Lupus Coagulation Inhibitor
Warfarin
Blood Coagulation
Prothrombin Time
Protein C
Partial Thromboplastin Time
Acenocoumarol
Heparin
Factor Xa
Phenindione
4-Hydroxycoumarins
Antithrombins
Thrombin Time
International Normalized Ratio
Thromboembolism
Protein S
Blood Coagulation Factors
Heparin, Low-Molecular-Weight
Thrombomodulin
beta-Alanine
Prothrombin
Antiphospholipid Syndrome
Vitamin K
Antithrombin III
Antibodies, Antiphospholipid
Antibodies, Anticardiolipin
Thrombophilia
Blood Coagulation Disorders
Venous Thromboembolism
Thromboplastin
Factor X
Hirudins
Factor V
beta 2-Glycoprotein I
Dicumarol
Activated Protein C Resistance
Atrial Fibrillation
Factor Va
Hemostasis
Platelet Aggregation Inhibitors
Rodent Control
Enoxaparin
Vitamin K Epoxide Reductases
Protein C Deficiency
Aspirin
Dermatan Sulfate
Heparin Cofactor II
Protein S Deficiency
Cardiolipins
Antithrombin III Deficiency
Hematoma
Drug Monitoring
Dalteparin
Lupus Erythematosus, Systemic
Coumarins
Stroke
Arthropod Proteins
Antithrombin Proteins
Factor VIIa
Hemorrhagic Disorders
Seaweed
Factor VIIIa
Citric Acid
Factor VII
Coagulation Protein Disorders
Fibrin
Treatment Outcome
Embolism
Fibrin Fibrinogen Degradation Products
Risk Factors
Blood Preservation
Heparinoids
Blood Specimen Collection
Heparitin Sulfate
Postoperative Hemorrhage
Phospholipids
Cerebral Hemorrhage
Hematoma, Subdural
Ancrod
Phaeophyta
Intracranial Embolism and Thrombosis
Pregnancy Complications, Hematologic
Chromogenic Compounds
Heart Valve Prosthesis
Disseminated Intravascular Coagulation
Ancylostoma
Protein C Inhibitor
Glycoproteins
Edetic Acid
Blood Platelets
Fibrinogen
Bleeding Time
Salivary Proteins and Peptides
Dose-Response Relationship, Drug
Prospective Studies
Factor IX
Heparin Lyase
Benzylamines
Factor IXa
Strongylida
Retrospective Studies
Receptors, Thrombin
Annexin A5
Hemostatics
Follow-Up Studies
Cobra Venoms
Viper Venoms
Factor VIII
Protamines
Blood Coagulation Factor Inhibitors
Hirudin Therapy
Drug Interactions
Vena Cava Filters
Galactans
Platelet Activation
Glycosaminoglycans
Annexins
Crotalid Venoms
Cerebrovascular Disorders
Complement Inactivator Proteins
Autoantibodies
Plasma
Sinus Thrombosis, Intracranial
Randomized Controlled Trials as Topic
Oral Surgical Procedures
Risk Assessment
Hexadimethrine Bromide
Nadroparin
Intracranial Hemorrhages
Chondroitin Sulfates
Platelet Aggregation
Pregnancy Complications, Cardiovascular
1-Carboxyglutamic Acid
Protein Binding
Hematology
Molecular Sequence Data
Platelet Factor 4
Clinical Trials as Topic
Structure-Activity Relationship
Drug Therapy, Combination
Receptor, PAR-1
Vitamin K 1
Agkistrodon
Thrombolytic Therapy
Elapidae
Thienopyridines
Fibrinopeptide A
Sulfotransferases
Phlebography
Drugs, Investigational
Drug Substitution
Drug Administration Schedule
Ischemic Attack, Transient
Thrombelastography
Pregnancy
Amino Acid Sequence
Intracranial Hemorrhage, Traumatic
Aptamers, Nucleotide
Pyrazoles
Antifibrinolytic Agents
Heart Diseases
Factor V Deficiency
Mixed Function Oxygenases
Inherited prothrombotic risk factors and cerebral venous thrombosis. (1/5820)
Fifteen patients with cerebral venous thrombosis were ascertained retrospectively. Their case notes were reviewed, and stored or new blood was assayed for factor V Leiden (FVL) mutation, prothrombin gene mutation 20201A, and 5,10 methylene tetrahydrofolate reductase (MTHFR) C677T mutation. A clinical risk factor was identified in 13 patients--the oral contraceptive pill (5), puerperium (1), HRT (1), mastoiditis (1), dehydration (1), lumbar puncture and myelography (1), carcinoma (1), lupus anticoagulant (2). In addition, two patients had the FVL mutation and five (one of whom also had the FVL mutation) were homozygous for the MTHFR mutation. The latter showed a higher than expected frequency compared to 300 healthy controls from South Wales (OR 3.15.95% Cl 1.01-9.83). No patient had the prothrombin 20201A mutation. Two patients died and three had a monocular visual deficit following anticoagulation (13) or thrombolytic (2) treatment, but there was no association between the presence of a primary prothrombotic risk factor and outcome. These results confirm the importance of investigating patients for both clinical predisposing factors and primary prothrombotic states. (+info)Anticoagulant heparan sulfate precursor structures in F9 embryonal carcinoma cells. (2/5820)
To understand the mechanisms that control anticoagulant heparan sulfate (HSact) biosynthesis, we previously showed that HSact production in the F9 system is determined by the abundance of 3-O-sulfotransferase-1 as well as the size of the HSact precursor pool. In this study, HSact precursor structures have been studied by characterizing [6-3H]GlcN metabolically labeled F9 HS tagged with 3-O-sulfates in vitro by 3'-phosphoadenosine 5'-phospho-35S and purified 3-O-sulfotransferase-1. This later in vitro labeling allows the regions of HS destined to become the antithrombin (AT)-binding sites to be tagged for subsequent structural studies. It was shown that six 3-O-sulfation sites exist per HSact precursor chain. At least five out of six 3-O-sulfate-tagged oligosaccharides in HSact precursors bind AT, whereas none of 3-O-sulfate-tagged oligosaccharides from HSinact precursors bind AT. When treated with low pH nitrous or heparitinase, 3-O-sulfate-tagged HSact and HSinact precursors exhibit clearly different structural features. 3-O-Sulfate-tagged HSact hexasaccharides were AT affinity purified and sequenced by chemical and enzymatic degradations. The 3-O-sulfate-tagged HSact hexasaccharides exhibited the following structures, DeltaUA-[6-3H]GlcNAc6S-GlcUA-[6-3H]GlcNS3(35)S+/-6S-++ +IdceA2S-[6-3H]Glc NS6S. The underlined 6- and 3-O-sulfates constitute the most critical groups for AT binding in view of the fact that the precursor hexasaccharides possess all the elements for AT binding except for the 3-O-sulfate moiety. The presence of five potential AT-binding precursor hexasaccharides in all HSact precursor chains demonstrates for the first time the processive assembly of specific sequence in HS. The difference in structures around potential 3-O-sulfate acceptor sites in HSact and HSinact precursors suggests that these precursors might be generated by different concerted assembly mechanisms in the same cell. This study permits us to understand better the nature of the HS biosynthetic pathway that leads to the generation of specific saccharide sequences. (+info)Warfarin therapy: evolving strategies in anticoagulation. (3/5820)
Warfarin is the oral anticoagulant most frequently used to control and prevent thromboembolic disorders. Prescribing the dose that both avoids hemorrhagic complications and achieves sufficient suppression of thrombosis requires a thorough understanding of the drug's unique pharmacology. Warfarin has a complex dose-response relationship that makes safe and effective use a challenge. For most indications, the dose is adjusted to maintain the patient's International Normalized Ratio (INR) at 2 to 3. Because of the delay in factor II (prothrombin) suppression, heparin is administered concurrently for four to five days to prevent thrombus propagation. Loading doses of warfarin are not warranted and may result in bleeding complications. Interactions with other drugs must be considered, and therapy in elderly patients requires careful management. Current dosing recommendations are reviewed, and practical guidelines for the optimal use of warfarin are provided. (+info)Exosites 1 and 2 are essential for protection of fibrin-bound thrombin from heparin-catalyzed inhibition by antithrombin and heparin cofactor II. (4/5820)
Assembly of ternary thrombin-heparin-fibrin complexes, formed when fibrin binds to exosite 1 on thrombin and fibrin-bound heparin binds to exosite 2, produces a 58- and 247-fold reduction in the heparin-catalyzed rate of thrombin inhibition by antithrombin and heparin cofactor II, respectively. The greater reduction for heparin cofactor II reflects its requirement for access to exosite 1 during the inhibitory process. Protection from inhibition by antithrombin and heparin cofactor II requires ligation of both exosites 1 and 2 because minimal protection is seen when exosite 1 variants (gamma-thrombin and thrombin Quick 1) or an exosite 2 variant (Arg93 --> Ala, Arg97 --> Ala, and Arg101 --> Ala thrombin) is substituted for thrombin. Likewise, the rate of thrombin inhibition by the heparin-independent inhibitor, alpha1-antitrypsin Met358 --> Arg, is decreased less than 2-fold in the presence of soluble fibrin and heparin. In contrast, thrombin is protected from inhibition by a covalent antithrombin-heparin complex, suggesting that access of heparin to exosite 2 of thrombin is hampered when ternary complex formation occurs. These results reveal the importance of exosites 1 and 2 of thrombin in assembly of the ternary complex and the subsequent protection of thrombin from inhibition by heparin-catalyzed inhibitors. (+info)Sperm chemotaxis. (5/5820)
Communication between spermatozoa and egg before contact by chemotaxis appears to be prevalent throughout the animal kingdom. In non-mammalian species, sperm chemotaxis to factors secreted from the egg is well documented. In mammals, sperm chemotaxis to follicular factors in vitro has been established in humans and mice. The attractants of female origin in non-mammalian species are heat-stable peptides or proteins of various sizes, or other small molecules, depending on the species. Species specificity of the attractants in non-mammalian species may vary from high species specificity, through specificity to families with no specificity within a family, to absence of specificity. The mammalian sperm attractants have not been identified but they appear to be heat-stable peptides. The claim that progesterone is the attractant for human spermatozoa has failed to be substantiated, neither have claims for other mammalian sperm attractants been verified. The molecular mechanism of sperm chemotaxis is not known. Models involving modulation of the intracellular Ca2+ concentration have been proposed for both mammalian and non-mammalian sperm chemotaxis. The physiological role of sperm chemotaxis in non-mammalian species appears to differ from that in mammals. In non-mammalian species, sperm chemotaxis strives to bring as many spermatozoa as possible to the egg. However, in mammals, the role appears to be recruitment of a selective population of capacitated ('ripe') spermatozoa to fertilize the egg. (+info)Nonanticoagulant heparin prevents coronary endothelial dysfunction after brief ischemia-reperfusion injury in the dog. (6/5820)
