Tests on the topic: “Acute leukemia.” Clinical picture of patients with acute leukemia
- Acute leukemia– these are rapidly progressive diseases that develop as a result of impaired maturation of blood cells (white cells, leukocytes) in the bone marrow, cloning of their precursors (immature (blast) cells), the formation of a tumor from them and its growth in the bone marrow, with possible further metastasis ( spread of tumor cells through the blood or lymph into healthy organs).
- Chronic leukemia differ from acute ones in that the disease lasts for a long time, and occurs pathological production precursor cells and mature leukocytes, disrupting the formation of other cell lines (erythrocyte line and platelet). A tumor is formed from mature and young blood cells.
Leukemia can affect both adults and children. Men and women are affected in equal proportions. In different age groups meet different types leukemia. IN childhood, acute lymphoblastic leukemia is more common, at the age of 20-30 years - acute myeloblastic, at 40-50 years - chronic myeloblastic leukemia is more common, in old age– chronic lymphocytic leukemia.
Anatomy and physiology of bone marrow
Bone marrow is tissue found inside bones, primarily in the pelvic bones. This is the most main body, involved in the process of hematopoiesis (the birth of new blood cells: red blood cells, leukocytes, platelets). This process is necessary for the body to replace dying blood cells with new ones. Bone marrow consists of fibrous tissue(it forms the basis) and hematopoietic tissue (blood cells on different stages maturation). Hematopoietic tissue includes 3 cell lines (erythrocyte, leukocyte and platelet), which respectively form 3 groups of cells (erythrocytes, leukocytes and platelets). The common ancestor of these cells is stem cell, which starts the process of hematopoiesis. If the process of formation of stem cells or their mutation is disrupted, then the process of cell formation along all 3 cell lines is disrupted.
Red blood cells- these are red blood cells, contain hemoglobin, oxygen is fixed on it, with the help of which the cells of the body are nourished. With a lack of red blood cells, insufficient saturation of the body's cells and tissues with oxygen occurs, resulting in various clinical symptoms.
Leukocytes these include: lymphocytes, monocytes, neutrophils, eosinophils, basophils. They are white blood cells, they play a role in protecting the body and developing immunity. Their deficiency causes a decrease in immunity and the development of various infectious diseases.
Platelets are blood platelets that participate in the formation of a blood clot. A lack of platelets leads to various bleedings.
Read more about the types of blood cells in a separate article by following the link.
Causes of leukemia, risk factors
Exposure to a number of factors leads to a mutation (change) in the gene responsible for the development and maturation of young (blast) blood cells (along the erythrocyte, leukocyte and platelet pathways) or a mutation in the stem cell (the original cell that triggers the process of hematopoiesis), resulting in they become malignant (tumor). Rapid proliferation of tumor cells, disrupting the normal process of hematopoiesis and replacement healthy cells tumor.Risk factors leading to leukemia:
- Ionizing radiation: radiologists are exposed after the atomic bombing, radiation therapy, ultraviolet radiation;
- Chemical carcinogens: toluene, found in paints and varnishes; pesticides are used in agriculture; arsenic is found in metallurgy; some medications, for example: Chloramphenicol and others;
- Some types of viruses: HTLV (T - human lymphotropic virus);
- Household factors: car exhausts, additives in various food products, smoking;
- Hereditary predisposition To cancer diseases;
- Mechanical damage fabrics.
Symptoms of various types of leukemia
- For acute leukemia There are 4 clinical syndromes:
- Anemic syndrome: develops due to a lack of red blood cell production, many or some symptoms may be present. Manifests itself in the form of fatigue, pale skin and sclera, dizziness, nausea, rapid heartbeat, brittle nails, hair loss, pathological perception of smell;
- Hemorrhagic syndrome: develops as a result of a lack of platelets. Manifested by the following symptoms: first, bleeding from the gums, bruising, hemorrhages in the mucous membranes (tongue and others) or in the skin, in the form small dots or stains. Subsequently, as leukemia progresses, massive bleeding develops, as a result DIC syndrome(disseminated intravascular coagulation);
- Syndrome of infectious complications with symptoms of intoxication: develops as a result of a lack of leukocytes and with a subsequent decrease in immunity, an increase in body temperature up to 39 0 C, nausea, vomiting, loss of appetite, sudden weight loss, headache, general weakness. The patient is joined various infections: influenza, pneumonia, pyelonephritis, abscesses, and others;
- Metastases - Through the blood or lymph flow, tumor cells enter healthy organs, disrupting their structure, functions and increasing their size. First of all, metastases reach the lymph nodes, spleen, liver, and then other organs.
Erythroblastic acute leukemia, precursor cells are affected, from which red blood cells should subsequently develop. It is more common in old age and is characterized by a pronounced anemic syndrome; no enlargement of the spleen or lymph nodes is observed. In the peripheral blood, the number of erythrocytes, leukocytes and platelets, and the presence of young cells (erythroblasts) are reduced.
Monoblastic acute leukemia, the production of lymphocytes and monocytes is disrupted, and accordingly they will be reduced in the peripheral blood. Clinically, it is manifested by an increase in temperature and the addition of various infections.
Megakaryoblastic acute leukemia, platelet production is impaired. In the bone marrow, electron microscopy reveals megakaryoblasts (young cells from which platelets are formed) and an increased platelet count. A rare variant, but more common in childhood and has a poor prognosis.
Chronic myeloid leukemia, increased formation of myeloid cells, from which leukocytes are formed (neutrophils, eosinophils, basophils), as a result of which the level of these groups of cells will be increased. For a long time may be asymptomatic. Later, symptoms of intoxication appear (fever, general weakness, dizziness, nausea), and the addition of symptoms of anemia, enlargement of the spleen and liver.
Chronic lymphocytic leukemia, increased formation of lymphocyte precursor cells, as a result, the level of lymphocytes in the blood increases. Such lymphocytes cannot perform their function (development of immunity), so patients develop different kinds infections, with symptoms of intoxication.
Diagnosis of leukemia
- Decrease in hemoglobin level (normal 120g/l);
- Decrease in the level of red blood cells (normal 3.5-5.5 * 10 12 / l);
- Low platelets(norm 150-400*10 9 /l);
- Reticulocytes (young red blood cells) level decreases or are absent (normal 02-1%);
- Blast (young) cells >20% in acute leukemia, and in chronic leukemia it may be less (the norm is up to 5%);
- The number of leukocytes changes: in 15% of patients with acute leukemia it increases to >100*10 9 /l, other patients may have a moderate increase or even a decrease. The norm of leukocytes is (4-9*10 9 /l);
- Decrease in the number of neutrophils (normal 45-70%);
- Absence of band leukocytes, eosinophils and basophils;
- Increased ESR (normal 2-12mm/h).
