Acquired hemorrhagic coagulopathy
Classification of the main clinical situations in which there is a majority of acquired coagulopathies: 1) in the neonatal period: a) the deficit-To-vitaminsvitamin factors b) immune thrombocytopenia
Classification of the main clinical situations in which there is a majority of acquired coagulopathies: 1) in the neonatal period: a) the deficit-To-vitaminsvitamin factors b) immune thrombocytopenia
The disease occurs with increasing severe anaemia, fever, enlarged liver and spleen, and hemorrhagic diathesis phenomena in later stages of the disease.
The most characteristic symptom of acute intermittent porphyria are abdominal pain. Sometimes severe pain is preceded by a delay of menstruation. Often patients are, but not find the cause of the pain.
In acute porphyria affects the nervous system by type of severe polyneuritis. It begins with pain in the limbs, difficulty in movements associated with pain, and with symmetrical movement disorders, primarily in the muscles of the limbs.
In acute low-interest leukemia granulocytic-monocytic precursor cells in the agar give low efficiency of kolonialapologie, while at subleukemic the myelosis growth agar colonies has hyperplastic type - effectiveness of kolonialapologie high.
The basic principle of treatment of acute non-lymphoblastic leukemia adults is the rapid release of bone marrow tumor cells with a combination of cytotoxic drugs in adequate doses. A more rapid disappearance of blasts from the bone marrow leads to a more rapid recovery of normal hematopoiesis.
All cells in the human body are divided into 2 types - granulocytic and agranoulozitarna (granular and non-granular), these two groups, in turn, are divided into eosinophils, basophils, neutrophils (granulocyte), and lymphocytes (b - and T-type) and monocytes (agranoulozitarna). In the process of maturation and development (differentiation), all cells go through several stages, the first of which is the progenitor stage (lymphoblasts).
The clinical picture of acute megakaryoblastic leukemia mostly devoid of special features. The outcome of the disease there is suppression of the normal germs of myelopoiesis and other symptoms of the terminal stage. In some cases, acute megakaryoblastic leukemia may have clinical and hematologic picture of acute low-interest leukemia, and bone marrow histology - picture of myelofibrosis. This form of megakaryoblastic leukemia is characterized by a low percentage of blast cells in the bone marrow and blood, polymorphonuclear cell composition of bone marrow, often pronounced megakaryocytes in the bone marrow and diffuse myelofibrosis, and sometimes osteomyelosclerosis. Myelofibrosis usually not possible throughout the illness to receive a bone marrow punctate.
The clinical picture of this form of leukemia is not very different from acute myeloid leukemia, although often expressed intoxication and fever. Much more frequently complications associated with neutropenia, which are dominated by necrotic changes in the mucous membranes of the mouth and pharynx, aided by a characteristic of this form of acute leukemia leukemic infiltration of the gums, leading to hypertrophy of the papillae. Inflammation of the tongue may be due to the neutropenia.
The clinical picture of the UML are well known and manifested by the following syndromes: anemia, hemorrhagic and toxic, which are characterized by pale skin, severe weakness, dizziness, decreased appetite, fatigue, fever with no signs of catarrhal symptoms.
Acute posthemorrhagic anemia causes the first symptoms of collapse. The person has severe weakness, dizziness, pallor, dry mouth, cold sweat, vomiting. Decreases arterial and venous pressure, decreased cardiac output of blood, dramatically quickens the pulse. Filling pulse becomes weak.
The bone marrow unable to produce healthy red blood cells. Or leukopenia (low white cells) or leukocytosis (high white blood cell count) can be observed in the peripheral blood.
The clinical picture of amoebic liver abscess is almost similar to the pyogenic abscesses, however, the temperature is usually somewhat lower than in pyogenic abscesses, until joined by secondary infection. History data are usually available undergoing dysentery.
In the basis of hemolytic anemia have the value of the accumulation on the surface of red blood cells cholesterol and impaired updating of phospholipids of erythrocyte membranes.
Anemia occurs due to the violation of the synthesis of porphyrins. Lead inhibits enzymes involved in heme synthesis. As a result accumulates in the urine 6 aminolevulinate acid, and erythrocyte protoporphyrin. In connection with the violation of synthesis of heme increased serum iron concentration, it is deposited in the organs.
Hereditary and acquired anemia associated with impaired activity of enzymes involved in the synthesis of porphyrins and heme, hypochromic, with a high content of iron in the body and hemosiderosis bodies. Hereditary anemia are relatively rare, especially in men. The acquired form is most often associated with poisoning. Generally, the causes of acquired disorders of the synthesis of porphyrins are lead poisoning and deficiency of vitamin B6.
The disease is inherited in dominant type. The instability of the hemoglobin molecule is detected when the amino acid substitution relate to communication with globin gem, connection of a– and beta-globin chains between them.
B12-deficiency anemia develops relatively slowly and may be oligosymptomatic. Clinical signs of anemia are nonspecific: fatigue, fatigue, shortness of breath, dizziness, palpitations. Patients pale, subinterior.
The clinical picture of the disease is directly dependent on the localization of the defect in the chain of hemoglobin. So, hemoglobinopathies can be characterized by anaemia, or, conversely, increase the content of hemoglobin, and red blood cell in the blood. Quite often the disease is completely asymptomatic.
The clinical picture of idiopathic aplastic anemia may be different. Sometimes the disease begins acutely and progresses very quickly, almost defies any therapy. But more often it starts with a whimper, the patient adapts to anemia and turns to the doctor when the severity of pancytopenia significant. The clinical picture of depression of hematopoiesis consists of anaemia of varying depth, thrombocytopenia with all clinical manifestations thrombocytopenic syndrome (such as bruising, petechial skin rash, nasal, gingival bleeding, uterine bleeding). Often the consequence of severe neutropenia from pneumonia, ear inflammation and other inflammatory processes.
When acute onset autoimmune hemolytic anemia in patients appear rapidly increasing weakness, shortness of breath and palpitations, pain in the heart area, sometimes in lower back, fever and vomiting intense jaundice. During the chronic process is observed relatively satisfactory state of health of patients, even with profound anemia, often expressed jaundice, in most cases, enlargement of the spleen and sometimes the liver, alternating periods of exacerbation and remission.
This form of autoimmune hemolytic anemia, usually begins gradually, in more rare cases acute onset, the same as when agglûtininovaâ form. Hemoglobin decreased to 40-60 g/l. the Patient may be slightly jaundiced, although this form of jaundice is less than when agglûtininovaâ forms of anemia. The spleen is enlarged, almost half of patients, but this increase is negligible. Also 50 cases of patients with enlarged liver
In the bone marrow in most cases enlarged red sprout, but sometimes the number erythrokaryocytes decreases. Probably such crises are associated with a very large number of antibodies, resulting in the collapse not only of the peripheral blood erythrocytes, but also erythrokaryocytes. It cannot be excluded that at the heart of such crises, as in mikrosferocitoze and sickle cell anemia, involved infection with parvovirus.
Disease has a gradual increase in symptoms the main complaints that patients have, are the complaints of a General nature: lowering efficiency, weakness, malaise, cold intolerance. The majority of patients after exposure to the cold mark the blue, and then the whitening of the fingers, toes, and ears, tip of the nose. There is a sharp pain in the limbs. After a long stay in the cold in these patients often develop gangrene of the fingers.
It should be noted that myeloid leukemias are frequent in families with different genetic defects and individuals with genetic diseases non-neoplastic nature. For example, they are described with Marfan's syndrome, osteogenesis imperfect, with Gaucher disease. In hereditary diseases that affect the bone marrow, the likelihood of developing myeloid leukemia.