Agents that prevent clotting.
An antiphospholipid antibody found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.
An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.
A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.
The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.
Substances used to destroy or inhibit the action of rats, mice, or other rodents.
A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233)
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
Activated form of factor X that participates in both the intrinsic and extrinsic pathways of blood coagulation. It catalyzes the conversion of prothrombin to thrombin in conjunction with other cofactors.
An indandione that has been used as an anticoagulant. Phenindione has actions similar to WARFARIN, but it is now rarely employed because of its higher incidence of severe adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p234)
Substances found in many plants, containing the 4-hydroxycoumarin radical. They interfere with vitamin K and the blood clotting mechanism, are tightly protein-bound, inhibit mitochondrial and microsomal enzymes, and are used as oral anticoagulants.
Endogenous factors and drugs that directly inhibit the action of THROMBIN, usually by blocking its enzymatic activity. They are distinguished from INDIRECT THROMBIN INHIBITORS, such as HEPARIN, which act by enhancing the inhibitory effects of antithrombins.
Laboratory tests for evaluating the individual's clotting mechanism.
Clotting time of PLASMA mixed with a THROMBIN solution. It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. BATROXOBIN, a thrombin-like enzyme unaffected by the presence of heparin, may be used in place of thrombin.
System established by the World Health Organization and the International Committee on Thrombosis and Hemostasis for monitoring and reporting blood coagulation tests. Under this system, results are standardized using the International Sensitivity Index for the particular test reagent/instrument combination used.
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.
The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
Bleeding or escape of blood from a vessel.
Heparin fractions with a molecular weight usually between 4000 and 6000 kD. These low-molecular-weight fractions are effective antithrombotic agents. Their administration reduces the risk of hemorrhage, they have a longer half-life, and their platelet interactions are reduced in comparison to unfractionated heparin. They also provide an effective prophylaxis against postoperative major pulmonary embolism.
A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation.
An amino acid formed in vivo by the degradation of dihydrouracil and carnosine. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, the compound may be a false transmitter replacing GAMMA-AMINOBUTYRIC ACID. A rare genetic disorder, hyper-beta-alaninemia, has been reported.
Formation and development of a thrombus or blood clot in the blood vessel.
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
The presence of antibodies directed against phospholipids (ANTIBODIES, ANTIPHOSPHOLIPID). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (ANTIBODIES, ANTICARDIOLIPIN). Present also are high levels of lupus anticoagulant (LUPUS COAGULATION INHIBITOR).
A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.
Inflammation of a vein associated with a blood clot (THROMBUS).
Coumarin derivative that acts as a long acting oral anticoagulant.
The formation or presence of a blood clot (THROMBUS) within a vein.
A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.
Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals.
Antiphospholipid antibodies found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN.
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.
Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.
Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.
The giving of drugs, chemicals, or other substances by mouth.
Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS.
Coagulant substances inhibiting the anticoagulant action of heparin.
Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.
Storage-stable glycoprotein blood coagulation factor that can be activated to factor Xa by both the intrinsic and extrinsic pathways. A deficiency of factor X, sometimes called Stuart-Prower factor deficiency, may lead to a systemic coagulation disorder.
Single-chain polypeptides of about 65 amino acids (7 kDa) from LEECHES that have a neutral hydrophobic N terminus, an acidic hydrophilic C terminus, and a compact, hydrophobic core region. Recombinant hirudins lack tyr-63 sulfation and are referred to as 'desulfato-hirudins'. They form a stable non-covalent complex with ALPHA-THROMBIN, thereby abolishing its ability to cleave FIBRINOGEN.
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.
Agents that cause clotting.
A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.
An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases.
A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.
Activated form of factor V. It is an essential cofactor for the activation of prothrombin catalyzed by factor Xa.
The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
The reduction or regulation of the population of noxious, destructive, or dangerous rodents through chemical, biological, or other means.
Low-molecular-weight fragment of heparin, having a 4-enopyranosuronate sodium structure at the non-reducing end of the chain. It is prepared by depolymerization of the benzylic ester of porcine mucosal heparin. Therapeutically, it is used as an antithrombotic agent. (From Merck Index, 11th ed)
OXIDOREDUCTASES which mediate vitamin K metabolism by converting inactive vitamin K 2,3-epoxide to active vitamin K.
An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
A naturally occurring glycosaminoglycan found mostly in the skin and in connective tissue. It differs from CHONDROITIN SULFATE A (see CHONDROITIN SULFATES) by containing IDURONIC ACID in place of glucuronic acid, its epimer, at carbon atom 5. (from Merck, 12th ed)
A sulfated plasma protein with a MW of approximately 66kDa that resembles ANTITHROMBIN III. The protein is an inhibitor of thrombin in plasma and is activated by dermatan sulfate or heparin. It is a member of the serpin superfamily.
Compounds with a BENZENE fused to IMIDAZOLES.
Pyridine derivatives with one or more keto groups on the ring.
An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)
Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal SYPHILIS SERODIAGNOSIS.
An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis.
A collection of blood outside the BLOOD VESSELS. Hematoma can be localized in an organ, space, or tissue.