- Blood chemistry: nonspecific method, indicates changes in indicators as a result of damage to the liver and kidneys:
- Increased level of lactate dehydrogenase (normal 250 U/l);
- High ASAT (norm up to 39 U/l);
- High urea (normal 7.5 mmol/l);
- Promotion uric acid(normal up to 400 µmol/l);
- Increase in bilirubin ˃20 µmol/l;
- Decrease in fibrinogen
- Decrease in total protein
- Decreased glucose ˂ 3.5 mmol/l.
- Myelogram (punctate analysis bone marrow): is the method of choice for confirming acute leukemia
- Blasts (young cells) >30%;
- Low level erythrocytes, leukocytes, platelets.
- Trephine biopsy ( histological examination iliac bone biopsy): does not allow an accurate diagnosis, but only determines the proliferation of tumor cells, displacing normal cells.
- Cytochemical study of bone marrow punctate: detects specific blast enzymes (reaction to peroxidase, lipids, glycogen, nonspecific esterase), determines the variant of acute leukemia.
- Immunological method research: identifies specific surface antigens on cells, determines the variant of acute leukemia.
- Ultrasound internal organs: a nonspecific method that detects enlarged liver, spleen and other internal organs with metastases of tumor cells.
- Chest X-ray: is a nonspecific met, detects the presence of inflammation in the lungs when an infection is attached and enlarged lymph nodes.
Treatment of leukemia
Treatment of leukemia is carried out in a hospital.Drug treatment
- Polychemotherapy, used for antitumor effects:
- Transfusion therapy: red blood cell mass, platelet mass, isotonic solutions, for the purpose of correcting severe anemic syndrome, hemoragic syndrome and detoxification;
- General restorative therapy:
- used to strengthen the immune system. Duovit 1 tablet 1 time per day.
- Iron supplements, to correct iron deficiency. Sorbifer 1 tablet 2 times a day.
- Immunomodulators increase the body's reactivity. Timalin, intramuscularly 10-20 mg once a day, 5 days, T-activin, intramuscularly 100 mcg once a day, 5 days;
- Hormone therapy: Prednisolone at a dose of 50 g per day.
- Antibiotics wide range actions prescribed for the treatment of associated infections. Imipenem 1-2 g per day.
- Radiotherapy used to treat chronic leukemia. Irradiation of an enlarged spleen and lymph nodes.
Surgery
Involves bone marrow transplantation. Before the operation, preparation is carried out with immunosuppressive drugs (Prednisolone), total irradiation and chemotherapy. A spinal cord transplant provides a 100% recovery, but a dangerous complication can be graft rejection if it is incompatible with the host cells.Traditional methods of treatment
Usage saline dressings with 10% saline solution (100 g of salt per 1 liter of water). Soak the linen fabric in a hot solution, squeeze the fabric a little, fold it into four, and place it on sore spot or tumor, secure with adhesive tape.An infusion of crushed pine needles, dry onion skin, rose hips, mix all ingredients, add water, and bring to a boil. Leave for a day, strain and drink instead of water.
Drink juices from red beets, pomegranates, and carrots. Eat pumpkin.
Infusion of chestnut flowers: take 1 tablespoon of chestnut flowers, pour 200 g of water into them, boil and leave to infuse for several hours. Drink one sip at a time, you need to drink 1 liter per day.
A decoction of blueberry leaves and fruits is good for strengthening the body. Approximately 1 liter of boiling water, pour 5 tablespoons of blueberry leaves and fruits, leave for several hours, drink everything in one day, take for about 3 months.
ACUTE LEUKEMIA (LEUCOSIS ACUTA)
Leukemia - malignant disease hematopoietic tissue with the primary localization of the pathological process in the bone marrow. The term "leukemia" was proposed in 1921 by Ellerman. The works of domestic scientists (I. A. Kassirsky, A. I. Vorobyov, Yu. I. Lorie, A. F. Tur, N. S. K islyak, L. A. Makhonova, I. V. Koshel) contributed contribution to the development of leukemia as a science. In childhood, acute leukemia is diagnosed more often than any other tumor. Among all patients with malignant diseases of hematopoietic and lymphoid tissues, every tenth patient is a child. The peak incidence of leukemia in childhood occurs at the age of 2-5 years. The upward trend in the incidence of leukemia noted in recent decades and the continuing high mortality rate make the problem of leukemia in children especially relevant for practical healthcare. Etiology and pathogenesis. The causes of the leukemic process are not fully understood. Currently, the etiological role of ionizing radiation, chemical exogenous factors, and oncogenic viruses has been confirmed. The significance of hereditary predisposition to the occurrence of leukemia has been studied. The main provisions of the mutation theory and the bug concept are formulated. Ionizing radiation. The etiological connection of ionizing radiation with leukemia is convincingly confirmed by the tragedy of Hiroshima and Nagasaki. After the explosion of the atomic bomb, residents of these cities developed leukemia 13 times more often than residents of other areas of Japan. Chemical leukozogenic substances. Various chemical compounds are known, with the help of which it is possible to experimentally induce tumor process , including leukemia. These include polycyclic hydrocarbons, aromatic amines, azo compounds, and insecticides. Some exogenous substances have a leukosogenic effect: steroid compounds (sex hormones, bile acids, cholesterol, etc., as well as tryptophan metabolism products. Viral theory. According to the hypothesis of Hubner (1970), the cells of most vertebrate species contain genetic material of oncogenic viruses, But viral genetic characteristics are inhibited by cellular repressors of the macroorganism and the virus is in an inactive form. Under the influence of chemical carcinogens, radiation and other influences, cellular repressors “weaken" and the virus is activated, causing the development of leukemia. Thus, non-infected bacteria play a certain role in the development of the disease - a virus, but the state of control systems that suppress leukemic information in the cell.The viral etiology of leukemia in humans as an infectious epidemic process is evidenced by: a) the absence of disease upon contact with a patient with leukemia; b) the absence of leukemia in the recipient following an accidental blood transfusion from a patient with leukemia. The study of viral aspects of the etiology of leukemic growth in humans continues in various directions. Attempts are being made to confirm the viral nature of leukemia in humans by detecting a leukemia-specific antigen. Hereditary factor. It is assumed that some hidden genetic defect is inherited, in which the development of leukemia is possible under the influence of external and internal unfavorable factors. In 1960, Nowell and Hungerford (Philadelphia) first discovered that in patients with chronic myeloid leukemia one pair of chromosomes is almost 2 times less than normal. This shortened chromosome was called the Philadelphia chromosome (Phl) and belongs to the XXII pair. However, most researchers believe that a change in the chromosome set is not a cause, but a consequence of leukemia. The most common chromosomal anomaly is aneuploidy (change in the number of chromosomes), mainly of a hyperploid nature. Confirmation of the role of hereditary factors in the development of leukemia is familial, congenital leukemia and the disease of both identical twins with leukemia. If one of the monozygotic twins has acute leukemia, the probability of the other twin having the disease is 25%. It has been established that in families of persons with acute leukemia, the risk of developing the disease