What Is the Connection between Thrombosis and Embolism?

1. Venous thrombosis

Thrombosis and thromboembolism

This is a common senile disease. Thromboembolic diseases include thrombosis and embolism, which can occur anywhere in the heart cavity, arteries or veins in the blood circulation. If the blood coagulates to form a blood clot in a local area, it is called thrombosis; the formed thrombus detaches from the original position, and blocks other parts along the blood flow, which is called embolism.

Thrombosis and signs and symptoms of thromboembolism

1. Venous thrombosis

Most common. It is common in deep veins, such as the iliac vein, femoral vein, terminal mesenteric vein, and portal vein, and venous thrombosis of the lower limbs is particularly common in the elderly. The common causes are surgery, trauma, malignant tumors, and vasculitis. But most of the reasons are unknown. Thrombosis types are mostly red blood cell thrombosis and myofibrin thrombosis. Main manifestations are: 1 local swelling and pain of thrombosis 2 clinical abnormalities caused by blood circulation disorder at the distal end of the thrombus, such as edema, swelling and pain, skin color change, ascites, etc. 3 Pulmonary infarction caused by thrombosis.

2. Arterial thrombosis

It is more common in the cerebral arteries, mesenteric arteries, and limb arteries of the coronary arteries. Age is an important factor in coronary atherosclerotic heart disease. Coronary heart disease can also cause common heart disease in the elderly and directly threaten their lives. The high prevalence of cerebrovascular disease, high recurrence rate, and high disability bring great pain to middle-aged and elderly people. The type of thrombus is mostly platelet thrombus in the early stage, followed by fibrin thrombus. The clinical manifestations are: 1 The onset is more sudden, and there may be severe local pain, such as angina pectoris, headache, abdominal pain, and severe pain in the limbs. Shock, arrhythmia, disturbance of consciousness, and hemiplegia. 3 Thrombosis may cause cerebral embolism, myocardial infarction, renal embolism, spleen embolism and other related symptoms and signs, 4 clinical manifestations caused by ischemic necrosis of the donor tissue, such as fever.

Capillary thrombosis

Common in disseminated intravascular coagulation, snow mountain thrombocytopenic purpura, and hemolytic uremic syndrome. The manifestations often lack specificity, mainly including microcirculation disorders, skin and mucosal embolism necrosis, organ dysfunction, and bleeding tendency.

Causes of thrombosis and thromboembolic disease

1. Endothelial injury

The integrity of the vascular intima, the antiplatelet aggregation and anticoagulant activity of vascular endothelial cells are important conditions for maintaining blood flow. When vascular endothelial cells are damaged due to factors such as mechanical, infection immunity, and vascular autopathy, thrombosis can be promoted through the following mechanisms: 1 Reflex vasoconstriction and other factors slow blood flow, blood stasis, and 2 subendothelial tissue Exposure, vWF release, etc. lead to platelet adhesion, aggregation and release reactions in the vessel wall 3TF expression and release, exposure of collagen fibers under the subendothelium initiates the coagulation process, 4 endothelial platelet aggregation (prostacyclin I2, etc.) and anticoagulation Impaired function (heparin sulfate, etc.) and accelerates the coagulation process.

Platelet activation

The adhesion and aggregation of platelets outside the injured intima leads to platelet activation and release reactions. It participates in snow mountain formation through the following mechanisms: 1 platelet aggregation directly forms platelet thrombus, 2 releases PF-3 and participates in the coagulation process 3 starts arachidonic acid Metabolism, TXA2, etc., constrict blood vessels and platelet aggregation, 4 release SHT and ADP, etc., accelerate the two-phase aggregation of platelets 5 Under certain conditions, directly activate F, , start the coagulation process.

3.Initiation of the coagulation process

Under the condition of increased blood coagulation, coagulation process is initiated due to vascular endothelial damage, platelet activation and other factors, and promote thrombus formation: 1 coagulation activation, formation of fibrin thrombus, 2 thrombin formed during coagulation, feedback Accelerate the coagulation process, 3 thrombin and other activated fibrinogen, start the fibrinolytic process, 4 thrombin guides irreversible platelet aggregation and release response.