The process of observing, recording, or detecting the effects of a chemical substance administered to an individual therapeutically or diagnostically.
A low-molecular-weight fragment of heparin, prepared by nitrous acid depolymerization of porcine mucosal heparin. The mean molecular weight is 4000-6000 daltons. It is used therapeutically as an antithrombotic agent. (From Merck Index, 11th ed)
A class of Echinodermata characterized by long, slender bodies.
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Synthetic or naturally occurring substances related to coumarin, the delta-lactone of coumarinic acid.
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
Proteins synthesized by organisms belonging to the phylum ARTHROPODA. Included in this heading are proteins from the subdivisions ARACHNIDA; CRUSTACEA; and HORSESHOE CRABS. Note that a separate heading for INSECT PROTEINS is listed under this heading.
Absence or reduced levels of PROTHROMBIN in the blood.
An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance.
Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).
Multicellular marine macroalgae including some members of red (RHODOPHYTA), green (CHLOROPHYTA), and brown (PHAEOPHYTA) algae. They are widely distributed in the ocean, occurring from the tide level to considerable depths, free-floating (planktonic) or anchored to the substratum (benthic). They lack a specialized vascular system but take up fluids, nutrients, and gases directly from the water. They contain CHLOROPHYLL and are photosynthetic, but some also contain other light-absorbing pigments. Many are of economic importance as FOOD, fertilizer, AGAR, potash, or source of IODINE.
Activated form of factor VIII. The B-domain of factor VIII is proteolytically cleaved by thrombin to form factor VIIIa. Factor VIIIa exists as a non-covalent dimer in a metal-linked (probably calcium) complex and functions as a cofactor in the enzymatic activation of factor X by factor IXa. Factor VIIIa is similar in structure and generation to factor Va.
A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
Hemorrhagic and thrombotic disorders resulting from abnormalities or deficiencies of coagulation proteins.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The natural enzymatic dissolution of FIBRIN.
Blocking of a blood vessel by an embolus which can be a blood clot or other undissolved material in the blood stream.
Elements of limited time intervals, contributing to particular results or situations.
Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
The time required by whole blood to produce a visible clot.
The process by which blood or its components are kept viable outside of the organism from which they are derived (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).
The return of a sign, symptom, or disease after a remission.
Heparin derivatives. The term has also been used more loosely to include naturally occurring and synthetic highly-sulphated polysaccharides of similar structure. Heparinoid preparations have been used for a wide range of applications including as anticoagulants and anti-inflammatories and they have been claimed to have hypolipidemic properties. (From Martindale, The Extra Pharmacopoeia, 30th, p232)
The taking of a blood sample to determine its character as a whole, to identify levels of its component cells, chemicals, gases, or other constituents, to perform pathological examination, etc.
A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.
Hemorrhage following any surgical procedure. It may be immediate or delayed and is not restricted to the surgical wound.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.
Accumulation of blood in the SUBDURAL SPACE between the DURA MATER and the arachnoidal layer of the MENINGES. This condition primarily occurs over the surface of a CEREBRAL HEMISPHERE, but may develop in the spinal canal (HEMATOMA, SUBDURAL, SPINAL). Subdural hematoma can be classified as the acute or the chronic form, with immediate or delayed symptom onset, respectively. Symptoms may include loss of consciousness, severe HEADACHE, and deteriorating mental status.
An enzyme fraction from the venom of the Malayan pit viper, Agkistrodon rhodostoma. It catalyzes the hydrolysis of a number of amino acid esters and a limited proteolysis of fibrinogen. It is used clinically to produce controlled defibrination in patients requiring anticoagulant therapy. EC 3.4.21.-.
A division of predominantly marine EUKARYOTA, commonly known as brown algae, having CHROMATOPHORES containing carotenoid PIGMENTS, BIOLOGICAL. ALGINATES and phlorotannins occur widely in all major orders. They are considered the most highly evolved algae because of their well-developed multicellular organization and structural complexity.
Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures.
The co-occurrence of pregnancy and a blood disease (HEMATOLOGIC DISEASES) which involves BLOOD CELLS or COAGULATION FACTORS. The hematologic disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
Colorless, endogenous or exogenous pigment precursors that may be transformed by biological mechanisms into colored compounds; used in biochemical assays and in diagnosis as indicators, especially in the form of enzyme substrates. Synonym: chromogens (not to be confused with pigment-synthesizing bacteria also called chromogens).
A device that substitutes for a heart valve. It may be composed of biological material (BIOPROSTHESIS) and/or synthetic material.
A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.
A genus of nematode intestinal parasites that consists of several species. A. duodenale is the common hookworm in humans. A. braziliense, A. ceylonicum, and A. caninum occur primarily in cats and dogs, but all have been known to occur in humans.
A member of the serpin family of proteins that is found in plasma and urine. It is dependent on heparin and is able to inhibit activated PROTEIN C; THROMBIN; KALLIKREIN; and other SERINE ENDOPEPTIDASES.
Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.
Interventions to provide care prior to, during, and immediately after surgery.