increases almost 3 times. Observations have shown that a hereditary abnormality in tryptophan metabolism also poses a threat for leukemia in children. This is a particular risk factor for congenital leukemia. The discovery of a connection between Down's disease and leukemia made it possible to recognize the significance of hereditary influence on the origin of leukemia. With Down's disease, the possibility of developing acute leukemia increases by 20-30 times. Thus, the etiology of leukemia seems to be diverse, but the pathogenesis boils down to a violation of the information of division, differentiation of cells and their escape from the control of regulatory factors. The monoclonal theory of the development of hemoblastoses as tumors in general is generally accepted. According to this theory, leukemia cells are a clone - the offspring of one mutated cell. It is known that mutations occur almost continuously; on average, one cell mutates every hour. In healthy people, it is eliminated as a result of the inclusion of protective immune system, which reacts to these cells as foreign. The bug theory of leukemia pathogenesis considers the disease as a result of the proliferation of an uncontrolled clone of cells that have lost the ability to differentiate and mature. Consequently, the development of leukemia is possible due to an unfavorable combination of exposure to mutagenic factors and a weakening of the body’s defenses. Morphology. Leukemia is based on a hyperplastic, tumor-like process in the hematopoietic tissue with foci of leukemic metaplasia in varying degrees. personal organs and systems. Most often, pathological hematopoiesis occurs where it existed in the embryonic period: in the spleen, lymph nodes, and liver. The study of blast cells showed that the morphological substrate in acute leukemia is heterogeneous in different patients. A characteristic sign of acute leukemia is an increase in the number of blast cells in the bone marrow. Clinical picture. The disease usually begins unnoticed with appearance vague complaints of pain in bones and joints, fatigue, loss of appetite, sleep disturbance, increased body temperature. The skin and mucous membranes are pale, less often jaundiced, sometimes the skin acquires an earthy-greenish tint; Possible gingivitis, stomatitis - from catarrhal to ulcerative-necrotic. There is often a visible enlargement of the lymph nodes; they are of dense elastic consistency, painless, and not fused with the surrounding tissue. Sometimes the Mikulicz symptom complex is determined - a symmetrical increase in the lacrimal and salivary glands due to their leukemic infiltration. Such children have a puffy face and outwardly resemble patients with mumps. Hemorrhagic syndrome is one of the most striking and common signs of acute leukemia. Patients experience hemorrhages in the skin, mucous membranes, bleeding from the nose, gums, gastrointestinal tract, hematuria, and cerebral hemorrhages. Characteristic pain in the joints and bones is caused by leukemic infiltration of the synovial membrane and hemorrhages into the joint cavity. Damage to bone tissue is manifested by its diversity, the development of foci of destruction with damage to the epiphyses and diaphyses. A common symptom acute leukemia is hepatosplenomegaly. Cardiovascular disorders may be observed in the form of tachycardia, dullness of heart sounds, functional murmurs; expansion of the borders of the heart is less common. Pneumonia may develop in the lungs. Changes in the skin, mucous membranes, and internal organs are mainly caused by leukemic infiltration (Fig. 79). According to their course, leukemia is divided into acute and chronic. The terms “acute” and “chronic” leukemia reflect not temporary, but cytochemical differences. Distinguishing the stages of the leukemic process is necessary to determine therapeutic tactics. The first stage is the first attack of the disease. This period from the beginning clinical manifestations until the effect of the therapy is obtained. The second stage is remission. There are complete and incomplete remissions. With complete clinical hematological remission (duration of at least 1 month), there are no clinical symptoms, and the myelogram shows no more than 5% blast cells and no more than 30% lymphocytes. Incomplete clinical hematological remission is a condition in which clinical parameters and hemogram are normalized, but no more than 20% of blast cells remain in the bone marrow aspirate. The third stage is a relapse of the disease, caused by the return of the leukemic process. More often, a relapse of the disease begins with the appearance of extramedullary foci of leukemic infiltration in the testicles, nervous system, lungs, against the background of normal hematopoiesis. In the presence of hematological relapse, a significant number of patients do not present any complaints. In some children, relapse is diagnosed only on the basis of a bone marrow test. Less severe symptoms during the period of relapse of acute leukemia are associated with continuous complex treatment that inhibits the development of the leukemic process. In acute lymphoblastic leukemia, the state of remission is often interrupted by the development of a specific lesion of the nervous system - neuroleukemia syndrome. Neuroleukemia develops as a result of metastasis of blast cells into the nervous system, which apparently occurs in the initial period of the disease and is due to the fact that anti-leukemia drugs do not penetrate the blood-brain barrier. Most often, neuroleukemia is detected in patients with normal hematopoiesis. The clinical picture of neuroleukemia develops gradually. Dizziness appears headache, nausea, diplopia, pain in the spine and intercostal spaces. Some children experience a sharp increase in body weight in a short period of time, bulimia, and thirst, which is associated with damage to the diencephalic region. Rarely, neuroleukemia is detected by chance during a clinical examination of children. When examining the cerebrospinal fluid, hypertension, hypercytosis, an inconsistent increase in the amount of protein, and positive Hide and Panne-Apelt tests are detected. An auxiliary diagnostic method is fundus examination. Increasing swelling of the optic discs indicates a persistent increase intracranial pressure, associated not only with edema, but also in some cases with leukemoid infiltration of the brain. X-ray examination of the skull reveals compaction of bone tissue along the sutures, increased pattern of digital impressions, vascular patterns, and osteoporosis of the sella turcica. Laboratory data. Severe proliferation of blast cells is the main hematological feature of acute leukemia. In smears of bone marrow punctate, up to 90-95% of blast cells are detected, but the presence of more than 5% of them in bone marrow punctate suggests acute leukemia. A characteristic diagnostic criterion is leukemic gaping (hiatus leucaemicus), which is a break in hematopoiesis at early stage, as a result of which there are no transitional forms between the young cells that make up the main morphological substrate and the mature forms of leukocytes. The main hematological signs of acute leukemia are: 1) changes in the qualitative composition of white blood (the appearance of immature pathological forms); 2) anemia, 3) thrombocytopenia. Less permanent signs include changes in the number of leukocytes (increase or decrease), increased ESR. Depending on the number of leukocytes, 3 forms of acute leukemia are distinguished: 1) leukemic (the number of leukocytes is above 50,000); 2) subleukemic (the number of leukocytes from 10,000 to 50,000); 3) leukopenic (the number of leukocytes is below 10,000 per mm3). Using