BACKGROUND: Coronary endothelial dysfunction after brief ischemia-reperfusion (IR) remains a clinical problem. We investigated the role of heparin and N-acetylheparin, a nonanticoagulant heparin derivative, in modulating coronary endothelial function after IR injury, with an emphasis on defining the role of the nitric oxide (NO)-cGMP pathway in the heparin-mediated effect. METHODS AND RESULTS: Male mongrel dogs were surgically instrumented, and the effects of both bovine heparin and N-acetylheparin on coronary endothelial vasomotor function, expressed as percent change from baseline flow after acetylcholine challenge, were studied after 15 minutes of regional ischemia of the left anterior descending artery (LAD) followed by 120 minutes of reperfusion. In dogs treated with placebo (saline), coronary vasomotor function was significantly (P+info)Ex vivo evaluation of a Taylor-Couette flow, immobilized heparinase I device for clinical application. (7/5820)
Efficient and safe heparin anticoagulation has remained a problem for continuous renal replacement therapies and intermittent hemodialysis for patients with acute renal failure. To make heparin therapy safer for the patient with acute renal failure at high risk of bleeding, we have proposed regional heparinization of the circuit via an immobilized heparinase I filter. This study tested a device based on Taylor-Couette flow and simultaneous separation/reaction for efficacy and safety of heparin removal in a sheep model. Heparinase I was immobilized onto agarose beads via cyanogen bromide activation. The device, referred to as a vortex flow plasmapheretic reactor, consisted of two concentric cylinders, a priming volume of 45 ml, a microporous membrane for plasma separation, and an outer compartment where the immobilized heparinase I was fluidized separately from the blood cells. Manual white cell and platelet counts, hematocrit, total protein, and fibrinogen assays were performed. Heparin levels were indirectly measured via whole-blood recalcification times (WBRTs). The vortex flow plasmapheretic reactor maintained significantly higher heparin levels in the extracorporeal circuit than in the sheep (device inlet WBRTs were 1. 5 times the device outlet WBRTs) with no hemolysis. The reactor treatment did not effect any physiologically significant changes in complete blood cell counts, platelets, and protein levels for up to 2 hr of operation. Furthermore, gross necropsy and histopathology did not show any significant abnormalities in the kidney, liver, heart, brain, and spleen. (+info)Randomized, placebo-controlled trial of anticoagulant treatment with low-molecular-weight heparin for cerebral sinus thrombosis. (8/5820)
BACKGROUND AND PURPOSE: Treatment of cerebral sinus thrombosis with heparin is controversial. We conducted a double-blind, placebo-controlled multicenter trial to examine whether anticoagulant treatment improves outcome in patients with sinus thrombosis. METHODS: Patients were randomized between body weight-adjusted subcutaneous nadroparin (180 anti-factor Xa units/kg per 24 hours) and matching placebo for 3 weeks (double-blind part of trial), followed by 3 months of oral anticoagulants for patients allocated nadroparin (open part). Patients with cerebral hemorrhage caused by sinus thrombosis were also included. RESULTS: Sixty patients were enrolled, and none were lost to follow-up. In 1 patient the diagnosis proved wrong after randomization. After 3 weeks, 6 of 30 patients (20%) in the nadroparin group and 7 of 29 patients (24%) in the placebo group had a poor outcome, defined as death or Barthel Index score of <15 (risk difference, -4%; 95% CI, -25 to 17%; NS). After 12 weeks, 4 of 30 patients (13%) in the nadroparin group and 6 of 29 (21%) in the placebo group had a poor outcome, defined as death or Oxford Handicap Score of >/=3 (risk difference, -7%; 95% CI, -26% to 12%; NS). There were no new symptomatic cerebral hemorrhages. One patient in the nadroparin group had a major gastrointestinal hemorrhage, and 1 patient in the placebo group died from clinically suspected pulmonary embolism. CONCLUSIONS: Patients with cerebral sinus thrombosis treated with anticoagulants (low-molecular-weight heparin followed by oral anticoagulation) had a favorable outcome more often than controls, but the difference was not statistically significant. Anticoagulation proved to be safe, even in patients with cerebral hemorrhage. (+info)Thromboembolism can be caused by a variety of factors, such as injury, surgery, cancer, and certain medical conditions like atrial fibrillation. It can also be inherited or acquired through genetic mutations.
The symptoms of thromboembolism depend on the location of the clot and the severity of the blockage. They may include:
* Swelling or redness in the affected limb
* Pain or tenderness in the affected area
* Weakness or numbness in the affected limb
* Shortness of breath or chest pain if the clot has traveled to the lungs (pulmonary embolism)
* Dizziness, lightheadedness, or fainting
Thromboembolism can be diagnosed through a variety of tests, such as ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), and blood tests. Treatment typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, thrombolysis or clot-busting drugs may be used to dissolve the clot. Filters can also be placed in the vena cava to prevent clots from traveling to the lungs.
Prevention of thromboembolism includes:
* Moving around regularly to improve blood flow
* Avoiding long periods of immobility, such as during long-distance travel
* Elevating the affected limb to reduce swelling
* Compression stockings to improve blood flow
* Avoiding smoking and managing weight
* Taking anticoagulant medications if recommended by a healthcare provider.
Example sentence: The patient had a hemorrhage after the car accident and needed immediate medical attention.
There are several types of thrombosis, including:
1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.
The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:
1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic
Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.
The syndrome is typically diagnosed based on the presence of anticardiolipin antibodies (aCL) or lupus anticoagulant in the blood. Treatment for antiphospholipid syndrome may involve medications to prevent blood clots, such as heparin or warfarin, and aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation. In some cases, intravenous immunoglobulin (IVIG) may be given to reduce the levels of antibodies in the blood. Plasmapheresis, a process that removes antibodies from the blood, may also be used in some cases.
Antiphospholipid syndrome is associated with other autoimmune disorders, such as systemic lupus erythematosus (SLE), and may be triggered by certain medications or infections. It is important for individuals with antiphospholipid syndrome to work closely with their healthcare provider to manage their condition and reduce the risk of complications.
There are two main types of thrombophlebitis:
1. Superficial thrombophlebitis: This type of thrombophlebitis affects the superficial veins, which are located just under the skin. It is often caused by injury or trauma to the vein, and it can cause redness, swelling, and pain in the affected area.
2. Deep vein thrombophlebitis: This type of thrombophlebitis affects the deep veins, which are located deeper in the body. It is often caused by blood clots that form in the legs or arms, and it can cause symptoms such as pain, swelling, and warmth in the affected limb.
Thrombophlebitis can be caused by a variety of factors, including:
1. Injury or trauma to the vein
2. Blood clotting disorders
3. Prolonged bed rest or immobility
4. Surgery or medical procedures
5. Certain medications, such as hormone replacement therapy or chemotherapy
6. Age, as the risk of developing thrombophlebitis increases with age
7. Family history of blood clotting disorders
8. Increased pressure on the veins, such as during pregnancy or obesity
Thrombophlebitis can be diagnosed through a variety of tests, including:
1. Ultrasound: This test uses sound waves to create images of the veins and can help identify blood clots or inflammation.
2. Venography: This test involves injecting a dye into the vein to make it visible under X-ray imaging.
3. Blood tests: These can be used to check for signs of blood clotting disorders or other underlying conditions that may be contributing to the development of thrombophlebitis.
Treatment for thrombophlebitis typically involves anticoagulation therapy, which is designed to prevent the blood clot from growing larger and to prevent new clots from forming. This can involve medications such as heparin or warfarin, or other drugs that work by blocking the production of clots. In some cases, a filter may be placed in the vena cava, the large vein that carries blood from the lower body to the heart, to prevent clots from traveling to the lungs.
In addition to anticoagulation therapy, treatment for thrombophlebitis may also include:
1. Elevation of the affected limb to reduce swelling
2. Compression stockings to help reduce swelling and improve blood flow
3. Pain management with medication or heat or cold applications
4. Antibiotics if there is an infection
5. Rest and avoiding strenuous activities until the symptoms resolve.
In some cases, surgery may be necessary to remove the clot or repair the affected vein.