Proteins prepared by recombinant DNA technology.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
Proteins and peptides found in SALIVA and the SALIVARY GLANDS. Some salivary proteins such as ALPHA-AMYLASES are enzymes, but their composition varies in different individuals.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).
An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC 4.2.2.7.
Toluenes in which one hydrogen of the methyl group is substituted by an amino group. Permitted are any substituents on the benzene ring or the amino group.
Activated form of factor IX. This activation can take place via the intrinsic pathway by the action of factor XIa and calcium, or via the extrinsic pathway by the action of factor VIIa, thromboplastin, and calcium. Factor IXa serves to activate factor X to Xa by cleaving the arginyl-leucine peptide bond in factor X.
An order of nematodes of the subclass SECERNENTEA. Characteristics include an H-shaped excretory system with two subventral glands.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
A family of proteinase-activated receptors that are specific for THROMBIN. They are found primarily on PLATELETS and on ENDOTHELIAL CELLS. Activation of thrombin receptors occurs through the proteolytic action of THROMBIN, which cleaves the N-terminal peptide from the receptor to reveal a new N-terminal peptide that is a cryptic ligand for the receptor. The receptors signal through HETEROTRIMERIC GTP-BINDING PROTEINS. Small synthetic peptides that contain the unmasked N-terminal peptide sequence can also activate the receptor in the absence of proteolytic activity.
A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.
Agents acting to arrest the flow of blood. Absorbable hemostatics arrest bleeding either by the formation of an artificial clot or by providing a mechanical matrix that facilitates clotting when applied directly to the bleeding surface. These agents function more at the capillary level and are not effective at stemming arterial or venous bleeding under any significant intravascular pressure.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.
Venoms from SNAKES of the viperid family. They tend to be less toxic than elapid or hydrophid venoms and act mainly on the vascular system, interfering with coagulation and capillary membrane integrity and are highly cytotoxic. They contain large amounts of several enzymes, other factors, and some toxins.
Agents counteracting or neutralizing the action of POISONS.
Three or more consecutive spontaneous abortions.
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
A subnormal level of BLOOD PLATELETS.
A group of simple proteins that yield basic amino acids on hydrolysis and that occur combined with nucleic acid in the sperm of fish. Protamines contain very few kinds of amino acids. Protamine sulfate combines with heparin to form a stable inactive complex; it is used to neutralize the anticoagulant action of heparin in the treatment of heparin overdose. (From Merck Index, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p692)
Substances, usually endogenous, that act as inhibitors of blood coagulation. They may affect one or multiple enzymes throughout the process. As a group, they also inhibit enzymes involved in processes other than blood coagulation, such as those from the complement system, fibrinolytic enzyme system, blood cells, and bacteria.
Use of HIRUDINS as an anticoagulant in the treatment of cardiological and hematological disorders.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Mechanical devices inserted in the inferior vena cava that prevent the migration of blood clots from deep venous thrombosis of the leg.
Polysaccharides composed of repeating galactose units. They can consist of branched or unbranched chains in any linkages.
A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.
Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or N-acetylgalactosamine.
Family of calcium- and phospholipid-binding proteins which are structurally related and exhibit immunological cross-reactivity. Each member contains four homologous 70-kDa repeats. The annexins are differentially distributed in vertebrate tissues (and lower eukaryotes) and appear to be involved in MEMBRANE FUSION and SIGNAL TRANSDUCTION.
Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
The residual portion of BLOOD that is left after removal of BLOOD CELLS by CENTRIFUGATION without prior BLOOD COAGULATION.
Formation or presence of a blood clot (THROMBUS) in the CRANIAL SINUSES, large endothelium-lined venous channels situated within the SKULL. Intracranial sinuses, also called cranial venous sinuses, include the superior sagittal, cavernous, lateral, petrous sinuses, and many others. Cranial sinus thrombosis can lead to severe HEADACHE; SEIZURE; and other neurological defects.
Works about clinical trials that involve at least one test treatment and one control treatment, concurrent enrollment and follow-up of the test- and control-treated groups, and in which the treatments to be administered are selected by a random process, such as the use of a random-numbers table.
Organic esters of sulfuric acid.
Surgical procedures used to treat disease, injuries, and defects of the oral and maxillofacial region.
The qualitative or quantitative estimation of the likelihood of adverse effects that may result from exposure to specified health hazards or from the absence of beneficial influences. (Last, Dictionary of Epidemiology, 1988)
A synthetic polymer which agglutinates red blood cells. It is used as a heparin antagonist.
A heparin fraction with a mean molecular weight of 4500 daltons. It is isolated from porcine mucosal heparin and used as an antithrombotic agent. (From Merck Index, 11th ed)
Bleeding within the SKULL, including hemorrhages in the brain and the three membranes of MENINGES. The escape of blood often leads to the formation of HEMATOMA in the cranial epidural, subdural, and subarachnoid spaces.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
Derivatives of chondroitin which have a sulfate moiety esterified to the galactosamine moiety of chondroitin. Chondroitin sulfate A, or chondroitin 4-sulfate, and chondroitin sulfate C, or chondroitin 6-sulfate, have the sulfate esterified in the 4- and 6-positions, respectively. Chondroitin sulfate B (beta heparin; DERMATAN SULFATE) is a misnomer and this compound is not a true chondroitin sulfate.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
The co-occurrence of pregnancy and a cardiovascular disease. The disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
Found in various tissues, particularly in four blood-clotting proteins including prothrombin, in kidney protein, in bone protein, and in the protein present in various ectopic calcifications.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Inorganic salts of sulfuric acid.