4, reduced anticoagulant activity

Decreased physiological anticoagulant activity of the human body is an important condition for thrombosis. The common causes of decreased anticoagulant activity of the human body are: 1 AT- is reduced or lacking 2 PC and PS deficiency 3 Anti-protein caused by structural abnormalities such as FV c phenomenon (APC-R), o4 heparin cofactor (HC-) deficiency and so on.

5. Reduced fibrinolytic activity

Common clinical patients include: 1 abnormal plasminogen structure and function, such as abnormal plasminogenemia, 2 plasminogen activator (PA) release disorder, 3 plasminogen activator inhibitor ( PAI) is too much, these factors cause the body to reduce fibrin clearance ability, which is conducive to thrombosis and expansion.

6, abnormal blood flow

Systemic or local blood flow stasis and slowness caused by various reasons are important factors for thrombosis, such as hyperfibrinogenemia, hyperlipidemia, dehydration, high viscosity syndrome caused by increased red blood cells, and circulatory disorders. Thrombosis can be promoted through the following mechanisms: red blood cells aggregate to form red thrombus 2 promote adhesion and aggregation of platelets and endothelium, release reaction 3 damage the blood vessel endothelium, and start the coagulation process.

Thrombosis and the pathophysiology of thromboembolism

1. Endothelial injury

Platelet activation

3.Initiation of the coagulation process

4, reduced anticoagulant activity

Decreased physiological anticoagulant activity of the human body is an important condition for thrombosis. The common causes of decreased anticoagulant activity of the human body are: 1 AT- is reduced or lacking 2 PC and PS deficiency 3 Antiprotein caused by structural abnormalities such as FV c phenomenon (APC-R), o4 heparin cofactor (HC-) deficiency and so on.

5. Reduced fibrinolytic activity

6, abnormal blood flow

Diagnosis of thrombosis and thromboembolism

The main points of diagnosis of this disease are: 1. Basic diseases such as atherosclerosis, diabetes, kidney disease, pregnancy, thromboembolism, recent surgery and trauma, long-term use of contraceptives, etc. It should be noted that some elderly people are healthy but have a pre-thrombotic state. 2. Symptoms and signs of various thrombosis and thromboembolic diseases. 3. Imaging examinations such as angiography, vascular ultrasound Doppler, CT, MRI, electrical impedance, etc. 4. Hematological examination can be selected according to the above six factors of thrombosis, combined with the patient's condition. Thrombosis is mainly related to the state of hypercoagulability. Viable coagulology, coagulation activation molecular markers, AT-, APC-R and other aspects are detected. If thrombus formation involves vascular disease, endothelin, vWF, TM are feasible. , Angiography and imaging.

Thrombosis and thromboembolism treatment options

The purpose is to improve the prethrombotic state or hypercoagulable state, prevent the thrombus from expanding and new thrombus formation, dissolve the thrombus, reconstruct the blood flow channel, and restore the blood supply and function of related tissues and organs.

1. Treat basic diseases such as preventing and curing arteriosclerosis and controlling diabetes.

2, general treatment of bed rest, elevated venous thrombosis of the stump.

3. Symptomatic treatment includes pain relief and correction of organ failure.

4.Thrombotic drugs

(1) Anticoagulant therapy 1. Heparin and small molecular weight heparin: It is mainly used for the treatment of thrombotic diseases that have recently occurred. The initial dose is 10,000 to 20,000 U / d, instilled once every 8 hours, and AFTT is used as a monitoring index to adjust the dose in the future, so that AFTT is prolonged by 1-2 times, and the total course of treatment should not exceed 10 days. Small molecular weight heparin introduced in recent years has strong anti-factor Xa effect, weak antithrombin, less dependence on AT- and less thrombocytopenia, high bioavailability by subcutaneous injection (80%), and lower half-life. (24h) and other advantages have been widely used in clinical practice. The dose is 30,000 U / d, under the skin, 1-2 / d. 2. AT-: It is mainly used for those with low levels of AT-, which can enhance the anticoagulant effect of heparin and reduce the bleeding complications of heparin. The commonly used dose is 1500U / d, intravenous drip, 3-5d1 course. 3. Coumarins: Block vitamin B-dependent biosynthesis by competing with vitamin K. It is mainly used for the prevention of thrombosis and maintenance treatment after heparin anticoagulation therapy. Warfarin is commonly used. The first dose is 10-15 mg / d, and it is taken orally in divided doses, followed by 5-10 mg / d. PT is used as a monitoring indicator to adjust the dosage to extend PT by 1.5-2.0 times or INR = 2.0-3.0. Optimal therapeutic dose.

