Acquired platelet dysfunction

Introduction to acquired platelet dysfunction Acquired platelet dysfunction, also known as secondary thrombocytopenia, is a thrombocytopenia secondary to other diseases, involving a considerable number of diseases. Such as drug-induced immune thrombocytopenia, other immune thrombocytopenia such as Evans syndrome, chronic lymphocytic leukemia, various acute leukemia, lymphoma, systemic lupus erythematosus, rheumatoid arthritis, hyperthyroidism and so on. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: leukemia

Acquired platelet dysfunction

Abnormal platelet function (30%):

May be due to endogenous platelet defects, or may be caused by exogenous factors that alter normal platelet function. Platelet defects may be hereditary or acquired, and the coagulation phase of coagulation is tested. (PTT and PT) are normal (but not all) in most cases. Because of the widespread use of aspirin, which affects platelet function, acquired platelet dysfunction is common, and many other drugs can cause platelet dysfunction.

Abnormal bone marrow disease (25%):

Many clinical diseases (such as myeloproliferative diseases, uremia, macroglobulinemia, multiple myeloma, cirrhosis, and systemic lupus erythematosus) can also affect platelet function. Aspirin can make the bleeding time of normal subjects slightly Prolonged, but for patients with pre-existing platelet dysfunction or severe hemagglutination (eg, given a therapeutic dose of heparin or severe hemophilia), it can significantly prolong the bleeding time during surgical extracorporeal circulation when blood flows through Pumping the oxygenator can cause platelet dysfunction and prolonged bleeding time. Therefore, regardless of the patient's platelet count, as long as there is a large amount of bleeding and prolonged bleeding after cardiac surgery, platelet concentrate should be given. Platelet dysfunction appears to be mainly due to Platelet surface fibrinolysis is activated, leading to the loss of platelet membrane glycoprotein Ib and VWF binding sites. It is reported that aprotinin (a protease inhibitor that neutralizes plasmin activity) prevents bleeding during surgical cardiopulmonary bypass. Time prolongs and reduces blood transfusions.

Other reasons (20%):

Due to chronic renal failure, uremia patients may have an unexplained bleeding time. In effective dialysis, the bleeding time can be temporarily shortened after input of cryoprecipitate or desmopressin. Red blood cells or erythropoietin can be used to make red blood cells. The increase in the number can also shorten the bleeding time.

Acquired platelet dysfunction prevention

1. Actively participate in sports activities to enhance physical fitness and improve disease resistance.

2. Pay attention to prevent respiratory infections, measles, chickenpox, rubella and hepatitis, otherwise it is easy to induce or aggravate the condition.

3. In the acute phase or when there is a lot of bleeding, you should rest in bed, limit activities, and eliminate the fear of nervousness.

4. Avoid traumatic collisions, so as not to cause bleeding.

5. When the platelet count is lower than 20×10 ⁹ /L, it is necessary to closely observe the changes in the condition and prevent various trauma and intracranial hemorrhage.

6. Diet should be light, rich in nutrition, easy to digest, hematemesis, blood in the stool should be in a semi-flow diet, avoid hard food and crude fiber food, avoid spicy food, you can eat peanuts, red dates and other foods.

Acquired platelet dysfunction complications Complications leukemia

Severe patients may have hematemesis and blood in the stool. Very few patients may have intracranial hemorrhage, intracranial hypertension, and even coma.

Acquired platelet dysfunction symptoms common symptoms pale pale skin purpura nasal herpes fatigue tired

1. Drug-induced immune thrombocytopenia: There is an incubation period before the occurrence of bleeding symptoms. The short-term can occur within a few hours after taking the drug. The elderly can develop after a few months, usually 5-10 days, often accompanied by chills and fever. Headache, nausea, vomiting, etc.

Second, other immune thrombocytopenia: suffering from teaching systemic skin purpura, nasal discharge or female menorrhagia, fatigue, weakness, pale, dark urine, occasionally visible signs of kidney damage such as hypertension, hematuria, azotemia Etc., the symptoms of the nervous system are rare.

Third, a coagulopathy

1, aplastic anemia and bone marrow disease: a variety of causes of aplastic anemia, with reduced bone marrow megakaryocytes, decreased platelet production, etc., thrombocytopenia can be the earliest manifestation of aplastic anemia, also It may be that after treatment, hemoglobin and granulocytes return to normal, platelets have not recovered, and bone marrow disease such as cancer cells infiltrate with thrombocytopenia. Most of the tumor cells damage giant nucleus and thin legs, so platelet production is reduced. Can be clearly diagnosed, the former bone marrow hyperplasia, megakaryocytes decreased; the latter can be found tumor cells.