A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A CXC chemokine that is found in the alpha granules of PLATELETS. The protein has a molecular size of 7800 kDa and can occur as a monomer, a dimer or a tetramer depending upon its concentration in solution. Platelet factor 4 has a high affinity for HEPARIN and is often found complexed with GLYCOPROTEINS such as PROTEIN C.
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
Therapy with two or more separate preparations given for a combined effect.
The rate dynamics in chemical or physical systems.
A thrombin receptor subtype that couples to HETEROTRIMERIC GTP-BINDING PROTEINS resulting in the activation of a variety of signaling mechanisms including decreased intracellular CYCLIC AMP, increased TYPE C PHOSPHOLIPASES and increased PHOSPHOLIPASE A2.
A family of phylloquinones that contains a ring of 2-methyl-1,4-naphthoquinone and an isoprenoid side chain. Members of this group of vitamin K 1 have only one double bond on the proximal isoprene unit. Rich sources of vitamin K 1 include green plants, algae, and photosynthetic bacteria. Vitamin K1 has antihemorrhagic and prothrombogenic activity.
A genus of venomous snakes of the subfamily Crotalinae. Twelve species of this genus are found in North and Central America and Asia. Agkistrodon contortrix is the copperhead, A. piscivorus, the cottonmouth. The former is named for its russet or orange-brown color, the latter for the white interior of its mouth. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p336; Moore, Poisonous Snakes of the World, 1980, p75)
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
A family of extremely venomous snakes, comprising coral snakes, cobras, mambas, kraits, and sea snakes. They are widely distributed, being found in the southern United States, South America, Africa, southern Asia, Australia, and the Pacific Islands. The elapids include three subfamilies: Elapinae, Hydrophiinae, and Lauticaudinae. Like the viperids, they have venom fangs in the front part of the upper jaw. The mambas of Africa are the most dangerous of all snakes by virtue of their size, speed, and highly toxic venom. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p329-33)
Heterocyclic compounds that contain 4H,5H,6H,7H-thieno[2,3-c]pyridine as part of their structure.
Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin.
Enzymes which transfer sulfate groups to various acceptor molecules. They are involved in posttranslational sulfation of proteins and sulfate conjugation of exogenous chemicals and bile acids. EC 2.8.2.
Radiographic visualization or recording of a vein after the injection of contrast medium.
Drugs which have received FDA approval for human testing but have yet to be approved for commercial marketing. This includes drugs used for treatment while they still are undergoing clinical trials (Treatment IND). The main heading includes drugs under investigation in foreign countries.
The practice of replacing one prescribed drug with another that is expected to have the same clinical or psychological effect.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Bleeding within the SKULL induced by penetrating and nonpenetrating traumatic injuries, including hemorrhages into the tissues of CEREBRUM; BRAIN STEM; and CEREBELLUM; as well as into the epidural, subdural and subarachnoid spaces of the MENINGES.
Nucleotide sequences, generated by iterative rounds of SELEX APTAMER TECHNIQUE, that bind to a target molecule specifically and with high affinity.
Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.
Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. Several endogenous antiplasmins are known. The drugs are used to control massive hemorrhage and in other coagulation disorders.
Pathological conditions involving the HEART including its structural and functional abnormalities.
Proteins found in any species of helminth.
A deficiency of blood coagulation factor V (known as proaccelerin or accelerator globulin or labile factor) leading to a rare hemorrhagic tendency known as Owren's disease or parahemophilia. It varies greatly in severity. Factor V deficiency is an autosomal recessive trait. (Dorland, 27th ed)
Widely distributed enzymes that carry out oxidation-reduction reactions in which one atom of the oxygen molecule is incorporated into the organic substrate; the other oxygen atom is reduced and combined with hydrogen ions to form water. They are also known as monooxygenases or hydroxylases. These reactions require two substrates as reductants for each of the two oxygen atoms. There are different classes of monooxygenases depending on the type of hydrogen-providing cosubstrate (COENZYMES) required in the mixed-function oxidation.

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.

Oral anticoagulants (OACs) are taken by many people in pill or tablet form, and various intravenous anticoagulant dosage forms ... Common anticoagulants include warfarin and heparin. The use of anticoagulants is a decision based upon the risks and benefits ... Anticoagulants are often used to treat acute deep vein thrombosis. People using anticoagulants to treat this condition should ... Djulbegovic M, Lee AI (September 2018). "An Update on the "Novel" and Direct Oral Anticoagulants, and Long-Term Anticoagulant ...
Both words in the term "lupus anticoagulant" can be misleading: Most patients with a lupus anticoagulant do not actually have ... lupus anticoagulant and a history of thrombosis should be considered candidates for indefinite treatment with anticoagulants. ... Lupus anticoagulant in living systems causes a decrease in clotting time. The name derives from their properties in vitro, as ... Testing for lupus anticoagulant can also be indicated by a prolonged aPTT test that is unexplained. An aPTT is generally ...