cytochemical studies, they are divided into the following groups: 1) acute lymphoblastic, 2) acute myeloblastic, 3) acute myel omonocytic, 4) acute promyelocytic, 5) acute monoblastic leukemia, 6) acute erythromyelosis, 7) undifferentiated form of acute leukemia . Identification of the variant of acute leukemia is made by examining bone marrow punctate using cytochemical marker reactions: the glycogen-CHIK reaction, the granular form of which is pathognomonic for acute lymphoblastic leukemia; reaction to lipids with Sudan black B, characteristic of acute myeloblastic leukemia; reaction to Nonspecific esterase with a-naphthyl acetate, characteristic of monoblastic leukemia; reaction to peroxidase, alkaline and acid phosphatases. Identification of various cytomorphological forms of the disease has important when choosing a treatment method. Acute lymphoblastic leukemia. This is the most common type of leukemia in childhood (80%, all forms). Morphologically, in the bone marrow aspirate, and in the case of a generalized process, in the blood, a large number of lymphoblasts are found, which are of two types. Type 1 cells are round with a tender nucleus and nucleolus, with blue cytoplasm; Type 11 cells have a slightly coarser nucleus, the cytoplasm is often elongated in the form of a tail. Pitochemically, cells of types 1 and 11, like all lymphoid cells, do not contain myeloperoxidase or phospholipids. Type 1 leukemia cells are distinguished by a large accumulation of PAS-positive material (glycogen), the absence of acid phosphatase activity and weak activity of nonspecific α-naphthyl acetate esterase. Leukemia cells of type 11 have almost no granules of PHIK-positive material and are characterized by high activity of acid phosphatase and nonspecific esterase. According to the belonging of lymphoblastic cells to T- or B-lymphocytes, 3 subvariants of acute lymphatic leukemia are distinguished: T-cell, B-cell and O-cell. T-cell variant is characterized by an increase in peripheral and visceral lymph nodes, frequent damage to the thymus gland. Remission is short-lived, on average 16 months. In case of relapses, extramedullary localizations predominate (neu rolicosis, orchitis). Repeated remissions are rare. The average life expectancy is approximately 20 months. The B-cell variant occurs mainly in young children. Rapid generalization of the process is noted. Complete remission is achieved only in 28.5% of patients, its duration is no more than 6 months. life expectancy - 9-12 months. In terms of sensitivity to therapy and prognosis, this variant of leukemia in children is the least favorable. With the 0-cell variant, the best treatment results are observed. Remission is achieved in almost 95% of patients; average duration life - up to 3 years or more; in some children, complete recovery is possible. Acute myeloblastic leukemia. Leukemia cells are large in size, regular in shape, have a delicate nucleus and several nucleoli. High activity of myeloperoxidase and increased lipid content are noted. Glycogen is determined in myeloblasts in the form of fine granules. CHIC reaction is positive. Acute myeloblastic leukemia is characterized by a progressive course, severe intoxication, and constant enlargement of the liver. The course of the disease is usually severe, remission is achieved less frequently than with lymphoblastic leukemia, and is of shorter duration. The average life expectancy of children is within 17 months. Acute myelomonocytic leukemia. This disease is a variant of acute myeloblastic leukemia, since both monocytes and myeloblasts have one common precursor; ablast cells in both types of leukemia are very similar in morphological and cytochemical criteria. A specific cytochemical reaction in these variants is the determination of a-naphthyl acetate esterase inhibited by sodium fluoride. The population of myelomonocytic cells is also characterized positive reaction n and chloroacetate esterase, which is typical for neutrophil granulocytes. The effect of treatment, as with acute myeloblastic leukemia, is short-lived. Acute promyelocytic leukemia. This variant of acute leukemia is characterized by a high percentage of leukemic promyelocytes in bone marrow puncture, which are cytochemically characterized by high activity of myeloperoxidase, naphthol-A50-chloroacetate esterase and a-naphthyl acetate esterase, as well as a sharply positive reaction to acid phosphatase. The course is malignant. Severe hemorrhagic syndrome is typical for this variant of leukemia. Enlargement of the liver, spleen and lymph nodes is uncharacteristic. Rapid death is caused by manifestations of hemorrhagic syndrome. Complete remission is short and is observed in no more than 20% of patients. The average life expectancy does not exceed 12 months. Acute monoblastic leukemia. This is a rare variant of acute leukemia. It is characterized by large monoblasts with a round or oval nucleus with 2-3 nucleoli. Cyt plasma is gray-smoky in color. Reactions to peroxidase, lipids, and PAS reaction are inconsistent. A characteristic (marker) cytochemical sign of this variant of leukemia is the high activity of nonspecific esterase in blast cells (reaction with a-naphthyl acetate atom). Clinically, acute monoblastic leukemia is manifested by anemia, hemorrhagic rashes, and frequent enlargement of lymph nodes. In most patients, blood tests show a low white blood cell count. Often there is a specific skin lesion in the form of rounded papular infiltrates of a bluish tint ranging in size from 0.5 to 1 cm. Combined cytostatic therapy relatively rarely causes complete clinical hematological remissions. Acute erythromyelosis. This is one of the cellular variants of acute myeloid leukemia. Leukemic cells of the erythroid series, often multinucleated, are characterized by a sharply positive PAS reaction, high activity of acid phosphatase and nonspecific α-naphthyl cetate esterase. Of the clinical manifestations, signs of intracellular hemolysis attract attention. Most patients with erythromyelosis are refractory to treatment, remission occurs in a small percentage of cases, its average duration is up to 6 months, and life expectancy is not 12 months. Acute undifferentiated cell leukemia. This is a rare variant of leukemia. In this variant, leukemic transformation is observed at the level of a single stem cell, giving rise to both hematopoietic lineages - lymphoid and myeloid. This option cannot be differentiated due to limited methodological capabilities. Blast cells are quite large, sometimes irregular shape , with a medium and high nuclear-cytoplasmic ratio. The cytoplasm does not contain inclusions or granularity. The reaction to Sudan, peroxidase, nonspecific esterase, and the CHIC reaction are negative. Diagnosis and differential diagnosis. The presence of intoxication in the patient, severe pallor, polyadenia and hepatosplenomegaly require the exclusion of acute leukemia. Dynamic blood testing is mandatory. Detection of blast cells in the hemogram with the presence of a “leukemic gape” allows one to suspect acute leukemia. The examination of bone marrow puncture will be decisive for the diagnosis. In those rare cases when bone marrow examination does not provide clear data for diagnosis, it is necessary to conduct a histological examination of the bone marrow using trepanobiopsy. Detection of diffuse or large-focal blast infiltration in the bone marrow in violation of the normal ratio of hematopoietic germs, bone resorption confirms the diagnosis of acute leukemia. For differential diagnosis, first of all, it is necessary to exclude the leukemoid reaction that occurs in response to diseases such as sepsis, severe forms of tuberculosis, tumors, etc. In these