Thrombocytopenia: causes and treatment, pictures
Thrombocytopenia (thrombocytopenia) – reduced level of platelets (red blood platelets) in the blood to less than 150*109/l relative to the norm, which is within 180 – 320*109/L. Thrombocytopenia may be a separate disease (primary) or be a symptom of another disease (secondary or symptomatic).
Thrombocytopenia (thrombocytopenia) – reduced level of platelets (red blood platelets) in the blood to less than 150*109/l relative to the norm, which is within 180 – 320*109/L. Thrombocytopenia may be a separate disease (primary) or be a symptom of another disease (secondary or symptomatic). Platelets – fragments of cytoplasm megakaryocytes, they have no core. Formed in result of separation of small plots of megakaryocyte – maternal cells, a major cellular predecessor. In the body platelets perform several functions:
- involved in the formation of the primary platelet plugs;
- secrete compounds that narrow the lumen of the vessel;
- activate the blood clotting system, resulting in a fibrin clot.
That is why the shortage of platelets in the blood developing bleeding, often carrying a threat to the health and life of the patient.
The etiology and pathogenesis of thrombocytopenia
The main causes of the pathology:
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- education insufficient number of platelets (reduced products);
- increased destruction of platelets;
- the redistribution of platelets in which their number in the General circulation is sharply reduced;
- increased body’s need for platelets.
Education insufficient number of platelets
Thrombocytopenia arising from weak synthesis of platelets, divided into three groups:
- deficiency of megakaryocytes (by bone hypoplasia megakaryocytes);
- ineffective thrombocytopoiesis in which the precursor cells are formed in sufficient quantity, but the formation of a platelet from megakaryocyte almost does not occur;
- rebirth (metaplasia) megakaryocytes process.
The development of hypoplasia of the bone marrow with subsequent thrombocytopenia sometimes with such pathologies:
- megakaryocytes congenital hypoplasia as a result of severe genetic disorders – Fanconi aplastic anemia (constitutional pancytopenia) and amegakaryocytic thrombocytopenia;
- purchased insulated amegakaryocytic thrombocytopenic purpura;
- receiving cytotoxic drugs (myelosuppressive drugs) that have a direct impact on red bone marrow, inhibiting its functions;
- radiation sickness;
- the Chloramphenicol (provided that the patient has an idiosyncrasy – hypersensitivity to the drug);
- the use of certain other drugs (thiazide diuretics, interferon, estrogen);
- alcohol abuse (alcohol inhibits megakaryocytic process);
- the viruses of mumps, hepatitis A, b, C and HIV cause thrombocytopenia products;
- sometimes when vaccination with a live attenuated measles vaccine may develop transient thrombocytopenia;
- sepsis is a generalized inflammatory response caused by fungal or bacterial infections;
- weakly expressed thrombocytopenia can cause a state of hypoxia.
Failures in the processes of platelet production occur in the following cases:
- congenital deficiency thrombopoetin – a substance that stimulates the synthesis of platelet;
- the development of megaloblastic anemia due to vitamin B12 deficiency and folic acid;
- iron deficiency anemia (due to iron deficiency reduces the production of platelets and is not absorbed vitamin B12);
- infection of viral etiology;
- chronic alcoholism;
- congenital abnormalities, where there is a combination of thrombocytopenia and thrombocytopathy (autosomal dominant anomaly may Hegglin, syndrome Bernard-Soulier, Wiscot-Aldrich syndrome, etc.).
Rebirth megakaryocytes process occurs with such pathologies:
- cancer in the last stages, when metastases develop, penetrating into the bone marrow;
- malignant blood diseases (lymphoma, generalized plasmacytoma or disease Rusticola Calera, leukemias);
- myelofibrosis (replacement of fibrous tissue);
- sarcoidosis (replacement of specific granulomas).
Increased destruction (destruction) of platelets
The destruction of platelets – the most common cause in the development of thrombocytopenia. When there is an increased need for red blood platelets, bone marrow starts working in emergency mode. Develops over time, the hyperplasia of the tissue and increases the number of megakaryocytes. But if the platelets are destroyed faster than the time to enter the bloodstream new elements (i.e., compensatory mechanisms can’t cope with their task), there is a thrombocytopenia. Clinically, thrombocytopenia resulting from increased destruction of platelets in the pathogenesis divided into two groups: immunological and nonimmunological.