2, physical and chemical factors inhibit bone marrow: physical and chemical factors such as ionizing radiation, alkylating agents, antimetabolites, cytotoxic agents, etc. in the treatment of malignant tumors, thrombocytopenia is a common complication, or directly poison bone marrow cells, or immune response, Most of these factors cause diffuse bone marrow damage, and patients show a reduction in whole blood, but a few patients with megakaryocytes are more sensitive to radiation, because some diseases can only show thrombocytopenia and megakaryocytes decrease.

3, factors that selectively inhibit megakaryocytes: chlorothiazide drugs and their synergists can cause thrombocytopenia, in addition to the mechanism of platelet antibodies, but also by inhibiting the production of platelets, and the latter is more important, generally considered to be The role of pharmacology, patients with bone marrow suppression, megakaryocytes decreased, light asymptomatic patients can take up to 25 of this drug, individual pregnant women can cause congenital thrombocytopenia after taking this drug, the mother can be asymptomatic .

4, congenital megakaryocyte production is poor: the disease is rare, megakaryocytes and platelets are significantly reduced, often accompanied by congenital malformations, such as kidney, heart, bone, etc., the prognosis is poor, about 2 / 3 children died within 8 months Intracranial hemorrhage, maternal pregnancy with rubella, oral D860 can be a disease factor.

5, other: estrogen can occasionally cause no megakaryocyte thrombocytopenia, ethanol can inhibit platelet production, which is a common cause of long-term heavy drinking into thrombocytopenia, clinically rare bleeding, stop drinking, platelets can be restored .

IV. Ineffective thrombocytosis is common in some patients with megaloblastic anemia with partial vitamin B12 or folic acid deficiency. It is characterized by thrombocytopenia, some patients have bleeding tendency, some show reduced whole blood, and bone marrow megakaryocytes are normal or even increased. Therefore, for ineffective thrombocytopenia, platelets can return to normal with the treatment of poor young people.

5. Thrombopoietin deficiency This disease is caused by thrombocytopenia caused by congenital thrombopoietin deficiency. This disease is mostly hereditary. It has bleeding in infancy, platelet count is reduced, megakaryocyte number is normal, morphology and structure. No special changes.

Sixth, periodic thrombocytopenia This disease is a hemorrhagic disease caused by unexplained periodic thrombocytopenia. The disease is more common. Thrombocytopenia and platelet increase or normal alternate at regular intervals. The interval is usually 20 A 30-day, the disease is more common in women, its seizures are often consistent with menstruation, menstrual period thrombocytopenia, increased bleeding, megakaryocytes generally do not reduce, mainly skin and mucous membrane bleeding, no specific treatment.

7. Thrombocytopenia caused by spleen disease Under normal circumstances, one third of the body's platelets are arrested in the spleen. When there is splenomegaly, such as portal hypertension, Gaucher's disease, lymphoma, sarcoidosis, Folty syndrome, etc. The platelet count can be reduced, but the total amount of platelets in the body is not reduced. After injection: adrenaline, the platelet count can be significantly increased within a certain period of time. Sometimes, there may be factors of increased platelet destruction.

8. Infectious thrombocytopenia This disease is a thrombocytopenic bleeding disease caused by viruses, bacteria or other infections:

1, viral infection: viral infections that can cause thrombocytopenia include measles, rubella, herpes simplex, chickenpox, cytomegalovirus infection, viral hepatitis, flu, mumps, infectious mononucleosis, epidemic hemorrhagic fever, cat In the case of claw heat, dengue fever, etc., the virus can invade megakaryocytes, reduce platelet production, and the virus can also adsorb to platelets, resulting in increased platelet destruction; some patients with severe measles and epidemic hemorrhagic fever consume platelets due to disseminated intravascular coagulation.

2, bacterial infection: many bacterial infections can cause thrombocytopenia, including Gram-positive and negative bacterial sepsis, meningococcus, bacteremia, typhoid fever, tuberculosis, bacterial endocarditis, scarlet fever, brucellosis, Bacterial toxins inhibit platelet production, or increase platelet destruction, and may also increase platelet consumption due to toxins affecting vascular wall function. In short, patients with simple thrombocytopenia should consider the disease if there is a clear sign of infection. After primary infection control, Then the platelets recover.