cases, although hyperleukocytosis is detected in the peripheral blood, mature cells predominate in the leukegram and only occasionally single myelocytes appear, there is no “leukemic gaping”. There is no pronounced cell rejuvenation in the bone marrow aspirate. The changes disappear as you recover from the underlying disease. In the differential diagnosis of acute leukemia and agranulocytosis, hypoplastic anemia, Werlhof's disease, collagen diseases, infectious mononucleosis, the main criteria should be the results of a cytological examination of the bone marrow. Treatment. The goal of modern leukemia therapy is the complete eradication (destruction) of leukemia cells. This is achieved through the use of hormonal, cytostatic drugs and immunotherapy. A modern program for treating children with chemotherapy includes the following stages: 1) induction of remission; 2) consolidation (consolidation) of remission; 3) treatment during relapse. To date, various treatment regimens for acute leukemia in children have been developed, taking into account the characteristics of the kinetics of leukemic cells. The name of the regimens consists of the first letters of the drugs: VAMP (vincristine-2 mg/m2 once a week; amethopterin 20 mg/m2 once every 4 days; 6-mercaptopurine-100 mg/m2 daily; prednisolone-40 mg/m2 daily ); course - 10-14 days. CVAMP (cyclophosphamide - 200 mg/m2 every other day, vincristine, amethopterin, 6-mercaptopurine); course - 10-14 days. VPR (vincristine, prednisolone, rubomycin 60 mg/m2 - daily); course - 4-5 days. CPR (cyclophosphamide, prednisolone, rubomycin). CLA P (cyclophosphamide, L-asparaginase - 5000-7000 U/m2 per day, prednisolone); course - 10-14 days. In the treatment of acute leukemia, the method of synchronizing polychemotherapy is successfully used. It lies in the fact that under the influence of certain cytostatic drugs (cytorabine, methotrexate), the cell cycle is delayed, cells are blocked at a certain stage of the mitotic cycle, they accumulate, and then drugs are introduced that affect the cells in this phase. The method helps to increase the effectiveness of anti-leukemia therapy. To prevent neuroleukemia during intensive therapy according to the VAMP regimen, methotrexate is administered endolumbarally at a dose of 12 mg/m2, and X-ray or gamma therapy of the head area is also performed. The goal of modern therapy is not only to achieve remission, but also to prolong it as much as possible and increase the patient’s life. Since during the period of remission, 108-109 leukemia cells remain in the child’s body, supportive therapy is necessary. In this phase of the disease, it is most advisable to use antimetabolites (6-mercaptopurine, methotrexate). However, neither intensive nor maintenance therapy in most patients is able to restrain the progression of the process, so periodic intensification of treatment - reinduction - is justified. With it, various schemes are used for induction: VAMP, CAMP, etc. In the last 15 years, a new method of influencing the leukemic clone has been developed - immunotherapy, which consists in the maximum mobilization of the immune system of the patient’s body in order to eliminate the immunological inertia of the body by relation to a leukemic agent. Methods of active immunotherapy are used, designed to stimulate immune stimulation of the patient’s body; methods of passive immunotherapy based on the introduction of humoral immune factors (plasma, immunoglobulins) and methods of adaptive immunotherapy, consisting of the introduction of immunocompetent donor cells into the body (immune lymphocytes, bone marrow transplantation). By their nature, immunotherapy methods can be both specific using leukemic antibodies, and non-specific, when other antigens are used to stimulate the immune response - BCG anti-tuberculosis vaccine, smallpox vaccine, biologically active substances, in particular interferon, which shields the cell genome from penetration virus. Rational immunotherapy regimens are still being developed. The success of the treatment of acute leukemia is determined both by the prescription of antileukemic drugs and by measures for the prevention and treatment of complications caused by various, mainly infectious, diseases and the effect of cytostatic therapy. During treatment, patients may experience nausea, vomiting, and anorexia. The most serious complication of cytotoxic therapy is bone marrow suppression, as a result of which patients develop infectious complications: pneumonia, enteropathy, ulcerative necrotizing stomatitis, purulent otitis media. During this period, it is necessary to carry out intensive replacement therapy. Freshly preserved blood is transfused daily, leuka and thromboconcentrates are administered, broad-spectrum antibiotics and vitamins are prescribed. In case of deep myeloid depression, in order to prevent infectious complications, the patient is placed in a separate ward or box, where conditions are created that are as close to sterile as possible. The staff follows the rules of asepsis and antisepsis, as in operating units. Treating patients with acute leukemia is a difficult task; it is always long-term, and in some cases it is fraught with serious complications. In this regard, complete mutual understanding between the doctor and the patient’s parents is necessary. Advances in recent years in the treatment of acute leukemia make it possible to significantly prolong the life of a child, and in some patients to achieve a cure. About prevention. Prevention of acute leukemia has not been developed. When remission is achieved, maintenance therapy is necessary to prevent relapse of the disease. The patient should be under medical supervision. Control blood tests are carried out 2 times a month, sternal puncture - once every 2 months. The patient should be protected from infection; Sun exposure is contraindicated. The child must be exempted from physical education and preventive vaccinations. Forecast. The prognosis for acute leukemia is poor. The duration of the disease depends on the type of leukemia and the adequacy of therapy. Currently, the life expectancy of a child with acute leukemia ranges from 8-10 months to 4-5 years. IN last years There are cases of recovery from acute leukemia.
appear as if suddenly
among full health. In fact, it develops unnoticed or subacutely. Observed at
When a patient is admitted to a hospital, a severe symptom complex essentially means an already developed
phase of the disease (thus it is not acute onset disease, or rather, the “sharp end” of it).
The onset has no pathognomonic manifestations. Most often the disease develops
subacutely, over several weeks, and is characterized by gradually increasing general weakness,
fatigue, loss of body weight, unmotivated increase in body temperature. Some
less often, leukemia debuts acutely and occurs with a clinical picture of acute pneumonia, tonsillitis, or other
infectious disease. Often the first manifestation of the disease is hemorrhagic
syndrome (subcutaneous hemorrhages, nasal, uterine bleeding). In some patients
diagnosed during a routine blood test, when there are no complaints at all (preventive
inspection). It must be remembered that the onset of acute leukemia can be almost any
(hypertrophic gingivitis, stomatitis, migrating thrombophlebitis, sudden loss consciousness or
paraparesis in neuroleukemia, etc.).
Although the symptoms of the advanced stage are very diverse and cover almost all the most important
systems of the body, however, the main clinical picture is clearly outlined and typical, it consists of 6
main syndromes: 1) hyperplastic, 2) hemorrhagic, 3) anemic, 4) intoxication,
5) syndrome secondary immunodeficiency, 6) ulcerative-necrotic syndrome.