Interactions: Oral anticoagulants; rifampin. [...] U.S. Treatments: Conjugated estrogens are commonly prescribed for menopausal ...
Anticoagulants (blood thinners). Lofepramine may inhibit the metabolism of certain anticoagulants leading to a potentially ...
Response to anticoagulants". The New England Journal of Medicine. 276 (5): 265-8. doi:10.1056/NEJM196702022760505. PMID 6016063 ... Current treatments consist of a combination of antibiotics selected based on suspected pathogen(s), and anticoagulants. Though ... such as anticoagulant and antimicrobial therapy. Septic pelvic thrombophlebitis (SPT) is often associated with postpartum ...
Anticoagulants (e.g. Warfarin, Coumadin) or clopidogrel (Plavix) are often additionally prescribed following formation of a ...
... and other anticoagulants. These compounds in their saliva are especially effective on birds. Birds are their preferred prey ...
"Pharmacogenetics of oral anticoagulants". Pharmacogenetics. 13 (5): 247-252. doi:10.1097/00008571-200305000-00002. PMID ...
Arora N, Goldhaber SZ (2006). "Anticoagulants and transaminase elevation". Circulation. 113 (15): e698-702. doi:10.1161/ ...
... (xabans) are anticoagulants (blood thinning drugs), used to both treat and prevent blood clots in ... Andexanet alfa, a specific antidote to reverse the anticoagulant activity of direct Xa inhibitors in the event of major ... Chen, Ashley; Stecker, Eric; Warden, Bruce A. (7 July 2020). "Direct Oral Anticoagulant Use: A Practical Guide to Common ... ISBN 978-1-59259-658-4. Bauer, K. A. (6 December 2013). "Pros and cons of new oral anticoagulants". Hematology. 2013 (1): 464- ...
Daly AK, King BP (May 2003). "Pharmacogenetics of oral anticoagulants". Pharmacogenetics. 13 (5): 247-52. doi:10.1097/00008571- ...
Anticoagulants, cantharides (Spanish Fly) and recreational drugs (alcohol, heroin and cocaine) have been associated. Priapism ... Anticoagulants (heparin and warfarin). Antihypertensives (i.e., hydralazine, guanethidine and propranolol). Hormones (i.e., ...
Anticoagulants have been used. Low-dose aspirin has been used as an antiplatelet drug. Treatment strategies are being ...
... (trade name Bevyxxa) is an oral anticoagulant drug which acts as a direct factor Xa inhibitor. Betrixaban is FDA ... Compared to other directly acting oral anticoagulants betrixaban has relatively low renal excretion and is not metabolized by ... Sobieraj-Teague, M.; O'donnell, M.; Eikelboom, J. (2009). "New Anticoagulants for Atrial Fibrillation". Seminars in Thrombosis ...
Anticoagulants Anticoagulants exhibit variable interactions; monitoring coagulation indices is recommended to achieve the ...
"New parenteral anticoagulants in development". Therapeutic Advances in Cardiovascular Disease. 5 (1): 33-59. doi:10.1177/ ...
Anticoagulants are withheld if possible. Fasting is required 6 hours before the procedure and insulin requirement is reduced by ...
She's Being Treated with Anticoagulants." The Seattle Times. December 31, 2012. Retrieved August 30, 2016, from HighBeam ...
ISBN 978-0-7817-7153-5. "Lupus Anticoagulant". Family Practice Notebook. Archived from the original on 18 January 2013. ...
Anticoagulants: to reduce the risk of blood clots that could cause a heart attack or stroke. Anti-arrhythmics: to keep the ... "Anticoagulant medicines". nhs.uk. 2018-02-06. Retrieved 2020-01-23. Amin, Hina; Siddiqui, Waqas J. (2019). "Cardiomegaly". ...
Direct oral anticoagulants are newer types of anticoagulants that are available as oral medications and are widely used in non- ... Anticoagulants are medications that prevent the blood from forming clots and are also known as blood thinners. These ... Anticoagulants must be prescribed with caution as these medications can have negative health consequences for the developing ... "Anticoagulant medicines". nhs.uk. 6 February 2018. Retrieved 30 July 2020. Alshawabkeh L, Economy KE, Valente AM (October 2016 ...
Dabigatran is an anticoagulant that works as a direct thrombin inhibitor, and does not require blood tests for INR monitoring, ... To compensate for the increased risk of stroke, anticoagulants may be required. However, in the case of warfarin, if someone ... With the likely availability of new oral anticoagulants that avoid the limitations of warfarin (and may even be safer), more ... 2002). "Oral anticoagulants vs aspirin in nonvalvular atrial fibrillation: an individual patient meta-analysis". JAMA. 288 (19 ...
Anticoagulants may also threaten this species. In the Canary islands, it has become increasingly scarce due to loss of habitat ... Stone, W. B., Okoniewski, J. C., & Stedelin, J. R. (2003). Anticoagulant rodenticides and raptors: recent findings from New ...