It's important to note that early diagnosis and treatment of thrombophlebitis can help prevent complications such as infection, inflammation, or damage to the valves in the affected vein. If you suspect you or someone else may have thrombophlebitis, it is important to seek medical attention promptly.
Symptoms of venous thrombosis may include pain, swelling, warmth, and redness in the affected limb. In some cases, the clot can break loose and travel to the lungs, causing a potentially life-threatening condition called Pulmonary Embolism (PE).
Treatment for venous thrombosis typically involves anticoagulant medications to prevent the clot from growing and to prevent new clots from forming. In some cases, a filter may be placed in the vena cava, the large vein that carries blood from the lower body to the heart, to prevent clots from traveling to the lungs.
Prevention of venous thrombosis includes encouraging movement and exercise, avoiding long periods of immobility, and wearing compression stockings or sleeves to compress the veins and improve blood flow.
There are several types of thrombophilia, including:
1. Factor V Leiden: This is the most common inherited thrombophilia and is caused by a mutation in the Factor V gene.
2. Prothrombin G20210A: This is another inherited thrombophilia that is caused by a mutation in the Prothrombin gene.
3. Protein C and S deficiency: These are acquired deficiencies of protein C and S, which are important proteins that help to prevent blood clots.
4. Antiphospholipid syndrome: This is an autoimmune disorder that causes the body to produce antibodies against phospholipids, which can lead to blood clots.
5. Cancer-associated thrombophilia: This is a condition where cancer patients are at a higher risk of developing blood clots due to their cancer and its treatment.
6. Hormone-related thrombophilia: This is a condition where hormonal changes, such as those that occur during pregnancy or with the use of hormone replacement therapy, increase the risk of blood clots.
7. Inherited platelet disorders: These are rare conditions that affect the way platelets function and can increase the risk of blood clots.
8. Anti-cardiolipin antibodies: These are autoantibodies that can cause blood clots.
9. Lupus anticoagulant: This is an autoantibody that can cause blood clots.
10. Combined genetic and acquired risk factors: Some people may have a combination of inherited and acquired risk factors for thrombophilia.
Thrombophilia can be diagnosed through various tests, including:
1. Blood tests: These tests measure the levels of certain proteins in the blood that are associated with an increased risk of blood clots.
2. Genetic testing: This can help identify inherited risk factors for thrombophilia.
3. Imaging tests: These tests, such as ultrasound and venography, can help doctors visualize the blood vessels and look for signs of blood clots.
4. Thrombin generation assay: This test measures the body's ability to produce thrombin, a protein that helps form blood clots.
5. Platelet function tests: These tests assess how well platelets work and whether they are contributing to the development of blood clots.
Treatment for thrombophilia usually involves medications to prevent or dissolve blood clots, as well as measures to reduce the risk of developing new clots. These may include:
1. Anticoagulant drugs: These medications, such as warfarin and heparin, are used to prevent blood clots from forming.
2. Thrombolytic drugs: These medications are used to dissolve blood clots that have already formed.
3. Compression stockings: These stockings can help reduce swelling and improve blood flow in the affected limb.
4. Elevating the affected limb: This can help reduce swelling and improve blood flow.
5. Avoiding long periods of immobility: This can help reduce the risk of developing blood clots.
In some cases, surgery may be necessary to remove a blood clot or repair a damaged blood vessel. In addition, people with thrombophilia may need to make lifestyle changes, such as avoiding long periods of immobility and taking regular breaks to move around, to reduce their risk of developing blood clots.
Overall, the prognosis for thrombophilia is generally good if the condition is properly diagnosed and treated. However, if left untreated, thrombophilia can lead to serious complications, such as pulmonary embolism or stroke, which can be life-threatening. It is important for people with thrombophilia to work closely with their healthcare provider to manage the condition and reduce the risk of complications.
Types of Blood Coagulation Disorders:
1. Hemophilia A: A genetic disorder that affects the blood's ability to clot, leading to prolonged bleeding after injury or surgery.
2. Hemophilia B: Similar to hemophilia A, but caused by a deficiency of factor IX instead of factor VIII.
3. Von Willebrand Disease (VWD): A bleeding disorder caused by a deficiency of von Willebrand factor, which is needed for blood clotting.
4. Platelet Disorders: These include conditions such as low platelet count (thrombocytopenia) or abnormal platelet function, which can increase the risk of bleeding.
5. Coagulopathy: A general term for any disorder that affects the body's blood coagulation process.
Symptoms and Diagnosis:
Blood coagulation disorders can cause a range of symptoms, including easy bruising, frequent nosebleeds, and prolonged bleeding after injury or surgery. Diagnosis is typically made through a combination of physical examination, medical history, and laboratory tests such as blood clotting factor assays and platelet function tests.
Treatment and Management:
Treatment for blood coagulation disorders depends on the specific condition and its severity. Some common treatments include:
1. Infusions of clotting factor concentrates to replace missing or deficient factors.
2. Desmopressin, a medication that stimulates the release of von Willebrand factor and platelets.
3. Platelet transfusions to increase platelet count.
4. Anticoagulation therapy to prevent blood clots from forming.
5. Surgery to repair damaged blood vessels or joints.
Prevention and Prognosis:
Prevention of blood coagulation disorders is often challenging, but some steps can be taken to reduce the risk of developing these conditions. These include:
1. Avoiding trauma or injury that can cause bleeding.
2. Managing underlying medical conditions such as liver disease, vitamin deficiencies, and autoimmune disorders.
3. Avoiding medications that can interfere with blood clotting.
The prognosis for blood coagulation disorders varies depending on the specific condition and its severity. Some conditions, such as mild hemophilia A, may have a good prognosis with appropriate treatment, while others, such as severe hemophilia B, can have a poor prognosis without proper management.
Complications and Comorbidities:
Blood coagulation disorders can lead to a range of complications and comorbidities, including:
1. Joint damage and chronic pain due to repeated bleeding into joints.
2. Infection and sepsis from bacteria entering the body through bleeding sites.
3. Arthritis and other inflammatory conditions.
4. Nerve damage and neuropathy from bleeding into nerve tissue.
5. Increased risk of bleeding during surgery or trauma.
6. Emotional and social challenges due to the impact of the condition on daily life.
7. Financial burden of treatment and management costs.
8. Impaired quality of life, including reduced mobility and activity levels.
9. Increased risk of blood clots and thromboembolic events.
10. Psychological distress and anxiety related to the condition.
Conclusion:
Blood coagulation disorders are a group of rare and complex conditions that can significantly impact quality of life, productivity, and longevity. These disorders can be caused by genetic or acquired factors and can lead to a range of complications and comorbidities. Diagnosis is often challenging, but prompt recognition and appropriate treatment can improve outcomes. Management strategies include replacing missing clotting factors, using blood products, and managing underlying conditions. While the prognosis varies depending on the specific condition and its severity, early diagnosis and effective management can improve quality of life and reduce the risk of complications.
Deep Vein Thrombosis (DVT): DVT occurs when a blood clot forms in the deep veins of the body, usually in the legs. This can cause swelling, pain, and warmth in the affected area.
Pulmonary Embolism (PE): PE occurs when a blood clot from the deep veins of the body travels to the lungs, causing shortness of breath, chest pain, and coughing up bloody mucus.
The risk factors for VTE include:
* Prolonged immobility (e.g., long-distance travel or bed rest)
* Injury or surgery
* Age > 60 years
* Family history of VTE
* Cancer and its treatment
* Hormone replacement therapy or birth control pills
* Inherited blood-clotting disorders
* Inflammatory bowel disease
Prevention methods include:
* Moving around regularly during long-distance travel or bed rest
* Avoiding crossing your legs or ankles, which can restrict blood flow
* Wearing compression stockings during travel or when advised by a healthcare professional
* Elevating the affected leg when sitting or lying down
* Taking blood-thinning medication as prescribed by a healthcare professional
Early diagnosis and treatment of VTE can help prevent serious complications such as PE. Treatment options include anticoagulant medications, thrombolysis (dissolving the clot), and filtration devices.
The symptoms of pulmonary embolism can vary, but may include shortness of breath, chest pain, coughing up blood, rapid heart rate, and fever. In some cases, the clot may be large enough to cause a pulmonary infarction (a " lung injury" caused by lack of oxygen), which can lead to respiratory failure and death.
Pulmonary embolism can be diagnosed with imaging tests such as chest X-rays, CT scans, and ultrasound. Treatment typically involves medications to dissolve the clot or prevent new ones from forming, and in some cases, surgery may be necessary to remove the clot.
Preventive measures include:
* Avoiding prolonged periods of immobility, such as during long-distance travel
* Exercising regularly to improve circulation
* Managing chronic conditions such as high blood pressure and cancer
* Taking blood-thinning medications to prevent clot formation
Early recognition and treatment of pulmonary embolism are critical to reduce the risk of complications and death.
APC resistance can be caused by genetic or acquired factors and can lead to a range of clinical presentations, including:
1. Hereditary bleeding disorders: Familial APC resistance is caused by mutations in the APC gene and can result in severe bleeding, especially during childhood.
2. Acquired APC resistance: This can occur due to certain medical conditions, such as liver disease, sepsis, or cancer, which can impair APC function.
3. Drug-induced APC resistance: Certain medications, like anticoagulants, can reduce APC activity and lead to APC resistance.