Hyperplastic syndrome manifests itself as a moderate and painless increase
lymph nodes, slight enlargement of the spleen, liver (2-3 cm from under the edge of the costal arch).
Skin leukemic infiltrates (leukemia) may appear in the form of reddish-bluish plaques.
Hyperplastic syndrome is associated with diffuse proliferation of blast cells, this is a manifestation
extramedullary damage to lymph nodes, spleen, liver.
Anemic syndrome is manifested by dizziness, weakness, shortness of breath, tachycardia,
pallor skin, a decrease in hemoglobin and red blood cells (sometimes to critical numbers: Hb -
30 g/l, red blood cells 0.82 x 10!2/l). Anemia in acute leukemia is caused by:
1) inhibition of the erythroid germ of hematopoiesis in the bone marrow (this mechanism is clearly
manifests itself in acute non-lymphoblastic leukemia);
2) loss of red blood cells due to bleeding;
3) autoimmune hemolysis of erythrocytes, which is decisive in acute
lymphocytic leukemia (occurs with moderate jaundice, reticulocytosis, positive Coombs test).
Hemorrhagic syndrome manifests itself as hemorrhagic rashes on the skin and mucous membranes
membranes from single pinpoint and small-spotted to extensive hemorrhages and profuse
bleeding (nasal, uterine, gastrointestinal, etc.). The syndrome is caused by thrombocytopenia,
often very significant (hemorrhagic manifestations begin with a decrease in platelet levels
below 20 x 109/l). The causes of thrombocytopenia are:
1) inhibition of the megakaryocyte lineage of hematopoiesis;
2) loss of platelets due to bleeding;
3) destruction of platelets due to autoimmune processes;
4) consumption of platelets in disseminated vascular coagulation syndrome
Another reason hemorrhagic manifestations a patient with leukemia develops disseminated intravascular coagulation
syndrome due to consumption of blood clotting factors. Most often this process develops when
promyelocytic acute leukemia, since the release of promyelocyte granules due to their high
thrombogenicity triggers the coagulation cascade.
Intoxication syndrome is manifested by profuse sweating, weakness, low-grade fever
temperature, loss of body weight. This syndrome is caused by the breakdown of tumor cells due to
causing substances that cause a pyrogenic reaction and intoxication to enter the bloodstream.
Secondary immunodeficiency syndrome is observed in 80-85% of patients and is dangerous,
difficult-to-control complication. The most numerous group of infectious complications
bacterial origin, including pneumonia, sepsis, purulent processes. Last time
Severe infectious complications of viral and fungal origin have increased. Cause
immunodeficiency consists of granulocytopenia and inferiority of the lymphocytic immune system.
Ulcerative-necrotic syndrome is explained by leukemic infiltration of the submucosal layer,
malnutrition, tissue breakdown, formation of ulcers and necrosis. Sometimes ulcerative
necrotic changes in the oral cavity. Necrosis of the esophagus, stomach, small and large intestines is possible.
20% of patients develop paraproctitis.
Extramarrow manifestations of the disease include damage to the nervous system due to
tumor metastasis to meninges, the substance of the brain and nerve trunks that serves
complication of any leukemia. The clinical picture of neuroleukemia develops gradually and consists of
symptoms of increased intracranial pressure and local symptoms: meningoencephalic
syndrome (headache, nausea, vomiting, stiff neck, Kernig's sign),
pseudotumorous, dysfunction of cranial nerves, damage to peripheral nerves.
In all cases, when spinal tap high blast cytosis is detected (over 10 in 1 μl
cerebrospinal fluid).
The development of leukemic infiltration of the myocardium is indicated by the appearance of cardiac
insufficiency. It is preceded by dullness of heart sounds, decreased ECG voltage and negative
T waves, myocardial hypertrophy.
Lung damage - leukemic pulmonitis is characterized by the appearance of a dry cough,
increased temperature, dry wheezing. On the radiograph - the appearance of local enlargement
pulmonary pattern, small or large focal shadows. Specific infiltration is less common
pleura with effusion in pleural cavity. Diagnosis of this condition is difficult and complicated
necessity differential diagnosis with bacterial pneumonia.
When examining peripheral blood in patients with acute leukemia, the following are revealed:
hematological signs:
1) change in the number of leukocytes within a fairly wide range: from 0.1 x 109/l to 180 x 109/l;
2) the appearance of blast cells in the blood (at early stages blast cell diseases can still
absent in the peripheral blood, but there are already enough of them in the bone marrow; in peripheral blood
this time there is a decrease in all blood cells);
3) a decrease in the number of mature cells of the myeloid lineage in the absence of transitional forms
(“leukemic failure” - hiatus leukemicus);
4) in acute non-lymphoblastic leukemia, immature granulocytes can be detected:
promyelocytes, myelocytes, metamyelocytes, but their number is small (no more than 10%);
5) anemia varying degrees heaviness;
6) thrombocytopenia (observed in more than 90% of cases, while significant - less than 50
x 109/l - in more than half of them).
During puncture examination of the bone marrow, dozens of
percentage of blast cells - main diagnostic value has detection in the myelogram
more than 20% blast cells. A trephine biopsy (puncture of the iliac crest) is also performed.
These studies must be carried out before starting cytostatic therapy!
Once a diagnosis of acute leukemia has been made, it is necessary to determine its variant, since
Their treatment varies significantly. Three methods are used for differentiation - morphological,
cytochemical, cytogenetic (see classification).
Diagnostic criteria for acute leukemia:
1) the presence of relevant clinical syndromes;
2) the appearance of blast cells in the blood;
3) availability in general analysis blood "leukemic failure";
4) changes in white blood are combined with increasing anemia;
5) bone marrow is characterized by total or subtotal blast replacement (more
20% blasts).
Differential diagnosis is carried out with various hemoblastoses, infectious
mononucleosis, systemic diseases connective tissue(systemic lupus erythematosus,
other vasculitides).
Examples of diagnosis formulation
Acute lymphoblastic leukemia first attack, acute phase.
2. Acute myeloblastic leukemia from VI.2006. remission.
3. Acute lymphoblastic leukemia from VI.2005, the first relapse from X.2007.
For successful treatment the patient should be hospitalized in a hematological department
a hospital with conditions for chemotherapy. Established diagnosis is an indication
to the start of cytostatic therapy, since without treatment the average life expectancy of patients
is 3 months. Late diagnosis or wait-and-see tactics lead to a sharp deterioration
forecast.