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This form of disease is caused by the attack and subsequent destruction of platelets by the specific antiplatelet antibodies and immune complexes. Can be congenital and acquired disorders. Immunologic thrombocytopenia are divided into three groups:
- izoimmunnaya thrombocytopenia (developing production alloreactive antibodies that destroy «foreign» platelets when injected into the body, for example by blood transfusion or during pregnancy);
- autoimmune thrombocytopenia – the synthesis of autoantibodies that cause damage to own tissues and cells of the body;
- immune thrombocytopenia that develops after consuming certain drugs.
To isoimmune thrombocytopenia include congenital and acquired abnormalities:
- neonatal alloimmune thrombocytopenic purpura (a condition in which there is incompatibility between mother and fetus platelet indices);
- post-transfusion thrombocytopenic purpura (complication about a week after the procedure, blood transfusions);
- insensitive (refractory) patients to platelet transfusion, which is expressed in the absence of therapeutic effect (develops in cases of repeated blood transfusions).
Autoimmune thrombocytopenia there are primary (idiopathic, unknown etiology) and secondary (appearing under the influence of certain causes). The primary pathologies include acute and chronic autoimmune thrombocytopenic purpura. Secondary thrombocytopenic purpura is accompanied by many diseases, among which are:
- cancer of lymphoid tissue (Hodgkin’s disease, limfoleikoze, lymphoma, including non-Hodgkin’s);
- acquired autoimmune hemolytic anemia (Evans syndrome-Fisher);
- diseases connective tissue (systemic lupus erythematosus, rheumatoid arthritis);
- organ-specific autoimmune diseases – diseases in which there is a loss of certain organs (liver, digestive tract, joints, endocrine glands);
- viral diseases (HIV, rubella, herpes zoster).
Immune thrombocytopenia caused by medication
The list of drugs that can cause thrombocytopenia, is quite long. The main groups of such drugs:
- antibiotics (Ampicillin, Penicillin, Rifampicin, Gentamicin, Cephalexin);
- sulfonamides (Biseptol);
- nonsteroidal anti-inflammatory drugs;
- diuretics (Furosemide, Chlorthiazide);
- antidiabetic drugs (Tolbutamide, Chlorpropamide);
- drugs and narcotic painkillers (heroin, Morphine);
- antihistamines (Cimetidine);
- some medicines belonging to other groups, Ranitidine, heparin, quinidine, Methyldopa, Digitoxin, gold salts.
Thrombocytopenia neironnoi etiology can be divided into congenital and acquired. Congenital disease that leads to enhanced destruction of the platelets:
- preeclampsia during pregnancy in the mother;
- infectious processes;
- heart disease.
Acquired thrombocytopenia non-immune origin with increased destruction of platelets develop under the following conditions:
- the implantation of artificial heart valves, bypass grafting of blood vessels;
- expressed atherosclerosis;
- massive blood loss;
- metastases affecting the blood vessels;
- disease Marchiafava-Micheli (paroxysmal nocturnal hemoglobinuria acquired hemolytic anemia, in which there is a decrease in production, change of structure and the accelerated destruction of platelets);
- burn disease;
- hypothermia (hypothermia);
- influence of increased atmospheric pressure;
- Gasser disease (hemolytic uremic syndrome);
- infectious diseases;
- intravenous infusion of large volumes of solutions (massive transfusion), which develops thrombocytopenia breeding.
The redistribution of platelets
Forced redistribution leads to an excess of platelets in the body of the Deposit – the spleen. Develops hypersplenism (splenomegaly, up to 90% of platelets are in the spleen, although it is usually deposited only 1/3 of these cells). Deposition occurs for the following reasons:
- liver cirrhosis with portal hypertension;
- malignant pathology of the circulatory system (lymphomas, leukemias);
- infectious diseases (tuberculosis, malaria, endocarditis, etc.);
- hypothermia (hypothermia).
The advent of increased need for platelets
When a significant loss of platelets in the processes of thrombosis there is an increased need for them. This happens:
- when massive bleeding;
- during extracorporeal circulation (for example, when using an artificial kidney or extracorporeal circulation).