Diagnosis of APC resistance typically involves testing for APC activity in the blood, as well as genetic analysis to identify mutations in the APC gene. Treatment options for APC resistance depend on the underlying cause and may include:
1. Fresh frozen plasma (FFP): FFP can be used to replace missing or deficient APC in the blood.
2. Recombinant APC: This is a synthetic version of APC that can be used to replace missing or deficient APC.
3. Anticoagulants: These medications can help prevent blood clots and reduce the risk of thrombotic events.
4. Platelet inhibitors: These medications can help prevent platelet aggregation, which can contribute to bleeding.
Overall, APC resistance is a rare but important condition that can affect blood coagulation and increase the risk of bleeding or thrombotic events. Prompt diagnosis and appropriate treatment are essential to manage the condition effectively and prevent complications.
There are several risk factors for developing AF, including:
1. Age: The risk of developing AF increases with age, with the majority of cases occurring in people over the age of 65.
2. Hypertension (high blood pressure): High blood pressure can damage the heart and increase the risk of developing AF.
3. Heart disease: People with heart disease, such as coronary artery disease or heart failure, are at higher risk of developing AF.
4. Diabetes mellitus: Diabetes can increase the risk of developing AF.
5. Sleep apnea: Sleep apnea can increase the risk of developing AF.
6. Certain medications: Certain medications, such as thyroid medications and asthma medications, can increase the risk of developing AF.
7. Alcohol consumption: Excessive alcohol consumption has been linked to an increased risk of developing AF.
8. Smoking: Smoking is a risk factor for many cardiovascular conditions, including AF.
9. Obesity: Obesity is a risk factor for many cardiovascular conditions, including AF.
Symptoms of AF can include:
1. Palpitations (rapid or irregular heartbeat)
2. Shortness of breath
3. Fatigue
4. Dizziness or lightheadedness
5. Chest pain or discomfort
AF can be diagnosed with the help of several tests, including:
1. Electrocardiogram (ECG): This is a non-invasive test that measures the electrical activity of the heart.
2. Holter monitor: This is a portable device that records the heart's rhythm over a 24-hour period.
3. Event monitor: This is a portable device that records the heart's rhythm over a longer period of time, usually 1-2 weeks.
4. Echocardiogram: This is an imaging test that uses sound waves to create pictures of the heart.
5. Cardiac MRI: This is an imaging test that uses magnetic fields and radio waves to create detailed pictures of the heart.
Treatment for AF depends on the underlying cause and may include medications, such as:
1. Beta blockers: These medications slow the heart rate and reduce the force of the heart's contractions.
2. Antiarrhythmics: These medications help regulate the heart's rhythm.
3. Blood thinners: These medications prevent blood clots from forming and can help reduce the risk of stroke.
4. Calcium channel blockers: These medications slow the entry of calcium into the heart muscle cells, which can help slow the heart rate and reduce the force of the heart's contractions.
In some cases, catheter ablation may be recommended to destroy the abnormal electrical pathway causing AF. This is a minimally invasive procedure that involves inserting a catheter through a vein in the leg and guiding it to the heart using x-ray imaging. Once the catheter is in place, energy is applied to the abnormal electrical pathway to destroy it and restore a normal heart rhythm.
It's important to note that AF can increase the risk of stroke, so anticoagulation therapy may be recommended to reduce this risk. This can include medications such as warfarin or aspirin, or in some cases, implantable devices such as a left atrial appendage closure device.
In conclusion, atrial fibrillation is a common heart rhythm disorder that can increase the risk of stroke and heart failure. Treatment options depend on the underlying cause and may include medications, cardioversion, catheter ablation, or anticoagulation therapy. It's important to work closely with a healthcare provider to determine the best course of treatment for AF.
Word origin: [Latin] proteinus, "protein" + C, "deficiency"
Protein S is a vitamin K-dependent protein that is produced in the liver and circulates in the blood. It works by inhibiting the activity of thrombin, a clotting factor that helps to form blood clots. In people with protein S deficiency, there may be an overactivation of thrombin, leading to an increased risk of blood clots forming.
Protein S deficiency can be caused by several factors, including genetic mutations, vitamin K deficiency, and certain medical conditions such as liver disease or cancer. It is usually diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies.
Treatment for protein S deficiency typically involves replacing the missing protein with intravenous immune globulin (IVIG) or recombinant human protein S. In some cases, medications that inhibit thrombin activity, such as heparins or direct thrombin inhibitors, may also be used to reduce the risk of blood clots forming.
Preventing protein S deficiency involves ensuring adequate intake of vitamin K through dietary sources or supplements, managing underlying medical conditions, and avoiding factors that can increase the risk of bleeding or thrombosis, such as smoking, obesity, and inactivity.
In summary, protein S deficiency is a condition characterized by low levels of protein S, which increases the risk of developing blood clots. It can be caused by several factors and treated with replacement therapy or medications that inhibit thrombin activity. Prevention involves ensuring adequate vitamin K intake and managing underlying medical conditions.
People with ATIII deficiency may experience a range of symptoms, including:
* Prolonged bleeding after injuries or surgery
* Spontaneous bruising or petechiae (small red or purple spots on the skin)
* Nosebleeds or easy bruising
* Bleeding into the joints (hemarthrosis)
* Easy bleeding in the gastrointestinal tract
ATIII deficiency can be caused by inherited mutations in the ATIII gene or acquired due to certain medical conditions, such as liver disease, sepsis, or autoimmune disorders.
Diagnosis of ATIII deficiency involves blood tests to measure the level of antithrombin III activity and genetic testing to identify mutations in the ATIII gene. Treatment typically involves infusions of antithrombin III concentrates to replace the missing or abnormal protein, and management of underlying conditions that may be contributing to the deficiency.
In rare cases, individuals with severe ATIII deficiency may require regular infusions throughout their lives to prevent bleeding complications. However, with proper treatment and close monitoring, many people with ATIII deficiency can lead normal lives without significant limitations.
Intracranial hematoma occurs within the skull and is often caused by head injuries, such as falls or car accidents. It can lead to severe neurological symptoms, including confusion, seizures, and loss of consciousness. Extracranial hematomas occur outside the skull and are commonly seen in injuries from sports, accidents, or surgery.
The signs and symptoms of hematoma may vary depending on its location and size. Common symptoms include pain, swelling, bruising, and limited mobility. Diagnosis is typically made through imaging tests such as CT scans or MRI scans, along with physical examination and medical history.
Treatment for hematoma depends on its severity and location. In some cases, conservative management with rest, ice, compression, and elevation (RICE) may be sufficient. However, surgical intervention may be necessary to drain the collection of blood or remove any clots that have formed.
In severe cases, hematoma can lead to life-threatening complications such as infection, neurological damage, and organ failure. Therefore, prompt medical attention is crucial for proper diagnosis and treatment.
The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.
There are several subtypes of LES, including:
1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.
There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.
It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.
1. Ischemic stroke: This is the most common type of stroke, accounting for about 87% of all strokes. It occurs when a blood vessel in the brain becomes blocked, reducing blood flow to the brain.
2. Hemorrhagic stroke: This type of stroke occurs when a blood vessel in the brain ruptures, causing bleeding in the brain. High blood pressure, aneurysms, and blood vessel malformations can all cause hemorrhagic strokes.
3. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA is a temporary interruption of blood flow to the brain that lasts for a short period of time, usually less than 24 hours. TIAs are often a warning sign for a future stroke and should be taken seriously.
Stroke can cause a wide range of symptoms depending on the location and severity of the damage to the brain. Some common symptoms include:
* Weakness or numbness in the face, arm, or leg
* Difficulty speaking or understanding speech
* Sudden vision loss or double vision
* Dizziness, loss of balance, or sudden falls
* Severe headache
* Confusion, disorientation, or difficulty with memory
Stroke is a leading cause of long-term disability and can have a significant impact on the quality of life for survivors. However, with prompt medical treatment and rehabilitation, many people are able to recover some or all of their lost functions and lead active lives.
The medical community has made significant progress in understanding stroke and developing effective treatments. Some of the most important advances include:
* Development of clot-busting drugs and mechanical thrombectomy devices to treat ischemic strokes
* Improved imaging techniques, such as CT and MRI scans, to diagnose stroke and determine its cause
* Advances in surgical techniques for hemorrhagic stroke
* Development of new medications to prevent blood clots and reduce the risk of stroke
Despite these advances, stroke remains a significant public health problem. According to the American Heart Association, stroke is the fifth leading cause of death in the United States and the leading cause of long-term disability. In 2017, there were over 795,000 strokes in the United States alone.
There are several risk factors for stroke that can be controlled or modified. These include:
* High blood pressure
* Diabetes mellitus
* High cholesterol levels
* Smoking
* Obesity
* Lack of physical activity
* Poor diet
In addition to these modifiable risk factors, there are also several non-modifiable risk factors for stroke, such as age (stroke risk increases with age), family history of stroke, and previous stroke or transient ischemic attack (TIA).
The medical community has made significant progress in understanding the causes and risk factors for stroke, as well as developing effective treatments and prevention strategies. However, more research is needed to improve outcomes for stroke survivors and reduce the overall burden of this disease.
There are several types of hypoprothrombinemias, including:
1. Classical hemophilia A: This is the most common type of hypoprothrombinemia and is caused by a deficiency of factor VIII, which is converted to prothrombin in the liver.
2. Non-classical hemophilia A: This type is less severe than classical hemophilia A and is also caused by a deficiency of factor VIII.
3. Prothrombin gene mutation: This is a rare type of hypoprothrombinemia caused by a mutation in the PROTHROMBIN gene, which is responsible for the production of prothrombin.