The most commonly used anticoagulants in clinical practice, warfarin and the heparin series of anticoagulants and fondaparinux ... Inhibition of the synthesis or activity of Factor X is the mechanism of action for many anticoagulants in use today. Warfarin, ... Direct Xa inhibitors are popular anticoagulants. Polymorphisms in Factor X have been associated with an increased prevalence in ... The efficacy of heparin-based anticoagulants increases as selectivity for Factor Xa increases. LMWH shows increased ...
Warfarin, dabigatran, and edoxaban require the use of a parenteral anticoagulant to initiate oral anticoagulant therapy. When ... Some anticoagulants can be taken by mouth, and these oral medicines include warfarin (a vitamin K antagonist), rivaroxaban (a ... Lloyd NS, Douketis JD, Moinuddin I, Lim W, Crowther MA (March 2008). "Anticoagulant prophylaxis to prevent asymptomatic deep ... Beginning warfarin treatment requires an additional non-oral anticoagulant, often injections of heparin. Prevention of VTE for ...
Ruth Wexler is an American industrial chemist best known as a co-discoverer of apixaban, a marketed anticoagulant; and losartan ... "Factor XIa Inhibitors as New Anticoagulants". Journal of Medicinal Chemistry. 61 (17): 7425-7447. doi:10.1021/acs.jmedchem. ...
v t e (Anticoagulants, Human proteins, All stub articles, Biology stubs). ... Sinha, Gunjan (2013-12-01). "Regado's aptamer lines up against anticoagulants". Nature Biotechnology. 31 (12): 1060. doi: ...
Given this broad action of thrombin it stands as a good drug target for anticoagulant drugs such as heparin, warfarin and DTIs ... Direct thrombin inhibitors (DTIs) are a class of anticoagulant drugs that can be used to prevent and treat embolisms and blood ... Vitamin K antagonists are the most commonly used oral anticoagulants today and warfarin was the 11th most prescribed drug in ... Since both heparin and warfarin have their downsides the search for alternative anticoagulants has been ongoing and DTIs are ...
Factor Xa was identified as a promising target for the development of new anticoagulants in the early 1980s. In 1987 the first ... It wasn't until 1954 that it was approved for medicinal use in humans making warfarin the first oral anticoagulant drug. ... Because of these disadvantages there has been an urgent need for better anticoagulant drugs. For a modern society, convenient ... Another natural occurring direct Xa-inhibitor, the tick anticoagulant peptide (TAP), was discovered in 1990. It is a single- ...
This can be treated with anticoagulants. It may be injured by a variety of major trauma. It may also be damaged during surgery ...
Anticoagulants, Cardiovascular. Class Summary. These medications are used to prevent propagation of the clot to more extensive ... Studies indicate a tendency toward better outcome in patients treated with anticoagulant therapy than in those who are not ... Benamer HT, Bone I. Cerebral venous thrombosis: anticoagulants or thrombolyic therapy?. J Neurol Neurosurg Psychiatry. 2000 Oct ... and aPTT does not correlate with anticoagulant effect. ... treated with anticoagulants. In Einhaupls study, even patients ...
Anticoagulants, Cardiovascular. Class Summary. These medications are used to prevent propagation of the clot to more extensive ... Studies indicate a tendency toward better outcome in patients treated with anticoagulant therapy than in those who are not ... Benamer HT, Bone I. Cerebral venous thrombosis: anticoagulants or thrombolyic therapy?. J Neurol Neurosurg Psychiatry. 2000 Oct ... and aPTT does not correlate with anticoagulant effect. ... treated with anticoagulants. In Einhaupls study, even patients ...
Anticoagulant and antiplatelet drugs are blood thinners. They reduce risk of heart attacks and help keep blood clots from ... Anticoagulants and Drug-Food Interactions (National Jewish Health) * Blood Thinner Pills: Your Guide to Using Them Safely ( ... ClinicalTrials.gov: Anticoagulants (National Institutes of Health) * ClinicalTrials.gov: Heparin (National Institutes of Health ... Anticoagulants, such as heparin or warfarin (also called Coumadin), slow down your bodys process of making clots. ...
Case Objectives Review properties of newer target-specific oral anticoagulants (TSOACs) such as dabigatran, rivaroxaban, and ... Target-specific oral anticoagulants (TSOACs) have become viable alternatives to conventional oral anticoagulants and have the ... 6. Mani H, Kasper A, Lindhoff-Last E. Measuring the anticoagulant effects of target specific oral anticoagulants-reasons, ... The patient had been on rivaroxaban (a relatively new oral anticoagulant) as treatment for her DVT before admission, and thus ...
Anticoagulants, Cardiovascular. Class Summary. These agents are indicated in patients with VAD to prevent recurrent or ongoing ... Anticoagulant and antiplatelet agents are the drugs of choice (DOCs) to prevent thromboembolic disorders associated with ... Studies in recent years suggest that novel oral anticoagulants (NOACs) such as dabigatran, rivaroxaban, and apixaban may be ... Helsinki experience on nonvitamin K oral anticoagulants for treating cervical artery dissection. Brain Behav. 2015 Aug. 5(8): ...