Symptoms of thrombocytopenia
The main feature of the disease is the development of the hemorrhagic diathesis, in which the mucous membranes and the skin appears small rash hemorrhagic in the form of petechiae (pinpoint hemorrhages) or Achkasov up to 2 cm in diameter. The rash is painless, they do not have signs of inflammation. Their appearance is easy to trigger – just the minimum of injury to the vessels. Tight clothing, seams which cause friction, any injection, minor injuries – all can cause bruising and petechiae.
The lower the level of platelets in the blood, the harder manifestations of the hemorrhagic diathesis. In primary thrombocytopenia, serious bleeding occur only if the platelet count below 50*109/l. When thrombocytopenia occurs in the background of infectious processes, accompanied by fever, bleeding may occur at higher platelet counts.
The first signs of a worsening condition is the appearance of recurrent bleeding from the nose. In addition, increased bleeding of mucous membranes, primarily of the gums and oral cavity. Do women have heavy menstruation. The rash of hemorrhagic diathesis occur first in the legs and the anterior surface of the abdominal wall of the lower half of the body. As the progression of the disease can cause bleeding into the joints, digestive tract, metrorrhagia (uterine bleeding) and hematuria (blood in urine).
The higher rises the rash, the more unfavorable the prognosis. The upper half of the body, the face, especially hemorrhages in the conjunctiva are signs of worsening of the pathological process. The most severe consequences of bleeding in the retina of the eye that leads to vision loss, and hemorrhage in the brain or its membranes (stroke). While these symptoms are nonspecific and may accompany other pathologies (e.g., trombotsitopatii), then thrombocytopenia should be suspected in the case when there is a combination of hemorrhagic syndrome and reduced platelets in the blood.
Diagnosis of the disease
The physician must collect the most complete history, which he carefully asks the patient about the occurrence of bleeding in the past and when it happened. Suffered if the patient has hemorrhagic diathesis, what medications he was taking. Special attention is paid to questions about the presence of comorbidities (any diagnoses). Visually, the doctor evaluates the patient’s condition, the type and degree of the bleeding, localization of the rash, the amount of blood loss (excessive bleeding). Objective examination shows a positive sample «pinch», «harness» (on the fragility of blood vessels).
The diagnosis is confirmed by laboratory blood tests, which is determined not only platelets, but also platelet histogram, measure of anisocytosis (changes in size of platelets) and thrombocrit (percentage of platelets in the blood volume). The deviation of these indicators may indicate various pathological processes occurring in the body and caused thrombocytopenia.
Treatment of thrombocytopenia
The treatment of the disease depends on the causes that provoked it:
- the lack of vitamin B12 and folic acid are assigned the medication, diet, aimed at removing the deficiency;
- if thrombocytopenia occurred as a result of medication required their abolition and subsequent correction of treatment regimens.
In primary idiopathic purple children taken to adhere to the expectant management as the prognosis is often favorable, and remission occurs within six months without medical treatment. If the disease progresses (there is a decline of 20 thousand platelets/µl), with hemorrhagic syndrome increases (there hemorrhage in the conjunctiva, a rash on the face), shows the assignment of the steroids (Prednisolone). In this case, the effect of the drug seen in the first days of admission, and a week later the rash disappears completely. Over time, the number of platelets in the blood comes to normal.
In adults, idiopathic thrombocytopenia occurs quite differently. Recovery without medical therapy almost does not occur. In this case, the patients are also prescribed a course of treatment with Prednisolone, which usually lasts about a month. If the effect of therapy is not present, the doctor will immunotherapy – intravenous immunoglobulins (Sandoglobulin) in parallel with high doses of steroids. In the absence of remission within six months, you must hold a splenectomy – removal of spleen. Therapy of the secondary forms of thrombocytopenia is to treat the underlying pathology, but also to prevent the development of complications. When the platelet count reaches critical numbers, and the risk of hemorrhagic complications increases, prescribe a platelet transfusion and a course of Prednisone.
Diet for thrombocytopenia
Special diet with thrombocytopenia has not been developed. If there are no other diseases, doctors recommend the common table. This food should contain enough proteins, so vegetarianism when thrombocytopenia is strictly contraindicated.
Banned the use of any alcoholic beverages and foods, contain synthetic additives – preservatives, colorants, flavors, etc. During an exacerbation are shown sparing diet. During this period, should not eat hot and spicy dishes and smoked meats. Food and drinks should be warm, but in any case not hot.