4. Acquired hypoprothrombinemia: This type can be caused by liver disease, vitamin K deficiency, or other conditions that affect the production or function of prothrombin.
The symptoms of hypoprothrombinemias can vary depending on the severity of the disorder and can include prolonged bleeding after injury or surgery, easy bruising, and frequent nosebleeds. Treatment for hypoprothrombinemias usually involves replacing the missing clotting factor or addressing any underlying conditions that may be contributing to the deficiency. In severe cases, liver transplantation may be necessary.
There are several types of hemorrhagic disorders, including:
1. Hemophilia: A genetic disorder that affects the blood's ability to clot and stop bleeding. People with hemophilia may experience spontaneous bleeding or bleeding after injury or surgery.
2. von Willebrand disease: A mild bleeding disorder caused by a deficiency of a protein called von Willebrand factor, which is important for blood clotting.
3. Platelet disorders: Disorders that affect the platelets, such as thrombocytopenia (low platelet count) or thrombocytosis (high platelet count).
4. Bleeding and clotting disorders caused by medications or drugs.
5. Hemorrhagic stroke: A type of stroke that is caused by bleeding in the brain.
6. Gastrointestinal bleeding: Bleeding in the digestive tract, which can be caused by a variety of factors such as ulcers, inflammation, or tumors.
7. Pulmonary hemorrhage: Bleeding in the lungs, which can be caused by a variety of factors such as pneumonia, injury, or tumors.
8. Retinal hemorrhage: Bleeding in the blood vessels of the retina, which can be caused by high blood pressure, diabetes, or other eye disorders.
Symptoms of hemorrhagic disorders can vary depending on the specific condition and the location of the bleeding. Common symptoms include bruising, petechiae (small red spots on the skin), nosebleeds, gum bleeding, and heavy menstrual periods. Treatment for hemorrhagic disorders depends on the underlying cause and may include medications, blood transfusions, or surgery.
There are several types of coagulation protein disorders, including:
1. Hemophilia A: This is the most common type of bleeding disorder and is caused by a deficiency of factor VIII, a protein that plays a crucial role in blood clotting.
2. Hemophilia B: This is caused by a deficiency of factor IX, another important protein involved in blood clotting.
3. Von Willebrand disease: This is the most common bleeding disorder and is caused by a deficiency of von Willebrand factor, a protein that helps platelets stick together to form blood clots.
4. Platelet dysfunction: This is a rare condition where platelets do not function properly, leading to an increased risk of bleeding.
5. Protein C and protein S deficiencies: These are rare conditions caused by a deficiency of protein C and protein S, which are important proteins involved in blood clotting.
Symptoms of coagulation protein disorders can include easy bruising, frequent nosebleeds, bleeding gums, and prolonged bleeding after injury or surgery. Treatment for these disorders typically involves replacing the missing protein or modulating the body's immune system to prevent antibodies from attacking the protein. In some cases, treatment may also involve blood transfusions or medications to help regulate blood clotting.
It is important to note that coagulation protein disorders can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific disorder and the genetic mutation causing it. Genetic testing and counseling can help identify individuals at risk of inheriting these disorders and provide information on appropriate treatment and management options.
There are several types of embolism, including:
1. Pulmonary embolism: A blood clot that forms in the lungs and blocks the flow of blood to the heart.
2. Cerebral embolism: A blood clot or other foreign substance that blocks the flow of blood to the brain.
3. Coronary embolism: A blood clot that blocks the flow of blood to the heart muscle, causing a heart attack.
4. Intestinal embolism: A blood clot or other foreign substance that blocks the flow of blood to the intestines.
5. Fat embolism: A condition where fat enters the bloodstream and becomes lodged in a blood vessel, blocking the flow of blood.
The symptoms of embolism can vary depending on the location of the blockage, but may include:
* Pain or tenderness in the affected area
* Swelling or redness in the affected limb
* Difficulty breathing or shortness of breath
* Chest pain or pressure
* Lightheadedness or fainting
* Rapid heart rate or palpitations
Treatment for embolism depends on the underlying cause and the severity of the blockage. In some cases, medication may be used to dissolve blood clots or break up the blockage. In other cases, surgery may be necessary to remove the foreign substance or repair the affected blood vessel.
Prevention is key in avoiding embolism, and this can include:
* Managing underlying conditions such as high blood pressure, diabetes, or heart disease
* Avoiding long periods of immobility, such as during long-distance travel
* Taking blood-thinning medication to prevent blood clots from forming
* Maintaining a healthy weight and diet to reduce the risk of fat embolism.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
1. Injury to blood vessels during surgery
2. Poor suturing or stapling techniques
3. Bleeding disorders or use of anticoagulant medications
4. Infection or hematoma (a collection of blood outside the blood vessels)
5. Delayed recovery of blood clotting function
Postoperative hemorrhage can range from mild to severe and life-threatening. Mild bleeding may present as oozing or trickling of blood from the surgical site, while severe bleeding can lead to hypovolemic shock, organ failure, and even death.
To diagnose postoperative hemorrhage, a physical examination and medical history are usually sufficient. Imaging studies such as ultrasound, computed tomography (CT) or magnetic resonance imaging (MRI) may be ordered to evaluate the extent of bleeding and identify any underlying causes.
Treatment of postoperative hemorrhage depends on the severity and location of the bleeding. Mild bleeding may be managed with dressings, compression bandages, and elevation of the affected limb. Severe bleeding may require interventions such as:
1. Surgical exploration to locate and control the source of bleeding
2. Transfusion of blood products or fresh frozen plasma to restore clotting function
3. Use of vasopressors to raise blood pressure and perfuse vital organs
4. Hemostatic agents such as clotting factors, fibrin sealants, or hemostatic powder to promote clot formation
5. In some cases, surgical intervention may be required to repair damaged blood vessels or organs.
Prevention of postoperative hemorrhage is crucial in reducing the risk of complications and improving patient outcomes. Preventive measures include:
1. Proper preoperative evaluation and preparation, including assessment of bleeding risk factors
2. Use of appropriate anesthesia and surgical techniques to minimize tissue trauma
3. Conservative use of hemostatic agents and blood products during surgery
4. Closure of all bleeding sites before completion of the procedure
5. Monitoring of vital signs, including pulse rate and blood pressure, during and after surgery
6. Preoperative and postoperative management of underlying conditions such as hypertension, diabetes, and coagulopathies.
Early recognition and prompt intervention are critical in effectively managing postoperative hemorrhage. In cases of severe bleeding, timely and appropriate interventions can reduce the risk of complications and improve patient outcomes.
Symptoms of cerebral hemorrhage may include sudden severe headache, confusion, seizures, weakness or numbness in the face or limbs, and loss of consciousness. The condition is diagnosed through a combination of physical examination, imaging tests such as CT or MRI scans, and laboratory tests to determine the cause of the bleeding.
Treatment for cerebral hemorrhage depends on the location and severity of the bleeding, as well as the underlying cause. Medications may be used to control symptoms such as high blood pressure or seizures, while surgery may be necessary to repair the ruptured blood vessel or relieve pressure on the brain. In some cases, the condition may be fatal, and immediate medical attention is essential to prevent long-term damage or death.
Some of the most common complications associated with cerebral hemorrhage include:
1. Rebleeding: There is a risk of rebleeding after the initial hemorrhage, which can lead to further brain damage and increased risk of death.
2. Hydrocephalus: Excess cerebrospinal fluid can accumulate in the brain, leading to increased intracranial pressure and potentially life-threatening complications.
3. Brain edema: Swelling of the brain tissue can occur due to the bleeding, leading to increased intracranial pressure and potentially life-threatening complications.
4. Seizures: Cerebral hemorrhage can cause seizures, which can be a sign of a more severe injury.
5. Cognitive and motor deficits: Depending on the location and severity of the bleeding, cerebral hemorrhage can result in long-term cognitive and motor deficits.
6. Vision loss: Cerebral hemorrhage can cause vision loss or blindness due to damage to the visual cortex.
7. Communication difficulties: Cerebral hemorrhage can cause difficulty with speech and language processing, leading to communication difficulties.
8. Behavioral changes: Depending on the location and severity of the bleeding, cerebral hemorrhage can result in behavioral changes, such as irritability, agitation, or apathy.
9. Infection: Cerebral hemorrhage can increase the risk of infection, particularly if the hemorrhage is caused by a ruptured aneurysm or arteriovenous malformation (AVM).
10. Death: Cerebral hemorrhage can be fatal, particularly if the bleeding is severe or if there are underlying medical conditions that compromise the patient's ability to tolerate the injury.
Note: Hematoma is a collection of blood outside the blood vessels.
1. Atrial fibrillation (a type of irregular heartbeat)
2. Heart disease or valve problems
3. Blood clots in the legs or lungs
4. Infective endocarditis (an infection of the heart valves)
5. Cancer and its treatment
6. Trauma to the head or neck
7. High blood pressure
8. Atherosclerosis (the buildup of plaque in the arteries)
When a blockage occurs in one of the blood vessels of the brain, it can deprive the brain of oxygen and nutrients, leading to cell death and potentially causing a range of symptoms including:
1. Sudden weakness or numbness in the face, arm, or leg
2. Sudden confusion or trouble speaking or understanding speech
3. Sudden trouble seeing in one or both eyes
4. Sudden severe headache
5. Dizziness or loss of balance
6. Fainting or falling
Intracranial embolism and thrombosis can be diagnosed through a variety of imaging tests, including:
1. Computed tomography (CT) scan
2. Magnetic resonance imaging (MRI)
3. Magnetic resonance angiography (MRA)
4. Cerebral angiography
5. Doppler ultrasound
Treatment options for intracranial embolism and thrombosis depend on the underlying cause of the blockage, but may include:
1. Medications to dissolve blood clots or prevent further clotting
2. Surgery to remove the blockage or repair the affected blood vessel
3. Endovascular procedures, such as angioplasty and stenting, to open up narrowed or blocked blood vessels
4. Supportive care, such as oxygen therapy and pain management, to help manage symptoms and prevent complications.
1. Iron deficiency anemia: This is the most common hematologic complication of pregnancy, caused by the increased demand for iron and the potential for poor dietary intake or gastrointestinal blood loss.