The concept of cytostatic therapy for leukemia is based on two principles:
1) in the bone marrow there are simultaneously leukemic ones (sharply predominant in number)
and normal hematopoietic cells;
2) a necessary condition to obtain remission and restore normal
hematopoiesis is the eradication (destruction) of the leukemic cell clone, inevitably
accompanied by deep depression of hematopoiesis (agranulocytosis, thrombocytopenia and anemia).
It is known that proliferating cells successively go through 2 phases of mitosis
cycle: mitosis, the shortest, occupies 1% of the time of the entire mitotic cycle (lasting about 1 hour);
interkinesis, which consists of a postmitotic phase (G1), or a postmitotic rest phase, a phase
cell DNA synthesis (S), lasting 20-40 hours. In the premitotic phase (G2) lasting about 2 hours.
the cell contains a tetrashyoid amount of DNA. Total duration mitotic cycle
power cells for about 80 hours.
Based on the effect on cellular kinetics, all cytostatic drugs conditionally possible
divided into two groups: 1) cycle-specific - they can act in one or several phases
mitosis; 2) non-cyclospecific - chemical substances, the effect of which manifests itself regardless of
cycle. The latter disrupt the DNA structure of the cell at any functional stage (rest,
proliferation). These are mainly alkylating compounds.
It has been established that prednisolone promotes the accumulation of power cells in the G1 phase and at the beginning of
DNA synthesis, creating favorable conditions for effective action drugs that are most active in
S-phase. Vincristine is the only drug that destroys cells in the mitosis phase. This stage does not last
more than an hour, and the mitotic cycle time is 3 days. Therefore, frequent administration of the drug is not indicated, since
due to the lack of target cells in the mitotic phase, it will have a toxic effect on
healthy tissue. The concentration of the drug is maintained for 3 days. Optimal administration of the drug is one
once a week. Resting cells, previously considered not subject to cytostatic effects,
can serve as targets for cyclophosphamide and asparaginase. This data forms the basis for creating
programs (combination of cytostatics indicating the dose and frequency of administration) for the treatment of acute leukemia.
Treatment of acute lymphoblastic and non-lymphoblastic leukemia is fundamentally different, although
The stages of therapy are the same.
They include induction of remission, which begins immediately after establishment
diagnosis according to the program corresponding to the variant of leukemia, and ends with confirmation of remission with
using bone marrow puncture, lumbar puncture and clinical examination.
The next stage is the consolidation of remission, which involves consolidating what has been achieved
antitumor effect. This stage is the most aggressive and high-dose in terms of cytostatic
drugs. The goal of this period is to eliminate leukemia cells as completely as possible,
remaining after induction of remission.
Prevention of neuroleukemia - applies to all periods of treatment (induction
remission, consolidation, maintenance treatment). During the induction period, control is performed
diagnostic lumbar puncture, and then - prophylactic administration of cytostatic drugs
intrathecally (dexamethazone - 4 mg, cytarabine - 30 mg, methotrexate - 15 mg). Frequency
lumbar puncture depends on the chosen treatment program.
Maintenance therapy is carried out during remission of the disease. Its main goal is
in restraining control of the leukemia clone. It is carried out regardless of the type of leukemia.
captopurine 60 mg/m2 per day and methotrexate 20-30 mg/m2 once every 5 days. Therapy is interrupted at
during the first year once a month, in the next two years - once every three months intensively
courses of polychemotherapy.
The basis for the treatment of acute lymphoblastic leukemia of the “standard risk” group is
German polychemotherapy protocol HOELZER 1988 “Standard risk” group - patients who are not
having no adverse prognostic factors. “High risk” group - having
at least 1 risk factor. Risk factors include: age of patients over 35 years, baseline
leukocytes more than 30 x 109/l, initial leukopenic level of leukocytes less than 1.5 x109/l, absence
remission on the 28th day of therapy.
The most widely used treatment for acute non-lymphoblastic leukemia is
program “7+3” or “5+2”. This program uses cytarabine at a dose of 100 mg/m~ daily
for 7 or 5 days and rubomycin at a dose of 45 mg/m2 day for 3 or 2 days.
Accompanying therapy includes treatment of infectious complications. With them
is associated with up to 70% of deaths in patients with acute leukemia. The most common complications
bacterial origin (sepsis, acute pneumonia, local infections), and about 2/3 of them
caused by gram-negative flora. In 15-20% they are caused by viruses (herpes, cytomegalovirus).
The frequency of fungal infections is 25-70%. To prevent infectious complications
Broad-spectrum antibiotics, antifungal, and antiviral drugs are used.
In recent years, myelocytokines have been used to combat neutropenia. To them
include granulocyte colony-stimulating factor (filgrastim, lenograstim), granulocyte-
macrophage colony-stimulating factor (sargramostim). Myelocytokines are
polypeptides that accelerate the formation and maturation of neutrophils, eosinophils and monocytes.
The use of these drugs allows you to stimulate granulocytopoiesis and reduce the duration
critical neutropenia, reduce the number of life-threatening infectious complications that
1. Which of the following statements regarding the diagnosis of acute leukemia is correct:
a) the tumor substart is mature cells
b) the tumor substart is maturing cells
V) the substart of the tumor is immature, blast cells
2. LYMPHOADENOPATHY IS UNDERSTANDED:
a) lymphocytosis in peripheral blood;
b) high lymphoblastosis in the sternal punctate;
V) enlarged lymph nodes.
3. Acute myeloblastic leukemia is characterized by:
a) more than 5% of lymphoblasts in the sternal punctate;
b) the presence of gingivitis and necrotizing tonsillitis, more than 30% myeloblasts in the bone marrow;
c) hyperleukocytosis, thrombocytosis, significant enlargement of the liver and spleen.
4.WHAT FACTORS ARE THE BASIS OF THE PATHOGENESIS OF ACUTE
LEUKEMIA:
a) radial
b) chemical
c) chromosomal
d) formation of a pathological clone
d) all of the above
5. IF WHAT SIGN IS PRESENT DIAGNOSIS OF ACUTE LEUKEMIA?
IS IT BECOMING OBVIOUS?
a) anemia
b) ulcerative-necrotic lesions
c) enlarged lymph nodes
G) blastemia in peripheral blood and bone marrow
6. Patient, 36 years old. Suddenly there was weakness, fever, and headache. Diagnosed with "Flu". Within a few days the temperature returned to normal and the patient felt well. In the blood Hb is 131 g/l, er. 1.5 10 12 /l, leuk. - 21.9·10 9 /l, leuk., myeloc. - 1%, young - 10%, p. - 12%, village - 28%, eoz. - 2%, lymph. - 44%, mon. - 3%, ESR - 12 mm/h.
a) chronic lymphocytic leukemia
b) acute lymphocytic leukemia
c) lymphogranulomatosis
d) lymphocytoma
d) leukemoid reaction
7. A 44-year-old patient has been experiencing weakness for a month and a temperature of up to 37.8°C. Was treated with antibiotics without effect. Paleness of the skin. Otherwise no special features. In the blood: Hb - 90 g/l, er. -3.0·10 12 /l, leuk. - 3.3·10 9 /l, ESR - 40 mm/h, thrombus. - 100·10 9 /l. What study is most important to clarify the diagnosis?