(2) Anti-platelet drug treatment: 1. Aspirin: exerts anti-platelet aggregation effect by inhibiting cyclooxygenase, blocking arachidonic acid metabolism, and reducing the claim of TXA2. It is mainly used for the prevention of thrombosis and maintenance treatment after heparin application. The usual dose is 150-300mg / d, which is taken in divided doses. 2. Dipyridamole: by inhibiting phosphodiesterase or increasing adenosine cyclase activity, increase cAMP levels in platelets, inhibit platelet aggregation, and increase vascular procyclin (PGI2) claims and inhibit platelet TXA2 Generated effects. Dosage: 200-600mg / d, intravenous drip for 3-5d. Small doses are generally considered to have no therapeutic effect. 3. Ticlopidine: It is a specific anti-platelet aggregation agent. The mechanism of action is: Blocking platelet fibrinogen receptor (GPIb) binds to fibrinogen, enhances adenosyl cyclase activity, increases cAMP levels in platelets, stabilizes platelet membranes and reduces TXA2 synthesis. This medicine can be used for the prevention and treatment of thrombotic diseases. The commonly used dose is 250-500mg / d, taken orally or in divided doses, which can be used continuously for 5-7d and longer.

(3) Thrombolytic therapy is mainly used for newly formed thrombus or thromboembolism. Arterial thrombosis is best performed within 3 hours of onset, and no later than 6 hours. Venous thrombosis should also be performed within 24 hours of onset, no later than 5 days. 1, UK: A serine protease extracted from human urine or kidney cell culture fluid, which activates plasminogen to act as a thrombolytic agent. Since activated plasmin can simultaneously degrade fibrin in blood, Limits its clinical application. Common dose: the first dose of 40,000U / kg, intravenous injection, followed by 40,000U / h, continuous infusion for 1-3d 1 course. 2. SCU-PK: also known as pro-UK. It is now available in active recombination technology. This preparation has high affinity for plasmin bound to fibrin. Therefore, the selectivity of thrombolysis is better than WK. Common dose: 80 g of the first dose of hand, add 5% -10% glucose intravenous drip, 60-90min after the infusion is completed, then the dose is halved, 1 or 2 times a day, for 2-3 days.

3. t-PA: It can be produced by genetic recombination technology. Because its two changing structures have a strong affinity for fibrin, it can selectively activate plasminogen in the thrombus after administration, and then play a thrombolytic effect. Commonly used dose: the first dose of 100 g, intravenous injection, followed by continuous infusion at 50 g / h for a total of 2 hours, the second to third days can be reduced as appropriate.

4. APSAC: When the drug enters the bloodstream, its active center is blocked by acetyl groups, so it cannot activate plasminogen in the blood, and has no adverse effects of degrading fibrinogen. When it spreads to fibrin thrombus, it binds to the latter and re-exposes its active center through deacetylation, which plays the role of activating plasmin in the thrombus. Common dose: the first dose of 30mg, intravenous injection of 5mn, 6h can be repeated in equal amounts.

Thrombosis and thromboembolic medication safety

1. This disease is common in the elderly. Need to control blood pressure, blood lipids and reduce blood viscosity.

2. The patient should enter a low-fat, light diet to maintain smooth stool.

3, avoid tobacco, alcohol, spicy food, keep the stool smooth; avoid overeating, avoid excessive obesity.

4, regular living, regular work and rest, not overwork, is an important factor to maintain health.

5. Use pre-designated strategies to prevent VTE from occurring according to the risk stratification; drink enough water to avoid dehydration.