2. Thrombocytopenia: A decrease in platelet count, which can be mild and resolve spontaneously or severe and require treatment.
3. Leukemia: Rare but potentially serious, leukemia can occur during pregnancy and may require prompt intervention to ensure the health of both the mother and the fetus.
4. Thrombosis: The formation of a blood clot in a blood vessel, which can be life-threatening for both the mother and the baby if left untreated.
5. Hemorrhage: Excessive bleeding during pregnancy, which can be caused by various factors such as placenta previa or abruption.
6. Preeclampsia: A condition characterized by high blood pressure and damage to organs such as the kidneys and liver, which can increase the risk of hemorrhage and other complications.
7. Ectopic pregnancy: A pregnancy that develops outside of the uterus, often in the fallopian tube, which can cause severe bleeding and be life-threatening if left untreated.
In DIC, the body's normal blood coagulation mechanisms become overactive and begin to form clots throughout the circulatory system, including in small blood vessels and organs. This can cause a range of symptoms, including bleeding, fever, and organ failure.
DIC is often seen in sepsis, which is a severe infection that has spread throughout the body. It can also be caused by other conditions such as trauma, cancer, and autoimmune disorders.
Treatment of DIC typically involves addressing the underlying cause, such as treating an infection or injury, as well as supporting the body's natural clotting mechanisms and preventing further bleeding. In severe cases, hospitalization and intensive care may be necessary to monitor and treat the condition.
In summary, Disseminated Intravascular Coagulation (DIC) is a serious medical condition that can cause widespread clotting and damage to the body's organs and tissues. It is often seen in sepsis and other severe conditions, and treatment typically involves addressing the underlying cause and supporting the body's natural clotting mechanisms.
A condition in which spontaneous abortions occur repeatedly, often due to an underlying cause such as a uterine anomaly or infection. Also called recurrent spontaneous abortion.
Synonym(s): habitual abortion, recurrent abortion, spontaneous abortion.
Antonym(s): multiple pregnancy, retained placenta.
Example Sentence: "The patient had experienced four habitual abortions in the past year and was concerned about her ability to carry a pregnancy to term."
There are several possible causes of thrombocytopenia, including:
1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.
Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.
In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.
1. Stroke: A stroke occurs when the blood supply to the brain is interrupted, either due to a blockage or a rupture of the blood vessels. This can lead to cell death and permanent brain damage.
2. Cerebral vasospasm: Vasospasm is a temporary constriction of the blood vessels in the brain, which can occur after a subarachnoid hemorrhage (bleeding in the space surrounding the brain).
3. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches. It can lead to recurrent transient ischemic attacks (TIs) or stroke.
4. Cerebral amyloid angiopathy: This is a condition where abnormal protein deposits accumulate in the blood vessels of the brain, leading to inflammation and bleeding.
5. Cavernous malformations: These are abnormal collections of blood vessels in the brain that can cause seizures, headaches, and other symptoms.
6. Carotid artery disease: Atherosclerosis (hardening) of the carotid arteries can lead to a stroke or TIAs.
7. Vertebrobasilar insufficiency: This is a condition where the blood flow to the brain is reduced due to narrowing or blockage of the vertebral and basilar arteries.
8. Temporal lobe dementia: This is a type of dementia that affects the temporal lobe of the brain, leading to memory loss and other cognitive symptoms.
9. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL): This is a rare genetic disorder that affects the blood vessels in the brain, leading to recurrent stroke-like events.
10. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to decreased blood flow to the brain and increased risk of stroke.
It's important to note that this list is not exhaustive and there may be other causes of stroke and TIAs that are not included here. A proper diagnosis can only be made by a qualified medical professional after conducting a thorough examination and reviewing the individual's medical history.
Here are some possible clinical presentations and diagnostic procedures for intracranial sinus thrombosis:
Clinical Presentations:
* Headache (most common symptom)
* Fever
* Nasal congestion or swelling
* Pain in the face, particularly on one side
* Vision changes or blurriness
* Nausea and vomiting
Diagnostic Procedures:
1. Imaging studies (CT or MRI scans) to confirm the presence of a blood clot within a sinus and to rule out other conditions that may cause similar symptoms.
2. Endoscopy, which involves inserting a flexible tube with a camera into the nasal cavity to visualize the inside of the sinuses and to collect tissue or fluid samples for further examination.
3. Blood tests to check for infection or inflammation.
4. Sinus aspiration, which involves draining fluid from the affected sinus to determine if there is a blood clot present.
Treatment options for intracranial sinus thrombosis depend on the severity of the condition and may include antibiotics, anticoagulation medications, or surgical drainage of the affected sinus. In some cases, the condition may be life-threatening and require emergency treatment.
There are several types of intracranial hemorrhage, including:
1. Cerebral hemorrhage: Bleeding within the cerebral tissue itself, which can cause damage to brain cells and lead to a variety of complications.
2. Subarachnoid hemorrhage: Bleeding between the brain and the thin membrane that covers it (the meninges), which can cause severe headaches and other symptoms.
3. Epidural hemorrhage: Bleeding between the dura mater, a protective layer of tissue surrounding the brain, and the skull.
4. Subdural hemorrhage: Bleeding between the dura mater and the arachnoid membrane, which can cause severe headaches and other symptoms.
The symptoms of intracranial hemorrhage can vary depending on the location and severity of the bleeding, but may include:
* Sudden, severe headache
* Nausea and vomiting
* Confusion and disorientation
* Weakness or numbness in the face, arm, or leg
* Seizures
* Loss of consciousness
Diagnosis is typically made through a combination of physical examination, imaging tests (such as CT or MRI scans), and laboratory tests to determine the cause of the hemorrhage. Treatment depends on the location and severity of the bleeding, but may include medications to control symptoms, surgery to repair the source of the bleeding, or other interventions as needed.
Note: This definition is based on the current medical knowledge and may change as new research and discoveries are made.
Example sentence: "The patient experienced a transient ischemic attack, which was caused by a temporary blockage in one of the blood vessels in their brain."
Synonyms: TIA, mini-stroke.
Traumatic intracranial hemorrhage can be classified into several types based on the location and severity of the bleeding. These include:
1. Concussive hemorrhage: This type of hemorrhage is caused by a mild traumatic brain injury and is characterized by a small amount of bleeding in the brain tissue.
2. Contusional hemorrhage: This type of hemorrhage is caused by a direct blow to the head and is characterized by a larger amount of bleeding in the brain tissue.
3. Coup-contrecoup hemorrhage: This type of hemorrhage is caused by the force of the head striking one object and then bouncing back and striking another object, resulting in bleeding on both sides of the brain.
4. Definite hemorrhage: This type of hemorrhage is characterized by a well-defined area of bleeding in the brain tissue.
5. Diffuse hemorrhage: This type of hemorrhage is characterized by widespread bleeding throughout the brain tissue.
Symptoms of traumatic intracranial hemorrhage can vary depending on the location and severity of the bleeding, but may include headache, confusion, weakness or numbness in the limbs, seizures, and loss of consciousness. Treatment options for traumatic intracranial hemorrhage depend on the underlying cause of the bleeding and may include observation, medication, surgery, or a combination of these.
There are many different types of heart diseases, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries, which supply blood to the heart muscle, leading to chest pain or a heart attack.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, leading to fatigue, shortness of breath, and swelling in the legs.
3. Arrhythmias: Abnormal heart rhythms, such as atrial fibrillation or ventricular tachycardia, which can cause palpitations, dizziness, and shortness of breath.
4. Heart valve disease: Problems with the heart valves, which can lead to blood leaking back into the chambers or not being pumped effectively.
5. Cardiomyopathy: Disease of the heart muscle, which can lead to weakened heart function and heart failure.
6. Heart murmurs: Abnormal sounds heard during a heartbeat, which can be caused by defects in the heart valves or abnormal blood flow.
7. Congenital heart disease: Heart defects present at birth, such as holes in the heart or abnormal blood vessels.
8. Myocardial infarction (heart attack): Damage to the heart muscle due to a lack of oxygen, often caused by a blockage in a coronary artery.
9. Cardiac tamponade: Fluid accumulation around the heart, which can cause compression of the heart and lead to cardiac arrest.
10. Endocarditis: Infection of the inner lining of the heart, which can cause fever, fatigue, and heart valve damage.
Heart diseases can be diagnosed through various tests such as electrocardiogram (ECG), echocardiogram, stress test, and blood tests. Treatment options depend on the specific condition and may include lifestyle changes, medication, surgery, or a combination of these.
People with factor V deficiency may experience spontaneous bleeding or bruising, especially during childhood. The symptoms can range from mild to severe and may include:
1. Easy bruising
2. Nosebleeds
3. Bleeding gums
4. Heavy menstrual periods
5. Prolonged bleeding after injuries or surgery
6. Intestinal bleeding
7. Bleeding in the joints
Factor V deficiency is caused by a genetic mutation that affects the production of factor V protein. The disorder can be inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause symptoms. In some cases, the disorder may be caused by a mutation in both copies of the gene, leading to more severe symptoms.