Acquired platelet dysfunction

First, the bleeding time (BT) determination of the meaning of bleeding time is prolonged

1. Abnormal vascular structure or function: such as scurvy, telangiectasia, vascular pseudohemophilia (von Willebrand's disease).

2. Abnormal platelet count: thrombocytopenic purpura due to various causes, thrombocytosis.

3. Abnormal platelet function: such as platelet disease, thrombocytopenia.

4. Others: such as low/no fibrinogenemia, primary and secondary fibrinolysis, anticoagulant substances in the blood circulation.

Second, the significance of aspirin tolerance test

This test is an important method for diagnosing von Willebrand's disease. The bleeding time of the mild patients may still be normal, but the bleeding time may be prolonged after taking aspirin.

3. Capillary fragility test significance The new bleeding point is more than 10 positive, indicating an increase in capillary fragility, which can be seen in the following cases:

1. Abnormal capillary wall: such as hereditary hemorrhagic telangiectasia, allergic purpura, scurvy, infectious vascular purpura.

2. Decrease in platelet count: such as primary or secondary thrombocytopenic purpura.

3. Platelet function-deficient diseases: such as platelet weakness, platelet disease, drugs and certain diseases cause platelet-derived functional defects.

Fourth, the significance of vascular pseudohemophilia factor (VWF) determination

1. Vascular pseudohemophilia factor reduction is seen in: vascular pseudohemophilia, hemophilia carriers.

2. Increased vascular pseudohemophilia factor is found in:

(1) vascular endothelial injury, such as ischemic cardio-cerebral vascular disease, peripheral vascular disease.

(2) Hypercoagulable diseases such as nephrotic syndrome, pregnancy-induced hypertension, and uremia.

(3) Others such as major surgery, diabetes, hyperlipidemia, DIC, etc.

Determination of 6-keto-prostaglandin F1a (PG F1a) significance 6-keto-prostaglandin reduction

1. Congenital platelet arachidonic acid metabolism-deficient disease or oral non-steroidal anti-inflammatory drugs such as aspirin.

2. Hypercoagulable state and thrombotic diseases such as coronary heart disease, cerebral arteriosclerosis, cerebral thrombosis, diabetes, glomerular lesions, peripheral vascular thrombosis, etc.

Diagnosis and differentiation of acquired platelet dysfunction

diagnosis

First, bleeding time (BT) determination significance: prolonged bleeding time seen in vascular structural or functional abnormalities: such as scurvy, telangiectasia, von Willebrand disease (von Willebrand disease), abnormal platelet count: for various reasons Thrombocytopenic purpura, thrombocytosis, abnormal platelet function: such as platelet disease, thrombocytopenia, other: such as low/no fibrinogenemia, primary and secondary fibrinolysis, blood circulation Anticoagulant substances, etc.

Second, the significance of aspirin tolerance test: This test is an important method for the diagnosis of vascular pseudohemophilia, because the bleeding time of the mild patients can still be normal, but the bleeding time can be prolonged after taking aspirin.

Third, capillary fragility test significance: more than 10 new bleeding points are positive, indicating increased capillary fragility, can be seen in the following conditions: capillary wall abnormalities: such as hereditary hemorrhagic telangiectasia, allergic purpura, scurvy Infectious vascular purpura, decreased number of platelets: such as primary or secondary thrombocytopenic purpura, platelet function-deficient diseases: such as thrombocytopenia, thrombocytopenia, drugs and certain diseases cause platelet-derived functional defects .

Fourth, vascular pseudohemophilia factor (VWF) determination significance: vascular pseudohemophilia factor reduction seen in: vascular pseudohemophilia, hemophilia carriers, increased vascular pseudohemophilia factor seen in: (1) blood vessels Endothelial injury, such as ischemic cardio-cerebral vascular disease, peripheral vascular disease; (2) hypercoagulable disease, such as nephrotic syndrome, pregnancy-induced hypertension, uremia, etc.; (3) other major surgery, diabetes, hyperlipidemia, DIC Et,5,6-keto-prostaglandin F1a (PG F1a) determination of 6-keto-prostaglandin reduction found in congenital platelet arachidonic acid metabolism-deficient disease or oral non-steroidal anti-inflammatory drugs such as aspirin; Status and thrombotic diseases such as coronary heart disease, cerebral arteriosclerosis, cerebral thrombosis, diabetes, glomerular lesions, peripheral vascular thrombosis, etc.

Differential diagnosis

The disease needs to be differentiated from primary thrombocytopenia.

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