people is more than 80 % the total number of bile pigments. It is believed, that education BDG occurs mainly in the liver, and BMG can be synthesized outside of the liver (in the cells of the mononuclear phagocytes other bodies system).

Formation of conjugates bilirubin with glukuronova acid improves the solubility and maintenance from the body-soluble toxic substances.

Conjugates bilirubin (BDG and BMG total), being soluble, capable of directly reacting with diazoreaktivom — diazotirovat'sja. Therefore, this faction is called direct bilirubin, While free bilirubin, being insoluble in water connection, cannot directly diazotirovat'sja and is called indirect bilirubin. The nature of the reaction of bilirubin with diazoreaktivom does not depend on its connection with protein, and is in direct dependence on the complex of bilirubin with glukuronova acid.

Normal blood serum contains on average 17 micromole/l total bilirubin, of which only 10 — 15 % included in direct fractions. Indirect bilirubin cannot pass through the renal corpuscles, and so the urine of a healthy person does not contain this pigment. The emergence of bilirubin in the urine indicates the increase in the blood straight to his faction and, usually, is the breach of excretion of bile pigments in the guts.

For the detection of bilirubin in the urine sample used Harrison and Rosina.

Sample Harrison based on the oxidation of bilirubin in biliverdin under the influence of an oxidizer (reagent Fouche) with the formation of coloured substances.

Alkaline urine need to acidify slightly a few drops of concentrated acetic acid.

Sample Rosina — quality sample for bilirubin in urine, based on the oxidation of bilirubin in the urine under the influence of biliverdin 1 % alcohol solution of iodine.

In a healthy person, this sample is negative. When hematuria and after reception of antipyrine it becomes positive. To avoid errors in all cases of doubt, it is necessary to conduct sample Fouche.

Increasing concentrations of bilirubin in the blood leads to the development of jaundice and bilirubinurii. Most liver disease is jaundice leading clinical symptom, Therefore, the recognition of its nature is of great importance for the diagnosis and therapy of tactics.

By the nature of the violation bilirubinovogo Exchange and mechanism of occurrence There are four main types of jaundice: parenhimatoznuju, mechanical, haemolytic and kon'jugacionnuju, or enzymatic.

When parenhimatoznoj jaundice in the blood increased direct and indirect bilirubin fractions, most often, with a predominance of first. The amount of bilirubin in the blood and urine of urobilin promoted, and the number of sterkobilina in the feces is reduced to varying degrees and depending on the disease and its severity. The leading mechanism of metabolic disorders of bilirubin and its derivatives with parenhimatoznoj jaundice is a violation of the excretion of bile pigments in the guts (decreased activity gljukuronil- transferase, providing kon'jugaciju bilirubin, While there is a, but it is not the leading factor) .

When the mechanical jaundice in the blood there is giperbilirubinemia, caused by an excess of direct and indirect bilirubin. The amount of bilirubin in the urine increases, and urobilin is not changed. The content of sterkobilina in Calais is greatly reduced or completely absent. The main mechanism of metabolic disorders of bile pigments is block their removal in the guts.

When hemolytic jaundice as a result of the increased destruction of red blood cells in the blood increased indirect bilirubin content. Urine bilirubin is missing. Because conjugation and excretion of bilirubin can occur with maximum speed, the content of sterkobilina in Calais reaches considerable values (to 1800 mg per day), can increase the level of urobilin in urine.

Kon'jugacionnaja jaundice develops as a result of failure of the process of conjugation in the liver. Indirect bilirubin accumulates in the blood (to 171 mmol / l). Urine bilirubin is missing, urobilin is within normal limits, sterkobilina content in feces is lowered. Neonatal jaundice is also a consequence of enzyme deficiency gljukuroniltransferjezy some children due to temporary immaturity of liver cells. On the expiry of 10-15 days after the birth of enzyme deficiency, usually, filled and jaundice passes.

Urobilinovye body-urobilinogen, urobilin

Getting to jelchew in intestine, bilirubingljukuronidy are exposed to bacterial flora and the other constituent parts of bile. With the participation of glucuronidase enzyme from disrupted bilirubingljukuronidov glucuronic acid and the resulting free bilirubin is restored to urobilinogenov, or phone urobilinovyh. Depending on the place of education urobilinogena part of it comes from the portal vein in the liver, where either broken before the connection dipirrol'nyh, or rejekskretiruetsja. The other part of the urobilinogena, appearing mainly in the distal colon, on the gemorroidal'nym veins enters the general circulation and excreted from the body by the kidneys. Alfresco urine urobilinogen is oxidized spontaneously to urobilin. Content in the daily amount of urobilin urine healthy person ranges from 1 to 4 mg.