There is no cure for factor V deficiency, but treatment options are available to manage the symptoms. These may include:
1. Desmopressin, a medication that stimulates the release of von Willebrand factor, which helps to improve clotting.
2. Fresh frozen plasma or cryoprecipitate, which contain factors V and VIII, can be given intravenously to replace missing clotting factors.
3. Surgical intervention may be necessary in some cases, such as when bleeding is severe or persistent.
4. Lifestyle modifications, such as avoiding contact sports and taking precautions to prevent injuries, can also help manage the condition.
Early diagnosis and treatment of factor V deficiency are crucial to prevent complications and improve quality of life. If you suspect you or your child may have factor V deficiency, consult a healthcare professional for proper evaluation and management.
1. Infection: Bacterial or viral infections can develop after surgery, potentially leading to sepsis or organ failure.
2. Adhesions: Scar tissue can form during the healing process, which can cause bowel obstruction, chronic pain, or other complications.
3. Wound complications: Incisional hernias, wound dehiscence (separation of the wound edges), and wound infections can occur.
4. Respiratory problems: Pneumonia, respiratory failure, and atelectasis (collapsed lung) can develop after surgery, particularly in older adults or those with pre-existing respiratory conditions.
5. Cardiovascular complications: Myocardial infarction (heart attack), cardiac arrhythmias, and cardiac failure can occur after surgery, especially in high-risk patients.
6. Renal (kidney) problems: Acute kidney injury or chronic kidney disease can develop postoperatively, particularly in patients with pre-existing renal impairment.
7. Neurological complications: Stroke, seizures, and neuropraxia (nerve damage) can occur after surgery, especially in patients with pre-existing neurological conditions.
8. Pulmonary embolism: Blood clots can form in the legs or lungs after surgery, potentially causing pulmonary embolism.
9. Anesthesia-related complications: Respiratory and cardiac complications can occur during anesthesia, including respiratory and cardiac arrest.
10. delayed healing: Wound healing may be delayed or impaired after surgery, particularly in patients with pre-existing medical conditions.
It is important for patients to be aware of these potential complications and to discuss any concerns with their surgeon and healthcare team before undergoing surgery.
Anticoagulant
Lupus anticoagulant
Polyestriol phosphate
Lofepramine
Septic pelvic thrombophlebitis
Sticky platelet syndrome
White-winged vampire bat
Omeprazole
Hepatotoxicity
Direct factor Xa inhibitors
CYP3A4
Priapism
Multisystem inflammatory syndrome in children
Betrixaban
Methylprednisolone
Semuloparin sodium
Cerebral angiography
Diplomatic illness
Synovial fluid
Cardiomegaly
Drugs in pregnancy
Management of atrial fibrillation
Long-eared owl
Factor X
Deep vein thrombosis
Ruth R. Wexler
REG1
Discovery and development of direct thrombin inhibitors
Discovery and development of direct Xa inhibitors
Confluence of sinuses
Cerebral Venous Thrombosis Medication: Anticoagulants, Cardiovascular, Thrombolytics
Cerebral Venous Thrombosis Medication: Anticoagulants, Cardiovascular, Thrombolytics
Blood Thinners | Anticoagulants | MedlinePlus
New Oral Anticoagulants | PSNet
Vertebral Artery Dissection Medication: Anticoagulants, Cardiovascular, Antiplatelet Agents, Cardiovascular, Thrombolytics
Bald eagle's death puts anti-coagulant rodenticides under fire
Worldwide Anticoagulants Industry to 2025 - Featuring Bayer, Bristol-Myers Squibb, Boehringher Ingelheim and Daiichi Sankyo
Anticoagulant rodenticides
Practical considerations in the use of novel oral anticoagulants for stroke prevention in nonvalvular atrial fibrillation
Anticoagulants Market: Rise in Prevalence of Cardiovascular and Kidney Diseases to Drive Market
Thrombosis Associated with Procainamide-Induced Lupus Anticoagulant | Acta Haematologica | Karger Publishers
New oral anticoagulants drive ACC consensus on bleeding - The Hospitalist
Oral anticoagulants in older adults with atrial fibrillation. | Scholars@Duke
British Library EThOS: Anticoagulant rodenticides and non-target wildlife : an ecological evaluation of permanent baiting in...
Factors influencing primary care physicians' prescribing behavior of anticoagulant therapy for the management of patients with...
KAKEN - Research Projects | The New therapy of placental insufficiency ~ Endothelial progenitor cells for angiojenesis and new...
EN
The incidence of symptomatic thrombus in TKA patients has no correlation with use of anticoagulants after discharge - Authorea
Prevention Strategies | BSI | Guidelines Library | Infection Control | CDC
Does grapefruit affect my medicine? - NHS
Interactions Between Travel Vaccines & Drugs | CDC Yellow Book 2024
Dental Procedures in Patients with Atrial Fibrillation and New Oral Anticoagulants | Radcliffe Cardiology
Risks and benefits of direct oral anticoagulants versus warfarin in a real world setting: cohort study in primary care -...
Zetia: Package Insert / Prescribing Information - Drugs.com
Anticoagulants: Direct factor inhibitors: Video | Osmosis
ANTICOAGULANT - English word
Pathophysiological Changes in the Hemostatic System and Anti... : Transplantation
Reversal of Newer Anticoagulants in Acute Hemorrhagic Stroke
Lupus Anticoagulant Index - Machaon Diagnostics
Time at home among nonvalvular atrial fibrillation patients treated with non-VKA oral anticoagulants vs warfarin - STATinMED
Warfarin12
- Anticoagulants, such as heparin or warfarin (also called Coumadin), slow down your body's process of making clots. (medlineplus.gov)
- For the past 60 years, vitamin K antagonists such as warfarin sodium have been the only available oral anticoagulant medications. (ahrq.gov)
- Patients who orally ingest a TSOAC are actively anticoagulated within several hours and, because the half-life of TSOACs is considerably shorter than that of warfarin, most of the anticoagulant effect will typically wear off within 1-2 days. (ahrq.gov)
- As was his usual practice, he scanned the medication list to be sure the patient was not on enoxaparin or warfarin or other traditional anticoagulants, but he did not review the rest of the list. (ahrq.gov)
- The most commonly prescribed anticoagulant is Warfarin. (prnewswire.com)
- The proliferation of oral anticoagulants (warfarin and DOACs) and growing indications for their use prompted the need for guidance on the management of these drugs," said Gordon F. Tomaselli, MD , chair of the writing committee, in an interview. (the-hospitalist.org)
- Oral anticoagulant therapy use in patients with atrial fibrillation (AF) remains suboptimal in Singapore, despite the availability of both warfarin and non-vitamin K antagonist oral anticoagulants (NOACs). (physiciansweekly.com)
- Patients on warfarin might need to reduce their anticoagulant dose or monitor their prothrombin time more closely while taking atovaquone-proguanil, although coadministration of these drugs is not contraindicated. (cdc.gov)
- OBJECTIVE: To investigate the associations between direct oral anticoagulants (DOACs) and risks of bleeding, ischaemic stroke, venous thromboembolism, and all cause mortality compared with warfarin. (ox.ac.uk)
- PARTICIPANTS: 132 231 warfarin, 7744 dabigatran, 37 863 rivaroxaban, and 18 223 apixaban users without anticoagulant prescriptions for 12 months before study entry, subgrouped into 103 270 patients with atrial fibrillation and 92 791 without atrial fibrillation between 2011 and 2016. (ox.ac.uk)
- 4,8,9 The vitamin K antagonist warfarin has been the most widely used oral anticoagulant since its introduction in 1954. (uspharmacist.com)
- Warfarin is an anticoagulant and blood thinner used to treat thrombotic disorders. (cdc.gov)
Direct oral anticoagulants2
- However, the growth of the market would be supported by numerous market trends such as rising prevalence of venous thromboembolism (VTE), direct oral anticoagulants (DOACs), etc. during the forecasted period. (prnewswire.com)
- Examples include vitamin K antagonists and direct oral anticoagulants (DOACs). (informedhealth.org)
NOACs7
- Studies in recent years suggest that novel oral anticoagulants (NOACs) such as dabigatran, rivaroxaban, and apixaban may be viable alternatives with similar efficacy and safety outcomes to vitamin K antagonists. (medscape.com)
- Limitations with vitamin K antagonists (VKAs), the current standard of care, have led to the development of novel oral anticoagulants (NOACs) that target either thrombin (dabigatran etexilate) or activated factor X (rivaroxaban, apixaban, and edoxaban). (nih.gov)
- The rise in adoption of Novel Oral Anticoagulants (NOACs) boosts market growth. (medgadget.com)
- Therefore, adoption rate of NOACs has increased in the global anticoagulant market. (medgadget.com)
- Since the introduction of anticoagulants antidotes such as idarucizumab in the market in 2015, acceptance of NOACs has increased, as these eliminate the risk of bleeding. (medgadget.com)
- DOACs are sometimes still called 'new (or novel) oral anticoagulants' (NOACs) because they have only been approved since the year 2008. (informedhealth.org)
- Oral bleeding after dental extraction in patients on non- vitamin K oral anticoagulants (NOACs) is a frequent problem. (bvsalud.org)
Apixaban3
- Review properties of newer target-specific oral anticoagulants (TSOACs) such as dabigatran, rivaroxaban, and apixaban. (ahrq.gov)
- The use of novel oral anticoagulants, including dabigatran, rivaroxaban, and apixaban, is not expected to cause significant interactions, and their use has been suggested as an alternative for patients in need of anticoagulation. (cdc.gov)