A) sternal puncture
b) level determination serum iron in blood
c) counting the leukocyte formula
d) stool analysis occult blood
d) irrigoscopy
8. A 27-year-old patient presented with multiple petechial hemorrhages on the skin and mucous membranes. In the blood: Hb - 100 g/l, er. - 3.1·10 12 /l, leuk. - 41·10 9 /l. There is a leukemic failure, a blood clot. - 15·10 9 /l, ESR - 46 mm/h. Diagnosis?
a) hemophilia
b) leukemoid reaction
V) acute leukemia
d) aplastic anemia
d) all of the above
9. A 37-year-old patient presented with weakness, sore throat, petechial hemorrhages on the skin and mucous membranes. In Hb - 90 g/l, er. - 2.1·1012/l, leuk.- 61·109/l. There is a leukemic failure, lymphoblasts - 70%, thrombus. - 30·10 9 /l, ESR - 56 mm/h. Diagnosis?
A) chronic leukemia,
b) leukemoid reaction
V) acute lymphoblastic leukemia
d) aplastic anemia
d) all of the above
10. A 32-year-old patient has been experiencing fever up to 38°C for a month, resistant to antibiotics, and hyperhidrosis. Revealed: increase cervical lymph nodes, neutrophilic leukocytosis, increased ESR to 50 mm/hour. What should be chosen to verify the diagnosis:
A) lymph node biopsy;
b) sternal puncture;
c) trial prescription of nonspecific anti-inflammatory therapy;
d) trial administration of corticosteroids.
11. When treating a patient with acute myeloblastic leukemia with drugs
choice is:
a) prednisolone;
b) cytosar, rubomycin “7+3”;
c) cyclophosphamide;
d) myelobromol.
12. When treating a patient with acute lymphoblastic drugs
choice is:
A) Helzer protocol;
b) cytosar, rubomycin “7+3”;
c) cyclophosphamide;
d) myelobromol.
13. In the treatment of NEUROLEUKEMIA they use the following drugs:
choice is:
A) dexamethasone, methotrexate, rubomycin;
b) Helzer protocol;
c) cytosar, rubomycin “7+3”;
d) cyclophosphamide;
e) myelobromol.
14. A patient with chronic myeloid leukemia receiving myelosan experiences a rapid increase in symptoms of intoxication, debilitating sweats, pain in the bones, joints, and abdomen. There are 45% blasts in the peripheral blood, which positions are correct?
A) The patient has a blast crisis.
b) The cause of the deterioration of the condition is an overdose of myelosan.
c) It is necessary to increase the dose of myelosan.
d) Treatment with cytostatics is indicated, as in acute leukemia.
e) Severe blastemia is characteristic of the terminal stage
chronic myeloid leukemia.
15. A 54-year-old man complains of weakness, sweating, weight loss, and a sensation of a foreign body in the left half of the abdomen. The skin and mucous membranes are pale. Lymph nodes are not enlarged. An enlarged, painful spleen is palpated. Hb-100 g/l, er-3.5 10 12 /l, color. indicator 0.9, platelets 380-10 9 /l leukemia. - 230-10 9 /l, basophils - 5.5%, eoz. - 9%, promyelocytes - 2%, myelocytes - 2%, metamyelocytes - 20.5%, pal. - 15%, seg. - 12%, lymph - 8.5%, ESR - 20 mm/h. Which positions are correct?
A) The most likely diagnosis is chronic myeloid leukemia.
b) Activity needs to be determined alkaline phosphatase leukocytes
c) Karyological research is uninformative,
d) Possible development of infiltrative and thrombotic complications
d)Eosinophilic-basophilic association of chronic myeloid leukemia.
16. Which method is the most informative for confirming myeloproliferative syndrome in chronic myeloid leukemia:
a) Leukocyte blood count, b) Sternal puncture,
V ) Trepanobiopsy of bone marrow,
d) Puncture of the lymph node,
d) Liver puncture.
17. Which is the most common clinical symptom chronic lymphocytic leukemia:
a) Fever.
b) Bleeding.
V)Enlarged lymph nodes.
d) Enlarged liver.
d) Enlarged spleen.
18. A sharp increase in leukocyte formula granulocytes and the appearance of a small number of immature forms is more often observed with:
a) Chronic myeloid leukemia.
b) Acute blood loss.
V)Acute inflammatory process.
d) Chronic lymphocytic leukemia.
d) Acute leukemia.
19. A 52-year-old patient has been experiencing pain in the left hypochondrium for a year and a half. Upon examination, small hemorrhages were found on the skin, an enlarged spleen protruding 7 cm from under the edge of the costal arch. Blood test: Hb-100 g/l, leukocytes -50x10 9 /l (myeloblasts -1%, promyelocytes - 1%, neutrophilic myelocytes - 3%, neutrophilic metamyelocytes - 8%, neutrophilic band - 12%, segmented -55%, eosinophils -5%, basophils - 2%, lymphocytes - 12%, monocytes -1%). Probable diagnosis:
a) Thrombophlebitic sppenomegaly.
b) Abscess of the spleen.
V) Chronic myeloid leukemia.
d) Liver cirrhosis.
d) Acute leukemia.
a) Antibiotics.
b) Cytostatic drugs.
c) Corticosteroids.
d) Fibrinolytic drugs.
e) Continue observation.
20. Which variant of peripheral blood parameters is more typical for the advanced stage of chronic lymphocytic leukemia?
a) Leukopenia with granulocytopenia.
b) Slight leukzoitosis, neutrophilia with a shift to the left;
c) Hyperleukocytosis, granulocytosis with a left shift to myelocytes and promyelocytes.
21. Which of the following diseases is more typical?
leukocytosis up to 300,000 - 400,00 x 10 9 /l?
a) Chronic myeloid leukemia.
b) Multiple myeloma.
G)Chronic lymphocytic leukemia.
c) Erythremia.
e) Osteomyelofibrosis.
22. In chronic lymphocytic leukemia, all of the following occur, except:
a) Splenomegaly.
b) Hepatomegaly.
c) Enlarged lymph nodes.
d) Leukocytosis with absolute lymphocytosis.
e) Myelosan is the drug of choice.
1c) 2c) 3b) 4e) 5d) 6e) 7a) 8c) 9c) 10a) 11b) 12a) 13a) 14a) 15a)b)e) 16c) 17c)18c) 19 c)b) 20 d) 21 g ) 22 g)