To identify high content in the urine urobilinovyh Tel-urobilinurii — there are different quality sample-Nejbaujera, Schlesinger, Floransa, Bogomolov.

Urobilinurija hemolytic anemia occurs when, liver diseases and some diseases of intestines. When urobilinurija hemolytic anemia is an important sign of an increased hemolysis, as in the case of its termination it disappears. At gemoglobinurii, malaria, scarlet fever, extensive myocardial heart attacks, excretion of large hemorrhage occurs urobilinurija hemolytic type.

Great diagnostic value is identification of urobilinurii diseases of the liver parenchyma. When epidemic hepatitis urobilinurija appears in the predzheltushnoj stage and grows in the early days of the appearance of jaundice. In the midst of illness when expressed jaundice and aholicheskom Kale (inside the liver stagnation) it disappears, appearing again with the recovery. In mild cases of infectious hepatitis two-phase appearance there is no urobilinurii. Disappears urobilinurija through 8-24 days. Long urobilinurija happens in chronic hepatitis, cirrhosis. Newborn jaundice is not accompanied by urobilinuriej. With the stagnant phenomena in the liver (decompensation of cardiac activity) urobilinurija is a distinctive sign. The absence of urobilin in urine in severe forms of jaundice may indicate acute yellow atrophy of liver. When obturative jaundice urobilin in the urine is missing.

When enterocolitis, zavorote guts intensified the process of rotting resorption urobilinogena through the mucous membranes of the intestines increases and increase urobilinurii.

Bile acids in urine

When ingested, bile in urine bilirubin is detected in it also bile acids. There are qualitative and quantitative samples determination of bile acids in urine. Qualitative samples based on a property of these acids, lowering the surface tension of liquids.

Blood and pigments of blood in urine

Distinguish the kidney (Renal) and vnepochechnuju (jekstrarenal'nuju) hematuria.

Renal hematuria can be organic and functional. Organic kidney hematuria is noted in acute nephritis, especially diffuse. When focal nephritis hematuria is low. Chronic nephritis accompanied by moderate hematuria. The appearance of hematuria in infectious diseases indicates a violation of the kidney. Hematuria occurs also when sharp kidney insufficiency, thrombosis of the Renal vein, systemic connective tissue diseases, accompanied by the defeat of kidneys. When Cardiac decompensation may occur long hematuria, that with the improvement of heart function disappears. Very rarely functional renal hematuria occurs when body with extremely strong stimuli.

Extrarenal hematuria appears in inflammatory processes in the urinary tract and injury. When pielite and pielocistite accompanied by piuriej and bacteriuria. Urolithiasis, urate kidney infarction, nefroblastome, gidronefroze, congenital anomalies of the kidneys, gipovitaminose C hematuria has different origins.

Haemoglobin in urine (hemoglobinuria) appears when gemoglobinemii. Kidney threshold plasma hemoglobin is 0,06 mmol / l. To identify gemoglobinurii should conduct a chemical reaction in the presence of hemoglobin in the urine and by microscopic examination of urine sediment to establish the absence of red blood cells. To do this, you can use the sample with amidopirinom or benzidine. The final nature of the pigment is determined by spectroscopy or spectrophotometry.

Hemoglobinuria may occur if severe vnutrisosudistom erythrocytes. Distinguish between primary and secondary gemoglobinuriju. To the primary are cold, mid-flight, pristupoobraznaya in paroxizmalna night gemoglobinurii (disease Markiafavy-Micheli) and etc. Secondary hemoglobinuria appears after transfusion incompatible blood, poisoning with aniline dyes, sulfanilamides, PASC-sodium, Mushrooms, xloroformom, strychnine, potassium hloratom and other substances, as well as severe infectious diseases (sepsis, scarlet fever, malaria, tifah), severe injuries, some types of hemolytic anemia, allergic diseases, acute yellow atrophy of liver.