There are many poison-free options for preventing and addressing rodent problems, said Sam Anderson, of Mass Audubon, in a statement.
PRNewswire/ -- The Global Anticoagulants Market: Size & Forecast with Impact Analysis of COVID-19 (2021-2025 Edition) report ... 2.1 Overview of Anticoagulants. 2.1.1 Types of Anticoagulants. 2.1.2 Novel Oral Anticoagulants. 3. Global Market Analysis. 3.1 ... 5.1 The US Anticoagulants Market Analysis. 5.1.1 The US Anticoagulants Market by Value. 5.1.2 The US Anticoagulants Market by ... 3.3.3 Global Other Anticoagulants Market by Value. 4. Global Anticoagulants Product Analysis. 4.1 Oral Anticoagulants Product ...
1995)‎. Anticoagulant rodenticides. World Health Organization. https://extranet.who.int/iris/restricted/handle/10665/37676 ...
... ... have led to the development of novel oral anticoagulants (NOACs) that target either thrombin (dabigatran etexilate) or ...
... October 9th, 2020 Transparency ... Anticoagulants prevent clot formation or enlargement of existing clots in the arteries or veins. Heparins, including ... The rise in adoption of Novel Oral Anticoagulants (NOACs) boosts market growth. NOACs target either factor Xa to avoid or to ... This condition is treated using anticoagulants. Increase in the number of people suffering from DVT and surge in number of ...
Alan F. List, Donald C. Doll; Thrombosis Associated with Procainamide-Induced Lupus Anticoagulant. Acta Haematol 1 January 1989 ... We suggest that thrombosis may complicate treatment with procainamide in patients who develop the lupus anticoagulant. ... A predisposition to thrombosis in patients with procainamide-induced lupus anticoagulants is previously unrecognized. We ... with procainamide who experienced acute thromboembolic events temporally associated with development ofthe lupus anticoagulant ...
Patients on oral anticoagulants who experience a bleeding event may be able to discontinue therapy if certain circumstances ... In most cases of GI bleeding, for example, current data support restarting oral anticoagulants once hemostasis is achieved, but ... However, "the extent of the use of multiple anticoagulants and antiplatelet agents was a bit surprising and complicates therapy ... "The proliferation of oral anticoagulants (warfarin and DOACs) and growing indications for their use prompted the need for ...
Oral anticoagulants in older adults with atrial fibrillation. ... Oral anticoagulants in older adults with atrial fibrillation. ... The following review summarizes the use of oral anticoagulants in older adults with AF, focusing on practical topics such as ...
Anticoagulant rodenticides and non-target wildlife : an ecological evaluation of permanent baiting in rural rat control ...
... despite the availability of both warfarin and non-vitamin K antagonist oral anticoagulants (NOACs). Primary care physicians ( ... PCP) decision-making to initiate and select appropriate anticoagulant medication is pivotal in reducing complications among ... Oral anticoagulant therapy use in patients with atrial fibrillation (AF) remains suboptimal in Singapore, ... This study explored the factors influencing PCPs decision-making in anticoagulant initiation and anticoagulant switch for ...
The New therapy of placental insufficiency ~ Endothelial progenitor cells for angiojenesis and new anticoagulant therapy. ...
Anticoagulants are medicines that prevent blood clots from forming in the bloodstream. ... What are anticoagulants?. Anticoagulants are medicines that prevent blood clots. from forming in the bloodstream. This reduces ... Anticoagulants are divided into different groups. The most suitable type of anticoagulant will depend on the medical condition ... Oral anticoagulants are very effective. When people use them, it takes a lot longer for their blood to clot. The medication ...
Many guidelines indicated that to continue using anticoagulant drugs to reduce the incidence of symptomatic venous thrombosis ( ... Background: Many guidelines indicated that to continue using anticoagulant drugs to reduce the incidence of symptomatic venous ... Conclusion: There is no enough evidence showed that the TKA patients given anticoagulant after hospital discharged had ... The incidence of symptomatic thrombus in TKA patients has no correlation with use of anticoagulants after discharge ...
Anticoagulants. Recommendation. Do not routinely use anticoagulant therapy to reduce the risk of catheter-related infection in ... Other anticoagulants, such as factor Xa inhibitors or direct thrombin inhibitors, have not been adequately assessed in terms of ... These agents are usually combined with a compound acting as an anticoagulant, such as heparin or EDTA. Most of these studies ... anticoagulants have been used to prevent catheter thrombosis and presumably reduce the risk of infection. ...
Anticoagulants. Anticoagulants are medicines that help to prevent blood clots. Theyre given to people at high risk of getting ... Its safer to drink grapefruit juice if youre taking the newer anticoagulants rivaroxaban, dabigatran, apixaban or edoxaban. ...
Anticoagulants. Patients on warfarin might need to reduce their anticoagulant dose or monitor their prothrombin time more ... Anticoagulants. Patients on warfarin might need to reduce their anticoagulant dose while taking doxycycline because of its ... Anticoagulants. Increased anticoagulant effects have been noted when azithromycin is used with warfarin; monitor prothrombin ... Anticoagulants. An increase in the international normalized ratio (INR) has been reported when levofloxacin and warfarin are ...