- It's safer to drink grapefruit juice if you're taking the newer anticoagulants rivaroxaban , dabigatran , apixaban or edoxaban . (www.nhs.uk)
Factor Xa inhibitors2
- vitamin K antagonists, DTIs, and factor Xa inhibitors, are the various anticoagulants available in the market. (medgadget.com)
- The emergence of direct-acting oral anticoagulants (DOACs) to prevent venous thromboembolism and the introduction of new reversal strategies for factor Xa inhibitors prompted the creation of an Expert Consensus Decision Pathway to update the version from 2017, according to the ACC. (the-hospitalist.org)
Rivaroxaban1
- The patient had been on rivaroxaban (a relatively new oral anticoagulant) as treatment for her DVT before admission, and thus the discontinuation of anticoagulation placed her at high risk for recurrent DVT or pulmonary embolism. (ahrq.gov)
Heparin2
- There's also an anticoagulant called heparin that can be given by injection. (prnewswire.com)
- Patients undergoing invasive procedures or having signs/symptoms of underlying coagulopathy or other increased risk of bleeding (due to other therapies such as coumarin anticoagulants, heparin, tPA, streptokinase, high dose aspirin, or nonsteroidal anti-inflammatory drugs) should be evaluated for hemorrhage. (medscape.com)
Types of anticoagulants2
- Newer types of anticoagulants are also available and are becoming increasingly common. (prnewswire.com)
- What types of anticoagulants are there? (informedhealth.org)
Oral16
- Per standard protocol, she was given enoxaparin (an anticoagulant injected subcutaneously) after surgery as a "bridge" until she could resume her oral anticoagulant. (ahrq.gov)
- More recently, target-specific oral anticoagulants (TSOACs) have become available for the treatment and prevention of thromboembolism and currently make up approximately 20% of new anticoagulant prescriptions. (ahrq.gov)
- The report also provides an analysis of injectable and oral anticoagulants available in the market. (prnewswire.com)
- A brief analysis of the US anticoagulants market has also been provided in terms of value and sales of top four oral anticoagulant drugs in the region. (prnewswire.com)
- Patients on oral anticoagulants who experience a bleeding event may be able to discontinue therapy if certain circumstances apply, according to updated guidance from the American College of Cardiology. (the-hospitalist.org)
- In most cases of GI bleeding, for example, current data support restarting oral anticoagulants once hemostasis is achieved, but patients who experience intracranial hemorrhage should delay restarting any anticoagulation for at least 4 weeks if they are without high thrombotic risk, according to the document. (the-hospitalist.org)
- Oral anticoagulants in older adults with atrial fibrillation. (duke.edu)
- The following review summarizes the use of oral anticoagulants in older adults with AF, focusing on practical topics such as drug metabolism, drug-drug interactions, co-morbidities and cost considerations in a complex payer environment. (duke.edu)
- Oral anticoagulants are much more effective than antiplatelets. (informedhealth.org)
- Oral anticoagulants are also taken as tablets. (informedhealth.org)
- What oral anticoagulants are there? (informedhealth.org)
- Oral anticoagulants are very effective. (informedhealth.org)
- The use of oral anticoagulants leads to a 7- to 10-fold higher risk of spontaneous intracranial hemorrhage. (uspharmacist.com)
- There are no currently available antidotes to any of the newer oral anticoagulants. (uspharmacist.com)
- Persons who use oral anticoagulants (OACs) have a 7- to 10-fold higher risk of spontaneous ICH compared with those not receiving treatment. (uspharmacist.com)
- Tranexamic acid and bleeding in patients treated with non-vitamin K oral anticoagulants undergoing dental extraction: The EXTRACT-NOAC randomized clinical trial. (bvsalud.org)
Global Anticoagulants Market8
- DUBLIN , Sept. 22, 2021 /PRNewswire/ -- The "Global Anticoagulants Market: Size & Forecast with Impact Analysis of COVID-19 (2021-2025 Edition)" report has been added to ResearchAndMarkets.com's offering. (prnewswire.com)
- The report provides an in-depth analysis of the global anticoagulants market with description of market size and growth. (prnewswire.com)
- Growth of the global anticoagulants market has also been forecasted for the period 2021-2025, taking into consideration previous growth outlines, growth drivers and the existing and forthcoming trends. (prnewswire.com)
- Bayer Group, Bristol-Myers Squibb, Boehringher Ingelheim and Daiichi Sankyo are some of the key players operating in the global anticoagulants market, who's Company Profiles has been done in the report. (prnewswire.com)
- The global anticoagulants market has increased progressively over the years and the market growth was bolstered in 2020 owing to spread of COVID-19 pandemic. (prnewswire.com)
- The global anticoagulants market is supported by various growth drivers such as growing geriatric population, rising global healthcare expenditure, increasing diabetic population, escalating number of cancer patient, rising prevalence of cardiovascular disease, etc. (prnewswire.com)
- According to the report, the global anticoagulants market was valued at US$ 21,759.3 Mn in 2018 and is projected to expand at a CAGR of 8.0% from 2018 to 2026. (medgadget.com)
- Increase in the number of people suffering from DVT and surge in number of surgeries are expected to drive the global anticoagulants market. (medgadget.com)
Antiplatelet4
- What Are Anticoagulants and Antiplatelet Agents? (medlineplus.gov)
- Anticoagulant and antiplatelet agents are the drugs of choice (DOCs) to prevent thromboembolic disorders associated with vertebral artery dissection (VAD). (medscape.com)
- Antiplatelet agents have been used effectively in treating VAD but are reserved for those patients who cannot tolerate or have contraindications to anticoagulants. (medscape.com)
- However, "the extent of the use of multiple anticoagulants and antiplatelet agents was a bit surprising and complicates therapy with each of the agents," he noted. (the-hospitalist.org)
Lupus anticoagulants3
- A predisposition to thrombosis in patients with procainamide-induced lupus anticoagulants is previously unrecognized. (karger.com)
- The lupus anticoagulant index has been shown to be sensitive to weak lupus anticoagulants. (machaondiagnostics.com)
- Lupus anticoagulants result in the prolongation of clotting times which correct with the addition of phospholipids. (machaondiagnostics.com)
Thrombosis3
- We suggest that thrombosis may complicate treatment with procainamide in patients who develop the lupus anticoagulant. (karger.com)
- Background: Many guidelines indicated that to continue using anticoagulant drugs to reduce the incidence of symptomatic venous thrombosis (SVT) in total knee arthroplasty (TKA) patients after discharged. (authorea.com)
- The presence of antiphospholipid antibodies, such as lupus anticoagulant, increases the risk of arterial thrombosis, venous thrombosis, thrombocytopenia and recurrent miscarriage. (machaondiagnostics.com)
Eliquis1
- Xarleto and Eliquis are two anticoagulants increasingly preferred by physicians. (medgadget.com)
Anticoagulation1
- clinical support services for anticoagulation monitoring and constraints in existing care model influenced PCPs in their anticoagulant prescription. (physiciansweekly.com)
Atrial1
- Factors influencing primary care physicians' prescribing behavior of anticoagulant therapy for the management of patients with non-valvular atrial fibrillation in Singapore: a qualitative research study. (physiciansweekly.com)
Medications1
- Anticoagulant medications help to prevent thrombi, or blood clots from forming. (osmosis.org)
Patients treated2
- Studies indicate a tendency toward better outcome in patients treated with anticoagulant therapy than in those who are not treated with anticoagulants. (medscape.com)
- We describe two patients treated with procainamide who experienced acute thromboembolic events temporally associated with development ofthe lupus anticoagulant. (karger.com)
Clots4
- Anticoagulants which are also known as blood thinners are drugs that are prescribed to prevent blood from clotting or stop existing clots from getting larger. (prnewswire.com)
- Anticoagulants work by interrupting the process involved in the formation of blood clots. (prnewswire.com)
- Anticoagulants prevent clot formation or enlargement of existing clots in the arteries or veins. (medgadget.com)
- Anticoagulants are medicines that help to prevent blood clots. (www.nhs.uk)
Medication1
- Primary care physicians' (PCP) decision-making to initiate and select appropriate anticoagulant medication is pivotal in reducing complications among patients with AF. (physiciansweekly.com)
Blood1
- Anticoagulants don't completely stop blood from clotting. (informedhealth.org)
Medicines1
- Anticoagulants are the most common medicines for treating DVT. (medlineplus.gov)
Typically1
- After a substantial ingestion of a long-acting anticoagulant, clinical signs of coagulopathy typically occur within 24-72 hours. (cdc.gov)
Consensus1
- Long-acting anticoagulant rodenticide poisoning: an evidence-based consensus guideline for out-of-hospital management. (cdc.gov)
Acute1
- After an acute unintentional ingestion of a long-acting anticoagulant, the majority of patients are entirely asymptomatic. (cdc.gov)
Detection1
- Detection of a long-acting anticoagulant (e.g., brodifacoum) in serum, plasma, or urine, as determined by commercial laboratory tests. (cdc.gov)
Potentially1
- Paradoxically, patients with ESKD (CKD stage 5) also show an increased bleeding tendency, as may be reflected by a 4% incidence of significant bleeding posttransplantation compared with 1% in general surgery, 1 , 4 which is potentially due to profound pro- and anticoagulant changes in ESKD patients. (lww.com)