Hemosiderin in urine – gemosiderinuriya – appears as a result of the prolonged increase of level of serum iron and development of renal gemosideroza. Hemosiderin is formed by reinforced breakup of hemoglobin, deposited in the cells of various parenchymatous organs, including epithelial kidney as dark granules, convert ferric-containing iron. Kidney epithelium, rich gemosiderinom, undergoes degenerative changes, sluschivaetsya, gets into the urine and, in so doing, partially destroyed. Hemosiderin is insoluble in urine. To identify gemosiderinurii explore urine sediment. When you add a solution of potassium zhelezistosinerodistogo in acidic Wednesday formed Blue granules size 1 - 3 m, found under the microscope.

Gemosiderinurija observed in chronic hemolytic anemia, paroxysmal nocturnal hemoglobinuria, Cooley's anemia, jeritroblastoze fruit, multiple transfusion eritrocitarna mass or whole blood, overdose of drugs, containing iron, and etc.

Porphyrins-urine – porfirinurija can be primary and secondary.

Primary porfirinurija occurs when a congenital breach of porphyrins, secondary porfirinurija appears on the background of existing diseases. A large part of the Porphyrin is absorbed from food (meat, vegetables), t. it is. has the exogenous origin. The source of endogenous porphyrins is a synthesis of them from glikokola and succinic acid. Through the stage of aminolevulinic acid and porfobilinogena porphyrins are formed, as sources for further synthesis of hemoglobin, myoglobin, respiratory enzymes. A small amount of porphyrins are formed in the process of splitting hromoproteidov. The synthesis of porphyrins passes through intermediate stages (koproporfiriny (I) and (III), uroporfiriny (I) and (III), protoporfirnny IX).

Porphyrins are pigments, in this connection When porfirinurii urine color is red. To identify porfobilinogenurii delete urobilinogen and derivatives of indole and skatola by chloroform extraction and butanol, where porphobilinogen nerastvorim, and carry out the reaction of Ehrlich with paradimetilaminobenzal'degidom (Red link is formed). To determine the Uro- and koproporfirinov used Spectrophotometric study.

Porfirinurija observed in acute intermittent porfirii, Gunther disease, chronic porfirijah. Secondary porfirinurija occurs when acute hepatitis, cirrhosis, severe febrile diseases, certain anemias (aplastic, hemolytic) and leukemia, avitaminozax (B₁, PP, B₂, B₆), lead poisoning, acetylsalicylic acid, sulfanilamides, aniline dyes, etc.

Myoglobin in urine

Myoglobin appears in the urine as a result of the collapse of muscle tissue. Represents the muscle pigment, the chemical structure similar to hemoglobin; Kidney threshold approximately 0,15 g / l. Myoglobin gives a positive reaction to the blood. Differentiate Myoglobin and hemoglobin spectrophotometry method using electrophoresis on paper or reaction passive gemoggljutinacii using jeritrocitarnogo diagnosticum (conjugate reagent red blood cells and antibodies against Myoglobin).

Myoglobinuria may occur if severe injuries with crushes of muscle tissue, jelektrotravme. Atraumatic dental myoglobinuria occurs when muscular atrophy, myocardial infarction, mioglobinovom miozite, carbon monoxide poisoning, thrombosis of blood vessels and muscles etc.

Indikan in urine

Indikan formed in the small intestine of tryptophan (indolaminopropionovoj acid). In the tissues of the indole is oxidized, becoming indoksil. As the toxic substance indoksil and gljukuronovymi acids and sulphur cleared. Generated indoksilsul'fat potassium and indoksilgljukuronovaja acid, provided kidneys, get the name of the urinary indikana.

In normal urine detected traces of indikana. At high relative density of urine concentration indikana increased. Indikan in urine is detected when used meat food. The level of indikana in the urine increases when constipation different etiology and especially in small bowel obstruction, you have rotting processes in the large intestine.

Increases the content of indikana in the urine also with bruchnom tife, a tuberculosis of guts, peritonitis, as well as in abscessah various localization (intensive decay of protein).

The basis for the identification of indikana in urine lies indoksilsul'fata property of potassium and indoksilgljukuronovoj acid in the presence of acid and oxidizing agent be broken down, and released indoksila-painted indigo blue.

Melanin-urine

The kidneys secrete colorless melanogen. Urine, contains melanogen, on air due to melanogena dark melanin. When you add to this the urine of ferric chloride, bromine water, potassium dichromate, dilute sulfuric acid appears blackish-brown staining.

Melanogen in the urine detected in patients with melanoma (especially in large quantities when melanoma metastasis to the liver), as well as in some poisoning (carbolic acid, lizolom).