Dental Procedures in Patients with Atrial Fibrillation and New Oral Anticoagulants / * Dental Procedures in Patients with ... Dental Procedures in Patients with Atrial Fibrillation and New Oral Anticoagulants Pepie Tsolka ...
OBJECTIVE: To investigate the associations between direct oral anticoagulants (DOACs) and risks of bleeding, ischaemic stroke, ... PARTICIPANTS: 132 231 warfarin, 7744 dabigatran, 37 863 rivaroxaban, and 18 223 apixaban users without anticoagulant ... Risks and benefits of direct oral anticoagulants versus warfarin in a real world setting: cohort study in primary care ... Risks and benefits of direct oral anticoagulants versus warfarin in a real world setting: cohort study in primary care ...
Coumarin Anticoagulants. If ezetimibe is added to warfarin, a coumarin anticoagulant, the International Normalized Ratio (INR) ...
Learn and reinforce your understanding of Anticoagulants: Direct factor inhibitors. ... Anticoagulants: Direct factor inhibitors Videos, Flashcards, High Yield Notes, & Practice Questions. ... Anticoagulant medications help to prevent thrombi, or blood clots from forming. These medications work by interfering with the ... While the most common anticoagulants like warfarin and heparin act on multiple coagulation factors, in this video were gonna ...
... words that start with anticoagulant, words that end with anticoagulant, anagrams of anticoagulant, how to spell anticoagulant, ... Anagrams of anticoagulant. Words containing the word ANTICOAGULANT. Nearby Words. anticly : anticoagulant : anticoagulants ... Words that rhyme with anticoagulant. anticoagulation anticoagulants anticolonials anticollision antiglobulins anticlinorium ... Suffixes of anticoagulant. nticoagulant ticoagulant icoagulant coagulant oagulant agulant gulant ulant lant ant nt Prefixes of ...
Anticoagulants. Anticoagulants that are subscribed can be roughly divided into 3 groups: heparins, vitamin K antagonists (VKA, ... Direct Oral Anticoagulants. More recently introduced anticoagulants are direct thrombin and FXa inhibitors. They inhibit serine ... Anticoagulant. Coagulation cascade ↑ fibrinogen level, associated with ↑ level of proinflammatory markers (eg, CRP, IL-6). ↑ TF ... Current anticoagulants mainly block proteases of the common pathway and thus affect all 3 stages of the coagulation process: ...
Oral Anticoagulants. Persons who use oral anticoagulants (OACs) have a 7- to 10-fold higher risk of spontaneous ICH compared ... There are no currently available antidotes to any of the newer oral anticoagulants. The use of blood products and other ... The use of oral anticoagulants leads to a 7- to 10-fold higher risk of spontaneous intracranial hemorrhage. With the ... Reversal of Newer Anticoagulants in Acute Hemorrhagic Stroke. Treavor T. Riley, PharmD, BCPS. Assistant Professor. Wingate ...
A lupus anticoagulant index of 10% or less is considered negative for lupus anticoagulant. A lupus anticoagulant index of 15% ... The lupus anticoagulant index has been shown to be sensitive to weak lupus anticoagulants. The presence of antiphospholipid ... Lupus anticoagulants result in the prolongation of clotting times which correct with the addition of phospholipids. ... antibodies, such as lupus anticoagulant, increases the risk of arterial thrombosis, venous thrombosis, thrombocytopenia and ...
Effectiveness and safety of non-VKA oral anticoagulants among nonvalvular atrial fibrillation patients with prior bleeding ... Time at home among nonvalvular atrial fibrillation patients treated with non-VKA oral anticoagulants vs warfarin. ...
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Newer types of anticoagulants are also available and are becoming increasingly common. (prnewswire.com)
  • What types of anticoagulants are there? (informedhealth.org)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Xarleto and Eliquis are two anticoagulants increasingly preferred by physicians. (medgadget.com)
  • clinical support services for anticoagulation monitoring and constraints in existing care model influenced PCPs in their anticoagulant prescription. (physiciansweekly.com)
  • 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)
  • Anticoagulant medications help to prevent thrombi, or blood clots from forming. (osmosis.org)
  • 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)
  • 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)
  • Primary care physicians' (PCP) decision-making to initiate and select appropriate anticoagulant medication is pivotal in reducing complications among patients with AF. (physiciansweekly.com)
  • Anticoagulants are the most common medicines for treating DVT. (medlineplus.gov)
  • After a substantial ingestion of a long-acting anticoagulant, clinical signs of coagulopathy typically occur within 24-72 hours. (cdc.gov)
  • Long-acting anticoagulant rodenticide poisoning: an evidence-based consensus guideline for out-of-hospital management. (cdc.gov)
  • After an acute unintentional ingestion of a long-acting anticoagulant, the majority of patients are entirely asymptomatic. (cdc.gov)
  • Detection of a long-acting anticoagulant (e.g., brodifacoum) in serum, plasma, or urine, as determined by commercial laboratory tests. (cdc.gov)
  • 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)